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Final Pharamcology > Cardiovascual System > Flashcards

Cardiovascual System Flashcards

0
Q

What are the u/e of ACE inhibitors?

A

HA, dizziness, abdo pain, confusion, renal failure and impotence. Also a DRY IRRITATING COUGH

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1
Q

What is the MOA of ACE inhibitors?

A

block the synthesis of angiotensin II (a potent vasoconstrictor) -
reduce aldosterone secretion from adrenal cortex (resulting in net water loss)

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2
Q

What is the MOA of Thiazide Diuretics?

A

Inhibit sodium and chloride reabsorption in the thick ascending loop and early distal tubule. Loss of Ions increases urine volume.

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3
Q

Name two ACE inhibitors?

A

Captopril -

Enalapril

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4
Q

What are the U/E of Thiazide Diuretics?

A

can cause hypokalemia

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5
Q

Name a Thiazide diuretic?

A

Chlorthiazide

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6
Q

What Thiazide diuretic can cause u/e hyponatremia, hypokalemia, hyperglycemia, hyperuricemia, hypercalcemia?

A

Chlorthiazide

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7
Q

What is the MOA of Loop Diuretics?

A

inhibit chloride reabsorption in the ascending loop of Henly.
(also treat pulmonary edema b/c potent rapid action)

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8
Q

Name two Loop Diuretics?

A

Furosemide, Ethacrynic Acid

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9
Q

What are the U/E of loop Diuretics?

A

hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hyperglycemia, hyperuricemia, OTOTOXICITY

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10
Q

What drugs are cause hyponatremia, hypocalcemia, hypomagnesemia, hyperglycemia, hyperuricemia, ototoxicity?

A

Furosemide, Ethacrynic Acid (most ototoxic)

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11
Q

What is the MOA of Cardia Glycosides?

A

inhibit Na+K+ATPase.

causing an increase in the level of sodium ions in the myocytes, leading to a rise in the level of intracellular Ca+. Sodium/calcium exchanger on the plasma membrane depends on a constant inward Sodium gradient to pump out calcium. Cardiac Glycosides decreases sodium concentration gradient and the subsequent calcium outflow, thus raising the Ca+ concentration in myocardiocytes and increasing the force of myocardial contraction.

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12
Q

Name a Cardiac Glycoside?

A

Digoxin

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13
Q

What is the precaution with Digoxin-Cardiac Glycosides?

A

narrow therapeutic margin

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14
Q

What are the U/E of Digoxin - Cardiac Glycosides toxicity?

A

arrhythmias, anorexia, nausea, diarrhea, drowsiness, fatigue, visual disturbances

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15
Q

What is the MOA of class I antiarrythmic drugs?

A

Na+ channel blockers.
block ssodium entry into the cell during depolarization. This decreases the rate of rise of phase 0 of the action potential.

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16
Q

What is the MOA of Class III antiarrythmic drugs?

A

K+ channel blockers -

prolong re-polarization. Useful in treating intractable ventricular arrhythmias

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17
Q

What is the MOA of class IV antiarrythmic drugs?

A

CA++ channel blockers -
slowing the inward calcium current to slow conduction and prolong the effective refractory period, especially in the AV node. Most effective against atrial arrhythmias.

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18
Q

What is a Class I Anti-arrhythmic drug?

A

Lidocaine - used for ventricular ;

Procainamide - used for atrial and ventricular

19
Q

What is a Class III Anti-arrhythmic drug?

A

Amiodarone - effective preventative for ventricular fibrillation and tachychardia

20
Q

What is MOA for organic nitrates in relieving angina?

A

dilate the large myocardial arteries to increase the blood supply of the heart.
Also reduces cardia preload by reducing venous tone.
nitrAtes ^ -> ^ nitrItes -> ^ nitric oxide -> ^ cGMP -> ^ dephosphorylation of myosin light chain -> vascular smooth muscle relaxation

21
Q

What is the organic nitrate and drug of choice for acute coronary spasm?

A

Nitroglycerine - administered SV for rapid onset of action (2 minutes)- can be administered transdermally for a longer duration of action

22
Q

What is the MOA of ß-blockers in relieving angina?

