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Year2 Renal > Exam 3 Linger- Intro to antiHTN agents > Flashcards

Exam 3 Linger- Intro to antiHTN agents Flashcards

1
Q

What is formula for MAP

A

CO x TPR

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2
Q

reflex tachycardia is a compensatory response from waht system

A

SAN

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3
Q

edema is a compensatory response from what system

A

renin activity

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4
Q

When do you initiate pharmacologic intervention with HTN

A

stage I classification

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5
Q

what anti HTN work on the vasomotor center in CNS

A

methyldopa, clinidine, guanabenz, guanfacine

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6
Q

What are the 4 main mech actions anti HTN

A

diuretics
agents that block Angiotensin
direct vasodilators
sympathoplegic agents (blockers)

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7
Q

What are the monotherapy options for patients with CKD

A

ACEI

ARB

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8
Q

what is monotherapy choice for black without CKD

A

thiazide or CCB

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9
Q

what is the monotherapy choice for nonblacks without CKD

A

thiazide diuretic, ACEI, ARB, CCB

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10
Q

how much of CO do kidneys receive

A

25%

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11
Q

What is actively reabsorbed in proximal tubule

A

sodium bicarb
sodium chloride
K
ALL glucose and AA

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12
Q

what is passivley reabsorbed in prox tubule

A

60% water

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13
Q

What enzyme is found in prox tubule that is key to HCO3 reabsorption

A

Carbonic anhydrase

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14
Q

What occurs in thin descending limb

A

water reabsorption

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15
Q

what occurs in thin ascending limb

A

impermeable to water and solutes

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16
Q

What occurs in thick ascending limb

A

impermeable to water
Na reabsorption
Na K 2Cl cotransporter which leaves - net charge so K leaks back out which will drive Mg and Ca back into cells

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17
Q

What occurs in distal convoluted tubule

A

impermeable to water
NaCl co transporter that is affected by thiazides
Ca reabsorbed by Ca channels that are regulated + by PTH

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18
Q

What occurs in collecting tubule

A

K secretion!
2 Na into cell ENaC
K and H out (metabolic alkalosis)

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19
Q

Where does aldosterone work and what is the effect

A

on collecting tubule
increases ENaC expression so increase Na reabsorption, more K and H secretion
water retention from Na reabsorption

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20
Q

Where does ADH work and what is the effect

A

increases amount of aquaporins in the collecting tubule to reabsorb water
no ADH the tubule is impermeable to water (dilute urine)

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21
Q

What is the effect of alcohol on ADH

A

prevents release of ADH

pee alot

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22
Q

How do diuretics work short term/long term

A

immediately cause volume contraction

over time–> have vasodilatory properties

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23
Q

What clinical situations are diuretics helpful in

A

heart failure, kidney disease, renal failure, liver disease, HTN, nephrolithiasis, hypercalcemia, diabetes inspidus

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24
Q

What are the carbonic anhydrase inhibitors

A
  • amides

e. g acetazolamide

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25
Q

what are the loop diuretics

A

Ethacrynic acid
furosemide
bumetanide
tosemide

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26
Q

What are the thiazide diuretics

A

-azides
HCTZ
chlothalidone and metolazone
indapamide!!

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27
Q

What are the K sparing diuretics

A

Aldosterone Antagonists= eplerenone and spironolactone “-one”
ENaC inhibitors: amilioride and triamterene

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28
Q

What are the osmotic diuretics

A

mannitol and isosorbide

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29
Q

What are the ADH antagonists

A

-vaptan

conivaptan, tolvaptan

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30
Q

Where do CA inhibitors act

A

proximal tubule primarily and prevent uptake HCO3
decrease the H inside cell needed to run Na H exchange
decrease Na reabsorption
acidosis

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31
Q

What are CA inhibitors used for

A

glaucoma, AMS and metabolic alkalosis

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32
Q

What are side effects of CA inhibitors

A

acidosis, hypokalemia
renal stones, paresthesias
sulfonamide HS

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33
Q

Where do loop diuretics work and result?

