Exam IV: Cardiovascular Drugs

Question 1

RAAS Drugs

Answer 1

1. Aliskiren: inhibit renin to Ang I
2. Captopril: inhibit Ang I to Ang II (ACE inhibitor)
3. Losartan: inhibit Ang II to aldosterone (ARB)

Adverse effects of all: hyperkalemia, angioedema, hypotension
Captopril: causes cough
Losartan: acute renal failure

Question 2

Captopril 5 Advantages

Answer 2

1. Anti fibrosis
2. Vasodilation
3. Increase prostaglandins
4. Increase Ang 1-7
5. Increase bradykinin levels – can cause the cough and angioedema

Question 3

Nitrates

Answer 3

use for acute angina
1. NTG (Nitroglycerin): organic and selective for dilating veins and coronary arteries, which causes a decrease in preload and afterload
Averse effects: headache, overt syncope, and hypotension (decrease O2 to heart)

2. SNP: inorganic and non-specific, so dilates veins and arteries
   Adverse effects: cyanide build up if liver not functioning properly

Question 4

Ca2+ Channel Blockers

Answer 4

1. Dihydropyridine: Nifedipine
2. Non-dihydropyridine: Verapamil and Diltiazem

Effects of both: dilate arterioles, increase coronary blood flow, no effect on venous beds
Non-dihydropyridine effects: selective for heart, so do not use for heart failure patients

Adverse Effects of both: edema

Question 5

Beta Blockers

Answer 5

Propanolol: beta 1 and beta 2; bad for asthma
Metropolol: beta 1 only

Adverse effects of both: impotence, bradycardia, and vivid dreams

Question 6

Alpha Receptors

Answer 6

Prazosin: alpha 1 antagonist that dilates arteries and veins; decreases preload, intact negative feedback, and decrease sympathetic flow; side effect is 1st dose postural hypotension

Clonidine: alpha 2 agonist that decreases sympathetic flow and side effect is dry mouth

Question 7

Loop Diuretics

Answer 7

affects the thick ascending limb of loop of Henle by blocking the Na/K/2Cl cotransporter
monotherapy for CHF

Furosemide: secreted by organic acid
Effects: decrease in Na/H2O, Cl, Mg, and K
alkalosis, gout, ear issues, and allergy causing necrosis of cells that may lead to death

Question 8

K-sparing Diuretics

Answer 8

affect the collecting ducts

Spironolactone: MR antagonist (aldosterone) thereby blocking the Na/K pump; antagonist of androgens
Amiloride: ENaC blocker secreted by organic base

Effects: increases K and Cl while causing acidosis

Question 9

Thiazide Diuretics

Answer 9

affects distal convoluted tubule by inhibiting the Na/Cl cotransporter

HCT: decreases Na/H2O, K, and causes alkalosis
secreted by organic acid
1st line diuretic for hypertension

Question 10

Treatment for Angina Pectoris

Answer 10

Effort Induced: nitrates, calcium channel blockers, and beta blockers

Variant: nitrates and calcium channel blockers

Question 11

Treatment for Heart Failure

Answer 11

Preload Reduction: loop diuretics (monotherapy), K sparing (combination), venodilators (nitrates)

Afterload Reduction: ACEI/ARB, beta antagonists

Not used:
Alpha receptor antagonists: because neurotransmitters would bind to beta instead and increase renin angiotensin system = bad
Ca channel blockers: it blocks Ca2+ channels reducing Ca2+ in cells and decreases contractility = bad

Question 12

Compensation for Heart Failure

Answer 12

1. Increase preload to increase SV to decrease HR while maintaining CO because CO = SV * HR
2. In heart failure no longer have enough blood pumped out aka increase in afterload, so increase vasoconstriction to increase BP to drive the blood flow through the tissues to decrease afterload
3. Increase contractility to make the contraction longer lasting thereby decreasing afterload, or the amount of blood left in the heart after contraction
4. HR isn’t as important because when reduced SV, sympathetic is increased more and more until maximized so that means HR is maximized and won’t go any higher