ncnmnotes

10/7/11 group art show

2011-09-30T15:08:00.001-07:00

The Bamboo Grove Salon presents a group art show organized around the Five Elements of Chinese Philosophy and Medicine on Friday October 7th from 6-10pm. Each of the five artists is depicting one of theelements with a different medium: painting, poetry, ceramics, music, and photography. Three of the artists are students at the National College of Natural Medicine and the other two are local Portland artists:

Eugene Lee- paintings (wood)

Tim Nelson- poetry (fire)

Wil LaBelle- ceramics (earth)

Loren Chasse- music (metal)

Erica Zelfand- photography (water)

Please join us for a celebration of art and life at the Bamboo Grove Salon, a beautiful artspace / teahouse / movement studio tucked away in the Southeast Waterfront. Refreshments will be served and beer, wine, tea are all available for purchase.

Bamboo Grove Salon bamboogrovesalon.com

October 7th 6-10pm

134 SE Taylor St

Portland OR

6-10PM

new website

2011-07-30T15:15:00.000-07:00

www.fermatawellness.com

paintings

2011-04-05T23:07:00.000-07:00

here is the statement i wrote up for the art show i had in march at the bamboo grove salon:

i started painting last spring when i went back to boston, MA for spring break. i don't remember why, but i picked up my mom's brushes and started experimenting with them-- my mom is an artist through and through, starting with painting as a young child and currently with ceramic arts. i've always looked up to her aesthetic sense: at once subtle and razor sharp, always tactful, and heavily influenced by the rhythms of nature. there are many artists on her side of the family and sometimes i feel that when i started painting last year the dormant genotype was finally able to express its phenotype. i was drawn to the tools that she had: simple chinese brush painting with one color and a grinding stick that you made ink with by grinding for 10 minutes before painting.

i began experimenting and immediately became addicted. my mom gave me a brush, ink, and some paper to bring back to portland. i began painting anything that came to mind; abstract patterns, trees, faces, whatever. it became a nightly ritual that calmed my mind down from the marathon of medical memorization that is the second year of NCNM.

once i felt the limits of my imagination, i found myself craving actual techniques-- so i bought a basic book on sumi-e brush painting techniques. it laid out step by step instructions on how to approach the basic brushstrokes, framed by the "four gentlemen": four different plants that contain the basic brushstrokes that form the foundation of technique for chinese brush painting. i fell madly in love with the tradition of chinese brush painting and in particular, painting bamboo. last september i took my first chinese calligraphy class at NCNM with Dr. Zhou and subsequently fell madly in love with calligraphy as well.

i love the simplicity of bamboo painting and that it keeps me honest. in the short period i've experimented with bamboo i've found that if i get too attached to a certain image and try and paint a certain way, it almost always ends up contrived and unnatural, and that the paintings that seem successful to me are always done in a relaxed state of body and mind. i love painting in one color and one theme and exploring the never-ending diversity of texture and emotion within these limitations. finally, i love the improvisatory aspect to it; it feels very similar to jazz improvisation to me- in that there is a good balance of technique and free improvisation. i hope you will enjoy these paintings as i have and that maybe it will spark an interest in chinese brush painting for yourself as well!

many blessings,

eugene

for inquiry about commissions email sunjae (at) fermatawellness (dot) com or call 978.201.1140!

pharmacology: dermatology

2010-12-01T22:33:00.001-08:00

the pharm lecture on some of the conventional drugs used to treat dermatologic conditions. there are a number of topical antimicrobials used to treat superficial skin infections; the most common might be neosporin, which is most effective against superficial bacterial infections, although has the potential to be ototoxic. muciprocin is used for impetigo as well as part of the treatment against MRSA-- in this treatment it is prophylactically applied to the nares to eradicate potential nasal infection from MRSA. ketoconazol is an antifungal that works by inhibiting sterol synthesis. glucocorticoids can be applied topically in cases of inflammation such as dermatitis, psoriasis, eczema, urticaria. application to the face should be avoided if possible, in particular because abruptly stopping could cause rosacea and perioral dermatitis.

treatment of acne involves drugs that reduce the hyperkeratinization and sebum production, as well as combat the propionobacterium that is associated with acne inflammation. vitamin A derivatives such as isoretinoin are particularly effective, although potentially teratogenic. finally, PUVA is a treatment used for psoriasis and stands for psoralen plus UV-A light-- psoralen is a compound that reacts with ultraviolet light. phototherapy is one step in the progression of the treatment of psoriasis, which also involves corticosteroids, vitamin D3, and TNF inhibitors.

questions
neosporin...
1. effective against MRSA or cellulitis?
2. what is neosporin?
3. indications for neosporin?
4. mechanism of action?
5. neosporin is also sometimes used with...
6. avoid use of...

muciprocin / bactroban...
7. used for...
8. effective against which microorganisms?
9. mechanism?
10. special instructions when treating MRSA?

ketoconazol / nizarol...
11. class?
12. indication?
13. mechanism of action?
14. side effect?

topical glucocorticoids...
15. should be avoided on what type of skin and why?
16. indications?
17. local side effects?
18. when applied to the face, has potential for which side effects?
19. indications for intralesional injection?

retinoids and acne...
20. structure?
21. effect on skin?
22. indications?
23. drug treatment strategy for acne?

tretinoin / retin A...
24. indication?
25. mechanism of action?
26. side effects?

isoretinoin / accutane...
27. indications?
28. mechanism of action?
29. recurrence of acne when drug is stopped?
30. contraindicated in...
31. measures taken to prevent negative effects from [30]?
32. potential GI side effect?

psoriasis...
33. immune system involvement in production of psoriatic skin lesions?
34. treatment of psoriasis involves stepwise progression of...
35. describe the phototherapy protocol.
36. what is PUVA?
37. other indications for PUVA?
38. side effects?

answers
1. no.
2. polymyxin B plus neomycin.
3. superficial bacterial skin infections. eyes and ear infection.
4. polymyxin disrupts bacterial cell membrane, bacitracin interferes with PDG's of cell wall.
5. corticosteroids.
6. otic solution, because of potential ototoxicity of neomycin.

7. impetigo, other bacterial skin infections.
8. bacteria, not viruses or fungi.
9. inhibits bacterial protein synthesis.
10. apply to the nasal nares as well as the infection site to eradicate potential nasal infection.

11. anti-fungal.
12. superficial fungal infection.
13. inhibits sterol synthesis.
14. skin irritation.

15. abraded unless with antimicrobials because of greater systemic absorption.
16. dermatitis, eczema, psoriasis,
17. skin atrophy
striae
telangiectasias
purpura
acneiform lesions
perioral dermatitis
18. rosacea and perioral dermatitis when stopped abruptly.
19. cystic acne
psoriasis
discoid lupus

20. vitamin A derivatives.
21. cellular proliferation and differentiation
immune function
inflammation
sebum production
22. SCC
actinic keratosis
cystic acne
23. salicylic acid, benzoyl peroxide, antibiotics, retinoids.

24. acne or photo damaged skin.
25. reduction of hyperkeratinization, thickening of epidermis, dermal collagen synthesis.
26. erythema
peeling
burning / stinging
photosensitivity

27. acne / acne rosacea, hidradenitis suppurativa
28. reduction of hyperkeratization, reduction of sebum production, reduction of propionobacterium acne.
29. 40% of patients within 6 months.
30. pregnancy.
31. two forms of birth control required for females of child bearing age on this medication.
32. ulcerative colitis.

33. immune cells move from the dermis to the epidermis, where they stimulate keratinization.
34. corticosteroids
vitamin D3
phototherapy
systemic therapy
TNF inhibitors
35. use ultraviolet A or B light source along with a psoralen drug such as methoxsalen
36. psoralen plus ultraviolet A.
37. vitiligo
T cell lymphomas
alopecia areata
urticaria pigmentosa
38. nausea, erythema, blistering
skin cancer, actinic keratosis.

pharmacology: angina drugs

2010-11-30T19:49:00.000-08:00

the lecture on the conventional drugs used to treat chest pain-- otherwise known as angina. there are three types of angina, stable, unstable, and prinzmetal / atypical. stable is brought on by exertion, relieved by rest, and palliated with vasodilators. unstable is pain that is increasing in frequency and severity, brought on by diminishing levels of exertion and not aided by vasodilators. prinzmetal is a type related to vasospasm of the coronary artery. out of these three types, stable angina is the most treatable by anti-angina drugs, which come in three classes: nitrates, calcium channel blockers, and beta blockers.

nitrates work by way of nitric oxide, a natural vasodilator that stimulates the guanyl cyclase enzyme which activates the cGMP pathway, producing smooth muscle relaxation and vasodilation. there are two classes of nitrates; nitroglycerins and isosorbide dinitrates. both are used in acute MI's as well as prophylaxis before exertional activity. nitroglycerins can be administered in a number of different ways; sublingually and IV for quick onset (1-2 minutes), topically and transdermally for longer duration (12-24 hours). side effects might include headache and hypotension, which is especially a danger for patients taking viagra simultaneously. isosorbide dinitrates are similar to nitroglycerins in their mechanism and indications but are longer lasting and slightly less potent.

beta blockers are agents that inhibit the beta adrenergic receptors in the heart, leading to less stimulation by catecholamines. this has several effects: decreased cardiac contractility and rate decreases oxygen demand, thereby reducing the risk for ischemia in a post-MI. propranolol is an example of a non-selective beta blocker, meaning it acts upon both the beta-1 receptors in the heart as well as the beta-2 receptors in the bronchi, causing potential for bronchoconstriction as a side effect. atenolol / tenormin is a beta blocker that is more selective for beta-1 receptors, allowing for less potential for bronchoconstriction. both have the danger of rebound hypertension if stopped abruptly.

another class of anti-angina drugs are calcium channel blockers, which inhibit the influx of calcium into myocardial cells. this has the effect dilating the cardiac and peripheral arteries, as well as lowering rate of contraction. amlodopine / norvasc is an example, which is indicated especially in variant angina due to vasospasm. NB: calcium channels should not be combined with beta blockers for danger of hypotension / bradycardia due to synergistic effects.

morphine disulfate is the number one drug of choice in pain relief in cases of unstable angina or an MI. it is administered intravenously and titrated until symptoms are lessened. it is an opiate receptor agonist which also causes peripheral vasodilation. thus it has the potential for hypotension, but its effects can be reversed through naloxone.

questions
nitrates...
1. what are the three classes of drugs used to treat angina?
2. mechanism of nitrate action?
3. two main classes of nitrate drugs?
4. two indications for nitroglycerin?
5. effect on preload?
6. which methods of administration have the quickest onset?
7. which methods of administration have the longest duration?
8. two main side effects of nitroglycerins?
9. which other drug is contraindicated for simultaneous use and why?
10. how does the potency of isosorbide dinitrate compare with nitroglycerin?

propranolol / inderal...
11. mechanism of action of beta blockers?
12. indications for beta blockers?
13. indications for propranolol?
14. potential effect on another organ system?
15. abrupt continuation may cause...
16. difference between propranolol and atenolol.

amlodopine / norvasc...
17. class / mechanism?
18. indication?
19. onset of action?
20. calcium channel blockers should not be combined with...

morphine sulfate...
21. mnemonic of protocol for patient with unstable angina?
22. morphine's effects are reversible via...
23. mechanism of action?
24. potential for what adverse effect?

answers
1. nitrates, beta blockers, calcium channel blockers. [NBC]
2. conversion of drug to nitrate ion, formation of nitric oxide, activation of guanyl cyclase, increased cGMP levels, smooth muscle relaxation, vasodilation. [nitrate, nitric, guanyl, cGMP, relaxation]
3. nitroglycerin / nitrostat
isosorbide dinitrate / isordil
4. acute MI relief or prophylaxis before exertion.
5. preload reduced due to relaxed peripheral venous tone.
6. sublingual and IV both have 1-2 minute onsets.
7. topical and transdermal.
8. headache and hypotension.
9. viagra because of the danger of severe hypotension.
10. lower potency.

11. beta blockers block the beta-1 cardiac receptors, leading to a decrease in cardiac contractility and rate, leading to a decrease in oxygen requirement.
12. acute MI to reduce infarct size as well as post MI.
13. post MI
hypertension
panic attacks
migraine headaches
14. potential blockage of beta-2 receptors in the bronchi, leading to bronchoconstriction.
15. rebound hypertension and tachycardia.
16. atenolol is a selective beta blocker whereas propranolol is not-- less chance for bronchoconstriction.

17. blocks influx of calcium into myocardial cells, thus dilating cardiac and peripheral arteries, as well as decreasing contractility and rate.
18. angina, especially variant / vasospastic. hypertension.
19. 3-6 hours.
20. beta blockers.

21. MONA
morphine if pain not relieved by nitrates
supplemental oxygen
sublingual nitroglycerin
aspirin.
22. naloxone.
23. opiate receptor agonist.
24. hypotension.

pharmacology: anti-virals

2010-11-28T14:52:00.000-08:00

the pharm lecture on the conventional meds used to treat viral conditions. these drugs are designed to specifically target an aspect of the viral reproduction mechanism-- whether it be interfering with viral binding with the host cell, replication within the host cell, or budding off of the host cell. the drugs used to treat influenza, for example, are neuramidase inhibitors, which is an enzyme that allows the virus to bud off the host cell. oseltamivir / tamiflu is an oral neuramidiase inhibitor and zanamivir / relenza is the inhaled form. both have to be taken within 48 hours of the onset of symptoms in order to be effective. amandatine / symmetrel is a drug that is no longer used for treatment of influenza A, but has found some use as treatment for mild to moderate parkinson's disease symptoms.

the herpes family of viruses, which includes HSV-1 and 2, and herpes zoster (the cause of chicken pox and shingles) is treated by drugs such as acyclovir / zofirax, which acts as a guanine analog that is incorporated into viral DNA and halts replication. this particular drug crosses the blood brain barrier and thus is effective against herpes encephalitis and herpes meningitis, although resistance is becoming more widespread. it is administered in oral, IV, and topical form, each with its own side effects. higher IV doses can cause transient renal insufficiency.

drugs used to treat HIV fall into several categories: fusion inhibitors, integrase inhibitors, reverse transcriptase inhibitors, and protease inhibitors. zidovadine / retrovir is an example of a reverse transcriptase inhibitor, and is a pyrimidine analog that halts RT's action when incorporated into viral DNA. saquinivir is a protease inhibitor (protease is the enzyme that HIV uses to break viral proteins into component parts to be assembled into new viral particles) which is used for both HIV and hep C patients. interferon alpha is a naturally occurring cytokine that stimulates anti-microbial activity in phagocytic cells. it is used to treat HIV as well as hep C, where it is combined synergistically with ribavarin, a nucleoside antiviral.

a few notes on vaccinations (some background here) there are in general at least 3 different types of vaccinations in terms of what is injected into the patient to mount an immune response: live attenuated (inactivated), killed, and protein fragment. the live vaccines have the strongest immune response but have a small potential for reactivation, whereas killed vaccines have no chance for reactivation but less of an immune response. influenza vaccines are either live attenuated or "trivalent inactivated". laiv / flumist is the attenuated influenza vaccine which is delivered nasally. HPV vaccines such as gardasil and cervarix are available to guard against HPV 16 and 18, the strains most likely to cause cervical cancer. gardasil also is effective as a vaccine against HPV 6 and 11, the strains likely to cause genital warts.

questions
oseltamivir / tamiflu...
1. type A influenza is referred to as...
2. two most common strains of type A influenza?
3. when must tamiflu be given in order to be effective?
4. tamiflu shown to be effective against which strains of influenza?
5. mechanism of action for tamiflu?
6. method of administration?
7. usual adult dosage?
8. common side effects?

zanamivir / relenza...
9. mechanism of action?
10. strains of influenza that zanamivir is effective against?
11. when must relenza be given in order to be effective?
12. method of administration?
13. not recommended when patient is in...
14. contraindicated in patients with history of...
15. side effects?

amandatine / symmetrel...
16. effective against which forms of influenza?
17. used for what other condition?

acyclovir / zofirax...
18. how many families of the herpes virus are there that infect humans?
19. acyclovir is only effective against...
20. mechanism of action?
21. method of administration?
22. can or cannot cross BBB?
23. higher IV doses can cause what side effect?

HIV: reverse transcriptase inhibitors...
24. four categories of HIV drugs?
25. current treatment combination for HIV?
26. what are the forms of reverse transcriptase inhibitors?
27. what category does zidovadine (AZT) / retrovir fall under?
28. mechanism of action of zidovadine?
29. another example of a nucleoside RTI?
30. advantages of nucleotide RTI's over nucleoside RTI's?
31. difference in mechanism for non-nucleoside RTI's?

HIV: protease inhibitors...
32. what function does viral protease have?
33. which two viruses are protease inhibitors used to treat?
34. example of protease inhibitor?
35. side effect of [34]?

HIV: interferons...
36. what are interferons?
37. interferons stimulate which immune cells to do what?
38. what are the types of interferons and what are they used for?
39. indications for interferon alpha?
40. mechanism of action?
41. what is pegylated interferon alpha?

ribavirin...
42. structurally similar to...
43. which family?
44. used synergistically with what other drug for what condition?
45. effectiveness against HIV / AIDS?

vaccinations...
46. 3 types of vaccinations?
47. advantages / disadvantages to the first type?
48. ...second?
49. disadvantage to third?
50. examples of third?
51. two types of influenza vaccines?
52. laiv / flumist is what type of vaccine? method of delivery?
53. two HPV vaccines?
54. both protect against which strains?
55. gardasil also protects against...

ånswers
1. seasonal flu.
2. H1N1 and H3N2.
3. before 48 hours after onset of symptoms.
4. H5N1-- avian flu.
5. neuramidase inhibition.
6. oral.
7. 75mg bid for 5 days.
8. headache
nausea / vomiting / abdominal effects
neurologic effects

9. neuramidase inhibitor.
10. influenza A and B, and avian flu.
11. before 48 hours after onset of symptoms.
12. inhaler.
13. nursing homes.
14. COPD / asthma.
15. nausea / vomiting.

16. no longer recommended for prophylaxis of influenza A.
17. mild to moderate symptoms of parkinson's disease.

18. eight.
19. actively replicating viruses, not latent viruses.
20. guanosine analog that is incorporated into viral DNA and stops viral synthesis.
21. PO, IV, topical ointment.
22. can; is used to treat herpes meningitis and encephalitis.
23. transient renal insufficiency.

24. reverse transcriptase inhibitors
protease inhibitors
fusion inhibitors
integrase inhibitors.
25. HAART (highly active antiretroviral therapy): at least 3 drugs in at least 2 of the categories:
2 non-nucleoside reverse transcriptase inhibitors plus
[1 nucleoside reverse transcriptase inhibitor OR protease inhibitor]
26. nucleoside, nucleotide, and non-nucleoside RTI's.
27. nucleoside reverse transcriptase inhibitor.
28. pyrimidine analog that is incorporated by reverse transcriptase into viral DNA, thus halting further replication.
29. acyclovir / zovirax.
30. fewer side effects.
31. instead of inhibiting reverse transcriptase at its active site, it binds at the "NNRTI pocket" site.

32. breaks the viral protein chains apart to be assembled into new viral particles.
33. HIV and hep C.
34. saquinavir / invirase.
35. mostly GI upset.

36. cytokines produced by immune cells in response to foreign agents.
37. macrophages and NK cells to elicit anti-microbial and anti-tumor responses.
38. interferon alpha-- hep C
interferon beta-- MS
interferon gamma-- chronic granulomatous diseases.
39. chronic hep B, C
HPV induced genital warts
kaposi's sarcoma
hairy cell leukemia
40. interferes with virus's ability to infect cells, inhibits viral RNA translation.
41. interferon alpha plus polyethylene glycol to make the medication last longer in the body

42. D-ribose sugar.
43. nucleoside anti-viral family.
44. with interferon alpha against hep C.
45. little to none.

46. live/attenuated, killed, protein fragment.
47. stronger immune response that lasts longer, but has a small potential for being reactivated.
48. weaker immune response but cannot be reverted to virulence.
49. weakest immune response of all vaccination types.
50. hep B and HPV.
51. live attenuated and trivalent inactivated.
52. live attenuated, delivered as nasal spray.
53. gardasil and cervarix.
54. HPV 16 and 18.
55. HPV 6 and 11, the strains that cause genital warts.

pharmacology: opthalmic drugs

2010-11-14T21:25:00.000-08:00

the pharm lecture for the conventional medications used to treat eye conditions. first, there are a number of medications that are used to assess in the diagnosis of various eye disorders: anesthetics such as opthane, staining agents such as flourescein dye (which is useful in diagnosing herpes keratitis), mydriatic agents such as homatropine, cycloplegics such as homeatropine, and miotic agents such as pilocarpine.

there are are several drugs available to combat the different types of conjunctivitis. tetrahydrozoline / visine is one that is focused on removing the redness from eyes and does so by a vasoconstrictive effect, combined with the astringent effect of zinc sulfate. azelastine / optivar is an H1 blocker that is used for allergic conjunctivitis. bacterial conjunctivitis can be combated with ocular polysporin-- a mix of bacitracin and polymyxin. viral conjunctivitis, specifically herpes simplex keratoconjunctivitis, can be combated with vidarabine / ara-a.

the main drug used to treat glaucoma is timolol / timoptic, which works by blocking ocular norepinephrine, which reduces the production of aqueous humor, thereby relieving the anterior chamber pressure. pilocarpine, the miotic agent mentioned above, might also be used in glaucoma for contraction of the ciliary muscles, which increases aqueous humor outflow.

questions
1. types of medications that aid in diagnoses of opthalmic conditions?
2. example of anesthetic?
3. example of staining agent?
4. example of mydriatic agent?
5. example of cycloplegic?
6. example of miotic agent?
7. [3] useful in diagnosing which condition?

tetrahydrozoline / visine...
8. indication?
9. mechanism?
10. side effects?

azelastine / optivar...
11. indication?
12. mechanism?

ketorolac / acular...
13. mechanism / class?
14. indication?
15. unlike ocular steroids...

antimicrobials...
16. which combination of antimicrobials might be given for a case of infectious conjunctivitis of bacterial origin?
17. which is specific for HSV?
18. which form of HSV is [17] specific for?

glaucoma...
19. timolol mechanism of action?
20. example of a miotic agent? mechanism?
21. mechanism of xalatan?
22. effect of cannabis on glaucoma?

answers
1. stains, mydriatics, miotics, cycloplegics, anesthetics.
2. opthane
3. flourescein dye.
4. homatropine.
5. homatropine.
6. pilocarpine.
7. dendritic figures of herpes keratitis.

8. relieve of redness.
9. vasoconstriction and astringent effects via tetrahydrozoline and zinc sulfate.
10. local irritation, rebound vasodilation.

11. allergic conjunctivitis.
12. blocks H1 receptor sites.

13. cyclooxygenase inhibitor.
14. ocular discomfort from swelling.
15. ketorolac does not increase risk for cataracts or glaucoma.

16. polysporin-- polymyxin and bacitracin.
17. vidarabine / ara-a
18. herpes simplex keratoconjunctivitis, not zoster.

19. blocks ocular norepinephrine release, which reduces production of aqueous humor.
20. pilocarpine. increased outflow of the aqueous humor by ciliary contraction.
21. prostaglandin receptor agonist that increases uveoscleral outflow, improving outflow of aqueous humor and reducing intraocular pressure.
22. relaxes trabecular network and increases flow, reducing intraocular pressure.

pharmacology: urinary medications

2010-11-14T15:11:00.000-08:00

the pharm lecture on the conventional medications used to treat various urinary conditions, mostly urinary incontinence. the medications used to treat incontinence are chosen depending on the type of incontinence: urge incontinence, which is caused by irritation or stimulation of the bladder's detrusor muscle, can be treated by anti-cholinergics such as oxybutynin and tolterodine, as well as an antidepressant imapramine. overflow incontinence, which is caused by retained urine leaking out of the bladder sphincter, is often related to BPH in men and therefore drugs such as tamsulosin and finasteride are used to relax prostate smooth muscle relaxation and prevent synthesis of dihydrotesterone, the hormone responsible for prostate enlargement, respectively. phenazopyridine is a drug that is used to reduce urinary lining irritation, and has the notable side effect of turning urine and tears yellow.

questions
intro...
1. two sets of bladder muscles?
2. best treatment for stress incontinence?
3. what is urge incontinence due to?
4. most common cause of "transient urge incontinence"?
5. urge incontinence plus symptoms of eye pain, muscle weakness would lead one to suspect what condition?

oxybutynin / ditropan...
6. class / mechanism of action?
7. indications?
8. side effects?

tolterodine / detrol...
9. class / mechanism?
10. comparison to oxybutynin?

imapramine / tofranil...
11. class?
12. mechanism?
13. used when for incontinence?
14. increased risk for what mental symptom?
15. overdose fatal due to what? especially in what age group?

overflow incontinence...
16. definition?
17. in men, overflow incontinence related to...
18. how are diabetes mellitus and MS related to overflow incontinence?
19. two categories of drugs that treat [17]? what do they do?

tamsulosin / flomax...
20. class / mechanism?
21. selectivity for...
22. side effect?

finasteride / proscar...
23. indication?
24. mechanism?
25. proscar is also used for...
26. which patient population should not even handle finasteride tablets and why?

cystitis...
27. dipstick findings...
28. urinalysis findings...
29. three common organisms involved in cystitis?
30. drug of choice to treat cystitis?

phenazopyridine / pyridium...
31. indicated for...
32. potential complication if used during infection?
33. side effects?

answers
1. detrusor around bladder wall, bladder sphincter muscles.
2. kegels.
3. involuntary loss of urine due to overactive detrusor.
4. cystitis.
5. MS.

6. anticholinergic (blocks M3 muscarinic receptor) prevents acetylcholine stimulation of detrusor muscle.
7. urge incontinence and hyperhidrosis.
8. dryness, dizziness, diminished sweating.

9. anticholinergic (blocks M2 and M3 muscarinic receptors)
10. marketed as having fewer side effects than oxybutynin, although this is questionable.

11. antidepressant.
12. blocks reuptake of serotonin and NE and diminishes smooth muscle uptake of acetylcholine.
13. during bed time for enuresis.
14. suicidal ideation.
15. heart block, children.

16. pressure from retained urine overcomes bladder sphincter muscles.
17. BPH.
18. both can reduce sensory input from bladder, allowing for overfilling, as well as decreasing neural input to detrusor muscle, allowing for retention.
19. alpha blockers relax smooth muscle, 5-alpha reductase inhibitors inhibit synthesis of dihydrotestosterone.

20. alpha 1 receptor antagonist leads to smooth muscle relaxation.
21. alpha 1 A receptors in prostate, instead of alpha 1 B in blood vessels.
22. possible retrograde ejaculation.

23. functional incontinence.
24. blocks conversion of testosterone into DHT.
25. male pattern baldness.
26. pregnant women-- category X drug that can be absorbed through the skin.

27. positive leukocyte esterase, nitrite, hemoglobin.
28. WBC's, RBC's, bacteria.
29. ecoli, staph, enterococci.
30. TMP-sulfa.

31. irritation of urinary tract lining.
32. analgesic effects may prevent awareness of infection spreading to kidneys.
33. turns urine and tears yellow / orange.

pharmacology: GI drugs

2010-11-14T13:40:00.000-08:00

the pharmacology lecture on the conventional drugs used to treat various GI disorders. the first category we covered was laxatives, of which there are several different types. psyllium / metamucil is a laxative that is made of crushed psyllium husks, which contain both soluble and insoluble fiber-- allowing for more bulk, and softer stool. docusate / colase is a stool softener laxative that acts as an anionic surfactant, effectively making the intestinal lining more slippery. it is also used to dissolve earwax in cases of a blocked ear canal. magnesium hydroxide is an osmotic laxative, causing water to come out into the intestinal lumen. finally, dulcolax is an agent that decreases constipation by increasing intestinal motility.

on the other hand, there are agents designed to stop diarrhea, in cases of acute diarrhea or chronic diarrhea related to IBS. these are all generally contraindicated in cases of diarrhea with fever, due to parasitic or bacterial infections, and in cases of severe colitis to avoid toxic megacolon. loperamide is a morphine analog acts to stimulate the µ-opiod receptors in the myenteric plexus, effectively slowing down peristalsis. diphenoxylate is another morphine analog which is often combined with atropine for its inhibitory effects on acetylcholine, and commonly causes dry mouth as a side effect.

the analogous drugs for suppressing / inducing outflow on the top part of the GI tube: anti-emetics and emetics. both classes work on the two brainstem centers that are involved in the vomiting response-- chemoreceptor trigger zone and the vomiting center (responsible for the motor mechanisms involved). both centers have receptors for various neurotransmitters, especially histamine, dopamine, and serotonin (type 3 and 4, known as 5HT3 and 5HTP4, respectively).

antiemetics are drugs that block one of these receptor types. patients with mild nausea / vomiting symptoms are better off taking anti-histamines such as benadryl, whereas severe symptoms are best treated with 5HT3 blockers (serotonin receptor type 3 blockers). another example of an anti-histamine used to treat nausea is meclizine / antivert, which has the unfortunate side effect of urinary retention due to bladder neck spasm. metaclopramide is an anti-emetic that is especially indicated in gastric stasis following surgery, and ondansetron is a serotonin receptor blocker that is indicated for nausea concurrent with chemotherapy. on the other end of the spectrum, ipecac is used to trigger emesis by stimulating the same medullary centers that the anti-emetics suppress. it is administered with large amounts of water and can start working in 10-30 minutes. side effects might include dizziness, dehydration, and abdominal spasm, even on an empty stomach.

some drugs designed to alleviate symptoms of gastritis: TUMS is the trade name for calcium carbonate, which raises gastric pH and therefore temporarily lessens mucosal irritation. zantac / ranitidine blocks the H2 receptors for histamine, one of the substances that trigger acid release (the others being gastrin and acetylcholine). omeprazole / prilosec is a proton pump inhibitor which leads to less acid production by parietal cells and therefore can alleviate symptoms but may also lead to malabsorption as well as decreased defenses against certain pathogens. to treat peptic ulcer disease specifically, a "triple therapy" can be given for 7-14 days, which consists of a proton pump inhibitor and two antibiotics (two to prevent resistance). alternatively, bismuth subsalicylate or a histamine blocker can be used instead of the proton pump inhibitor to damage the h. pylori's cell wall or decrease gastric acidity, respectively.

drugs used to treat IBD fall into several categories. an aminosalicylate drug like mesalamine works to decrease inflammation by inhibiting leukotriene production as well as acting as an antioxidant- but may also cause nephrotoxicity. it is absorbed in the small intestine, but can be found in pro-drug forms such as asacol or sulfalazine which are absorbed in the large intestine via pH or colonic bacteria mechanisms. antibiotics are also used to treat IBD- most commonly a combination of metronidazole and cipro. another category used for IBD is the corticosteroid class, such as prednisone, used to suppress inflammation and the immune system on many fronts. some things to keep in mind with prednisone are the potential for addisonian crisis and avascular necrosis. immunomodulator drugs are also used, such as azthioprine / immuran, which inhibits purine synthesis, and infliximib / remicade, which inhibits TNF-alpha (but may cause t-cell lymphoma and drug induced lupus).

questions
1. agents which stimulate peristalsis should be used with caution in cases of...√√
2. what method of administration is preferred in such cases?√√
3. insoluble fiber's effect on GI?√√
4. sources of insoluble fiber?X†
5. sources of soluble fiber?XX
6. compare the physiological benefits of soluble vs. insoluble fiber.√

metamucil...
7. made from...√√
8. indicated in...†√
9. might help reduce...X†
10. mechanism of action?√√
11. timeframe of action?†√
12. which form of metamucil is not gluten free?√√

docusate...
13. category?√X√
14. mechanism?XX√
15. effect on stools is seen how long after first dose?XXX
16. avoid oral use if what is suspected?√√
17. also used for...X√√

magnesium hydroxide...
18. two mechanisms?√
19. how long until effects are felt?X
20. may precipitate or exacerbate...X
21. people with chronic kidney disease at a greater risk for...X

bisacodyl / dulcolax...
22. mechanism of action?†X
23. onset of action?X
24. especially indicated in...†
25. side effects?X

loperamide...
26. analog of...X√
27. mechanism?√X
28. unlike other opioids, loperamide...√√
29. two indications?X√
30. contraindicated in...X√

diphenoxylate plus atropine...
31. mechanism?†X
32. common side effect?√√
33. contraindicated in...X√

anti-emetics intro
34. two brain centers involved in vomiting reflex?
35. both centers have what types of receptors?
36. mild symptoms are best addressed by which type of anti emetic?
37. moderate / severe symptoms are best addressed by which type of anti emetic?

meclizine / antivert...
38. mechanism of action...†
39. side effects?†
40. last side effect due to...√

metoclopramide / reglan...
41. why is reglan considered a "pro kinetic"?√
42. indications? (3)X
43. side effects?
44. contraindicated in which two disorders?

ondansetron / zofran and others...
45. mechanism?
46. indication?√
47. given when in relation to the second indication in [46]?†
48. another drug that can be used for nausea induced by chemotherapy?X
49. marijuana derivative anti-emetic?X

ipecac...
50. mechanism of action?√√
51. onset of action?√
52. given with large doses of...
53. side effects?

gastritis, calcium carbonate...
54. three substances that trigger gastric acid release?√
55. why might drinking milk to alleviate ulcer pain be counterproductive?√
56. mechanism of TUMS?√
57. potential GI effect?√
58. long term use might cause...√

ranitidine / zantac...
59. mechanism of action?√
60. indications?X
61. when would zantac be administered IV?X
62. which method of administration has more side effects?X

omeprazole / prilosec...
63. mechanism?√
64. how long is it used for GERD and PID?√
65. side effects?†
66. esomeprazole is...√

triple therapy...
67. what are the two forms of triple therapy?
68. what substance might be added to the therapy to inhibit h. pylori reproduction?
69. how long is triple therapy generally administered?

5-ASA / mesalamine...
70. mechanism of action? (3)
71. indications?
72. side effects?
73. absorption in the GI tract?
74. pro-drug forms of mesalamine?
75. different mechanisms of [74]?

antibiotics...
76. which form of IBD shows more benefit from antibiotics?
77. two of the most commonly prescribed antibiotics for IBD?
78. hallmarks / warnings for [77]?

prednisone...
79. provides full remission to approximately what percent of IBD patients?
80. side effect on bone?
81. pro-drug form?

azthioprine / immuran...
82. class?
83. indications?
84. mechanism of action?
85. side effect on bone?

infliximib / remicade...
86. mechanism?
87. dosing schedule?
88. complications?

answers
1. suspected bowel obstruction.
2. rectal administration.
3. increase bulk, shorten transit time, softens stool.
4. whole grain foods
nuts
seeds
bran
green beans
cauliflower
zucchini
celery
tomato skins
5. legumes
oats
barley
6. insoluble: adds bulk and softens stool. soluble: fermentation yields products that are beneficial to enterocytes.

7. ground psyllium husks.
8. constipation, IBS.
9. cholesterol, colon cancer risk, heart disease.
10. contains both soluble and insoluble fiber, adds bulk and softens stool.
11. may take several days.
12. metamucil wafers contain wheat flour.

13. stool softener.
14. anionic surfactant-- makes bowel wall more slippery.
15. 1-3 days.
16. intestinal obstruction.
17. clearing out earwax.

18. acts as an osmotic agent in intestines, drawing more water out into the lumen. also acts as antacid, raising gastric secretion pH.
19. around 6 hours.
20. electrolyte imbalances such as hypokalemia.
21. hypermagnesemia.

22. irritant laxative-- increases intestinal motility.
23. 2 to 6 hours.
24. constipation due to severe back pain, which decreases intestinal motility due to edema.
25. diarrhea, cramping, sweating, dependence.

26. morphine.
27. activation of µ-opiate receptors in myenteric plexus within GI tract slows peristalsis.
28. doesn't affect CNS opiate receptors.
29. acute diarrhea and chronic diarrhea in IBS patients.
30. parasitic or bacterial infections accompanied by fever.

31. morphine analog plus acetylcholine inhibitor leads to decreased peristalsis.
32. dry mouth.
33. diarrhea with fever, diarrhea due to parasites or bacterial infection.

34. both in brain stem: chemoreceptor trigger zone and vomiting center (responsible for the motor mechanisms).
35. histamine, dopamine type 2, serotonin type 3 and 4.
36. anti-histamines.
37. serotonin type 3 receptor blockers.

38. H1 receptor blocker.
39. drowsiness, dizziness, dry mouth, urinary retention.
40. bladder neck spasm.

41. because it moves the bolus from the stomach to the intestines.
42. moderate N/V
gastric stasis due to surgery or diabetic gastroparesis.
GERD
43. drowsiness, dizziness, headache.
44. parkinson's, bowel obstruction.

45. 5HT3 blocker.
46. severe nausea, patients on chemotherapy.
47. 30 mins before chemotherapy.
48. decadron.
49. dronobinol.

50. stimulates the same medullary centers that zofran and dronabinol suppress.
51. 10-30 mins.
52. water.
53. abdominal muscle spasm
dizziness
dehydration.

54. acetylcholine, histamine, gastrin.
55. because calcium stimulates chief cells to produce more acid.
56. neutralizing stomach acid.
57. potentially constipating.
58. osteoporosis.

