Day 2 Cardiology- Hypertension Flashcards
What are some disease states that cause hypertension?
What are some drugs that cause hypertension?
What is the MOA of diuretics?
sleep apnea, drug induced hypertension, CKD, primary aldostteronism, renovascular disease, chronic steroid therapy and cushings syndrome, pheochromocytomia, coarction of the aorta, thyroid or parathyroid disease
oral contraceptives, steroids, illicit drugs, sympathomimetics, NSAIDS, cyclosporine, erythropoeitin.
lower sodium reabsorption, plasma volume, stroke volume, cardiac output and blood pressure. Initial increase in vascular resistance but it eventually normalizes.
What are the thiazide diuretics to recognize? Loops?
What is the most popular antihypertensive? Can these be first line agents? Why?
What are some disadvantages of thiazide diuretics?
Chlorthalidone, Hydrochlorothiazide. Bumetanide, Furosemide, Torsemide.
Thiaizde diuretics. Yes, proven to reduce morbidity and mortality, can be used in combination therapy, useful to counteract side effects of other antihypertensives that induce salt and water retention.
Not enough diuresis for heart failure, possible additional cost if potassium needed, should not be used in GFR <30 ml/min, higher doses are associated with more side effects.
What are the side effects of thiazide diuretics?
What to monitor with thiazide diuretics?
What are the counseling pearls for thiazide diuretics?
Lower potassium, Magnesium. Raise calcium, uric acid, blood glucose, lipids. Cause sexual dysfunction.
electrolytes every 6 months or yearly, serum creatinine yearly, uric acid levels if the patient has gout or symptoms of gout, blood glucose and lipids yearly.
Take in the morning, avoid in patients with gout, avoid in patients with hyponatremia, not effective for patients with CrCl <30, increase in blood glucose is not a CI for use in diabetes.
What are some advantages of loop diuretics?
What are some disadvantages of loop diuretics?
What are some advantages to potassium sparing diuretics?
More potent, effective in renal dysfunction, also effective in AA and elderly.
Not as effective as thiazide diuretics in terms of hypotensive effect, no data on mortality reduction, nephrotoxicity and ototoxicity, lower potassium, magnesium, calcium. Raise uric acid, blood glucose, lipids.
additive hypotensive effect, reduce need for K supplement, sprionolactone has shown reduced mortality in HF, eplerenone has reduced mortality post MI, synergistic effects.
What are some disadvantages to potassium sparing diuretics?
What is the short acting ACEI?
What are the intermediate acting ACEI?
weak by themselves(diuretic and hypertensive), sprionolactone causes gynecomastia, increased risk of hyperkalemia.
Captopril
Benazepril, Enalapril, Moexipril, Quinapril, Ramapril.
What are the long acting ACEI?
What are the ACEI side effects?
When are ACEI CI’d?
Fosinopril, Lisinopril, Perindopril, Trandolapril
Angioedema, dry cough, dizziness, orthostatic hypotension, hyperkalemia, rash, taste disturbance(captopril), neutropenia, agranulocytosis(hematologic), Acute renal failure.
Pregnancy, bilateral renal artery stenosis, angioedema from previous ACEI.
What are some important ACEI drug interactions?
What to monitor for ACEI’s?
When are ACEI’s first line therapy?
Potassium sparing diuretics(hyperkalemia), Potassium supplementation, Lithium(may raise lithium levels), Salicylates(blunt BP lower effect), NSAIDS(blunt effect), Calcineurin inhibitors(blunt effect).
Check SrCr at baseline then 1-2 weeks later then annually. Electrolytes(especially potassium) every year(unless taking potassium sparing diuretic then do it more), Have patient self monitor cough.
Htn plus diabetes, left ventricular hypertrophy, MI, Stroke
What are ARB adverse effects?
What are ARB CI’s? Drug interactions?
What are therapeutic uses for ARB’s?
Dizziness, Orthostatic hypotension, hyperkalemia, acute renal failure, cough is common, less angioedema.
Pregnancy, Bilateral renal artery stenosis. Same as ACEI.
Similar to ACEI, less data for ARB’s.
What is the direct renin inhibitor?
What are the A/E’s of Aliskiren?
What are the DI and CI’s of aliskiren?
Aliskiren
poor bioavailability, dyspepsia, ab pain, cough(not as much as ACEI), angioedema, hyperkalemia, can increase uric acid levels.
Similar to ACEI, decrease effectiveness of furosemide. Don’t combine with ACEI or ARB, pregnancy, no data for renal artery stenosis.
What did the altitude study show?
What are the clinical pearls for ACEI’s?
What are the pearls for aliskiren?
Don’t combine with ACEI or ARB.
1st line blockade of RAAS, decreased efficacy in African Americans, Start with low doses and titrate up, doses should be maximized in HF patients, Adding HCTZ may have more effect on BP than just increasing ACE dose, ACEI plus NSAID is not a CI but use caution.
Doses >300 do not lower BP but do increase SE.
What are the non selective beta blockers?
What are beta blockers with ISA?
What are the mixed Alpha Beta blockers?
Nadolol, Propanolol, Timolol.
Acebutolol, Carteolol, Penbutolol, Pindolol
Carvediolol, Labetolol
What are the compelling indications for beta blockers?
What are the A/E’s of beta blockers?
What to watch for in elderly with beta blockers?
Systolic HF(bisoprolol, carvediolol, metoprolol succinate), Post MI
Fatigue, Exercise intollerance, Dizziness/hypotension, bradycardia, transient increase serum lipids and glucose, masks the s/s of hypoglycemia(exception sweating)(highest prevalence with non selective).
higher rates of orthostatic hypotension, no age adjustments, little difference between agents.
What to watch for in pregnancy with beta blockers?
What disease states to avoid?
What are the beta blocker clinical pearls?
Labetolol IV is choice, lactation compatible,Category C.
Reactive airway disease, Erectile Dysfunction.
Should be used post MI and for CHF, cardioselective have least overall side effects but can lose selectivity at higher doses, class effect in lowering BP, low and slow titration, can cause unopposed alpha stimulation in stimulant use and clonidine withdrawal, don’t abruptly stop.
What are the dihydropyridine side effects?
What are the non-dihydropyridine side effects?
What are the alpha 1 receptor blocker side effects?
Dizziness, Flushing, Edema, Headache, reflex sympathetic stimulation, short acting nifedipine is associated with harmful CV effects.
Cardiac Conduction Abnormalities,exacerbate HF in patients with pre exisiting conditions, constipation.
First dose phenomenon, Reflex tachycardia, Fluid and sodium accumulation, CNS effects.
What are the alpha 1 receptor blockers place in therapy?
What are the central alpha 2 receptor agonists?
What are the side effects of the central alpha 2 receptor agonists?
NOT used as 1st line agent, effective for symptomatic relief of BPH, doxazosin can increase HF and death in all hat trial.
clonidine, methyldopa.
Sodium and fluid retention, dry mouth, CNS effects, orthostatic hypotension, rebound hypertension on abrupt stop, hepatitis and hemolytic anemia with methyldopa.