A

thick ascending limb
block Na K 2Cl
dec Na absorption so dec K secretion and dec Mg Ca reabsorption

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34
Q

what are side effects of loop diuretics

A

hypokalemia, alkalosis, hypocalcemiam hypomagenesemia, hyperuricemia, ototoxicity, sulfonamide HS

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35
Q

what are loops worked for

A

edema, herat failure, HTN, ARF, anion overdosem hypercalcemic states

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36
Q

why are loops good for kidney stones

A

flushing out tubules even though excreting more Ca

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37
Q

which loop does not contain sulfa

A

ethacrynic acid

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38
Q

where do thiazides work and effect

A

DCT
inhibit NaCl
decrease Na reabsorption
enhance reabsorption Ca from volume contraction

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39
Q

why are thiazides helpful in kidney stones

A

increase Ca reabsorption

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40
Q

what are thiazides used for

A

HTN, mild heart failure, nephrolithiasis, nephrogenic DI

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41
Q

what are the side effects of thiazides

A

hypokalemia, alkalosis, hyperCa, hyperuricemia, hyperglycemia, hyperlipidemia, sulfa HS

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42
Q

what patient population should you be careful with thiazides

A

DM and gout

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43
Q

How do the aldosterone antagonist diuretics work

A

block R which usually increases ENaC. therefore decreases expression and dec Na reabsorption, dec K secretion

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44
Q

how do the othe rK sparing diuretics work (not aldosterone antagonist)

A

directly inhibit ENaC

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45
Q

What are the side effects of aldosterone R antagonist diuretics

A

hyperkalmia, acidosis, anti-androgenic effects

gynecomastia in men

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46
Q

what are the indications to use aldosterone R block diuretic

A

hyperaldosteronism
adjunct to save K with other diuretics
female hirsutism
heart failure

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47
Q

what are indications to use direct ENaC inhibitors

A

lithium induced nephrogenic DI (amiloride)

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48
Q

which diuretics increase body pH (alkalosis)

A

loop and thiazide

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49
Q

What are the ACEI durgs

A

-pril
captopril
enalapril
enalaprilat

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50
Q

what are the ARB drugs

A

-sartans
losartan
valsartan

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51
Q

what drugs block renin secretion

A

clonidine and propanolol by blocking the B1 R on the juxtaglomerular cells

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52
Q

what drug is a direct renin inhibitor

A

aliskiren

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53
Q

what is the effect of AngII on pituitary

A

increase ADH secretion

54
Q

describe physical effects of ANG II on heart

A

vascular and cardiac hypertrophy remodeling

55
Q

what is the rapid pressor response to ANG II? slow pressor?

A

rapid is systemic vasoconstriction

slow is the altered renal function (aldosterone and Na reabsorption)

56
Q

What are the effects of ACEI

A

block conversion ANG I to ANG II

prevent degradation of bradykinin

57
Q

What are ACEI used for

A

HTN, heart failure, L ventricular dysfunction, prophylaxis of future CV evens like MI, CAD, stroke
nephropathy (DM +/-)

58
Q

what are the results of ACE I systemically

A

lower TPR
dec MAP both systolic and diastolic
no change SV or CO

59
Q

do ACEI affect baroReceptor

A

no

60
Q

what are the adsverse effects of ACEI

A

cough, angioedema (reduced metabolism bradykinin)
hyperkalmeia, ARF
hypotension
teratogenic
proteinuria, skin rash, altered sense of taste

61
Q

what are the drug interactions of ACEI

A

antacids, capsaicin NSAIDs, K+ sparing diuretics, digoxin, lithium, allopurinol

62
Q

Why are ACEI renal protective

A

vasodilate efferent arterioles more to reduce back pressure on glomerulus

63
Q

why are ACEI used for renal disease until GFR is <5%

A

because will decrease GFR even more, harmful

64
Q

What are the risk factors for ACEI induced ARF

A

MAP insufficiency
volume depletion
renal vascular disease (b/l stenosis) (PAD)
vasoconstrictor agents (cyclosporin and NSAIDs)

65
Q

What are the ANG II R and effects

A

AT1 and AT2
AT1 is GPCR smooth muscle contraction
AT2 causes production NO and causes smooth muscle dilation

66
Q

ACEI affect what ANG II R?