59. H2 receptor blocker.
60. PUD, gastritis, GERD.
61. burn victim.
62. IV.

63. inhibits hydrogen/potassium ATPase pump of parietal cells.
64. GERD: 2-8 weeks. PID: 1-2 weeks.
65. increased pH can cause malabsorption of nutrients and minerals as well as lowering defenses against certain pathogens.
66. an enantiomer of omeprazole.

67. proton pump inhibitor, bismuth based.
68. lactoferrin.
69. 7-14 days.

70. inhibit leukotriene production, anti-prostaglandin, anti-oxidant.
71. IBD.
72. N/V, diarrhea, abdominal pain, nephrotoxicity.
73. small intestine, doesn't reach colon.
74. asacol and sulfasalazine.
75. asacol based on higher pH in colon and sulfasalazine based on bacterial in colon.

76. crohn's.
77. metronidazole and ciprofloxin.
78. metro-- N/V, do not drink alcohol while taking. cipro-- tendon rupture, affinity for calcium.

79. 35-50%.
80. avascular necrosis, especially femur and humerus.
81. budenoside / enterocort.

82. immunomodulator.
83. IBD, RA, post-transplant.
84. inhibiting purine synthesis leads to an anti-proliferative effect and induction of t-cell apoptosis.
85. suppresses bone marrow, increasing susceptibility to infection.

86. inhibits TNF-alpha
87. IM or SQ dosing every 2 or 4 weeks.
88. t-cell lymphoma, drug induced lupus.

pharmacology: tuberculosis drugs

2010-11-14T13:37:00.001-08:00

the pharm lecture on the conventional treatment for TB. first a few facts: over one third of the world is exposed to TB, 90% of which are asymptomatic-- yet 50% of untreated cases are fatal. the pathognomonic signs are "rust colored sputum" and microscopically, the "red snapper" sign. the 4 drugs used in combination to treat TB are rifampin, isoniazid, pyrazinamide, and ethambutol. isoniazid, a drug activated by catalase, acts to prevent mycolic acid synthesis in the mycobacterial cell wall. side effects include rash, hepatitis, CNS effects, peripheral neuropathy (caused by deficiency of pyridoxine, the synthesis of which is blocked by isoniazid), as well as sideroblastic anemia.

the three other drugs used to treat TB: rifampin is a drug that inhibits RNA polymerase, preventing protein translation within mycobacterial cells. it is used both in TB as well as MRSA. its unique side effect is that it turns urine and tears a yellow color, and might cause fever / GI upset / rash / hepatotoxicity. pyrazinamide is a nicotinamide analog, and ethambutol works via the same mechanism as isoniazid. for a strain of TB to be labeled as "resistant", it must be resistant to at least isoniazid and rifampin. MDR-TB, or multidrug resistant tuberculosis is currently treated with a 7 drug protocol which might be modified after sensitivity testing is performed.

questions
1. how much of the world's population has been exposed to TB bacterium?
2. what percentage of people infected with TB are asymptomatic?
3. death rate for untreated TB cases?
4. pathognomonic morphological sign?
5. what are the 4 drugs used as standard treatment for TB?
6. which antibiotics are ineffective against the "resistant" strains?

isoniazid...
7. activation?X
8. mechanism?X
9. contraindicated in what patients?X
10. side effects?
11. effect on blood?
12. competes with which enzyme to produce which side effect?
13. what measures should be taken to combat [12]?

rifampin...
14. indications?
15. mechanism?
16. characteristics?
17. side effects?

misc...
18. pyrazinamide is an analog of...
19. ethambutol mechanism?
20. drugs used for TB can also be used for what other condition?

MDR-TB...
21. defined as...
22. standard CDC treatment?

answers
1. over one third.
2. 90%.
3. 50%.
4. red snapper.
5. RIPE:
rifampin
isoniazid
pyrazinamide
ethambutol
6. rifampin and isoniazid.

7. prodrug activated by catalase.
8. INH inhibits mycolic acid synthesis in cell wall.
9. liver disease due to load on the liver.
10. rash
hepatitis
CNS effects
peripheral neuropathy
11. sideroblastic anemia.
12. competes with an enzyme that produces pyridoxine, responsible for peripheral neuropathy.
13. pyridoxine supplementation.

14. tuberculosis
MRSA
n. meningitides
15. inhibits RNA polymerase which prevents protein translation.
16. causes body urine and tears to become yellow.
17. fever
GI upset / N / V
rash
hepatotoxicity

18. nicotinamide.
19. same as isoniazid.
20. leprosy.

21. TB that is resistant to at least isoniazid and rifampin.
22. 7 drug treatment: SHREZ MC
streptomycin
hydrazine
rifampin
ethambutol
pyrazinamide
moxifloxacin
cycloserine

pharmacology: antibiotics

2010-10-25T09:32:00.000-07:00

the pharm lecture on the conventional use of antibiotics. first, an introduction to the different terms and ideas in the world of antibiotics. there are a whole host of antibiotics, with a huge variety of structure and function depending on the microorganism targeted. bactericidal agents are drugs that actively kill microbes whereas bacteriostatic agents simply halt the growth and proliferation of microbes. minimum inhibitory concentration, or MIC, is the minimum concentration of an antibiotic required to have inhibitory action. besides low concentration, antibiotics can fail to work due to a number of factors, such as a failure to reach target, enzymatic inactivation, as well as specific ways that the microbe can develop resistance: conjugation (DNA that confers resistance passed from cell to cell), mutation (spontaneous), and transduction (DNA carried into microbe via bacteriophage). host conditions also play a factor-- pus, hematomas, abscesses all inactivate different classes of antibiotics.

the first class of antibiotics are the sulfonamides; an example is sulfamethoxazole. sulfonamides act by competitively antagonizing PABA in bacterial cells, blocking the synthesis of folic acid, required for DNA replication. since it halts reproduction of microbes it is considered a bacteriostatic, not bacteriocidal agent. it spreads everywhere in the body, including the CSF, and has a range of side effects: headache, skin changes (rashes and photosensitivity). it is sometimes combined with another folic acid inhibitor, trimethoprim, in a ratio of 5:1 sulfamethoxazole : trimethorpim. this combination might be indicated in more severe presentations and specifically for prophylaxis of pneumocystis carinii in patients with AIDS. the side effects are similar, but the combination creates more hypersensitivity, especially in the skin, which can be covered in papulomacular lesions that are pruritic and sandpaper like. general side effects from folic acid disruption are megaloblastosis, leukopenia, thrombocytopenia, and steven johnson's syndrome.

penicillins are another class of antimicrobials that work via beta-lactam rings that bind to penicillin proteins and disrupt the peptidoglycan layer in the bacterial cell walls. they are thus bactericidal, and are effective against a wide variety of gram positive bacteria. it is the antibiotic most commonly associated with allergies, although it is estimated that only about 20% of patients with reported allergies actually have them. "penicillin g" is an example, although it is not as widely used anymore due to widespread resistance in the form of microbes that produce beta lactamase. amoxicillin is a penicillin derivative with a beta lactam ring, thiazolaine ring, and side chains. being a penicillin drug, amoxicillin works to inhibit the peptidoglycan cross links in the bacterial cell walls, and it is spread through all tissues except for the CSF (as opposed to the sulfonamides). it is sometime prescribed in combination with clavulanate, which is an inhibitor of beta-lactamase, thus overcoming the microbes that are resistant to penicillin. side effects of this combination can include GI distress such as diarrhea, and pseudomembranous colitis is a severe diarrhea that is caused by clostridium difficile and associated with amoxicillin / clavulanate use.

cephalexin is in the cephalosporin drug class, which is similar to penicillin in that the mechanism involves a beta-lactam ring disrupting the peptidoglycan layer of the bacterial cell wall. due to the similar mechanisms, cephalosporins have similar side effect profiles to penicillin and also might need to be avoided in patients with penicillin allergies. another note: the first generation of cephalosporins are more specific for gram positive organisms while the second and third generations are more specific for gram negative organisms. drug resistance, as with penicillin, can occur via bacterial production of beta lactamase or modification of PDG. it is indicated in bronchitis, acute ENT infections.

macrolides are another class of antibiotics that work via a macrocytic lactone ring, which binds to the bacteria's 50S ribosomal subunit, making in an effective bacteriostatic agent as well as a bactericidal agent at higher concentrations. it has a similar coverage spectrum to penicillin, but covers more organisms such as chlamydia, mycobacterium, mycoplasma, and ricksettia. it also tends to be accumulated in leukocytes and thus transported to the site of infection. it is common to have GI upset (nausea and vomiting), which can be offset by an enteric coating that is sometimes available.

azithromax is another macrolide, having a multi-membered lactone ring that binds to the 50S ribosomal subunit. it is unique because of its long, 68 hour half life and easy dosing regimen-- a "z pack" has 6 pellets, 2 of which are taken on the first day, followed by 1 per day for the next 4 days. it is indicated for ENT infections, pneumonia, sinusitis, as well as for infection with atypical organisms such as mycoplasma and chlamydia. side effects are similar to erythromycin but with much less GI disturbances.

tetracyclines are another class of antibiotics (tetra because of the four hydrocarbon ring structure) that work by binding to the 16S part of the 30S bacterial ribosomal subunit, inhibiting protein translation. it is less effective these days due to widespread resistance and is mainly used for severe acne / rosacea. it is contraindicated in pregnancy and in children and can also permanently stain teeth. patients on tetracyclines should avoid dairy and calcium as they will interfere with absorption due to chelation. tetracycline specifically can be used in outpatient care for lyme's patients, and are also effective against organisms that have resistance to agents that work on the cell wall (ie penicillins), such as legionella, mycobacterium, chlamydia, ricksettia, plasmodium.

another drug class that binds to the 30S ribosomal subunit is the aminoglycoside class, of which gentamycin is a representative member. it has a relatively narrow coverage spectrum, mainly treating aerobic gram negative organisms-- in particular pseudomonas. it is also used mainly in severe, systemic conditions such as septicemia and is generally switched to a less toxic alternative once the causative organism is identified. side effects might include irreversible nephrotoxicity as well as ototoxicity.

quinolones such as ciproxin are another class that work by yet another mechanism-- this time by disrupting the microbial DNA gyrase enzyme, which is involved in uncoiling of DNA in the replication process. it has an affinity for intracellular organisms such as legionella and mycoplasma, and was also used as an anthrax treatment during the anthrax scares. quinolones chelate calcium and deposit into collagen and bone and thus are contraindicated in children and pregnancy. due to their collagen disruption they are associated with tendon injury, in particular the achilles tendon. it also reduces the breakdown of caffeine and affects the senses of taste and smell.

imidazoles are a class of drugs that are activated only upon intracellular processing by certain organisms: gram negative anaerobes (clostridium, bacteroids, fusobacterium), or protozoa. they work by disrupting the DNA helical structure and thus preventing reproduction. side effects might include GI upset, headache, thrush, and metallic taste in the mouth. it also interferes with alcohol metabolism by inhibiting acetaldehyde dehydrogenase, leading to a buildup of acetaldehyde in the body when alcohol is consumed (and thus a much amplified hangover feeling).

lincosamides-- derived from an actinomides species and is similar to macrolides but also works against actinomycetes, plasmodium, mycoplasma. it is rather toxic and is also associated with clostridium difficile related diarrhea. it is sometimes used topically for treatment of acne.

vancomycin is an glycopeptide antibiotic that is used as a "last resort" drug for severe conditions such as pseudomembranous colitis (only after metronidazole is shown to be ineffective) and against MRSA. like penicillin it works by disrupting the peptidoglycan layer of the bacterial cell walls, although it binds to a different site than the beta lactam in penicillin. it is usually given IV although may be given orally if treating c. difficile in the gut. side effects include "red man syndrome" and shock due to massive histamine release.

speaking of MRSA... MRSA are staph that are resistant to beta lactams (penicillins and cephalosporins) and come in two flavors-- community acquired, which can be treated with sulfas, tetracyclines, and clindamycin, and hospital acquired, which can only be treated with vancomycin.

muciprocin is another drug used against MRSA's which are originally derived from pseudomonas flourescens. it works by inhibiting incorporation of isoleucine into the cell walls of gram negative bacteria. it is used topically in such skin conditions as impetigo, boils, folliculitis.

some last notes on additional antibiotics: bacitracin targets gram positive organisms by inhibiting the transfer of cell wall precursors from the cell membrane to the cell wall. polymyxin kills gram negative bacteria by altering the cell membrane permeability, causing increased water uptake to the point of cell death. polysporin is the combination of polymyxin and bacitracin, while neosporin has both and adds neomycin, and aminoglycoside to the mix. this is the triple antibiotic cream that is used to treat superficial bacterial infections.

questions
1. difference between bactericidal vs. bacterioistatic agents?
2. classes of antibiotics that are naturally derived?
3. types of microbial resistance?
4. what are three categories of target inactivation? describe each mechanism.
5. what is the minimum inhibitory concentration?
6. pus might inactivate which antibiotics?
7. how might a hematoma inhibit antibiotics?
8. how might abscesses inhibit antibiotics?

sulfamethoxazole...
9. class?√√√√√
10. mechanism of action?√√√√√
11. bacteriostatic or bactericidal?√√√√√
12. spread throughout body?√√√√√
13. indicated in which conditions?X√XX†††
14. side effects?X√√√√√
15. sometimes combined with...X√√√√√
16. ratio of [15]?√√√√√√
17. when might [15] be specifically indicated?√√√√√√
18. how do the side effects of [15] compare to sulfamethoxazole?√√√√√√
19. skin morphology?√√√√√√
20. side effects associated with folic acid synthesis disruption?†√√√√√√

penicillins...
21. target which organisms?X√√
22. what type of antibiotics are penicillins? mechanism of action?√
23. is penicillin bactericidal or bacteriostatic?√
25. ∂escribe the prevalence of penicillin allergies.√
26. if a patient has true allergy to penicillin...√
27. penicillin g ineffective against...X√√
28. what is added to IM penicillin g?
29. side effects of penicillin g?X√X√

30. what is amoxicillin?√√√
31. mechanism of action?√√√
32. 2 mechanisms for bacterial resistance of amoxicillin?√√
33. distribution in the body?√√
34. indications for amoxicillin?XXX√XX
35. side effects?X†√†√
36. sometimes combined with what? mechanism of action?X√√√√
37. side effects?X√√√√
38. second of [37] caused by what microbe?√√

cephalexin...
39. bactericidal or bacteriostatic?X√√
40. mechanism?√X√
41. how do the generations of cephalosporins differ in their actions?√√√
42. the spectrum of coverage is similar to which other drug?X√√√
43. 2 mechanisms of resistance?√ √√
44. indications?XXX††
45. side effects?XXX√√

macrolides...
46. active constituent of macrolides?†√√
47. mechanism of action?√√√
48. bacteriostatic or bactericidal?√†√
49. unique transport mechanism within body?√√√
50. compare the coverage spectrum with penicillin.†X††√
51. indications for erythromycin?XXX
52. erythromycin needs to be dosed...√√√
53. common side effects?√√
54. most tablets are...√√

azithromax...
55. why is azithromax so popular?√√√√
56. active molecular constituent?XX√√√
57. mechanism of action?XX√√√
58. what is the half life of azithromax?√√√√√
59. typical dosing?√√√√√
60. indications?X√√√
61. compare the side effects of azithromax and erythromycin.X√√√√
62. helpful to dose concurrently with...√√√√√

tetracyclines...
63. molecular structure?√√
64. mechanism of action?√X√X√
65. usage is less effective due to...√√
66. most common use?XX√√√
67. all tetracyclines can do what in the oral cavity?X√
68. contraindicated in which populations?√√
69. shouldn't be given concurrently with...X√
70. reason for [69]?√√
71. is tetracycline bacteriostatic or bactericidal?XX√√√
72. effect on skin?XX√√
73. useful in outpatient care for...√√√
74. effective against organisms that are resistant to...√†X
75. examples of [74]?X√X√

aminoglycosides...
76. mechanism of action?√√√X†√√
77. indicated for which organisms?√√√X√√
78. most frequently indicated for what condition?√√√X√X
79. what is the usual course of dosing for aminoglycosides?√√√√
80. gentamycin MOA?√√√√
81. what patients in particular are susceptible to [77]?√√√√
82. method of administration?√√√√
83. side effects?√√√X√X

quinolones...
84. mechanism of action?X√X√
85. has an affinity for which organisms?X√X√
86. most severe side effect?√√X√√
87. ciproxin associated with what disease?X√√
88. affinity for what body tissue?√√√
89. affinity for injury of what body part?√√√
90. reduces breakdown of...X√√√
91. affect on the senses?√√√

imidazoles...
92. mechanism of imidazoles?X√√√√
93. describe how metronidazole is activated.√√√√√
94. indications?X√X
95. examples of anaerobic bacteria?X†
96. side effects?X†
97. interaction with alcohol?√√

lincosamides...
98. what are these drugs derived from?X√√√
99. coverage spectrum? (similar to which drug class)X†√√
100. side effects?XX√X
101. clindamycin used topically for?X√√√

vancomycin...
102. indication?X√
103. which organisms in particular might this drug be indicated for?√√√
104. mechanism of action?X√√
105. what form of adminstration?√√√
106. alternate administration? why?√√√
107. side effects?X√
108. should only be used to treat pseudomembranous colitis after...√√

MRSA...
109. what are MRSA's?√
110. two categorizations?√
111. first category is susceptible to which drugs?√
112. second?√

mupirocin...
113. derived from...X√√
114. mechanism of action?XXX
115. administered...X√√
116. effective against which types of organisms?XXX
117. used in what conditions?X†

misc...
118. MAO of bacitracin?√√
119. bacitracin targets which organisms?X√
120. bacitracin used for what conditions?XX
121. polymyxin MAO?√√
122. polymyxin effective against which organisms?√√
123. polysporin is...√√
124. neosporin is...X√

name the drug or class with these characteristics...
125. beta lactam ring√√√√√
126. intracellularly activatedXXX√√√
127. altering bacterial cell membrane permeabilityX√√√
128. transported in leukocytesX√√√√√
129. outpatient care in lyme's diseaseXX√√√√
130. treatment of pneumocystis carinii in AIDSX√X√√
131. aerobic gram negativesXXX√
132. steven johnson's syndrome√√
133. severe acne / rosaceaX√X√
134. red man syndromeXX√
135. DNA gyrase√
136. folic acid synthesis inhibition√
137. causes pseudomembranous†
138. metallic taste in the mouth√
139. chelates calcium and stains teeth√
140. other medication to avoid if have penicillin √
141. last resort for pseudomembranous colitis√
142. blocks isoleucine incorporation into cell walls√
143. 50S ribosomal subunitX
144. irreversible nephrotoxicity√
145. drug with long half life√
146. 30S ribosomal subunitX

answers
1. bactericidal agents kill, while bacteristatic agents simply halt the growth.
2. penicillins
cephalosporins
macrolides
tetracyclines
aminoglycosides
3. failure to reach target
inactivated by enzyme
microbial target area inactivated
4. conjugation (genes from cell to cell), mutation, transduction (bacteriophage carries DNA into microbe).
5. the bare minimum concentration of the drug that is needed to inhibit the growth of the organism.
6. aminoglycosides. [squirting bragg's on pus]
7. hemoglobin can inhibit some drugs such as tetracyclines and penicillin. [heme tetracycline penicillin][H T P][blood on the toilet paper]
8. the low pH of abscesses inactivate some antibiotics such as the macrolides. [abscesses macrolides][looking at an abscess closely with the macro mode]

9. sulfonamide.
10. competitively inhibits PABA, which is used in the synthesis of folic acid, which is required in DNA replication.
11. bacteriostatic.
12. everywhere, including CSF.
13. UTI, otitis media, bronchitis,
14. GI upset
headache
skin changes-- rash, photosensitivity.
15. trimethoprim-- another folic acid inhibitor.
16. 5:1 sulf to tri
17. besides the indications in question 13, it might also be indicated for pneumocystiss carinii prophylaxis in HIV patients.
18. markedly increased hypersensitivity, especially of the skin.
19. raised papulomacular appearance, feels like sandpaper, pruritic.
20. megaloblastosis
leukopenia
thrombocytopenia
stevens johnson's syndrome

21. gram-positive bacteria.
22. beta-lactams.
23. inhibiting formation of peptidoglycan cross links in bacterial cell wall.
24. bactericidal.
25. penicillin is the drug that is most reported in relation to allergies, but it is estimated that only 20% actually have an allergy.
26. all the cillin's should be avoided, and maybe the cephalosporin group as well.
27. many gram negative anaerobes, all beta-lactamase producing organisms.
28. procaine.
29. neutropenia, nephrotoxicity.

30. penicillin derivative that contains thiazolaine ring, beta-lactam ring, side shains.
31. binds to penicillin binding protein and inhibits protein synthesis in cell wall.
32. beta-lactamase or modification of penicillin binding protein.
33. everywhere except CSF.
34. UTI's, lower respiratory infections, skin infections, ENT infections .
35. GI issues, although less than ampicillin.
36. clavulanic acid, in order to prevent beta-lactamase inhibition.
37. GI distress, pseudomembranous colitis.
38. clostridium difficile.

39. bactericidal.
40. same as penicillin; disrupting the PDG element in bacterial cell walls.
41. first generation-- gram positive. second and third generation-- gram negative. [turning to the dark side after the first generation]
42. amoxicillin.
43. beta lactamase production or modifications of PDG.
44. ENT infections
bronchitis
skin infections
prophylaxis
45. GI effects
yeast overgrowth.

46. macrocytic lactone ring.
47. inhibition of bacterial protein synthesis by binding to the 50S ribosomal subunit.
48. only bactericidal at high concentrations.
49. accumulate within leukocytes and therefore are carried to site of infection.
50. similar to but slightly wider than penicillin: includes chlamydia, mycoplasma, mycobacteria, ricksettia. [cmmr][come here!]
51. respiratory tract infx
syphilis
chlamydia
gonorrhea
52. 4 times a day.
53. GI distress-- N/V
54. enteric coated to offset GI side effects.

55. long half life and easy dosing schedule.
56. many membered lactone ring.
57. macrolides: lactone ring binds to 50S ribosomal subunit, blocking protein synthesis.
58. 68 hours.
59. two tablets day one, one tablet day 2-5.
60. ENT infections, sinusitis, pneumonia, bronchitis
mycoplasma, chlamydia
61. similar but with far less GI distress.
62. probiotics.

63. four hydrocarbon ring structure.
64. inhibits cell growth by binding to the 16S part of the 30S ribosomal subunit.
65. widespread bacterial resistance.
66. severe acne and rosacea.
67. permanently stain teeth.
68. children younger than 8-15, pregnant women.
69. calcium or dairy.
70. the tetracyclines chelate with calcium / dairy in the gut and markedly diminish absorption.
71. bactericidal.
72. photosensitivity.
73. lyme's disease.
74. agents with cell wall activity (ie penicillins).
75. mycoplasma
chlamydia
legionella
ricksettia
plasmodium
[mclrp][LaMe CRaP]

76. binds to the 30S bacterial ribosomal subunit and interferes with protein translation.
77. aerobic, gram negative bacteria such as pseudomonas.
78. serious infections such as septicemia.
79. once causal organism is identified therapy is switched to a less toxic drug.
80. binds to 30S and 50S ribosomal subunit, interfering with protein synthesis.
81. burn victims.
82. IV.
83. potentially irreversibly nephrotoxic and ototoxic.

84. inhibits bacterial DNA gyrase.
85. intracellular residing organisms such as legionella, mycoplasma.
86. tendon damage or rupture especially when used in combination with prednisone.
87. anthrax.
88. chelates calcium, deposited in bone and cartilage.
89. achilles tendon.
90. caffiene.
91. affects taste and smell.

92. disrupts the helical structure of DNA.
93. it is taken up into certain organisms that activate the pro-drug intracellularly into its active form.
94. infections of anaerobic bacteria or protozoa.
95. bacteroids, fusobacterium, clostridium. [bfc][big f...]
96. GI upset
headache
metallic taste in the mouth
thrush
97. inhibits acetaldehyde dehydrogenase, the enzyme that breaks down the breakdown product of alcohol.

98. species of actinomides.
99. similar to macrolides but also effective against actinomycetes, plasmodium, mycoplasma.
100. c. diff associated diarrhea, toxicity.
101. acne.

102. used in prophylaxis and treatment of severe gram positive bacterial infection. generally used as a last resort.
103. c. difficile and MRSA.
104. inhibition of peptidoglycan polymerization (distinct from penicillin mechanism)
105. IV, because not absorbed well orally.
106. oral if treating difficult case of pseudomembranous colitis.
107. red man or red neck syndrome.
108. metronidazole is shown to be ineffective.

109. multi-resistant staph aureus; staph that is resistant to beta lactams.
110. community acquired and healthcare acquired.
111. sulfa drugs (trimethorprim / sulfamethoxazole), tetracyclines, clindamycin.
112. vancomycin.

113. pseudomonas flourescens.
114. halts incorporation of isoleucine into bacterial proteins.
115. topically.
116. gram negative bacteria including MRSA.
117. impetigo, boils, folliculitis.

118. interferes with the transfer of cell wall precursors from the cell membrane to the cell wall.
119. gram positive.
120. superficial skin and eye infections.
121. binds to bacterial cell membrane and increases permeability, causing increased water uptake and death of bacteria.
122. gram negative.
123. bacitracin and polymyxin.
124. bacitracin and polymyxin and neomycin.

125. penicillins
126. metronidazole
127. polymyxin
128. macrolides
129. tetracyclines
130. sulfonamides
131. aminoglycosides
132. sulfonamides.
133. tetracycline
134. vancomycin
135. quinolones
136. sulfonamides
137. amoxicillin plus clavulanate
138. metronidazole.
139. tetracycline
140. cephalosporins
141. vancomycin
142. mupirocin
143. macrolides
144. gentamycin
145. azithromycin
146. tetracycline and aminoglycosides.

homeopathy III: thuja

2010-10-23T20:36:00.000-07:00

some study questions on the homeopathic remedy thuja occidentalis.

questions
1. etiology of thuja. †
2. characteristic while answering / speaking... √
3. closely related to which remedy?√
4. two questions to ask thuja patients in an interview.√
5. eccentric or conformist?√
6. similarities to calc carb?√
7. similarity to lycopodium?√
8. role of lying?√
9. hard for thuja to believe what about others?√

10. left or right sided?√
11. worse with what weather?√
12. worse at what time?√
13. worse with which foods?√
14. relationship to smallpox?√
15. skin on the face?√
16. hair?√
17. hair in women?√
18. nasal symptoms?X
19. aversion to which family of veggies?√
20. 3 female genitalia symptoms?√
21. keynote urinary symptom?√
22. prostatic symptoms?√
23. skin conditions?X
24. worse with what weather?√

25. easy dislocation of what in children?√
26. dreams of...√
27. what happens during the course of the night?√
28. sweat?√
29. abdomen feels as if...√
30. worse or better with motion?√
31. worse or better with warmth?√
32. worse or better with open air?√

answers
1. suppression of warts
vaccination
gonorrhea
abuse, mistreatment
2. sentence might dwindle off into a mumble.
3. metorrhinum.
4. 1-- whether they think they are lovable if someone truly knew them inside. 2-- whether they feel attractive.
5. conformist.
6. worse with cold and damp
craves sweets
warts
7. lack of self esteem.
8. very good at lying, may even start to believe their own lies.
9. that they are sincere.

10. left.
11. damp.
12. 1-3PM
13. onions, garlic, tea.
14. thuja is worse after smallpox vaccination.
15. greasy, pale, waxy, acne.
16. greasy, or dry and sticking up.
17. hair growth on the face.
18. thick green catarrh.
19. brassicas.
20. urethral discharge
history of gonorrhea
left ovarian pain.
21. forked urinary stream.
22. dribbling, waking to urinate.
23. warts, especially around anus and horny warts around hands. condylomata.
24. cold and damp.

25. easy dislocation of hip joint in children.
26. falling, dead people.
27. wakes at 3AM and is sleepless.
28. profuse, like onions or honey. only on uncovered parts.
29. animal were alive inside.
30. worse.
31. better.
32. better.

homeopathy III: nat mur

2010-10-23T19:45:00.000-07:00

some study questions on the homeopathic remedy natrum muriaticum, homeopathic salt.

questions
mental/emotional...
1. central idea in nat mur?†
2. describe the way a nat mur patient might talk about an emotional experience.√
3. nat mur is a main remedy for which rubric? (ailments from...)
4. in what way does Lot's wife (from the Bible) represent nat mur?√
5. relationship to music?√
6. relationship to crying?√
7. consolation?√
8. "goal in life is to"...√
9. how is nat mur like a "stuck door"?√
10. relationship to sunlight?√
11. characteristic fear?√
12. typical occupations?†
13. how do nat mur patients act when romantically attracted to someone?√
14. what is one thing that can break down the inhibitions of a nat mur patient?√

physical...
15. in which system(s) is retention found for nat mur patients?X√
16. body temperature?√
17. describe the typical nat mur headache. X√√
18. nasal symptoms?X†√√
19. facial features?√
20. typical throat symptom?X√
21. thirsty for what type of drinks?√
22. unique urinary characteristic?√
23. skin features?X√
24. food cravings? (6)XX√
25. food aversions? (4)X√
26. miasm?XX√

answers
1. introversion due to vulnerability to emotional injury.
2. unemotional, objective tone.
3. ailments from disappointed love.
4. dwelling on past disagreeable experiences.
5. very sensitive to music.
6. cries only when alone, but resists crying in general.
7. aggravates.
8. not be hurt, and avoid hurting others.
9. the tendency to keep emotions inward to the point where they burst out in inappropriate ways periodically (hysteria, awkward laughing), similar to the way a stuck door will suddenly burst open after pulling incessantly.
10. bothered by sunlight.
11. fear of robbers.
12. counseling, ministry, social work (sympathy)
13. reserved.
14. alcohol; wine.

15. urinary retention, constipation, amenorrhea.
16. tend to be warm, worse with heat.
17. headache 10am-3pm coming and going with the sun.
18. coryza like raw egg whites. allergic rhinitis symptoms.
19. oily skin, pimples, and herpetic eruptions around lips.
20. lump in throat. related to grief.
21. cold water.
22. can't pee in front of others.
23. eczema, urticaria, herpes.
24. bitter, beer, sour, salt, fish, milk.
25. bread, meat, coffee, tobacco.
26. psoric and syphilitic.

homeopathy III: staphysagria

2010-10-23T18:53:00.001-07:00

some study questions on the homeopathic remedy staphysagria...

questions
1. staph is used to treat...
2. etiologies for staphysagria?
3. haughty or humble?
4. emotion seen in later stage of staphyagria?
5. sensitive to...
6. commonality between causticum and staph?
7. confrontations might cause...
8. one patient archetype to consider?
9. worse from suppression of...
10. refined or coarse?
11. keynote of doing what when alone?
12. what type of depression?
13. aggression can be linked to...
14. a remedy for intense...
15. miasm?

16. indicated for any neurological problem brought on by...
17. indicated for what type of children?
18. indicated for complaints following first...
19. first remedy to consider for what bladder condition?
20. indicated for complaints from stretching...
21. staph temperature?
22. worse from letting the mind dwell on...
23. better after? (3)
24. head feels like...
25. head symptoms especially after...
26. hair symptom?
27. eye symptom?
28. mouth symptoms? (2)

29. food cravings?
30. thirst level?
31. colic following what? (3)
32. rectum symptoms?
33. type of GU pain?
34. keynote in honeymoon cystitis?
35. males: impotence after...
36. remedy for psoriasis following...
37. keynote: something about afternoons...
38. perspiration?

answers
1. wounds and scars, wounds that penetrate, wounds that do not heal properly.
2. humiliation, mortification, injury to ego, ailments from physical abuse, ailments from domination.
3. more often humble.
4. anger.
5. rudeness, grief.
6. etiology of repeated grief.
7. physical and emotional spasms, speechlessness.
8. battered women.
9. anger.
10. refined.
11. talking to themselves.
12. resigned sadness, not suicidal.
13. sexuality.
14. sexual fantasies, especially with masturbation.
15. sycotic.

16. suppressed grief or anger.
17. children who become autistic or retarded from slight suppression.
18. coition.
19. honeymoon cystitis.
20. sphincters.
21. not distinct-- either hot or cold.
22. sexual objects.
23. hard pressure, breakfast, warmth.
24. block of wood.
25. sexual excesses, coition.
26. alopecia after grief.
27. long lasting sties on eyelids.
28. tooth decay, apthous ulcers

29. sweets, milk, bread, tobacco.
30. low thirst.
31. anger, cold drinks, or least food or drink.
32. painful hemorrhoids, especially after suppressed anger.
33. stinging, stitching, shooting pain.
34. burning in urethra when not urinating.
35. sexual excess.
36. grief or mortification.
37. aggravated by afternoon naps.
38. profuse, with rotten egg smell.

homeopathy III: mercurius

2010-10-19T20:48:00.000-07:00

some study questions about the homeopathic remedy mercurius, which is homeopathically diluted and potentized mercury.

questions
1. kent suggests what about the use of mercury?
2. mercury state can be summed up by which words?XX
3. temperature disposition?√
4. temperature aggravation?√
5. only thing that helps the mercury patient when disturbed by their environment is...√
6. what time of day aggravates?√
7. aggravated by lying on the...√
8. glands?√
9. miasm?√
10. what type of discharges?√
11. quality of discharges?√
12. nervous system symptoms?√
13. tendency towards formation of...√
14. how can acute wounds for mercury be distinguished from aconite / belladonna?√

15. similarity to arsenicum album?√
16. delusional feeling as if...√
17. headache sensation?√
18. headache aggravation?XX
19. appearance of tongue?X√
20. thirst?√
21. what type of taste in the mouth?√
22. mercury can be as important as pulsatilla in which disorder?√
23. mercury is a major remedy for which disorder involving the tongue?√

24. eye symptoms worsened by...√
25. cravings?√
26. food aversions?√
27. PMS characteristics?√
28. lactation?√
29. consider in cases of which STD?√
30. bone involvement?√
31. skin symptoms?√

32. merc-cor indicated for...√
33. merc-iodatum flavum indicated for...√
34. merc-iodatum rubrum indicated for...√

answers
1. not to use more than twice in the winter to treat colds.
2. debility, sluggishness, weakness, oversensitivity.
3. very chilly, but easily overheated.
4. aggravated by the least cold, as well as by heat.
5. lying down and resting.
6. aggravated at night.
7. right side.
8. swollen, inflamed, tender, hardened.
9. syphilitic.
10. profuse, especially saliva and sweat.
11. offensive, acrid.
12. fine tremors, epilepsy, emaciation.
13. pus.
14. both are initially red and inflammed, but mercury then turns to pus formation and is slow in healing.

15. anxious restlessness.
16. he had committed a crime.
17. band around head.
18. worse night and worse in a draft.
19. indented, swollen, flabby.
20. intense thirst for cold drinks.
21. metallic.
22. otitis media.
23. stuttering.

24. heat, radiant heat.
25. bread and butter, alcohol.
26. sweets, diary.
27. anxious restlessness before menses, milk in the breast during menses.
28. mastitis during lactation.
29. syphilis.
30. destructive bone diseases such as osteomyelitis.
31. severe itching, worse from heat of the bed.

