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Treatment goals for HTN therapy

ultimate goal is to reduce morbidity/mortality

DASH diet

Dietary Approaches to Stop HTN, low fat, low sodium, can reduce BP up to 8-14mmHg

Lifestyle modifications for reducing BP

DASH diet, weight loss (apple vs pear shape, BMI >27=increased BP), smoking cessation (reduces BP in 20-30mins), alcohol restriction(2/day men, 1/day women, can reduce BP by 2-4mmHg), sodium restriction (<2.4grams/day, can reduce BP by 2-8mmHg), physical activity (30mins aerobic on most days, can reduce BP by 4-9mmHg), biofeedback/relaxation, caffeine reduction

T or F: all BP drugs reduce the BP by the same amount

TRUE: all BP meds give about the same result, therapy choice is made by concurrent medical conditions and drug treatments, SE profile, cost, demographics, previous drug therapy failures

Initial drug choice for ppl with stage 1 HTN and no compelling indications

thiazide diuretics are first line. may add ACEI, ARB or CCB or any combo

intial drug choice for ppl with stage 2 HTN and no compelling indications

two drug combo, usually includes a thiazide diuretic and either ACEI, ARB or CCB

treatment choice for pt with HTN and left ventricular dysfunction

First line: diuretic and ACEI then add B blocker. Second line: ARB or aldosterone antagonist

treatment choice for pt with HTN and post MI

First line: B blocker then ACEI or ARB. Second line: aldosterone antagonist

treatment choice for pt with HTN and coronary disease

First line: B blocker then ACEI or ARB. Second line: CCB or diuretic

treatment choice for pt with HTN and diabetes

First line: ACEI or ARB. Second line: diuretic. Third line: B blocker, CCB

treatment choice for pt with HTN and chronic kidney disease


treatment choice for pt with HTN and recurrent stroke prevention

diuretic + ACEI or ARB

how often should K and Creat be taken for pts on HTN therapy

1-2 times/year

how often should patients be seen if their BP is not yet stable


how often should patients be seen if they have reached their BP goal and are stable

Q 3-6 months

the main antihypertensive drugs

Diuretics (thiazides and loop), ACEI/ARB, CCB, B blockers, peripheral alpha blockers

thiazide diuretics

drug of choice for HTN, MOA=inhibits NA reabsorption in distal tubule thereby increasing H2O and NA excretion which leads to decreased blood volume, they also do have some indirect vasodilation long term, 3-4 wks for full effect, ppl with CrCL<30 will not have response (except for metolazone)

Thiazide agents

HCTZ(12.5-25mg daily), chlorthalidone (12.5-25mg daily), metolazone(2.5-5mg daily, ok for renal pts), indapamide(1.25-2.5mg daily, neutral lipid effects)

Loop diuretics

drug of choice for renal insufficiency and CHF, MOA=inhibits Na reabsorption in the Loop of Henle and causes some vasodilation long term,

Loop diuretic agents

furosemide, bumetanide, torsemide

K sparing diuretics

drug of choice for those that experienced hypokalemia, MOA depend on agent

K sparing diuretic agents

Triamterene/amiloride MOA=inhibits Na reabsorption in the collecting duct thru the Na/K ATPase pump, Spironolactone/eplerenone MOA=aldosterone receptor antagonist (more potent then triam/amil but slower onset of action

adverse effects of diuretics

Hypokalemia (<3.5 tx is supplement), hyperuricemia, hypercalcemia (thiazides), glucose intolerence (thiazides >25mg), photosensitivity, hyponatremia, hypomagnesemia, hypochloremia, hyperkalemia (K sparing/ACEI/K supplement), increased LDL and triglycerides (not indapamide), sex dysfunction, orthostatic hypotension, gynecomastia (spironolactone)

which diuretic is preferred for most patients according to JNC7?

thiazide diuretics

which antihypertensive is preferred in African Americans and why?

diuretics work well because African Americans tend to have decreased renins which cause blood volume dependent HTN

which diuretic is preferred in patients with CrCL <30mL/min?

avoid thiazide and K sparing, use loop and metolazone

which diuretic has a benefit for osteoporosis?

thiazides because they slow bone demineralization

T or F: diuretics can cause lithium toxicity

TRUE kidneys will hold on to lithium in place of Na

what should be monitored while a patient is on diuretic therapy?

