AntiHypertensives and Diuretics Flashcards

1
Q

regular exercises causes what

A

decreased heart rate and concentration of circulating catechoalmines, increases HDL and increases ANP release

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2
Q

what are the four classes of anti-hypertensive medications

A

diuretics
sympatholytics
vasodilators
renin-angiotensin system antagonists

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3
Q

why are patients noncompliant with medications

A

largely asymptomatic and benefit is not immediate

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4
Q

what are the two beta blockers that are cardioselective

A

atenolol

metoprolol

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5
Q

what are the 3 beta blockers that are vasodilating agents

A

carvedilol
labetalol
nebivolol

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6
Q

what are the agents with instrinsic sympathomimmetic activites (ISA)

A

pindolol

acebutolol

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7
Q

what is the primary mechanisms for using beta blockers for treatment of hypertension

A

beta 1 decreases myocardial contratility which therefore decreases Cardiac ouput by decreaseing HR and contractility, leading to decreased renin secretion, decreased AngII and decreased TPR

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8
Q

what are the clinical effects of beta blockers

A

decreased heart rate (negative chronologic effect)
decreased contractility
decreased renal renin secretion

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9
Q

beta blockers are effective when the following comorbidities are present

A

ischemic heart disease
heart failure
dissecting aneurism of the thoracic aorta

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10
Q

_______are inferior to diuretics when used in elderly or african american hypertensive patients

A

beta blockers

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11
Q

beta blockers are contraindicated in

A

acute decompensated heart failure and asthma patients

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12
Q

adverse effects of beta blockers

A

elevated TG and decreased HDL
bronchospasm
fatigue, cold extremities, vivid dreams
impotence, hyperglycemia and raynauds phenomenon may be worsened

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13
Q

beta blocker metabolism is ________indirectly by decreasing hepatic blood flow secondary to decreased CO

A

decreased

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14
Q

what drugs have additive effects with beta blockers and may cause excessive negative inotropic and AV nodal efffects

A

verapamil, lidocaine, and other negative inotropes

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15
Q

in general how do Vasodialtors work

A

decrease vascular resistance by eliciting a compensatory response and work best with other HT meds that oppose compensatory responses

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16
Q

example of strict venodialtors

A

nitrates

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17
Q

examples of arteriolar dilators

A

hydralazine, minoxidil and calcium channel blockers

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18
Q

what is the MOA of ACE inhibitors

A

inhibits the synthesis of angiotensin II and increased bradykinin and decreases circulating levels of aldosteron

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19
Q

what are some examples of long acting ACEI

A

trandolapril and ramipril

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20
Q

long acting ACE-I are preferred in

A

young, white asian

patient with high plasma renin

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21
Q

trandolaprim and ramipril are contraindicated in

A

pregnancy

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22
Q

ACE-I are effective in patients with the following comorbidities

A

acute MI
congestive HF
risk of Cardiovascular diseases

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23
Q

______are useful against chronic kidney diseases and in hypertensive patients with diabetic neuropathy

A

ACE-I

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24
Q

are potassium sparing or potassium wasting diuretics bad with ACE-I

A

potassium sparing

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25
Q

examples of dentrimental drug interactions with ACE-I’s

A

potassium supplements
all potassium sparing diureetics
NSAIDS cause salt and water retention increase K+ in plasma
ARB’s

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26
Q

contraindications with ACE-I

A

angioedema
pregnancy
bilateral renal artery stenosis, renal failure

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27
Q

what are the adverse effects of ACE-I

A
first dose hypertension
dry cough
angioedema
increased serum K
developmental defects
hypoglycemia
functional renal failure in pts with renal stenosis
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28
Q

the ACE-I’s are the

A

Apirls

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29
Q

what are the ARB’s

A

the “sartans”–losartan, candesartan, olmesartan, valsartan

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30
Q

what is the mechanism of action for ARB’s

A

inhibits angiotensin 2 receptors which decreases aldosterone levels, decreasing plasma volume and total peripheral resistance

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31
Q

what are the side effects of ARBS

A

less increase K- than Ace

less potential for angioedema or cough, everything else is the same

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32
Q

________is a direct renin inhibitor

A

aliskiren

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33
Q

What are the three available calcium channel blockers for hypertension

A

dihydropyridines
verapamil
diltaizem

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34
Q

slows AV nodal conduction

A

verapamil

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35
Q

clinical effects of calcium channel blockers

A

vasodilation and decreased totoal TPR, decreased cardiac contractility and slows AV nodal conduction

