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Nefrologia PT > Hypertension > Flashcards

Hypertension Flashcards

1
Q

acceptable increase in creatinine within first 2 months of aceinhibitor therapy

A

30%

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2
Q

First line therapy: Acei

A

Htn with hf and systolic dysfunction
type 1 dm and proteinuria
mi or cad
new af
left ventricular dysfunction
hd

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3
Q

selectively antagonize Ang Ii at the AT1 receptor

A

ARB

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4
Q

B1 selective

A

Atenolol, Metoprolol, Bisoprolol, Acebutolol

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5
Q

Nonselective + A blockade or other mechanism

A

Labetalol Carvedilol Nebivolol

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6
Q

coexisting heart failure and htn

A

B blocker

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7
Q

inhibit entry of calcium or its mobilization from intracellular stores, lower peripheral resistance

A

Calcium channel blockers

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8
Q

Most potent vasodilator among ccb

A

dihydropyridines - amlodipine, nifedipine

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9
Q

augment atrial natriuretic peptide release

A

ccb

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10
Q

important tx option for renal transplant recipients - reduces initial graft nonfunction by attenuating ischemic and reperfusion injury, preserves long term renal function by protecting against cyclosporine nephrotoxicity

A

CCBs

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11
Q

cause of edema in dihydropyridines

A

uncompensated precapillary vasodilation

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12
Q

crosses the blood brain barrier and have a direct agonist effect in a2 adrenergic receptors in the midbrain and brainstem

A

central adrenergic agonist

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13
Q

most common adverse effect of a agonist

A

dry mouth

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14
Q

decrease peripheral vascular resistance, act directly on vascular smooth muscle

A

direct acting vasodilators

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15
Q

direct vasodilator reserved for severe or intractable hypertension

A

minoxidil

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16
Q

common adverse effect of minoxidil

A

hypertrichosis

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17
Q

associated with development of sle (direct vasodilator)

A

hydralazine

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18
Q

derivative of spironolactone that is approx 24x less potent in blocking mr than spironolactone

A

eplerenone

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19
Q

Bp target < 60

A

< 140/90

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20
Q

Bp target > 60 yo

A

< 150/90

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21
Q

Ideal therapy for older patients

A

vasodilators - ace/arb + hctz, ccb

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22
Q

optimal therapy in pregnant

A

a-methyldopa, hydralazine or bblocker

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23
Q

angina tx

A

Bblocker, nitrates, ccb
reduce hr and induce vasodilation

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24
Q

Lvh htn tx

A

hctz acei ccb arb
avoid vasodilators
reduce sbp

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25
Q

systolic dysfunction htn tx pharma consideration

A

reduce afterload and preload
acei, arb, hctz, bblocker, aldactone

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26
Q

diastolic dysfunction

A

improve myocardial compliance
bb, ccb, acei arb
avoid loop diuretics

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27
Q

MI

A

reduce heart rate, bb, acei

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28
Q

inability to reach desired bp goal despite the use of 3 optimally dosed drugs, one of which is a diuretic or need for four or more medications yo reach desired goal

A

Resistant htn

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29
Q

most common cause of resistant htn

A

non adherence

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30
Q

most potent parenteral vasodilator - dilates arteriolar resistance and venous capacitance vessels

A

sodium nitroprusside

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31
Q

degree of pressure gradient between aorta and poststenotic renal artery before measurable release of renin develops

A

10-20mmhg

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32
Q

critical lesions require how much of luminal obstruction before hemodynamic effects are detected

A

70-80%

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33
Q

Effects of angiotensin II

A

vasoconstriction
renal Na retention
aldosterone secretion
Vascular effects
Sns
myocardial effects

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34
Q

affects the intima or fibrous layers of the vessel wall, F, smoking, classically away from renal artery, string of bead appearance

A

fibromuscular disease, medial fibroplasia

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35
Q

most common cause of renovascular disease, at origin of artery

A

atherosclerosis

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36
Q

appear in the midportion of the vessel, strong predilection for the R renal artery

A

medial fibroplasia

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37
Q

syndromes associated with renovascular hypertension

A
  1. Early or late onset htn
  2. acceleration of treated essential htn
  3. Deterioration of renal function in treater essential htn
  4. Acute renal failure during treatment of hypertension
  5. Flash pulmonary edema
  6. Progressive renal failure
  7. Refractory congestive cardiac failure
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38
Q

lateralizafion is defined as a ratio of more than ___ between the renin activity of the stenotic kidnet and the nonstenotic kidney

A

1.5

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39
Q

used to monitor after renal revascularizarion to monitor restenosis and target vessel patency

A

Doppler studies

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40
Q

gold standard for definition of vascular anatomy and stenotic lesions in kidney

A

Intra arterial angiography

41
Q

resistive index that reflects intrinsic parenchymao and small vessel disease in the kidney that does not improve after revascularizarion

A

> 80

42
Q

Most frequently reported complication after ptra and stenting

A

Minor - groin hematoma and puncture site trauma

43
Q

Creatinine and size of kidneys which will unlikely benefit from surgical or endovascilar procedures

A

Crea > 3 cm, Small kidneys < 8 cm

44
Q

Indications for revascularizarion

A

circulatory congestion
deteriorating kidney function
bilateral high grade ras
solitary functioning kidney
uncontrolled hypertension

45
Q

Screening in primary hyperaldosteronism

A

Plasma aldosterone concentration to renin activity: ARR of 30

46
Q

False positives Arr

A

K and Na loading, bb, nsaid, ckd

47
Q

False negative primary hyperaldosteronism

A

HypoK, diuretics, acei, arb, ccb

48
Q

confirmatory tests for Pa

A

Saline loading
oral Na loading
fludricortisone
Captopril challenge

49
Q

+ saline loading test

A

plasma aldosterone > 10 ng/ml (2L in 4h)