BP, renal function, electolytes, glucose, uric acid

Patient education points about diuretics include....

take in AM, if BID take 2nd dose in afternoon, watch for muscle cramps/weakness

Hypokalemia treatment

K rich foods (dried fruit, bannana, cantaloupe, orange juice, cooked spinach, potatoes), salt substitutes (Mrs. Dash or Mortons) KCl supplements

Angiotensin Converting Enzyme Inhibitors (ACEI) MOA

MOA=blocks ACE which decreases angiotensin II which causes vasodilation, decreases ADH, decreases LVH effects and decreases aldosterone also ACEI inhibit the kinase enzyme which causes an increase in bradykinins which causes vasodilation and cough

What are the ACEI agents?

enalapril, ramipril, moexipril, benazepril, quinapril, lisinopril, trandolapril, perindopril, fosinopril (dual metabolism), captopril (HTN urgency)

Angiotensin II Receptor Blockers (ARBs) MOA

MOA=inhibit angiotensin II receptors, no effect on bradykinins so no cough

What are the ARB agents?

losartan, valsartan, irbesartan, candesartan, telmisartan, eprosartan, olmesartan, azilsartan

adeverse effects of ACEI and ARBs

angioedema, rash, neutropenia, metallic taste, sex dysfunction, cough (not ARB), hyperkalemia, orthostatic hypotension, hypotension is also using diuretic

patient populations where ACEI or ARBs are a good choice

diabetes, renal insufficiency, acute coronary syndromes, post MI, cerebrovascular disease, CHF, work better in Caucasians than AA

patient populations where ACEI and ARBs are contraindicated

pregnancy, past angioedema, bilateral renal artery stenosis, concurrent K sparing diuretics or K supplements

why should ACEI not be used by those taking NSAIDS?

they will cause decreased blood flow to the kidneys because NSAIDS will inhibit PG and cause vasoconstriction of vessels to kidneys and ACEI will cause vasodilation of vessels leaving kidneys

what should be monitored when patients are on ACEI or ARB

BP, SCr (may increase transiently but will normalize in 2 weeks), BUN, K SE

direct renin inhibitor

Aliskiren (tekturna) 150-300mg also Tekturna HCT (combo with HCTZ)

precautions with aliskiren use

renal insufficiency, hyperkalemia, angioedema

counseling points for aliskiren

take with full glass of water, avoid high fat meals as this will decrease absorption, avoid during pregnancy

calcium channel blockers MOA

MOA= blocks inward movement of Ca across cell membranes, relaxes smooth muscle

cardioselective CCB

nondihydropyridines, cause vasodilation, depress cardiac contractility, inhibit AV conduction

cardioselective CCB agents

verapamil, diltiazem

vasoselective CCB agents

dihydropyridines, nifedipine, nicardipine, isradipine, felodipine, amlodipine, nisoldipine, clevidipine

adverse effects of nondihydropyridines

some peripheral edema, bradycardia, orthostatic hypotension, constipation (verapamil), AV conduction disturbances

patient populations that CCB work well

geriatrics, African Americans, IHD

populations to avoid CCB

GERD, CHF (can use amlodipine or felodipine, dihydropyridines will cause edema, verapamil/diltiazem will decrease HR and CO)

drug interactions of CCB

verapamil>diltiazem inhibits 3A4, use with cautions with B blockers due to heart block, caution with grapefruit juice

stimulation of alpha 1 receptors will cause....

vasoconstriction...thus an alpha 1 receptor blocker will cause vasodilation

stimulation of beta 1 will cause.....

increase in HR and force...thus a beta1 receptor blocker will cause a decrease in HR ....decrease in CO....decrease in BP

stimulation of beta 2 will cause....

vasodilation, bronchodilation

Beta blockers/alpha-beta blockers MOA

MOA=blocke beta receptors.....decrease HR, decrease CO, increase TPR

beta blocker agents

atenolol, bisoprolol, betaxolol, metoprolol, nebivolol, nadolol, propranolol, timolol, acebutolol, penbutolol, pindolol, labetalol, carvedilol

what types of B blockers are preferred in asthma, PVD and DM?

