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Pharmacology > Cardio drugs > Flashcards

Cardio drugs Flashcards

0
Q

Fenofibrate

A

Fibrate

MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis

EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL

SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones

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1
Q

Gemfibrozil

A

Fibrate

MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis

EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL

SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones

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2
Q

Choleselevam

A

Bile acid resin

MOA: prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more.

EFFECTS: moderately decreases LDL, slightly increases both HDL and TGs

SIDE EFFECTS: patients hate it–it tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones

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3
Q

Niacin

A

MOA: inhibits lipolysis in adipose tissue; reduces hepatic VLDL
synthesis

EFFECTS: moderately decreases LDL, moderately increases HDL, slightly decreases TGs

SIDE EFFECTS: red, flushed face, which is decreased by aspirin or long term use, hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbates gout)

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4
Q

Ezetimibe

A

MOA: prevents cholesterol absorption at small intestine brush border

EFFECTS: decreases LDL

SIDE EFFECTS: rare increase in LFTs, diarrhea

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5
Q

Propranolol

A

Class II antiarrhythmic

MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval

USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Can cause exacerbation of vasospasm in prinzmetal angina. Treat overdose with glucagon

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6
Q

Metoprolol

A

Class II antiarrhythmic

MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval

USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Metoprolol can cause dislipidemia. Treat overdose with glucagon

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7
Q

Atenolol

A

Class II antiarrhythmic

MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval

USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon

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8
Q

Isosorbide dinitrate

A

MOA: vasodilates by increasing NO in vascular smooth muscle–>increased cGMP and smooth muscle relaxation. Dilates veins»arteries. Decreases preload. Undergoes extensive first pass metabolism.

USES: angina, acute coronary syndrome, pulmonary edema.

TOXICITY: reflex tachycardia (treat with B blockers), hypotension, flushing, headache, tolerance.

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9
Q

Diltiazem

A

Non-selective CCB; results in vasodilation, negative iototropic (non-dihydropyridine)

MOA: blocks voltage-dependent L-type calcium channels of cardiac and smooth muscle

CLINICAL USE: hypertension, angina, Raynaud phenomenon, atrial fibrillation

TOXICITY: cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation,

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10
Q

Nifedipine

A

Dihydropyridine CCB

MOA: block voltage-dependent L-type calcium channels of smooth muscle

CLINICAL USE: hypertension, angina, Raynaud phenomenon

TOXICITY: cardiac depression AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation

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11
Q

Verapamil

A

Non-dihydropyridine CCB

MOA: blocks voltage-dependent L-type calcium channels of cardiac muscles

CLINICAL USES: hypertension, angina, atrial fibrillation/flutter

TOXICITY: cardiac depression, AV block, flushing, peripheral edema, dizziness hyperprolactinemia, and constipation

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12
Q

Amlodipine

A

Dihydropyridine CCB

MOA: block voltage-dependent L-type calcium channels of smooth muscle

CLINICAL USE: hypertension, angina, Raynaud phenomenon

TOXICITY: cardiac depression AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, and constipation

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13
Q

NA nitroprusside

A

Short-acting. Increases cGMP via direct release of NO. Can cause cyanide toxicity (releases cyanide). Used for hypertensive emergencies

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14
Q

Hydralazine

A

MOA: increases cGMP–> smooth muscle relaxation. Vasodilates arterioles>veins leading to after load reduction

USES: severe HTN, CHF. First line therapy for HTN in pregnancy, with methyldopa. Frequently co administered with a B blocker to prevent reflex tachycardia

TOXICITY: compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus-like syndrome

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15
Q

Carvedilol

A

Sympatholytic, alpha and beta receptor antagonist
Class II antiarrhythmic

MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval

USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon

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16
Q

Digoxin

A

Cardiac glycoside

MOA: direct inhibition of Na/K ATPase leading to indirect inhibition of Na/Ca exchanger/antiport. Increases intracellular calcium–>positive inotropy. Stimulates vagus nerve–>decreased HR

USES: CHF (increases contractility), atrial fibrillation (decreases conduction at AV node and depression of SA node)

TOXICITY: cholinergic-nausea, vomiting, diarrhea, blurry yellow vision. ECG-increased PR interval, decreased QT interval, ST scooping, T wave inversion, arrhythmia, AV block. Can lead to hyperkalemia, which indicates poor prognosis.

