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What is the normal blood pressure (BP)?
- systolic BP (pressure taken when heart is contracting) <120mmHg
- diastolic BP (pressure taken when heart is realxing) <80mmHg
What is hypertension (HTN)?
SBP>140 and DBP>90mmHg or any condition that requires antihypertensive tx.
Whats the name of the guidelines used to classify HTN?
T/F: primary (essential) HTN is due to an unknown cause
What are some secondary causes of HTN?
- renovascular disease
- primary aldosteronism
- cushing syndrome
- aortic coarctation
- drugs (steroids and estrogens, alcohol, cocaine, cyclosporine, tacrolimus, sympathomimetics, erythropoietin, licorice, MOA inhibitors, tricyclic antidepressants, NSAIDS)
What is pre-HTN?
- SBP: 120-139 or
- DBP: 80-89mmHg
- if pt. has no compelling indications, then no drug tx. needed yet
What is stage-1 HTN?
- SBP: 140-159 or
- DBP: 90-99
- initiate tx. with: thiazide diuretics, or ACEI,ARB,BB,CCB or combos
What is stage-2 HTN?
- SBP: >or equal to 160 or
- DBP: > or equal to 100
- initiate tx. with 2 drug combos (most of the time a thiazide and ACEI or ARB or BB or CCB)
T/F: Stethoscope is placed over brachial artery to meassure BP
What is the goal BP for diabetic pt. and pt. with chronic kidney disease?
What are major cardiovascular risk factors?
- obesity (BMI>30)
- physical inactivity
- microalbuminuria or GFR<60
- age (>55 for M; >65 for F)
- family history or premature cardiovascular disease (M<55;F<45 years old)
HTN affects what organs?
- Heart (left ventricular hyperthrophy, angina or prior MI, prior coronary revascularization, HF)
- Brain (sroke or transient ischemic attack)
- Kidney (chronic kideny disease or end stage renal disease)
- Vascular system (peripheral arterial disease)
- Eyes (retinopathy)
Whats the non-drug tx. for HTN?
- lifestyle modifications:
- loose weight, limit alcohol intake, increase exercise, decrease sodium intake, maintain enough of intake of potassium, magnesium, and calcium, stop smoking, decrease cholesterol and saturated fat intake
DASH diet (dietary approaches to stop HTN)
What the initial therapy for HTN for pt. without compelling complications?
T/F: for pt. who are 20/10mmHg greater than their goal BP, 2 drug combo tx. should be strongly considered
Whats the MOA of thiazide diuretics?
inhibit sodium reabs. in distal tubule which will cause increased excretion of sodium, water, potassium, and hydrogen
What are ex. of thiazide or thiazide like diuretics?
Look at pg. 164
What are pt. counseling points on thiazide diuretics?
- take early to avoid nocturia
- use sunblock
- may increae blood sugar
- report muscle cramps (may indicate decreased potassium levels)
What are drug interactions with thiazide diuretics?
steroids, NSAIDs blunt effect of thiazides, class IA or III antiarrhythmic(that prolong QT) may cause torsade de pointes with diuretic induced hypokalemia, probenecid and lithium
Whats the MOA of loop diuretics?
inhibit sodium and chloride reabs. in ascending loop of henle, which causes increased exprection of water, sodium, chloride, magnesium, and calcium
What are ex. of loop diuretics?
- bumetanide (Bumex)
- furosemide (Lasix)
- torsemide (Demadex)
- look at pg. 164
What are pt. counseling tips with loop diuretics?
- take early to avoid nocturia
- may increase blood sugar in pt. with DM
- report musle cramps (hypokalemia)
- hypotension (rise slowly)
What are drug interactions with loops?
aminoglycosides(may percipitate ototoxicity), NSAIDS, class IA or III antiarrhythmics, probenecid
Whats the MOA of potassium sparing diuretics? and ex. of drugs
interfere with potassium and sodium exchange in distal tubule, decrease calcium excretion and increase magnesium loss
- amiloride (Midamor)
- triamterene (Dyrenium)
What are counseling tips for pt. on potassium sparing diuretics?
