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Pharmacology > Week 4: Medications > Flashcards

Week 4: Medications Flashcards

1
Q

In hypertension, what is the MOA and Effects for Thiazide diuretics (hydrochlorothiazide, lorthalidone)

A

MOA: Block Na/Cl transporter in renal distal tubule convoluted tubule
Effects: reduce blood volume

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2
Q

In hypertension, what is the MOA of loop diuretics (furosemide)

A

MOA: block Na/K/2Cl transporter in renal loop of Henle

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3
Q

In Hypertension, what is the MOA and Effects of spironolactone and eplerenone?

A

MOA: block aldosterone receptor in the renal collecting tubule
Effects: increase Na excretion and decrease K excretion

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4
Q

In hypertension, what is the MOA of ARBs (-sartan)

A

MOA: block AT1 angiotensin receptors

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5
Q

in hypertension, what is the MOA and Effects of ACE inhibitors (-pril)

A

MOA: inhibit angiotensin-converting enzyme
effects: reduce angiotensin II levels, reduce vasoconstriction and aldosterone secretion, increase bradykinin

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6
Q

In hypertension, what is the MOA and Effects of renin inhibitors (aliskiren)

A

MOA: inhibits enzyme activity of renin
Effects: reduces angiotensin I and II and aldosterone

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7
Q

In Hypertension, what is the MOA and Effects of Centrally acting sympathoplegics (Clonidine, methyldopa)

A

MOA: activate a2 adrenoceptors
Effects: reduce central sympathetic outflow, reduce norepinephrine release from noradrenergic nerve endings

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8
Q

In hypertension, what is the MOA and effects of the sympathetic nerve terminal blockers (reserpine)

A

MOA: blocks vesicular amine transporter in noradrenergic nerves and depletes transmitter stores
Effects: reduce all sympathetic effects, especially cardiovascular and reduce BP

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9
Q

In hypertension, what is the MOA of the sympathetic nerve terminal blockers (guanethidine, guanadrel)

A

MOA: interferes with amine release and replaces norepinephrine in vesicles

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10
Q

In hypertension, what is the MOA and effects of ‘a’ blockers (-zosin)

A

MOA: selectively block a1 adrenoceptors
Effects: prevent sympathetic vasoconstriction, reduce prostatic smooth muscle tone

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11
Q

in hypertension, what is the MOA and effects of b-blockers (-olol, -lol)

A

MOA: block b1 receptors (carvedilol also blocks a receptors; nebivolol also releases nitric oxide)
Effects: prevents sympathetic cardiac stimulation; reduce renin secretion

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12
Q

In angina pectoris, what is the MOA and Effects of nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)

A

MOA: releases nitric oxide in smooth muscle, which activates guanylyl cyclase and increase cGMP
Effects: smooth muscle relaxation, especially in vessels. vasodilation decreases venous return and heart size. may increase coronary flow in some areas and in variant angina

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13
Q

In angina pectoris, what is the MOA and Effects of beta blockers (propranolol, atenolol, metoprolol)

A

MOA: nonselective competitive antagonist at B adrenoceptors
Effects: decrease HR, CO, and BP. decreases myocardial oxygen demand

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14
Q

in angina pectoris, what is the MOA and Effects of Calcium Channel Blockers (verapamil, diltiazem)

A

MOA: nonselective block of L-type calcium channels in vessels and heart
Effects: reduced vascular resistance, cardiac rate, and cardiac force results in decreased oxygen demand

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15
Q

in angina pectoris, what is the MOA of Calcium Channel Blockers
(-dipine)

A

MOA: block of vascular L-type calcium channels> cardiac channels

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16
Q

In angina pectoris, what is the MOA and Effects of Ranolazine?

A

MOA: inhibits late sodium current in the heart. also may modify fatty acid oxidation at much higher doses
Effects: reduces cardiac oxygen demand; fatty acid oxidation modification could improve efficiency of cardiac oxygen utilization

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17
Q

Clinical applications of thiazide diuretics (hydrochlorothiazide, lorthalidone)

A

CA: hypertension; mild heart failure

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18
Q

Clinical applications of loop diuretics (furosemide)

A

severe hypertension
heart failure

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19
Q

clinical applications of spironolactone, eplerenone

A

aldosteronism
heart failure
hypertension

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20
Q

clinical applications and toxicities of ACE inhibitors (-prils)

A

hypertension
heart failure
diabetes
tox: angioedema, hyperkalemia, renal impairment, teratogenic