A

AT1 and AT2 because block production ANGII

67
Q

ARBS block what ANG II R?

A

just AT1 so does not increase NO and bradykinin. only blocks smooth muscle constriction

68
Q

what are ARBs used for

A

HTN, diabeitc nephropathy, HF , L ventricular dysfunction after AMI, prophylaxis

69
Q

what are adviser effects ARBs

A

not cough or angioedema

but otherwise same as ACEI

70
Q

What is a big difference of ACEI and ARB

A

ACEI icnrease bradykinin

ARB no influence on bradykinin

71
Q

How does aliskiren work

A

inhibits renin so blocks conversion angiotensinogen to ANG I

72
Q

What are the feedback loops from aliskiren

A

rise in plasma renin levels

ONLY drug that decreases renin activity

73
Q

What are the DHP CCBs

A

-dipines
amlodipine
nifedipine

74
Q

what are the non-DHP CCBs

A

diltiazem

verapamil

75
Q

What are the K channel openers

A

diazoxide and minoxidil

they hyperpolarize membrane

76
Q

what are the dopamine agonists that vasodilate

A

fenoldapam

77
Q

what are the NO donors

A

hydralazine
nitroprusside
organic nitrats: nitroglycerin and isosorbide dinitrate

78
Q

What channel to CCB work on

A

L type

79
Q

What is the predominant effect on DHP CCB

A

arteriolar vasodilation

decrease TPR

80
Q

what is the predominant effect of non-DHP CCB

A

prominent Cardiac effects

decreased CO

81
Q

which CCB has greatest negative inotropic effect on heart

A

verpapamil and then diltiazem

82
Q

Which CCB decrease rate of SA node depolarization and slow the AV node conduction

A

verapamil and diltiazem

83
Q

What is important about pharmkinetics of CCBs

A

high first pass effect

84
Q

whatare the side effects of CCBs

A

dizziness, hypotension, HA, flushing, nausea, peripheral edema, coughing, wheezing pulmonary edema

85
Q

what is a specfiic side effect to verapamil

A

constipation

86
Q

what drugs can you not concurrently use with verapamil or diltiazem

A

beta blokcers because AV block

87
Q

what patients should not be prescribe the non-DHP CCBs

A

ventricular dysfunction, SA or AV nodal conduction defects or a systolic pressure less than 90

88
Q

What are the clinical uses of CCBs

A

HTN, HTN EM, Angina

89
Q

What is the MOA of K channel openers

A

increased K permeability leading to hyperpolarization of smooth m membrane
reduce probability of contraction

90
Q

What are the adsverse effects of minoxidil

A

HA, sweating, hypertrichosis

reflex tachycardia and ema

91
Q

What must you prescribe with minoxidil to prevent reflex tachycardia and edema

A

beta blocker and diuretic

92
Q

how does fenoldopam work

A

dilate afferent renal artery

93
Q

what are the side effects of fenoldopam

A

tacycardia, HA and flusing

94
Q

when is fenoldapam used

A

HTN EM and post-operative HTN

95
Q

what are major contraindications for fenoldopam

A

avoided in patients with glaucoma because increase intraocular P

96
Q

What is the MOA of hydralazine

A

release NO from endothelium and vasodilate arterioles

97
Q

what are the clinical uses of hydralazine

A

HTN in pregnancy with methyldopa concurrently
heart failure
HTN EM

98
Q

what are the adverse effects of hydralazine

A

fluid and Na retention
HA, nausea, anorexia, sweting, flushing, palpitations
reflex tachy can provoke angina
lupus like syndrome!

