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Cardiovascular > Drugs to treat Hypertension > Flashcards

Drugs to treat Hypertension Flashcards

1
Q

define sympathoplegic

A

drugs used to treat HTN and anxiety which inhibit the postsynaptic transmission of SNS signaling

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2
Q

General MOA’s for drugs used to treat HTN

A

Diuretics, Sympathoplegics, Vasodilators, Angiotensin agonists, Renin inhibitor

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3
Q

Name the categories of Sympathoplegics

A

Drugs which inhibit CNS sympathetic outflow (Clonidine) Ganglionic blockers (trimethaphan and hexamethonium) Drugs that act at nerve terminals (guanethidine) Alpha and beta antagonists (prazosin, propranolol)

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4
Q

Name the vasodilators

A

hydralazine , caclium channel blockers (nefidipine and verapamil) parenteral vasodilators (nitroprusside)

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5
Q

name the diurectics

A

Thiazides–>HCTZ–>good for mild HTN Loop diuretics–> Furosemide (lasix)–>used in mod/severe and HTN emergencies

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6
Q

name the angiotensin antagonists

A

Ace inhibitors ARB’s

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7
Q

name the renin inhibitor

A

aliskiren tekamlo (aliskiren and amlodipine)

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8
Q

Compensatory response to diuretics

A

minimal

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9
Q

COmpens. response to beta blockers

A

minimal

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10
Q

Compensatory response to alpha1-ganglionic blockers-clonidine-methyldopa

A

salt and water retension *slight tachycardia with alpha 1 blockers (prazosin, tarazosin, doxazosin)

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11
Q

Compens. mechanism to hydralazine

A

salt and water retention, mild tachycardia

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12
Q

compensatory mechnanism to minodoxil

A

marked water and salt retention, marked tachycardia

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13
Q

compensaotry change to nefidipine and verapamil

A

minor salt and water retention

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14
Q

compensatory change to nitroprusside

A

salt and water rentention

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15
Q

compensatory change to ACE/ARB’s

A

minimal

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16
Q

Sympathoplegics all work by reducing what

A
  1. venous tone (increasing compiance) 2. Heart rate 3 contractility 4. CO. 5. TPR
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17
Q

most patients with HTN have normal CO, therefore their HTN rests

A

on increases TPR

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18
Q

Drugs that act at the baroreceptor site

A

WE CURRENTLY HAVE NONE

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19
Q

CNS active agents

A

clonidine and methyldopa

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20
Q

Clonidine and Methyldopa MOA

A

–>decreasing CO and TPR –>activation of alpha 2 receptors quickening the onset of negative feedback control and inhibiting NE release

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21
Q

Methyldopa active form

A

methyl-norepinephrine converted in the brain

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22
Q

sudden discontinuation of clonidine can cause

A

rebound HTN

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23
Q

tx of rebound HTN from clonidine withdrawl

A

clonidine reintroduction addisiotn of alpha 2 blocker–>phentolamine

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24
Q

drugs that depletes NE sotres

A

resperidine–>contraindicated in pregnancy

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25
Q

drugs that deplete stores and inhibit release

A

guanethidine guanadrel

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26
Q

name the alpha 1 receptor blockers

A

prazosin tarazosin doxazosin *moderately effective

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27
Q

name the non-selective alpha blockers

A

phentolamine phenoxybenzamine

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28
Q

phenoxybenzamine and phentolamine are of no use in tx of chronic HTN bc

A

they have a large risk of CV stimulation –>they are non-specicific–>ALPHA 1 BLOCKADE AND ALPHA 2 INHIBIBITON INCREASES SYMPATHETIC TONE AND PREVENTS THE NEGATIVE FEEDBACK OF THE ALPHA 2 RECEPTOR

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29
Q

MAJOR PROBLEM with alpha 1 antagonists

A

ist done orthostatic hypotension *also useful to treat BPH

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30
Q

vasodilators act via 4 mechanisms

A
  1. release of NO 2. opening of potassium channels resulting in hyperpolarization 3. binding to D1 (dopaminergic) 4. blockage of calcium channels
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31
Q

Name the memprane stabalizing beta blockers

A

Propranolol Acetobutalol Carvedilol

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32
Q

Name the beta blockers with ISA

A

Propranolol Acetabutalol Pindolol *partial beta 1 agonist

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33
Q

non-specific beta blockers

A

NPPPT +carteolol

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34
Q

Specific Beta Blockers

A

A-N *except carteolol

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35
Q

Beta blockers initially decrease cardiac output but eventually decrease TPR via what likley mechanism

A

inhibit renin release from JGS cells which are beta 1 receptor dependent for activation

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36
Q

Hydralazine and Minidoxil are more effective on

A

veins rather than arteries (therfore would have a greater effect on edema than the the others)

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37
Q

Hydralazine MOA

A

secretion of NO (EDGFR) *never used at high doses

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38
Q

Hydralazine can cause what side effect

A

Hydralazine Induced Systemic Lupic Erythematous–>subsides with attenuation of drug

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39
Q

Minidoxil MOA

A

extremely efficacious–>used in severe HTN –>prodrug that its metabolite (minidoxi sulfate) inhibits potassium channel opening–>hyperpolarizes and relaxes smooth muscle