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36
Q

clinical uses for calcium channel blockers

A

generally effective in elderly patients, african americans and patients from the caribbean, angina, and decreased rrisk of myocardial infract and stroke in HT pts and used in atrial arrhthmias

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37
Q

Iv ________can cause circulatory collapse in paitnets treated concurrently with beta blockers

A

verapamil

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38
Q

adverse effects of calcium channel blockers

A

well tolerated, short acting preparations, ankle swelling is common, can exacerbate heart failure and constipation

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39
Q

what is the main physiologic mechanisms of action for nitrates

A

venous vasodilation

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40
Q

_____is given IV for severe hypertensive emergencies in the ICU

A

sodium nitroprusside

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41
Q

sodium nitroprusside requires

A

co administration with a beta blocker

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42
Q

prolonged use of sodium nitroprusside can result in

A

cyanide toxicity

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43
Q

it dilates the arterioles ONLY resulting in rapid fall in BP leading to profound reflex tachycardia and increased CO

A

diazoxide

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44
Q

what are the adverse effects of diazodie

A

hypotension, hyperglycemia, salt and water retenion

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45
Q

diazoxide is contraindicated in

A

ischemic heart disease, reflex sympathetic response can promoke angina and cardiac failure

46
Q

what is the mechanism for fenoldopam

A

D1 agonist which dialates arterioles

47
Q

what are the adverse effects of fenoldopam

A

reflex tachycardia, headache and flushing

48
Q

what are the indications for fenoldopam

A

reflex tachycardia, headache, and flushing

49
Q

is used with a beta blocker in CAD pts to prevent ischemia

A

hydralazine

50
Q

used for treatment of severe refractory hypertension

A

hydralazine

51
Q

combine with a nitrate in african americans CHF patients for added benefit

A

hydralazine

52
Q

what drug has retianed a place in severe hypertension during pregnancy

A

hydralazine

53
Q

long term therapy of what drug can produce systemic lupus like symptoms in susceptible pts especially low acetylators

A

hydralazine

54
Q

is a prodrug that works via sulfate metabolite which activates K+ channels and relaxes vascular smooth muscles-predominately arteriolar dilator

A

minoxidil

55
Q

linked to causing hirsuitism and coarseness of facial features (used with caution in female patients)

A

minoxidil

56
Q

minixidil should be combined with what for better results in severe refractory hypertensive pts esp renal failure pts

A

beta blocker and loop diruetic

57
Q

example of alpha adrenergic blocker

A

doxazosin

58
Q

what is the MOA of alpha adrenergic blockers

A

relaxes vascular smooth muscles by preventing NE from interacting with alpha 1 receptors

59
Q

what are the adverse effects of alpha adrenergic blockers

A

first dose hypotension
postural hypotension
urinary incontinence

60
Q

what are the systemic alpha 1 selectives

A

prazosin, doxasin and terazosin

61
Q

what are the alpha 1 and alpha 2 blockers

A

phenoxybenzamine, phentolamine

62
Q

_________is combined with propranol to treat clonidine withdrawal syndrome

A

phentolamine

63
Q

use is limited by severe postural hypotension and is useful only as an add on to treat resistant hypertension

A

prazosin

64
Q

alpha methyldopa

A

Taken up by adrenergic nerve terminals and converted to α-methyl norepinephrine in the CNS where α2 receptors are stimulated to decrease sympathetic out flow to the periphery-

65
Q

DOC for hypertension in pregnancy

A

alpha methyldopa

66
Q

adverse effects of alpha methyldopa

A

drowsiness, depression, hepatitis, immune hemolytic anemia and fever

67
Q

toxicity of clonidien results in

A

xerostomia and sedation

68
Q

MOA and class for clonidine

A

centrally acting sympatholytic reducing sympathetic outlfow to the heart, blood vessels and the kidneys

69
Q

what are the three main causes of peripheral edema

A

cardiac failure
hepatic disease
renal disease

70
Q

the majority of sodium gets reabsorbed in the

A

proximal tubule

71
Q

what percentage of sodium gets reabsosrbed in DCT

A

7%

72
Q

what percentage of sodium the proximal tubule gets reabsorbed

A

65%

73
Q

what % of sodium gets reabsorbed in the collecting duct

A

2-3%

74
Q

what percentage of sodium gets reabsorbed in the ascending loop of henle

A

25%

75
Q

what part of the nepron does carbon anhydrase inhibitors work on

A

proximal convoluted tubule

76
Q

what part of the kidney do loop diruetics wokr on

A

loop of henle (ascneding)

