Lec 15 HTN Flashcards

1
Q

What are cutoff numbers for hypertension in normal person?

A

systolic BP > 140 mmHg and/or

diastolic BP > 90 mmHg

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2
Q

How do you diagnose hypertension?

A

2 readings separated apart

pt should not ingest caffeine or smoke for 30 min before reading

sit for 5 min with arm at heart level before BP is checked

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3
Q

What is prevalence of hypertension?

A

more prevalent with age

about 30% of population

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4
Q

What are the 4 systems determine of BP regulation?

A
  • heart [CO]
  • peripheral vasculature [tone]
  • kidney [regulate blood volume]
  • hormones/reflexes [modulate]
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5
Q

What is role of heart in BP regulation?

A

provides CO that fills the vascular tree

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6
Q

What is role of peripheral vasculature in BP regulation?

A

vascular tone/resistance –> modulates tone from heart

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7
Q

What is role of kidney in BP regulation?

A
  • regulates intravascular volume

- essential to maintain chronic HTN state –> w/out renal involvement cannot maintain HTN

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8
Q

What is equation for BP [MAP]?

A

MAP = CO * TPR

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9
Q

What is equation for CO?

A

CO = HR*SV

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10
Q

What factors determine SV?

A
  • contractility
  • venous return [preload]
  • afterload
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11
Q

What factors determine venous return [preload]?

A

blood volume

venous tone

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12
Q

What is renal regulation of BP?

A

kidneys sense drop in BP –> secrete renin –> converts angiotensinogen to AT1 –> ACE converts to AT II

ATII:

  • -> directly increase BP by constriction
  • -> causes aldosterone release –> Na/H2O retention –> increase volume
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13
Q

What is essential hypertension?

A

cause of HTN cannot be explained == multiple etiologies together increasing CO or TRP

makes of 90% of HTN

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14
Q

What is secondary hypertension?

A

hypertension attributed to definable cause

makes up 10% of HTN

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15
Q

What is pressure natriuresis?

A

homeostatic mechanism by which if you increase BP –> get increase urine volume and Na excretion –> decrease blood volume –> pressure back to normal

this process is blunted in kidneys of pt with HTN

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16
Q

What is baroreceptor reflex?

A

baroreceptors = in aortic arch and carotid sinuses; sense increase in stretch of aorta due to pressure –> baroreceptors stimulated –> increase PNS and inhibit SNS–> vasodilation + decrese HR and co –> BP drops back to normal

== moment to moment modulation of blood pressure

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17
Q

What nerves carry baroreceptor signals?

A

CN IX carries from carotid sinus

CN X from aortic arch

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18
Q

What are causes of essential hypertension?

A
  • genetics
  • black > white > asian
  • systemic abnormalities: sympathetic overactivity in response to stimulus, abnormally vasoconstricted
  • renal: excess Na/H2O retention, hormone dysregulation [normal renin level in HTN pt]
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19
Q

Is diastolic or systolic or both HTN most prevalent?

A
  • in young people mostly isolated diastolic HTN
  • as you get older = more and more isolated systolic HTN

b/c chronic exposure to hemodynamic stress, vessels stiffer, increase calcification –> higher systolic when push the blood into aorta but don’t have sufficient elastic recoil –> low diastolic

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20
Q

What are some clinical clues that should make you think it might be secondary HTN?

A
  • very young < 20 yo
  • new HTN after age 50 in someone who never had problem before
  • severe rapid onset
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21
Q

What are major causes of secondary HTN?

step1

A

mostly renal disease including fibromuscular dysplasia in young patient

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22
Q

What are renal causes of secondary HTN?

A
  • parenchymal damage to kidneys –> decrease # of functioning nephrons –> secrete less Na/H2O –> more blood volume –> CO/BP up
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23
Q

What lab findings if renal cause of secondary HTN?

A
  • high serum creatinine

- abnormal urinalysis

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24
Q

What is renovascular cause of 2ndary HTN?

A

renal artery stenosis due to atherosclerosis or fibromuscular dysplasia

stenosis –> reduced renal blood flow –> more renin –> RAAS = vasoconstriction + Na retention

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25
Q

What is treatment of renovascular secondary HTN?

A

ACE inhibitors

renal artery revascularization

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26
Q

What are clinical signs of renovascular hypertension?

A

abdominal bruit

unexplained hypokalemia [due to overactive aldosterone]

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27
Q

What is aortic coarctation?

A

congenital narrowing of aorta

28
Q

What should you think it pt with HTN and way higher BP in arms than legs?

A

aortic coarctation causing secondary HTN

coarctation located distal to left subclavian

29
Q

What should you think if pt with HTN and lower BP in left vs right arm?

A

aortic coarctation causing secondary HTN

coarctation located at origin of left subclavian

30
Q

What happens in aortic coarctation associated hypertension?

A
  • reduced blood flow to kidneys –> stimulate RAAS –> higher level Ang II and vasoconstriction
31
Q

What are signs that hypertension might be due to aortic coarctation?

A
  • blood pressure discrepancy
  • midsystolic murmur
  • rib notching on CXR= collaterals
32
Q

What is pheochromocytoma? how does it cause HTN?

A
  • catecholamine-secreting tumor
  • release NE/E –> vasoconstriction + tachycardia
  • have palpitations/tachy/headache
  • diagnose based on catecholamine level in serum/urine
33
Q

What is treatment for pheochromocytoma?