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21
Q

clinical applications of ARBs (-sartans)

A

hypertension
heart failure

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22
Q

clinical applications of renin inhibitor, aliskiren

A

hypertension

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23
Q

clinical applications of centrally acting sympathoplegics (clonidine, methyldopa)

A

hypertension
clonidine also used in drug withdrawl

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24
Q

clinical applications of sympathetic nerve terminal blockers (reserpine, guanethidine, guanadrel)

A

hypertension, but rarely used
tox:
Reserpine (psychiatric depression, GI disturbances)
Guanethidine, guanadrel ( severe orthostatic hypotension, sexual disfxn)

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25
Q

clinical applications and toxicity of “a” blockers (-zosins)

A

hypertension
BPH
tox: orthostatic hypotension

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26
Q

Clinical applications of B-Blockers (-olol, -lol)

A

hypertension
heart failure
coronary disease

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27
Q

clinical applications and toxicity of nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)

A

CA: angina: sublingual (acute), Oral/transdermal (prophylaxis), IV (acute coronary syndrome)
Tox: orthostatic hypotension, tachycardia, headache
synergistic hypotension with sildenafil

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28
Q

clinical applications and toxicity of Beta Blockers (propranolol, atenolol, metoprolol)

A

CA: prophylaxis of angina
Tox: asthma, AV Block, acute HF, sedation
additive effect with all cardiac depressants

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29
Q

Clinical applications and toxicity of Calcium channel blockers (verapamil, diltiazem)

A

CA: prophylaxis of angina, HTN, arrhythmias
Tox: AV block, Acute HF, constipation, edema
additive effects with other cardiac depressants/hypotensive drugs

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30
Q

Clinical applications and toxicity of calcium channel blockers (nifedipine, -dipine)

A

CA: prophylaxis of angina and treatment of HTN but prompt release of nifedpine is CI
Tox: excessive hypotension, baroreceptor reflex tachycardia

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31
Q

Clinical applications and toxicity of Ranolazine

A

CA: prophylaxis of angina
Tox: QT interval prolongation, nausea, constipation, dizziness
Interactions: inhibitors of CYP3A increase ranolazine concentration and DOA

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32
Q

In heart failure, what is the MOA and Effects of loop diuretics (furosemide)

A

MOA: decreases NaCl and KCl reabsorption in thick ascending limb of the loop of Henle in the nephron
Effects: increased excretion of salt and water, reduces cardiac preload and afterload, reduces pulmonary and peripheral edema

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33
Q

in heart failure, what is the MOA of hydrochlorothiazide

A

MOA: decrease NaCl reabsorption in the distal convoluted tubule

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34
Q

Clinical applications and toxicity of fursoemide?

A

CA: acute and chronic HR, severe hypertension, edema
Tox: hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfa allergy

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35
Q

clinical applications and toxicity of hydrochlorothiazide

A

CA: mild chronic failure, mild-moderate hypertension, hypercalciuria
TOX: hypokalemia, hyperglycemia, hyperuricemia, hyperlipidemia, sulfa allergy

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36
Q

in heart failure, what is the MOA and Effects of aldosterone antagonist (spironolactone)

A

MOA: blocks cytoplasmic aldosterone receptors in collecting tubules of nephron
Effects: increased salt and water excretion, reduces remodeling

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37
Q

Clinical applications and toxicity of spironolactone (aldosterone antagonist)

A

CA: chronic HR, aldosteronism (cirrhosis, adrenal tumor), HTN
Tox: hyperkalemia, antiandrogen action (gynecomastia)

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38
Q

in heart failure, ACE inhibitors (-prils) MOA and Effects:

A

MOA: inhibits ACE, reduces all formation by inhibiting conversion of AI to AII
effects: arteriolar and venous dilation, reduces aldosterone secretion, reduces cardiac remodeling

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39
Q

Clinical applications and toxicity of ACE inhibitors (-pril)

A

CA: chronic HR, HTN, Diabetic renal disease
Tox: cough, hyperkalemia, angioneurotic edema

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40
Q

In heart failure, the MOA and Effects of ARBs (-sartans)

A

MOA: antagonize all effects at AT1 receptors
effects: arteriolar and venous dilation, reduces aldosterone secretion, reduces cardiac remodeling

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41
Q

Clinical applications and toxicity of ARBs (-sartan)

A

CA: used in patients intolerant to ACE inhibitors
Tox: hyperkalemia, angioneurotic edema