B 1 selective

what types of B blockers are preferred in patients with bradycardia?

those with Intrinsic sympathomimetic activity

what types of B blockers shoud be avoided in those with migraines and angina?

those with Intrinsic sympathomimetic activity

some SE of B blockers

fatigue, insomnia, bizarre dreams, sex dysfunction, decreased exercise tolerance

what should be monitored when on B blockers

BP, HR, lipid profile, SE

peripheral alpha 1 antagonists MOA

MOA= blocks post-synaptic alpha 1 receptors leading to vasodilation, decreased BP (preload and afterload reducers)

peripheral alpha 1 antagonist agents

prazosin, terazosin, doxazosin

SE of peripheral alpha 1 blockers

1st dose syncope, dizziness, weakness, HA, reflex tachycardia, Na/H2O retention, priapism, icreases HDL, decreases LDL
*=not an adverse effect

when should peripheral alpha 1 blockers be taken?

dose at HS

which patient populations do well on alpha 1 blockers?

those with BPH, those with hyperlipidemia

which patient population should avoid alpha 1 blockers?

elderly.....risk of falls

central alpha 2 agonists MOA

MOA= stimulates alpha receptors in the CNS inhibiting sympathetic outflow to the heart, kidneys and periphery....decrease in BP

central alpha 2 agonist agents

methyldopa, clonidine, guanabenz, guanfacine

patient counseling points when using clonidine patch

leave patch on for 7 days, rotate sites non hairy, non shaved

how do you switch a patient from PO clonidine to clonidine patch?

day1-place patch and 100% of oral dose, day 2-50% of oral dose, day 3-25% of oral dose, day 4-no PO dose

clonidine patch strengths

TTS-1 is 0.1mg/24hr clonidine, TTS-2 is 0.2mg/24hr clonidine, TTS-3 is 0.3mg/24hr clonidine

adeverse effects of central alpha 2 agonists

orthostatic hypotension, sedation, dizziness, xerostomia, Na/H2O retention, sex dysfunction, hemolytic anemia, fatigue, rebound HTN, depression, increased LFT (methyldopa)

which antihypertensive agent can also be used for menopause symptoms?


which antihypertensive agent can also be used for smoking cessation?


which antihypertensive agents can be used in ADHD associated tics?

clonidine, guanfacine

what is the central alpha 2 agonist preferred in pregnancy?


adrenergic agonist MOA

MOA= inhibit catecholamine release from peripheral sites....decreased HR and decrease BP

adrenergic agonist agent


adverse effects of reserpine

orthostatic hypotension, diarrhea, sex dysfunction, nasal congestion, depression, sedation , fatigue, bradycardia, Na/H2O retention

direct vasodilator MOA

MOA= cause direct vasodilation of arterial smooth muscle

direct vasodilator agents

hydralazine, minoxidil

T or F: direct vasodilators should be given as monotherapy

FALSE: they should be given with B blocker and diurectic

what is one important SE of direct vasodilators?

reflex tachycardia

if patient is coming off of clonidine and B blocker, which should be d/c'd first?

taper and d/c B blocker, then taper and d/c clonidine

which antihypertensives can cause rebound HTN and should therefore be tapered?

central alpha 2 agonists (clonidine) and B blockers...taper over 4-5 days

T or F: BP meds may be stepped down if BP is stable

TRUE: if BP is under stable control for 6-12 months we can decrease the dosage or the # of drugs

what antiHTN should be avoided in DM?

BB, thiazides

what antiHTN should be avoided in asthma/COPD?

nonselective BB

what antiHTN should be avoided in hyperlipidemia?

BB w/o ISA, diuretics(use with caution)

what antiHTN should be avoided in PVD?

nonselective BB

what antiHTN should be avoided in CHF?

CCB, nonselective BB

what antiHTN should be avoided in IHD?

direct vasodilators (hydralazine and minoxidil)

T or F: diruetics are the best agent to use in gout

FALSE: use diuretics with caution in gout and hyperurecemia

what are the best antiHTN to use in renal insufficiency?

metolazone, loops, ACEI, ARBs, hydralazine

what are the best antiHTN agents to use in a patient who has tachycardia?

BB w/o ISA, cardioselective CCB

what antiHTN can exacerbate GERD?


what antiHTN can cause gynecomastia?

spironolactone....thus good for hyperaldosteronism

what antiHTN agent should be used in someone with tremor?


what are some good agents to use in patients with migraines?

CCB (verapamil), BB(non ISA and lipid soluble), clonidine

which antiHTN should be avoided in pregnancy?

ACEI, ARBs, aliskiren (teratogenic), CCB( can cause contractions in 3rd trimester)

what antiHTN are the best for use in peds?

ACEI, BB and diuretics

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