32. more intense, excoriating presentations of mercury.
33. sore throat with more inflammation on the right side.
34. sore throat with more inflammation on the left side.

botanical medicine: cardiovascular herbs

2010-10-19T20:41:00.000-07:00

this lecture covered the herbs used to treat various cardiovascular conditions. allium sativa, or garlic, is one example; it affects the vascular system by several proposed mechanisms, including stimulating intracellular activity of nitric oxide synthase, which produces nitric oxide, a potent vasodilator. it also works to inhibit the cyclooxygenase enzyme, which produces inflammatory mediators from arachadonic acid- this effect is perhaps more pronounced with raw garlic. on the other hand, the oil produced from steaming garlic is high in sulphur compounds such as diallyl disulfide, which are thought to be antimicrobial and mucolytic. it might be helpful for diabetics by making more insulin available in circulation by competing for insulin binding sites in the liver. finally, garlic is thought to increase NK cells, thereby boosting innate immunity.

angelica sinensis, or dong quai as it is known in chinese medicine (as a blood mover / yin tonic) is another herb useful for cardiovascular conditions. it has vasodilating effects due to nicotinic acid and antispasmodic effects due to ferulic acid, which is thought to have calcium channel blocking effects. it is relaxing for uterine tissue and thus is indicated in some female hormonal conditions such as cramping and dysmenhorrea.

crataegus oxycantha, or hawthorne is an herb that is useful both in acute care as well as long term chronic management of cardiac cases. it has positive inotropic effects (increasing myocardial contractility), stabilizes capillaries via flavonoids, acts as a natural calcium channel blocker via procyanidins (which inhibits phosphodiesterase), and lowers blood pressure by inhibiting ACE and thus aldosterone.

gingko biloba is an herb commonly associated with increased mental clarity, which is thought to be due to increased cerebral artery perfusion. it also has beneficial effects on the vascular system, increasing coronary artery perfusion, enhancing peripheral vasodilation and also acting as an antioxidant via flavonoids and super oxide dismutase. because of its antioxidant effect it can be indicated in cases of hypoxic tissue damage.

one of the few herbs that is indicated specifically for hypotension rather than hypertension is selenicerues grandiflora, or cactus as it is commonly known. it is indicated in cases of weak heart muscle, as in CHF, mitral / aortic insufficiency, and even some arrhythmias. it is used more for functional, rather than organic disorders, and is especially indicated for a sensation of a heavy band in the chest.

a couple herbs with specific applications: leonurus cardiaca is a cardiotonic that is specific for the pelvic area and the vasculature, much like angelica (see above). thus it is used in cases of palpitations associated with pelvic pain, hormonal imbalances, or menstrual complaints. it might also have beta-blocking activity as well as improving blood viscosity. mentha piperita is an herb used specifically when angina occurs after a heavy meal, accompanied by digestive complaints such as gas and bloating. it is in fact part of the "glyconda formula", an eclectic formula used to treat cardiovascular complaints associated with gastrointestinal symptoms.

there are a number of herbs used to treat various pathologies of the peripheral vasculature. yarrow is an astringent that can be applied topically to wounds as well as internally; where it has vasodilatory effects in the peripheral vasculature and vasoconstrictive effects in the uterus. horse chestnuts aids in venous return and is therefore indicated in disorders such as varicose veins, and also has immune modulating effects via lectins. pineapple contains the sulfur-rich bromelain, which is thought to have thrombolytic effects, so much so that it might be used pre-surgery to reduce the risk of clots.

other peripheral vascular herbs: capsella (shepard's purse) is an herb used to stop chronic bleeding, especially uterine bleeding. stone root is a specific for constipation due to vascular engorgement of rectal mucosa and is also specific for congestion of oral, urinary, rectal mucosa. witch hazel is an astringent that can be applied topically or ingested, indicated for pale, engorged, congested tissues. hypericum is better known for its emotionally uplifting effects but also aids in venous stasis and varicosities due to the high flavonoid content. ruscus is in the lily family and contains rescogenins that have vasoconstrictive and anti-inflammatory effects. red clover is more commonly used to for female hormonal balance, but it also has circulatory actions, via the coumarins it contains, which improve blood lipids, reduce inflammation and reduce platelet aggregation. vaccinium, or bilberry contain anthocyanosides which have powerful antioxidant properties, and are stabilizing for capillaries as well. veratrum is an herb that can be used carefully in acute or severe cases of hypertension, indicated in a bounding pulse or flushed face. at higher doses, it acts as an emetic and thus must be used cautiously.

questions...
allium sativa...
1. what compounds does garlic contain that affect vascular endothelium?
2. how does garlic thin blood?
3. raw garlic has more of what effect?
4. which compounds are in garlic oil and result from steam processing?
5. how does garlic affect blood sugar?
6. garlic's effect on the immune system?
7. garlic's effect on inflammation?

angelica sinensis...
8. which family is angelica in? what compound is found in high quantities in this family?
9. antispasmodic effects due to which compound? what does this compound do?
10. vasodilating effects due to which compound?
11. used in chinese medicine for what purpose?

crataegus oxycantha, monogyna...
12. chemical consituents in crataegus?
13. describe the overall effect of hawthorne on the CV system.
14. flavonoids in hawthorne have what effect?
15. indicated for hyper or hypotension?
16. mechanism for lowering blood pressure?
17. mechanism for calcium channel blocking effects?
18. hawthorne berries are high in what compounds in the spring vs. the fall?
19. useful in CHF along with which other nutrient?

ginkgo biloba...
20. increases blood flow to...
21. main active constituent?
22. antioxidant actions via...
23. also used for what conditions due to cerebral perfusion?
24. why indicated for diabetics?

selenicereus grandiflorus...
25. indicated for hyper or hypotension?
26. indicated for functional or organic disorders?
27. specifically indicated for what chest sensation?

leonurus cardiaca...
28. what areas of the body is motherwort specific for?
29. leonurus injections were shown to improve...
30. 2 specific indications for leonurus.

mentha piperita...
31. most indicated for...
32. part of which formula?
33. contraindicated in which patients? why?

peripheral vasculature herbs...
34. yarrow's action in the peripheral vasculature?
35. yarrow's action on the uterus?
36. yarrow's topical effect?
37. horse chestnut's effect on vasculature?
38. [37] attributed to what compound?
39. horse chestnut immune effect via which compounds?
40. pineapple high in which compound?
41. pineapple used pre-surgery for...

more peripheral vasculature herbs...
42. shepard's purse used for...
43. capsella might be contraindicated in pregnancy because of...
44. capsella also contraindicated in people with...
45. stone root specific for which areas?
46. specific GI condition that might benefit from stone root?
47. witch hazel indicated in...
48. hypericum high in which compound?
49. cardiovascular indications of hypericum?
50. mechanism of action for hypericum?
51. what family is ruscus in?
52. active constituents of ruscus? actions?
53. indications for ruscus? affinity for which tissue?

54. active constituent in red clover?
55. effect of [54]?
56. active constituents in vaccinium?
57. effect of [56]?
58. why is bilberry particularly indicate for diabetics?
59. active constituents of veratrum viride?
60. effect of [59]?
61. veratrum effect at high doses?
62. black haw's effect is similar to what other herb?

answers
1. nitric oxide like compounds.
2. by inhibiting platelet aggregation.
3. it is more of a inhibitor.
4. diallyl disulfide and diallyl trisulfide.
5. competes with insulin binding sites on liver, allowing for more insulin to be in circulation, allowing for blood sugar stabilization.
6. increases NK cells.
7. COX inhibitor.

8. umble family, coumarins.
9. ferulic acid; ca-channel blocking effects.
10. nicotinic acid.
11. blood mover and blood builder.

12. flavonoids, tannins, organic acids, sterols, purines, triterpines.
13. normalize blood pressure, positive inotropic activity, diuresis.
14. stabilize capillaries to reduce permeability and fragility.
15. both.
16. inhibits ACE, which leads to a decrease in aldosterone and thus decreased water retention.
17. procyanidins inhibits phosphodiesterase, which breaks down cAMP, leaving higher calcium levels.
18. amines (spring) vs. bioflavonoids.
19. CoQ10.

20. cerebral arteries, carotid arteries.
21. flavonoids; ginkgo heterosides.
22. super oxide dismutase, flavonoids.
23. tinnitus or ear congestion.
24. to increase peripheral perfusion and prevent retinopathy, nephropathy, gangrene, etc.

25. hypotension.
26. functional.
27. band squeezing the chest.

28. pelvis and vasculature.
29. blood viscosity.
30. heart palpitations associated with pelvic pain or hormonal imbalance such as hyperthyroid.
e31. angina that occurs after eating accompanied by digestive symptoms.
32. glyconda.
33. patients with GERD, due to relaxing effects on LES.

34. peripheral vasodilator.
35. promotes constriction of uterine blood vessels.
36. astringent; aids in wound healing.
37. increases venous returns.
38. coumarins.
39. lectins have many immune modulating effects.
40. bromelain.
41. to reduce risk of clotting.

42. to stop chronic bleeding, especially from the uterus.
43. alkaloids.
44. high blood pressure.
45. oral, urinary, rectal mucosa.
46. constipation due to vascular engorgement of rectal mucosa.
47. pale, engorged, congested tissues.
48. hypericin, a bright red flavonoid.
49. venous stasis, varicosities.
50. hypericin and other flavonoids strengthen venous wall integrity, prevent free radical damage and enzymatic breakdown of collagen.
51. lily family.
52. ruscogenins: vasoconstrictive and anti-inflammatory effects.
53. peripheral vasculature, varicosities and hemorrhoids.

54. coumarin.
55. improve blood lipids, reduce inflammation and platelet aggregation.
56. flavonol glycosides-- anthocyanosides.
57. antioxidant and capillary stabilization.
58. because of its specificity for the eyes, fighting the effects of diabetic retinopathy.
59. veratrine.
60. potent hypotensive; circulatory depressant.
61. emesis.
62. cramp bark: uterine relaxant, relaxes peripheral blood vessels.

pharmacology: cardiovascular drugs

2010-10-17T12:56:00.000-07:00

the lecture about the conventional medications used to treat cardiac arrhythmias. the electrical conduction system of the heart can be affected in many different ways and there are several classes of drugs, each with a unique mechanism that targets different portions of the cardiac cycle [see questions 4-9]. quinidine is in class Ia, which works to slow the phase 0 depolarization, thereby prolonging action potential and slowing conduction. it is indicated in atrial fibrillation, atrial flutter, and some other arrhythmias, but tends to be avoided due to its high side effect profile; GI upset, cinchonism (a host of symptoms including nausea/vomiting, tinnitus, headache, disorientation), and torsade de pointes (an abnormal heart rhythm normally found in ventricular tachycardia where the peaks and troughs of the Q wave are equidistant from the baseline).

mexiletine is indicated in ventricular arrhythmias and recurrent ventricular tachycardia post-MI. it is class 1b; still a sodium channel blocker like quinidine but acts upon phase 3 repolarization instead of phase 0. side effect include drowsiness, confusion, and pro-arrhythmic potential. flecainide is used for supra-ventricular arrhythmias; arrhythmias that have an origin above the ventricles. the main side effect is its pro-arrhythmic potential; thus it is contraindicated in patients with a history of an MI or ventricular arrhythmia related to an acute ischemic event.

atenolol is a drug in class II anti-arrhythmics, drugs which diminish phase 4 repolarization by acting as beta-adrenergic blockers, thus decreasing sympathetic tone in the myocardium. it is indicated in tachyarrhythmias, a-flutter, a-fib, hypertension, angina, among other conditions, and stabilizes heart rate by the mechanism mentioned above; resulting in decreased automaticity in the various pacemaker cells in the heart. side effects might include drowsiness, bradycardia, dizziness, hypotension.

amiodarone is a typical class III anti-arrhythmic drug, causing a K+ channel blockade that results in prolonged phase 3 repolarization. it is indicated for arrhythmias with a ventricular origin and contains high amounts of iodine, which can cause blue-gray discoloration of the skin as a side effect. other side effects include dizziness / light headedness and pulmonary fibrosis.

the last class of anti arrhythmic, class IV, is represented by verapamil; these are drugs that block calcium channels, resulting in slowed phase 0 depolarization, which results in decreased AV conduction and a slower heart rate. side effects might include flushing, dizziness, hypotension.

there are other drugs that do not fall into the 6 major classes; one such drug is adenosine, which is produced endogenously from the breakdown of ATP. pharmacologically, adenosine has the effect of lengthening the refractory period and decreasing automaticity in the AV node by acting directly on the sinus pacemaker cells and vagal nerve terminals. it is administered by IV and can work as quickly as 15 seconds. it is the drug of choice for patients with PSVT (paroxysmal supraventricular tachycardias).

atropine is a drug derived from the nightshade belladonna which is used in cases of severe bradycardia with hypotension. it works by competitively inhibiting muscarinic acetylcholine receptors, thus blocking parasympathetic activity. thus it can also be used orally to treat diarrhea due to its effect of slowing peristalsis. it is also an effective antidote to organophosphate poisoning; these pesticides work by inhibiting acetylcholinesterase, leaving an abundance of acetylcholine-- while atropine works to block the effects of acetylchoine in the synapse.

digoxin is an anti-arrhythmic derived from the plant digitalis lanata and is classified as a cardiac glycoside. it both increases cardiac contractility as well as lowering conductivity, leading to a more stable, stronger heart beat. it works by inhibiting the Na/K ATPase and allowing for more intracellular influx of Na and Ca, as well as increasing the AV node's sensitivity to vagal stimulation. an overdose can cause "digitalis intoxication" which has a host of symptoms which might include bradycardia, fatigue, nausea, vomiting, blurred vision. digibind is used in such cases, an antibody formulated against digoxin (harvested IgG from sheep that are immunized with digoxin) which forms complexes that can be excreted via the kidneys.

questions
1. what are the five phases of the cardiac rhythm?
2. how does the origin of the arrhythmia correspond with prognosis?
3. common causes of arrhythmias?
4. describe the mechanism for the anti-arrhythmic drug class Ia.
5. describe the mechanism for the anti-arrhythmic drug class Ib.
6. describe the mechanism for the anti-arrhythmic drug class Ic.
7. describe the mechanism for the anti-arrhythmic drug class II.
8. describe the mechanism for the anti-arrhythmic drug class III.
9. describe the mechanism for the anti-arrhythmic drug class IV.

quinidine...
10. what class is quinidine?
11. indications?
12. mechanism of action?
13. side effects?
14. what is cinchonism?
15. what is torsade de pointes?

mexiletine...
16. what class is mexiletine? what is the mechanism?
17. indications?
18. side effects?

flecainide...
19. class? mechanism?
20. indications?
21. side effects?
22. contraindicated for which patients?

atenolol...
23. class?
24. indications?
25. mechanism of action?
26. side effects?

amiodarone...
27. indicated for...
28. mechanism of action?
29. contains high amounts of...
30. [29] results in what side effect?
31. other side effects?

verapamil...
32. which class? mechanism?
33. side effects?

adenosine...
34. drug of choice for which disorder?
35. breakdown product of...
36. mechanism of action?
37. acts directly on...
38. increases vagal tone by...
39. method of administration? onset of action?

atropine...
40. derived from...
41. cardiac use is for treatment of...
42. mechanism of action?
43. oral atropine can be used for...
44. can act as an antidote for...
45. symptoms of organophosphate poisoning?
46. specific antidote for atropine overdose? mechanism?

digoxin...
47. belongs to which family of drugs?
48. derived from which plant?
49. difference between digoxin and digitoxin?
50. mechanism of action?
51. effect on AV node?
52. effect on kidneys?
53. effect on EKG?
54. what is digitalis intoxication?
55. what is digibind?

answers
1. sodium channels open
sodium channels close, potassium channels begin to open
calcium and potassium channels open
calcium channels close
return to resting membrane potential
[Na, Na/K, Ca/K, Ca, return]
2. arrhythmias that originate in the atrias are generally more benign while ventricular arrhythmias are generally fatal within minutes.
3. ischemic damage
electrolyte disturbances
pH imbalance
4. sodium channel blockade: slow phase 0 depolarization-- prolong action potential and slow conduction.
5. sodium channel blockade: shorten phase 3 repolarization and decrease action potential duration by blocking sodium channels.
6. sodium channel blockade: markedly slow phase 0 depolarization.
7. diminish phase 4 repolarization, thus depressing automaticity.
8. prolong phase 3 repolarization without altering phase 0.
9. slow phase 4 depolarization and slow conduction, particularly at the AV node.

10. class Ia.
11. a-flutter, a-fib, AV and ventricular arrhythmias.
12. diminished inward flow of sodium at phase 0 results in decreased automaticity and a longer refractory period.
13. arrhythmias
GI symptoms: nausea, diarrhea, vomiting
cinchonism
torsade de pointes
14. nausea / vomiting
tinnitus
headache / disorientation
psychosis.
15. abnormal rhythm of ventricular tachycardia; peaks and troughs of Q wave are equidistant from baseline.

16. class 1b: blocks open sodium channels and shortens phase 3 repolarization.
17. ventricular arrhythmias, recurrent v-tach post MI.
18. drowsiness, confusion, pro-arrhythmias.

19. class Ic- sodium channel blocker.
20. supraventricular arrhythmias, WPW syndrome.
21. pro-arrhythmic.
22. patients with history of MI or ventricular arrhythmia due to acute ischemic event.

23. class II.
24. tachyarrhythmias
a-flutter, fib
PSVT
hypertension
angina
25. reduced sympathetic myocardial tone.
26. bradycardia, hypotension, fatigue, dizziness.

27. ventricular arrhythmias.
28. potassium channel blockade; prolong phase 3 repolarization.
29. iodine.
30. blue-gray skin discoloration.
31. dizziness, light headedness, pulmonary fibrosis.

32. class IV-- calcium channel blocker, slows phase 0 depolarization resulting in slowed AV conduction.
33. dizziness, flushing, hypotension, headaches.

34. PVST.
35. ATP.
36. prolongs refractory period and decreases automaticity in AV node.
37. sinus pacemaker cells and vagal nerve terminals
38. working between the SA and AV nodes.
39. IV, 15 seconds.

40. belladonna.
41. bradycardia and hypotension.
42. competitive inhibitor of muscarinic AcH receptors; blocks parasympathetic pathway.
43. diarrhea due its effect of slowing peristalsis.
44. pesticides that inhibit acetylcholinesterase.
45. SLUDGE:
salivation, lacrimation, urination, diarrhea, gastric distress, emesis
46. physostigmine; a reversible acetylcholinesterase inhibitor.

47. cardiac glycosides.
48. digoxin lanata.
49. digitoxoin has a longer half life and higher potential for toxicity.
50. inhibits Na/K ATPase, leads to more influx of Na and Ca intracellularly, allowing for higher contractility while decreasing conductivity and thereby stabilizing heart rate.
51. increases sensitivity to vagal stimulation.
52. increases renal perfusion.
53. flattening or inversion of t wave.
54. cardiac symptoms such as bradycardia, heart block
GI symptoms such as N/V, anorexia and diarrhea
eye symptoms such as blurred vision, double vision
55. antibodies specific to digoxin used to clear digoxin from the body after intoxication.

modern living

2010-10-15T22:04:00.000-07:00

just read a short article on physorg.com which basically proposes that cancer is a recent evolutionary development, mainly due to the poor diet and pollution that is endemic in industrialized society. reminded me of the first chapter of the neijing; the yellow emperor asking why people in modern times ("modern" being before the 1st century BCE) tended to live much shorter lives than their ancestors.

here's the entire chapter, courtesy of fiveelement.com

Chapter 1: THE UNIVERSAL TRUTH

In ancient times the Yellow Emperor, Huang Di, was known to have been a child prodigy. As he grew he showed himself to be sincere, wise, honest and compassionate. He became very learned and developed keen powers for observing nature. His people recognized him as a natural leader and chose him as their emperor.

During his reign, Huang Di had discussions concerning medicine, health, lifestyle, nutrition, Taoist cosmology with his ministers, including Qi Bo, and others. Their first conversation began with Huang Di asking, “I’ve heard that in the days of old everyone lived one hundred years without showing the usual signs of aging. In our time, however, people age prematurely, living only fifty years. Is this due to a change in the environment, or is it because people have lost the correct way of life?”

Qi Bo replied, “In the past, people practiced the Tao, the Way of Life. They understood the principle of balance as represented by the transformations of the energies of the universe. They formulated exercises to promote energy flow to harmonize themselves with the universe. They ate a balanced diet at regular times, arose and retired at regular hours, avoided overstressing their bodies and minds, and refrained from overindulgence of all kinds. They maintained well-being of body and mind; thus, it is not surprising that they lived over one hundred years.”

“These days, people have changed their way of life. They drink wine as though it were water, indulge excessively in destructive activities, drain their jing - the body’s essence that is stored in the Kidneys - and deplete their qi. They do not know the secret of conserving their energy and vitality. Seeking emotional excitement and momentary pleasures, people disregard the natural rhythm of the universe. They fail to regulate their lifestyle and diet, and sleep improperly. So it is not surprising that they look old at fifty and die soon after.”

“The accomplished ones, of ancient times, advised people how to guard themselves against disease-causing factors. On the mental level, one should remain calm and avoid excessive desires and fantasies, recognizing and maintaining the natural purity and clarity of the mind. When internal energies are able to circulate smoothly and freely, and the energy of the mind is not scattered, but is focused and concentrated, illness and disease can be avoided.”

“Previously, people led a calm and honest existence, detached from undue desire and ambition; they lived with an untainted conscience and without fear. They were active, but never depleted themselves. Because they lived simply, they knew contentment, as reflected in their diet of basic but nourishing foods, and clothing that was appropriate to the season but never luxurious. Since they were happy in their position in life, they did not feel jealousy or greed. They had compassion for others and were helpful and honest, free from destructive habits. They remained unshakable and unswayed by temptations, and they were able to stay centered even when adversity arose. They treated others justly, regardless of their level of intelligence or position.”

Huang Di asked, “I’ve heard of people in ancient times, spoken of as the immortals, who knew the secrets of the universe and held the world in the palm of their hands. They extracted essence from nature and practiced Qi Gong and various stretching and breathing exercises, and visualizations, to integrate body, mind and spirit. They remained undisturbed and thus attained extraordinary levels of accomplishment. Can you tell me about them?”

Qi Bo responded, “The immortals kept their mental energies focused and refined, and harmonized their bodies with the environment. So they did not show typical signs of aging and were able to live beyond their biological limitations.
“Not so long ago there were people known as achieved beings who had true virtue, understood the Way of Life, and were able to adapt to and harmonize with the universe and the seasons. They too were able to keep their mental energy through proper concentration.

“These achieved beings did not live like ordinary humans, who tended to be hard on disease-causing factors. On the mental level, one should remain themselves. They were able to travel freely to different times and places since they were not governed by conventional views of time and space. Their sense of perceptions were supernormal, going far beyond the sight and hearing of ordinary humans. They were also able to preserve their life spans and live in full health, just as the immortals did.

“There was a third type of a person, known as the sage. The sages lived peacefully under Heaven and Earth, following the rhythms of the planet and the universe. They adapted to society without being swayed by fashions and trends. They were free from emotional extremes and lived a balanced, contented existence. Their outward appearance, behavior and thinking did not reflect the conflicting norms of society. the sages appeared busy but were never depleted. Internally they did not overburden themselves. they abided in calmness, recognizing the empty nature of existence. The sages lived over one hundred years because they did not scatter or disperse their energies.

“A fourth type were the natural people who followed the Tao, the Way of Life, and were called naturalists. They lived in accordance with the rhythmic patters of the seasons: Heaven and Earth, moon, sun and stars. They aspired to follow the way of the ancient times, choosing not to lead excessive lifestyles. They, too, lived plainly and and enjoyed long life."

homeopathy III: causticum

2010-10-11T13:49:00.000-07:00

study questions for the homeopathic remedy causticum...

questions
1. causticum is prepared from which materials?
2. which acute conditions treated with causticum?
3. causticum burns might have which concomitants?
4. Jeremy Sherr describes causticum as...
5. dry vs. wetness?
6. important neurological remedy for which conditions?
7. some etiologies for causticum?
8. some aggravations for causticum?
9. some ameliorations for causticum?
10. describe the quality of causticum's anxiety.
11. anxiety worse at what time?
12. may have an internal conflict with...
13. describe an archetypal life path for causticum.
14. what is a unique causticum mistake with regards to language?

15. head symptoms?
16. eyes?
17. ears?
18. affinity for which joint in the head?
19. throat conditions?
20. hunger?
21. food cravings / dislikes?
22. rectum?
23. fear of which animals?

answers
1. calcium carbonate and potassium sulfate.
2. scalds / burns-- especially deep ones.
3. urinary frequency / burning, restlessness.
4. old age, a slowing down of life. a person who has worked all day and is weary at the close of the day.
5. more a dry remedy, worse with wetness.
6. weakness and paralysis.
7. ailments from cold exposure (air, water)
overuse or exertion
longstanding grief, fright, worry
8. cold winds
dry weather
coffee
menses
extremes of temperature
9. rainy / damp weather
warmth
heat of the bed
swallowing cold wtaer
10. free floating, vague.
11. twilight.
12. control / self control.
13. young anarchist becomes lawyer.
14. spoonerisms.

15. empty space between the forehead and the brain.
16. heaviness, ptosis, paralysis.
17. abundance of earwax with foul odor.
18. TMJ.
19. loss of voice from laryngeal paralysis.
20. may vanish at the sight of food.
21. cravings for smoked meats / aversion to sweets.
22. tendency towards ineffectual urging, BM's are easier standing up.
23. dogs.

homeopathy III: arsenicum album

2010-10-11T13:48:00.000-07:00

some study questions for the homeopathic remedy arsenicum album...

questions
1. describe what is at the core of arsenicum album.
2. dependency on others for...
3. impulse to...
4. relationship to others in terms of power balance?
5. fearful dreams might especially be of...
6. other types of dreams?
7. personal organization?
8. [7] is a manifestation of what?
9. "anger when he spoke of..."
10. five delusions?

11. beyond which level of homeopathic dilution is arsenicum no longer poisonous?
12. similarity to nat mur?
13. similarity to rhus tox?
14. describe the quality of restlessness that arsenicum patients experience.
15. describe the selfishness of arsenicum.
16. they can accumulate...
17. energy level characteristics?
18. suicidal impulses motivated by...
19. sleep disorders around what time?
20. delusions that he will never be...
21. relationship to knifes?
22. appropriate for middle aged women who...
23. anxiety / panic attacks around what time?

24. kids have desire to be...
25. unique aspect of suicidal nature?
26. what miasm does arsenicum belong to?
27. a high potency (10M) is recommended in which special cases?
28. body temperature?
29. desires which foods?
30. thirsty for what?
31. which side is favored?
32. tendency to...
33. discharges are...
34. better or worse from lying?
35. better or worse from seashore?
36. used for fainting from...

37. dry or wet?
38. general appearance?
39. in acute headaches, wants...
40. eyes.
41. HEENT: one of three most common remedies for...
42. colds accompanied by...
43. colds palliation and provocation?
44. feeling of what in the lungs?
45. GI symptoms affect which area of the GI tract?
46. appearance of the tongue?
47. stomach symptoms alleviated by...
48. type of gastroenteritis associated with arsenicum?
49. for which other GI pathology is arsenicum the go to remedy?
50. desires or detests sweets?
51. GU symptoms?

answers
1. insecurity and vulnerability.
2. security.
3. murder.
4. can be dictatorial and demanding.
5. cancer.
6. misfortune, great exertion, danger, accidents.
7. very fastidious.
8. inner insecurity, need for control.
9. her complete recovery.
10. delusions he's offended people
everyone is looking at her
everything she touches is contaminated
body will putrefy
that he murdered someone

11. 6X
12. dreams of robbers
13. restlessness with desire for motion.
14. anxious, weak restlessness.
15. self indulgence.
16. doctors.
17. exaggerated weakness from least effort causes immediate loss of energy.
18. hopelessness and despair.
19. 2-3 AM
20. happy in his own house.
21. afraid to see knives, for fear of what they might do with them.
22. fall to pieces when children leave home.
23. 12-1AM

24. held on to and carried quickly.
25. suicide by setting oneself on fire.
26. syphillis.
27. in someone whose time has come to die but has conflict due to a fear of death.
28. very chilly, yet desires fresh air.
29. sourness, olive oil, hard liquor.
30. sips of warm tea or hot water with lemon.
31. right side.
32. bleed.
33. offensive, acrid, scanty.
34. worse.
35. worse.
36. the slightest cause.

37. dry.
38. thin and wiry, like a racehorse.
39. head cool.
40. burning, inflammation.
41. common cold.
42. chilliness, weakness, fatigue.
43. worse outside, better warm room.
44. smoke.
45. mouth to anus.
46. white, as if painted.
47. warm drinks.
48. viral, with simultaneous vomiting and diarrhea.
49. food poisoning.
50. averse to sweets.
51. swelling and burning.

homeopathy III: lycopodium

2010-10-04T12:18:00.000-07:00

some study questions for the remedy lycopodium.

questions
1. what is lycopodium made of?
2. lycopodium especially affects which systems?
3. appearance of lycopodium infants?
4. infants usually suffer from...
5. infants' actions upon waking?

6. physicality vs. mental.
7. describe the lycopodium countenance.
8. body shape?
9. what head symptom is characteristic of lycopodium?

10. underlying mental state is one of...
11. relationship to public speaking?
12. relationship to power and responsibility?
13. consideration for others?
14. intimacy patterns?
15. sexual dysfunctions?
16. does lycopodium enjoy being alone?

17. lycopodium is sensitive to...
18. what time of day aggravates?
19. left or right sided remedy?
20. what type of clothing?
21. temperature disposition?
22. what type of heat ameliorates vs. aggravates?
23. GI symptoms?
24. motion aggravates or ameliorates?

25. headache might be precipitated by...
26. ears?
27. nose?
28. mouth?
29. sore throat is ameliorated and aggravated by...
30. in abdomen-- right sided...
31. urine appearance?
32. urinary symptoms in children?
33. female symptoms-- right sided...
34. aggravated or ameliorated by coition?

35. modalities are similar to which other remedy?
36. extremities-- right sided...

answers
1. inert club moss spores.
2. alimentary tract, GU tract, liver, genitals.
3. wrinkled appearance.
4. colic and constipation.
5. infants are irritable upon waking and immediately demand feeding.

6. lycopodium is more of a mental remedy; these patients are not very physically inclined or athletic.
7. wrinkled, frowning, emaciated.
8. pear shaped; can be emaciated on top and normal / plump on bottom.
9. premature graying of hair.

10. cowardice.
11. dreads public speaking but generally gives exceptional performances.
12. seek power but avoid having responsibility.
13. lyc's might have an "unknowing selfishness", a self-centerdness and self-directed ambition that is oblivious to others' pain or comfort.
14. strong sexual impulses without having true intimacy; one night stands instead of long term relationships.
15. male: impotency or erectile dysfunction. female: inability to achieve orgasm.
16. prefers not to be alone, but wants others to be slightly removed-- wants someone in the next room or house.

17. themselves, to music, to sentiment.
18. 4-8PM.
19. right sided remedy.
20. tight clothing aggravates.
21. chilly, worse cold drinks and food.
22. most heat ameliorates, but cool, fresh air ameliorates.
23. flatulence, easy satiety, gastritis, stomach cancer.
24. restlessness is ameliorated by motion.

25. great hunger.
26. thick otorrhea, otitis media, eczema behind ears.
27. sinusitis with pain at root of the nose, thick yellow discharge with yellow green crusts.
28. dry without thirst.
29. worse with cold drink, better with warm drink.
30. hernia.
31. "red sand in urine".
32. enuresis.
33. ovarian neuralgia
34. aggravated.

35. rhus tox-- better warm, better motion,
36. sciatica.

pharmacology: respiratory drugs

2010-10-04T10:46:00.000-07:00

this lecture covered the conventional drugs used to treat respiratory conditions such as asthma. there are several classes of asthma treating drugs, including adrenergic agonists, anti-cholinergics, methylxanthines, etc. which can be grouped into 2 categories: drugs that reduce inflammation, and drugs that relax bronchial smooth muscle. bronchial smooth muscle tone is increased with increased sympathetic activity; epinephrine is a sympathetic neurotransmitter that decreases asthmatic symptoms by this mechanism. since it acts non-selectively, it also acts on beta-1 receptors, causing cardiac symptoms such as palpitations, and on alpha-1 receptors, causing dry mouth and hyperglycemia. in general, the bronchodilating group of asthma drugs are the type used for anaphylaxis / status asthmaticus, while the inflammation reducing drugs are better for longer term, less acute treatments.

then there are drugs that specifically bind to beta-2 agonists, and using the same mechanism above induces dilation of bronchial smooth muscle. these include albuterol, proventil, and salmeterol-- the latter is longer acting and is used more for chronic conditions. these drugs are mainly administered by inhalation, and delivery can be improved by the use of "spacers" which allow for smaller, slower velocity to reach the lungs.

anticholinergics are another class of asthma drugs that act by competitively inhibit the acetylcholine neurotransmitter at muscarinic receptor sites, inducing sympathetic bronchodilation. as opposed to epinephrine or beta-2 agonists, anticholinergics are best used for maintenance as opposed to acute conditions. atrovent and theophylline are two examples of anticholinergics; the former is chemically similar to atropine (from the plant belladonna) and the latter is similar to caffeine.

corticosteroids are also used as asthma treatment when bronchodilators are not effective by themselves. they are potent anti-inflammatories; blocking phospholipase A2, the enzyme which mediates the release of arachidonic acid, the precursor of inflammatory mediators such as leukotrienes and prostaglandins. thus, they decrease the activity of macrophages, eosinophils and t-lymphocytes, as well as decreasing capillary permeability and thus edema systemically (not specific for bronchial tissue). the main danger of corticosteroids is disruption of the body's natural cortisol production via the HPA axis; abrupt discontinuation of corticosteroids might result in an addisonian crisis due to the body's inability to produce ACTH.

corticosteroids also suppress immunity in general, leading to increased susceptibility to infection. one of the side effects of beclovent, an inhaled corticosteroid, is an increased incidence of oral thrush. prednisone is an oral corticosteroid which, compared to inhaled steroids, has more chance of producing systemic side effects, such as hyperglycemia, fat redistribution (same as in cushing's syndrome, a condition of excess cortisol production), osteoporosis, in addition to the potential for the addisonian crisis.

leukotriene inhibitors such as zafirlukast are a newer class of asthma drugs which block leukotriene receptors D4 and E4 in bronchial smooth muscle, thereby reducing inflammation and allowing for bronchodilation. it is also used in the treatment of chronic cases as opposed to anaphylaxis. side effects include headache, Gi upset, possibly increased respiratory infections.

antitussives such as codeine block the medullary centers that are involved in the cough response. the two antitussives that we discussed, codeine and dextramethorphan, are related to morphine: codeine is broken down into morphine while dextramethorphan is a synthetic morphine derivative. besides being addictive, these drugs have other side effects, drowsiness and constipation being among the chief complaints. dextramethorphan is milder than codeine in terms of constipation and and addictive properties.

another major category of respiratory drugs are drugs used to treat allergic rhinitis. antihistamines such as benadryl block histamine H1 receptors and cross the blood brain barrier, causing drowsiness, while medications such as claritin perform the same action while being large enough to not cross the BBB. both cause dryness of mucous membranes and thus are contraindicated in asthma, when a mucolytic (n-acetyl cysteine?) and moistening agent is preferred.

nasal corticosteroids can also be used to depress the inflammatory response locally, such as beconase or rhinocort, although can result in local irritation and nosebleeds, as well as increased susceptibility to nasal candidiasis. nasal alpha agonists are also used to combat allergic rhinitis, such as phenylephrine / afrin, but are highly addicting due to the rebound symptoms that occur as soon as the medication is stopped.

questions
intro...
1. describe the different roles of the autonomic nervous system in terms of bronchoconstriction and bronchodilation.
2. what are the two general mechanisms of action for asthma drugs?
3. epinephrine indications...
4. epinephrine mechanism of action?
5. side effects of epinephrine?
6. method of delivery?

beta-2 agonists...
7. albuterol, proventil mechanism of action?
8. methods of administration and timing of action for each?
9. inhaled administration might be improved by...
10. when is use of salmeterol / serevent indicated?
11. onset and duration of action of salmeterol?
12. side effects of salmeterol?

anticholinergics...
13. anticholinergics are similar in structure to...
14. action of anticholinergics?
15. when are anticholinergics indicated?
16. example of anticholinergic?
17. what is an example of an anticholinergic that has been replaced by beta agonists / corticosteroids?
18. what class of drug does [17] belong to?
19. what other substance is [17] similar to?

corticosteroids...
20. mechanism of action?
21. acute or chronic cases?
22. main side effect?
23. secondary side effects?
24. examples of inhaled corticosteroids?

specific corticosteroids...
25. indication for beclovent?
26. 2 mechanisms of action for beclovent?
27. beclovent's effect on bronchial smooth muscle?
28. oral side effect of inhaled beclovent?
29. indications for prednisone?
30. side effects of prednisone?

leukotriene inhibitors...
31. mechanism of action?
32. two examples?
33. indications for leukotriene inhibitors?
34. zafirlukast used more commonly in which population?
35. side effects?
36. inhibits which other enzyme?

antitussives...
37. mechanism of antitussives?
38. codeine is broken into...
39. side effects?
40. what does the DM in robitussin DM stand for?
41. what class of drug is DM?
42. how do DM antitussives compare to narcotic analgesic tussives in terms of side effects?

antihistamines...
43. MAO of benadryl?
44. benadryl relationship with BBB?
45. why is benadryl contraindicated for asthma?
46. example of a non-drowsy antihistamine?
47. MAO of [46]?
48. how is [46] non-drowsy?
49. common side effect of [46]?

nasal sprays...
50. two examples of nasal corticosteroids?
51. mechanism of action?
52. side effects?
53. two examples of nasal alpha-agonists?
54. most significant side effect?

answers
1. sympathetic= bronchodilation. parasympathetic= bronchoconstriction.
2. bronchodilators and inflammation suppressors.
3. emergent treatment of asthma, status asthmaticus, anaphylaxis.
4. beta-2 adrenergic receptor stimulation leads to increased cAMP levels leads to smooth muscle relaxation and bronchodilation.
5. B-1 agonist effects include tachycardia, anxiety, arrhythmias, palpitations. alpha-1 agonist effects include dry mouth and hyperglycemia.
6. subcutaneous, IV, IM, inhalation, endotracheal tube.

7. beta-2 agonist causes increased cAMP levels resulting in bronchial smooth muscle dilation.
8. periorally-- 30 minutes onset and 4-8 hour duration. inhaled-- 15 mins onset and 2-3 hour duration.
9. spacer which allows for smaller, slower velocity particles.
10. for long term treatment of asthma.
11. 20-30 min onset, 12 hour duration.
12. headache, cough.

13. atropine from belladonna.
14. competitively antagonize AcH at muscarinic receptor sites, resulting in sympathetic bronchodilation.
15. maintenance as opposed to acute cases.
16. ipratropium / atrovent.
17. theophylline.
18. methylxanthine / xanthines bronchodilators.
19. caffiene.