42
Q

In heart failure, the MOA and effects of beta blockers (carvedilol, metoprolol, bisprolol, nebivolol)

A

MOA: competitive blocks B1 receptors
effects: slows heart rate, reduces BP

43
Q

Clinical applications and toxicity of beta blockers (carvedilol, metoprolol, bisprolol, nebivolol)

A

CA: chronic HR (to slow progression); reduce mortality in moderate to severe HR
Tox: bronchospasms, bradycardia, AV block, acute cardiac decompensation

44
Q

In heart failure, the MOA and effects of digoxin (cardiac glycoside)

A

MOA: NA+/K+-ATPase inhibition results in reduced Ca2+ expulsion and increased Ca2+ stored in sarcoplasmic reticulum
Effects: increases cardiac contractility; cardiac parasympathomimetic effect (slowed sinus HR, slowed AV conduction)

45
Q

Clinical applications and toxicity of digoxin ( cardiac glycosides)

A

CA: chronic symptomatic heart failure, rapid ventricular rate in atrial fibrillation, does not reduce mortality, but does reduce rehospitalization
Tox: nausea, vomiting, diarrhea, cardiac arrhythmias

46
Q

In heart failure, venodilator (isosorbide dinitrate) MOA and effects:

A

MOA: releases nitric oxide; activates guanylyl cyclase
effects: venodilation, reduces preload and ventricular stretch

47
Q

Clinical applications and toxicity of venodilator (isosorbide dinitrate):

A

CA: acute and chronic HR; angina
Tox: postural hypotension, tachycardia, Headache

48
Q

In heart failure, arteriolar dilator (hydralazine) MOA and effects:

A

MOA: probably increases NO synthesis in endothelium
effects: reduces blood pressure and afterload; results in increased cardiac output

49
Q

Clinical applications and toxicity of arteriolar dilator (hydralazine):

A

CA: hydralazine plus nitrates may reduce mortality in African Americans
tox: tachycardia, fluid retention, lupus-like syndrome

50
Q

In heart failure, combined arteriolar and venodilator (nitroprusside) MOA and effects:

A

MOA: releases NO spontaneously; activates guanylyl cyclase
effects: marked vasodilation; reduces preload and afterload

51
Q

clinical applications and toxicity of combined arteriolar and venodilator (nitroprusside):

A

CA: acute cardiac decompnesation; hypertensive emergencies (malignant hypertension)
Tox: excessive hypotension, thiocyanate and cyanide toxicity

52
Q

In heart failure, Dobutamine MOA and effects:

A

MOA: beta1-selective agonist; increases cAMP synthesis
Effects: increases cardiac contractility, output

53
Q

Clinical applications and toxicity of dobutamine:

A

CA: acute decompensated HF
tox: IV ONLY; arrhythmias

54
Q

In heart failure, dopamine MOA and Effects:

A

MOA: dopamine receptor agonist; higher doses activate B and A adrenoceptors
Effects: increases renal blood flow; higher doses increase cardiac force and blood pressure

55
Q

Clinical applications and toxicity of dopamine:

A

CA: acute decompensated HF
tox: IV ONLY; arrhythmias

56
Q

In heart failure, milrinone (bipyridines) MOA and Effects:

A

MOA: phosphodiesterase type 3 inhibitor; decrease cAMP breakdown
effects: vasodilator; lower peripheral vascular resistance

57
Q

Clinical applications and toxicity of milrinone:

A

CA: actue decompensated HF
tox: IV ONLY; arrhythmias

58
Q

In heart failure, natriuretic peptide (nesiritide) MOA and Effects:

A

MOA: activates BNP receptors, increases cGMP
Effeects: vasodilation, diuresis

59
Q

Clinical applications and toxicity of natriuretic peptide (nesiritide):

A

CA: acute decompensated failure
Tox: renal damage, hypotension

60
Q

In heart failure, neprilysin inhibitor (sacubitril) MOA and Effects:

A

MOA: inhibits neprilysin, thus reducing breakdown of ANP and BNP
Effects: vasodilator

61
Q

Clinical applications and toxicity of neprilysin inhibitor (sacubitril):

A

CA: chronic HF, combination reduces mortaility and rehospitalization in HFrEF
tox: used only in combination with ARB – hypotension, angioedema

62
Q

Sacubitril is used only in combination with what drug? why?