99
Q

what is Tx for lupus like syndrome created by hydralazine use

A

withdrawl of drug

100
Q

What is MOA of nitroglycerin

A

dilates arterial and venous vessels
decrease TPR and venous return
decrease pre and afterloads

101
Q

what are the adverse effects of nitroprusside

A

excessive hypotension, cyanide poisoning

102
Q

what are the adverse effects of nitrates

A

orothostatic hypotension, syncope, throbbing HA

103
Q

when is nitroprusside used

A

HTN EM. IV only

104
Q

What are the main nonselective Beta blockers

A

propanolol timolol, nadolol, carteoolol, penbutolol

pindolol

105
Q

What are the B1 selective beta blockers

A

atenolol, metoprolol esmolol, bisoprolol, betaxolol

acebutolol, nebivolol

106
Q

what are the alpha and beta blockers

A

carvedilol, labetalol

107
Q

what are the alpha 1 blockers

A

prazosin
doxasin
terazosin

108
Q

what are the a2 agonists (central acing

A

clonidine, methyldop, guanabenz, guanfacine

109
Q

what to alpha blockers do

A

block vasoconstriction

110
Q

what is the purpose of B1 selective blockers

A

cardioselective

111
Q

what is labetalol used for

A

IV in severe HTN

acceptable option for HTN during pregnancy

112
Q

which non selective beta blockers have vasodilatory effects

A

carteolol, carvedilol, labetalol

113
Q

which selevtice beta blockers can induce peripheral vasodilation

A

betaxolol, nebivolol

114
Q

what beta blocker is given IV for pre-operative tachycardia and HTN, HTN EM, arrhythmias

A

esmolol

115
Q

what are the pharmodynic effects of alpha 1 selective blockers

A

decrease TPR, decrease venous return, decrease preload
does not inc HR or CO
does not inc NE release(still have neg feedback from alpha2)
relazes smooth muscle in prostate

116
Q

what are the adverse effects of alpha 1 selective blockers

A

postural hupotension and syncope

usually given at bedtime to minimize hypotension

117
Q

What occurs after injection of clonidine

A

increase BP via peripheral a2B

decreased BP due to central a2A

118
Q

how does oral clonidine cause decreased BP

A

decreased CO preload

119
Q

what is the clinical use of clonidine

A

essential HTN

adjunct for narcotic, alcohol and tobacco withdrawal

120
Q

what are the sideeffets of clonidine

A

dry mouth, sedation, impotence, depression

121
Q

what occurs if sudden withdrawl of clonidine

A

HTN crisis

122
Q

what are side effects of methyldopa

A

sedation, dry mouth, sexual dysfunction, postural hypotension, anemia

123
Q

what are some HTN medications used in pregnancy

A

methyldopa,
beta blockers: labetalol, pindolol, metoprolol
CCB: nifedipine, nicardipine

124
Q

What durgs are contraindication in pregnancy

A

ACEI, ARBs, alkiskren

nitroprusside

125
Q

What drugs are used for HTN EM

A

vasodilators: Na nitroprusside
nitroglycerin, niardipine, celivdipine, fenoldopam, hydralazine, enalaprilat
adrenergic antagonists: labetalol, metoprolol, esmolol, phenolamine

126
Q

What drugs are used as initial mono therapy

A

thiazide
ACEI or ARB( always in CKD +/- DM)
CCB
beta blockers if indicated

127
Q

pregnant patient has liver disease, which medication is contraindicated

A

methyldopa

128
Q

patient has HTN and BPH, what drug should you give him

A

alpha blocker

129
Q

patient has HTN and osteoporosis, what drug should you give him

A

thiazide

130
Q

patient has hyperthyroidism and HTN was drug should you give him

A

beta blocker

131
Q

What are compelling indications to use beta blocker and non-DHP CCB together

A

atrial fibrillation or flutter

angina

Year2 Renal (20 decks)

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