points final study guide (partial)

a study guide for those of us in Points III lecture class:

QUESTIONS

EXTRAORDINARY VESSELS 

1. extraordinary vessels first appear in completion in which text?

2. some general characteristics of the 8 extras?

3. yangwei (yang linking)'s illness is of...

4. yinwei (yin linking)'s illness is of...

5. yinqiao (yin motility)'s illness is of...

6. yangqiao (yang motility)'s illness is of...

7. chong's illness is of...

8. du's illness is of...

9. ren's illness is of...

10. dai's illness is of...

11. chong goes alongside which channel in the leg...

12. merges with which channel where?

13. chong links up and passes...

14. ren mai starts where?

15. ren mai main branch?

16. du mai starts where? 

17. du mai first branch?

18. du mai second branch?

19. du mai third branch?

20. du connects with which organs?

21. du connects with what else (that no other extra does)?

22. which points do the ren and du link up at?

23. Ren/Du system might be related to which system in Western physiological terms?

24. confluent point of chong mai?

25. indications?

26. confluent point of the ren mai?

27. indications?

28. confluent point of the du mai?

29. indications?

30. confluent point of the dai mai?

31. indications?

32. confluent point of the yinwei mai?

33. indications?

34. confluent point of yangwei mai?

35. indications?

36. confluent point of yinqiao mai?

37. indications?

38. confluent point of yangqiao mai?

39. indications?

DIVERGENT CHANNELS

1. list four functions of the divergent channels

2. in zang/fu paired divergent channels, where do the the zang divergent channels always end up merging?

3. except for BL/KD divergent channels, all divergent channels go to...

4. where does the BL divergent channel start?

5. exit point for BL/KD?

6. exit point for GB/LV?

7. exit point for ST/SP?

8. exit point for SI/HT?

9. exit point for TB/PC?

10. exit point for LI/LU?

SINEWS

1. the three foot yang sinew channels all pass through which part of the body and which acupuncture point? 

2. 2 points at which the LI sinew channel is different than the primary channel?

3. where do the three hand yang channels more or less all pass through?√

4. 3 foot yin sinews all pass through the... √

5. 3 hand yin all go to the...√

6. how does the direction of the jing jin differ as compared to the primary channels?√

7. the jingjin gather in which parts of the body, generally?√ 

8. which jingjin gather at the genitals?√

notable symptoms of jingjin of...

9. hand taiyin (LU)?√

10. hand yangming (LI)?†

11. foot yangming (ST)?

12. foot taiyin (SP)?√ 

13. hand shaoyin (HT)?√

14. hand taiyang (SI)?X

15. foot taiyang (BL)?√

16. foot shaoyin (KD)?

17. hand jueyin (PC)?

18. hand shaoyang (TB)?

19. foot shaoyang (GB)?

20. foot jueyin (LV)?

21. which jingjins correspond to the ear?

22. which jingjins correspond to the genitals?

six needling techniques from the neijing...

23. fenci?√

24. huici?√

25. fuci?√

26. guanci?X√

27. heguci?√

28. huozhen?√

29. what is jin cuo feng?

30. jin is healthiest in what temperature?

31. jin depends on nourishment of... 

REGULAR MERIDIANS

1. describe the course of the lung channel before it emerges at LU-1.√ 

2. if the channel is shaken, then what happens?√

3. describe the course of the LI channel.√ 

4. channel is shaken, what happens?††

5. how many branches off of the stomach channel?√√√

6. describe the course of the stomach channel from beginning to the first branch.√√ 

7. describe the first branch.√√

8. via which point does the stomach channel get to ST 9?√√

9. second branch?√X

10. third branch?√

11. fourth branch?√

12. fifth branch? √

13. when this channel is shaken, what happens?√

14. where do the spleen and liver channels cross on the lower leg?√√

15. where does the spleen intersect with the ren mai?√ 

16. first branch of spleen?†

17. second branch of spleen?X√

18. when this channel is shaken, what happens?†

19. 4 herbs for "opening the ghosts door / drive damp out of the pores"?√√

20. three branching points for the origination of the heart channel?√√√

21. heart primary channel links with what other channel, and where?√√√

22. when this channel is shaken, what happens?††

23. where does the SI channel first branch off from the course of the points?√√

24. where does it go from there?†

25. describe the second branch?√ 

26. describe the third branch?√

27. when channel is shaken...