FACTORS PREDISPOSING TO TOXICITY: renal failure (decreased excretion), hypokalemia (permissive for digoxin binding at K+ binding site on Na/K ATPase), verapamil, amiodarone, quinidine (decreases digoxin clearance, displaces digoxin from tissue-binding sites)

ANTIDOTE: slowly normalize k+, cardiac pacer, anti digoxin Fab fragments, mg++

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17
Q

Disopyramide

A

Class 1A antiarrhythmic

MOA: increases AP duration and increases effective refractory period, increases QT interval. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

TOXICITY: heart failure, thrombocytopenia, torsades de pointes due to increased QT interval

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18
Q

Procainamide

A

Class 1A antiarrhythmic

MOA: increases AP duration and increases effective refractory period, increases QT interval. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

TOXICITY: reversible SLE-like syndrome, thrombocytopenia, torsades de pointes due to increased QT interval

19
Q

Quinidine

A

Class 1A antiarrhythmic

MOA: increases AP duration and increases effective refractory period, increases QT interval. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

TOXICITY: cinchonism (headache, tinnitus), thrombocytopenia, torsades de pointes due to increased QT interval

20
Q

Lidocaine

A

Class 1B antiarrhythmic

MOA: Class 1A antiarrhythmic

MOA: decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: acute ventricular arrhythmias (especially in post-MI), digitalis-induced arrhythmias

21
Q

Flecainidine

A

Class 1C antiarrhythmic

MOA: significantly prolongs refractory period in AV node. Minimal effect on AP duration. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

TOXICITY: proarrhythmic, especially post-MI (contraindicated).

22
Q

Propafenone

A

Class 1C antiarrhythmic

MOA: significantly prolongs refractory period in AV node. Minimal effect on AP duration. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: SVTs, including atrial fibrillation. Only as a last resort in refractory VT.

TOXICITY: proarrhythmic, especially post-MI (contraindicated).

23
Q

Amiodarone

A

Class III. Antiarrhythmic (has class I, II, III, and IV effects)

MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.

USES: atrial fibrillation, atrial flutter, ventricular tachycardia

TOXICITY: pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight), corneal deposits, skin deposits resulting in photodermatitis, neurological effects, constipation, cardiovascular effects (bradycardia, heart block, CHF) **remember to check PFTs, LFTs, and TFTs when using amiodarone.

24
Q

Class II anti arrhythmics

A

Beta blockers; decrease SA and AV nodal activity by decreasing camp, decreasing calcium concentrations; suppresses abnormal pacemakers by decreasing slope of phase 4; AV node is particularly susceptible leading to increased PR interval on EKG

Use: atrial flutter, a fib, AV nodal reentry; first line of drugs (with CCBs) for RATE control of Afib; decreases mortality rate post MI

25
Q

Sotalol

A

Class III. Antiarrhythmic

MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.

USES: atrial fibrillation, atrial flutter, ventricular tachycardia

TOXICITY: torsades de pointes, excessive B blockade

26
Q

Verapamil

A

Class IV anti arrhythmic; oral; blocks cardiac calcium channels; anti-anginal as well; slows phase 4 depolarization in SA, AV node and increases refractory period of AV node

Use: v fib (rate control), AV nodal re entry, SVT

Side effects: can cause/ exacerbate hypotension, GI upset, peripheral edema, increases serum digoxin

27
Q

Diltiazem

A

Class IV anti arrhythmic; calcium channel blocker preferentially vascular over cardiac

Use: a fib, AV nodal reentry, SVT

Side effects: exacerbates hypotension

28
Q

Adenosine

A

Increases K+ out of cells leading to hyperpolarizing the cell and decreased Calcium influx. Drug of choice in diagnosing/abolishing SVT. Very short acting (~15 sec). Adverse effects include flushing, hypotension, chest pain. Effect blocked by theophylline and caffeine.

ADVERSE EFFECTS: flushing, hypotension, chest pain, sense of impending doom, bronchospasm.