- take early in day and after meals
- avoid foods high in potassium (hyperkalemia)
- may increase blood sugar
- sex dysfunction is possible
What are drug interactions with potassium sparing diuretics?
- ACEI may increase hyperkalemia
- indomethacin and cimetidine
What the MOA of aldosterone receptor blocker- Spironolactone (Aldactone)?
- competes with aldasterone for receptor sites in distal tubule, incerease sodium and water excretion and conserving potassium
- SE: hypotension, report new fluid retention
- DI: otc sympathomimetics, tricyclic antidepressants
- -avoid in pt. with pheochromocytoma, CHF, angina,cerebrovascular disease
Whats the MOA of centrally active alpha2 agonist?
- decrease sympathetic outflow to cardiovascular system by agonistic activity on alpha 2 receptor
- ex: clonidine (Catapres)
- methyldopa (Aldomet)
- guanabenz acetate (Wytensin)
- guanfacine (Tenex)
What are pt. counseling tips on alpha2 agonists and DI?
- SE: hypotension, fluid retention, flu symptoms with methyldopa, exercise sedation precautions
- DI: use cautiously with other sedating drugs, caution use in pt. with CVA, recent MI, angina..
Whats the MOA of peripherally acting alpha1 adrenergic blockers?
- MOA: block alpha1 which cause vasodilation of arteries and veins
- Ex: doxazosyn (Cardura), prazosin(Minipres), terazosin(Hytrin)
- SE: hypotension, dizzy, priapism
- DI: NSAIDS
Whats the MOA of BB?
- MOA:block secretion of renin, decrease cardiac contractility, decrease HR
- Ex. drugs end on -olol pg.168
- SE: hypotension,decreased exercise tolerance, bronchospasm, bradycardia,hypogalcemia
- DI: nondihydropyridines may increse effect(toxicity) of BB
What are ex. of direct vasodilators of peripheral arterial smooth muscle?
pt. counseling tips?
- hydralazine(Apresoline), minoxidil(Loniten)
- Counseling: hypotension, hirsutism(with monoxidil),report weight gain
- DI: use in caution in pt. with pulmonary HTN,renal failure CHF,CAD,or recent MI
Whats the MOA of CCB?
inhibit influx of calcium ions through channels in vascular smooth muscle, thus relax coronary and peripheral arteries
What are ex. of nondihydropiridines and SE?
- SE: gingivial hyperplasia,constipation(verapamil),hypotension
What are ex. of dihydropyridines and SE?
- others on pg169
- SE:ankle edema,flush,gingivial hyperplasia
What are the interactions with CCB?
- use in caution in pt. on BB and nondihydropyridines-may increase CHF and bradycardia
- caution in pt. with disturbances in SA and AV node
- avoid grape fruit juice
What the MOA of ACEI and ARBS?
ex. of drugs?
- MOA: ACEI-inhibit conversion from angiotensin 1 to 2
- ARBS-inhibit binding of angiotensin II to angiotensin II receptors
- ex. are on pg.170
- PC: dizzy,hypotension,swelling,hyperkalemia
- Interactions: NSAIDS,potassium drugs will increase risk of hyperkalemia, avoid in pt. with bilateral renal artery stenosis or stenosis in single kidney, avoid in pregnancy
Whats the MOA of direct renin inhibitor?
- MOA:inhibit human renin, thus decrease plasma renin activity and inhibit conversion of angiotensin to angio.-1
- ex. aliskiren(Tekturna)
- PC:hypotension, diarrhea, swelling
- Interactions: cyclosporine,potassium drugs may increase risk of hyperkalemia, ketokonazole, avoid in preganant women
T/F: Classification and tx. of hypertensive urgency and emergency is determined by presence or absence of acute target damage (Not by BP)
What is hypertensive emergency?
- BP>180(SBP) or >120(DBP) with acute or ongoing target organ damage
- goal is to reduce mean arterial pressure by no more than 25% within min to hrs (reach BP of 160/100 within 2-6hrs)
- tx: pg 173
What is hypertensive urgency?
- accelerated elevations in BP in absence of new or progressive target organ damage, thus immediate lowering of BP is not required
- ex. of drugs used is on pg.173
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