A

decrease the oxygen demands of the myocardium by lowering both the rate and force of contraction of the heart

23
Q

What are the contraindications when using ß-blockers for angina?

A

contraindicated in patients with COPD, asthma, diabetes, severe bradycardia, peripheral vascular disease.

24
Q

How should the use of ß-blockers be discontinued?

A

dose should be gradually tapered off over 5-10 days to avoid reboudn angina or hypotension.

25
Q

Which group of antihypertensive drugs useful in treating diabetes patients?

A

ACE inhibitors do not affect glucose levels so are good for diabetes patients.

ACE inhibitors useful in hypertension that is a result of increased rennin levels.

26
Q

Which group of antihypertensive drugs is useful in patients of African American decent?

A

Calcium Channel Blockers

27
Q

Which group of antihypertensive drugs is useful for patients with angina?

A

ß-blockers

28
Q

Which group of antihypertensive drugs are used for pregnant women?

A

central acting adrenergic drugs like METHYLDOPA .

29
Q

What are the important antiplatelet drugs?

A

Aspirin, Clopidegrol, Abciximab

30
Q

What is the MOA of aspirin?

A

inhibits platelet aggregation by inhibiting thromboxane A2 synthesis in the platelets and thus prolongs bleeding time.

31
Q

What is the MOA of Clopidegrol?

A

blocks platelet aggregation by irreversibly inhibiting the binding of ADP to its receptor on platelets. This inhibits the activation of GP IIb/IIIa receptors required for platelets to bind to fibrinogen.

32
Q

What is the action of Heparin?

A

interferes w the clotting factor activation in both the intrinsic and extrinsic pathways, principally by binding to antithrombin III w the subsequent rapid inactivation of coagulation factors especially thrombin and factor Xa.

33
Q

What is the main u/e of Heparin?

A

hemorrhage

34
Q

What is the antidote to a heparin-induced hemorrhage?

A

protamine

35
Q

What is the MOA of oral anticoagulants?

A

they antagonize vitamin K, interfere w the synthesis of vitamin K dependent clotting factors (II, VII, IX, X) - intrinsic clotting pathway is vitamin K dependent

36
Q

Name an oral anticoagulant?

A

warferin

37
Q

What does a thrombolytic drug do?

A

they lyse already formed clots

38
Q

What is the MOA of Thrombolytic drugs?

A

activate plasminogen to plasmin. Plasmin digests fibrin forming degradation products. most effective if initiated early after clot formation.

39
Q

Name two thrombolytic drugs?

A

streptokinase -

tissue plasminogen activator (t-PA)

40
Q

What drug is used to treat anemia from end-stage renal failure?

A

erythropoietin -

synthesized in the KD in response to hypoxia or anemia to stimulate erythropoiesis

41
Q

What drug is used in megaloblastic anemia?

A

Cyanocobalamin aka Vitamin B 12 -

lacking intrinsic factor and unable to absorb vit b12

42
Q

What is the MOA of HMG-CoA reductase inhibitors? What does it treat?

A

Antihyperlipidemic; first choice for Tx of patients with hypercholesterolemia.

HMG-CoA reductase is a precursor of cholesterol - the inhibitor prevents the reductase enzyme from rate-limiting cholesterol synthesis.

HMG-CoA reductase inhibitor decrease LDL, VLDL and TG.
Increases HDL.

43
Q

Name two kinds of HMG-CoA reductase inhibitors and their U/E.

A

Simvastatin ; Atrovastatin ; Rosuvastatin -

LV Fx abnormalities, myopathy, rhabdomyolysis.

cannnot be taken w grapefruit juice

44
Q

What is the MOA of Niacin? What category of drug is this?

A

antihyperlipidemic drug ;

MOA: strongly inhibist lipolysis in adipose tissue.
Decreases LDL, VLDL, TG
increases HDL

45
Q

What are the U/E of Niacin?

A

flush and pruritus

46
Q

What is the MOA and drug category of Ezetimibe?

A

Anithyperlipidemia - cholesterol absorption inhibitor ;

MOA: inhibit intestinal absorption of dietary and biliary cholesterol.
decrease LDL and TG
increase HDL

Final Pharamcology (8 decks)

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