Cardiovascual System Flashcards
(47 cards)
What are the u/e of ACE inhibitors?
HA, dizziness, abdo pain, confusion, renal failure and impotence. Also a DRY IRRITATING COUGH
What is the MOA of ACE inhibitors?
block the synthesis of angiotensin II (a potent vasoconstrictor) -
reduce aldosterone secretion from adrenal cortex (resulting in net water loss)
What is the MOA of Thiazide Diuretics?
Inhibit sodium and chloride reabsorption in the thick ascending loop and early distal tubule. Loss of Ions increases urine volume.
Name two ACE inhibitors?
Captopril -
Enalapril
What are the U/E of Thiazide Diuretics?
can cause hypokalemia
Name a Thiazide diuretic?
Chlorthiazide
What Thiazide diuretic can cause u/e hyponatremia, hypokalemia, hyperglycemia, hyperuricemia, hypercalcemia?
Chlorthiazide
What is the MOA of Loop Diuretics?
inhibit chloride reabsorption in the ascending loop of Henly.
(also treat pulmonary edema b/c potent rapid action)
Name two Loop Diuretics?
Furosemide, Ethacrynic Acid
What are the U/E of loop Diuretics?
hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hyperglycemia, hyperuricemia, OTOTOXICITY
What drugs are cause hyponatremia, hypocalcemia, hypomagnesemia, hyperglycemia, hyperuricemia, ototoxicity?
Furosemide, Ethacrynic Acid (most ototoxic)
What is the MOA of Cardia Glycosides?
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.
Name a Cardiac Glycoside?
Digoxin
What is the precaution with Digoxin-Cardiac Glycosides?
narrow therapeutic margin
What are the U/E of Digoxin - Cardiac Glycosides toxicity?
arrhythmias, anorexia, nausea, diarrhea, drowsiness, fatigue, visual disturbances
What is the MOA of class I antiarrythmic drugs?
Na+ channel blockers.
block ssodium entry into the cell during depolarization. This decreases the rate of rise of phase 0 of the action potential.
What is the MOA of Class III antiarrythmic drugs?
K+ channel blockers -
prolong re-polarization. Useful in treating intractable ventricular arrhythmias
What is the MOA of class IV antiarrythmic drugs?
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.
What is a Class I Anti-arrhythmic drug?
Lidocaine - used for ventricular ;
Procainamide - used for atrial and ventricular
What is a Class III Anti-arrhythmic drug?
Amiodarone - effective preventative for ventricular fibrillation and tachychardia
What is MOA for organic nitrates in relieving angina?
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
What is the organic nitrate and drug of choice for acute coronary spasm?
Nitroglycerine - administered SV for rapid onset of action (2 minutes)- can be administered transdermally for a longer duration of action
What is the MOA of ß-blockers in relieving angina?
decrease the oxygen demands of the myocardium by lowering both the rate and force of contraction of the heart
What are the contraindications when using ß-blockers for angina?
contraindicated in patients with COPD, asthma, diabetes, severe bradycardia, peripheral vascular disease.