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40
Q

compensation for minidoxil requires

A

concurrent beta blocker treatment *can cause hirsutism

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41
Q

Ca channel blockers (L-type)

A

Nefidipine Verapamil DIltizem

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42
Q

prototypical dihydroproline channel blockers

A

nefidipine *others include amlodipine, felodipine, isradipine

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43
Q

DHP channel blockers MOA

A

reduce cardiac output by inhibiting calcium influx during depolarization–>slower HR, less contractility

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44
Q

why are CA channel blockers preferred over Minidoxil and Hydralazine

A

less side effects—> fewer compensatory changes

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45
Q

Parenteral vasodilator used in HTN emergencies

A

nitroprusside

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46
Q

nitroprusside MOA

A

release of NO from the drug molecule itself leading to vessel relaxation and rapid decrease in BP *half life is in minutes so must be consinuously infused

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47
Q

MInidoxil must be administered with

A

a beta blocker bc it causes severe tachycardia

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48
Q

third generation specific beta blocker

A

nebivolol and bisoprolol

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49
Q

name the direct vasodilators

A

minidoxil

nitroprusside

diazoxide

fenoldapam

50
Q
A
51
Q

pharmacologic effects of alpha 1 blockers

A

decrease tpr

reduce bp

relieve symptoms of BPH (relax bladder and prostate)

increase HDL

lower HDL

beneficial in insulin resistance

52
Q

side effects of alpha one blockers

A

first fose postural hypotension

53
Q

are alpha 1 blockers recommended as first line tx of HTN according to ALLLHAT

A

NO

54
Q

Beta blockers with MSA

A

PAC-M

propranolol

acebutolol

carvedilol

metoprolol

55
Q

beta blockers with ISA

A

APT-T

prindolol

propranolol

timolol

acebutolol

56
Q

may be useful in pt.’s with severe brady cardia

A

ISA agents

partial beta1 agonist

–>acts as a antagonist and agonist simultaenously (concentration dependent effect)

57
Q

cardioselectivity beta blockers

A

A-N

atenolol, metoprolol (mentioned specifically)

58
Q

non selective beta blockers

A

tomolol

pindolol

proprnaolol

59
Q

MOA for a beta blocker with no ISA

A

block beta-1 adrenergic recpetors

decrease heart rate and contractility–>decrease CO

block beta 1 AR in JGA–>decrease renin output

60
Q

this class of drugs works well in pt.’s with TN and hihg renin output

A

beta blockers with no ISA

61
Q

“provides effective therapy for all grades of HTN”

A

beta blockers with no ISA effect

62
Q

do beta blockers cause salt retention

A

NO–>can be administered without a diuretic

BB + diuretic is additive effect

63
Q

compelling indications of use for BB’s

A

CHF and MI, Ischemic Heart Disease

64
Q

preferred Hypertensive in pt.’s with hyperthyroidism and migraines

A

beta blockers

65
Q

Side effects of beta blockers

A

cold extremities–>worsens periph. arterial insuff.

bradycardia–>will slow it down too much, slows AV nodal condunction

bronchospasm –>need beta 2 to be agonized in asthma

bad dreams/depression

Hypoglycemia–>only seen in NSBB’s

Blocks HSL in lipocytes–> increases LDL, Reduces HDL increases Trigs

66
Q

Prolonged beta blocker and abrupt cessation of therapy will cause

A

Tachycardia–> use increases beta adrenergic receptor density–>stoppage of therapy will cause a large increase in CO

*withdraw slowly

67
Q

3rd generation beta blockers with Beta and Alpha blocking ability

A

LCN

Labetalol

Carvedilol

Nebivolol

68
Q

non-selective beta and alpha1 antagonist

A

labetolol

carvedilol

69
Q

beta blocker given IV for HTN emergencies

A

labetolol

70
Q
A
71
Q

highly selective beta1 antagonist with NO mediated vasodilation

A

nebivolol

72
Q

useful in HTN with metabolic syndrome

A

nebivolol

–>antioxidant activity with increased carb and lipid metabolism

IncreasesSV

maintains CO and systemic blood flow

73
Q

3rd generation beta blocker useful for CHF and HTN

A

carvedilol

74
Q

decreases mortality and morbity in patients with CHF and HTN

A

carvedilol

75
Q

3rd gen. BB which protects membranes from lipid peroxidation

A

carvedilol

–>antioxidant, binds and scavenges ROS’s

76
Q

dry cough from ACEI is caused by

A

inibition of bradykinin breakdown

–>there are bradykinin recptors which become overstimulated in the nasopharynx

77
Q

ace inhibitors on the kidney

A

increase renal blood flow without increasing GFR

78
Q

ACE-I which is renoprotective in diabetics

A

captopril

->increases syntheis of prostaglandins–>deleays progression of renal disease in Diabetics

79
Q

is posutral hypertension associated with ace inhibitors

A

no–>they leave the baroreceptor reflex intact

-

80
Q

most powerful vasocontrctor known

A

ATII

81
Q

side effects of ACE-I

A

exacerbate hypotension in volume depleted/sodium depleted pt.’s

HYPERKALEMIA–>avoid potassium sparing diuretics

dry cough–>brady

angioedema–>brady (vasodilator)

fetotoxicity (so are statins and arbs)

