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.
Showing posts with label pharmacology. Show all posts
Showing posts with label pharmacology. Show all posts
Wednesday, December 1, 2010
Tuesday, November 30, 2010
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.
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.
Sunday, November 28, 2010
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.
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.
Sunday, November 14, 2010
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.
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.
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.
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
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
Monday, October 25, 2010
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.
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.
Sunday, October 17, 2010
pharmacology: cardiovascular drugs
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.
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.
Monday, October 4, 2010
pharmacology: respiratory drugs
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.
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
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.
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.
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