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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
clinical applications and toxicity of "a" blockers (-zosins)
hypertension BPH tox: orthostatic hypotension
26
Clinical applications of B-Blockers (-olol, -lol)
hypertension heart failure coronary disease
27
clinical applications and toxicity of nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
CA: angina: sublingual (acute), Oral/transdermal (prophylaxis), IV (acute coronary syndrome) Tox: orthostatic hypotension, tachycardia, headache *synergistic hypotension with sildenafil*
28
clinical applications and toxicity of Beta Blockers (propranolol, atenolol, metoprolol)
CA: prophylaxis of angina Tox: asthma, AV Block, acute HF, sedation *additive effect with all cardiac depressants*
29
Clinical applications and toxicity of Calcium channel blockers (verapamil, diltiazem)
CA: prophylaxis of angina, HTN, arrhythmias Tox: AV block, Acute HF, constipation, edema *additive effects with other cardiac depressants/hypotensive drugs*
30
Clinical applications and toxicity of calcium channel blockers (nifedipine, -dipine)
CA: prophylaxis of angina and treatment of HTN but prompt release of nifedpine is CI Tox: excessive hypotension, baroreceptor reflex tachycardia
31
Clinical applications and toxicity of Ranolazine
CA: prophylaxis of angina Tox: QT interval prolongation, nausea, constipation, dizziness Interactions: inhibitors of CYP3A increase ranolazine concentration and DOA
32
In heart failure, what is the MOA and Effects of loop diuretics (furosemide)
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
33
in heart failure, what is the MOA of hydrochlorothiazide
MOA: decrease NaCl reabsorption in the distal convoluted tubule
34
Clinical applications and toxicity of fursoemide?
CA: acute and chronic HR, severe hypertension, edema Tox: hypovolemia, hypokalemia, orthostatic hypotension, ototoxicity, sulfa allergy
35
clinical applications and toxicity of hydrochlorothiazide
CA: mild chronic failure, mild-moderate hypertension, hypercalciuria TOX: hypokalemia, hyperglycemia, hyperuricemia, hyperlipidemia, sulfa allergy
36
in heart failure, what is the MOA and Effects of aldosterone antagonist (spironolactone)
MOA: blocks cytoplasmic aldosterone receptors in collecting tubules of nephron Effects: increased salt and water excretion, reduces remodeling
37
Clinical applications and toxicity of spironolactone (aldosterone antagonist)
CA: chronic HR, aldosteronism (cirrhosis, adrenal tumor), HTN Tox: hyperkalemia, antiandrogen action (gynecomastia)
38
in heart failure, ACE inhibitors (-prils) MOA and Effects:
MOA: inhibits ACE, reduces all formation by inhibiting conversion of AI to AII effects: arteriolar and venous dilation, reduces aldosterone secretion, reduces cardiac remodeling
39
Clinical applications and toxicity of ACE inhibitors (-pril)
CA: chronic HR, HTN, Diabetic renal disease Tox: cough, hyperkalemia, angioneurotic edema
40
In heart failure, the MOA and Effects of ARBs (-sartans)
MOA: antagonize all effects at AT1 receptors effects: arteriolar and venous dilation, reduces aldosterone secretion, reduces cardiac remodeling
41
Clinical applications and toxicity of ARBs (-sartan)
CA: used in patients intolerant to ACE inhibitors Tox: hyperkalemia, angioneurotic edema
42
In heart failure, the MOA and effects of beta blockers (carvedilol, metoprolol, bisprolol, nebivolol)
MOA: competitive blocks B1 receptors effects: slows heart rate, reduces BP
43
Clinical applications and toxicity of beta blockers (carvedilol, metoprolol, bisprolol, nebivolol)
CA: chronic HR (to slow progression); reduce mortality in moderate to severe HR Tox: bronchospasms, bradycardia, AV block, acute cardiac decompensation
44
In heart failure, the MOA and effects of digoxin (cardiac glycoside)
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
Clinical applications and toxicity of digoxin ( cardiac glycosides)
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
In heart failure, venodilator (isosorbide dinitrate) MOA and effects:
MOA: releases nitric oxide; activates guanylyl cyclase effects: venodilation, reduces preload and ventricular stretch
47
Clinical applications and toxicity of venodilator (isosorbide dinitrate):