82
Q

MOA for ARB’s

A

selectively block ATII type I receptors which are responsible for all the effects of ATII

cause vasodilation and increase Na/Water retention

(thus decrease TPR, plasma volume, CO, and BP)

no effect on bradykinin breakdown

83
Q

pt. on ACE-I develops intolerable cough

A

put him on a ARB’s

84
Q

ARB-prodrug metabolized into an active roduct

A

LOSARTAN

85
Q

MOA for Losartan

A

competitive inhibitor of TXA2 receptor (therfore inhibitor of platelet aggrgation)

increases uric acid secretion

*irbesartan, valsartan, temlasartan do NOT increase uric acid secretion

86
Q

ARB useful in tx of gout

A

losartan

87
Q

main side effect of ARB’s

A

fetotoxicity

88
Q
A
89
Q

name the three classes of L type caclium channel blockers

A

Phenylalkylamines (Verapamil)

Benzothiazepines (diltizem)

Dihydropirines (nefidipine, amlodipine)

90
Q

CLASS/DRUG relatively selective for myocardium–>less effective at vasodilation

A

verapamil (phenyalkamine)

91
Q

CLASS/DRUG intermediate between phenyalkyamines and dihydropyridines for myocardial antagonist/vasodilaition

A

Diltiazem: Benzothiazepines

92
Q

CCB most specific for vasodilation

A

Amlodipine, Nefidipine (dihydropyridines)

–.selectively block L-type Ca2+ channels in the vasculature

(they are unable to depolarize..unabe to contract–>therfore they are vasodilated)

decrease TPR and arterial pressure

93
Q
A
94
Q

does nefidipine cause postural HTN

A

NO, baroreceptor relfex is left intact

95
Q

drugs most useful in pt.’s with HTN and LOW RENIN output

such as the elderly and AA’s

A

nefidipine and amlodipine

dihydropyridines

96
Q

MOA for alpha 2 selective AGONISTS

clonidine, guanfacine

A
  • decreases sympathetic impulses from RVLM to heart & blood vessels.
  • decrease in peripheral vascular resistance and decrease in HR.

–>the nerve terminal becomes negatively feedback inhibited quicker

97
Q

side effects of alpha 2 agonists

A

sedtion , drowsiness, fatigue,

98
Q

clonidine withdrawl leads to

A

severe HTN

*withdraw slowly

99
Q

MOA for hydralazine

A

selective arteriolar smooth muscle relaxer

*triggers baroreflexive sympathetic output–> tachycardia and renin release

100
Q

uses of hydralazine

A

IV in eclampsia

101
Q

side effects in hydralazine

A

Autoimmune hemolytic anemia

angina

tachycardia

palpitations

102
Q
A
103
Q

hydralazine is usually used with

A

BB and diuretics

104
Q

minodoxil MOA

A

relaxes arteriolar smooth muscle by OPENING K-atp channels

dilates arterioles but not veins–>causes reflex tachy and activates renin secretion

–>stuck in the inactive-open stage

–>depolarazation cannot happen

105
Q

side effect of minodoxil

A

hirsutism

increased renin

106
Q

MOA for nitroprusside

A

given IV for Malignant HTN

–>forms NO with stimulates smooth muscle production fo cGMP

–>CAUSES RELAXATION AND DECREASE IN BP

107
Q

direct dilator that dilates veins and arteries

A

nitroprusside–increases venous pooling

decreases afterload–>increases CO in CHF due to left heart failure

**hydralazine is specific to the arteriolar circulation

108
Q
A
109
Q

augments the action of ALL anti-HTN’s

A

diuretics

with BB’s decreases mortality in pt.’s with HTN

110
Q

which pt.’s show better response to thiazides

A

pt.s with volume dependent HTN (with low renin levels)

111
Q

HTN drug that has secondary protective effect in CAD

A

beta blockers

*useful in pt.’s with HTN, tachycardia, HIGH CO, and/or high renin

–>less effective in african americans and elderly

hyperthyroidism, migraine glaucoma

112
Q

considered standard tx option used with diuretics and ACEI

A

bisoprolol

–>34%mortality benefit

113
Q
A
114
Q

ACE-i’s and ARB’s work best in

A

young ppl with htn due to high renin output

115
Q

ace inhibitor with someone who has low renin outut

elderly and AA’s

requires what

A

co-admin with diuretic

116
Q

should be initial antihypertensive drug in Diabetic pt.’s with HTN

A

ACE-I or ARB

then CCB in 2nd drug needed

117
Q

HTN drug choice in pt’s with non-diabtic nephroathy

A

captopril

118
Q

pt.’s prone to CHF should be prescribed

A

ACE-I or ARB

119
Q

specific for relaxation of coronary vessels

A

dihyropyridines

120
Q

very useful in low-renin output HTN pt.’s

A

CCB’s

121
Q

can CCB’s be safely used in DM pt.’s

A

yes

Cardiovascular (6 decks)

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