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CVR Biweekly 2 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

no obvious cause; risk factors include overweight, sedentary lifestyle and high salt diet

A

primary hypertension

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2
Q

increased bp due to either medical condition or medication

A

secondary hypertension

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3
Q

causes include renovascular disease, aldosteronism, pheochromocytoma

A

secondary hypertension

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4
Q

> 130 mmHg SBP OR >80 mmHg

A

hypertension

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5
Q

as we age, there is an increased risk for what

A

CAD (coronary artery disease)

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6
Q

most common form of HTN

A

diastolic HTN

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7
Q

ages 30-50
DBP elevated (above 80 mmHg)

A

diastolic HTN

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8
Q

after age of 55
systolic bp elevated (>140)

A

isolated systolic HTN in older adults

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9
Q

17-25 yrs old
overactive sympathetic NS
increased CO

A

isolated systolic HTN in young adults

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10
Q

MAP=

A

CO x TPR (SVR)

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11
Q

blood volume controlled by kidney

A

CO

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12
Q

respond to rapid change in bp (3 things)

A

baroreceptor reflex
chemoreceptors
CNS ischemic response

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13
Q

respond to longterm changes in BP and have infinite gain

A

kidneys

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14
Q

a lot of the time due to renal dysfunction

A

hypertension

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15
Q

how kidneys respond to low bp

A

increase fluid retention
RAS activation
vasoconstrict

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16
Q

when factors alter the pressure natriuresis and diuresis relationship, what happens

A

changes in bp will follow (HTN)

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17
Q

AV fistula closure ultimately causes

A

increase in CO and MAP

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18
Q

how to decrease blood volume

A

diuresis and natriuresis

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19
Q

when fistula is repaired what happens

A

TPR increased (venous pressure increases and pumps blood to heart)

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20
Q

3 main functions of kidney

A

glomerular filtration
tubular reabsorption
tubular secretion

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21
Q

net effect of the 3 stages of kidney function

A

what gets excreted as urine

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22
Q

what increases GFR (glomerular filtration rate)

A

vasodilation of afferent arteriole and vasoconstriction of efferent arteriole

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23
Q

normal natriuresis steep curve remains the same regardless of what intake (BP remains normal)

A

increased salt intake

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24
Q

what happens when you decrease filtering capacity of kidney

A

bp becomes salt sensitive

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25
Q

what happens when you elevate pre-glomerular resistance

A

GFR decreases and BP is elevated

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26
Q

what happens to MAP if renal mass is decreased

A

nothing

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27
Q

if you eat salt w/ impaired kidney filtration

A

bp changes (salt-sensitive)

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28
Q

due to decreased NO and impaired vasodilation

A

endothelial dysfunction

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29
Q

what happens in endothelial dysfunction

A

stop making NO, and start making ROS (vasoconstrictors)

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30
Q

what happens as a response to endothelial dysfunction

A

vascular remodeling

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31
Q

what happens as an effect of vascular remodeling

A

decrease in arterial radius
increase in resistance
increase in bp

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32
Q

cross sectional wall area has no change; just decreased lumen size

A

eutrophic

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33
Q

increased in cross sectional wall area and decreased lumen size

A

hypertrophic

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34
Q

3 factors leading to SNS overactivity

A
  1. deactivation of baroreceptors
  2. increase in activation of stimulatory inputs
  3. circulating Ang II
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35
Q

targets of SNS activity in HTN

A

arterial tone
adrenal medulla
RAS

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36
Q

most powerful system for regulating bp and body fluid volume

A

Renin-Angiotensin-Aldosterone system

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37
Q

powerful vasoconstrictor and stimulates production of aldosterone

A

Angiotensin II

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38
Q

renal baroreceptors

A

juxtaglomerular cells in afferent arterioles

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39
Q

what is released by JG cells to increase pressure

A

renin

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40
Q

angiotensin receptor blockers

A

ARBs

41
Q

net effect of Ang II induced vasoconstriction

A

decrease in diameter and increase in bp

42
Q

effect of Ang II binding to AT1R

A

increase in Ca2+ and decrease in NO

43
Q

key mediator of natriuresis

A

Ang II

44
Q

stimulates production of aldosterone and ADH which contribute to volume regulation

A

Ang II

45
Q

Na+ intake increases, level of Ang II does what and why

A

decreases to vasodilate and get Na+ out of system

46
Q

putting patients on ARBs or ACEIs does what

A

makes them salt sensitive b/c blocked Ang II which is key regulator

47
Q

highly effective in preventing hyperfiltration in pt’s @ high risk for glomerulosclerosis and nephron loss (diabetes)

A

Ang II blockade

48
Q

when RAS is blocked, what happens to MAP when increase in salt intake

A

increases

49
Q

aldosterone is produced where

A

in adrenal gland

50
Q

2 channels activated by aldosterone in the kidney

A

Na+/K+ ATPase and ENaC

51
Q

promotes Na+ retention(and water) and K+ elimination by kidney

A

Aldosterone

52
Q

increases ENaC (Na+ reabsorption)

A

Aldosterone

53
Q

released from hypothalamus, promotes water reabsorption at the collecting duct; triggered release by Ang II too

