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104 Cards in this Set

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Primary HTN
-90% of cases
-aka Essential HTN
-Not due to identifiable causes
-can't be cured
Secondary HTN
-10%
-due to another identifiable cause
Goals of HTN Therapy
-Reduce morbidity/mortality
-Prevent CCD and TOD
modify other cardiovasc. risk factors
What are the BP goals?
general <140/90
Diabetic, CRI <130/80
Non-Pharm Therapies
weight reduction
salt restriction
smoking cessation
alcohol restriction (1 oz. for males and .5 oz. for females)
exercise (30-45 min, 3-4xweek
adequate intake of K, Mg, Ca
low fat, low cholesterol diet
NL BP classification
SBP <120 and DBP <80
Tx for NL BP
encourage lifestyle modification, no HTN meds
Pre-HTN classification
SBP 120-139 or DBP 80-89
Tx for Pre-HTN
lifestyle modification, no HTN meds
Stage I HTN classification
SBP 140-159 or DBP 90-99
Tx for Stage I HTN
lifestyle modification, Thiazide diuretic for most, consider ACE, ARB, BB, CCB
Stage II HTN classification
SBP >160 or DBP >100
Tx for Stage II HTN
lifestyle modification, 2 drug combo with thiazide diuretic for most, plus ACE, ARB, BB, CCB
What are compelling indications for HTN? Tx for any classification with compelling indications
CRI or DM
diuretics, ACE, ARB, BB, CCB as needed
If pt. is not at goal BP and has had no response or troublesome side effects, what is the next step
substitute another drug from a different class
If pt. is not at goal BP and has had inadequate response, but tolerated the drugs well, what is the next step
add a 2nd agent for different class (diuretic is not already used)
If either of these pt. are still not at goal BP, what is the next step
continue optimizing dosages or adding agents from other classes until BP is achieved

or may need to refer to a HTN specialist
when is Tx initiated with 2 drugs
BP >20/10mmHg above the goal
Uncomplicated HTN
thiazide diuretic for most pt., except ACE-I in white males (ALLHAT trial)
Tx in the elderly
-more sensitive than younger pt.
-req. lower intial and maintenance doses
-more gradual and longer intervals btwn dose adjustments or addition
-presence of orthostasis
-impaired renal and hepatic fxn
-decr. beta-adrenergic fxn
What is the principle Tx in Caucasians and why?
BB and ACE-I because high-renin system
What is the principle Tx in AA pt. and why
diuretics and CCB because low-renin system
T/F Pre-menopausal women are at same risk for HTN as males
False--they are at lower risk because the presence of endogenous estrogen has a protective risk, but post-menopausal women are at equal risk compared to men
Estimates of Compliance
-daily or 2x a day
-combination products to simplify regimes
-avoid agents with potential for rebound HTN (clonidine)
which is the most cost-effective anti-HTN drug
diuretic
Diuretics initial MOA
initially decr. plasma volume (SV), which will decr. CO and thus decr. BP
Diuretics MOA after continued use
decr. peripheral vascular resistance, thereby decr. BP
What are the 3 types of diuretics
Thiazide, loop, and potassium sparing
Thiazide efficacy
-AA > whites
-very effective in elderly
-synergy with ACE, ARB, BB
-useful in pt. w/ uncomplicated HTN, ISH, osteoporosis (retains Ca)
Thiazide Adverse Reactions
Electrolyte disturbance
Hyperuricemia
hyperglycemia
photosensitivity
impotence, dehydration, dizziness, nausea, polyuria
If pt. is not at goal BP and has had inadequate response, but tolerated the drugs well, what is the next step
add a 2nd agent for different class (diuretic is not already used)
If either of these pt. are still not at goal BP, what is the next step
continue optimizing dosages or adding agents from other classes until BP is achieved

or may need to refer to a HTN specialist
when is Tx initiated with 2 drugs
BP >20/10mmHg above the goal
Uncomplicated HTN
thiazide diuretic for most pt., except ACE-I in white males (ALLHAT trial)
Tx in the elderly
-more sensitive than younger pt.
-req. lower intial and maintenance doses
-more gradual and longer intervals btwn dose adjustments or addition
-presence of orthostasis
-impaired renal and hepatic fxn
-decr. beta-adrenergic fxn
What is the principle Tx in Caucasians and why?