20. inhibition of phospholipase A2 which blocks the release of arachidonic acid, the precursor of inflammatory mediators. also inhibits histamine and kinin activity.
21. chronic.
22. starts to shut off the HPA feedback loop for cortisol production
23. increased susceptibility to infections, hyperglycemia, bone loss, insomnia.
24. beclomethasone / beclovent , vanceril.

25. when asthma can not be controlled by bronchodilators.
26. decreasing activity for inflammatory cells (macrophages, eosinophils, t lymphocytes), decreases capillary permeability.
27. no direct effect on smooth muscle.
28. oral thrush.
29. COPD, worsening asthma.
30. fat redistribution, hyperglycemia / diabetes, osteoporosis, addisonian crisis.

31. blocking leukotriene receptors (E4, D4) in bronchial smooth muscle.
32. zafirlukast / accolate, montelukast / singulair.
33. chronic asthma, prophylaxis.
34. pediatrics.
35. headache, GI upset, increased respiratory infections in older populations.
36. cytochrome p450 enzymes.

37. decreases sensitivity of medullary cough centers.
38. morphine.
39. drowsiness, constipation, GI upset, dependence.
40. dextromethorphan.
41. morphine derivative.
42. DM less addictive, less constipation.

43. blocking H1 receptors.
44. readily crosses BBB.
45. because benadryl will dry and thicken secretions and asthma needs moistening and mucolytics.
46. claritin / loratadine.
47. same as [43].
48. doesn't cross BBB.
49. dry mouth. dryness of mucous membranes.

50. beclomethasome / beconase
budesonide / rhinocort
51. decreases inflammatory mediators in nasal mucosa.
52. irritation, nose bleeds, sore throats, candidiasis.
53. phenylephrine / afrin
oxymetazoline / long acting afrin
54. rhinitis medicosum: rebound effect after taking nasal alpha agonists.

pharmacology: antihypertension drugs

2010-10-04T10:37:00.000-07:00

this pharm lecture focused on the conventional medications designed to control blood pressure, of which there are many. the first category is diuretic medications, controlling blood pressure by modifying the kidney's filtration functioning. thiazide diuretics such as hydrodiuril act on the thick ascending loop and early distal tubule to inhibit sodium and chloride reabsorption, thereby increasing water excretion and lowering blood pressure. they also increase calcium and uric acid levels by acting on the proximal tubule. thus, the side effect of thiazide diuretics are hypokalemia, hyponatremia, and hypercalcemia / hyperuricemia. they are commonly used in conjunction with ACE inhibitors and beta blockers.

loop diuretics such as lasix are the most potent of all the types of diuretics and work by blocking the Na/K/Cl cotransporter system in the loop of Henle. they have similar side effects to thiazide diuretics; hypokalemia, hyponatremia, etc. in terms of potency, they are stronger than thiazide diuretics and thus the preferred diuretic in renal disease or hypertensive emergencies.

potassium sparing diuretics such as aldactone inhibit sodium / chloride reabsorption but also promote potassium reabsorption and therefore are sometimes used in conjunction with potassium wasting diuretics such as loop diuretics. it is a direct antagonist to aldosterone. because of the potential for hyperkalemia these medications should be avoided in patients who are taking potassium supplements, or other medications that raise potassium levels such as ACE inhibitors or ARB's.

these diuretics all work by promoting the excretion of fluid from the kidneys, thereby reducing the body's total fluid volume and thus lowering blood pressure. another mechanism that is used to lower blood pressure is via blocking the beta-2 receptors in the heart, which ultimately lowers cardiac output and therefore lowers blood pressure. "beta blockers" such as propanolol are non-specific, meaning they will also affect the beta receptors on peripheral vasculature, causing dilation, as well as the beta receptors on bronchial smooth muscle (the same ones that asthma medications seek to stimulate), causing bronchoconstriction. thus these medications must be used cautiously with patients who have respiratory issues. even the never, "cardio-selective" atenolol which preferentially seeks the beta-2 receptors in the heart also cause non-selective effects at higher doses. all beta blockers can cause CNS depression, sexual dysfunction, and bradycardia-- if acute episodes occur, this can be treated with glucagon, which antagonizes beta blockers' effects between the SA and AV node.

another class of drugs, alpha-1 adrenergic antagonists, block the alpha-1 receptors on peripheral vasculature smooth muscle to cause dilation, which causes a decrease in total peripheral resistance, thus lowering blood pressure. BPH patients might also be benefitted by the relaxation of the bladder neck / prostate. prazosin / minipress is an example, as well as reserpine (which is derived from the alkaloids of rauwolfia).

calcium blockers work by blocking the influx of calcium into smooth muscle cells of the peripheral vasculature as well as cardiac muscle cells, promoting relaxation and dilation, thereby lowering peripheral resistance. they might also have a "negative inotropic effect", which can diminish cardiac output - thus care is needed when administering to patients with CHF or bradycardia. verapamil / isopten is one example, and is indicated for hypertension, CHF, and angina-- in particular, atypical angina due to vasospasm. calcium blockers can be sometimes be used in combination with beta blockers in order to wean a patient off of beta blockers, which have much more severe withdrawal symptoms in the form of rebound hypertension, etc.

there are a couple classes of drugs that work on the renin / angiotensin system- first is the ACE inhibitors (angiotensin converting enzyme inhibitors). as the name suggests, these drugs block the conversion of angiotensin I to angiotensin II, a hormone that facilitates water retention on a large scale in the body. they are particularly effective for diabetics with hypertension due to their actions to counteract diabetic nephropathy by reducing glomerular capillary pressure. ACE inhibitors tend to raise K+ levels, thus one must not use a potassium sparing diuretic in combination, although other diuretics seem to potentiate their actions. the other mechanism that ACE inhibitors have is to prevent the degradation of bradykinins, which leads to a common side effect of a dry cough, since bradykinins stimulate the medullary cough reflex.

other drugs that works with the renin / angiotensin system are angiotensin II receptor blockers such as losartan / cozaar. although the mechanism is different (blocking the receptors as opposed to blocking the conversion of angiotensin II, and no bradykinin involvement) the profile is similar to ACE inhibitors in that they are good for diabetic patients with hypertension, can cause hyperkalemia, and are contraindicated in pregnancy.

questions
introduction...
1. how does "hypertension beget hypertension"?
2. mechanism of thiazide diuretics?
3. indication of thiazide diuretic?
4. thiazide diuretics often used in conjunction with...
5. what occurs at the proximal tubule with thiazide diuretics?
6. thiazide side effects?
7. examples of thiazide diuretics?
8. what supplement in recommended with thiazide diuretics?

loop diuretics...
9. example of loop diuretic?
10. physiological mechanism?
11. side effects of loop diuretics?
12. loop diuretics are the preferred form of diuretics for...
13. loop diuretics can be used to treat what other condition?
14. how do loop diuretics compare in strength to other diuretics?
15. lasix should be avoided in patients with what allergy?

potassium sparing diuretics...
16. example of a PSD?
17. mechanism of action?
18. direct antagonist to...
19. avoid use with patients who are on...

beta blockers...
20. general mechanism of action?
21. if the beta blocker is non selective, what other effects might it have?
22. which beta blockers are selective and which are not?
23. disadvantages to beta blockers?
24. why is abrupt discontinuation not recommended?
25. besides hypertension / cardiac symptoms, what else is propranolol used for?
26. what can be administered to counter the effects of a beta blocker induced acute bradycardia?

alpha-1 adrenergic antagonists...
27. example of an alpha antagonist?
28. mechanism of action?
29. how can these medications additionally benefit patients with BPH?
30. what is an herb that has alpha-1 adrenergic effects?

calcium channel blockers...
31. mechanism of action?
32. what is the "negative inotropic effect"?
33. what is an example?
34. what are the specific indications for [33]?
35. side effects?
36. how do rebound effects compare for calcium vs. beta blockers?

ACE inhibitors...
37. two mechanisms for ACE inhibitors?
38. ACE inhibitors often the drug of choice in treating...
39. least likely of the anti-hypertensives to cause...
40. effect on electrolytes?
41. ACE inhibitors work well in combination with...
42. number one side effect? why?
43. other side effect?
44. pregnancy?

angiotensin II blockers...
45. how does the mechanism differ from ACE inhibitors?
46. example of an AII blocker?

direct vasodilators...
47. mechanism of action?
48. examples of direct vasodilators?
49. side effects for the first example in [48]?
50. side effects for the second example in [48]?

answers
1. prolonged hypertension results in smooth muscle hypertrophy and proliferation in arterioles, which increases total peripheral resistance, thereby raising blood pressure.
2. inhibit sodium and chloride reabsorption in the thick ascending loop and early distal tubule, thereby increasing sodium and water excretion in the urine.
3. mild hypertension with chronic edema.
4. beta blockers and ACE inhibitors.
5. holding back of calcium and uric acid.
6. decreased Na, K, Mg. increased Mg, Ca.
7. hydrochlorthiazide / hydrodiuril.
8. potassium.

9. furosemide / lasix.
10. block the Na/K/Cl cotransporter system in ascending loop of henle.
11. hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hyperglycemia, hyperuricemia.
12. patients with renal disease and hypertensive emergencies.
13. hypocalcemia.
14. generally stronger.
15. sulfonamide allergies.

16. spironolactone / aldactone.
17. inhibits Na/Cl reabsorption while promoting potassium reabsorption.
18. aldosterone.
19. ACE inhibitors, potassium supplements, ARB's.

20. reduce beta-1 receptors in the heart, causing decreased cardiac output.
21. if it affects beta-2 receptors, peripheral vasculature will be dilated and bronchial smooth muscle will constrict.
22. propanolol is non-selective, atenolol is.
23. CNS effects, sexual dysfunction, bradycardia.
24. because of rebound tachycardia / hypertension due to upregulation of beta receptors during the period of medication.
25. stage fright and migraine headache prophylaxis.
26. glucagon-- blocks the beta blocker action between the SA and AV node.

27. prazosin / minipress
28. blockage of alpha-adrenergic sites in peripheral vasculature causes dilation.
29. relaxation of smooth muscle around bladder neck and prostate, allowing urine to pass more easily.
30. rauwolfia alkaloids have peripheral adrenergic blocking effects.

31. blockage of influx of calcium into smooth muscle cells around peripheral vasculature as well as cardiac cells causes dilation, thereby lowering peripheral resistance.
32. a side effect of calcium channel blockers-- decreased cardiac output. thus these medications might be contraindicated for patients with CHF or bradycardia.
33. verapamil / isopten
34. hypertension, angina (especially atypical), CHF
35. flushing, headache, hypotension.
36. calcium blocker rebound effects are much less.

37. 1) block conversion of angiotensin I to angiotensin II. 2) prevent degradation of bradykinins, reducing peripheral vascular resistance.
38. diabetic patients with hypertension.
39. sexual dysfunction in males.
40. tends to increase potassium levels.
41. diuretics.
42. dry irritating cough, due to bradykinin stimulation of the medullary cough reflex.
43. angioedema, especially of tongue and oropharyngeal area.
44. never-- category X.

45. block the angiotensin II receptors, and no involvement of bradykinins.
46. lozartan / cozaar.

47. opening potassium channels in vascular smooth muscle.
48. minoxidil, hydralazine.
49. hirusitism.
50. drug induced lupus syndrome.

pharmacology: antilipidemics

2010-10-02T19:54:00.001-07:00

this lecture went into the conventional antilipidemic drugs, indicated when patients have high cholesterol levels (high LDL, low HDL, or high total cholesterol levels). there are five classes of antilipidemic drugs: niacin, fibrates, HMG-CoA reductase inhibitors, bile acid binding resins, and cholesterol absorption blockers. The first category, niacin, is given in the form of Vitamin B3, or alternatively, inositol hexaniacinate (considered safer both in the short and long term). niacin is thought to decrease VLDL production in the liver as well as increase its clearance in the serum.

fibrinates, a class of drugs that are derived from fibric acid, are mainly indicated for high TG levels; their main action is to lower TG levels, while also raising HDL levels. the side effects might include liver damage, gallstones, GI upset, myalgias, and rhabdomyolysis. the main fibrinate is called gembibrate / lopid, and it is contraindicated in patients with preexisting liver or gall bladder problems.

statin drugs are a popular category of antilipidemics that act on the HMG-CoA reductase enzyme, which is the first enzyme in cholesterol synthesis. although statins are effective at lowering cholesterol levels, they are not without side effects, the most common being muscle soreness / weakness, thought to be related to HMG-CoA's involvement in CoQ10 synthesis. a severe side effect is rhabdomyolysis which might lead to acute renal failure in some cases. GI symptoms and erectile dysfunction are two other potential side effects from statins as well. they are contraindicated in patients with liver disease, as well as in pregnancy and lactation, and may interact with fibrinates, anti-fungals, macrolides, protease inhibitors. statins can also be used prophylactically during MI's, strokes, or episodes of unstable angina, especially in DM II patients.

the next class of antilipidemics are bile acid sequestrants, which bind to bile salts and form insoluble complexes which are excreted in the feces. the net effect is cholesterol excretion in the stool and secondarily, lowering of LDL blood levels due to a compensatory upregulation of LDL receptors. questran is an example-- side effects include constipation, bloating, and malabsorption of fat soluble vitamins, folic acid, or other medications.

the last class is cholesterol absorption blockers, which are used in conjunction with statins when their cholesterol lowering actions are insufficient. the main side effect is diarrhea (although myalgias and arthralgias can also occur), requiring patients on these medications to wear dark pants and panty liners when starting these medications. along with bile acid sequestrants, cholesterol absorption blockers are considered category C for pregnancy; underresearched and not recommended.

questions
introduction and niacin...
1. how do change in percentage levels of HDL and LDL affect myocardial infarction risk?
2. what are the five categories of antilipidemics?
3. what does niacin do that is unique among lipid lowering medications?
4. what are the longer term side effects of niacin?
5. two potential MOA's for niacin?
6. what tests might be monitored in patients on niacin?
7. niacin is contraindicated in...
8. what is currently considered the safest form of niacin?

fibrinates...
9. what are the actions of fibrinates?
10. side effects?
11. examples of fibrinates?
12. main indication for fibrinates?
13. contraindicated in...

statin drugs...
14. what is the enzyme blocked by statin drugs? what does it do?
15. most common complaints from statin users?
16. severe potential side effect of statins? what might be a complication?
17. what is a potential mechanism for statins' relationship to rhabdomyolysis?
18. side effects besides [question 15]?
19. contraindications for statin drugs?
20. potential drug interactions?
21. examples of statin drugs?
22. besides cholesterol lowering, what else are statin drugs indicated for?
23. what lab test might be run if rhabdomyolysis is suspected in a patient taking lipitor?
24. lipitor contraindicated in...

bile acid sequestrants...
25. general mechanism of action?
26. how do bile acid sequestrants lower LDL levels?
27. often used in conjunction with...
28. example of bile acid sequestrants?
29. side effect of [question 28]?
30. use in pregnancy?

cholesterol absorption inhibitors...
31. example of a CAI?
32. often used in conjunction with what other class? when?
33. side effect of CAI's?
34. use in pregnancy?

answers
1. 1% increase in HDL decreases MI risk 3-4%. 1% decrease in LDL decreases MI risk 2%.
2. niacin, firates, HMG-CoA reductase inhibitors, bile acid binding resins, cholesterol absorption blockers. [never forget his bad cholesterol]
3. lowers alpha-lipoprotein(a) levels.
4. liver damage
retinal damage
gout
rhabdomyolysis [liver, eye, uric, muscle] [See Ur Life Strength vanish]
5. mainly unknown, but may be related to decreased VLDL synthesis in liver and increased VLDL clearance in plasma.
6. liver function and glucose.
7. DM, liver disease, peptic ulcer disease.
8. inositol hexaniacinate.

9. decrease liver's TG production, increase HDL levels.
10. liver damage / gall stone formation
nausea / diarrhea / GI upset
rhabomyolysis / myalgias
[LV/GB, ST/SP, PC/TB] [wood, earth, fire]
11. gemfibrozol / lopid, fenobibrate / lofibra. [stupid gemstone, lofi fennel]
12. elevated TG levels.
13. pre-existing GB/LV disease.

14. HMG-CoA reductase, the enzyme that catalyzes the first step of cholesterol synthesis.
15. muscle soreness and weakness.
16. rhabdomyolysis which might lead to acute renal failure.
17. HMG-CoA is also involved in CoQ10 production, which is an enzyme involved in oxidative phosphorylation-- ultimately interfering with muscle cell function and contributing to their degeneration.
18. abdominal pain / nausea / diarrhea
headache
erectile dysfunction
19. liver disease, pregnancy, lactation.
20. fibrinates, macrolides, oral antifungals, protease inhibitors. [mac pro: filled with fungus fiber]
21. atorvastin / lipitor
fluvastatin / lescol
lovastatin / mevacor
22. prophylaxis during MI's, stroke, unstable angina, especially in DM II patients.
23. CPK levels.
24. pregnant women-- category X.

25. bind cholesterol and form insoluble complexes which are ultimately excreted.
26. a compensatory mechanism increases the number of LDL receptors, thereby removing LDL from blood.
27. niacin.
28. cholestryramine / questran
29. bloating, constipation, malabsorption of fat soluble vitamins, folic acid.
30. category C; not adequately studied, but recommended to avoid use.

31. ezetimibe / zetia.
32. statins, when they aren't working to lower serum cholesterol.
33. diarrhea, myalgias, arthralgias.
34. category C.

homeopathy III: calc carb

2010-09-27T14:07:00.000-07:00

here are some study questions for the remedy we studied this week: calc carb. the remedy is essentially depicted by an overweight, overworked, task oriented person.

questions
1. calc carb is made from...
2. which miasm does calc carb belong to? how does it match the miasm's character?
3. two words that capture the essence of the calc carb state?
4. calc carb's world is seen as a series of never ending...
5. greatest fear is...
6. relationship to insanity?
7. relationship to change?
8. fast or slow?
9. weakness of ...
10. unique language trait?
11. food cravings?

12. one word that describes the physical disposition?
13. temperature disposition?
14. difference of temperature of calc carb children and adults?
15. ability to exercise?
16. better with what form of human contact?
17. time of day that aggravates?
18. how are the joints affected?

19. two body types?
20. head characteristics?
21. headaches from...
22. another prominent symptom related to HEENT?
23. throat symptoms?
24. eyes?
25. ears?
26. type of mucous?
27. mouth?
28. dentition?

29. appetite/thirst?
30. cravings?
31. averse to which foods?
32. BM's?
33. all arthritic pains aggravated by...
34. what do calc carb's do with their feet at night?
35. respiratory symptoms?

36. females: major remedy for...
37. aggravated or ameliorated by coition?
38. sleep is characterized by...
39. wrinkles on face?

40. infants and consolation?
41. kent described a circle of which remedies?

answers
1. inner lining of oyster shell.
2. psora-- a remedy of weakness, insecurity, anxiety.
3. overwhelmed and overexertion.
4. tasks.
5. inability to function, leading to a piling up of work.
6. fear of going insane, but rarely actually insane.
7. aggravated by change.
8. slow.
9. mind.
10. may "confound" words.
11. soft eggs, chalk, dairy products.

12. leucophlegmatic.
13. cold, aggravated by cold.
14. children are generally warmer than adults.
15. worse with any exertion.
16. touching, rubbing, scratching.
17. 1-3pm.
18. low back pain and arthritis.

19. overweight type that gets winded easily. or thin sun laborers with wrinkles on face.
20. perspiration on occiput.
21. eyestrain, overexertion, being chilled.
22. vertigo.
23. swollen glands, sore throat, swollen tonsils.
24. sticky discharge, glandular feeling, blocked tearducts in infants.
25. all types of otitis.
26. thick, yellow.
27. apthae, canker sores, thrush.
28. may be delayed in children.

29. big.
30. sweets, soft eggs, salt, cold drinks, milk, oysters, ice cream, cheese.
31. meat, spicy foods, milk, fat.
32. constipation without urgency, or diarrhea from malabsorption or allergies.
33. cold / damp.
34. put socks on initially then take them off in the middle of the night because their feet are burning hot.
35. tubercular.

36. menorrhagia.
37. aggravated.
38. nightmares, especially in children. insomnia due to thinking about tasks for next day.
39. vertical and horizontal, forms square in lean types.

40. aggravated by consolation.
41. calc carb to lyc to sulphur.

homeopathy III: aurum

2010-09-19T14:48:00.000-07:00

the first class of homeopathy III with Dr. Elmore. besides the orientation spiels we went over two case studies that demonstrated key aspects of the homeopathic remedies aurum and nat mur, which are fairly similar. the first case was a 31 year old female that came initially complaining about her allergies, but further questioning revealed deep stress, mainly centering around a dysfunctional marraige--to a man she married almost out of obligation, because he could pay off the massive debt she had accrued. although she couldn't stand him (in fact spent every night outside because she didn't want to be in the house with him), she felt that leaving him would be a betrayal and thus had been living in distress the entire marraige. her current state was one of profound depression to the point of suicidal notions, which she kept from others. she had lost her "inner light", which only came back when thinking about leaving her husband. another poignant aspect of her character was that as a young child, she took care of younger siblings after the mother abandoned the family.

the fastidiousness, emotional insularity and feelings of loyalty and betrayal were all indicative of nat mur, but it was then revealed to the class that this patient also loved the sun, which is decidedly not characteristic of nat mur-- instead, the remedy given to this patient was aurum, which is apparently the leading remedy for patients with suicidal tendencies. aurum patients hold themselves to extremely high standards and have to do things right in all aspects of their lives. the combination of their idealism and suicidal notions (losing the fear of death) makes teenagers the most likely aurum patients. here are some study questions based on Dr. Elmore's readings of aurum:

questions
1. central theme of aurum is...
2. personality type?
3. two remedies that might be confused with aurum?
4. miasm?
5. how does the miasm physically manifest?
6. how does the miasm manifest mentally / emotionally?
7. suicidal thoughts may arise in aurum patients when...

8. occupation ameliorates or aggravates?
9. how much do aurum patients share of their suffering to others?
10. relationship to religion?
11. relationship to death?
12. aurum state might be brought on by loss of...
13. aurum patient can't stand...
14. aurum imagines that... resulting in...
15. relationship to physical pain?

16. relationship to music?
17. what time of day aggravates aurum patients?
18. relationship to sunshine?
19. sleep?

20. nasal symptoms?
21. aurum is a main remedy for which HEENT disorder?
22. eye symptoms?
23. affect on glands?
24. testicles?
25. uterus?
26. chest symptoms?

27. in what particular way are aurum children similar to nat. mur children?
28. relationship to friends?
29. time course of aurum?
30. what are the salts of aurum?

answers
1. depression and loathing of life.
2. perfectionists.
3. nux vomica and natrum muriaticum.
4. syphilitic.
5. destruction of bones and tissue.
6. depression, suicidal thoughts.
7. in a high place or any other precarious situation.

8. ameliorates.
9. nothing; others may not know of their suffering at all.
10. despair of religious salvation -- praying for hours on end.
11. no fear of death, desires death.
12. finances or property.
13. contradiction.
14. he neglected his duty, resulting in guilt.
15. intense pain, causing suicidal thoughts.

16. often ameliorates.
17. sunset to sunrise.
18. desires sunshine.
19. insomnia.

20. boring pain at the root of the nose.
21. mastoiditis.
22. photophobia, corneal ulcers, conjunctivitis, sore / bruised sensation. [look-- PCC]
23. swelling and hypertrophy.
24. swelling and indurated, especially right side.
25. prolapse due to heaviness and congestion of uterus.
26. dyspnea, asthma, angina.

27. easily hurt.
28. few friends, doesn't share much with them.
29. since it is a metal remedy, takes a longer time to act.
30. aurum arsenicum, muriaticum, iodatum, sulphuricum [ars mur iod sul] [aura of siam]

two down, four to go

2010-08-11T12:29:00.000-07:00

just did a little redesign on this site and scanning over the entries from the past two years made me think about how fast the time has gone. i'm 1/3 of the way through my education here at NCNM and as expected, it feels like i both got here yesterday and that i've been here for a decade. here are some little tidbits of knowledge i've gleaned over these two years.

• portland is full of coffeeshops, bikers, and naturopathic clinics
• the kidneys are complicated. the liver is complicated. all of our organs are little universes that for the most part, defy our comprehension
• the first two years of studying naturopathy is essentially cramming as much basic science information into one's head as humanly possible
• the most impressive clinicians (to me) are the ones who are flexible with their ideas and able to navigate their body of knowledge with agility
• homeopathy is an impossible thing to represent accurately
• botanical medicine is much more empirical than one might imagine
• there are people in my school that are exceedingly knowledgeable and competent and can compare to some of my best college professors
• there are people in my school that i wouldn't trust to change my toilet paper
• coffee doesn't really help anything, ever
• meditation helps everything, always
• jumping into cold water outside is one of my favorite things to do now
• the onslaught of information in the first two years can suppress the desire to ask questions about material. it's difficult enough to just ingest the material, let alone digest it well and ask an intelligent, probing question.
• spinal adjustments are extremely satisfying to perform
• the "etiology" of the majority of pathological conditions is unknown or poorly elucidated at best, even in conventional textbooks
• doing massage (shiatsu, in my case) has proven to be essential as a supplement for learning about the muscles and bones and rhythms of the body during these two years
• relationships never turn out how you plan them
• my impression so far of what naturopathy aims to be: [naturopathy] = [conventional medical knowledge] + [herbal and energetic modalities] - [symptom suppression techniques]

chinese cosmology III: notebook project

2010-08-11T11:56:00.000-07:00

1
this semester we learned about the four "humanity" organs: pericardium, triple burner, gall bladder, and liver. this painting shows the organ clock and the positions of these four organs, starting with pericardium at the rightmost position, representing lunar month 9 and 7-9PM, and ending with liver in the leftmost position, representing lunar month 12 and 1-3AM. each position has an association with an earthly branch, which itself has an association with an element.

earthly branches
pericardium: xu (earth)
triple burner: hai (water)
gall bladder: zi (water)
liver: chou (earth)

the red lines represent the 6 conformation correspondences. pericardium and liver are part of the jueyin wood conformation, while triple burner and gall bladder are part of the shaoyang fire conformation.

each organ is also assigned to a zang fu pairing, which has its own elemental association. thus, each organ is associated with three different elements: 5 element, 6 conformation, and 12 earthly branches. they are as follows:

pericardium: fire / wood / earth
triple burner: fire / fire / water
gall baldder: wood / fire / water
liver: wood / wood / earth

2
the pericardium is full of gate symbolism, which this painting represents. on a physiological level, the pericardium's job is to protect the heart from external pathogens, and its meridian wraps around the heart like a barrier. acupuncture point PC6 is aptly named "the last door before the emperor". the protection that the pericardium provides might be seen as analogous to the blood brain barrier's function in western medicine.

the pericardium's close relationship to the heart is also suggested by its three names: xin bao (the sac around the heart), xin zhu (heart master / that which sees mastership of the heart), and dan zhong (surrendered minister that follows commands that others will not).

on an emotional level, the pericardium is thus involved with romantic relationships, about intimacy. there are two pathologies associated with intimacy that are represented by the red horizontal arrows in the painting. on the one hand, there is the pathology of being closed off to one's emotions and overly intellectual, achieving a Kafka-esque neuroticism in relationships.

on the other hand, there is the pathology of having the gates to one's heart constantly flung open and having no barrier to new and potentially harmful relationships. prostitution is a crystallized example of this pathology. thus the pericardium must be looked at when addressing trauma related to intimacy (as opposed to the bladder, which is more associated with general emotional trauma).

the arrow pointing upwards represents the fact that achieving balance within romantic relationship along the pericardial axis will allow the partners use the relationship in its full potential; as a vehicle for divine connection, an enhanced experience of unity with the universe.

3
the tidal hexagram associated with the pericardium is hexagram 23, the character of which implies, "stripping naked", or "peeling off the peel". the time of day associated with the hexagram is 7-9pm, a time when intimacy between partners occurs; a time for stripping naked. (the theme of intimacy is also depicted in the river zhang, which is made up of two rivers that end up interweaving together)

the time of year, month 9, also has a similar energy; during this time, nature "sheds its clothing", and the leaves on the trees that turned brilliant colors during autumn now start to wither and fall to the ground. during this time nature "has only one goal-- to conserve the life force" and pump everything underground in preparation for the wintertime.

the ninth month is also traditionally the month for marriage, another tie in with the theme of romantic union. one of the pericardium's archetypes is the pure female virgin about to get married, which is on an axis opposite the clock pair of the pericardium, the stomach-- whose archetype is the hormonal, debaucherous teenage male.

4
the stellar constellations associated with the pericardium are also associated with the same themes of intimacy and heart protection. all three refer to spots on a constellation of a dragon-- fang, the breast of the dragon, di, the chest of the dragon, and xin, the heart of the dragon.

the strong connection to the chest and breast within these constellations is indicative of the pericardium's energetic connection to the breasts; breast cancer is oftentimes a pericardium pathology. in fact, hormonal function in women in general can partly be attributed to the pericardium, although some other organs might be more closely associated. uterine fibroids is another example of a hormonally based pathology that is associated with the pericardium.

the character for fang also refers to the ancillary chambers of a house, where sex with concubines with occur. sex therefore has a strong association with the pericardium. incidentally, the animal associated with the pericardium is the dog, whose genitals are used in sex tonics. scorpio, the western counterpart to the pericardium time of year, is also notably associated with strong sexual energy.

5
this painting represents the triple burner's elusive function in the body, which is perhaps the most difficult organ to depict because it basically has no single analogue in simple anatomical terms. in general, triple burner is the function within the body that serves to connect the spaces between cells and organs. accordingly, the painting represents two of the many examples of triple burner manifestations in the body; the lymph channels, draining fluid from the extracellular matrix around cells, and the nervous system, connecting and coordinating all parts of our body to our central command center.

the middle channel represents the river luo, which is the river that is purported to hub together the other rivers (acting similar to the nervous system), as well as a drainage canal for the yellow river (acting similar to the lymph channels)

the triple burner's networking function can be seen in personality traits as well; the person with a triple burner personality is the "networker"-- in a group setting, this person connects everyone to each other and knows everyone. sometimes this function can be pathological and come at the expense of knowing true intimacy, resulting in a charismatic, sociable mask covering up a loneliness that only that person knows.

6
the triple burner is not only involved with connecting on a horizontal level, within one system, but it is also involved in connecting on a vertical, hierachical level. it is in charge of connecting with the universe, the microcosm with the macrocosm. this painting depicts the state that must be realized to achieve this connection; wu wei-- doing without doing, in the flow.

the person in bed represents the time associated with the triple burner, 9-11, a time when nature takes us into sleep, which is the ultimate wu wei state. our bodies are completely relaxed, our breathing gets deep and slow, and we merge with our subconscious, at the very least.

in the middle of the flow is the tidal hexgram associated with the triple burner, hexagram 2. this hexagram is "kun", and its meaning is again "in the flow". it is also a symbol of a grave and related to peaceful awareness of death, that is afforded by the unity of the wu wei state. (a metaphor for the TB function of proper transition / awareness of death is the structure of the pyramids; the long passageways into the pyramids and the elaborate, temple-like interiors suggest a transition with the next realms, rather than a hiding from them.)

the two dots on either side of the flow in the painting represent the stellar constellations wei and ji, which are on either side of the milky way, and also part of the milky way, representing the theme of "in the flow" as well.

7
this painting represents two examples of the relationship between the triple burner and the other organs. the bladder and the triple warmer can both be likened to the roots on a tree, but the bladder is more the large taproot (as it is concerned with circulating energy up the spine in the microcosmic orbit), whereas the triple burner is represented by the root network that connects adjacent plants.

secondly, the kidney and the triple burner can be represented by a battery (or spark plug) and a circuit; the kidney is the central power source and the triple burner provides the channels in which energy can flow. the kidney and triple burner are the pair most closely associated with adrenal function in western medicine. thus some states of adrenal fatigue can be related to these organ networks (although many cases are conflated with thyroid dysfunction).

8
the tidal hexagram of the gall bladder is hexagram 24: fu. it has one yang line under 5 yin lines and represents the energetic momentum at this time of year; yang is returning. the hexagram, when split into two trigrams, also represents thunder under the earth, which is represented by the painting.

the bottom layers of the painting represent the thunderous yang energy deep under the earth. each layer gets progressively more tame, and by the time the surface is reached, the manifestation of what is deep underground is simply rolling hills. the hilly landscape is also reminiscent of gansu province, which the gall bladder's river wei is purported to come from. this province is full of desert like landscapes full of burial mounds that poke up like hills; suggestive of a force about to burst from underneath.

the valleys between the hills in the painting are also suggestive of vertical caves-- caves are an important part of gall bladder symbolism. nature is beginning to come out of the caves during this time of year, out of hibernation. the life force reached the deepest place in the previous month and now is beginning to push back upwards.

9
the gall bladder's emotional function is highly related to decision making; the initial drive that starts a process. people who are unable to make a decision are likely to have a deficiency in the gall bladder network. it is also linked with leadership styles. this painting represents the clock pairs of gall bladder and heart, which form an axis that depicts two styles of leadership. on the one hand, heart leadership is wise, loving, and prioritizes the connection with all members of the group. on the other hand, gall bladder leadership is pushy, about efficiency and organization, and about making decisions rapidly. (the pushy nature of the gall bladder leader is mirrored in part by the gall bladder's physiological function; it serves to move energy in the body and flush out phlegm.)

these two styles are represented by the bamboo leaves- the heart bamboo leaves are falling downwards, representing the more relaxed heart leader and the gall bladder leaves are pushing upwards, representing the wood nature of the gall bladder leadership. bamboo in general might be an archetype for the wood organs, as it is rapidly growing, yet highly flexible. it is also hollow in the middle, which points to the heart function of being an "empty vessel", not having any private agenda as a leader.

another archetype of the gall bladder is the "jihad official". this official has a flag with truth written on it; as the name implies, this truth is often radical or cultish, and the official pursues it with the devotion of a cult leader. thus those who have a tendency to follow charismatic religious leaders or dive into esoteric religious beliefs might be related to gall bladder dysfunction.

10
this painting depicts an old myth about how the months were set in the zhou dynasty; all the animals were lined up on one side of a river and it was determined that the first animal to cross would be assigned to the first month. as the story goes, the rat, in all its cleverness, asked the ox for a ride across, and just as the ox was about to reach the other shore, jumped off and won the contest. the rat thus represents the gall bladder energy of cleverness. incidentally, the gall bladder meridians zig zag along the brain, furthering the mind connection.

the rat and the ox are also the animals for the gall bladder and liver, which are intricately related. if the gall bladder is about the initial push, the liver is about long term endurance. another notable relationship is the gall bladder and the small intestine: both are related to one's internal compass, but the SI has more of a mental, spiritual focus while the gall bladder has more of a visceral nature.

11
in contrast to the triple burner's maxim of "in the flow", the livers energy is decidedly "against the flow", as this painting depicts. hexagram 19 is the tidal hexagram associated with the liver and has two yang lines pushing up against 4 yin lines, and the chinese character means "to advance". the liver thus represents endurance, working for work's sake, without necessarily seeing the light at the end of the tunnel.

the river associated with the liver is the river sheng, which, unlike all the other rivers in china, flows east to west, against gravity. (a side note-- this river is also full of toads, which symbolically represent the liver's detoxifying properties, as toads have mucous membranes on the outside and are highly susceptible to environmental toxicity)

the liver's elemental associations for the five element and six conformation systems are both wood; further exemplifying the quality of pushing against the flow. the energy of the jueyin wood network might represented well by a single blade of grass pushing up towards the sun, bringing water upwards against gravity.

in this painting the liver energy is represented by the single red fish, swimming against the flow of the school of black fish.

12
the endurance that is associated with the liver is a womanly endurance. this painting depicts the symbol for a woman with many complex symbols inside of it, which represent the hormonal reality that renders the female body capable of feats of endurance such as childbirth. the arrow to the right represents the drive to go forward as well as suggesting that this quality might be channeled in males as well, although our physiologies might be different.

however, there is a stronger association with the female archetype than the male with the liver. another connection: the emotion associated with the liver is anger, and the character associated with anger depicts a woman being suppressed-- suggesting that the essence of liver anger is the heart of a suppressed woman, about to burst forth. also, the source of prenatal energy in women is the liver (and the kidneys in men).

xi wang mu is an archetypal liver woman character; a legendary tribal leader who led her tribe with eternal youthfulness and shamanistic wisdom. she was also, according to myth, wore a leopard mask, and howled at the moon-- representing perfectly the physiological qualities of "nu"-- healthy emotional expression.

the ox is yet another symbol of the endurance that liver energy represents; it toils in the fields tirelessly and as the jueyin conformation suggests, works best when pulling against some resistance. as mentioned before, while the gall bladder is important for making initial decisions, the liver is crucial for carrying out plans long term. the liver is therefore also represented by the general, the official in charge who plans and strategizes and delegates orders to the gall bladder's platoon seargent, who then executes the orders on the ground.

