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Pharmacology > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

0
Q

What are the mechanisms that maintain cardiac reserve in heart failure?

A

Compensatory or Adaptive mechanisms

  • Frank-Starling mechanism: the contractility of heart increases in response to an increase in the volume of blood filling the heart
  • activation of sympathetic nervous system
  • the renin-angiotensin-aldosterone mechanism
  • myocardial hypertrophy and remodeling
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1
Q

When does heart failure occur?

A

Heart failure occurs when the heart muscle can no longer pump enough blood to meet demands of body. It most often develops insidiously during the end stage of many forms of chronic heart disease, such as hypertension, valvular heart disease, ischemic heart disease (e.g. following myocardial infarction), etc.

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2
Q

What is the role of physiologic compensatory mechanism in the progression of HF?

A
  1. When cardiac function is impaired, the compensatory physiologic mechanisms maintain arterial pressure and perfusion of vital organs by maintaining normal cardiac output in the face of heart disease. But their capacity to do so may ultimately be overwhelmed. Moreover, superimposed pathological changes in the heart muscles causes further functional disturbances.
  2. Chronic activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis is associated with remodeling of cardiac tissue, characterized by loss of myocytes, hypertrophy, and fibrosis. The geometry of the heart becomes less elliptical and more spherical, interfering with the ability to efficiently function as a pump. This prompts additional neurohumeral activation, creating a vicious cycle that, if left untreated, leads to death…
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3
Q

What are the symptoms of Left Heart Failure?

A

Dyspnea from pulmonary congestion

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4
Q

What are the symptoms of Right Heart Failure?

A

peripheral edema

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5
Q

What are the 3 major events to which the treatment of heart failure is targeted?

A
  1. decreasing cardiac workload
  2. controlling excess fluid
  3. enhancing myocardial contractility
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6
Q

What are the 5 groups of drugs that can reduce the cardiac workload in heart failure?

A
  1. Angiotensin-converting enzyme (ACE) inhibitors
  2. Angiotension II Receptor Antagonists
  3. Direct Vasodilators
  4. Beta-Blockers
  5. Spironolactone
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7
Q

What does ACE Inhibitors do? What is MOA of ACE Inhibitors?

A

ACE Inhibitors –> improve symptoms, slow the progression of heart failure, and prolong survival. Also used in tx of hypertension.

ACE Inhibitors MOA:

  • blocks the synthesis of angiotension II, a potent vasoconstrictor
  • reduce aldosterone secretion from adrenal cortex resulting in net water loss
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8
Q

What are the 3 benefits of ACE inhibitors in heart failure patients?

A

3 benefits of ACE inhibitors:

  1. improves symptoms
  2. slow the progression of heart failure
  3. prolongs survival
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9
Q

Give examples of ACE Inhibitors:

A
  1. Captopril (Capoten): Infrequently causes aganulocytosis or neutropenia.
  2. Enalapril (Vasotec)
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10
Q

What are the major side effects of ACE Inhibitors?

A

headache, dizziness, abdominal pain, confusion, renal failure, and impotence

can also cause a dry, irritating cough

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11
Q

What is MOA for Angiotensin II Receptor Antagonisits?

A

These drugs interfere with the binding of angiotensin II with its receptors. They do not produce cough. Also used in the treatment of hypertension.

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12
Q

Example of Angiotensin II Receptor Antagonists:

A

Losartan (Cozaar)

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13
Q

MOA of Direct vasodilators and example?

A

MOA of direct vasodilators: directly relax arterioles

Minoxidil (Loniten)

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14
Q

What is dual action of Minoxidil?

A

Minoxidil (Loniten) –> side effects - unwanted hair growth; also marketed for topical treatment of male pattern baldness

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15
Q

What is MOA of Beta-Blockers?

A

blocks sympathetic nervous system

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16
Q

What is the MOA of Spironolactone? In what cases of heart failure is it used?

A

Antagonizes aldosterone

-reserved for advanced cases of heart failure…

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17
Q

What is the purpose of using diuretics in heart failure patients? What are the 3 groups of diuretics?

A

Diuretics are almost always used to control excess fluid accumulation in heart failure. Heart failure is associated with retention of sodium and water. Control of excessive fluid accumulation can relieve symptoms, but do not stop progression of disease.

  1. Thiazide diuretics
  2. Loop diuretics
  3. potassium sparing diretics
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18
Q

What is MOA of Thiazide Diuretics? Example? What are undesirable side effects of Thiazide Diuretics? What happens if you give to gout patients?

A

MOA of Thiazide Diuretics: inhibits sodium and chloride reabsorption in the thick ascending loop and early distal tubule. This loss of ions increases urine volume. This causes hypokalemia (low potassium in blood).