BB and ACE-I because high-renin system
What is the principle Tx in AA pt. and why
diuretics and CCB because low-renin system
T/F Pre-menopausal women are at same risk for HTN as males
False--they are at lower risk because the presence of endogenous estrogen has a protective risk, but post-menopausal women are at equal risk compared to men
Estimates of Compliance
-daily or 2x a day
-combination products to simplify regimes
-avoid agents with potential for rebound HTN (clonidine)
which is the most cost-effective anti-HTN drug
diuretic
Diuretics initial MOA
initially decr. plasma volume (SV), which will decr. CO and thus decr. BP
Diuretics MOA after continued use
decr. peripheral vascular resistance, thereby decr. BP
What are the 3 types of diuretics
Thiazide, loop, and potassium sparing
Thiazide efficacy
-AA > whites
-very effective in elderly
-synergy with ACE, ARB, BB
-useful in pt. w/ uncomplicated HTN, ISH, osteoporosis (retains Ca)
Thiazide Adverse Reactions
Electrolyte disturbance
Hyperuricemia
hyperglycemia
photosensitivity
impotence, dehydration, dizziness, nausea, polyuria
Loop efficacy
-weak anti-HTN
-maybe useful in pt. with renal insufficiency
-useful in pt. with CHF
Loop adverse effects
similar side effects as Thiazide, except decr. Ca and lipid and glucose abn. not as severe
Potassium Sparing Efficacy
-often not effective for HTN
-used in combo with thiazide to decr. incidence of hypokalemia
What drugs are the exception to the rule of not using K sparing and when?
-spironolactone--used in severe CHF
-Eplerenone--used in severe CHF and post-MI
K sparing adverse effects
incr. K
spironolactone--gynecomastia
What side effect do all diuretics potentially have
increase Scr and BUN
may cause gout attack
Diuretic drug interactions
-ACE-I: precipitous fall in BP, renal insufficiency
-K sparing diuretics + ACE/ARB: increases risk of hyperkalemia
Beta Blockers MOA
-decr. HR and CO
-block renin release and decrease plasma volume
Beta Blockers Efficacy
-young > elderly
-good in combo w/ diuretic (the alpha-blocker)
-smoking may decr. efficacy
-useful in pt. w/ concomitant A-tachy, AFib, angina, migraine, throtoxicosis, peri-operative HTN, s/p MI, benign essential tremor, CHF
BB precautions/Side effects
-bronchospasm in pt. w/ asthma or COPD
-Bradycardia, AV block
-fatigue, decr. exercise tolerance, depression
-incr. TG, decr. HDL
-hyperglycemia
-erectile dysfunction
In diabetics, what are the precautions/side effects for using BB
-blunts natural response to hypoglycemia
-masks symptoms of hypoglycemia
What peripheral vascular precautions/side effects exist for BB
-acts at the B2 receptors of arterioles causing vasoconstriction
-this can:
may worsen Raynaud's dz
may worsen intermittent claudication
BB drug interactions w/ decongestants
antagonize the effects of BB; can raise BP
BB drug interactions w/ Verapamil/dilitazem
risk of significant bradycardia, AV block
BB drug interactions w/ NSAIDs and COX-2 inhibitors
blunt antihypertensive effects
BB drug interactions w/ thyroid hormones
antagonistic effect
BB drug interactions w/ Digoxin/Digitoxin
incr. risk for bradycardia
what can abrupt discontinuation of BB cause
-rebound HTN
in pt. w/ CAD, may produce unstable angina, MI , or even death
-need to taper over 14 days
BB Contraindications
-asthma, COPD
-avoid labetalol in liver dz
-2nd/3rd degree heart block
-sick sinus syndrome
-? PVD
-do not start in pt. with acute heart failue
alpha-1, beta blockers
similar to other BB, but also has alpha-blockade which produces more orthostasis
Example of alpha-1, beta blockers
-Labetalol--inidicated in pregnancy
-Carvedilol--indicated in heart failure
alpha-1 blockers
-reduces vasc. resistance from sympathetic activation--decr. PVR
-vasodilation--induces smooth msc. relaxation, no reflex tachy
alpha-1 blockers efficacy
-improves lipid profile
-useful in pt. w/ BPH, hyperlipidemia
-tolerance may occur over time
alpha-1 blockers precautions/side effects
-1st dose syncope, orthostasis (esp. in elderly)
-h/a