A

valsartan - valsartan inhibits action of angiotensin on its receptors

63
Q

In arrhythmias, Effects of Procainamide

A

Class 1A Action - Sodium Channel Blocker:
slows conduction velocity and pacemaker rate.
prolongs action potential duration and dissociates from sodium channels with intermediate kinetics
direct depressant effects on SA and AV nodes

64
Q

Clinical applications and toxicity of Procainamide

A

most atrial and ventricular arrhythmias
second drug of choice for most sustained ventricular arrhythmias associated with acute MI
TOX: NAPA implicated in torsades de pointes in patients with renal failure
hypotension, long-term therapy produces reversible lupus-related symptoms

65
Q

In arrhythmias, effects and MOA of Lidocaine?

A

CLass 1B Action-Sodium Channel blocker:
MOA: sodium channel blockade
Effects: blocks activated and inactivated channels with fast kinetics

66
Q

Clinical applications and toxicity of lidocaine?

A

CA: ventricular tachycardia and for prevention of ventricular fibrillation after cardioversion
TOX: neurologic symptoms
reduce dose in patients with HF or liver disease

67
Q

In arrhythmias, MOA and effects of Flecaininde?

A

Class 1C:Sodium channel blocker
MOA: sodium channel blockade
Effects: dissociates from channel with slow kinetics

68
Q

Flecaininde Clinical applications and toxicity?

A

CA: supraventricular arrhythmias in patients with normal heart. do not use in ischemic conditions (post MI)
Tox: proarrhythmic

69
Q

in arrhythmias, MOA and Effects of propranolol

A

Class 2 - Sympatholytic
MOA: B-Adrenoceptor blockade
Effects: direct membrane effects (sodium channel block) and prolongation of action potential
slows SA node automaticity and AV node conduction velocity

70
Q

In arrhythmias, Clinical applications and toxicity of propranolol

A

CA: atrial arrhythmias and prevention of recurrent infarction and sudden death
Tox: asthma, AV blockade, acute HR

71
Q

In arrhythmias, effects of Dofetilide?

A

Class 3: Prolongation of ADP
Effects: prolongs action potential, effective refractory period

72
Q

Clinical applications and toxicity of Dofetilide.

A

CA: maintenance or restoration of sinus rhythm in atrial fibrilation
Tox: torsades de pointes (initiate in hospital with monitoring)

73
Q

In arrhythmias, the effects of Amiodarone?

A

Effects: prolongs action potential duration and QT interval
slows HR and AV node conduction

74
Q

Clinical applications and toxicity of Amiodarone?

A

CA: serious ventricular arrhythmias and supraventricular arrhythmias
Effects: bradycardia and heart block in diseased heart, peripheral vasodilation, pulmonary and hepatic toxicity. hypo/hyperthyroidism

75
Q

in arrhythmias, the MOA and effects of Verapamil?

A

Class 4: calcium channel blocker
MOA: calcium channel blockade
Effects: slows SA node automaticity and AV nodal conduction velocity
decreases cardiac contractility
reduces BP

76
Q

Clinical applications and toxicity of Verapamil?

A

CA: supraventricular tachycardias, HTN, Angina
Tox: caution in pt with hepatic dysfxn

77
Q

In arrhythmias, effects of Adenosine?

A

Effects: very brief, usually complete AV Blockade

78
Q

Clinical applications and toxicity of Adenosine?

A

CA: proxysmal supraventricular tachycardias
Tox: flushing, chest tightness, dizziness

79
Q

In arrhythmias, effects of Magnesium

A

Effects: normalizes or increases plasma Mg2+

80
Q

Clinical applications and toxicity of magnesium

A

CA: torsades de pointes. digitalis-induced arrhythmias
TOX: muscle weakness in overdose

81
Q

in arrhythmias, MOA and effects of potassium

A

MOA: increase K+ permeability
Effects: slows ectopic pacemaker
slows conduction velocity in heart

82
Q

Clinical applications and toxicity of Potassium

A

CA: digitalis-induced arrhythmias, arrhythmias associated with hypokalemia
Tox: reentrant arrhythmias, fibrillation or arrest in overdose

83
Q

in diuretics, carbonic anhydrase inhibitors (acetazolamide) MOA and Effects:

A

MOA: inhibition of the enzyme prevents dehydrations of H2CO3 and hydrations of CO2 in the proximal convoluted tubule
Effects: Reduce reabsorption of HCO3−, causing self-limited diuresis. hyperchloremic metabolic acidosis. reduce body pH, . reduce intraocular pressure

84
Q

Clinical applications and toxicities of acetazolamide?

