Hypertension Flashcards

1
Q

HTN risk factors

A

Age

Genetics

Diabetes and dyslipidemia

African American race

CKD

Excessive alcohol intake

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2
Q

avg arterial blood pressure during normal flow

A

90mm hg

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3
Q

systole hemodynamics

A

pressure in arteries increase

heart pumps blood into arterial system

wall of the arteries stretch

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4
Q

diastole

A

recoil elasticity of vessel

forces blood out and into the capillaries

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5
Q

minimum diastolic pressure

A

70-80 mmHg

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6
Q

maximum systolic pressure

A

110-120

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7
Q

BP regulation depends on

A

cardiac output and peripheral vascular resistance

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8
Q

cardiac output impact on BP

A

affected by sodium intake, renal function, mineralocorticoids

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9
Q

peripheral vascular resistance

A

dependent upon sympathetic nervous system, humoral factors, local vasculature autoregulation

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10
Q

inotrope

A

strength of contraction

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11
Q

chronotrope

A

beats per minute

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12
Q

after load

A

force heart exerts to overcome peripheral resistance

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13
Q

short term BP regulation (systems?)

A

neural

humoral

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14
Q

neural short therm BP control

A

baroreceptors and chemoreceptors (O2, CO2, H+) in carotids and aorta to determine response

acts on vagus n. to DECREASE HR
acts on sympathetic n. to INCREASE HR and tone

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15
Q

humoral BP control

A

RAAS promotes water retention and ADH vasoconstricts and decreases water loss

directly increases HR, contractility, vascular tone

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16
Q

long term BP control

A

kidney

regulates pressure around an individual set point

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17
Q

how is BP elevated?

A

hydrostatic pressure

widespread arteriolar vasoconstriction

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18
Q

normal BP

A

systolic less than 120

diastolic less than 80

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19
Q

prehypertension

A

120-139 systolic/ 80-89 diastolic

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20
Q

hypertension stage 1

A

systolic 140-159 or diastolic 90-99

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21
Q

hypertension stage 2

A

systolic > 160, diastolic > 100

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22
Q

isolated systolic HTN

A

BP is >140/<90

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23
Q

isolated diastolic HTN

A

<140/>90

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24
Q

hypertensive urgency

A

BP at or above 180/120 with NO end organ damage

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25
Q

hypertensive emergency

A

evidence of impending or progressive target organ dysfunction

at or above 180/120

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26
Q

neurological HTN damage (4)

A

hypertensive encephalopathy

cerebrovascular accident (stroke)

subarachnoid hemorrhage

intracranial hemorrhage

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27
Q

cardiac end organ damage

HTN

A

myocardial ischemia/infarction

acute left ventricular dysfunction

acute pulmonary edema

aortic dissection

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28
Q

other hypertensive emergencies

A

acute renal failure/insufficiency

hypertensive retinopathy

pre-eclampsia/eclampsia

microangiopathic hemolytic anemia

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29
Q

diagnosis of HTN

A

must see provider 2x

initial (if 180- dx)

then come back for several random checks and then review with provider in 3 weeks

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30
Q

non-dippers

A

failure of BP to decrease nocturnally

confers a cardiovascular disease risk

31
Q

younger patients and HTN risk

A

diastolic BP is most closely associated with CV risk

32
Q

older adults and HTN risk

A

older adults typically have isolated systolic HTN

adults over 60- BP remains primary determiner of CV risk

33
Q

African Americans and HTN

A

HTN that is more responsive to sodium intake, obesity, and diet

younger pts have more severe HTN than older

vulnerable to strokes and HTN kidney disease

3-5 times as likely ot have renal complications and end stage kidney disease

34
Q

HTN classifications

A

primary or secondary

90-95% are primary

35
Q

resistant HTN

A

typically secondary HTN

uncontrolled BP while on meds from 3+ drug classes (and one is a thiazide diuretic)

36
Q

secondary HTN etiologies

A
  1. CKD
  2. polycystic kidney disease
  3. renal artery stenosis
  4. coarctation of aorta
  5. thyroid dz
  6. pheochromocytoma
  7. primary hyperaldosteronism
  8. medication
37
Q

renal disease and secondary HTN

A

CKD- mc cause

PCKD - large size of kidneys

both have lo GFR and can’t be reversed

38
Q

renal artery stenosis

A

renovascular HTN

caused by arteriosclerosis in men and fibromuscular dysplasia in women

constant RAAS activation

39
Q

when do you suspect renal artery stenosis

A

suspect if AKI with imitation of ACEI/ARD, refractory HTN, recurrent flash pulmonary edema, abdominal bruit

