Hypertension and CVS Therapeutics Flashcards
Where and how does mannitol work?
In the proximal convoluted tubule and the descending loop, it works by increasing the osmolarity of the lumen fluid. It is filtered and not reabsorbed.
Acetazolamide
Carbonic anhydrase inhibitor, decreases NaCO3 resorption, makes urine alkaline, not used for hypertension but for epilepsy.
Furosemide
Loop diuretic, inhibits NKCC pump in the ascending loop, more Na in the lumen so water follows
Bumetanide
Loop diuretic, inhibits NKCC pump in the ascending loop, more Na in the lumen so water follows
What are some problems you see with loop diuretics?
Hypokalemia, aldosterone sensitive Na/K exchanger, pulls Na back into the body at the expense of K. Hypokalemia can cause heart arrhythmias
Hydrochlorothiazide
Thiazide, works in the distal convoluted tubule, inhibits the Na/Cl co transporter, more Na and H2O in the lumen. SE hypokalemia
Chlorthialindone
Thiazide, works in the distal convoluted tubule, inhibits the Na/Cl co transporter, more Na and H2O in the lumen. SE hypokalemia
What are some issues resulting from hypokalemia?
Arrhythmias and decreased insulin secretion leading to hyperglycemia
What are the 2 K sparing diuretics?
Spironolactone and amiloride, weak diuretics so used in combination with other diuretics. Don’t give with ACE inhibitors because it increases hyperkalemia
How does amiloride work?
It blocks the aldosterone sensitive Na/K exchanger
How does spironolactone work?
It blocks aldosterone itself so it has the same effect as amiloride
Clonidine
Alpha 2 agonist, receptors in the medulla (autoreceptor), reduces sympathetic tone resulting in decreased BP (more parasympathetic). SE xerostomia and sedation
Mecamylamine
Nicontinic Neuronal antagonist, shuts down both sympathetic and parasympathetic, rarely used.
Guanethidine
Used for resistant hypertension, depletes NE in sympathetic nerve terminals so when nerve gets stimulated there is no effect. SE orthostatic hypotension and diarrhea
What are the cardioselective beta blockers?
Atenolol and Metoprolol
What are the non cardioselective beta blockers?
Propranolol and Nadolol
Propranolol also inhibits the stimulation of renin production by catecholamines (beta 1) so it also effects the renin-angiotensin-aldosterone pathway
What are the beta and alpha 1 blockers?
Labetalol and carvedilol
What are the cardioselective alpha blockers? (alpha 1 antagonists)
Prozosin and Terazosin
What are the non cardioselective alpha blocker? (mixed alpha antagonists)
Phentolamine and Phenoxybenzamine
What is the direct vasodilator that caused NO release for endothelium or from the drug itself?
Hydralazine
What direct vasodilator drug (3) cause reduction of Ca influx?
Verapamil, Diltiazem, and Nifedipine (smooth muscle relaxation)
What direct vasodilator drug causes hyper polarization of smooth muscle membranes?
Minoxidil (opens K channels causing the hyperpolarization)
T/F Direct vasodilators cause hypotension?
F. They do not effect they baroreceptors or the sympathetic reflexes
Captopril
ACE inhibitor, aldosterone sensitive Na/K exchanger doesn’t get activated causing a hyperkalemia
What are the 2 ways ACE inhibitors cause decrease in BP?
They stop the conversion of angiotensin I to angiotensin II, which stops aldosterone secretion therefore more water is secreted. They also cause an increase in bradykinin concentration which cause vasodilation themselves and through increased prostaglandin production.
Losartan
Angiotensin II inhibitor, no bradykinin effects. SE hyperkalemia
Nitroglycerine
Metabolized to NO, causes vasodilation and reduces O2 consumption of heart. SE orthostatic hypotension, tachycardia, throbbing headache
Amyl nitrate
Metabolized to NO, causes vasodilation and reduces O2 consumption of heart. SE orthostatic hypotension, tachycardia, throbbing headache
Ca channel blockers?
Verapamil, diltiazem, and nifedipine. Effect L-type Ca channels, blocks contraction of smooth and cardiac muscles. SE cardiac depression and bradycardia, flushing and dizziness (vasodilation)
Non selective beta blocker?
Propranolol, used prophylactically. Toxicities, asthma and acute heart failure
Cardioselective beta blocker?
Atemolol, less risk for bronchospasm (b1 selective)
Statins
Lovastatin, Atorvastatin, and Simvastatin. Competitive inhibitors of HMG-COA reducatase. Reduce synthesis of cholesterol and have most effect of LDL (some effect of tryglicerides)
SE Liver toxicity, weakness in skeletal muscles that can become permanent (increase creatine kinase)
Fenobrate
Increases oxidation of fats in liver and muscles, reduces VLDL modest effect on LDL, increases HDL, and reduces triglycerides
SE GI symptoms
Niacin
Decreases triglycerides and LDL, tolerance develops. SE mild flushing
Cholersteramine
Reduces reabsorption of bile acids and metabolites
SE constipation and bloating
Ezetimibe
Inhibits intestinal absorption of cholesterol and reduces LDL
Digitalis
Provides cardiac glycosides such as digoxin, orally effective, Increases intracellular Ca and cardiac contractility, increases blood ejection
SE premature depolarization, ectopic beats (arrhythmias), effects all excitable tissues
Milrinone
Works similar to digitalis, increases contractility and Ca flux
Dobutamine
Beta 1 adrenoreceptor agonist can cause arrhythmias
Furosemide
No positive ionotropic effects, reduces NaCl and H2O retention, reduces venous pressure and ventricular preload
Captopril
Reduce peripheral resistance by reducing salt and water retention
Hydralazine
Vasodilator, smooth muscle relaxant
Metoprolol
Beta blocker, reduces HR and blocks sympathetic N.S.
Procainamide
Na channel blocker, slows action potential conduction, can cause new arrhythmias, works for both atrial and ventricular arrhythmias, not first choice
Quinidine
Similar to procainamide
Lidocaine
Low toxicity, effective against infarct-related arrhythmias, 1st choice for ventricular arrhythmias
Amiodarone
Prolong refractory time, tx ventricular arrhythmias and atrial fibrillation. SE pulmonary fibrosis
What are the 4 classes of drugs used to treat arrhythmias?
Na channel blockade
Block sympathetic autonomic effects on the heart
Prolong refractory time
Ca channel blockade
