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.
Showing posts with label beta blockers. Show all posts
Showing posts with label beta blockers. Show all posts
Tuesday, November 30, 2010
Monday, October 4, 2010
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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