B4.043 - Pharmacology of Drugs to treat Hypertension Flashcards

1
Q

What are common types of end organ damage that can be caused by hypertension

A

MI Stroke Renal Failure Death

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2
Q

what is the most common etiology of HT

A

Primary aka we dont know really

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3
Q

epidemiological evidence shows involvement of what factors in HT

A

genetic inheritance phycological stress environmental dietary factors

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4
Q

high prevalence of HT is driven by what factors

A

increased age of population obesity high salt intake

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5
Q

what are steps you need to take to be sure you’re getting an accurate measurement on BP

A

Pt. should avoid caffeine, exercise, smoking 30 minutes prior No talking during measurement Remove clothing covering cuff location placement Use validated device with correct cuff size Support patients arm Record BP on both arms at first visit

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6
Q

what is stage 1 hypertension

A

systolic 130-139 diastolic 80-89

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7
Q

what is stage 2 hypertension

A

systolic > 140 diastolic >90

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8
Q

what is elevated BP

A

120-129, <80

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9
Q

what demographic is more likely to have HT and worse HT

A

african americans

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10
Q

what drug intervention do african american patients respond to

A

calcium channel blockers and diuretics

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11
Q

what drug classes should you not start treatment of HT with

A

ACE inhibitors, Beta blockers they are better for add on therapy

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12
Q

what do diuretics do

A

Deplete body of sodium and reduce blood volume

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13
Q

what do agents that interact with angiotensin do

A

reduce peripheral vascular resistance

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14
Q

what do direct vasodilators do

A

relax vascular smooth muscle and dilate resistance

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15
Q

what do sympatholytic agents do

A

reduce peripheral vascular resistance, inhibit cardiac function, and increase venous pooling

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16
Q

what should you always start with therapy wise in hypertensive patients

A

lifestyle change

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17
Q

why can drug treatments for HT be a hard sell

A

the patients are usually asymptomatic so they dont feel the need to take anything

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18
Q

what is the most common cause of treatment failure

A

Non-compliance

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19
Q

primary agents used in treatment of HT

A

thiazide diuretics ACE I/ARBs CCBs

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20
Q

what are thiazides

A

inhibit NaCl reabsorption in distal convoluted tubule

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21
Q

what are 2 main clinical uses for thiazides

A

1.) At low dose to lower BP 2.) at high dose second to loop diuretics in congestive heart failure

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22
Q

what are some drug names of thiazides

A

Hydrochlorothiazide Chlorthaidone Indapamide Metolazone

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23
Q

what is the preferred thiazide

A

chlorothalidone because fo the long t1/2 and proven trial reduction of CV disease

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24
Q

how do thiazides treat nephrolithiasis and nephrogenic diabetes insipidus

A

to reduce urinary calcium concentration and to reduce polyuria and polydipsia; paradoxical effect due to plasma volume reduction

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25
Q

what are side effects of thiazide diuretics

A

Hyperglycemia

Hyperlipidemia

Hyperuricemia

Hypercalcemia

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26
Q

what are the drug classes that affect the renin angiotensis system

A

ACE Is

ARBs

Aldosterone inhibitors

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27
Q

why are ACE I more efficient than ARBs

A

Bradykinin is inactivated by ACEs so an ACE I will increase bradykinin and can lead to vasodilation

28
Q

what are the ACE Is

A

Benazepril

captopril

enalapril

fosinopril

lisinopril

moexopril

perindopril

quinapril

ramipril

trandolapril

29
Q

what ACEI is an active drug

A

captopril

30
Q

What is a side effect of ACEIs

A

coughing - due to increased bradykinin

31
Q

what demographic are ACE most effecting in

A

middle aged caucasion

diabetes patients

32
Q

what are the major AEs of ACE inhibitors

A

Dry hacking, non productive cough

Hyperkalemia

Angioedema and anaphylaxis

33
Q

what are ACEIs not supposed to be used with and when are they contraindicated

A

Do not use in combo with ARBs

Avoid in pregnancy especially in 2nd and 3rd trimerster

34
Q

what are the ARBs

A

Azilsartan

candesartan

eprosartan

irbesartan

losartan

olmisartan

telmisartan

valsartan

35
Q

what are two major differences between ARBs and ACEIs

A
  1. more specific than ACE Is (dont affect bradykinin)
  2. More complete inhibition of angiotensis action
36
Q

what are AEs for ARBs and how do they differ from ACEIs

A

Pretty much the same except no coughing

Hyperkalemia

reduced renal function

pregnancy

37
Q

what are the calcium channel blockers

A

Verapamil

diltiazem (mainly at heart)