A

ADH

54
Q

inserts aquaporins in collecting duct to allow water to flow out

A

ADH

55
Q

atrial myocytes store and release this in response to stretch

A

ANP

56
Q

promotes natriuresis (loss of Na+ and water)

A

ANP

57
Q

HTN that has identifiable cause typically linked to kidney

A

secondary HTN

58
Q

renovascular cause (decreased) filtering ability

A

secondary HTN

59
Q

alters Na+ and water handling can cause secondary HTN

A

aldosteronism

60
Q

excess secretion of glucocorticoids from adrenal gland; cause of secondary HTN

A

Cushing syndrome

61
Q

NE or Epi (catecholamine) secreting tumor; can cause secondary HTN

A

Pheochromocytoma

62
Q

stenosis and string of beads effect on kidneys

A

low perfusion; so kidneys will increase volume by increasing AngII; bp increases

63
Q

patients with this have high bp, and elevated Na+ reabsorption

A

hyperaldosteronism

64
Q

what percentage of weight loss can help someone w/ HTN and not use medicine

A

5%

65
Q

3 things visceral obesity can lead to (cause HTN)

A

RAS activation
increase SNS activity
renal compression

66
Q

released from fat cells and will increase sympathetic activity

A

leptin

67
Q

risk factor for metabolic syndrome

A

HTN

68
Q

what grade confirms HTN emergency and has narrowing of arteries, hemorrhage, cotton wool spots and exudates while looking at eye

A

grade 3

69
Q

what does it mean if you can’t see optic disc

A

edema

70
Q

sodium nitroprusside (used for HTN emergency) produces what 2 things

A

NO and cyanide

71
Q
A

HTN emergency

72
Q

bp for HTN urgency

A

180/120

73
Q

bp for HTN emergency

A

greater than 180/120 (220/130)

74
Q

bp >/= 180/120 w/ no signs of end-organ damage

A

HTN urgency

75
Q

diastolic bp >130 means what

A

HTN emergency; organ damage

76
Q

main drugs to administer for HTN emergency

A

labetalol, nitroprusside, nicardipine

77
Q

1st hour goal of bp when gradually lowering during HTN emergency

A

decrease by 10%
diastolic bp at 110

78
Q

6 hour goal when lowering bp in HTN emergency

A

160/100

79
Q

2-3 days goal when lowering bp in HTN emergency

A

PO drugs
nicardipine + (ACEIs, ARBs)
Enalapril, Losartan

80
Q

a combined a1 and beta blocker

A

Labetolol

81
Q

what to administer to patient after bp has been brought under control from HTN emergency to overcome drug resistance

A

IV Furosemide

82
Q

why gradually lower bp

A

to keep brain perfused and autoregulating

83
Q

A 42-year-old woman in her second trimester of gestation requires antihypertensive therapy for her chronic hypertension. Which of the following is NOT safe to prescribe to her?

A

Aliskiren

84
Q

Which of the following drugs is the best choice for a patient with hypertensive emergency and A-V block?

A

Nitroprusside; (-LOLs contraindicated for heart blocks)

85
Q

triad of sweating, palpitations, and high bp

A

pheochromocytoma

86
Q

what catecholamine is produced more in pheochromocytoma

A

NE

87
Q

catecholamines are produced from what

A

Chromaffin cells of the adrenal medulla

88
Q

what will reverse effects of sodium nitroprusside overdose (cyanide poisoning)

A

sulfur

89
Q

A 53-year-old woman complains of headaches and blurry vision of 12 hours duration. Her BP is 240/130 mm Hg. Labs show BUN 32 mg/dL and creatinine 4 mg/dL. A novel drug for hypertensive emergencies that causes arteriolar dilation, increased renal perfusion and increased natriuresis is prescribed. This drug is similar in action to:

A

Fenoldapam (targets a1 receptor)

90
Q

dopamine low dose effect

A

D1 agonism (increases renal function and GFR)

91
Q

intermediate dose of dopamine

A

B1 agonism (increase HR, contractility)

92
Q

higher dose of dopamine does

A

a1 agonism (vasoconstriction-increase bp)

93
Q

drug that causes vasoconstriction only(a1 agonist)

A

phenylephrine

94
Q

drugs contraindicated in bilateral renal artery stenosis

A

ACEIs/ARBs (would cause even more hypoperfusion)

95
Q

3 HTN drugs contraindicated in pregnancy

A

ACEIs/ARBs and Aliskiren (hypoperfusion of fetal kidneys)

96
Q

for elevated bp of 120-129/<80 how do you treat patient

A

non-pharmacologic therapy

97
Q

for stage 1 HTN (130-139/80-89) with no risk of CVD, how do you treat patient

A

non-pharmacologic therapy

98
Q

for stage 1 HTN (130-139/80-89) with a risk of CVD, how do you treat patient

A

non-pharmacologic therapy + BP lowering meds

99
Q

for stage 2 HTN (>/=140/90) how do you treat patient

A

non-pharmacologic therapy + BP lowering meds

CVR Biweekly 2 (15 decks)

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