28. where does the first branch of the BL channel arise and where does it go?√√

29. where does the BL channel go after BL-67?√√√

30. when channel is shaken...X††

31. kidney channel begins where?√√√

32. KD meets with the DU where?√√√

33. where does it go after that?√√√

34. where does it intersect with the REN?√√√

35. first branch?√√√

36. second branch?√√√

37. what happens when KD channel is shaken?X†

38. describe the first branch of the GB.X

39. how does the GB channel end at its most distal end?

40. when this channel is shaken...

______________________




ANSWERS

1. nanjing. 

2. no pairing

mostly in the center of the body

no hand / foot differentiation

no special relationship between zang/fu

3. chills and fever

4. pain in the heart

5. yang flaccidity and yin spasm

6. yin flaccidity and yang spasm

7. counterflow qi and internal urgent pain

8. spinal spasm and syncope

9. internal binds, hernias, masses

10. abdominal fullness, sensation of sitting in water

11. kidney (great luo of shaoyin)

12. stomach channel at ST30

13. 12 meridians' blood and qi

14. uterus / lower abdomen, emerges from REN-1

15. arises in pelvic cavity, goes up spine

16. lower abdomen, emerges from perineum

17. lower abdomne to genitals, around anus, interior of spinal column, into kidneys

18. lower abdomen, winds around external genitals, heart, winds around mouth, to below middle of eye. 

19. enters at BL-1, follows BL channel up head, enters brain, emerges at DU-16, bifurcates and follows BL channel from BL-12, into kidneys

20. kidney (in first and third branches), heart

21. brain

22. REN-1, REN-24, DU-1, DU-28

23. neuroendocrine system. 

24. SP-4 gongsun

25. food stagnation

stabbing pain in chest

counterflow qi

26. LU-7, lieqi

27. dead fetus retention

pain of genitals

xuan qi (cold phlegm accumulation)

28. SI-3, houxi

29. cold / exterior damage

stiff neck / spine

30. GB-41, zulinqi

31. surface wind pruritis

hand/foot numbness

swollen/painful throat

deafness

32. PC-6

33. fullness in chest/diaphragm

lumbar pain 

34. TB-5 waiguan. 

35. fever/chills

joint pain

visual dizziness

36. KI-6

37. throat obstruction

alcoholic bi syndrome

constipation

38. BL-62

39. spastic pain in abdomen / back

postpartum spontaneous sweats 

DIVERGENT CHANNELS

1. strengthens zang/fun interior/exterior channel connection

connects parts of the body (heart and kidney)

distributes qi to the neck and head

helps explain certain acupuncture points

2. the yang channel

3. the throat

4. the anus. 

5. BL-10 tian zhu 天柱 heavenly pillar

6. SI-17 tian rong 天容 heavenly appearance  

7. ST-9 ren ying 人迎 man's welcome

8. SI-16 天窗 tian chuang heavenly window

9. TB-16 天牖 tian you heavenly window

10. LI-18 扶突 fu tu support the prominence 

SINEWS

1. knees, ST-12

2. crosses over deltoid and goes to spine, and also makes a headband across the head

3. the shoulder / scapula, then the neck. 

4. genitals

5. diaphragm

6. they always start from extremities and move proximally and superiorly. 

7. bones and joints, to promote proper movement. 

8. three foot yin and foot tai yang.

9. hematemesis

10. limited neck rotation

11. deviated mouth/eyes, lower eyelid paralysis, spasm of spine

12. deep pain in the spinal cord

13. spasm and decreased ROM of little finger

14. scapular pain that radiates to the neck, facial paralysis, neck pain radiating to back of the ear. 

15. eversion of the ankle, popliteal spasm, back arching spasm

16. arching back spasm

17. difficult shoulder abduction. 