13
this painting represents some of the energetic functions of the liver in the body. the red drops and flow represents the blood, which the liver has a pivotal role managing. the liver can be likened to a manager in a warehouse of blood, ushering the blood in and out when needed. the three drops of blood in each outlet represent three substances; blood, tears, and hormones (as described above the liver has a close connection with hormones, and tears are an expression of emotional reality made possible by hormones, and contain hormone metabolites as well).

the liver and the pericardium together govern the hormones and blood. jue ni represents a pathological condition of these two organ networks, resulting in blood rushing up in the wrong direction; leading to such conditions as stroke. another organ network that is related to blood flow is the small intestine, which is in charge of all the narrow passageways-- however it is more related to venous, retreating flow, while the liver is related to the pushing, arterial flow.

the overall painting describes another function of the liver, that it is in charge of coursing and draining. the two receiving channels represent the fact that the liver can aid in draining stagnant energy from two areas: the digestive spleen/stomach system, as well as emotional well being, preventing stagnant depressive states. (not depicted by the painting is another physiological function of the liver: the liver contains the hun spirits, which are ethereal spirits that follow the shen and come out in full force during sleep)

music: a song dedicated to studying for the NPLEX part I

2010-08-11T11:49:00.001-07:00

recorded the night before the NPLEX part I, after weeks of studying my brains out.

lab dx III final review questions

2010-06-17T11:37:00.000-07:00

HCG is produced by the synctiotrophoblast cells of the fetal placenta. levels begin rising about 1 week after conception; serum levels are detectable 1-2 days after implantation and urine levels are detectable 3-4 days afterwards. HCG levels are useful for monitoring the viability of a pregnancy; normally, levels should double every 48 hours. if the rate of increase is less than 66% / 48 hours, ectopic pregnancy is suspected. false positives can be caused by hematuria / proteinuria while false negatives can be caused by dilute urine or early timing of testing.

other tests: if gestational diabetes is suspected, a glucose challenge screening test is performed at 24-28 weeks. if this test is above 140mg/dl, an OGTT is then administered.

[didn't have a chance to write up the rest of the summaries, my apologies]

questions
1. HCG is produced by...√
2. when does HCG production begin?√
3. when is serum and urinary HCG present in detectable amounts? √√
4. what are factors that could produce false negative results in urine pregnancy tests?†
5. what are factors that could produce false positives in urine pregnancy tests?†
6. what is the normal rate of increase for serum quantitative HCG tests?√

7. how might ectopic pregnancy be detected by serum quantitative HCG test?†
8. what is the significance of decreased HCG levels?†
9. how long after an ectopic pregnancy is removed would HCG levels return to normal? √√√
10. what are other reasons why HCG levels might be elevated? √√√
11. how do HgB, HcT, and CMP values change during pregnancy?√
12. what is the test for gestational diabetes and when is it performed? √√√√√
13. what is the indication for performing a full OGTT test when gestational diabetes is suspected?

14. at what point during a pregnancy are group B strep cultures collected? √√XX√
15. what is the purpose of collecting triple screens and quad screens? √√√
16. when are triple and quad screens collected? √√X†
17. what is the most common reason for increased AFP levels? √√√
18. what is the pH of vaginal secretions vs. amniotic fluid? √√√

19. why would the ABO or Rh test be administered to neonates? √√√
20. why would the direct coombs test be administered to neonates? √√√
21. what bilirubin values are associated with kernicterus and jaundice? √√√
22. when and how are thyroid tests performed on neonates? √√√
23. what is the PKU test and how is it administered? √√√
24. describe what happens with a phenylalanine hydroxylase deficiency. √√√
25. what can cause a false positive PKU test? X√†

26. what is the LD50? √√√
27. what are the best testing choices for short term vs. long term toxic material exposure? √√√
28. what are some routes of absorption for heavy metals? √√√
29. what are some ways in which heavy metals impair proper metabolic functioning? XX√√√
30. what are the effects of lead toxicity? XX√√
31. how would lead toxicity show up on a CBC? XX√√√
32. what are normal lead blood levels in children and adults? X√√√

33. what is the principle behind the "provocative challenge test" of heavy metals? √√
34. which tests should be performed before administration of DMSA? √√
35. what is the order of heavy metals that are bound by DMSA? √√
36. what is the method for assessing the "natural method of heavy metal elimination"? √√
37. what are the symptoms of cholinesterase pesticide toxicity? √√√
38. how is glyphosphate exposure monitored? √√

39. how is exposure to agent orange (chlorophenoxy) monitored? √X
40. what is the metabolite of benzene in the body? XX
41. what about toluene? √√
42. and what about ketones? √√
43. where are solvents generally stored in the body? √√
44. when is nitrite/nitrate toxicity suspected? √√
45. what occurs with nitrate/nitrite toxicity? √X

46. what is the therapeutic index? √
47. how many "half lives" are required after starting drug therapy to achieve "steady state" generally? √
48. what are peak and trough levels? √
49. what are the active ingredients in cocaine and opiates? X

answers
1. synctiotrophoblast cells of fetal placenta.
2. 7 days after conception, 1 day after implantation.
3. serum: 1-2 days after implantation, urine: 3-4 days after implantation.
4. dilute urine, early timing in pregnancy.
5. proteinuria, hematuria, excess pituitary gonadotropin production, HCG containing drugs.
6. doubles every 48 hours.
7. 66% rate of increase every 48 hours.
8. increased chance of miscarraige, non-viable pregnancy.
9. 4 weeks.
10. multiple embryos
tumors
gestational trophoblastic diseases
hydatidiform moles
choriocarcinomas
11. all get lower due to higher blood volume.
12. glucose challenge screen at 24-28 weeks
13. when the initial screening test is >140mg/dl.

14. 35-37 weeks.
15. to assess for risks of neural tube defects, trisomy 21, trisomy 18.
16. 16-18 weeks gestation.
17. neural tube defects.
18. vaginal: 4.5-5.5. amniotic fluid: 7.0-7.5.

19. ABO: when the mother is type O. Rh: when the mother is Rh-.
20. when the mother is type O, Rh-, or if the baby has jaundice.
21. >2.5 mg/dl jaundice, >15 mg/dl kernicterus.
22. heel stick at 3 days.
23. test for deficiency of phenylalanine hydroxylase, via heel stick at 3 days.
24. buildup of phenylalanine in the brain causes brain damage.
25. prematurity, lack of proper nutrition, phenylpyruvic acid buildup and spillage into urine.

26. lowest dose for a toxic substance which will kill 50% of people.
27. short term is best tested through blood, long term through urine or hair.
28. skin, ingestion, inhalation, eyes.
29. disruption of enzymes, cell membrane transport processes, mitochondrial function, neuronal function. [membrane, energy, nerves]
30. inhibition of heme synthesis, globin synthesis, and porphobilinogen synthesis.
31. basophilic stippling, microcytic hypochromic anemia, accumulation of delta ALA
32. <10>Fe3+)

46. ratio of median toxic dose (MD50) over median effective dose (ED50).
47. 4-5 half lives.
48. peak levels achieved 1-2 hours after oral intake or 1/2 hour after IV, and is used to monitor toxicity levels. trough levels achieved 15-30 minutes before next dose, and used to monitor therapeutic levels.
49. cocaine: benzoylecgoin
opiates: conguated glucuronide.
50.

pathology IV: CNS

2010-06-14T11:32:00.000-07:00

congenital brain anomalies are among the most common birth defects, affecting 10 in 1000 live births. anencephaly is one example, the lack of growth of a brain due to a neural tube defect. its incidence has gone down in recent years because of the knowledge that folic acid supplementation pre-conception can significantly reduce the risk of developing anencephaly. microcephaly refers to abnormally small brain development, and can be due to fetal alcohol syndrome, trisomy 13, or HIV/rubella. polymicrogyri is a condition of excess gyri due to decreased white matter.

hydrocephalus is a condition of increased CSF, generally due to blocked drainage. this might be due to stenosis of the cerebral aqueduct or the foramen Monroe. it is associated with spina bifida and can be identified due to increased cerebral ventricals. normal pressure hydrocephalus is a variant that has intermittently elevated CSF pressure.

spina bifida is another congenital anomaly that results in failure of closure of the dorsal vertebral column, or its overlying skin. it is associated with elevated alpha fetal protein and might be linked to abdominal radiation and congenital rubella. sequelae might include paralysis and incontinence. there are several variants; spina bifida occulta refers to a missing vertebal segments without herniation, while a meningocele is an outpouching of the meninges, and a myelomeningocele is herniation of both the meninges and spinal cord.

cerebral palsy is a movement disorder due to damage to the motor centers of the brain, and most commonly develops in premature infants due to maternal infection during pregnancy. the most common type is spastic CP, which results in an "equinus deformity". patients with this variant are most likely to be able to walk, whereas patients with spastic quadriplegia are least likely to be able to walk. spastic quadriplegia affects all limbs equally and might be accompanied by hemiparetic tremors, which are uncontrollable shaking that affects one side of the body. morphological features of the brain affected by cerebral palsy might include paraventricular leukomalacia (necrosis and softening of paraventricular white matter) and gliosis (neuronal death and astrocyte proliferation).

meningitis is an infection of the meningeal layers which affects 17,000 people per year in the US. viral infections are the most common cause and are generally self limiting. on the other hand, bacterial meningitis is a medical emergency and is most commonly caused by strep pneumonia, e.coli, neisseria meningococci, h. influenza, and listeria monocytogenes. the main signs and symptoms include headache, fever, stiff neck, photophobia, and petechiae, among other things.

CSF analysis can serve to differentiate between the forms of meningitis. in bacterial meningitis, "opening pressure" will be increased, glucose will be decreased, and leukocytosis might be present. viral meningitis might have normal opening pressure, a lower degree of leukocytosis (100 WBC/mm^3 as opposed to 1000),

h. influenza is a meningitis that is caused by the haemophilus influenza bacteria type B, not to be confused with the virus that causes influenza. it is often caused by URI's which then travel through the bloodstream and infect the brain. the top demographic is 6-9 year olds who have recurrent URI's, are in day care, and Native Americans and Inuits have a particularly high incidence. potential complications are hearing loss, seizures, learning / speech / behavioral abnormalities, hydrocephalus.

cryptococcal meningitis is caused by cryptococcus neoformans, which is a yeast that is found in soil worldwide. those who have compromised immune systems are at greatest risk for contracting this disease. microscopy might reveal circular yeast bodies and CSF might grow cryptococcus cultures. fundoscopy might also reveal granulomas and papilledema.

viral meningitis generally follows a systemic viral infection, most commonly by arboviruses. other viruses also play roles, such as HSV-1. VM has a predilection for the temporal lobes, causing hemorrhage.

carcinomatous meningitis is a type of meningitis that is caused by tumors in and around the nervous system, commonly spread from lung, breast cancer, or melanoma. symptoms include headache, mental status changes, difficulty with vision/hearing/swallowing, and loss of sensation. fever is absent unless infection is present as well. CM is diagnosed definitively by tumor cells in the CSF.

brain abscesses are collections of pus, inflammatory / immune cells, and other material that accumulates in the brain due to infection, generally from multiple organisms. streptococcus is the most common cause in adults, and gram negative bacteria a common cause of abscess in infants. abscesses occur when infection causes inflammation, which then is walled off and increases in size, blocking blood flow to the area and causing necrosis of tissue and accumulation of immune cells.

questions
anatomy review...
1. how many pairs of nerves extend from the spinal cord?√√
2. what are the meningeal layers from outside to inside?√√
3. what is the space between the dura and arachnoid mater filled with?√√

congenital forebrain anomalies...
4. how common are birth defects related to the brain compared to other organs?√√
5. anencephaly is due to... √√
6. what is a supplement that might be helpful in reducing the risk for anencephaly and when should it be taken?√√
7. what are the potential etiologies for microcephaly?X†√
8. what is polymicrogyri? X†√

hydrocephalus...
9. what is hydrocephalus? what is commonly due to?XX†√
10. what condition is hydrocephalus associated with?XX√√
11. what is the imaging hallmark of hydrocephalus?X√√
12. describe how hydrocephalus might develop.X√
13. what is normal pressure hydrocephalus?X√√

spina bifida...
14. how common is brain hypoxia?x√
15. what is spina bifida?√√
16. what is a marker that is elevated in spina bifida?√√
17. what are two potential etiologies for spina bifida?XX
18. what are two major sequelae for spina bifida?X†
19. describe the various presentations of spina bifida. which is the most common?X†

cerebral palsy...
20. what is cerebral palsy?√√
21. when does most cerebral palsy develop?√√
22. which demographic is associated with cerebral palsy?√√
23. what is the most common type of CP?X√√
24. what is a characteristic PE finding for spastic hemiplegia?†√√
25. describe the hallmarks of spastic quadriplegia?X√√
26. some children with spastic quadriplegia have...X√√

cerebral palsy morphology, prognosis, sequelae...
27. what are two morphological signs in cerebral palsy?†X
28. what is PVL?X
29. what is gliosis?X√

meningitis introduction...
30. what are the most common causes of meningitis?√√
31. what is the difference in prognosis between viral and bacterial meningitis?√√
32. what are the most common bacterial strains that cause meningitis? X√√
33. how many cases of meningitis occur each year? X√√
34. what is the most common cause of bacterial meningitis for neonates?√√
35. what is the most common cause of bacterial meningitis for infants, adolescents, and young adults?√√
36. what is the most common cause of bacterial meningitis for the elderly?√√
37. what are the main signs and symptoms of meningitis?√

CSF diagnosis...
38. how can the "opening pressure" of CSF differentiate between causes of meningitis?√√
39. describe the white blood cell count in bacterial vs. viral meningitis?√√
40. what are the findings for a cell differential in the CSF of bacterial vs. viral meningitis?†√√
41. describe the CSF to glucose ratio for the different types of meningitis.√
42. describe the protein levels in the various types of meningitis. X√
43. the latex agglutination test is most sensitive for detecting which microorganism?√√

meningococcal meningitis...
44. how common is this form of meningitis?√√
45. what is a characteristic histomorphological feature of MM?X√√†
46. describe the exudate characteristics in MM. X√√√
47. describe the gross morphological changes in MM. X√√
48. what is a dermatological manifestation of MM? X√√
49. what are the potential complications of MM? XX†√

h. influenza meningitis...
50. what is the age of peak incidence for this disease?√√√
51. may follow...√√√
52. what are some risk factors for h. influenza meningitis?√√√
53. which demographic has a higher risk for h. flu meningitis?X√XX
54. what are the potential complications for h. flu meningitis?X√X

aseptic meningitis...
55. what is aseptic meningitis?√√√
56. which two viruses are the most common causes of aseptic meningitis?X√√†
57. what are the symptoms that characterize aseptic meningitis?†√√√

cryptococcal meningitis...
58. what is the etiological agent in CM?√√√√
59. what are the demographics at risk for CM?√√√X
60. which lab tests are used to diagnose CM?†√√√
61. what is another PE finding that can aid in the diagnosis of CM?††X†√

viral meningitis...
62. what are the different types of viral meningitis? √√√√
63. most cases arise as complications of...√√√√
64. what is the most common cause of VM?√XXX√√√√
65. which virus is responsible for 10-20% of cases of VM?√X√X√√√√
66. what is a distinct morphological feature of VM?√XXX√√√√

carcinomatous meningitis...
67. what are the most common non-hematologic causes of CM?√√
68. what are the symptoms of CM?X
69. how is CM diagnosed?†√
70. 1/3 of the patients have...√
71. what percentage of CM patients have fever?√√

brain abscess...
72. what is a brain abscess?√√
73. which demographic has a higher incidence for brain abscesses?√√
74. what is the etiology of most brain abscesses?√√
75. what is the most common bug that causes brain abscesses?√√
76. which is found more commonly in infant brain abscesses, gram negative or positive bacteria?√√
77. describe the pathophysiology of brain abscesses.√√
78. what is the morphology of an aspergillus brain abscess?√

neurocysticercosis...
79. what is neurocysticercosis?√√√
80. what is the morphology of neurocysticercosis?√√√

neurosyphilis...
81. what is neurosyphilis caused by? √√√
82. which variant is associated with the middle cerebral artery or the branches of the basilar artery?√†√√
83. which variant is associated with widespread infection of parenchyma?√††
84. which variant is associated with demyelination and fibrosis of the posterior column of the spinal cord?√†X
85. what are gummas?†√√
86. what is the jarisch-herxheimer reaction? what is the prognosis?√√√

progressive multifocal leukoencephalopathy...
87. what is PML caused by? XX√√√
88. what is PML? X√√√√
89. what are some symptoms of PML? X†√X
90. what is the gross morphological feature of PML? X††√XX√

subacute sclerosing panencephalitis...
91. what is SSPE caused by? X√√√
92. describe the course of SSPE. X√√√
93. what is a sign of poor prognosis for SSPE patients?√√√√
94. how is diagnosis of SSPE made? XX√
95. what is a morphological sign of SSPE? XX†X

poliomyelitis...
96. describe the infectious process in poliomyelitis.√√
97. what is post polio syndrome?√√

rabies...
98. what occurs in 1-3 months after rabies exposure? √√
99. what are some symptoms of rabies? √√
100. what is the diagnostic sign for rabies? †√√

AIDS dementia complex...
101. when during the course of AIDS does ADC emerge?√√
102. what are some nonspecific symptoms of ADC?√√
103. what are some late symptoms of ADC?√√
104. describe the pathophysiology of ADC.√√
105. what are the morphological changes of ADC?X√

reye's syndrome...
106. what is reye's syndrome characterized by?†√
107. what is reye's syndrome associated with?√√√

cerebrovascular disease...
108. how prevalent is cerebrovascular disease?√
109. what factors does the survival of ischemic tissue depend on?√
110. describe the histopathology of a stroke within the first 12-24 hours.√
111. describe the histopathology of a stroke at 24 hours.√
112. describe the histopathology of a stroke from 2-14 days.√
113. which heart condition is associated with ischemic stroke?
114. which artery is commonly affected by thrombosis leading to ischemic stroke?
115. what is the leading cause of hemorrhagic stroke?

answers
1. 31 pairs.
2. dura mater, arachnoid mater, pia mater.
3. CSF.

4. most common, 10 in 1000 live births.
5. neural tube defect.
6. folic acid pre-conception.
7. fetal alcohol syndrome, trisomy 18, congenital rubella, congenital HIV.
8. excess gyri due to decreased white matter.

9. excess CSF due to drainage problem.
10. spina bifida.
11. enlarged ventricles.
12. stenosis of the cerebral aqueduct or foramen of monroe.
13. a variant that has enlarged cerebral ventricles but only intermittent elevations of CSF pressure.

14. over 1/3 of the 30,000 children per year in the US that are born with congenital heart disease.
15. failure of closure of dorsal vertebral column or overlying skin.
16. AFP.
17. radiation to the abdomen and congenital rubella.
18. paralysis and incontinence.
19. spina bifida occulta: missing portion of dorsal vertebral body.
meningocele: herniation of the meninges but not the spinal cord.
myelomeningocele: herniation of meninges with spinal cord. most common.

20. a movement disorder related to damage to movement centers of the brain.
21. during pregnancy, due to a maternal infection.
22. premature infants, 8 months or less.
23. spastic.
24. equinus deformity, causing walking on the ball of one foot.
25. all four limbs equally affected, least likely to be able to walk.
26. hemiparetic tremors.

27. paraventricular leukomalacia and gliosis.
28. softening and necrosis of paraventricular white matter due to lack of blood supply.
29. neuronal cell death and phagocytosis, astrocyte proliferation.

30. viral infection, bacterial infection.
31. viral is generally self resolving, bacterial is generally emergency.
32. ecoli, strep pneumonia, h. influenza, neisseria meningitis, listeria monocytogenes. [ESHNL][HESNL][SHENL][SIENL][SENIL]
33. 17,000.
34. ecoli.
35. neisseria meningococci, strep pneumonia.
36. strep pneumonia.
37. fevers, headache, stiff neck, sensitivity to light and sound, petechiae.

38. increased in bacterial, normal in viral, variable in fungal and tubercular.
39. more than 1,000 / mm^3 in bacterial, more than 100/mm^3 in viral.
40. PMN's in bacterial, lymphocytes in other forms of meningitis.
41. decreased to normal in bacterial, normal in viral, decreased in fungal and tubercular.
42. increased in bacterial, fungal, tubercular, normal to increased in viral.
43. h. influenza.

44. most common form in children, second most common form in adults.
45. gram negative diplococci inside neutrophils
46. neutrophilic exudate that causes yellow/tan clouding of meninges.
47. prominent dilated vessels, edema and focal inflammation in the cortex.
48. rapidly spreading petechial rash.
49. mental retardation, permanent brain damage, hydrocephalus, myocarditis, waterhouse-friderichsen syndrome. [brain brain water water heart]

50. 6-9 months.
51. upper respiratory infection
52. recurrent URI's, daycare.
53. native americans and inuits.
54. hearing loss
seizures
learning / behavioral problems
hydrocephalus
[flu hear seize learn water] [hear the fluid water's seizing behavior]

55. signs and symptoms of meningitis are present but no bacteria is cultured in CSF.
56. coxsackie and echovirus.
57. headache, fever, inflammation of the meninges.

58. cryptoccal neoformans, a yeast that is found in soil around the world.
59. those with compromised immune systems.
60. india ink stain microscopy might reveal circular yeast bodies. CSF grows cryptococcus cultures.
61. fundoscopy: papilledema and granuloma.

62. focal, multifocal, diffuse.
63. systemic viral infections.
64. arboviruses transmitted by mosquitos and ticks.
65. HSV.
66. predilection for hemorrhage of the temporal lobe.

67. lung, breast cancer, melanoma.
68. headache
mental status changes
vision / hearing / swallowing difficulty
loss of sensation
69. presence of tumor cells in CSF.
70. headache.
71. only those with supervening infection.

72. mass of immune cells, pus, other material that accumulates in the brain due to infection.
73. immune compromised, first four decades of life.
74. generally more than one microorganism.
75. streptococcus.
76. negative.
77. infection causes inflammation and fibrosis, which leads to mass effect and blockage of blood flow to area, leading to necrosed tissue.
78. relatively slender hyphae with 45 degree angle branches.

79. infection of CNS by larvae of pork tapeworm, taenia solium.
80. multiple calcifications and viable cysts in brain parenchyma.

81. treponema pallidum infection.
82. meningovascular syphilis.
83. paretic syphilis.
84. tabes dorsalis.
85. meningeal granulomas which are well circumscribed masses of granulation tissue resulting from a cell mediated response to treponema.
86. a reaction from the treatment of treponema, resulting in headache, fever/chills, nausea. generally disappears in 24 hours.

87. members of the papovavirus family, usually JC virus.
88. rare demyelinating disease that results in the loss of oligodendrocytes.
89. memory, vision, mental function, coordination loss.
90. irregular areas of granularity in the white matter.

91. a rare complication of measles.
92. develops 1-20 years after measles.
93. deterioration of neurological function.
94. rubeola IgG antibody.
95. white matter hemorrhage and gliosis.

96. virus transmitted via oral/fecal route, replicates in nasopharynx and lymph tissues, leading to viremia, which then turns neurotropic and destroys neurons in the anterior horn and brainstem.
97. recurrent bouts of muscle weakness that occur 20-50 years after the initial polio episode. more of an "autoimmune reaction" than a reactivation of virus.

98. virus travels from peripheral nerves to the brain. time depends on depth and location of bite.
99. headache
irritability
salivation
water intolerance
muscle spasm
100. negri bodies within neurons.

101. late in the process, when CD4 count starts to drop.
102. difficulty concentration
poor coordination, muscle weakness
103.
104. uncertain, but: HIV infects CNS macrophages, which release substances that cause nerve dysfunction and death.
105. cortical atrophy and ventricular enlargement.
106. fever, vomiting
fatty infiltration
swelling of kidneys and brain
107. a previous infection and treatment using aspirin.

108. most prevalent neurologic disorder in terms of mortality and morbidity, third leading cause of death in US.
109. duration of ischemia
rapidity of onset of ischemia
magnitude of ischemia
collateral circulation
110. red neurons: vacuolated, eosinophilic neuronal cytoplasm.
111. neutrophilic infiltrate at the edge of the lesion.
112. neutrophilic / macrophage infiltrate, gliosis.
113. atrial fibrillation.
114. middle cerebral artery.
115. HTN.

pathology IV: skeletal muscle

2010-06-10T11:29:00.000-07:00

muscular atrophy: can be generalized, as in prolonged bedrest, or localized, as in immobilization of a body part with a cast. neurogenic atrophy is muscle atrophy that is due to the lack of innervation of muscle fibers, which then necrose-- and can be mixed in next to healthy muscle fibers. neurogenic atrophy might result in contracture due to the reduced resistance of opposing muscle groups.

congenital myopathies are genetic disorders of muscle that present early on and have an insidious progression. they result in general muscle weakness and might have a connection with diet, as elucidated in "breaking the vicious cycle", which describes a possible connection between muscle weakness and intake of simple carbohydrates. duchenne's is one of many types of muscle dystrophy which develops early on and is generally fatal by the 20's. it results from an x linked genetic defect which leads to an absence of dystrophin, a component of the membrane of skeletal muscle. this leads to dysfunctional membrane permeability, which leads to excess calcium levels, cloudy swelling, and ultimately cell death.

myasthenia gravis is an autoimmune neuromuscular condition that results from antibodies to the acetylcholine receptors in neuromuscular junctions. the hallmark symptom is muscle weakness that is worse with activity and better with rest. there is also a strong association with thymic abnormalities, such as hyperplasia or thymomas. histomorphology includes large clusters of lymphocytes and pale / atrophic muscle fibers.

lambert-eaton syndrome is another autoimmune neuromuscular condition in which antibodies to the presynaptic calcium channels are produced, leading to decreased acetylcholine release. it is strongly associated with lung cancer-- in particular oat cell cancer of the lung, and generally appears first on the upper legs and upper arms. diagnosis is made by antibody tests, nerve stimulation tests, and chest xray to detect lung cancer. in contrast to MG, patients with LES might experience greater strength in the beginning of a mild exertion.

dermatositis is an idiopathic inflammatory connective tissue disorder which also has skin and muscle involvement. half of cases are associated with paraneoplastic syndrome. histomorphological signs include perivascular inflammatory infiltrate of mixed B and T cells, and perifascicular musclar atrophy. characteristic signs and symptoms include neck extensor weakness, periorbital heliotrope rash, grotton's sign (purple/red papular rash on the dorsal side of fingers).

questions
muscular atrophy...
1. what might cause generalized vs. localized atrophy?
2. what might atrophy be masked by?
3. what is neurogenic atrophy?
4. describe the morphology of neurogenic atrophy.
5. neurogenic atrophy might result in...

congenital myopathies...
6. describe the onset and course of most congenital myopathies.
7. what is a diet that might have a connection with muscle tone and what is the book in which these findings were presented?
8. what are the signs / symptoms of congenital myopathies?

muscle dystrophies...
9. how many forms of muscle dystrophies are there? which is most common?
10. muscular dystrophies are characterized by...
11. what is the etiology of duchenne's?
12. which gender is associated with duchenne's?
13. describe the pathophysiology of duchenne's.
14. what is the typical age of onset for duchenne's?
15. describe the distribution of duchenne's.
16. what is "pseudohypertrophy"?
17. describe the histomorphology of the early and late stages of duchenne's.
18. what is the prognosis of duchenne's?

myasthenia gravis...
19. what is the etiology of myasthenia gravis?
20. what is the hallmark symptom of MG?
21. there is an association between MG and...
22. what is the histomorphology of MG?
23. how is diagnosis of MG made?

lambert-eaton syndrome...
24. where is LES first noticed?
25. 60% associated with...
26. what is the etiology of LES?
27. describe the symptom picture of patients with LES.
28. how is LES diagnosed?

dermatositis...
29. what is dermatositis?
30. what is the etiology of dermatositis?
31. besides muscle weakness, how is dermatositis diagnosed?
32. what are the 2 characteristic histomorphological signs of dermatositis?
33. what are the characterizing signs/symptoms of dermatositis?
34. what is grotton's sign?

polymyositis...
35. what is the main difference between polymyositis and dermatositis?
36. which muscles are affected in polymyositis?
37. what is a sign that occurs in 1/3 of patients that indicates poor prognosis?
38. what is a common presentation of a patient with polymyositis?
39. what is the histomorphology of polymyositis?
40. describe the composition of the inflammatory infiltrate in polymyositis.

answers
1. generalized: lying in bed for a long time. localized: wearing a cast.
2. fat deposition in between muscle fibers.
3. muscle atrophy as a result of decreased nerve supply.
4. areas of atrophied tissue mixed with healthy tissue.
5. contractures due to reduced resistance in opposing muscle groups.

6. generally early onset and gradual progression.
7. specific carb diet, in "breaking the vicious cycle".
8. generalized or proximal muscle weakness, hypotonia.

9. hundred's, duchenne's.
10. progressive skeletal muscle weakness.
11. defective gene on X chromosome that leads to inability to produce dystrophin, a skeletal muscle membrane protein.
12. almost exclusively in boys.
13. absence of dystrophin leads to membrane permeability changes which leads excess calcium and ROS, cloudy swelling and ultimately to cell death.
14. 2-6yo.
15. proximal large muscles and spreads to all voluntary muscles.
16. muscle that is replaced by fat and thus appears to be hypertrophied.
17. early: scattered inflammatory cells. late: pseudohypertrophy.
18. wheelchair bound by age 12, generally fatal by 20's.

19. autoimmune condition in which antibodies are produced against the acetylcholine receptors at the neuromuscular junctions, resulting in an inhibition of acetyl choline's stimulatory activity.
20. muscular weakness that worsens with activity and improves with rest.
21. thymic abnormalities such as thymic hyperplasia.
22. large collections of lymphocytes, and pale/atrophic necrotic muscle fibers.
23. history, PE, and two positive diagnostic tests: serum antibodies, nerve stimulation studies, tensilon injection studies.

24. upper legs/upper arms.
25. oat cell cancer of the lung.
26. antibodies to the presynaptic calcium channels, resulting in inhibition of Ach release.
27. greater strength with initial exertion but weakness upon prolonged exertion.
28. chest x ray for lung involvement, antibody tests, nerve conduction studies.

29. connective tissue disease with muscle and skin involvement.
30. unknown, although 50% have an association with paraneoplastic syndrome.
31. skin involvement, elevated CPK, ESR, EMG, and muscle biopsy.
32. mixed B/T cell perivascular inflammatory infiltrate and perifascicular muscle atrophy.
33. neck extensor weakness
dysphagia / aspiration
periorbital heliotrope rash
grotton's sign
34. symmetrical purple/red papular rash over dorsal aspect of finger joints.

35. no skin involvement in polymyositis.
36. symmetric proximal muscles, especially neck flexors.
37. oropharyngeal and esophageal involvement.
38. inability to rise from a seated position.
39. pale and enlarged muscle fibers, surrounded by macrophages.
40. cytotoxic T8 lymphocytes.

CPD III: musculoskeletal part II

2010-05-24T08:40:00.000-07:00

discoid lupus is a chronic skin condition that manifests as erythematous, round, scaly lesions 5-10mm in diameter that are common on the cheeks, ears, scalp, and the bridge of the nose. the etiology is unclear, though sunlight seems to be a trigger. it is more common in females 3:1, and usually appears in the third decade. other symptoms may appear such as atrophy and telangiectasias, as well as mouth ulcers in some. ddx's might include SLE, seborrheic dermatitis, rosacea, lichen planus, most of which can be ruled in or out via atrophic features or distribution of lesions on the body.

systemic lupus erythematosus (SLE) is an autoimmune disease that affects many systems of the body that is thought to involve antinuclear antibodies and a type III hypersensitivity response. it has a predilection for females and african americans and affects 1 in 2000 people. etiology is unclear, although genetic factors are presumed, and some environmental triggers have been identified, such as certain medications (procainamide, hydralazine, quinidine), sunlight, infection, silicone implants.

the most characterizing symptom for SLE is the butterfly rash across the face, although this might be absent in some patients. because SLE is a systemic disease, it can manifest in many different ways- ulcerations in the mouth / nasal cavity, xerostomia, polyserositis (inflammation of the serous membranes, leading to pleuritis / peritonitis / etc), recurrent respiratory infections, kidney failure, and very commonly, polyarthralgia that are symmetric and non deforming. diagnosis is by presence of characterizing symptoms as well as ANA tests.

scleroderma is a condition that results from abnormal fibrosis and collagen deposition. it can come in different variants; the diffuse type is more severe, rapid onset, with more internal organ involvement and widespread skin thickening. on the other hand, the CREST variant is more common and less severe-- CREST stands for calcification, raynaud's, esophageal dysfunction, sclerodactyly, and telangiectasias. patients with scleroderma might have hard, taut, shiny skin and faces that resemble mask-like textures, as well as subcutaneous calcifications. joints might have a friction rub, especially the knees. esophageal issues resulting from LES dysfunction might result in dysphagia, acid reflux, and barrett's esophagus. cardiovascular changes might include arrhythmias and pericarditis, while respiratory changes might include pleurisy, pulmonary hypertension, and dyspnea. diagnosis is made by presence of characteristic major and minor symptoms: the one major symptom is sclerotamous skin changes proximal to the MCP joints, and the minor symptoms are sclerodactyly, pulmonary fibrosis, and digital pitting scars. lab tests commonly reveal positive antibodies- ANA and anti-centromere in most cases, and anti-Scl-70 might be present in 30%, indicating pulmonary fibrosis.

polymyalgia rheumatica is a seronegative musculoskeletal condition that mainly presents as muscle pain in the neck, shoulders, or pelvic girdle muscles (as opposed to the joints). it might also result in weight loss, profound morning stiffness, fever, malaise. lab findings would be seronegative, with an increased ESR, and possibly normochromic / normocytic anemia. it is often treated with a 5 day burst of steroids, which may alleviate symptoms greatly. a severe complication is temporal arteritis, which will cause a severe headache and could ultimately lead to blindness.

polyarteritis nodosa is a vasculitis of the small and medium sized artery, with secondary ischemia of the affected tissues. it is an autoimmune condition that affects middle aged males most commonly. this condition affects the whole body and therefore has a presentation that is difficult to diagnose because it mimics many other conditions. the most common symptoms are fever, headache, weight loss, asthma, chest / abdomen pain, renal issues (hypertension, edema, failure), peripheral neuropathy. labs would reveal high WBC count, proteinuria and hematuria.

mixed connective tissue disorder (MCTD) is a combination of scleroderma, lupus, and polymyositis that mostly affects females in the 4th decade of life. it can cause: sausage digits and lupus like rashes, non deforming arthritis, muscle weakness / pain, decreased peristalsis in the esophagus, dyspnea, pulmonary hypertension, pericarditis. diagnosis is by ANA and anti-U1RNP.

ankylosing spondylitis is an inflammatory arthritis that preferentially affects males 15-30 and is fairly well localized to the lower spine, SI joints, ribcage, and eyes. it is usually made worse by prolonged rest and better by motion-- thus morning activities are particularly difficult for AS patients, who present with severe heel pain. ribcage pain might prevent full respirations and cause asthma like symptoms. uveitis might occur as well, resulting in ciliary injection and photophobia. a patient with AS will have a loss of lumbar lordosis and compensatory thoracic accentuation, stooped posture, and abnormal gait. lab findings are seronegative, elevated ESR, and positive HLA-B27. diagnosis is made by xray of the SI joints. ddx's include herniated disc and DISH syndrome.

psoriatic arthritis is a type of arthritis that affects 20% of sufferers of psoriasis, resulting in inflammation of the DIP joints, sausage digits, and nail discoloration / pitting. there are different types that vary in distribution and severity; the most common (50% of cases) are symmetrical, presenting similarly to RA. next is asymmetrical, which is milder and affects less than 3 joints at a time. lab findings are seronegative, increased ESR / CRP, may have positive HLA B27.

reiter's syndrome, aka reactive arthritis, is an arthritis that is secondary to infection such as GU infection or gastroenteritis. it affects males preferentially and seems to have the HLA B27 connection as well. main symptoms are captured by the phrase "can't see, can't pee, can't dance with me"- uveitis, urethritis (milder than that of an STD), and arthritis which is generally an asymmetric polyarthralgia of the lower extremities. severe cases will also develop back pain. RS patients may also develop mucocutaneous, painless lesions in the mouth, tongue, glans penis, and bottom of the feet, as well as hyperkeratosis on the soles of the feet and palms.

osteoarthritis is the most common connective tissue disease that is degenerative in nature: meaning RF-seronegative, non-inflammatory. if under 45, OA is associated with males and if over 55 OA is associated with females. etiological factors are varied and can include microtrauma, infection, malabsorption, genetic factors, endocrine imbalances. the cartilage of an OA patient undergoes erosion via fissuring and pitting, causing osteophytes / bone spurs to form (as adaptive physiology to prevent movement of the affected joint). common locations are the knee, hip, fingers (PIP=bouchard's nodes, DIP=heberden's nodes), spine (C5-7 and L4-5 in particular). some features distinguish OA from RA: the morning stiffness is not as bad, and OA is more of a deep, poorly localized pain. PE findings might include joint swelling / effusion / crepitus, abnormal gait / ROM / deformation, and tenderness to palpation. OA diagnosis is made definitively by xray.

infectious arthritis is arthritis secondary to an infection: in young children this is commonly caused by staph, h. flu, and in adults it is commonly caused by staph, strep, pneumonia, or gonococci. the typical presentation is rapid onset of swelling / tenderness / decreased ROM / redness of a single joint with fever and leukocytosis. the most common location is the knee, but IA often affects the hip, shoulder, wrist, and phalanges. it is diagnosed by a CBC w/ differential and a synovial fluid biopsy.

lyme disease is an infectious condition caused by borelia burgdorferi carried by deer ticks, largely in the northeast. the characteristic symptom is the bullseye lesion: erythema chronicum migrans, which appears 3-30 days after exposure. lyme disease might also affect other systems, causing neurological symptoms (meningitis or encephalitis, chorea, ataxia, peripheral neuropathy), cardiovascular symptoms (AV blocks, pericarditis, cardiomegaly), and myalgias/arthalgias (sudden swelling of a single large joint). CDC recommends a two step diagnosis process: antibody titer test, then western blot.

the last condition of this week was osteomyelitis: infection of the bone via a longstanding condition such as prostatitis, UTI, or open wound. osteomyelitis develops slowly over the course of several months and presents as severe back pain and perivertebral spasm. it is not accompanied by fever or leukocytosis, and is diagnosed by elevated ESR and xray, which would show spotty demineralization of bone.

questions
discoid lupus...
1. what etiological factor commonly precedes the initial lesions of DL?
2. what is the most common age and gender that DL affects?
3. describe the skin lesions in DL.
4. where are the body areas commonly affected in DL?
5. what is a concomitant symptom in DL?
6. are anti-DNA antibodies present or absent?
7. what are some ddx's for DL?
8. how can most of the ddx's be ruled out?