CA: acute and chronic HR; angina Tox: postural hypotension, tachycardia, Headache
48
In heart failure, arteriolar dilator (hydralazine) MOA and effects:
MOA: probably increases NO synthesis in endothelium effects: reduces blood pressure and afterload; results in increased cardiac output
49
Clinical applications and toxicity of arteriolar dilator (hydralazine):
CA: hydralazine plus nitrates may reduce mortality in African Americans tox: tachycardia, fluid retention, lupus-like syndrome
50
In heart failure, combined arteriolar and venodilator (nitroprusside) MOA and effects:
MOA: releases NO spontaneously; activates guanylyl cyclase effects: marked vasodilation; reduces preload and afterload
51
clinical applications and toxicity of combined arteriolar and venodilator (nitroprusside):
CA: acute cardiac decompnesation; hypertensive emergencies (malignant hypertension) Tox: excessive hypotension, thiocyanate and cyanide toxicity
52
In heart failure, Dobutamine MOA and effects:
MOA: beta1-selective agonist; increases cAMP synthesis Effects: increases cardiac contractility, output
53
Clinical applications and toxicity of dobutamine:
CA: acute decompensated HF tox: IV ONLY; arrhythmias
54
In heart failure, dopamine MOA and Effects:
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
Clinical applications and toxicity of dopamine:
CA: acute decompensated HF tox: IV ONLY; arrhythmias
56
In heart failure, milrinone (bipyridines) MOA and Effects:
MOA: phosphodiesterase type 3 inhibitor; decrease cAMP breakdown effects: vasodilator; lower peripheral vascular resistance
57
Clinical applications and toxicity of milrinone:
CA: actue decompensated HF tox: IV ONLY; arrhythmias
58
In heart failure, natriuretic peptide (nesiritide) MOA and Effects:
MOA: activates BNP receptors, increases cGMP Effeects: vasodilation, diuresis
59
Clinical applications and toxicity of natriuretic peptide (nesiritide):
CA: acute decompensated failure Tox: renal damage, hypotension
60
In heart failure, neprilysin inhibitor (sacubitril) MOA and Effects:
MOA: inhibits neprilysin, thus reducing breakdown of ANP and BNP Effects: vasodilator
61
Clinical applications and toxicity of neprilysin inhibitor (sacubitril):
CA: chronic HF, combination reduces mortaility and rehospitalization in HFrEF tox: used only in combination with ARB -- hypotension, angioedema
62
Sacubitril is used only in combination with what drug? why?
valsartan - valsartan inhibits action of angiotensin on its receptors
63
In arrhythmias, Effects of Procainamide
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
Clinical applications and toxicity of Procainamide
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
In arrhythmias, effects and MOA of Lidocaine?
CLass 1B Action-Sodium Channel blocker: MOA: sodium channel blockade Effects: blocks activated and inactivated channels with fast kinetics
66
Clinical applications and toxicity of lidocaine?
CA: ventricular tachycardia and for prevention of ventricular fibrillation after cardioversion TOX: neurologic symptoms reduce dose in patients with HF or liver disease
67
In arrhythmias, MOA and effects of Flecaininde?
Class 1C:Sodium channel blocker MOA: sodium channel blockade Effects: dissociates from channel with slow kinetics
68
Flecaininde Clinical applications and toxicity?
CA: supraventricular arrhythmias in patients with normal heart. do not use in ischemic conditions (post MI) Tox: proarrhythmic
69
in arrhythmias, MOA and Effects of propranolol
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
In arrhythmias, Clinical applications and toxicity of propranolol
CA: atrial arrhythmias and prevention of recurrent infarction and sudden death Tox: asthma, AV blockade, acute HR
71
In arrhythmias, effects of Dofetilide?
Class 3: Prolongation of ADP Effects: prolongs action potential, effective refractory period
72
Clinical applications and toxicity of Dofetilide.
CA: maintenance or restoration of sinus rhythm in atrial fibrilation Tox: torsades de pointes (initiate in hospital with monitoring)
73
In arrhythmias, the effects of Amiodarone?
Effects: prolongs action potential duration and QT interval slows HR and AV node conduction
74
Clinical applications and toxicity of Amiodarone?