A

CA: Glaucoma, mountain sickness, edema with alkalosis
TOX: Metabolic acidosis, renal stones, hyperammonemia in cirrhotic

85
Q

In diuretics, MOA and Effects of SGLT2 inhibitors (canagliflozin)

A

MOA: Inhibition of sodium/glucose cotransporter (SGLT2) in the PCT results in decreased Na+ and glucose reabsorption
Effects: Inhibition of glucose reabsorption lowers serum glucose concentration, and reduced Na+ reabsorption causes mild diuresis

86
Q

Clinical applications and toxicities of Canagliflozin

A

CA: Diabetes mellitus; approved for the treatment of hyperglycemia, not as a diuretic
Tox: not recommended in severe renal or liver disease

87
Q

in diuretics, MOA and effects of loop diuretics (furosemide):

A

MOA: Inhibition of the Na/K/2Cl transporter in the ascending limb of Henle’s loop
Effects: Marked increase in NaCl excretion, some K wasting, hypokalemic metabolic alkalosis, increased urine Ca and Mg

88
Q

Clinical applications and toxicities of furosemide (loop diuretics):

A

CA: Pulmonary edema, peripheral edema, heart failure, hypertension, acute hypercalcemia, anion overdose
Tox: Ototoxicity, hypovolemia, K wasting, hyperuricemia, hypomagnesemia

89
Q

in diuretics, MOA and effects of thiazide diuretics (hydrochlorothiazide):

A

MOA: Inhibition of the Na/Cl transporter in the distal convoluted tubule
effects: Modest increase in NaCl excretion * some K wasting * hypokalemic metabolic alkalosis * decreased urine Ca

90
Q

Clinical applications and toxicity of hydrochlorothiazide:

A

CA: Hypertension, mild heart failure, nephrolithiasis, nephrogenic diabetes insipidus
Tox: Hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, hyponatremia

91
Q

in diuretics, MOA and Effects of K-Sparing (spironolactone) diuretics:

A

MOA: Pharmacologic antagonist of aldosterone in collecting tubules * weak antagonism of androgen receptors
Effects: Reduces Na retention and K wasting in kidney * poorly understood antagonism of aldosterone in heart and vessels

92
Q

Clinical applications and toxicity of spironolactone?

A

CA: Aldosteronism from any cause * hypokalemia due to other diuretics * post–myocardial infarction
Tox: Hyperkalemia, gynecomastia (spironolactone, not eplerenone) * additive interaction with other K-retaining drugs

93
Q

In diuretics, MOA and effects of K-sparing (amiloride) diuretics:

A

MOA: Blocks epithelial sodium channels in collecting tubules
Effects: Reduces Na retention and K wasting * increases lithium clearance

94
Q

Clinical applications and toxicity of Amiloride?

A

CA: Hypokalemia from other diuretics * reduces lithium-induced polyuria * Liddle syndrome
Tox: Hyperkalemic metabolic acidosis

95
Q

in diuretics, MOA and effects of osmotic diuretics (mannitol)

A

MOA: Physical osmotic effect on tissue water distribution because it is retained in the vascular compartment
effects: Marked increase in urine flow, reduced brain volume, decreased intraocular pressure, initial hyponatremia, then hypernatremia

96
Q

Clinical applications and toxicity of mannitol:

A

CA: Renal failure due to increased solute load (rhabdomyolysis, chemotherapy), increased intracranial pressure, glaucoma
Tox: Nausea, vomiting, headache

97
Q

in diuretics, MOA and effects of Vasopressin (Conivaptan) diuretics:

A

MOA: Antagonist at V1a and V2 ADH receptors
Effects: Reduces water reabsorption, increases plasma Na concentration, vasodilation

98
Q

Clinical applications and toxicities of Conivaptan:

A

CA: Hyponatremia, congestive heart failure
Tox: Infusion site reactions, thirst, polyuria, hypernatremia

99
Q

In diuretics, MOA and Effects of vassopressin (tolvaptan) diuretics:

A

MOA: Selective antagonist at V2 ADH receptors
Effects: Reduces water reabsorption, increases plasma Na concentration

100
Q

Clinical applications and toxicities of Tolvaptan

A

CA: Hyponatremia, SIADH
Tox: Polyuria (frequency), thirst, hypernatremia

Pharmacology (5 decks)

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