50
Q

+ oral sodium loading test

A

urinary aldosterone > 12-14 mcg/day (6g/day for 3-5 days)

51
Q

+ fludrocortisone suppression test after 0.1 mg of fludrocortisone every 6 hrs for 4 days

A

+ if upright plasma aldo > 6 ng/dL and renin/cortisol low

52
Q

+ captopril challenge test after 20-25 mg

A

+ plasma aldosterone elevated and unchanged after 1 amd 2h

53
Q

initial study in subtype testing of pa

A

adrenal ct

54
Q

small hypodense nodule (2 cm in diameter)

A

Aldosterone producing adenoma

55
Q

normal adrenals or nodular changes

A

Idiopathic hyperaldosteronism

56
Q

> 4 cm, heterogenous, indistinct margins, hemorrhage and necrosis

A

Aldosterone producing adrenal ca

57
Q

medical management for GRA

A

low dose dexa/pred

58
Q

11B-hydroxysteroid dehydrogenase deficiency

A

licorice

59
Q

htn hypoK inappropriate kaliuresis with low aldosterone and renin

A

liddle syndrome

60
Q

headache, sweating, hypertension in paroxysms

A

Pheochromocytoma

61
Q

tx of pheochromocytoma

A

alpha blocker - phentolaminr or phenoxybenzamine

62
Q

screening for acromegaly

A

Insulin like growth factors

63
Q

tx for aortic dissection

A

bblocker plus nitroprusside
120 mmhg in 20 mins

64
Q

phenomenon where a mild increase in blood pressure results in a concomitant increase in Na excretion

A

Pressure natriuresis

65
Q

factor produced by adipocytes found to impair nitric oxide synthesis and enhances endothelin 1 production favoring the devt ko htn in obesity

A

resistin

66
Q

when decreased causes insulin resistance, decreased induction of enos, increased sympathetic activity

A

adiponectin

67
Q

When increased heightens sns

A

leptin

68
Q

causes Na retention causing increased bp

A

angiotensinogen

69
Q

isolated office htn, high bp in the office and normal bp in the out of office environment

A

White coat htn

70
Q

normal bp in the office, increased outside

A

masked htn

71
Q

difficult to control bp with 3 optimally dose drugs one of which is a diuretic, need for 4 or more medications

A

resistant htn

72
Q

orthostatic hypotension is defined as a drop of more than how many mmhg in BP after 3 mins of standing

A

20/10

73
Q

labile htn and hypotensive symptoms

A

home bp monitoring

74
Q

gold standard when patients have home bp values that are borderline

A

abpm

75
Q

monitor orthosatic htn

A

home bp

76
Q

supine htn and average levels of bp

A

abpm

77
Q

autosomal dominant disorder with htn, met alk, low aldo and low renin, increased bp with aldactone intake

A

hypertension brachydactyly syndrome

78
Q

hypokalemia, met acid with normal renal fxn, htn

A

gordon syndrome

79
Q

hypok, met alk, low plasma aldosterone and renin, enac mutation

A

liddle syndrome

80
Q

hypok met alk low plasma and aldosterone, mutation in 11B hydroxysteroid dehydrogenase type 2

A

Apparent mineralocorticoid excess

81
Q

Mutation in MR, hypok and met alk, low aldosterone and renin, increased bp due to pregnancy or aldactone intake

A

Geller syndrome

82
Q

mutationnof hypertension brachydactily syndrome

A

phosphodiasterasr E3a

83
Q

short fingers, stature; brainstem compression from
vascular tortuosity in the posterior fossa

A

htn brachydactyly syndrome

84
Q

patients who lack normal BP dip of 20% during sleep

sleep bp that falls by less than 10% compared with awake levels

A

nondippers

85
Q

cut off of high renin

A

6.5 ng/mL/hr

86
Q

medication of choice high levels of renin

A

acei, arbs, renin inhibitors, bblockers

87
Q

Low levels of renin tx of choice

A

diuretics, aldosterone antagonists, ccbs or a blockers

88
Q

when to work up for secondary htn

A

htn younger than 30 with no family hx of htn
> 55 yo with new onset htn, worsening of bp control, recurrent flash pulmo edema, abdominal bruit, inc of more than 30% after raas blocker

89
Q

treatment of primary hyperaldosteronism

A

verapamil, hydralazine, peripheral a adrenoreceptor antagonists

90
Q

cut off size to consider adrenal adenocarcinoma

A

> 4 cm

91
Q

diffuse hyperplasia of aldosterone producing cells within adrenal cortex

A

idiopathic hyperaldosteronism

92
Q

enlarged limbs of one or both adrenal glands > 10 mm thick

A

Unilateral adrenal hyperplasia

93
Q

Management for acute aortic dissection

A

sbp < 120 within 20 mins
Bblocker and vasodilator

94
Q

bp target for htn with hemorrhage

A

10-15% reduction over 1-2 hrs

95
Q

bp target for major hematuria or kidney injury

A

0-25% reduction in map over 1-12 h

96
Q

Bp target for hypertensive enceph

A

25% over 2-3 h

97
Q

bp target for acute head injury

A

0-35% reduction over 2-3h with nitroprusside

98
Q

LIDDLE

A

Autosomal dominant, gain of function mutation do ENaC in the collecting tubules
HTN due to increased Na+ retention, hyporenin/hypoaldosteronism due to volume expansion, but hypokalemia and metabolic alkalosis due to facilitated renal K+ and H+ secretion in the collecting tubules via the favorable electrochemical gradient generated by the enhanced Na+ reabsorption through ENaC.
Treatment: low-sodium diet and direct ENaC inhibitors such as amiloride and triamterene.

Nefrologia PT (112 decks)

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