Amlodipine

Felodipine

Isradipine

Nicardipine

Nifedipine

Nimodipine

Nisoldipine

38
Q

what is an improtant AE of peripheral Ca blockers

A

reflex tachycardia

39
Q

what is special about verapamil and diltiazem

A

they act on heart (SA and AV conduction directly)

SOOOOOO no reflex tachycardia but potentially bradycardia

40
Q

what are peripheral antagonists

A

block receptors at nerve endings

41
Q

what are central agonists

A

stimulate medullary receptors

42
Q

cardioselective beta blockers

A

Atenolol

betaxolol

bisoprolol

metoprolol

43
Q

what are teh cardioselective and vasodilatory beta blockers

A

nebivolol

44
Q

what are the non cardioselective beta blockers

A

nadolol

propranolol

45
Q

what are the beta blockers with intrinsic sympathomimemtic acitvity

A

acebutolol

penbutolol

pindolol

carteolol

46
Q

what are the drugs that are combined alpha and beta blockers

A

carvedilol (alpha 1 antagonists, clocks calcium entry)

labetalol (alpha 1 antagonist)

47
Q

beta blockers are more effective in what demographic

A

caucasian and young hypertensives

48
Q

beta adrenergic antagonists can be combined with what and for what purpose

A

antihypertensive drugs to counteract:

  1. reflex tachycardia
  2. increased renin secretion caused by thiazide and loop diuretics
49
Q

how do beta blockers affect atherogenesis

A

can predispose bc of increaseing plasma TGs and decreasing HDL

50
Q

what do beta blockers do to exercise tolerance

A

in angina treatment - helps

in HF treatment - may hurt bc of reduced CO –> earlier onset of fatigue

51
Q

why do beta blockers have a significant risk of new onset diabetes

A

beta blockade delays recovery of nromoglycemia because it inhibits hyperglycemic response mediated by epi

52
Q

what can abrupt cessation of beta blockers cause

A

tachycardia

hypertension

angina

MI

53
Q

what are the direct renin inhibitors

A

aliskiren

54
Q

what are drugs that block renin secretion

A

clonidine

55
Q

what are the alpha 1 adrenergic antagonists

A

Doxazonsin

Prazosin

Terazosin

56
Q

what happens to BP in pts on alpha 1 adrenergic antagonists

A

falls bc of decreased peripheral resistance

57
Q

centrally acting sympatholytic drugs

A

clonidine

methyldopa

guanfacine

58
Q

what do centrally acting sympatholytic drugs do

A

act in CNS as agonist on presynapyic alpah 2 recetpros in breain stem and reduce peripheral vascular resistance

59
Q

sudden withdrawal of clonidine can cause what

A

hypertensive crisis, headache. termor, abdominal pain

60
Q

what are the direct vasodilators

A

hydralazine

sodium nitroprusside

diazoxide

fenoldopam

analaprilat

nicardipine

61
Q

how do direct vasodilators work

A

act directl yon vascular smooth muscle to cause relaxtion and lowe BP by reducing vascular resistance `

62
Q

AEs of vasodilators

A

headaches

reflex tachy

fluid retention

flushing

palpitations

dizziness

63
Q

what can hydralazine cause as an AE

A

lupus like syndrome

64
Q

what is an AE of minoxidil

A

hypertrichosis

topical ointment to treat male baldness (rogaine)

65
Q

recommendatins for treatmen in pregnancy

A

beta blocker (labetalol) or CCB (nifedipine); methyldopa and hyralazine may also be used