Example: Chlorthiazide (Diuril)

Undesirable side effects: hyponatremia, hypokalemia, hypoglycemia, hyperuricemia, hypercalcemia

Can cause an increase in levels of uric acid in blood, so if you give to gout patients it will increase gout…

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19
Q

What is MOA of Loop Diuretics? Example? What are the undesirable side effects?

A

MOA of Loop Diuretics: They inhibit chloride reabsorption in the ascending loop of Henle. They are used in the treatment of pulmonary edema because of their potent and rapid action.

Examples:
Furosemide (Lasix)
Ethacrynic Acid (Ethacrynate): *** most ototoxic

Undesirable side effects: hyponatremia, hypokalemia, hypomagnesemia, hyperglycemia, hyperuricemia, ototoxicity

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20
Q

What is the MOA of Potassium Sparing Diuretics? Examples? What is the undesirable effect of these drugs?

A

MOA of Potassium Sparing Diuretics: They enhance sodium excretion and retain potassium by an action in the distal tubule. They are often used in combination with the other diuretics to help maintain potassium balance.

Example: Spironolactone (Aldactone)

Undesirable effect: hyperkalemia

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21
Q

Name 3 categories of drugs that enhance the contractility of heart in heart failure patients.

A
  1. cardiac glycosides
  2. sympathomimetics
  3. phosphodiasterase inhibitors
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22
Q

What is MOA of cardiac glycosides? Example? What is the importance of its therapeutic index?

A

MOA of cardiac glycosides: they inhibit NA+-K+-ATPase. This causes an increase in the level of sodium ions in the myocytes, which leads to a rise in the level of intracellular calcium ions. This occurs because sodium/calcium exchanger on plasma membrane depends on the constant inward sodium gradient to pump out calcium. Digoxin decreases sodium concentration gradient and the subsequent calcium outflow, thus raising the calcium concentration in myocardiocytes. Thus the force of mycardial contraction is increased.

Example: Digoxin (Lanoxin)

Important: The cardiac glycosides have a low therapeutic index which means that they plasma concentration that causes serious toxicity is only slightly higher than the therapeutic dose. Toxicity resulting from cardiac glycosides can be manifested by – arrhythmias; anorexia, nausea, and diarrhea; drowsiness and fatiguel visual disturbances…

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23
Q

What are the 3 groups of drugs used in treatment of angina pectoris?

A
  1. organic nitrates
  2. Beta Blockers
  3. Calcium Channel Blockers
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24
Q

What is angina pectoris?

A

Angina pectoris occurs when coronary blood flow is insufficient to meet the oxygen demands of the myocardium leading to ischemia. It is due to an imbalance between the supply (perfusion) and demand of the heart for oxygenated blood.
>90% of cases are due to coronary artery atherosclerosis
In the setting of coronary artery obstruction, ischemia can be aggravated by an increase in heart energy demand as occur in conditions, such as increased heart rate (tachycardia)

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25
Q

What are 3 types of angina pectoris?

A
  1. stable
  2. unstable
  3. prinzmetal or variant angina
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26
Q

What is mechanism of organic nitrates?

A

MOA of organic nitrates:

  • they dilate the large myocardial arteries to increase the blood supply of the heart
  • also reduces cardiac preload by reducing venous tone
  • nitrates increase nitrites increase nitric oxide increase cGMP increase dephosphorulation of myosin light chain increase vascular smooth muscle relaxation
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27
Q

What are the common side effects of organic nitrates?

A

Side effects of organic nitrates: headache and postural hypotension

28
Q

What is the interaction between organic nitrates and sildenafil (Viagra)?

A

Sildenafil potentiates the action of nitrates thereby causing dangerous hypotension. An interval of at least 6 hours between ingestion of the two drugs is recommended.

29
Q

What is the drug of choice for acute coronary spasm? What is common route of administration?

A

Nitroglycerine is the drug of choice for acute coronary spasm. It is useful in treating all forms of angina.
It is often administered sublingually for rapid onset of action (2 min), but can be applied transdermally for a longer duration of action.

30
Q

What is MOA of Beta Blockers in relieving angina pectoris? Which group of patients they are particularly useful? How these drugs should be withdrawn?

A

MOA of Beta Blockers: they decrease the oxygen demands of myocardium by lowering both the rate and the force of contraction of the heart.
Cardioselective beta blockers are preferred. They suppress the activation of the heart by blocking B1 receptors.
They are particularly useful in the treatment of patients with myocardial infarction and have been shown to prolong survival.

Contraindication: patients with asthma, diabetes, severe bradycardia, peripheral vascular disease or COPD

Caution: Do not discontinue B-blocker therapy abruptly. They dose should be gradually tapered off over 5-10 days to avoid rebound angina or hypotension.

31
Q

What is MOA of calcium channel blockers with angina pectoris? Give Example.