77
Q

where do thiazides work

A

distal convoluted tubule

78
Q

where do potassium sparring diruetics work

A

collecting duct

79
Q

where do osmotic diruetics work

A

proximal tubule and descending loop of henle

80
Q

what are the four thiazides

A

chlrothalidone, hydrochlrothiazide, indapamide, and metolazone

81
Q

Act at the luminal surface of the cortical (proximal)
diluting segment of the distal convoluted tubule and
early collecting duct to inhibit the Na+/Cl+ cotransporter.

A

thiazides

82
Q

what are the loop diruetics

A

bumentadine, fuorsemide, torsemide

83
Q

Bind to the Na+/K+/2Cl- cotransporter complex at the luminal border of the
thick ascending limb of the loop of Henle, and inhibit Cl- re-absorption.

A

loop diuretics

84
Q

what are the three aldosterone antagonists

A

eplernone, spironolactone and spironolactone/hctz

85
Q

what are the potassium sparing diuretics

A

amiloride, tramterene or both drugs and hctz

86
Q

what class is acetazolamide

A

carbonic anhydrase inhibitor

87
Q

_____________interferes with the small proportion of sodium that is reabsorbed in the proximal tubule in exchange for Hydrogen

A

acetazolamide

88
Q

________exerts osmotic activity within the proximal renal tubule and particuarly the descending limb of the loop of Henle and limits passive tubular water reabsorption

A

mannitol

89
Q

what remains the basis of treatment in patients with congestive heart failure

A

diuretics and ACE inhibitors

90
Q

why can loop diruetics also be used to treat hypercalcemia

A

because they also cause increased urinary calcium excretion

91
Q

patients on loop diruetics should also receive

A

potassium supplements or a potassium sparring agent

92
Q

what is a common adverse side effect of treatment with high dose IV diuretics

A

acute gout

93
Q

act on the cortical diluting segment of the nephron

A

thiazide diuretics

94
Q

thiazides are often ineffective in what patient population

A

elderly patients

95
Q

what are the side effects of thiazide diuretics

A

hyponatremia and hypokalemia are commonly assoc with higher doses of thiazide diuretics

96
Q

metolazone is contraindicated in

A

liver failure patients

97
Q

if patient has chronic or severe CHF in the presence of renal impairment what should you do

A

give thiazide like diuretic and combine it with a loop diuretic but only under close supervision!!!

98
Q

what are the potassium sparing diuretics

A

amiloride and triamterine and spironolactone (competitive aldosterone inhibitor)

99
Q

potassium sparing diruetics must be used in caution in patients receiving _____because of the risk for hyperkalemia

A

ACE I

100
Q

what are the risk factors for hyperkalemia

A

spironolactone greater than 50
high dose ACE-I
evidence of renal failure

101
Q

pt has MI should give

A

beta antagonist and ACE-I

102
Q

pt has isolated systolic hypertension in elderly then give

A

diruetics, ACE-I, ARBS, dihydropyridines, and calcium antagonists

103
Q

drugs used to treat CHF

A

ACE-I
diruetics
beta blockers

104
Q

drugs use to treat uncomplicated hypetension

A

diuretics, ACE-I, ARB, and CCA

105
Q

thiazides are contraindicated in

A

renal insufficiency and diabetics

106
Q

what drug to you give for sulfa allergy

A

ethacrynic acid

107
Q

__________are reserved for patients whose creatinine levels are above 2mg %

A

loop dirutics

108
Q

large doses of ethacrynic acid can cause

A

otoxicity

109
Q

increased cholesterol has been reported with the use of thiazide diuretics but one of them is better than the others

A

imdapamide

110
Q
ACE inhibitors  
Antipsychotics
Beta-blockers
Ethanol
Ca-channel blockers
Antiadrenergic agents
 are known to
A

increase antihypertensive effects

111
Q
ASA/NSAIDs
Anticonvulsants
Bile acid resins
Sympathomimetics
(e.g., albuterol, 
dobutamine, etc).
A

know to decrease antihypertensive effects