Drugs to treat HTN Flashcards

1
Q

htn damages

A

bv in kidney, heart, and brain which leads to end organ damage- MI, stroke, renal failure, death

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2
Q

main risk of htn tied to

A

inc in systolic blood pressure- progressive stiffening of arterial circulation

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3
Q

htn stage 1 at

A

130-139 or 80-89

If 10 yr risk for HD >10%, lifestyle changes and meds

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4
Q

htn stage 2 at

A

> 140 or >90

2 medications of different classes

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5
Q

BP=

A

BP=CO x TPR

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6
Q

Primary agents used in tx of htn

A
  • thiazide diuretics
  • ACE inhibitors
  • ARBs
  • Calcium channel blockers
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7
Q

Thiazide diuretics

A

-Inhibit NaCl reabsorption in distal convoluted tubule
-low dose for htn
high dose for CHF
-Hydrochlorothiazide
-chlorthalidone, indapamide, metaolazone
-all are sulfonamides

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8
Q

Chlorothalidone

A

preferred thiazide because of long 1/2 life and research

-more effective as antihtn in AAs and elderly

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9
Q

AE of thiazides

A
  • hypokalemic metabolic alkalosis
  • hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia (GLUC)

If ED occurs, sildenafil can be added (PDE5 inhibitor)

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10
Q

Ang II causes

A

vasoconstriction by inc peripheral vascular resistance causing inc blood pressure

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11
Q

aldosterone causes

A

inc sodium and water retention–>inc blood pressure

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12
Q

ACE inhibitors

A
  • prils
  • lower bp by inhibiting ACE which conv ang I to ang II
  • decreases peripheral vascular resistance and leads to increased bradykinin (AE of coughing and angioedema)
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13
Q

Therapeutics of ACE inhibitors

A

lower BP w/o compromising blood supply to brain heart or kidneys

  • does not cause reflex sympathetic activation
  • effective orally for monotherapy
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14
Q

ACE inhibitors first choice tx for htn pts with

A

diabetes, chronic renal disease, or lv hypertrophy

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15
Q

ACEI AE

A

hyperkalemia, cough, angioedema, anaphylaxis

  • do not use in comb with ARBs
  • contraindicated in pregnancy
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16
Q

Angiotensin Receptor Antagonists

A
  • sartan
  • more specific than ACE inhibitors because do not affect bradykinin
  • more complete inhibition of angiotensin action (other enzymes than ACE can also generate ang II)
  • similar AE except coughing (hyperkalemia, reduced renal fxn, contra in pregnancy)
17
Q

Calcium Channel Blockers- cardiac

A

Verapamil (strongest cardiac effect) and diltiazem act on heart (in between nifedipine and verapamil)

  • no reflex tachycardia because they depress SA and AV node
  • can cause Myocardial depression- bradycarida- bad in HF
18
Q

Peripheral Calcium channel blockers- Dihydropyridines

A
  • amlodipine, nicardipine, nifedipine (strongest vasodilator), etc.
  • strongest vasodilators
  • most likely to produce reflex tachycardia

-can cause headache, flushing, dizziness, peripheral edema

19
Q

Calcium channel blockers

A

-block slow calcium channels will reduce intracellular Ca–> relax arteriolar smooth muscles–> vasodilation and lower BP
-especially used in elderly and AA (along with thiazides)
-

20
Q

Sympatholytic drugs

A

not recommended for monotherapy because of AE- postural hypotension and sodium retention

21
Q

Cardioselective b blockers

A

atenolol, betaxolol, bisoprolol, metoprolol

22
Q

cardioselective and vasodilatory b blockers

A

Nebivolol (NO production)

23
Q

Noncardioselective b blockers

A

Nadolol, propranolol

24
Q

b blockers- intrinsic sympathomimetic activity

A

b2 agonists: acebutolol, penbutolol, pindolol

w/ NO production: carteolol

25
Q

b blockers- combined a and b receptors

A

carvedilol (a1 antagonist, blocks Ca entry) and labetalol (a1 antagonist

26
Q

how do b blockers work

A

lower BP by blocking b-adrenergic receptors in-
heart to reduce CO
kidneys to reduce renin secretion
CNS to reduce sympathetic vasomotor tone

-used with other antihtn to counteract reflex tachycardia caused by vasodilators and increased renin secretion by thiazide and loop diuretics

27
Q

AE of b blockers

A
  • worsen symptom sin pts with reduced myocardial reserve, asthma, peripheral vascular insuff, diabetes (delays recovery of normoglycemia bc inhibits hyperglycemic responses mediated by epinephrine)
  • decrease exercise tolerance in HF pts
  • predispose to atherogenesis
  • GI or CNS minor AE
  • tachycardia with abrupt cessation
28
Q

Aliskiren

A

orally active renin inhibitor

  • dose dep reduction of blood pressure
  • no generic
  • avoid in pregnancy, do not combine with ACE or ARB
29
Q

Drugs that block renin secretion

A

Clonidine- reduce renal sympathetic nerve activity

beta- blocker- block intra and extra renal receptors involved in neural control of renin secretion

30
Q

Doxazosin, prazosin, terazosin

A

a1 adrenergic antagonist

  • reduces NE induced vasoconstriction to dilate both arteries and veins
  • BP falls because of decreased PR
  • AE: orthostatic hypotension
31
Q

Centrally acting sympatholytic drugs

A

Clonidine, methyldopa, guanfacine

  • last line because of significant CNS adverse effects
  • act in CNS as agonist on presynpatic a2 receptors and reduce peripheral vascular resistance
  • withdrawal of clonidine may result in hypertensive crisis
  • methyldopa limited to pregnancy
32
Q

oral direct vasodilators

A

Hydralazine or minoxidil (K channel opener)

- both selectively dilate arteries (not venous)

33
Q

IV direct vasodilators

A

sodium nitroprusside (NO, both arteries and veins), diazoxide (activate K channels and hyperpolarize, arteries only), fenoldopam (dopa agonist, selective for arteries), enalaprilat (ACEI), nicardipine (CCB), hydralazine (preeclampsia)

34
Q

direct vasodilators

A
35
Q

AE of vasodilators

A

hypotension, headaches, reflex tachycardia

  • elderly with CAD- hydralazine or minoxidil may induce anginal attacks and MI
  • hydralazine may cause lupus like syndrome
  • minoxidil causes hypertrichosis (hair growth)
36
Q

Tx in pregnancy

A

b- blocker (labetalol) or CCB (nifedipine); methyldopa or hydralazine may also be used