A

MOA of calcium channel blockers: they block calcium influx into the smooth muscle cells of the arteries causing them to dilate.

common side effects are: headache, dizziness, hypotension, etc…

Example: Diltiazem (Cardizem)
Amlodipine (Norvasc)

32
Q

Name the group of drugs to treat hypertension.

A

Antihypertensives:

  1. Diuretics
  2. B-Blockers
  3. ACE Inhibitors
  4. Angiotensin II Receptor Antagonists
  5. Calcium Channel Blockers
  6. Alpha Blockers
  7. Central Acting Adrenergic Drugs
  8. Drugs affecting neurotransmitter uptake or release
  9. Direct Vasodilators
  10. Drugs used in hypertensive crisis (Hypertensive urgency and emergency)
33
Q

What is MOA of diuretics in lowering blood pressure? What is first line drug therapy for hypertension?

A

MOA of diuretics in lowering blood pressure: eliminate excess salt and water from body

Currently recommended as first-line therapy for hypertension unless there are compelling reasons to choose another agent

34
Q

What is MOA of Beta Blockers in lowering blood pressure? What concomitant disease with Beta-Blockers are particularly useful?

A

MOA of Beta Blockers in lowering blood pressure: they prevent sympathetic stimulation of the heart thereby causing decreased heart rate and cardiac output.
Similar to the ACE inhibitors, beta-Blockers may not be effective in lowering BP in African Americans
beta-Blockers may be particulary useful in patients with angina or those with migraines…

35
Q

Examples of Beta Blockers for hypertension:

A

Atenolol (Tenormin): B1 antagonist

Metoprolol (Lopressor): B1 antagonist

36
Q

What 2 groups of hypertensive patient ACE inhibitors are particularly useful?

A

ACE inhibitors are useful in hypertension that is a result of increased renin levels…
Because they do not affect glucose levels, ACE inhibitors are also used in the treatment of diabetes patients with hypertension.

37
Q

Which group of hypertensive patient Calcium channel blockers are particularly useful?

A

Calcium channel blockers are particularly useful in the treatment of hypertensive African Americans.

38
Q

Which drug is suitable to treat pregnant hypertensive patients?

A

Central acting adrenergic drugs are used to treat hypertensive pregnant women.

39
Q

Name the drugs used in hypertensive emergencies? What is the MOA of sodium nitroprusside? (Direct vasodilator)

A

Sodium nitroprusside - given via IV causes prompt vasodilation; capable of reducing BP in all patients regardless of cause of hypertension
Labetalol
Fenoldopam

40
Q

What is hypertensive urgency vs hypertensive emergency?

A

Hypertensive urgency - systolic bp is > or = 180/diastolic bp is > or = 110, but no associated organ damage

Hypertensive emergency - systolic bp is > or = 180/ diastolic bp is > or = 120, with evidence of associated organ damage, such as stroke, MI, angina pectoris, encephalopathy, cerebral hemorrhage etc.

41
Q

What is MOA of class I anti-arrhythmic drugs? Give examples.

A

MOA of class I anti-arrhythmic drugs: they block sodium entry into the cell during depolarization. This decreases the rate of the rise of Phase 0 of the action potential.

Class 1a: are useful in tx of atrial and ventricular arrhythmias (all-purpose antiarrhythmics).
-Procainamide (Pronestyl)

Class 1b: are used for the tx of ventricular arrythmias (ventricular tachycardia, ventricular fibrillation, and ventricular ectopy
-Lidocaine (Xylocaine)

Class 1c: are used for chronic suppression of ventricular arrhythmias (as opposed to acute tx of patients with ventricular arrhythmias, which is the roll of class 1b agents.

42
Q

What is the MOA of Class II anti-arrhythmic drugs? Give examples.

A

MOA of Class II antiarrhythmic drugs (beta-adrenoreceptor blockers): are particularly useful in suppressing the tachyarrhythmias that result from increased sympathetic activity. They stabilize cardiac membrane, slow down conduction through SA and AV nodes, and increase the refractory period.
-Propranolol (Inderal): most commonly used to tx patients with arrhythmias.

43
Q

What is the MOA of class IV anti-arrhythmic drugs?

A

MOA of class IV anti-arrhythmics: Calcium channel blockers: by slowing the inward calcium current, these drugs slow conduction and prolong the effective refractory period, especially in the AV node. They are most effective against atrial than ventricular arrhythmias.

44
Q

What are the 3 phases of hemostasis?

A
  1. Vascular
  2. platelet
  3. coagulation
45
Q

What is MOA of aspirin?

A

MOA of aspirin: inhibits platelet aggregation by inhibiting thromboxane A2 in the platelets, and thus prolongs bleeding time
-reduces the risk of MI and stroke

46
Q

What is MOA of Clopidegrol (Plavix)?