CA: serious ventricular arrhythmias and supraventricular arrhythmias Effects: bradycardia and heart block in diseased heart, peripheral vasodilation, pulmonary and hepatic toxicity. hypo/hyperthyroidism
75
in arrhythmias, the MOA and effects of Verapamil?
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
Clinical applications and toxicity of Verapamil?
CA: supraventricular tachycardias, HTN, Angina Tox: caution in pt with hepatic dysfxn
77
In arrhythmias, effects of Adenosine?
Effects: very brief, usually complete AV Blockade
78
Clinical applications and toxicity of Adenosine?
CA: proxysmal supraventricular tachycardias Tox: flushing, chest tightness, dizziness
79
In arrhythmias, effects of Magnesium
Effects: normalizes or increases plasma Mg2+
80
Clinical applications and toxicity of magnesium
CA: torsades de pointes. digitalis-induced arrhythmias TOX: muscle weakness in overdose
81
in arrhythmias, MOA and effects of potassium
MOA: increase K+ permeability Effects: slows ectopic pacemaker slows conduction velocity in heart
82
Clinical applications and toxicity of Potassium
CA: digitalis-induced arrhythmias, arrhythmias associated with hypokalemia Tox: reentrant arrhythmias, fibrillation or arrest in overdose
83
in diuretics, carbonic anhydrase inhibitors (acetazolamide) MOA and Effects:
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
Clinical applications and toxicities of acetazolamide?
CA: Glaucoma, mountain sickness, edema with alkalosis TOX: Metabolic acidosis, renal stones, hyperammonemia in cirrhotic
85
In diuretics, MOA and Effects of SGLT2 inhibitors (canagliflozin)
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
Clinical applications and toxicities of Canagliflozin
CA: Diabetes mellitus; approved for the treatment of hyperglycemia, not as a diuretic Tox: not recommended in severe renal or liver disease
87
in diuretics, MOA and effects of loop diuretics (furosemide):
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
Clinical applications and toxicities of furosemide (loop diuretics):
CA: Pulmonary edema, peripheral edema, heart failure, hypertension, acute hypercalcemia, anion overdose Tox: Ototoxicity, hypovolemia, K wasting, hyperuricemia, hypomagnesemia
89
in diuretics, MOA and effects of thiazide diuretics (hydrochlorothiazide):
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
Clinical applications and toxicity of hydrochlorothiazide:
CA: Hypertension, mild heart failure, nephrolithiasis, nephrogenic diabetes insipidus Tox: Hypokalemic metabolic alkalosis, hyperuricemia, hyperglycemia, hyponatremia
91
in diuretics, MOA and Effects of K-Sparing (spironolactone) diuretics:
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
Clinical applications and toxicity of spironolactone?
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
In diuretics, MOA and effects of K-sparing (amiloride) diuretics:
MOA: Blocks epithelial sodium channels in collecting tubules Effects: Reduces Na retention and K wasting * increases lithium clearance
94
Clinical applications and toxicity of Amiloride?
CA: Hypokalemia from other diuretics * reduces lithium-induced polyuria * Liddle syndrome Tox: Hyperkalemic metabolic acidosis
95
in diuretics, MOA and effects of osmotic diuretics (mannitol)
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
Clinical applications and toxicity of mannitol:
CA: Renal failure due to increased solute load (rhabdomyolysis, chemotherapy), increased intracranial pressure, glaucoma Tox: Nausea, vomiting, headache
97
in diuretics, MOA and effects of Vasopressin (Conivaptan) diuretics:
MOA: Antagonist at V1a and V2 ADH receptors Effects: Reduces water reabsorption, increases plasma Na concentration, vasodilation
98
Clinical applications and toxicities of Conivaptan:
CA: Hyponatremia, congestive heart failure Tox: Infusion site reactions, thirst, polyuria, hypernatremia
99
In diuretics, MOA and Effects of vassopressin (tolvaptan) diuretics:
MOA: Selective antagonist at V2 ADH receptors Effects: Reduces water reabsorption, increases plasma Na concentration
100
Clinical applications and toxicities of Tolvaptan
CA: Hyponatremia, SIADH Tox: Polyuria (frequency), thirst, hypernatremia

Pharmacology (5 decks)

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