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CVR Biweekly 2 > Hypertension > Flashcards

Hypertension Flashcards

(99 cards)

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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
what happens when you elevate pre-glomerular resistance
GFR decreases and BP is elevated
26
what happens to MAP if renal mass is decreased
nothing
27
if you eat salt w/ impaired kidney filtration
bp changes (salt-sensitive)
28
due to decreased NO and impaired vasodilation
endothelial dysfunction
29
what happens in endothelial dysfunction
stop making NO, and start making ROS (vasoconstrictors)
30
what happens as a response to endothelial dysfunction
vascular remodeling
31
what happens as an effect of vascular remodeling
decrease in arterial radius increase in resistance increase in bp
32
cross sectional wall area has no change; just decreased lumen size
eutrophic
33
increased in cross sectional wall area and decreased lumen size
hypertrophic
34
3 factors leading to SNS overactivity
1. deactivation of baroreceptors 2. increase in activation of stimulatory inputs 3. circulating Ang II
35
targets of SNS activity in HTN
arterial tone adrenal medulla RAS
36
most powerful system for regulating bp and body fluid volume
Renin-Angiotensin-Aldosterone system
37
powerful vasoconstrictor and stimulates production of aldosterone
Angiotensin II
38
renal baroreceptors
juxtaglomerular cells in afferent arterioles
39
what is released by JG cells to increase pressure
renin
40
angiotensin receptor blockers
ARBs
41
net effect of Ang II induced vasoconstriction
decrease in diameter and increase in bp
42
effect of Ang II binding to AT1R
increase in Ca2+ and decrease in NO
43
key mediator of natriuresis
Ang II
44
stimulates production of aldosterone and ADH which contribute to volume regulation
Ang II
45
Na+ intake increases, level of Ang II does what and why
decreases to vasodilate and get Na+ out of system
46
putting patients on ARBs or ACEIs does what
makes them salt sensitive b/c blocked Ang II which is key regulator
47
highly effective in preventing hyperfiltration in pt's @ high risk for glomerulosclerosis and nephron loss (diabetes)
Ang II blockade
48
when RAS is blocked, what happens to MAP when increase in salt intake
increases
49
aldosterone is produced where
in adrenal gland
50
2 channels activated by aldosterone in the kidney
Na+/K+ ATPase and ENaC
51
promotes Na+ retention(and water) and K+ elimination by kidney
Aldosterone
52
increases ENaC (Na+ reabsorption)
Aldosterone
53
released from hypothalamus, promotes water reabsorption at the collecting duct; triggered release by Ang II too
ADH
54
inserts aquaporins in collecting duct to allow water to flow out
ADH
55
atrial myocytes store and release this in response to stretch
ANP
56
promotes natriuresis (loss of Na+ and water)
ANP
57
HTN that has identifiable cause typically linked to kidney
secondary HTN
58
renovascular cause (decreased) filtering ability
secondary HTN
59
alters Na+ and water handling can cause secondary HTN
aldosteronism
60
excess secretion of glucocorticoids from adrenal gland; cause of secondary HTN
Cushing syndrome
61
NE or Epi (catecholamine) secreting tumor; can cause secondary HTN
Pheochromocytoma
62
stenosis and string of beads effect on kidneys
low perfusion; so kidneys will increase volume by increasing AngII; bp increases
63
patients with this have high bp, and elevated Na+ reabsorption
hyperaldosteronism
64
what percentage of weight loss can help someone w/ HTN and not use medicine
5%
65
3 things visceral obesity can lead to (cause HTN)
RAS activation increase SNS activity renal compression
66
released from fat cells and will increase sympathetic activity
leptin
67
risk factor for metabolic syndrome
HTN
68
what grade confirms HTN emergency and has narrowing of arteries, hemorrhage, cotton wool spots and exudates while looking at eye
grade 3
69
what does it mean if you can't see optic disc
edema
70
sodium nitroprusside (used for HTN emergency) produces what 2 things
NO and cyanide
71
HTN emergency
72
bp for HTN urgency
180/120
73
bp for HTN emergency
greater than 180/120 (220/130)
74
bp >/= 180/120 w/ no signs of end-organ damage
HTN urgency
75
diastolic bp >130 means what
HTN emergency; organ damage
76
main drugs to administer for HTN emergency
labetalol, nitroprusside, nicardipine
77
1st hour goal of bp when gradually lowering during HTN emergency
decrease by 10% diastolic bp at 110
78
6 hour goal when lowering bp in HTN emergency
160/100
79
2-3 days goal when lowering bp in HTN emergency
PO drugs nicardipine + (ACEIs, ARBs) Enalapril, Losartan
80
a combined a1 and beta blocker
Labetolol
81
what to administer to patient after bp has been brought under control from HTN emergency to overcome drug resistance
IV Furosemide
82
why gradually lower bp
to keep brain perfused and autoregulating
83
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?
Aliskiren
84
Which of the following drugs is the best choice for a patient with hypertensive emergency and A-V block?
Nitroprusside; (-LOLs contraindicated for heart blocks)
85
triad of sweating, palpitations, and high bp
pheochromocytoma
86
what catecholamine is produced more in pheochromocytoma
NE
87
catecholamines are produced from what
Chromaffin cells of the adrenal medulla
88
what will reverse effects of sodium nitroprusside overdose (cyanide poisoning)
sulfur
89
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:
Fenoldapam (targets a1 receptor)
90
dopamine low dose effect
D1 agonism (increases renal function and GFR)
91
intermediate dose of dopamine
B1 agonism (increase HR, contractility)
92
higher dose of dopamine does
a1 agonism (vasoconstriction-increase bp)
93
drug that causes vasoconstriction only(a1 agonist)
phenylephrine
94
drugs contraindicated in bilateral renal artery stenosis
ACEIs/ARBs (would cause even more hypoperfusion)
95
3 HTN drugs contraindicated in pregnancy
ACEIs/ARBs and Aliskiren (hypoperfusion of fetal kidneys)
96
for elevated bp of 120-129/<80 how do you treat patient
non-pharmacologic therapy
97
for stage 1 HTN (130-139/80-89) with no risk of CVD, how do you treat patient
non-pharmacologic therapy
98
for stage 1 HTN (130-139/80-89) with a risk of CVD, how do you treat patient
non-pharmacologic therapy + BP lowering meds
99
for stage 2 HTN (>/=140/90) how do you treat patient
non-pharmacologic therapy + BP lowering meds

CVR Biweekly 2 (15 decks)

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