SLE overview...
9. what is SLE?
10. what are the demographic / gender groups most likely to have SLE?
11. what are three etiological categories for SLE?
12. what are some environmental triggers for SLE?
13. what are the most common drugs that are associated with SLE?
14. what is the most characterizing symptom for SLE?

SLE symptom presentation and diagnosis...
15. 40% of SLE patients have...
16. SLE patients might have ulcerations in which locations?
17. what symptoms might cause a SLE patient to be confused with sjogren's?
18. what is the most common symptom of SLE? what condition presents in a similar way?
19. how might SLE manifest in the respiratory system?
20. what are common UA findings for SLE patients?
21. which serous membranes might be affected in SLE? what is this condition called?
22. how common is raynaud's in SLE patients?
23. what is the screening test for SLE?

scleroderma overview...
24. what is scleroderma?
25. how common is scleroderma in the US? which gender is more affected?
26. how does the age of onset for scleroderma compare to SLE?
27. what is the more severe variant of scleroderma? what is it characterized by?
28. what are the hallmarks of CREST syndrome?

scleroderma presentation...
29. describe the distribution of skin changes in scleroderma.
30. describe the morphology of skin changes in scleroderma.
31. what are some other skin changes that might accompany a scleroderma patient?
32. what is a PE sign that might be picked up in the joints of a scleroderma patient?
33. what are the typical GI manifestations of scleroderma?
34. what are the cardiovascular changes in scleroderma?
35. what are the respiratory manifestations of scleroderma?

scleroderma diagnosis...
36. which lab markers are present in over 90% of scleroderma patients?
37. how common is a positive anti Scl-70 antibody and what is it associated with?
38. what is the major diagnostic criteria for scleroderma?
39. what are the three minor diagnostic criteria for scleroderma?

polymyalgia rheumatica...
40. which gender and age is more prone to developing polymyalgia rheumatica?
41. describe the distribution of pain in PR.
42. what are some concomitant symptoms in PR?
43. in the shoulder girdle, are proximal or distal muscles more likely to be affected?
44. what are the lab findings associated with polymyalgia rheumatica?
45. what is a treatment that can serve as a diagnosis for PR?
46. what is an important, severe concomitant that might result from PR?
47. what are the diagnostic criteria for [46]?
48. [46] might lead to...
49. what is the prognosis for PR?

polyarteritis nodosa...
50. what is polyarteritis nodosa?
51. which gender and age is most commonly affected by PN?
52. what is the etiology of PN?
53. why is PN so difficult to diagnose?
54. what are the most common symptoms of PN?
55. what would labs for PN reveal?

mixed connective tissue disease...
56. MCTD is a combination of...
57. which age and gender is most commonly affected by MCTD?
58. what are the dermatological manifestations of MCTD?
59. how does MCTD manifest in the joints?
60. and the muscles?
61. and the esophagus?
62. pulmonary stuff?
63. heart?
64. what are the lab findings for MCTD?

ankylosing spondylitis...
65. what is AS?
66. which gender and age is most commonly affected by AS?
67. what is a genetic marker that is often positive in AS?
68. what are the body areas commonly affected by AS?
69. describe the severity of the morning symptoms of AS.
70. how does movement / rest affect AS patients?
71. why does AS present with asthma?
72. what are the eye symptoms that AS patients present with?
73. what are the PE findings for AS?
74. what are the lab findings for AS?
75. how is diagnosis of AS confirmed?
76. what are the ddx'es for AS?
77. what are the treatment goals for AS?

psoriatic arthritis...
78. what percentage of chronic psoriasis patients develop PA?
79. what percentage of PA patients develop ankylosing spondylitis?
80. describe the distribution and morphology of PA.
81. what are the different types of PA? which is most common?
82. what are the lab findings for PA?

reiter's syndrome...
83. what is reiter's syndrome? what is it also called?
84. what are the etiological agents identified for RS?
85. what is the difference between the people prone to developing sexually transmitted vs. dysenteric RS?
86. what are the signs / symptoms of RS?
87. how does the urethritis differ from that of an STD?
88. describe the arthritis in RS.
89. what are the dermatological manifestations of RS?

osteoarthritis...
90. how common is osteoarthritis?
91. what age and gender is most commonly affected by OA?
92. what are some etiological factors for OA?
93. describe what happens to the bones and joints in OA.
94. which vertebral junctions are particularly prone to developing [93]?
95. what are the most common locations for osteoarthritis?
96. what are Heberden's and Bouchard's nodes?
97. what are the symptoms/signs that differentiate OA from RA?
98. what are some PE findings for OA?
99. how is OA diagnosed?
100. what are the ddx's for OA?
101. what are the treatment strategies for OA?

infectious arthritis...
102. what are the most likely microorganisms responsible for IA in young children?
103. what are the most likely microorganisms responsible for IA in adults?
104. what is the typical presentation of IA?
105. what are the most common locations for IA?
106. how is IA diagnosed?

lyme disease...
107. what are the infectious agents in lyme disease?
108. what is the characteristic symptom of lyme disease? when does it appear?
109. what are the neurological signs of lyme disease?
110. what are the CV symptoms of lymedisease?
111. 50% of patients with lyme disease have...
112. what is the two step diagnostic method advocated for identification of lyme disease by the CDC?
113. what are some ddx's for lyme disease?

osteomyelitis...
114. what is the etiology of osteomyelitis?
115. describe the time course of osteomyelitis.
116. what are the signs and symptoms of osteomyelitis?
117. is osteomyelitis accompanied by fever? what about leukocytosis?
118. what labs are used to diagnose osteomyelitis?

answers
1. sunlight.
2. females in 30's.
3. erythematous, round, scaly papules with follicular plugging. 5-10mm.
4. cheeks, bridge of nose, scalp, ears.
5. many mouth ulcers.
6. absent.
7. SLE
rosacea
seborrheic dermatitis
photosensitivity
lichen planus
8. via lack of atrophic features or a different distribution pattern.

9. an type III hypersensitivity response which results in immune complex deposition and antinuclear antibody formation affecting many systems of the body.
10. young females, african americans.
11. genetic predisposition (not clarified), environmental triggers, drug reactions.
12. medications
stress
sunlight
infection
silicone implants
13. procainamide, hydralazine, quinidine.
14. butterfly rash.

15. photosensitive skin eruptions.
16. oral and nasal.
17. parotid enlargement and xerostomia.
18. polyarthralgia and arthritis, similar to rheumatoid arthritis presentation.
19. recurrent respiratory infections.
20. proteinuria, hematuria, cellular elements.
21. polyserositis: pleuritis, pericarditis (and myocarditis), peritonitis.
22. 1/3.
23. ANA test, UA.

24. rare chronic disease characterized by excess collagen deposition in various tissues.
25. 300,000 in US, 4 times more likely females.
26. slightly older; 30's to 40's.
27. diffuse scleroderma, a rare variant that develops rapidly and has widespread skin thickening and greater lung / GI damage.
28. calcinosis
raynaud's
esophageal dysfunction
sclerodactyly
telangiectasia

29. most commonly on the distal portions of upper extremities, but may be all over the body.
30. taut, shiny, hyperpigmented. face becomes mask like.
31. subcutaneous calcifications and telangiectasias.
32. friction rubs over joints, especially knees.
33. esophageal dysfunction which leads to dysphagia, acid reflux, and may progress to barrett's esophagus (1/3 of patients)
34. arrythmias, abnormal EKG, pericarditis.
35. fibrosis, pulmonary hypertension, pleurisy.

36. ANA, anti centromere antibodies,
37. 30%, pulmonary fibrosis.
38. scleromatous skin changes proximal to the MCP joint.
39. digital pitting scars, sclerodactyly, bibasilar pulmonary fibrosis.

40. females (2:1) over 50.
41. symmetric distribution in neck, shoulder, and pelvic girdle muscles.
42. morning stiffness
weight loss
fever, malaise
43. proximal.
44. seronegative, ESR over 40, may have normochromic/normocytic anemia.
45. if a 5 day burst of steroids helps, it is likely PR.
46. temporal arteritis.
47. age over 50, new onset, temporal artery abnormality (tenderness or diminished pulse), elevated ESR, biopsy.
48. blindness.
49. 90% recover within 2 years.

50. vasculitis of the small and medium arteries and secondary ischemia of the affected tissues.
51. middle aged males.
52. autoimmune/hyperimmune response.
53. because it mimics many other diseases and has a insidious onset.
54. fever
abdominal pain
peripheral neuropathy
renal hypertension / edema / failure
angina / MI / CV issues
weight loss
headache
asthma
55. high WBC's, proteinuria, hematuria.

56. scleroderma, lupus, polymyositis.
57. 80% females in 4th decade.
58. sausage fingers, lupus like rashes.
59. non deforming arthritis.
60. weakness, maybe tenderness.
61. decreased peristalsis.
62. dyspnea, hypertension.
63. pericarditis.
64. high ANA and high titers of anti-U1RNP.

65. an inflammatory arthritis primarily affecting spine and SI joints.
66. males 3:1, 15-30 years old.
67. HLA-B27.
68. heels, spine, rib cage, eyes.
69. prolonged morning stiffness, and heel pain that causes most AS patients to not want to walk.
70. prolonged rest makes worse, movement makes stiffness better.
71. because the rib pain makes breathing difficult.
72. uveitis: ciliary injection, photophobia.
73. reduced lumber range of motion, accentuated thoracic curve, loss of lumbar lordosis, stooped posture, abnormal gait, shallow breathing.
74. seronegative, increased ESR, positive HLA-B27.
75. xray of SI joints.
76. herniated disk, DISH syndrome.
77. prevent joint fusion via regular movement and stretching.

78. 20%.
79. 1/3.
80. DIP's, sausage digits, nail pitting and discoloration.
81. symmetric, asymmetric, arthritis mutilans, spondylitis, DIP predominant. symmetric accounts for 50%.
82. seronegative, increased ESR, CRP, may have positive HLA B-27.

83. reactive arthritis; arthritis that develops secondary to an infection elsewhere in the body such as a GU infection or gastroenteritis.
84. HLA-B27, male gender, white race (connected to HLA-B27)
85. sexually transmitted: young men, chlamydia trachomatis. dysenteric: women, children, elderly. shigella, salmonella, campylobacter, yersinia.
86. uveitis, urethritis, arthritis. [can't see, can't pee, can't dance with me]
87. less painful / more mild.
88. asymmetric polyarthritis that affects larger joints of lower extremities and toes.
89. mucocutaneous lesions- small, painless ulcers in the mouth, tongue, glans penis, bottom of feet. may also develop hyperkeratotic lesions on soles of feet and palms.

90. most common connective tissue disease.
91. under 45: males more affected. over 55: females more affected.
92. genetic, autointoxication, malabsorption, endocrine imbalance, microtrauma, surgery.
93. pitting/fissuring erosions of articular cartilage, formation of osteophytes / bone spurs.
94. C6-C7, L4-L5.
95. knee, hip, fingers.
96. H: DIP involvement. B: PIP involvement.
97. morning stiffness not as bad
deep, poorly localized pain
better with rest, worse with use
might have night time pain
98. tenderness to palpation
joint swelling / effusion / crepitus
ROM limitation / abnormal gait
valgus / varus deformities
99. lab tests are largely uninformative (may have increased ESR). diagnosis by xray.
100. psoriatic arthritis
ankylosing spondylitis
reiter's
RA
101. largely palliation of pain, although glucosamine sulfate can help if taken for a long time. exercise is the most helpful.

102. staph, h influenza, gram- bacilli. [staff, flu, negative]
103. staph, strep, pneumonia, gonococci. [staff, strip, new, gone]
104. rapid onset, unilateral, single hot / swollen / painful joint with fever and decreased ROM.
105. knee, shoulder, wrist, hip, phalanges.
106. CBC with diff: leukocytosis. biopsy of synovial fluid.

107. borelia burgdorferi carried through the deer tick.
108. erythema chronicum migricans, 3-32 days after tick bite.
109. lymphocytic meningitis, encephalitis, chorea, ataxia, cranial neuritis, peripheral neuropathy.
110. AV block, pericarditis, cardiomegaly
111. myalgias/arthralgias that present as sudden swelling of a single large joint.
112. test for antibody titers, then do western blot.
113. juvenile RA
hepatitis
herpes zoster
infectious arthritis
reiter's syndrome

114. an underlying condition that makes the patient more prone to chronic infection such as an open wound, chronic prostatitis or chronic UTI's.
115. slow onset over several months.
116. severe back pain and paravertebral spasm.
117. no.
118. increased ESR and xray would show cloudy/spotty demineralization of bone.

CPD III - thyroid and parathyroid conditions

2010-05-10T07:28:00.000-07:00

we started the second week of endocrine with a look at parathryoid and calcium issues. calcium levels are regulated hormonally by 3 main agents: PTH from the parathyroid, activated vitamin D from the kidneys, and calcitonin from the thyroid. PTH has four main actions: increases osteoclastic activity, increases reabsorption of calcium in the kidneys, decreases reabsorption of phosphate in the kidneys, and stimulates activation of vitamin D in the kidneys. whereas PTH has the effect of raising serum calcium levels, calcitonin (secreted from the C cells of the thyroid) lowers them by inhibiting osteoclastic bone resorption.

parathyroid hormone can be secreted in excess in many conditions, categorized by 1º, 2º, 3º. 1º is usually due to a parathyroid adenoma and results in osteoporosis, kidney stones, abdominal symptoms, and fatigue (bones, stones, groans, moans). it may also be asymptomatic and found by elevated serum calcium levels. hypercalcemia can also be caused by other conditions such as multiple sclerosis and sarcoidosis, in which case PTH levels would be low due to negative feedback to the parathyroid. 2º hyperparathyroid is often due to renal failure, which causes chronically low levels of calcium, resulting in compensatory PTH secretion. 3º refers to hypercalcemia from autonomous PTH secretion.

on the other end, hypoparathyroidism is mainly caused by surgical procedures-- such as removing part of the thyroid in grave's disease. signs and symptoms might include neuromuscular instability, parkinsons-like movements, and muscle tetany. the characteristic signs on a PE are chvosek (tapping on the TMJ causes contraction of the periorbital or perioral muscles) or trousseau's sign (carpal pedal spasm from occluding forearm blood supply).

the thyroid gland produces thyroid hormone mostly in the form of T4, most of which is bound to TBG in the blood. hypothyroidism can be due to primary causes (autoimmune dysfunction of the thyroid itself), secondary (dysfunction of anterior pituitary secretion of TSH), or tertiary (dysfunction of hypothalamic secretion of TRH), though the latter two are relatively rare. primary hypothyroidism can affect newborns, and cretinism can develop if thyroid hormones are low during the first few weeks of life, resulting in mental retardation, short stature, puffy facial features, among other symptoms.

for adults, hypothyroidism occurs more frequently in females, and is most commonly due to autoimmune disease, although outside the US can also be attributed to iodine deficiency. besides the signs and symptoms related to slowed metabolism (decreased circulation, energy, hair loss, etc), one might also notice follicular hyperkeratosis-- red bumps over the hair follicles on the outer arms, which is related to a defect in vitamin A synthesis, as well as diminished DTR's. lab values would show decreased levels of T4 but increased levels of TSH. secondary hypothyroidism results from pituitary dysfunction, causing low TSH and T4/T3 levels but high TRH levels. patients might present with signs of general pituitary dysfunction, or an intracranial mass (such as pituitary adenoma symptoms).

hyperthyroidism manifests with signs of metabolic excess such as heat intolerance, weight loss, irritability, warm/moist skin, muscle tremors, high cardiac output, etc. the most common cause is autoimmune via antibodies to the thyroid's TSH receptors as in grave's disease. grave's patients might also present with pretibial myxedema, a skin thickening specific to the legs. hyperthyroid states are diagnosed by testing for antibodies against the thyroid as well as checking radioactive iodine uptake. high uptake plus positive antibodies means primary / autoimmune hyperthyroid. high uptake plus negative antibodies can mean plummer's syndrome, toxic thyroid nodules that can stimulate thyroid hormone production. low uptake plus negative antibodies can indicate thyroiditis.

four types of thyroid cancer have been identified: papillary is the most common and has a relatively good prognosis. follicular is more malignant and makes up 15% of thyroid cancers. medullary involves proliferation of c-cells and subsequent elevation of calcitonin levels. anaplastic / undifferentiated type is the most rare and has the worst prognosis.

questions
physiology...
1. what are the three hormones that are in charge of calcium regulation and where are they secreted from?
2. what steps would be taken in order to make a diagnosis of hyperparathyroid from a patient with high calcium levels?
3. what are the four main actions of PTH?
4. what are the actions of calcitonin and where is it secreted from?

hyperparathyroid states...
5. what is 1º hyperparathyroidism usually due to?
6. what are the signs and symptoms of 1º hyperparathyroidism?
7. besides hyperparathyroidism, what are some other causes of hypercalcemia?
8. in general, how high or low are PTH levels in hypercalcemia that is not of parathyroid origin?
9. what is the most common cause of 2º hyperparathyroidism?
10. what is the mechanism of pathogenesis for 2º hyperparathyroidism?
11. what is the hallmark of 3º hyperparathyroidism?

hypoparathyroid...
12. what is the most common cause of hypoparathyroidism?
13. what are the signs / symptoms of hypoparathyroidism?
14. what are the classic PE findings for hypoparathyroidism?
15. describe the first sign from question 14.
16. describe the second sign from question 14.

thyroid physiology review...
17. which cells in which gland is TSH made in?
18. TSH levels are mainly regulated by...
19. what are the three proteins that carry thyroid hormones in the blood?

hypothyroidism intro...
20. what is the difference between primary, secondary, and tertiary hypothyroidism?
21. what is peripheral hypothyroidism?
22. what are some etiologies for primary hypothyroidism?
23. hypothyroid is the number one reversible cause of...
24. what is cretinism and what are its manifestations?

primary hypothyroidism...
25. which gender is hypothyroidism more common in?
26. what are the most common causes of adult hypothyroidism in the US and the world?
27. what is follicular hyperkeratosis and what is it due to?
28. what is a common PE finding for hypothyroidism?
29. what are the lab values for the thyroid hormones in hypothyroidism?

secondary hypothyroidism...
30. what is a condition associated with secondary hypothyroidism?
31. what are the signs / symptoms of a patient with secondary hypothyroidism?
32. what åre the typical lab values for a patient with secondary hypothyroidism?
33. what is a contraindication for thyroid hormone replacement therapy?

hyperthyroidism...
34. what are some of the symptoms of hyperthyroidism?
35. what are some PE findings for hyperthyroidism?
36. what is the most common cause of hyperthyroidism?
37. what is the mechanism for the condition in question 36?
38. what is a symptom associated with the condition in question 36 that manifests on the extremities?
39. how is the cause of hyperthyroidism determined diagnostically?
40. according to the method in question 39, primary hyperthyroid would be characterized by...
41. according to the method in question 39, plummer's syndrome would be characterized by...
42. according to the method in question 39, thyroiditis would be characterized by...

other thyroid pathologies...
43. what are the 4 types of thyroid cancer?
44. which thyroid cancer is the most common?
45. which is more malignant, follicular or papillary?
46. the medullary type is characterized by proliferation of which cell?
47. how does anaplastic thyroid cancer present?

answers
1. PTH from parathyroid, calcitonin from thyroid, and activated vitamin D from the kidneys.
2. recheck. check for high ionized calcium levels. check for high PTH levels.
3. stimulates osteoblastic activity
inhibits reabsorption of phosphate in the kidneys
stimulates reabsorption of calcium in the kidneys
stimulates activation of vitamin D in the kidneys
4. secreted from C cells of the thyroid, decreases serum calcium by decreasing bone resorption via osteoclasts.

5. parathyroid adenoma.
6. bones, stones, abdominal moans, groans.
7. multiple sclerosis, paget's disease, vitamin D intoxication, sarcoidosis.
8. low because of negative feedback to the parathyroid.
9. renal disease.
10. depressed serum calcium leads to overcompensation via PTH secretion.
11. development of autonomous hypersecretion of PTH, causing hypercalcemia.

12. surgically induced.
13. neuromuscular instability, parkinsons-like movements, tetany.
14. chvosek and trousseau's sign.
15. tapping around the TMJ causes contraction of muscles around the mouth or eyes.
16. "carpal pedal spasm" resulting from occluding blood supply to forearm for several minutes.

17. thyrotroph cells of the anterior pituitary.
18. T3 levels.
19. TBG, transthyretin, albumin.

20. primary is a dysfunction in secretion of the thyroid gland itself, secondary is dysfunction in secretion of TSH from AP, tertiary is dysfunction in secretion of TRH from hypothalamus.
21. peripheral resistance to thyroid hormones, or reduced T4 to T3 conversion, or excess rT3.
22. congenital
iodine deficiency related (goitrogens)
thyroid ablation
23. depression.
24. primary hypothyroid during the first few weeks of life, resulting in mental retardation, short stature, puffy facial features, dry skin, myxedema.
25. females.
26. autoimmune, and iodine deficiency.
27. red bumps over the hair follicles on the outer arm, due to vitamin A synthesis defect.
28. diminished DTR's
29. high TSH, low T4.

30. sheehan's.
31. symptoms of deficiency of other pituitary hormones, or intracranial mass.
32. high TRH, low TSH, low T4 and T3.
33. adrenal cortisal insufficiency / addison's, MI, thyrotoxicosis

34. heat intolerance
irritability
weight loss
exophthalmos
35. may have goiter
warm, moist skin
conjunctival injection
high cardiac output
tremor
fast DTR's
36. grave's disease.
37. antibody against TSH receptor causes constant stimulation of thyroid gland.
38. skin thickening on the legs: pretibial myxedema.
39. testing for antibodies to thyroid plus radioactive iodine uptake.
40. high uptake and positive antibodies.
41. high uptake and negative antibodies.
42. low uptake and negative antibodies.

43. papillary, follicular, medullary, anaplastic.
44. papillary.
45. follicular.
46. c cells that produce calcitonin.
47. rapid and painful enlargement of the thyroid, poor prognosis.

GPA prep- respiratory and HEENT

2010-05-05T10:03:00.000-07:00

URI: upper respiratory infection caused either by bacteria or a virus, leading to congestion, sneezing, rhinorrhea, discharge, malaise. if bacterial in origin, a URI might be more likely to present with fever / chills and yellow/green mucopurulent discharge. if viral in origin a URI might present with clear rhinorrhea. diagnosis is by the jones criteria, rapid strep test, and microscopic smear of exudates.

asthma: can be extrinsic (allergic, to molds, pollens, etc), or intrinsic (infectious, emotional, etc.). usually results in coughing (worse at night), wheezing, dyspnea, sputum production. PE findings might include tachypnea, tachycardia, accessory muscle use, and if severe, pulsus paradoxus and muscle wasting. lung auscultation will reveal prolonged expiratory phase with expiratory wheezing, diminished breath sounds. a skin exam might also be performed to confirm signs of atopy (eczema, dermatitis).

sinusitis is an inflammation of the sinuses due to infection or allergies. it can result in a painful pressure in the sinus area from the swelling of the mucous membranes if associated with a URI. typical signs and symptoms might include swelling / tenderness over the affected sinus, malaise, toothache, severe frontal headache, swollen eyelids. on PE, one might find erythematous nasal mucosa and sinuses that do not transilluminate. labs might be useful to rule out periapical abscess (using xray) or to confirm chronic sinusitis (using CT scan).

bronchitis is an inflammation of the bronchial tree, either secondary to an infection, asthma, irritant, or primary/chronic. if infectious in origin, bronchitis is likely due to a bacterial URI, while common irritants might be organic solvents, ammonia, dust, chlorine. symptoms are similar to an infectious URI: coryza, malaise, f/c, myalgia, etc. the cough often progresses from a dry, non-productive, to a sputum producing cough. on a respiratory exam, one might hear scattered rhonchi, crackling/wheezing, moist rales.

pneumonia is an acute infection of the lung, and can be from a variety of different sources- bacterial, viral, or mycoplasmal. adults are more likely to get bacterial pneumonia, while young adults and children are more likely to get mycoplasmal or viral. risk factors include cigarette smoke, young/old age, immunocompromised, recurrent URI's, physical debilitation. patients might present with fever / chills, nausea / vomiting, pleurisy / dyspnea, productive cough with rusty colored sputum and an increased pulse and respiratory rate. a lung exam might reveal signs of lung consolidation: dullness to percussion, increased tactile fremitus, whispered pectriloquy, and bronchial breath sounds / crackles. ddx's might include bronchitis, goodpasture's, asthma, cystic fibrosis.

some notes on the different types of headaches. doing a good history is vital to determining the cause of the headache, as well as determining the location and radiation patterns. tension headaches are more likely to be described as a band-like pain around the occiput, whereas migraines are more frontal. pain around or in the eyes might be due to a cluster headache, and pain in the face is likely from trigeminal neuralgia. unilateral head pain on the side of the head could be from temporal arteritis. papilledema or A/V nicking on a fundoscopic can indicate serious conditions such as intracranial hemorrhage or malignant hypertension, respectively.

hay fever aka allergic rhinitis is inflammation of the mucosa of the eyes and nasal passageways, leading to rhinorrhea, itchy / burning eyes and nasal congestion. it is often due to seasonal allergens such as pollen and will present bilaterally. a skin test might be useful to check for signs of atopy in the form of dermatitis, etc. differentials might include sinusitis, acute rhinitis, vasomotor rhinitis, and cocaine use.

conjunctivitis is an inflammation of the conjunctiva of the eyes and can be bacterial, viral (pink eye), or allergic / irritant in nature. signs include conjunctival injection (superficial dilated vessels away from the iris), pruritis, discharge, hyperemic and swollen lids. if symptoms are bilateral, the origin is more likely to be infectious or allergic while unilateral symptoms suggest toxic/chemical/mechanical causes. a culture of secretions can be useful in differentiating the cause of conjunctivitis: bacterial related secretions would contain PMN's, viral would contain leukocytes, and allergic would contain eosinophils.

strep throat is the result of infection via type A beta-hemolytic strep. it manifests as swollen, sore throat with fever and L/A. the jones criteria, used to diagnose strep, requires at least 2 of the following: fever above 100.4F po, no cough, pseudomembrane, tonsillar exudate. strep can also be diagnosed via a rapid strep test or throat culture. ddx's might include pharyngitis, mono, peritonsilar abscess, and diptheria.

vertigo is more of a symptom and can be due to several different causes, including benign paroxysmal positional vertigo, meniere's vestibular neuronitis, and other CNS disorders. episodic vertigo is more likely to be BPPV, while vertigo that lasts for hours / days is more likely to be meniere's or vestibular neuronitis. vertigo can also be associated with symptoms such as nausea / vomiting, tinnitus, and nystagmus-- which if unilateral and horizontal indicates benign causes and if variable indicates CNS disorders.

questions
URI...
1. what is the etiology of a URI?
2. what are some typical signs / symptoms of a URI?
3. what are some features that might distinguish a URI of bacterial vs. viral origin?
4. what labs should be performed for the diagnosis of a URI?

asthma...
5. what are three major features of asthma?
6. what is the difference between intrinsic and extrinsic asthma?
7. what are the major signs and symptoms of asthma?
8. what are some typical PE findings for asthma?
9. what signs might indicate a severe case of asthma?
10. what are the common findings for a lung exam on a patient with asthma?
11. why might a skin exam be performed on a patient suspected of having asthma?

sinusitis...
12. what is sinusitis?
13. what are the typical signs and symptoms of sinusitis?
14. what are some typical PE findings for sinusitis?
15. which labs might be performed to aid in a diagnosis of sinusitis?

bronchitis...
16. what is bronchitis?
17. what are the most common etiological agents for bronchitis?
18. the symptoms of infectious bronchitis are similar to...
19. describe the progression of the cough in infectious bronchitis.
20. severe cases of bronchitis might also present with...
21. what might be heard on a respiratory exam for bronchitis?
22. where in the lung might these sounds be heard?

pneumonia...
23. what is pneumonia?
24. what are three different types of pneumonia?
25. which type is most common in adults? young adults / children?
26. what are some risk factors for pneumonia?
27. what are the signs and symptoms for pneumonia?
28. what are the signs one would expect to find on a lung exam of a pneumonia patient?
29. what are some ddx's for pneumonia?

headaches...
30. what are some causes of head pain?
31. where do tension headaches usually present? how is the sensation described?
32. a frontal headache is more likely what type of headache?
33. a periorbital or deep orbital pain is most likely due to what type of headache?
34. pain in the face is likely due to...
35. unilateral head pain on the side of the head is likely due to...
36. patients with temporal arteritis might also present with what concomitant symptom?
37. what are some physical exams that one should perform on a patient that presents with head pain?

hay fever...
38. what is hay fever?
39. what are two useful questions to ask a patient suspected of hay fever?
40. what are the signs and symptoms of hay fever?
41. why might a skin test be performed in patients suspected of hay fever?
42. what are the differentials for hay fever?

conjunctivitis...
43. "pink eye" is...
44. what are the signs and symptoms of conjunctivitis?
45. what do bilateral vs. unilateral symptoms suggest about the origins of conjunctivitis?
46. what PE exams would be useful in diagnosing conjunctivitis?
47. what labs would you order with a patient suspected of conjunctivitis?

strep throat...
48. what is the etiology of strep throat?
49. what are the signs/symptoms of strep throat?
50. what are the jones criteria for diagnosing strep throat?
51. what are the lab tests used to diagnose strep throat?
52. what are the ddx's for strep throat?

vertigo...
53. episodic vertigo is more likely to be...
54. vertigo that lasts hours or days is more likely to be...
55. vertigo that is sudden onset and lasts for minutes is more likely to be...
56. what are the signs and symptoms associated with vertigo?
57. how can the type of nystagmus differentiate between potential causes of vertigo?

answers
1. viruses or bacteria invading upper respiratory tract, causing inflammation of the mucosa.
2. congestion, sneezing, rhinorrhea, post-nasal drainage, malaise.
3. bacterial more likely to have fever / chills and yellow green mucopurulent discharge. viral more likely to have clear rhinorrhea.
4. rapid strep test if jones criteria met, microscopic smear of exudates.

5. airway obstruction
inflammation
irritability / hypersensitivity
6. extrinsic is to allergy to external factors such as mold, pollen, etc. intrinsic is non allergic- from infections or emotional or other internal causes.
7. coughing, especially at night
wheezing, shortness of breath, DOE
sputum production
8. tachypnea, tachycardia, diaphoresis, wheezing, accessory muscle use.
9. weight loss, wasting, pulsus paradoxus.
10. prolonged expiratory phase, expiratory wheezing and diminished breath sounds.
11. to look for signs of atopy: dermatitis, eczema, other allergic skin conditions.

12. inflammation of the paranasal sinuses due to infection or allergy.
13. swelling / tenderness
malaise
toothache
frontal headache
swollen eyelids
14. erythematous nasal mucosa, sinuses do not transilluminate.
15. CT scan for chronic sinusitis
xray of teeth apices to rule out periapical abscess
CBC

16. an infection of the bronchial tree, either secondary to an infection, asthma, irritant, or primary / chronic.
17. infectious: bacterial URI
irritant: organic solvents, ammonia, dusts, chlorine
18. infectious URI symptoms: coryza, malaise, fever/chills, myalgia, etc
19. begins as dry and non productive, then develops into a productive cough.
20. 101-102 degree fevers.
21. scattered rhonchi, crackling/wheezing, moist rales.
22. at the base for crackling / rales.

23. infection of the lung.
24. bacterial, viral, mycoplasma.
25. bacterial most common in adults, mycoplasma in young adults and children.
26. immunocompromised
young or old age
recurrent URI's
cigarette smoke
physical debilitation
27. fever / chills
pleurisy / dyspnea
productive cough with rusty sputum
tachycardia, tachypnea
N/V
malaise / myalgia
28. increased tactile fremitus
dullness to percussion
bronchial breath sounds
whispered pectriloquy
crackles
[touch dull bronchial whisper crackle]
[fremitus dullness whisper bronchial crackles] [touch the dull whisker to hear the bronchial crackles]
29. bronchitis
asthma
cystic fibrosis
goodpasture's

30. vasomotor instability
muscle tension
hypoglycemia
infection
trauma
mass lesion
cerebral hemorrhage
31. occiput, band-like.
32. migraine
33. cluster
34. trigeminal neuralgia.
35. temporal arteritis.
36. polymyalgia rheumatica.
37. vitals, M/S, eye exam, sinsuses, neurological exam.

38. also known as allergic rhinitis; an inflammatory process involving the nasal and throat mucosa, as well as the conjunctiva in response to various allergens.
39. do your symptoms appear seasonally? are they bilateral?
40. rhinorrhea
burning, itchy, watery eyes
nasal / sinus congestion
41. to check for signs of atopy: dermatitis, eczema.
42. sinusitis, acute rhinitis, vasomotor rhinitis, cocaine use.

43. viral conjunctivitis.
44. superficial dilated vessels in conjunctiva
pruritis
discharge
hyperemia, swelling of lids
45. bilateral more likely allergic / infectious. unilateral more likely toxic/chemical/mechanical.
46. vitals, lymph nodes, EENT, (heart, lungs)
47. culture of secretion: bacterial would contain PMN's, viral would contain lymphocytes, allergic would contain eosinophils.

48. pharyngitis caused by group A beta-hemolytic streptococcus.
49. sore throat
fever
no cough
cervical L/A
injected / erythematous mucous membranes
exudate / pseudomembrane
50. fever over 100.4 po, no cough, tonsilar exudate, pseudomembrane.
51. rapid strep test and throat culture.
52. viral / bacterial pharyngitis
infectious mononucleosis
diptheria
peritonsilar abscess

53. BPPV
54. meniere's, vestibular neuronitis
55. brain or vascular disease.
56. spinning sensation/disequilibirum
nystagmus
N/V
tinnitus
57. unilateral horizontal nystagmus is more likely benign, variable nystagmus likely due to a CNS disorder.