A

MOA of Clopidegrol: blocks platelet aggregation by irreversibly inhibiting the binding of ADP to its receptors on platelets and thus inhibit the activation of GP IIb/IIIa receptors required for platelets to bind to fibrinogen; thus it blocks platelet aggregation.

47
Q

What is MOA of Abeiximab?

A

MOA of Abeiximab (Reopro): prevents platelet aggregation by blocking the binding of fibrinogen to the glycoprotein IIb/IIIa receptor on surface of the platelet.

48
Q

Classify anticoagulant drugs:

A
  1. Heparin and LMWH (low molecular weight heparin)
  2. Oral anticoagulants
  3. Thrombin inhibitors
49
Q

What is MOA of Heparin and LMWH?

A

MOA of Heparin and LMWH: Interfere with the clotting factor activation in both the intrinsic and extrinsic pathways;
the principal anticoagulant actions of heparin are a result of its binding to antithrombin III with the subsequent rapid inactivation of coagulation factors, esp. thrombin and Xa.
LMWH are extracted from heparin. These agents have larger anti-factor activities than heparin, which permits them to be used at lower doses… In addition they have greater bioavailability after subcutaneous injection and have a longer half-life than heparin.

50
Q

What is the difference between heparin and LMWH?

A

The LMWH are extracted from heparin. These agents have a larger anti-factor activities than heparin, which permits them to be used at lower doses. In addition, they have greater bioavailability after subcutaneous injection and have a longer half-life than heparin.

51
Q

What is the major adverse effect of anticoagulant?

A

hemorrhage

52
Q

What is antidote for heparin poisoning?

A

Protamine is a specific heparin antagonist that can be used to treat heparin-induced hemorrhage.

53
Q

What is the MOA of oral anticoagulants, such as warfarin?

A

MOA of oral anticoagulants: They antagonize Vitamin K , interfere with the Vitamin K -dependent clotting factors (II, VII, IX, X)

54
Q

What is the MOA of hirudin or argatroban?

A

Inhibit clotting… Hirudin is derived from medicinal leech

55
Q

What is MOA of Thrombolytic drugs?

A

They activate plasminogen to plasmin. Plasmin digests fibrin forming degradation products…
-Clot dissolution is more likely if therapy is initiated early after clot formation. Clots become more difficult to lyse as they age.

56
Q

What are thrombolytic drugs?

A

Streptokinase

Tissue plasminogen activator (t-PA)

57
Q

What are the drugs that are used to treat bleeding?

A

Aminocaproic acid –> inhibits plasminogen activation
Tranexamic acid –> inhibits plasminogen activation
Ptotamine sulphate –> antagonizes heparin
Vitamin K –> can overcome the anticoagulant effects of oral agents
Aprotinin –> blocks plasmin

58
Q

What is anemia and how are drugs chosen for anemia?

A

Anemia is defined as a plasma hemoglobin level that is below normal.
There are many causes of anemia. Before tx, the cause needs to be determined.

59
Q

What are the drugs used to treat anemia of end-stage renal failure?

A

Epoetin alpha, darbepoetin alpha are human recombinant erythropoietin effective in the treatment of anemia caused by end-stage renal disease.

60
Q

What are the drugs used to treat megaloblastic anemia?

A

Cyanocobalamin (Vitamin B12)

61
Q

Classify Antihyperlipidemic drugs:

A
  1. HMG-CoA reductase inhibitors: ***first choice of tx for high cholesterol
  2. Fibrates
  3. Niacin
  4. Bile acid sequestrants
  5. Cholesterol absorption inhibitors
62
Q

What are first choice tx for hypercholesterolemia?

A

HMG-CoA is the first choice for hypercholesterolemia

Drugs: Simvastin (Zocor); Atrovastatin (Lipitor - most potent); Rosuvastatin (Crestor - most potent)

63
Q

What are the adverse effects of HMG-CoA?

A
  • Liver fx abnormalities, myopathy, rhabdomyolysis (disintegration of muscle), etc.
  • Concomitant use of grapefruit juice
64
Q

What do HMG-CoA do to different factions of cholesterol?

A

They decrease cholesterol, LDL, VLDL and Triglycerides (TG)

increase HDL…

65
Q

What is MOA of Niacin? Adverse effects?

A

Niacin strongly inhibits lipolysis in adipose tissue; decreases cholesterol, TG, LDL, VLDL and increases HDL.

Adverse effects of Niacin - flush and pruritis

66
Q

What is MOA of bile acid sequestrants?

A

MOA of bile acid sequestrants: They bind to bile acids in small intestine and prevent their reabsorption. This causes liver to use cholesterol to make more bile acids.

67
Q

What is MOA of Ezetimibe?

A

MOA of Ezetimibe (Zetia): is a cholesterol absorption inhibitor: they inhibit intestinal absorption of dietary and biliary cholesterol.

Pharmacology (7 decks)

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