29
Q

Nimodipine

A

Dihydropyridine CCB

MOA: block voltage-dependent L-type calcium channels of smooth muscle

CLINICAL USE: subarachnoid hemorrhage (prevents cerebral vasospasm). hypertension, angina, Raynaud phenomenon

TOXICITY: peripheral edema, flushing, dizziness, constipation, gingival hyperplasia

30
Q

Nitroglycerin

A

MOA: vasodilates by increasing NO in vascular smooth muscle–>increase in cGMP and smooth muscle relaxation. Dilates veins»arteries. Decreases preload.

USES: angina, acute coronary syndrome, pulmonary edema

TOXICITY: reflex tachycardia (treat with B blockers), hypotension, flushing, headache, “Monday disease” in industrial exposure: development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure. Must have a nitrate-free interval.

31
Q

Statins

A

MOA: inhibits conversion of HMG-CoA to mevalonate

EFFECTS: significantly lowers LDL, slightly increases HDL, slightly decreases TGs

SIDE EFFECTS: hepatotoxicity, rhabdomyolysis

32
Q

Cholestyramine

A

Bile acid resin

MOA: prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more.

EFFECTS: moderately decreases LDL, slightly increases both HDL and TGs

SIDE EFFECTS: patients hate it–it tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones

33
Q

Colestipol

A

Bile acid resin

MOA: prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more.

EFFECTS: moderately decreases LDL, slightly increases both HDL and TGs

SIDE EFFECTS: patients hate it–it tastes bad and causes GI discomfort, decreases absorption of fat soluble vitamins, cholesterol gallstones

34
Q

Clofibrate

A

Fibrate

MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis

EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL

SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones

35
Q

Bezafibrate

A

Fibrate

MOA: upregulate LPL leading to increased TG clearance. Activates PPAR-alpha and induces HDL synthesis

EFFECTS: greatly decreases TGs, slightly decreases LDL, slightly increases HDL

SIDE EFFECTS: myositis (increased risk with concurrent statins), hepatotoxicity, cholesterol gallstones

36
Q

Mexiletine

A

Class 1B antiarrhythmic

MOA: Class 1A antiarrhythmic

MOA: decreases AP duration. Preferentially affects ischemic or depolarized Purkinje and ventricular tissue. Slows or blocks conduction (especially in depolarized cells). Decreases slope of phase 0 depolarization and increases threshold for firing in abnormal pacemaker cells.

USES: acute ventricular arrhythmias (especially in post-MI), digitalis-induced arrhythmias

36
Q

Esmolol

A

Class II antiarrhythmic–very short acting

MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval

USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon

37
Q

Timolol

A

Class II antiarrhythmic

MOA: decreases SA and AV nodal activity by decreasing cAMP, decreases calcium currents. Suppress abnormal pacemakers by decreasing slope of phase 4. AV node particularly sensitive–increases PR interval

USES: SVT, slowing ventricular rate during atrial fibrillation and atrial flutter

TOXICITY: impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alteration). May mask the signs of hypoglycemia. Treat overdose with glucagon

38
Q

Ibutilide

A

Class III. Antiarrhythmic

MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.

USES: atrial fibrillation, atrial flutter

TOXICITY: torsades de pointes

38
Q

Dofetilide

A

Class III. Antiarrhythmic

MOA: increases AP duration, increases ERP. Used when other antiarrhythmics fail. Increases QT interval.

USES: atrial fibrillation, atrial flutter

39
Q

Class IV antiarrhythmics

A

CCBs-verapamil and diltiazem

MOA: decrease conduction velocity; increase ERP, increase PR interval

USES: prevention of nodal arrhythmias (e.g. SVT), rate control in atrial fibrillation

TOXICITY: constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

40
Q

Mg++

A

Effective in torsades de pointes and digoxin toxicity

41
Q

Indomethacin

A

NSAID used to close PDA (inhibits PGE1 and 2)

42
Q

Isosorbide mononitrate

A

MOA: vasodilates by increasing NO in vascular smooth muscle–>increased cGMP and smooth muscle relaxation. Dilates veins»arteries. Decreases preload. Isosorbide dinitrate Undergoes extensive first pass metabolism. This is an active metabolite of isosorbide dinitrate–oral bioavailability is close to 100%

USES: angina, acute coronary syndrome, pulmonary edema.

TOXICITY: reflex tachycardia (treat with B blockers), hypotension, flushing, headache, tolerance.

Pharmacology (13 decks)

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