CPD III- endocrine II: adrenals

2010-05-03T08:17:00.000-07:00

some review of kidney / adrenal physiology. the adrenals are endocrine organs that lie on top of the kidneys and are divided into the adrenal cortex and medulla. the adrenal medulla can be described as "a gland within a gland" and mostly secretes epinephrine, although nor-epinephrine and small amounts of dopamine are also secreted. the adrenal cortex is subdivided into three "zones", each secreting a different hormone- the zona glomerulosa secretes minerocorticoids such as aldosterone, zona fasiculata secretes glucocorticoids such as cortisol, and the zona reticularis secretes sex steroids such as DHEA, androgens, and small amounts of estrogen / cortisol.

addison's disease refers to adrenal hypofunction and can be primary or secondary. primary is due to damage to the adrenal cortex itself, usually due to autoimmune causes. this can result in decreased cortisol as well as aldosterone production, leading to hypoglycemia, hyponatremia, and hyperkalemia. the serum levels of ACTH will be extremely high but levels of cortisol will be extremely low in these patients. signs and symptoms might include weakness, dehydration, anorexia, hypotension, hyperpigmentation due to stimulation of melanocytes by ACTH. primary addison's can be confirmed with the ACTH stimulation test- patients with a damaged adrenal cortex will not respond to exogenous ACTH administration. secondary addison's is a shortage of ACTH, usually from damage to the pituitary from trauma, surgery, radiation, or tumors. this patient would have low levels of cortisol as well, but also low levels of ACTH and normal aldosterone secretion. also, because ACTH levels are low, melanocytes would not be stimulated and this results in hypopigmentation, contrasting with the hyperpigmentation seen in primary addison's.

an addisonian crisis results when a patient who has been taking exogenous glucocorticosteroids is unable to produce cortisol intrinsically due to lower ACTH levels when the glucocorticosteroids have been stopped. this patient may take weeks to months to acclimate, during which severe symptoms of weakness, nausea/vomiting, dehydration, hypoglycemia may occur.

cushing's syndrome is on the opposite side from addison's, representing adrenal hyperfunction. most cases are iatrogenic, from long term exogenous use of glucocorticosteroids. cushing's disease is a specific type which involves a pituitary adenoma that produces ACTH. ACTH may also be produced in ectopic cancer sites- lung cancer cells in particular. patients with cushing's will present with weight gain, especially around the abdomen, as well as moon facies, buffalo hump, and hypertension. aldosterone production may also be affected, leading to hypokalemia and hypertension as well. diagnosis can be confirmed by the dexamethasone test, in which the cortisol production in response to dexamethasone is measured-- normally it is suppressed, but in cushing's patients, it is unaffected.

conn's syndrome is hyperfunction of the adrenals specific to the zona glomerulosa- resulting in aldosterone hyperproduction. this generally results in hypertension and hypokalemia and is due to a adrenal adenoma. lab results might include high serum aldosterone, low potassium, and low renin (suppressed in response to high blood volume). a patient suspected of conn's might go through the aldosterone suppression test, in which IV fluid is introduced into the body and aldosterone levels are monitored-- if they are not inhibited as they should be in response to the extra fluid volume, they probably have conn's syndrome.

congenital adrenal hyperplasia is an underproduction of cortisol due to a deficiency of enzymes that regulate cortisol production. due to the shunting of cortisol precursor to androgen precursors such as 17-hydroxyprogesterone, these patients will have signs and symptoms of androgenism: hirsuitism, abnormal menses and infertility in females and precocious sexual development in males. they might also have short stature due to the premature closure of the epiphyseal growth plates. lab tests would look for increased levels of 17-ketosteroids and treatment involves exogenous administration of cortisol.

a pheochromocytoma is an catecholamine producing adenoma of the adrenal medulla which results in increased renin secretion, leading to severe hypertension which is resistant to blood pressure lowering regimens. the classic presentation is a patient with episodes of hypertension with intermittent episodes of hypotension, with headache, sweating, mental status changes, and hypermetabolism. a pheochromocytoma is generally diagnosed by the 24 hour urinary catecholamine test, meta-nephrine levels, and the clonidine suppression test.

questions
physiology...
1. what are the three zones of the adrenal cortex?
2. what do the cells of the adrenal medulla secrete?
3. what do the three zones of the adrenal cortex secrete?
4. describe the chain of production of ACTH.

addison's disease...
5. what is primary addison's disease?
6. what is the most common cause of primary addison's disease?
7. why might primary addison's lead to hypotension?
8. what are the signs and symptoms of primary addison's disease?
9. which areas of the body are more prone to developing hyperpigmentation in primary addison's?
10. what is the characteristic lab picture of a patient with primary addison's?
11. what are some other lab markers that might be abnormal in a patient with primary addison's?
12. what is the test that can be performed that will confirm the diagnosis of primary addison's?
13. what is the etiology of secondary addison's?
14. what is the sign that can differentiate secondary and primary addison's?

addisonian crisis...
15. what is an addisonian crisis?
16. what are the symptoms of an acute addisonian crisis?

cushing's syndrome...
17. what is the difference between cushing's syndrome and cushing's disease?
18. what are the causes of cushing's disease?
19. what is a potential cause for cushing's disease not related to the pituitary or adrenals?
20. what are the signs and symptoms for cushing's syndrome?
21. what are the lab findings for a patient with cushing's?
22. what is a test that can confirm the diagnosis of cushing's syndrome? how does it work?

conn's syndrome...
23. what is conn's syndrome?
24. what is the typical presentation of a patient with conn's syndrome?
25. what are the abnormal lab results of a patient with conn's syndrome?
26. what is a test that confirms the diagnosis of conn's syndrome?

congenital adrenal hyperplasia...
27. what is CAH?
28. what is the most common enzyme involved in CAH?
29. why might CAH lead to virilization?
30. how might CAH affect females?
31. how might CAH affect males?
32. why might CAH lead to short stature?
33. what is the lab test that can help diagnose CAH?

pheochromocytoma...
34. what is a pheochromocytoma?
35. what is the classic presentation of a patient with a pheochromocytoma?
36. what are the signs and symptoms of a patient with a pheohromocytoma?
37. what are the lab tests useful in diagnosing a pheochromocytoma?
38. what is a test that can be used to confirm the diagnosis of a pheochromocytoma?

answers
1. zona glomerulosa, fasiculata, reticularis.
2. mostly epinephrine, some nor-epinephrine, a little dopamine.
3. glomerulosa: minerocorticoids such as aldoesterone
fasiculata: glucocorticoids such as cortisol
reticularis: androgens such as DHEA
4. hypothalamus secretes CRH in response to stress, triggering pituitary to release ACTH, which acts on the adrenal glands.

5. adrenal insufficiency due to a damaged adrenal gland.
6. autoimmune destruction of the adrenal cortex.
7. because damage might include the zona glomerulosa, which would result in an underproduction of aldosterone, a hormone that facilitates water reabsorption in the kidneys.
8. WOAHH:
weakness
often dehydrated
anorexia
hypotension
hyperpigmentation / bronze skin
9. palmar creases, buccal mucosa, elbows and knees.
10. extremely low cortisol levels and high ACTH levels.
11. hypoglycemia, hyponatremia, hyperkalemia.
12. ACTH stimulation test: patients with primary addison's should not respond to administration of ACTH exogenously.
13. insufficient ACTH production by the anterior pituitary due to trauma, surgery, radiation, tumors.
14. secondary patients have pallor instead of hyperpigmentation because of low ACTH levels.

15. removal of long term exogenous administration of glucocorticoids leading to inability to produce cortisol due to low ACTH levels.
16. weakness
nausea/vomiting
dehydration
hypoglycemia

17. cushing's syndrome refers to adrenal hyperfunction generally whereas cushing's disease is a type of cushing's syndrome that refers to a pituitary adenoma.
18. generally from longterm exogenous administration of glucocorticoids.
19. ectopic sites that produce ACTH, such as lung cancer cells.
20. weight gain, especially mid abdominal
moon facies / buffalo hump
hypertension
21. hyperglycemia
secondary diabetes
hypertension / hypokalemia
22. 6 hour or overnight dexamethasone suppression test. normally cortisol production should be inhibited by administration of dexamethasone.

23. an increase in aldosterone production from an adrenal adenoma without cortisol increases.
24. hypertension.
25. high serum aldosterone
hypokalemia
low serum renin
26. aldosterone suppression test: administer extra IV fluid and watch for the lack of aldosterone suppression.

27. underproduction of cortisol due to deficiency of enzymes related to cortisol synthesis.
28. 21-hydroxylase.
29. because the decreased cortisol precursor production will lead to increased synthesis of other precursors, one of which is an androgen precursor, 17-hydroxyprogesterone.
30. symptoms of androgenism: hirsuitism, abnormal menses, infertility.
31. precocious development.
32. because high androgen levels also lead to premature closure of the epiphyseal growth plates.
33. serum levels of 17-ketosteroids such as 17-hydroxyprogesterone.

34. catecholamine producing tumor.
35. episodes of severe hypertension followed by hypotension.
36. headache
diaphoresis
mental status changes
hypermetabolism
postural hypotension
37. 24 hour urinary catecholamines and meta-nephrines
38. clonidine suppression test.

CPD III- endocrine I: hypothalamus, pituitary

2010-05-03T08:13:00.000-07:00

this lecture began our introduction to diagnosis of endocrine disorders, courtesy of dr. marcus miller.

the hypothalamus is the endocrine organ that receives information from the CNS and in turn stimulates the pituitary to release hormones. it carries a set of hormones as well, including TRH, CRH, GnRH, GHRH, somatostatin, ADH, oxytocin, and dopamine. [quick note: somatostatin acts as a GHRH antagonist, and dopamine acts as a prolactin antagonist] the hypothalamus is connected via nerves as well as blood to the pituitary, which is divided into 3 lobes, anterior (makes up 80%), intermediate, and posterior. the posterior pituitary acts as a storage for ADH and oxytocin, and the intermediate lobe also contains hormones such as the melanocyte stimulating hormone. because of the pituitary's location in the sella turcica, pituitary adenomas might lead to bitemporal hemianopsia due to the upward growth and subsequent impingement on the optic chiasm.

the anterior pituitary's general function is to stimulate peripheral endocrine organs such as the thyroid and regulate growth and lactation. it does this by release of a variety of hormones, including growth hormone, LH / FSH, TSH, prolactin, and ACTH. ACTH is responsible for stimulating cortisol production from the adrenals. LH stimulates ovulation and progesterone production in females and prolactin has the opposite effect, while also stimulating lactation.

the posterior pituitary is made up of modified nerve fibers, axons, and glial cells extending from the supraoptic and paraventricular nuclei from the hypothalamus. as mentioned before, the axons of the posterior pituitary store two hormones made in the hypothalamus, ADH and oxytocin. ADH's main action is in the kidney, stimulating water reabsorption in the distal tubules, while oxytocin stimulates lactation and uterine contraction, among other things.

hypopituitarism means decreased output of pituitary hormones and can be due to a variety of causes-- oftentimes the cause for panhypopituitarism (equal reduction in all AP hormones) is iatrogenic-- either through radiation to the head or surgery that reduces blood flow. other causes might include destructive processes such as inflammation or infection, hemochromatosis, malignancy. hypopituitarism can also result in dwarfism, which comes in several varieties as well- if resulting from panhypopituitarism, body proportions will be normal, while a selective GH deficiency might result in abnormal proportions. achondroplastic dwarfism is a third type that is not related to hypopituitarism (and therefore is unresponsive to GH supplication).

some pituitary pathologies: pituitary apoplexy is a hemorrhage into a pre-existing adenoma, resulting in a sudden onset headache and diplopia. severe cases might also lead to ischemic necrosis and may even result in death. the most common cause of ischemic necrosis is sheehan's syndrome, although patients with this syndrome may have a range of outcomes, ranging from asymptomatic to death. sheehan's syndrome is a situation where the already hypoxic pituitary in pregnant women (due to an increase in pituitary size without increased vasculature) is further compromised by obstetric hemorrhage, leading to vasospasm and ischemic necrosis.

pituitary adenomas are the most common cause of hyperpituitarism, although a good portion of pituitary adenomas are non functional and can remain undetected. they can be macro (greater than 1cm) or micro (less than 1cm) and comprise 10% of all intracranial neoplasms. functional adenomas are generally composed of one cell type and secrete a single hormone. the most common functional adenomas are: prolactinoma, ACTH producing, gonadotropin producing, and growth hormone producing.

the most common type of adenoma produces prolactin and is composed of weakly staining acidophilic cells-- within which prolactin can be detected in the secretory granules. in females, the effects of a prolactinoma are what one would expect from increased prolactin levels: amenorrhea, diminished libido, ovarian cysts (due to inhibition of ovulation), galactorrhea. in males, prolactinomas might manifest asymptomatically, or decreased libido. prolactinomas might be diagnosed by high serum prolactin levels, and an MRI will confirm the presence of one as small as 2mm.

growth hormone producing adenomas are the second most common type. they are measured / diagnosed primarily by increased IGF-1 levels, from increased hepatic production due to GH stimulation. GH excess can lead to a variety of signs/symptoms, including diabetes, HTN, hyperglycemia, CHF, gonadal dysfunction, and muscle weakness. if the adenoma is functional before growth plate closure, the result is pituitary giantism, in which body size is increased and arms / legs are disproportionately long. if the adenoma is function after growth plate closure, the result is acromegaly, which has its own characteristics: enlarged hands, feet, face (nose broadens, teeth get further apart, jaw protrudes), and organomegaly. GH producing adenomas are diagnosed via IGF-1 levels as well as the GH suppression test, in which GH levels do not drop as they should in response to glucose administration.

empty sella syndrome describes any condition in which the sella turcica is enlarged but not filled with pituitary tissue. risk factors include pregnancy, obesity, and hypertension. ESS is caused by increased intracranial pressure which leads to CSF entering the sella turcica, compressing the pituitary against its walls. presentation might be asymptomatic, or may have papilledema. ESS might also be due to a surgical procedure or radiation which has enlarged the sella turcica.

excess ADH production may be related to posterior pituitary dysfunction and can result in dysfunction in the water balance in the body. syndrome of inappropriate ADH describes such a condition, which can also be caused by ectopic sites, generally from cancer cells. the signs and symptoms might be limited to reduced urine, and the diagnosis might be made by highly concentrated urine, decreased plasma osmolality, and hyponatremia.

diabetes insipidus is a condition which results from ADH deficiency; either from an underproduction from the hypothalamus (central) or dysfunctional ADH receptors in the kidney (nephrogenic). DI results in polyuria and polydipsia, with the polyuria generally exceeding the polydipsia. central might be caused by surgery/trauma, tumors, infection, sheehan's syndrome, while nephrogenic might be caused by chronic renal disease, lithium, among other things. a useful test for distinguishing central, nephrogenic DI, and psychogenic polydipsia is the water deprivation test. after depriving water, patients with psychogenic polydipsia will have increased osmolality while the other two conditions will not. after administration of ADH, psychogenic polydipsia and central DI will increase urine osmolality (increased reabsorption produces more concentrated urine), whereas nephrogenic will remain the same.

questions
hypothalamus and pituitary...
1. what is the relative prevalence of endocrine issues related to the hypothalamus, pituitary, and thyroid?
2. what are the hormones released by the hypothalamus?
3. what is the effect of these hormones on the pituitary?
4. where is the pituitary gland located?
5. what is the pituitary gland covered by?
6. how might a pituitary adenoma lead to loss of peripheral vision?
7. what are the divisions of the pituitary? which division predominates?
8. describe the general function of the posterior pituitary.
9. describe the function of the intermediate pituitary.
10. dopamine exerts inhibitory control over which other hormone?

anterior pituitary...
11. what are the hormones released by the anterior pituitary?
12. what is a better marker for checking growth hormone activity than a simple serum growth hormone level test?
13. describe the general function of the hormones released by the anterior pituitary.
14. what does ACTH do?
15. what does LH do in males and females?
16. what does prolactin do?

posterior pituitary...
17. describe the structure / content of the posterior pituitary.
18. what are the two hormones that are stored in the axons of the posterior pituitary?
19. what does ADH do?
20. what does oxytocin do?

hypopituitarism and dwarfism...
21. most cases of hypopituitarism are the result of...
22. what are some other potential causes of hypopituitarism?
23. what are the two types of pituitary dwarfism?
24. what is achondoplastic dwarfism?

acute pituitary pathologies...
25. what is pituitary apoplexy?
26. what are the symptoms of a pituitary apoplexy?
27. what are the complications of a severe case of pituitary apoplexy?
28. sheehan's syndrome is the most common cause of...
29. describe the pathophysiology of sheehan's syndrome.

pituitary adenoma...
30. pituitary adenomas are the most common cause of...
31. pituitary adenomas are usually...
32. what percentage of intracranial neoplasms are pituitary adenomas?
33. what age range is most common for pituitary adenomas?
34. functional adenomas are usually...
35. what is the difference between a macro and microadenoma?
36. are males more likely to present with a macro or microadenoma?
37. what are the most common types of functional adenomas?

prolactinoma...
38. most prolactinomas are composed of...
39. prolactin can be detected within...
40. what are the signs and symptoms of a prolactinoma in females?
41. what percentage of secondary amenorrhea cases are due to prolactinomas?
42. what are the signs / symptoms of a prolactinoma in males?
43. what are some labs and imaging techniques useful in diagnosing prolactinomas?
44. what is a naturopathic treatment option for prolactinoma?

growth hormone producing adenoma...
45. persistent oversecretion of GH stimulates...
46. what are the signs and symptoms of a GH producing adenoma?
47. how is a GH producing adenoma classified if it is functional before vs. after growth plate closure?
48. describe the body proportions of a patient with pituitary gigantism.
49. what are the signs and symptoms of a patient with acromegaly?
50. what are the lab tests used to diagnose GH producing adenomas?
51. how can a GH producing adenoma be differentiated from hyperglycemia?

corticotroph adenoma...
52. what is a corticotroph adenoma?
53. what is the difference between cushing's syndrome and cushing's disease?

empty sella syndrome...
54. what is the empty sella syndrome?
55. what are the risk factors for ESS?
56. what is the etiology of ESS?
57. what are the signs/symptoms of ESS?
58. what is secondary ESS?

syndrome of inappropriate ADH...
59. what is SIADH?
60. what are some etiological factors that might lead to SIADH?
61. what are the signs / symptoms of SIADH?
62. what are the lab results for SIADH?

diabetes insipidus...
63. what are the two causes of diabetes insipidus?
64. what are the signs and symptoms of DI?
65. what are some etiologies of central DI?
66. what is a drug that might cause nephrogenic DI?
67. what is a test that can distinguish between central DI, nephrogenic DI, and psychogenic polydipsia?
68. what is one possible treatment for DI?

answers
1. hypothalamus problems are much rarer than pituitary and thyroid.
2. TRH
CRH
GnRH
GHRH
somatostatin
dopamine
ADH
oxytocin
3. stimulates pituitary, except for somatostatin and dopamine.
4. the sella turcica.
5. dura mater, except for the a thin opening which conveys a stalk from the hypothalamus.
6. the upward growth of a pituitary tumor will impinge on the optic chiasm, which will block the optic pathways responsible for peripheral vision bilaterally.
7. anterior, intermediate, posterior lobes. anterior is 80%.
8. storage unit for oxytocin and ADH.
9. also contains hormones or precursor to hormones such as melanocyte stimulating hormone and a hormone that increases aldosterone production.
10. prolactin.

11. growth hormone
LH and FSH
TSH
prolactin
ACTH.
[G L/F T P A] [go left, pa]
12. IGF-1 levels.
13. stimulates peripheral endocrine organs and regulates growth and lactation.
14. stimulates cortisol production in the adrenals.
15. stimulates ovulation and progesterone production in females, stimulates testosterone production in males.
16. promotes lactation and suppresses ovulation and fertility.

17. a modified neural network consisting of modified glial cells, nerve fibers, and axonal processes extending from the supraoptic and paraventricular nuclei of the hypothalamus.
18. ADH and oxytocin.
19. stimulates water reabsorption in distal tubules of nephron.
20. regulates lactation and uterine contraction.

21. radiation or surgery which reduce blood flow to the brain.
22. destructive lesions
destructive processes
impingement from malignancy
infection
hemochromatosis
sarcoidosis
23. resulting either from deficiency of all AP hormones or just GH, in which body proportions remain normal and abnormal, respectively.
24. genetic dysfunction of fibroblasts that results in abnormal cartilaginous development.

25. sudden hemorrhage into an existing pituitary adenoma.
26. sudden onset headache and diplopia.
27. ischemic necrosis, death.
28. ischemic necrosis of the pituitary.
29. in pregnant women, the anterior pituitary enlarges without corresponding vasculature increase. this hypoxic state combined with an obstetric hemorrhage can cause vasospasm of the blood supply and ultimately ischemia and necrosis.

30. hyperpituitarism.
31. non functional, isolated lesions with no associated neoplasms.
32. 10%.
33. 30-60.
34. made of one cell type that produces one hormone.
35. greater than or less than 1 cm.
36. macro because of the greater chance of adenoma remaining undetected due to the lack of hormonal feedback as compared to women.
37. prolactinoma, ACTH cell adenoma, gonadotropin adenoma, growth hormone adenoma
[pro act gon grow] [functionally proactive: go and grow!]

38. weakly staining acidophilic cells.
39. secretory granules within cytoplasm of cells.
40. diminished menses or amenorrhea
diminished libido
infertility
ovarian cysts
galactorrhea
[prolact amen libido infertility cysts galact] [amen; all infertile cysts in the galaxy now have libidos]
41. roughly 25%.
42. asymptomatic, or decreased libido / sperm count.
43. serum prolactin and MRI.
44. botanicals that have phytoestrogenic or progesterone agonist effects.

45. hepatic secretion of IGF-1
46. hyperglycemia, DM, HTN, CHF, gonadal dysfunction, muscle weakness/arthritis. [sugar sugar blood blood nads muscles]
47. before: pituitary giant
after: acromegaly
48. bigger body size with disproportionately long arms and legs.
49. disproportionately large hands, feet, face
enlargement of heart, thyroid, liver, adrenals
jaw protrusion
spreading of teeth
broadening of nose
"spade like" hands
50. IGF-1 levels and the GH suppression test.
51. in the GH suppression test of a hyperglycemic patient, GH will be suppressed, but won't be in a patient with a GH producing adenoma.

52. an adenoma that produces ACTH, leading to adrenal hypersecretion of cortisol.
53. cushing's syndrome describes a state of hypercortisolism, of which cushing's disease is a specific type related to a corticotroph adenoma.

54. any condition that leads to an enlarged sella turcica not filled with pituitary tissue.
55. obese females
multiple pregnancies
hypertension
[fat fetus food]
56. increased intracranial pressure leads to CSF entering the sella turcica and compressing pituitary against wall.
57. asymptomatic, may see papilledema.
58. ESS due to surgical procedure or radiation that has enlarged the sella turcica.

59. excess secretion of ADH by ectopic sites.
60. cancer (lung, breast, prostate), head trauma, narcotics.
61. oliguria with no other signs.
62. highly concentrated urine, low plasma osmolality, hyponatremia.

63. deficiency of ADH either by hypothalamus underproduction or kidney unresponsiveness.
64. polyuria, polydipsia.
65. trauma
surgery
tumor
infection
sheehan's
66. lithium.
67. the water deprivation test.
68. oxytocin.

pathology IV- male genitalia quiz

2010-04-30T14:48:00.000-07:00

a study guide for the pathology quiz on male genitalia. we started with a review of various conditions that can affect the male genitalia: phimosis refers to an inability to retract the foreskin of the penis, often due to adhesions formed from undifferentiated tissue in children less than 3 years old. paraphimosis is an inability of the foreskin to fold over the glans. condyloma acuminata are genital warts, caused by HPV strains 6 and 11, appearing as sessile or pedunculated, red papillary outgrowths on the coronal sulcus, inner prepuce, glans, or perianal area.

bowen's disease is commonly caused by HPV 16 and 18 and manifests as single, gray-white plaques with shallow ulcerations and crusting, either on the shaft of the penis or the scrotum. histologically, one might see dysplastic epithelium, scattered mitosis above the basal layer, and nuclear atypia.

bowen's might lead to squamous cell carcinoma, which might also be caused by HPV strains 16 / 18, or simply poor hygeine. SCC typically affects men 40-70 and manifests as painless lesions that may bleed. early lesions may just be epithelial thickening with some fraying / fissuring, while late or untreated lesions may develop into papules, ulcers with ragged and heaped up margins.

some assorted testicular disorders that we've already covered in CPD: cryptorchidism is an undescended testicle which can be associated with hormonal disorders of deficient LHRH and "trisomy 13". it might also be related to exposure to anti-androgenic compounds such as phthalates in plastics and tagamet, which is used to treat plantar warts and peptic ulcers. cryptorchidism increases the risk for infertility as well as testicular cancer of the fully descended side. hydroceles are serous fluid filled masses that can be caused by inflammation (sports) as well as structural / developmental abnormalities. varicoceles result from dilatation of the panpiniform plexus and is also associated with sports such as extreme mountain biking or soccer.

benign prostatic hypertrophy is nodular hyperplasia of the periurethral region of the prostate. it is associated with some dietary factors: deficiency of lycopene, nettles, zinc, EFA's, and amino acids- as well as dietary excess of alcohol, cadmium, cholesterol, and pesticides. the main growth factor for the prostate is DHT, which is converted from testosterone by 5-alpha reductase; cadmium and cholesterol both increase 5-alpha reductase activity, thus contributing to BPH. two other hormonal influences: estrogen increases stroma susceptibility to hyperplasia and prolactin increases androgen uptake.

prostate cancer is the most common type of cancer in men, generally of the type adenocarcinoma. it affects men over 50 with some racial demographic trends: asians tend to have a lower incidence and african americans have a higher incidence. genetic factors that have been identified are the p53 gene and hypermethylation of glutathione S-transferase. a diet high in arachidonic acid (found in meat products) can also be a risk factor. dietary protective factors might include lycopene, vitamin A and E, selenium, soy, and possibly fish oil. the lesions themselves are gritty and firm nodules on the posterior aspects of the lateral lobes, and if metastasis occurs, the bones are a high possibility-- osteoblastic lesions are a common finding in the lumbar / thoracic spine, femur, pelvis, ribs.

questions
various conditions...
1. what is phimosis?
2. how is phimosis related to age?
3. what is paraphimosis?
4. what is the etiology of condyloma acuminata?
5. what is the morphology of condyloma acuminata?
6. what locations are condyloma acuminata commonly found?
7. ∂escribe the histopathology of condyloma acuminata.

bowen's disease...
8. what age does bowen's disease usually affect?
9. what are the most common etiological agents for bowen's disease?
10. describe the morphology of the lesions in bowen's disease.
11. what locations are affected in bowen's disease?
12. what are some histopathological features of bowen's disease?

SCC...
13. what are the most common etiologies for SCC?
14. where are SCC lesions located?
15. describe the morphology of early SCC lesions.
16. describe the morphology of late SCC lesions.
17. what age does SCC generally occur in?
18. what is the relationship to regional lymph nodes and metastasis of SCC?
19. what is the clinical presentation of SCC?

various testicular disorders...
20. what are some intrinsic risk factors for cryptorchidism?
21. what are some extrinsic risk factors for cryptorchidism?
22. what are the sequelae for cryptorchidism?
23. what is a hydrocele and what is it commonly due to?
24. how common in a varicocele?
25. what are examples of types of hobbies that are associated with varicoceles?
26. which side is more commonly affected by varicoceles?

benign prostatic hypertrophy...
27. what are some etiological factors for BPH related to dietary deficiency?
28. what are some etiological factors for BPH related to dietary excess?
29. what is the mechanism by which cadmium and cholesterol are related to BPH?
30. what are DHT and 5-alpha reductase and how are they involved in BPH pathophysiology?
31. what is the effect of estrogen and prolactin in the prostate?

prostate cancer...
32. how common is prostate cancer?
33. what age group does prostate cancer affect?
34. what are the demographic groups that have high and low risks for developing prostate cancer?
35. what are two genetic factors that have been identified as etiological agents in prostate cancer?
36. what is a dietary risk factor for prostate cancer?
37. what are some protective factors for prostate cancer?
38. what is the most common location for prostate cancer?
39. what is the morphology of the lesions in prostate cancer?
40. what is a common area for metastasis and what are the type of lesions found?

testicular cancer...
41. testicular cancer cells are most commonly derived from which cell line?
42. germ cell vs. non germ cell derived testicular cancer: which is more likely malignant?
43. what is the racial trend for incidence of testicular cancer?
44. what is the serum marker for a seminoma?
45. which condition is a seminoma associated with?
46. what is the prognosis for a seminoma?
47. what is the prognosis for an embryonal carcinoma?
48. what are the serum markers for an embryonal carcinoma?
49. which age group does the yolk sac tumor affect?
50. what are the serum markers for a yolk sac tumor?
51. are teratomas considered benign or malignant?
52. what are the serum markers for a teratoma?
53. what is the prognosis for a choriocarcinoma?
54. which age group is lymphoma most common?

answers
1. abnormal tightness of the prepuce that prevents retraction over the glans.
2. may be related to adhesions from lack of tissue differentiation that occurs before ~3 years.
3. tissue gets stuck behind the glans.
4. HPV 6 and 11
5. sessile or pedunculated, red papillary outgrowths that may be verrucous or flat.
6. coronal sulcus, inner prepuce, glans, perianal.
7. acanthosis, koilocytosis, intact basement membrane.

8. over 35yo.
9. HPV 16 and 18.
10. solitary thickened gray/white plaque with shallow ulcerations and crustin.
11. the shaft or scrotum.
12. dysplastic epithelium
scattered mitosis above basal layer
nuclear abnormalities: large, odd shaped, or multiple.

13. bowen's disease, HPV 16 + 18
14. most on the glans or the inner surface of the prepuce.
15. epithelial thickening with fraying and fissuring.
16. papules and large, infected ulcers with ragged, heaped up margins.
17. 40-70yo.
18. regional nodes may be swollen without spread of SCC.
19. painless lesions that bleed.

20. hormonal disorders of deficient LHRH
trisomy 13
21. phthalates (in plastic)
tagamet (used to treat plantar warts and peptic ulcers)
22. increased risk for testicular cancer
increased risk for infertility
23. build up of serous fluid in the scrotum, from trauma or due to structural abnormalities.
24. 10% of men have them.
25. extreme mountain biking and soccer players.
26. mostly left side.

27. lycopene
nettles
zinc
EFA's
amino acids
28. alcohol
pesticides
cadmium
cholesterol
29. increase in 5-alpha reductase activity.
30. testosterone is converted by 5-alpha reductase to DHT, which is the main prostatic growth factor.
31. estrogen increases stroma susceptibility and prolactin increases androgen uptake.

32. the most common cancer in males.
33. after 50 years old.
34. low risk in asians, high risk in african americans.
35. loss of p53 gene, hypermethylation of glutathione S-transferase.
36. high arachidonic acid content.
37. lycopene
vitamin A, E
fish oil
soy, selenium
38. posterior aspect of lateral lobes.
39. gritty, firm nodules.
40. osteoblastic bone lesions characteristic of boney metastasis to lumbar/thoracic, femur, pelvis, ribs.

41. germ cells.
42. germ cells.
43. whites: blacks 5:1
44. HCG.
45. cryptorchidism.
46. good with removal of affected testes. >95%.
47. worse than seminoma; tends to grow rapidly and spread outside the testicle.
48. HCG or AFP.
49. children under 3yo.
50. AFP.
51. benign until puberty, malignant afterwards.
52. no increase in HCG or AFP levels.
53. poor; fast growing.
54. over 65yo.

CPD III: kidneys, part II

2010-04-25T21:32:00.000-07:00

the second week on the kidney: beginning with tubular disorders. the normal function of the renal tubules is reabsorption of various electrolytes, thus many tubular disorders result in excess amounts of these materials in the urine. fanconi's syndrome is a congenital or acquired syndrome that is often fatal by the 20's that leads to dysfunction of the proximal tubule, resulting in cystinosis, glucosuria, phosphaturia, aminoaciduria, bicarbonate wasting. cystinuria and aminoaciduria are failed reabsorption of cysteine or amino acids in general, leading to excess excretion in the urine. in both, cystine crystals might form and create symptoms similar to that of a patient with renal colic. wilson's disease is a rare congenital disease that involves copper deposition in the tubules, along with the liver, brain, and RBC's. the pathognomonic sign for wilson's disease is the "kayser fleischer" rings seen in the eye.

renal glucosuria is a tubular dysfunction that results in spilling of glucose into the urine despite normal or low blood glucose levels. it is often asymptomatic and might be found by glucose in the urine after a 24 hour fast. renal acidosis is another condition that involves acidosis which might be due to impaired secretion of H+ in the distal tubule or impaired reabsorption of bicarbonate in the proximal tubule. the latter might be associated with potassium wasting and muscle dysfunction as well. potassium absorption can also be affected by tubular dysfunction, as seen in bartter's and liddle's syndrome. nephrogenic diabetes insipidus is a congenital and generally fatal disease that might show up in infants in which the kidney's ADH receptors are dysfunctional, resulting in polydipsia, polyuria and hypotonic urine.

diabetic nephropathy is a complication that occurs in about 1/3 of cases of diabetes mellitus which involves glycosylation of the nephron and the dysfunction that results. it might occur 15-20 years after a diagnosis of DM and might be heavily influenced (or prevented) by diet and lifestyle factors early on. the first signs are not overt and may include increased GFR and mild proteinuria. patients with stage II DN will see a drop in GFR, more noticeable proteinuria (resulting in edema symptoms as well), and increasing hypertension. stage III is the last stage, the last few years of a ~20 year process which involves greatly reduced GFR, massive proteinuria, hypertension, and retinopathy. patients with severe DN are at increased risk for infections as well due to the higher glucose levels in the urine.

polycystic kidney disease is a hereditary disorder that results in multiple bilateral cysts that increase size and decrease function of the kidneys. it can manifest as proteinuria, mild hematuria, low back pain, infection, and colic due to formation of stones. late stage, it might also be accompanied by hepatic involvement such as portal HTN and esophageal varices. it will show proteinuria and hematuria on lab diagnosis, as well as pyuria which might appear even without infection. 50% of patients with PKD will end up with renal failure in 10 years.

interstitial tubular disorder is another possible tubular dysfunction that occurs due to drug toxicity or hypersensitivity- most commonly from seizure medication. these drugs can affect both the tubules and the interstitial space, causing a variety of symptoms including that of tubular dysfunction, renal failure, UTI, as well as a host of dermatological manifestations depending on the causative agent. labs might resemble an infection without the presence of bacteria: eosinophilia, proteinuria, hematuria. a patient with ITD would present clinically with enlarged kidneys.

cystitis is a UTI of the bladder, commonly due to vaginal uptake in women and chronic bacterial prostatitis in men. it manifests mostly through urinary symptoms: frequency, urgency, dysuria, occasional hematuria, and possibly suprapubic or lower back pain. there are generally no remarkable PE findings other than general achiness. a UA might show turbid urine and possibly hematuria.

if acute infection reaches the kidneys, acute pyelonephritis results. this condition is more common in girls / pregnant women or patients who have urethral instrumentation. it is most commonly due to e.coli, klebsiella, enterobacter and proteus, which may be present in a urine culture in excess of 100,000 / ml. symptoms include fever/chills/nausea/vomiting, as well as kidney tenderness and enlargement, and possible urinary symptoms as well. lab tests might show neutrophilia, bacteruria, and presence of WBC casts is a pathognomonic sign.

untreated or poorly managed acute pyelonephritis might lead to chronic pyelonephritis, which in turn may lead to chronic renal failure if fibrosis is widespread enough. these patients have a vague and inconsistent clinical presentation, sometimes having fever, abdominal/flank pain, and obstructive symptoms. a PE for a patient with CP should include checking for HTN and anemia symptoms, as well as edema, CVA tenderness, and palpation of the kidney and bladder. definitive diagnosis is made by IVU.

interstitial cystitis is a disorder of the bladder lining, related to dysfunction of the GAG layer. rather than an infectious origin, IC is commonly triggered by such foods as cranberry juice, potassium rich foods, coffee, alcohol, tomatoes, etc. it presents as a more severe cystitis, with urgency, frequency, and severe abdominal pain which can be severe enough to limit sexual activity. diagnosis is made by excluding other bladder conditions and can be made definitively by bladder wall biopsy, which would show hunnel's patches: tiny ulcerations.

a urinary calculi is a stone in the ureter, commonly made of calcium oxalate, struvite, uric acid, or cystine. they appear more frequently in men and are often idiopathic, although several risk factors have been identified- such as low water intake, excess vitamin C intake, and a sedentary lifestyle. people with UC will present with episodes of severe, colicky flank pain that may radiate down to the thigh, as well as hematuria and urinary symptoms. a UA might show hematuria, pyuria, and crystals-- a 6 sided crystal points to a stone made of cystine.

some notes on cancers of the kidney and bladder: most kidney tumors are adenocarcinomas, which are commonly caused by drugs and environmental toxins and might present asymptomatically due to the high functional reserve of the kidneys. wilm's tumor mostly affects children and may present as an asymptomatic mass. neuroblastoma is a systemic, often fatal condition which affects the kidney as well and can be identified by blackness around the eyes. bladder tumors are most often caused by cigarette smoking, and can cause hematuria, secondary infection, flank pain with obstructive symptoms. the conventional treatment strategy is sloughing off of cancer cells via instillation of BCG within the bladder.

questions
various tubular disorders...
1. what is fanconi's syndrome?
2. what is the prognosis for patients with fanconi's syndrome?
3. what is cystinuria?
4. patients with cystinuria can present similarly to which condition?
5. what is aminoaciduria?
6. cystine renal stones in a patient with aminoaciduria might indicate...
7. how is aminoaciduria diagnosed?
8. what is wilson's disease?
9. wilson's disease might present similarly to...
10. what is the pathognomonic sign for wilson's disease?
11. what is the prognosis for patients with wilson's disease?
12. if diagnosed early, what might be of benefit to patients with wilson's disease?

more tubular disorders...
13. what is renal glucosuria?
14. how is renal glucosuria diagnosed?
15. what is renal acidosis?
16. renal acidosis from proximal tubule dysfunction often accompanies which disease?
17. distal tubule dysfunction is often accompanied by...
18. what is bartter's syndrome?
19. what is liddle's syndrome?
20. what is nephrogenic diabetes insipidus?
21. what are the signs and symptoms of nephrogenic diabetes insipidus?

diabetic nephropathy...
22. what is diabetic nephropathy?
23. describe the hallmarks of the first stage of diabetic nephropathy. how long after DM diagnosis is the onset?
24. what are the hallmarks of the second stage of diabetic nephropathy?
25. what are the hallmarks of the third stage of diabetic nephropathy?
26. patients with diabetic nephropathy are more prone to...
27. what is the treatment strategy for patients in stage I DN?
28. what is the survival rate for stage II or III DN patients who need dialysis?

polycystic kidney disease...
29. what is polycystic kidney disease?
30. what are the signs and symptoms of PKD?
31. what are some symptoms that might appear late in the course of PKD?
32. what are the lab results for PKD?
33. what is the prognosis for PKD?

interstitial tubular disease...
34. what is ITD?
35. what are medications that commonly trigger ITD?
36. what are the signs and symptoms of ITD?
37. what are some typical lab results for a patient with ITD?
38. what is a PE finding one might find on a patient with ITD?

renal / urinary tract infections...
39. what are some general symptoms of a lower UTI?
40. what are some general symptoms of an upper UTI?
41. blood borne infections are more likely seen in which demographic?
42. what are some physiological mechanisms that fight against infections in the urinary tract?
43. what are some factors that predispose an individual to getting a UTI?

cystitis...
44. what is a common etiology of cystitis for females?
45. what is the most common etiology of cystitis for males?
46. what are the typical cystitis PE findings?
47. what are the signs and symptoms of cystitis?
48. what are some lab findings for cystitis?

acute pyelonephritis...
49. which demographic is AP most common in?
50. which microorganisms are most commonly implicated in AP?
51. what are the signs and symptoms of AP?
52. what are the lab markers one might see with an AP patient?
53. a urine culture might show...

chronic pyelonephritis...
54. CP accounts for what percentage of renal failure cases?
55. what is CP caused by?
56. how does CP lead to renal failure?
57. what is the symptom picture for CP?
58. CP symptoms might appear similarly to what other condition?
59. what should be checked for on a PE of a patient with CP?
60. definititve diagnosis of CP is made by...
61. what are some strategies for improving kidney health?

interstitial cystitis...
62. what gender is more affected by IC?
63. what is the pathophysiology of IC?
64. what are some common foods that irritate IC?
65. how does IC present clinically?
66. 60% of patients with IC experience...
67. how long does IC generally take to diagnose?
68. what are the diagnostic criteria for IC?
69. what is the pathognomonic sign for IC?
70. what is unique about the UA for patients with IC?

urinary calculi...
71. which gender is more prone to UC?
72. 75% of urinary calculi are due to what etiology?
73. 20% of urinary calculi are due to...
74. what are the most common types of stones found in UC?
75. what are the signs and symptoms of UC?
76. what might be found on a urinalysis of UC?
77. 6 sided crystals in a UA of UC is indicative of...
78. what are some risk factors for UC?

cancer...
79. what percentage of kidney tumors is represented by adenocarcinomas?
80. what are some etiological agents in adenocarcinoma of the kidneys?
81. what are the signs / symptoms of adenocarcinoma?
82. wilm's tumor is most common in which demographic?
83. wilm's tumor most commonly presents as...
84. what is a characteristic sign for neuroblastoma?
85. what is a common etiology for bladder cancer?
86. what are the signs and symptoms of bladder cancer?

answers
1. congenital or acquired dysfunction of proximal tubule that results in cystinosis, glucosuria, phosphaturia, aminoaciduria, and bicarbonate wasting.
2. most die in 20's.
3. impaired reabsorption of cysteine in the tubules which causes increased urinary excretion and formation of cystine calculi.
4. renal colic.
5. impaired absorption of all amino acids.
6. chronic renal failure.
7. excess amino acids and cystine crystals on UA.
8. a rare congenital disorder which involves copper deposition in various places in the body such as the renal tubules, liver, brain, RBC's.
9. hepatitis.
10. kayser fleischer rings.
11. generally poor due to late diagnosis.
12. treatment with zinc.