18. facial paralysis / spasm, curling of tongue

19. fourth toe spasm radiating to lateral knee, facial paralysis

20. limited motion of knee joints, impotence 

21. ST, SI, TB, GB (the three hand yang and foot yangming)

22. SP, LR, KD, ST (the three foot yin and foot yangming)

23. fenci: needles inserted in space between muscles

24. huici: relaxes the tendons

25. fuci: shallow insertion to treat cold spasm 

26. guanci: rapid insertions on the end of tendons 

27. heguci: the foot of a chicken one

28. huozhen: fire needles

29. jin is separated or in disorder. 

30. warm. 

31. qi and blood. 

REGULAR MERIDIANS

1. originates in middle burner

descends to connect with LI

returns and traverses diaphragm

penetrates lung

ascends to throat

emerges from LU-1

2. gasping / coughing 

frequent, scanty urination. 

3. starts at LI1, then follows course of points until LI-15:

goes around shoulder to da jue 

goes to superclavicular fossa

branches off:

1) connects with lung

goes down to diaphragm and LI

2) passes through neck

reaches cheek

enters gum of lower teeth

curves around lip 

crosses sides at the philtrum

joins ST channel at LI20 

4. toothache, swelling of the neck, yellow eyes. 

5. 4 or 5 branches depending on what you consider a branch...(4 according to lingshu according to Qin)

6. originates in LI20

goes to BL1

goes to ST1-3

goes to philtrum (DU26-28)

circles lips and meets REN-24

goes to ST-5

7. keeps going up to ST8 and meets DU24

8. via ST-5, not ST-8. 

9. separates from ST-5

enters ST-12

goes to DU-14

descends through diaphragm

enters stomach, connects with spleen

10. emerges from pyrloric orifice of stomach

descends within abdomen

rejoins at ST-30

11. separates at ST-36

ends at lateral aspect of middle toe

12. separates at ST-42

ends at medial side of big toe

links with SP-1, spleen channel 

stomach branches summary:

a) the one that goes up to ST8 (really just part of the channel?)

b) the one that separates at ST5, goes to dajue and down to spleen

c) the one that starts in the middle of the stomach

d) the one that separates from ST36

e) the one that separates from ST42

13. yangming-like symptoms, essentially. 

14. 8 cun above MM. 

15. REN 3,4 and REN 10

16. ascends through diaphragm

runs along esophagus

spreads to lower surface of tongue.

17. ascends from stomach, passes through diaphragm, links with heart. 

18. tongue stiffness or pain

body heaviness / swelling

watery diarrhea

jaundice

19. ge gen

cang zhu

ma huang

du huo 

20. all start at the heart.

a) heart to small intestine

b) heart up esophagus, to tissues surrounding eyes

c) heart to lungs to HT 1

21. only links with SI channel at HT 9 

22. dry throat

painful hearts

yellow eyes

painful upper arm

23. SI 13

24. da jue

supraclavicular fossa

heart

stomach

small intestine

25. ascends from ST-12

neck to GB-1 to SI-19

26. cheek to lateral side of the nose

merges with BL-1 (taiyang!)

27. sore throat 

swollen chin / jaws

stiff neck / shoulder

shoulder / upper arm pain 

28. bai hui to temples. 

29. kidney channel. 

30. head / spine pain

loins are broken 

eversion of the ankle?

31. begins below little toe, then goes to KD1

32. DU1

33. up the spine

into the kidneys

into the bladder

34. REN 3,4, 7

35. emerges from kidneys

goes through liver / diaphragm

enters the lung

ends at root of tongue

36. separates at the lung

goes to heart

pericardium 

ends at REN 17

37. disease where one is hungry but doesn't want to eat

anxiety in the heart

heat in the mouth or on the bottom of the foot

38. emerges behind ear

does a lot of random stuff in the side of the face

intersects ST-9 and rejoins main channel in ST-12

descends into chest

meets P-1

connects with Liver, GB

encircles genitals 

meets bladder channel at the sacral foramen points

goes to DU-1

emerges at GB 30

39. separates from GB 41, goes to medial tip of big toe and joins with liver channel. 

40. bitter taste in the mouth

headache

goiter

10/7/11 group art show

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

www.fermatawellness.com

paintings

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

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

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

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

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

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

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

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

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...àX
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.