Cardiovascular Drugs General Overview

Based off of Nkembo Cardiovascular Pharmacology lecture & Hyperlipidemia pharmacology

Diuretic MOA

Increase the rate of urine flow

Most common adverse effects of diuretics

potassium depletion

Main Diuretics and their types

furosemide: loop
Chlorothiazide: thiazide

Amiloride: potassium sparing

When are Diuretics used clinically

hypertension and Congestive heart failure (edema)

ARBs work at which receptor

AT1

Renin Inhibitor example and MOA

Aliskiren: Directly inhibits renin thereby preventing the

formation of angiotensin I and II

When are Renin Inhibitors used clinically

patients with high-renin HTN or primary HTN

Sulfhydryl ACEI example

captopril (capoten)

Captopril main side effect

rashes and loss of taste

ACE Dicarboxylate inibitor examples

Lisinopril (prinivil, zestril) & Enalapril

T/F lisinopril requires bioactivation

false

Enalapril clinical pearl

long acting, requires bioactivation

two ACEI that do not require bioactivation

captopril & lisinopril

Fosinopril clinical pearl

only ACEI not eliminated by kidneys

Common adverse effects of ACEI

dry cough, hypokalemia, skin rash, hypotension, altered taste

MOA of ACE inhibitors

block the enzyme ACE, decrease the secretion of aldosterone, resulting in decreased

sodium and water retention, reduce both cardiac preload and afterload

ARB examples

valsartan, irbesartan, losartan, candesartan

Losartan clinical pearl

requires bioactivation

CCB Non-DHP examples

verapamil & Diltiazem

CCB dihydropyridines examples

amlodipine and nifedipine

Calcium Channel Blocker MOA

Inhibit calcium influx into arterial smooth muscle cells

Calcium Channel blocker common adverse effects

flushing, hypotension, nasal congestion, headache, and dizziness

CCB 1,4- DHPs side effects

Palpitations, chest pain, and tachycardia

Centrally Acting α-2 agonist examples

methyldopa & clonidine

Methyldopa clinical pearl

used for HTN in pregnancy

β-Adrenergic Receptor Blockers (Beta blocker) MOA

Bind and block the binding of norepinephrine and epinephrine to these receptors, causing inhibition of normal sympathetic effects.

Propranolol side effects

CNS side effects, such as dizziness, confusion, or depression. (lipid-soluble)

α1 – Adrenergic Receptor blocker examples

quinoxalines: Prazosin, Terazosin, Doxazosin

MOA of α1 – Adrenergic Receptor blocker

They cause vasodilation, decreased blood pressure and decreased peripheral resistance.

α1 – Adrenergic Receptor blocker clinical pearl

have not been shown to be beneficial in heart failure or angina

Ace inhibitors end in

-pril

ARBs end in

-sartan

Dihydropyridine CCBs end in

-pine

alpha blockers end in

-azosin

Oral Vasodilators

hydralazine & minoxidil

Vasodilator drawback

can lead to renal retention of sodium and water, increasing blood volume and cardiac output

When can low dose aspirin be given to an ASCVD risk patient

higher ASCVD risk and is NOT at increased bleeding risk

Beta-Blockers work in what part of the body

Nervous system ( sympathetic nervous system , norepinephrine, HR/contractility )

ACEIs, ARBs, ARNI, & MRAs work on what part of the body

kidneys ( renin, RAAs activation, sodium/water retention)

Which drug classes directly addresses sodium/water retention

Diuretics, SGLT2I

ARNI example

Entresto ( sacubitril/valsartan)

Mineralocorticoid Receptor Antagonists (MRA) example

spironolactone (Aldactone)

Adverse effects of HMG CoA reductase inhibitors

liver failure, myopathy, contraindicated in pregnancy/lactation

What enzyme are statins metabolized by

CYP3A4 (except pravastatin)

Contraindications for statins

Pregnancy/lactation, liver disease

Ezetimibe (zetia) MOA

Lowers plasma cholesterol levels by inhibiting the absorption of cholesterol at the brush border of the small intestine

Statin MOA

competitive inhibitors of HMG CoA reductase, the rate- limiting step in cholesterol synthesis

Ezetimibe selectivity is good because

It does not interfere with the absorption of triglycerides, lipid-soluble vitamins, or other nutrients

Mechanism of action of Niacin (nicotinic acid)

strongly inhibits lipolysis in adipose tissue, thereby reducing the production of

free fatty acids

Niacin (nicotinic acid) therapeutic uses:

treatment of familial hyperlipidemias and other severe hypercholesterolemia.

• reduces LDL and is the one of the most effective agents for increasing HDL.

Mechanism of action of Fibrates

Bind to peroxisome proliferator response elements, which ultimately leads to decreased triglyceride concentrations through increased expression of lipoprotein lipase.
Decrease Plasma triglyceride levels

Ezetimibe Class

Cholesterol Absorption Inhibitor

Fibrate examples

Gemfibrozil, Fenofibrate

Bile acid sequestrants example

Cholestyramine, Colestipol and Colesevelam

Bile acid sequestrants MOA

Bind (hold or sequester) bile acids and increase their fecal elimination with beneficial effects of lowering serum cholesterol levels

Proprotein convertase subtilisin/ kexin type 9 inhibitors (PCSK9) example

Alirocumab and evolocumab (repatha)

Proprotein convertase subtilisin/ kexin type 9 inhibitors (PCSK9) MOA

inhibiting the PCSK9 enzyme making more LDL receptors are available to clear LDL-C from the serum.

Omega-3 fatty acids MOA

Inhibit VLDL and triglyceride synthesis in the liver.

Ezetimibe efficacy

Lowers LDL by about 25%

When should evolocumab be used over ezetimibe

patient has no cost concerns, can handle injection, LDL needs to decrease by more than 25%