-dizziness
alpha-1 blockers dosing compliance
start low and titrate slowly to avoid orthostasis
alpha-1 blocker drugs
Doxazosin
Terazosin
Prazosin
alpha-1 blockers pt. education
-take at bedtime in supine position
-avoid driving for 12-24 hrs. after any change in meds
-change positions slowly
ACE-I/ARB efficacy
-less effective as monotherapy in AA
-good in combo
-effective in mild-severe HTN
-lipid neutral
-beneficial effects on glucose/insulin sensitivity
-useful in CHF, DM, s/p MI< high coronary dz risk, renal insufficiency
ACE-I/ARB precautions/side effects
-cough (less w/ ARB)
-renal--incr. Scr, BUN, hyperkalemia
-CI in bilat. renal a. stenosis
-angioedema
-hypotension
-metallic taste
-fetal death (CI in pregnancy)
ACE-I/ARB drug interactions
-ACE-I: precip. fall in BP
-NSAIDs/ASA/COX-2: inhibit anti-HTN effects of ACE-I
-K sparing drugs: incr. risk of hyperkalemia
-lithium: incr. risk for toxicity
Calcium Channel Blockers
-decreases PVR
-different effects on HR, contractility, AV-nodal contraction
2 types of CCB
1. nondihydropyridine
2. dihydropyridine
non-dihydropyridine drugs
verapamil and diltiazem
dihydropyridine (DHP) drugs
amlodipine
felodipine
isradipine
nifedipine
nisoldipine
CCB efficacy
-AA > whites
-mild-severe HTN
-DHP--useful in ISH, angina
-non-DHP--useful in diastolic dysfxn, migraine, angina, a-tachy, Afib, DM w/ proteinuria
CCB contraindications
systolic heart failure or heart block: verapamil and diltiazem
Central Adrenergic Inhibitors MOA
-stim. central postsynaptic alpha-2 receptors in the brain
-decr. sympathetic activity to periphery, decr. plasma NE, decr. PVR
-suppress plasma renin activity
Central Adrenergic Inhibitors drugs
clonidine
methyldopa
guanfacine
guanabenz
Central Adrenergic Inhibitors Efficacy
-very potent, not 1st line Tx
-use w/ diuretic sec. to Na/fluid retention
-best not to use w. preipheral alpha-1 blockers
Clonidine
rapid onset,good for HTN urgency
Methyldopa
drug of choice in pregnancy
Central Adrenergic Inhibitors Precautions/Side Effects
withdrawal syndrome (rebound HTN)
Central Adrenergic Inhibitors Drug Interactions
abrupt discontinuation of clonidine can cause life-threatening HTN crisis
Direct Vasodilators
-decr. PVR (afterload)
-reflex tachycardia
-Na and water retention
-direct smooth msc. relaxation and dilation of arterioles
Direct Vasodilators drugs
Hydralazine
Minoxidil
Direct Vasodilators Efficacy
-decr. DBP > SBP
-not as monotherapy, not 1st line
-very useful in resistant HTN
Hydralazine
good for pt. w/ systolic HF
Minoxidil
-more potent than hydralazine
-useful for pt. w/ renal insufficiency who are refractory to all other Tx
Direct Vasodilators precautions/side effects
-lupus-like syndrome
-hypotension
-reflex tachycardia (need BB)
-edema (need diuretic)
Minoxidil side effects
-hair growth
-precipitate angina in pt. w/ CAD
Useful drug combinations
BB + diuretic
ACE + diuretic
ARB + diuretic
CCB + ACE
Pre-clampsia
-presents after 20wks.
-HTN >140/90 w/ proteinuria, hyperuricemia, coag abn.
-can be fatal for mother and fetus
Tx for pre-clampsia
-delivery, bed rest, activity restriction
-IV hydralazine or IV labetalol
-Nifedipine IR oral has been used, but not FDA approved
HTN urgency
-benefit from reducing BP w/in 24-48 hrs.
-DBP >120mmHg w/ min. to no TOD, usually asymptomatic
-not life-threatening
TX for HTN urgency
-Avoid nifedipine and other CCB (short-acting)
-use fast acting drug ORAL agents
-Captopril
-Clonidine
-Labetalol
-Prazosin
HTN emergency
-DBP >120 mmHg and symptomatic
-life-threatening
Drug-induced caused of HTN emergency
-MAO-I and tyramine interactions
-overdose w/ phenyclidine, cocaine, LSD (ilicit drugs)
Tx goals
-immediate BP reduction to a safe value to prevent/limit TOD and death
- decr. MAP by 20-25% w/in 2 hrs., then goal of 160/100mmHg
-avoid rapid reduction in BP bc can cause ischemic damage
Tx for HTN emergency
IV route:
-Na nitroprusside
-Nicardipine
-Labetalol
-Fenoldopam
-Nitroglycerine (acute MI)
-Hydralazine (pregnancy)
-Diazoxide (obsolete)