13. inherited condition that involves low blood glucose combined with excess excretion of glucose.
14. normal or low serum glucose but glucose in urine after overnight fast.
15. chronic acidosis which results either from impaired resorption of bicarbonate in proximal tubule or impaired secretion of H+ in distal tubule.
16. fanconi's syndrome, wilson's disease, multiple myeloma, vitamin D deficiency, heavy metal toxicity.
17. potassium wasting and the resulting muscle dysfunction.
18. hypokalemia due to dysfunction in thick ascending loop of henle.
19. rare disorder that resembles primary aldosteronism with hypertension and hyperkalemic alkalosis.
20. dysfunction of ADH receptors on the kidney.
21. polydipsia, polyuria, hypotonic urine.

22. a complication that occurs in about a third of cases of diabetes mellitus resulting from glycosylation of the nephron.
23. may appear 15-20 years after DM diagnosis; undetectable increase in GFR, mild proteinuria.
24. decreased GFR
proteinuria
edema due to low protein
hypertension.
25. azotemia (increases seen in BUN and creatinine)
GFR less than 1/3
massive proteinuria
hypertension
retinopathy
26. infections due to higher glucose levels in urine, neurogenic bladder, hypertension.
27. watch diet: low sugars, high vegetables
monitor blood pressure
watch for retinal fundus changes
28. 2-3 years.

29. an autosomal dominant or recessive disease that results in multiple bilateral cysts that increase the size and reduce the function of the kidneys.
30. asymptomatic, or
lumbar pain
hematuria
infection
colic due to stones [back blood bugs stones] [bloody stones on the back of bugs]
31. hepatic symptoms: portal HTN, esophageal varices.
32. proteinuria, occasional hematuria, pyruria (even without infection)
33. 50% chance for kidney failure in 10 years.

34. acute renal failure due to drug reaction / hypersensitivity that affects tubules and interstitial tissue.
35. seizure medications.
36. variable:
UTI sxs
tubular dysfunction sxs
oliguria
urticaria, photosensitivity, erythema nodosum, epidermal necrolysis
37. eosinophilia, proteinuria, hematuria, but no bacteria.
38. enlarged kidneys.

39. more urinary symptoms: dysuria, frequency, urgency, hematuria, etc. suprapubic pain.
40. kidney tenderness, fever/chills, N/V, sometimes diarrhea.
41. IV drug users.
42. immune response via WBC's and antibodies, urine acidity, and voiding.
43. congenital malformations (hypospadias)
poor or ineffective hygiene
frequent intercourse, anal sex
high urine pH
catheterization
low water intake
high carb diet / diabetes

44. uptake of bacteria from vagina.
45. chronic bacterial prostatitis.
46. patient in general distress and malaise, but not as severe as pyelonephritis.
47. dysuria, urgency, frequency, nocturia
suprapubic and lower back pain
48. turbid urine and occasional hematuria.

49. girls / pregnant women, or patients with catheterization.
50. e.coli, klebsiella, proteus, enterobacter.
51. fever/chills, N/V
flank pain, kidney tenderness and enlargement
urinary frequency / urgency in 1/3.
52. elevated neutrophils, bacteria, WBC casts in the urine.
53. more than 100,000 organisms / ml.

54. 2-3%.
55. recurrent acute pyelonephritis.
56. CP leads to fibrosis which decreases renal function, ultimately leading to chronic renal failure.
57. vague, inconsistent. may have
fever
flank / abdominal pain
obstructive symptoms
58. chronic interstitial nephritis.
59. signs of HTN, anemia, edema, CVA tenderness, palpation of kidneys and bladder.
60. IVU.
61. drink more water (up to half your weight??)
regulate protein intake
reduce unnecessary medications

62. females 10:1.
63. disruption of interior lining of the bladder, related to dysregulation of GAG layer. may also be abnormal accumulation of mast cells.
64. cranberry
coffee / tea
alcohol / tobacco
tomatoes
potassium
65. as a more severe cystitis:
frequency, urgency (enough to keep housebound) and severe abdominal pain
66. pain with intercourse.
67. 4.5 years on avg.
68. exclusion of other bladder conditions
irritative voiding
specific cystography changes or
aggravation from potassium
69. hunner's patches: tiny ulcerations seen in bladder wall biopsy.
70. consistently free of bacteria, unlike many other bladder conditions; not infective.

71. 3-4 times more common in males.
72. idiopathic.
73. uric acid abnormalities.
74. calcium oxalate, struvite, uric acid, cystine.
75. hematuria
episodes of severe, spastic, colicky pain that may radiate from flank to thigh
urinary symptoms: urgency, frequency, dysuria.
76. may have hematuria, pyuria, crystals.
77. cystine crystals.
78. low fluid intake
sedentary lifestyle
excess vitamin C
low vitamin B6, mg

79. 86%.
80. drugs
heavy metals
radiation
viruses
lifestyle factors: smoking, coffee, etc.
81. often asx because of high functional reserve of kidneys, but may present with colic, hematuria.
82. children.
83. asymptomatic mass.
84. black under the eyes.
85. smoking.
86. hematuria
infection
obstructive symptoms, flank pain

CPD III: kidneys part I

2010-04-19T07:29:00.000-07:00

the kidney unit in CPD III. we started with some introductory notes about diagnosis and the general symptom picture. labs that are helpful in the diagnosis of kidney conditions include urinalysis (can detect infection, RBC's, casts, etc), CBC, and chem screen (BUN and creatinine are useful measures of glomerular function). imaging studies might include xray, US, IVU, depending on the condition suspected. some typical symptoms associated with kidney conditions: UTI's commonly present with a triad of symptoms, urinary frequency, urgency, dysuria. chills/fever in association with these symptoms might indicate involvement of the upper urinary tract. urethral discharge in males is most likely due to GC/chlamydia infection. nocturia might be indicative of BPH, or simply reflect excess nighttime fluid consumption- consider nocturia seriously if it is a sudden change for the patient. enuresis, bedwetting, can be primary or secondary- patients with secondary enuresis might only have episodes followed by breaks of 6 months or more and are more likely due to psychological as opposed to physiological factors. incontinence comes in three flavors- overflow from incomplete emptying due to obstruction, stress from increased pressure, and urge from decreased CNS inhibition.

renal colic, or kidney stones, often cause severe unilateral pain in a crescendo-decrescendo pattern that radiates from the kidney / flank area to the lower abdomen and bladder, and sometimes as far down as the knee. patients might also present with nausea/vomiting, hematuria, and urinary frequency, as well as chills/fever if an infection is involved. diagnosis is made by UA and imaging, in particular US and IVU.

polyuria can be a physiologic response to an increased osmolar load, in which case the major concern is loss of electrolytes. it can also point to certain underlying pathologies such as diabetes insipidus, which leads to an underproduction of ADH by the pituitary. nephrogenic diabetes insipidus can also result in polyuria- in this condition, the kidney's ADH receptors are non functioning.

oligouria and anuria are conditions of decreased urine and can be from pre-renal, renal, or post renal causes. pre-renal causes can include dehydration, as well as any condition that decreases blood flow to the kidney such as CHF or hemorrhage. renal causes are grouped under the acronym VINDICATE: vascular lesions, inflammatory lesions, neoplasm, degenerative conditions, intoxication, congenital disorders, autoimmune, trauma, endocrine causes. post renal: MINNT-- malformations, inflammatory, neoplasm, neurological, trauma.

some notes about the various colors of urine and what they might indicate: normal color is yellow, although bright / concentrated yellow might indicate dehydration or B vitamins. overly clear might indicate glomerular dysfunction as in chronic glomerulonephritis, or simply polydipsia. cloudy white might be indicative of infection as the cloudiness might be bacteria or pus. red might be RBC's but can also be from certain foods such as beets.

as the kidneys are primarily responsible for maintaining fluid volume in the body, systemic edema symptoms often point to kidney filtration issues. pitting edema refers to a type in which fluid can be displaced, forming transient "pits", whereas in non-pitting, fluid can not be displaced- this is often due to local trauma such as a bee sting. in general edema formation can occur via four mechanisms- increased capillary pressure, increased capillary permeability, decreased plasma proteins, and lymph obstruction. edema symptoms may also point to other organ systems, in particular heart dysfunction (recall that RCHF leads to systemic edema), thyroid (hypothyroid myxedema), hepatic (look for jaundice, ascites, palmar erythema), and might even be due to a worm found in pork, trichinosis if seen periorbitally.

acute renal failure describes a situation marked by rapidly increasing azotemia plus oliguria / anuria. as with azotemia, the cause may be pre-renal (CHF), renal (glomerulonephritis), or post renal (bladder outlet obstruction, BPH). clinically, it manifests as lethargy, pulmonary edema, CHF, hypertension, and oliguria. diagnosis is made via chem screen, CBC, and UA-- most helpful is the rapid and steady increase of creatinine (as well as BUN). if oliguria / anuria persists for more than 3 days, this is an indicator of poor prognosis; conventional emergency treatment might require dialysis and complete kidney rest.

whereas acute renal failure might produce sudden increases in BUN / creatinine, chronic renal failure might show mild elevations for month long periods. there are many risk factors that contribute to CRF, such as glomerulonephritis, cardiovascular disease, SLE, pyelonephritis, etc. clinical presentation can be divided by the stage of disease: CRF initially presents with nonspecific / vague symptoms, or fatigue / mental haze. the intermediate stage presents with bad taste in mouth, muscle spasm/convusion/neuropathy, pruritis, nausea / vomiting. the late stage presents with cardiovascular issues such as hypertension, CHF, pericarditis, as well as skin issues such as uremic frost and yellow/brown complexion. in addition to the BUN / creatinine levels, one might expect to see normochromic / normocytic anemia (deficient erythropoetin production), waxy casts on a UA, and imbalanced electrolytes. these patients are generally put on dialysis long term (200,000 in the US) with dietary / fluid intake monitoring- in particular, avoiding high protein intake.

nephrotic syndrome results from a dysfunctional or damaged glomerular basement membrane, leading to loss of proteins and hyperlipidemia. it can be primary from diseases such as immune complex nephritides, or secondary to systemic illness such as diabetes mellitus. patients might present with frothy urine, marked edema periorbitally and peripherally, muscle wasting due to lack of protein, and respiratory symptoms. diagnosis is made by UA, chem screen, CBC- UA might show proteins, cellular elements, casts. chem screen might show hyperlipidemia, hyperalbuminemia, and CBC might show microcytic anemia.

acute glomerulonephritis is another form of glomerular dysfunction, this time from immune complex deposition from previous infection, such as an untreated strep throat infection. it commonly affects children and young adults and is relatively rare in adults over 50. although it has mild proteinuria as nephrotic syndrome does, the hallmark of AG is hematuria and presence of RBC casts in the UA. the decreased glomerular function also leads to increased sodium retention, which ultimately increases blood volume and may lead to hypertension or CHF. children have a good chance of recovery from AG but will always have an increased risk for HTN-- thus an adult who has unexplained HTN might have had acute glomerulonephritis earlier in life. chronic glomerulonephritis might result from longstanding acute glomerulonephritis and might develop insidiously- patients might asx, but with occasional proteinuria and hematuria, with RBC casts on a UA. steadily increasing BUN might also be observed over months or years.

goodpasture's is a near fatal glomerular disease that has a predilection for young males. the hallmark signs are lung and renal hemorrhage that results in hemoptysis and hematuria. labs have the combined characteristics of nephrotic syndrome and glomerulonephritis: hematuria / RBC's, but also with protein / casts in UA, along with increased BUN / creatinine. patients might also present with headache, malaise, and anorexia. the prognosis for goodpasture's is poor, and patients with this condition rarely live past their 20's.

idiopathic primary renal hematuric/proteinuric syndrome is diagnosed when there is mild gross or microscopic hematuria and proteinuria without any clear explanation. the etiology may be related to IgA towards the glomeruli, as well as buerger's disease and febrile URI's. this condition has a preference for males and children-- most recover but like acute glomerulonephritis have an increased lifetime risk for hypertension and renal insufficiency.

henoch-schoenlein purpura is similar to IPRHPS but with marked skin, GI, and joint involvement- the characteristic purpura lesions are symmetrically distributed on the extensor surfaces. GI symptoms might include abdominal pain, vomiting, and joint pain may occur at the ankles, hands, feet. HSP generally follows a viral infection, such as an acute viral URI. lab findings might show hematuria / proteinuria, occult blood, and increased ESR. HSP is self limiting, generally within 6 weeks, although 10-20% of patients might develop chronic renal failure.

questions
diagnosis...
1. what are some helpful lab tests to consider when ruling in or out kidney related pathologies?
2. what are two components of a chem screen that can give an indication of kidney function?
3. what are the imaging techniques used to diagnose kidney conditions?
4. what is the "triad of symptoms" seen in UTI's?
5. what might chills/fever indicate in a patient with the triad of symptoms for a UTI?
6. leukocyte casts in a UA might indicate...
7. what is the most common cause of urethral discharge in males?
8. what might nocturia be indicative of?
9. what is the difference between primary and secondary enuresis?
10. what are the different types of incontinence?

renal colic...
11. describe the pain sensation in renal colic.
12. describe the typical radiation patterns seen in renal colic pain.
13. what are some concomitant symptoms seen in renal colic?
14. what is a typical PE of a patient with RC?
15. what would labs show for RC?
16. what are the imaging studies used to diagnose RC?

polyuria...
17. what are some pathological conditions associated with polyuria?
18. why does diabetes insipidus cause polyuria?
19. what is nephrogenic diabetes insipidus?

oligo / anuria...
20. what are some prerenal causes of oligouria or anuria?
21. what are some renal causes of oligouria / anuria?
22. what are some post renal causes of oligouria / anuria?

what might be indicated by urine that is...
23. colorless.
24. cloudy white.
25. yellow.
26. orange.
27. red.
28. blue/green.
29. brown/black.

edema...
30. what is the difference between pitting and non-pitting edema?
31. what is a common cause of non-pitting edema?
32. what are four pathophysiological mechanisms for edema formation?
33. what are some hepatic symptoms or conditions that might be associated with edema?
34. what is a thyroid related etiology for edema?
35. what is the relationship between edema and pork?

acute renal failure...
36. what is acute renal failure?
37. what are the major etiologies of acute renal failure?
38. what are some "pre-renal" causes of acute renal failure?
39. what are some "renal" causes of acute renal failure?
40. what are some "post-renal" causes of acute renal failure?
41. what are some of the signs and symptoms of acute renal failure?
42. what are some labs that aid in the diagnosis of acute renal failure?
43. if anemia is present in acute renal failure, what type of anemia would it be?
44. what is a marker for prognosis of acute renal failure?
45. what is the conventional treatment strategy for acute renal failure?

chronic renal failure...
46. what are some risk factors for CRF?
47. how many patients in the US are currently on dialysis long term?
48. what are the early signs / symptoms for CRF?
49. what are the intermediate stage signs/symptoms for CRF?
50. what are the late stage signs/symptoms for CRF?
51. what are the lab tests used to diagnose CRF?
52. what are some electrolyte imbalances one might expect to see in CRF?
53. what is the connection between CRF and chronic anemia?
54. what are some treatment strategies for CRF?

nephrotic syndrome...
55. what is nephrotic syndrome?
56. which gender is more affected by nephrotic syndrome?
57. what are the etiologies of nephrotic syndrome?
58. what are the signs and symptoms of nephrotic syndrome?
59. what might one expect to find on a UA of a pt with NS?
60. what might one expect to find on a chem screen of a pt with NS?
61. what is the connection between nephrotic syndrome and hyperlipidemia?
62. what might be a finding on a CBC of a pt with NS?
63. what are some PE findings for NS?

acute glomerulonephritis...
64. what is AG? what are the hallmarks of AG?
65. what age group is most commonly affected by AG?
66. what is the etiology of AG?
67. how long after an episode of untreated strep throat might AG appear?
68. what are the signs/symptoms of AG?
69. what is the lab finding that is diagnostic for AG?
70. what might be seen in fundoscopy of a pt with AG?
71. what is the prognosis for children with AG?

chronic glomerulonephritis...
72. what is chronic glomerulonephritis?
73. what is a typical presentation for chronic glomerulonephritis?

goodpasture's syndrome...
74. which demographic is most commonly affected by goodpasture's syndrome?
75. what are the hallmark signs and symptoms of GS?
76. what are the concomitant symptoms of GS?
77. what are common lab findings for GS?
78. what is the prognosis of goodpasture's syndrome?

idiopathic primary renal hematuric/proteinuric syndrome...
79. what is IPRHPS?
80. what are some possible etiologies of IPRHPS?
81. what demographic is most closely associated with IPRHPS?
82. what might be a predisposing factor for IPRHPS?
83. what might lab findings show for IPRHPS?
84. what is the prognosis for IPRHPS?

henoch-schoenlein purpura...
85. what is HSP?
86. what is the etiology of HSP?
87. what are the signs and symptoms of HSP?
88. what are some lab findings one might expect to find with HSP?
89. what is the prognosis of HSP?

answers
1. UA, culture, CBC, chem screen.
2. BUN and creatinine: both excreted by the kidneys and therefore can be a rough indicator for glomerular function.
3. Xray, US, IVU.
4. urinary frequency, urgency, pain.
5. upper UTI.
6. renal parenchyma infection.
7. GC chlamydia.
8. early disease, excess fluid consumption in evening, BPH, interstitial cystitis.
9. in secondary, there might be a period of dryness (over 6 months)-- more likely due to psychological factors.
10. overflow (obstruction of urinary tract leads to incomplete emptying), stress (increased intraabdominal pressure), urge (decreased CNS inhibition).

11. severe, unilateral, crescendo-decrescendo pain.
12. from flank/kidney around to lower abdomen, follows course of urinary tract and sometimes radiates down further, as far as knee.
13. chills/fever
N/V
hematuria
frequency
14. unremarkable or flank tenderness.
15. hematuria with or without pyuria / bacteruria.
16. xray, US, IVU (for kidney and ureter).

17. diabetes insipidus, nephrogenic diabetes insipidus, psychogenic polydipsia.
18. in DI, the pituitary underproduces ADH, a hormone that allows for water reabsorption in the kidney- thereby leading to greater urine output.
19. a condition where the kidney's receptors for ADH are not functioning.

20. dehydration, hemorrhage, CHF.
21. VINDICATE:
vascular lesions
inflammatory lesions
neoplasm
degenerative
intoxication
congenital disorders
autoimmune (most common)
trauma
endocrine
22. MINNT:
malformations
inflammation
neoplasms
neurological disorders
trauma

23. polydipsia, chronic glomerulonephritis, diabetes inspidis/mellitus.
24. phosphates, epithelial cells, bacteria/pus.
25. B vitamins.
26. urobilinogen, bile, pyridium, carrots.
27. beets, or RBC's.
28. certain drugs (thymol, phenol, indigo blue), pseudomonas.
29. bilirubin, hemoglobin.

30. in pitting, fluid can be displaced and transient "pits" are formed. in non-pitting, edema is so severe that fluid can not be displaced.
31. trauma causes coagulation of proteins such as fibrinogen.
32. increased capillary pressure (blood clots, CHF)
increased capillary permeability (CHF)
decreased plasma proteins (burns, nephrosis, low protein intake)
lymph obstruction (lymph node removal, parasites)
33. jaundice
ascites
spider nevi
red nose
palmar erythema
34. there is a marked increase in water retention in hypothyroid myxedema.
35. trichinosis is a worm found in pork that is associated with periorbital edema.

36. rapidly increasing azotemia plus oliguria.
37. 60-70% extrinsic factors: trauma, drugs, surgery, obstruction, etc.
20-30% due to intrinsic factors: acute glomerulonephritis, SLE, goodpasture's, etc.
38. renal failure that results from inadequate renal perfusion due to factors upstream from the kidney: CHF, hemorrhage, etc.
39. decreased renal blood flow, reduced glomerular filtration, or renal obstruction.
40. bladder outlet obstruction, BPH, tumors.
41. lethargy
pulmonary edema
CHF
hypertension
oliguria
42. chem screen: steadily increasing creatinine is diagnostic. also see BUN increase.
CBC to check for anemia and infection
UA to check for RBC's, WBC's, casts.
43. normocytic normochromic.
44. oliguria / anuria for more than 3 days indicates very poor prognosis; may be fatal.
45. dialysis to allow kidney to recover, or severe limitation of fluid and electrolyte intake.

46. glomerulonephritis
cardiovascular diseases such as arteriosclerosis, HTN
SLE, diabetes
congenital abnormalities (polycystic kidney)
pyelonephritis
47. about 200,000.
48. non-specific
fatigue
nocturia
mental haze
49. muscle twitching, aches, convulsions
neuropathy
bad taste in mouth
N/V
pruritis
50. uremic frost
GI ulcers / bleeding
tissue wasting
yellow / brown skin
hypertension / CHF / pericarditis
51. chem screen would show mild / moderate elevations of BUN/creatinine over months
CBC would show normocytic / normochromic anemia,
UA might show waxy casts
52. decreased calcium, increased phosphorous, potassium, CO2.
53. kidney failure leads to improper erythropoetin production.
54. dietary and fluid intake monitoring - decrease protein and increase carb intake.

55. damage to the glomerular basement membrane that causes hyponaturia, proteinuria, hypoalbuminemia, lipiduria, hyperlipidemia.
56. males.
57. primary nephrotic disease such as immune complex nephritides or underyling systemic disease such as diabetes mellitus.
58. frothy urine
edema
muscle wasting
abdominal pain
SOB/DOE
[basement pee edema muscle stomach breath] [basement flooded with pee- use your stomach muscles and blow it out]
59. cellular elements, protein, casts.
60. hyperalbuminemia and hyperlipidemia.
61. the liver increases lipid production (cholesterol) concurrently with protein production in an attempt to normalize protein levels from the protein loss incurred in nephrotic syndrome.
62. microcytic anemia.
63. periorbital and peripheral edema
muscle wasting
parallel white lines on nails
orthostatic hypotension

64. glomerular dysfunction which causes decreased GFR and increased Na retention, leading to hematuria and hypertension.
65. young children older than 3 or young adults. rare in >50yos.
66. previous infection which causes immune complex deposition in glomeruli.
67. 1-6 weeks.
68. hematuria / oliguria
flank pain
mild edema
hypertension
69. RBC casts on a UA.
70. retinal hemorrhages.
71. 90% chance of recovery but increased risk for HTN remains throughout lifetime.

72. diffuse sclerosis of glomeruli and insidious loss of kidney function.
73. asx, with no abnormal lab results except for occasional proteinuria and hematuria. steadily increasing BUN over years.

74. young males 9:1.
75. renal and lung hemorrhage-- hemoptysis and hematuria.
76. headache, malaise, anorexia.
77. increased BUN/creatinine, RBC, protein on UA, microcytic anemia on CBC.
78. poor, patients rarely live past 20's.

79. presence of protein and RBC's in urine with no explanation.
80. glomerular IgA deposition, buerger's disease.
81. 6:1 males, children/young adult most common.
82. febrile URI.
83. hematuria, proteinuria, increased IgA.
84. many children recover but have an increased lifetime risk for hypertension and renal insufficiency.

85. similar to IPRHPS but with skin, joint, and GI involvement.
86. often follows a viral infection, acute URI.
87. symmetrically distributed purpura on extensor surfaces
arthritis
GI distress- vomiting, pain, occult blood
hematuria, proteinuria
88. increased ESR
hematuria / proteinuria
occult blood
89. self limiting in 1-6 weeks. 10-20% have chronic renal failure.

pathology IV: female genitalia

2010-04-16T17:20:00.001-07:00

some notes for the pathology test on the female reproductive system.

ovarian cysts-- made up of unruptured graffian follicles or ruptured graffian follicles that immediately reseal. they can be follicular (first 2 weeks of cycle, estrogen related), or luteal (second 2 weeks of cycle, progesterone related). within follicular cysts there is also a subcategory of "cystic follicles" which refers to small, common, physiological cysts less than 2cm, generally filled with serous fluid. luteal cysts are the product of failure of degeneration of the corpus luteum, and rupture of these may lead to peritoneal irritation.

PCOS is a condition we learned about in CPD II and is basically the combination of anovulation and androgenism. theca lutein cells of the ovaries, along with the adrenals, overproduce androstenedione which is then converted to testosterone and estrogen in the periphery. anovulation produces low levels of progesterone and a LH:FSH ratio of 3:1 instead of the normal 1:3. one possible mechanism for the hyperandrogenism is via dysfunction of cytochrome P450c17, which is the enzyme involved in the rate limiting steps for synthesis of androgens. a common allopathic treatment, metformin, seems to work via this pathway, related to reduction of insulin levels.

ovarian tumors are relatively common neoplasms that are more likely to be malignant in 40-60 year olds. risk factors that can increase incidence include nulliparity, family history, BRCA1 and 2 mutations, gonadal dysgenesis. there is also a connection between ovarian adenocarcinoma and abnormal expression of the her2/neu oncogene. the WHO classification of ovarian tumors is based upon the tissue of origin: epithelial, germ cell, or sex cord.

mullerian epithelial tumors are derived from the coelemic mesothelial layer and come in three main flavors: serous, endometroid, and mucinous-- cells that are related to uterine tubes, endometrium, and the cervix, respectively. the more developed the epithelial growth is, the greater likelihood for malignancy. symptoms for tumors may include abdominal pain and GI distress, urinary symptoms, and may progress to ascites and peritoneal implants for carcinoma. the benign mullerian tumors are generally unilateral with no epithelial thickening and abundant cilia / papillae, while the malignant tumors are bilateral with large amounts of tissue mass, increased complexity and stratification of the epithelium, which may also show nuclear atypia.

questions
ovarian cysts...
1. ovarian cysts are generally made up of...
2. what age and demographic is most likely to have ovarian cysts? what percentage has regular vs. irregular menstrual cycles?
3. what is the relationship between hypothyroidism and ovarian cysts?
4. what are some risk factors for ovarian cysts?
5. what is "mittelschmerz"?
6. what are the two different types of ovarian cysts and what distinguishes them?
7. what are the two different types of follicular cysts and what distinguishes them?
8. what is hyperthecosis?
9. what are luteal cysts due to?
10. what is the histological apperance of luteal cysts?
11. rupture of luteal cysts may lead to...

PCOS...
12. what is the pathophysiological connection between PCOS and theca lutein cells?
13. what is a typical hormone imbalance seen in PCOS and why?
14. what is cytochrome P450c17 and how is it related to PCOS?
15. full expression of PCOS may require...
16. what is the morphology of PCOS?

ovarian tumors...
17. in what age group are malignant ovarian tumors more common?
18. what are some risk factors for developing ovarian tumors?
19. what is a genetic marker for ovarian adenocarcinomas that can indicate poor prognosis?
20. epithelial tumors are usually...
21. what is the WHO classification of ovarian tumors based upon?

mullerian epithelial tumors...
22. what germ layer are mullerian epithelial tumors derived from?
23. what are the three major types of mullerian epithelial tumors? what cell types are they from?
24. risk of malignancy increases as...
25. what are the symptoms of a mullerian epithelial tumor?
26. what are the symptoms of a mullerian epithelial carcinoma?
27. what is the morphology of benign mullerian epithelial tumors?
28. what is the morphology of a malignant mullerian epithelial tumor?

serous tumors...
29. describe the morphology of serous tumors.
30. what percentage of serous tumors are benign or borderline malignant?
31. what are "psammoma" bodies?
32. what is the most common type of malignant ovarian tumor?

mucinous tumors...
33. what portion of ovarian neoplasms do mucinous tumors account for?
34. what percentage of mucinous tumors are malignant?
35. what is the histomorphology of mucinous tumors?
36. what are pseudomyoma peritonei?

endometroid tumors...
37. what percentage of ovarian neoplasms do endometroid tumors account for?
38. most endometroid tumors are...
39. describe the morphology of endometroid tumors.
40. what is "seeding" in the context of ovarian neoplasms?

cancer markers...
41. what is CA-125?
42. what is the relationship between tubal ligation, oral contraceptives and the risk of cancer?

teratomas...
43. what are mature/benign dermoid cysts derived from?
44. about 1% of dermoids undergo...
45. what is the morphology of an immature/malignant dermoid?
46. what are the most common monodermal teratomas?
47. what is the average ages that are affected by immature and mature teratomas?
48. what is the cell of origin of a struma ovarii?
49. what is the cell of origin of an ovarian carcinoid?
50. what is carcinoid syndrome?

yolk sac...
51. what is the cell of origin for yolk sac tumors?
52. what is a schiller-duval structure?
53. what markers are present in yolk sac tumors?

granulosa cell tumors...
54. does granulosa theca cell secretion indicate malignancy?
55. what are some other conditions that might result from granulosa cell tumors?

meig's syndrome...
56. meig's syndrome is associated with...
57. what cell type is overproduced in meig's syndrome?
58. what is meig's syndrome called when malignant?
59. what is the clinical presentation of meig's syndrome?

abnormal pregnancy, placental issues...
60. what are the most common sites of implantation for ectopic pregnancies?
61. what are the major risk factors for ectopic pregnancy?
62. what is the clinical presentation of an ectopic pregnancy?
63. what is a hydatidiform mole?
64. what is the difference between a complete and partial molar pregnancy?
65. what is the morphology of a molar pregnancy?
66. what are the risk factors for choriocarcinoma?
67. describe the course of a choriocarcinoma.

answers
1. unruptured graffian follicles or ruptured follicles that immediately reseal.
2. women of childbearing age: 50% with irregular cycles, 30% with regular cycles.
3. TSH is similar to HCG and stimulates the growth of cysts.
4. smoking
ovarian cancer
hormonal imbalance
early menarche
nulliparity
tamoxifen
[s o h e n t] [hes not]
5. unilateral sharp pain that occurs during ovulation in 25% of women that can be related to rupture of a follicular cyst.
6. ovarian and luteal, during the first 2 weeks and second 2 weeks of the menstrual cycle, respectively.
7. cystic follicles: small, common, physiological, less than 2cm, filled with serous fluid.
follicular cysts: larger than 2cm and may cause pain.
8. outer theca cells with increased cytoplasm and pale appearance which may cause increased estrogen production and an abnormal endometrium.
9. failure of corpus luteum to degenerate.
10. rim of bright yellow luteal tissue with luteinizing granulosa cells.
11. peritonitis.

12. theca lutein cells produce androstenedione (also produced in the adrenals) which is then converted into testosterone and estrone.
13. LH:FSH ratio is 3:1 instead of 1:3 due to deficient progesterone due to anovulation.
14. cytochrome p450c17 is a rate limiting enzyme involved in androgen synthesis that can be functionally abnormal in PCOS.
15. insulin resistance and a defect in androgen synthesis.
16. gray-white ovaries that are twice the normal size with thickened superficial cortex and numerous subcortical cysts 0.5-1.5cm.

17. 40-60yo.
18. nulliparity
family history
BRCA1, BRCA2 mutations
"gonadal dysgenesis" in children
[tumors parity family broca gonads] [risk for tumors in the broca family assessed by gonad parties]
19. high levels of expression from her2/neu gene.
20. bilateral.
21. tissue of origin: epithelial, germ cell, sex cord.

22. coelomic mesotheium.
23. serous (tubal), endometriod (endometrium), and mucinous (cervix).
24. discernable epithelial cell growth increases.
25. abdominal pain and enlargement
urinary frequency and dysuria
GI complaints
26. weight loss / cachexia
ascites with peritoneal implants of exfoliated tumor cells
27. unilateral, no epithelial thickening, abundant cilia and papillae
28. bilateral, large amounts of tumor mass, increased complexity and stratification of epithelium, nuclear atypia.

29. lined with tall, columnar ciliated epithelium, filled with clear serous fluid.
30. 75%.
31. concentric calcifications
32. serous cystadenocarcinoma.

33. 25%.
34. 15% malignant.
35. columnar epithelial cells with apical mucin and no cilia.
36. cancer of the peritoneum.

37. 20%.
38. carcinomas.
39. tubular glands that look like endometrium.
40. the spread of a ovarian neoplasm to the peritoneal cavity by bits of malignant tissue that resemble salt or spots.

41. high molecular weight glycoprotein that is present in greater than 80% of serous and endometrial carcinomas.
42. both decrease the risk for cancer by 50%.

43. ectodermal differentiation of totipotent cells.
44. malignant transformation of any one of the component elements.
45. more primordial / embryonic tissue, bulky tumors with smooth external surface.
46. struma ovarii, carcinoid.
47. immature- 18yo. mature- young women during reproductive years.
48. germ cell tumor, mature thyroid tissue.
49. germ cell tumor, intestinal epithelial cell.
50. cutaneous flushing and cramps
diarrhea, cramping, nausea, vomiting
cough, weeding, dyspnea
hepatomegaly

51. malignant germ cells differentiated towards extraembryonic yolk sac structure.
52. glomerular-like structure that involves central blood vessels surrounded by germ cells in a space surrounded by germ cells.
53. AFP, alpha 1 antitrypsin

54. potentially, in 5-25% of cases.
55. precocious puberty
endometrial hyperplasia, carcinoma
cystic breast disease

56. sex cord stromal tumors, such as fibroma thecomas.
57. basal cell.
58. fibrosarcoma.
59. pain, pelvic mass, ascites, hydrothorax.

60. uterine tubes (90%)
ovary
abdominal cavity
corona of tubes
61. PID with chronic salpingitis.
peritubal adhesions
leiomyoma
IUD
62. acute onset of severe abdominal pain ~6 weeks after normal menstrual flow.
63. cystic swelling of chorionic villi with variable trophoblastic growth.
64. complete is diploid, from sperm, no viable embryo. partial is triploid or more, viable embryo for several weeks.
65. may see fetal parts in partial mole
uterus filled with delicate, grape like edematous villi.
66. hydatidiform mole (complete)
previous pregnancy / abortion
67. invades myometrium
penetrates adjacent vasculature
metastasizes to lungs, vagina, brain, bone marrow, liver, kidney