A

surgical resection

alpha and beta blockade

34
Q

What are endocrine causes of secondary hypertension?

A

too much Ne/E –> pheochromocytoma

too much aldosterone –> primary [conn syndrome] or secondary [renin secreting tumor]

too much cortisol [Cushing]

35
Q

How do you differentiate between primary and secondary aldosteronism as cause for HTN

A

primary = conn syndrome = adrenal adenoma or hyperplasia adrenal glands –> high aldosterone so suppresses renin
= high ratio aldosterone:renin

secondary = renin secreting tumor –> lots of renin –> causes lots of aldosterone
= low ration ald:renin

36
Q

Why does cushing syndrome cause HTN?

A
  • excess cortisol stimulates RAAS

also have: round face, central obesity, prox muscle weakness

37
Q

how does hyperthyroidism cause HTN?

A
  • cardiac hyperactivity/high HR –> increase BP/blood volume
38
Q

how does hypothyroidism cause HTN?

A

diastolic hypertension

increase in peripheral vascular resistance

39
Q

What medications/drugs cause HTN?

A
  • oral contraceptives
  • glucocorticoids
  • erythropoetin
  • sympathetomimetics [OTC cold remedies]
  • alcohol
  • cocain
40
Q

What are consequences of chronic HTN?

A

physio/structural derangements - increase work of heart, arterial damage, loss of elasticity, endothelial dysfunction

41
Q

How much does CV risk change with each increase in 20/10 mmHG BP increment?

A

doubles

42
Q

What are cardiac effects of HTN?

A

ventricular hypertrophy due to high afterload –> ventricular stiffness –> diastolic HF

CAD: HTN –> development atherosclerosis –> decreased myocardial O2 supply –> increased work

43
Q

Is most common form of heart failure in elderly diastolic or systolic?

A

diastolic

44
Q

What is hemorrhagic stroke?

A

rupture microaneurysms induced by long-standing HTN

45
Q

What is ischemic stroke?

A

thrombosis of atherosclerotic plaque in cerebral vessel –> get embolism of plaque which causes ischemia

46
Q

What is aortic aneurysm? Where is it usually found?

A

prominent abnormal aortic dilation
most common in abdominal below level of renal arteries

if it ruptures you die

associated with HTN

47
Q

What is aortic dissection?

A

ripping between intima and media in aorta; can be in ascending or descending aorta

high mortality

associated wtih HTN

48
Q

What is a hypertensive urgency?

A

SBP > 180 or DBP > 110 without evidence of end-organ damage

need immediate evaluation but does not need hospital admission

49
Q

What is hypertensive emergency?

A

severe HTN [SBP > 180, DBP > 110] with evidence of acute organ damage

need immediate hospitalization

50
Q

What are symptoms of hypertensive emergency

A
  • hypertensive encephalopathy = mental status changes, headache, blurred vision
  • SOB [pulm edema]
  • papilledema on fundoscopy
51
Q

What does it mean if abnormal K in HTN?

A

sign of too much aldosterone –> may be primary or secondary aldosteronism or renovascular problem

52
Q

What are non-pharm treatments for HTN?

A
  • weight [each 10 kg = 5-20 mmHG drop in BP]
  • exercise
  • diet
  • salt restriction < 6g/day
53
Q

Why give a diuretic in HTN? For who?

A
  • decrease circulating volume, CO
  • give in mild-moderate HTN with normal renal function
  • good for uncomplicated HTN
54
Q

Why give Beta blocker in HTN? For who?

A
  • reduce HR and contractility –> reduce CO + decrease renin

- reduces mortality if you’ve had MI or in heat failure

55
Q

What are side effects of beta blockers?

A

bronchospasm [asthma], fatigue, sex effects

56
Q

Why give alpha-2 adrenergic agonists in HTN?

A

Reduce sympathetic outflow

poor side effects, dont usually use

57
Q

Why give alpha 1 antagonists in HTN?

A

sympatholytic
relaxes smooth muscle + reduces prostatic enlargement

= good for older men

58
Q

What meds do you give if primary essential uncomplicated HTN?

A
  • diuretics
  • ACE inhibitors/ARBs
  • Ca channel blockers
59
Q

What meds do you give f HTN with CHF?

step1

A
  • diuretics
  • ACE inhibitors/ARBs
  • beta blockers in compensated
  • aldosterone antagonists [spirinolactone]
60
Q

What meds do you give if HTN with DM?

step1

A
  • ACEI/ARBs = main b/c protects against diabetic nephropathy
  • Ca channel blockers
  • diuretics
  • b blcokers
  • a blockers
61
Q

Why do you give ACE inhibitor in HTN?

A

reduce mortality in pts with acute MI, chronic HF or at high risk for vascular disease

good for diabetic nephropatyn

side effects = dry cough, hyperkalemia

62
Q

When do you use spironolactone?

A

in symptomatic heart failure for HTN

mech = aldosterone blockade

63
Q

When do you use eplerenone?

A

in pt with acute MI complicated by heart failure

= aldosterone blockade

64
Q

What med for HTN pt pos-MI?

A

give beta blocker

65
Q

What med for HTN if chronic kidney disease?

A

ACEI/ARB

66
Q

What med for HTN might you avoid in woman of child bearing age

A

ACE-I = teratogenic

67
Q

Who should you be cautious about prescribing diuretics?

A

elderly = susceptible to dehydration