40
Q

contraction of aorta

A

uncommon cause of secondary HTN

suspect if UE pulses and BP are higher than LE BP

41
Q

medications that cause secondary HTN

A

ethanol

illicit drug use

estrogens

ephedra/pseudoephedrine

black licorice or licorice root

42
Q

prehypertension history

A

asymptomatic increase in CO and intermittently elevated BP

43
Q

early HTN history

A

persistently increased peripheral resistance

44
Q

possible mechanisms causing HTN (6)

A
  1. sympathetic N.s. hyperactivity
  2. genetics
  3. reduced adult nephron mass
  4. sodium intake
  5. immunologic
  6. cardiac manifestations
45
Q

sympathetic NS hyperactivity and HTN

A

over activity of sympathetic tone leads to increased vascular tone and HTN

46
Q

sodium intake and HTN

A

increased salt intake triggers increase in BP that promotes increased natriuresis

brings BP up to basal levels

47
Q

diseases that contribute to HTN (9)

A
  1. obesity
  2. sleep apnea
  3. cigarette smoking
  4. alcohol
  5. lack of exercise
  6. immune system activation
  7. polycythemia
  8. increased salt intake
  9. NSAIDs
48
Q

obesity HTN

A

associated with increase in intravascular volume, cardiac output, activation of RAAS, increased sympathetic outflow

lowers BP modestly

49
Q

cigarette smoking and HTN

A

raises BP by increasing plasma norepinephrine and synergistic effect of smoking and high BP on CV risk

50
Q

alcohol and HTN

A

raises BP

increasing plasma catecholamines

can be difficult to control in alcoholics

51
Q

vascular remodeling and HTN

A

increased after load causes increased arterial wall stiffness, increased systolic BP, widened pulse pressures

decrease coronary perfusion pressures, increased myocardial O2 consumption, hypertrophy of left vent myocytes

52
Q

steps in cardiac decline due to HTN (awk. phrasing but what happens first, second and third)

A
  1. left ventricle hypertrophy
  2. diastolic dysfunction
  3. systolic dysfunction
53
Q

left ventricle hypertrophy

A

left ventricle muscle gets thicker so that the heart can pump more strongly against the elevated pressure

increased risk of premature death and morbidity

54
Q

diastolic dysfunction

A

incomplete passive relaxation of stiff hypertrophied left ventricle

less space to go in

55
Q

cerebral auto regulation of BP

A

ability of vasculature to maintain constant cerebral blood flow across wide range of perfusion pressure

56
Q

cerebral auto regulation and HTN

A

when chronic HTN present, CNS becomes accustomed to elevated perfusion pressures
therefore more prone to cerebral ischemia when BP/flow decreases

57
Q

CNS auto regulation and HTN tx

A

pts with longstanding HTN

can be just as dangerous to lower their BP too precipitously as it is to let it stay elevated

can cause ischemia (too low) or edema (too high)

58
Q

chronic HTN and the kidney

A

causes pathologic sclerotic changes in kidney

endothelial cell dysfunction and impaired vasodilation

alters auto regulation of blood flow to glomerulus and is instead affected by systemic arterial pressure

volume expansion is main cause

59
Q

in patients with vascular disease, HTN is the result of (kidney)

A

activation of RAAS

secondary to tissue ischemia

volume expansion and activation of system is believed to be cause of HTN with chronic renal failure

60
Q

RVHT

A

occurs when there is complete or partial vascular occlusion of a renal artery

RAAS Is activated by kidney with low blood flow

hyerreninemia promotes conversion of angiotensin I to angiotensin II = severe vasoconstriction and aldosterone release

61
Q

CV risk factors

A
tobacco use 
diabetes mellitus 
obesity 
lack of exercise 
elevated LDL 
>55 (men) or >65 (women) 
GFR <60 
microalbuminuria 
family hx
62
Q

prescription drugs causing drug induced HTN

A
NSAIDS 
psych meds 
migraine meds
high dose OCs 
pseudoephedrine
63
Q

situations w/prescriptions drug causing drug induced HTN

A

b- blockers without alpha blocker first when treating cocaine induced HTN or pheo

64
Q

street drugs or other causing drug induced HTN

A

cocaine
cocaine withdrawal
narcotic withdrawal
st. john’s wort

65
Q

diagnostic HTN work up

A
urinalysis 
fasting blood glucose 
CBC
electrolytes 
fasting lipids 
baseline EKG
66
Q

HTN target

general population

A

<140/90

  • under 60 = <150/90
67
Q

HTN target

80+

A

<150/90

68
Q

HTN target

Diabetics Mellitus

A

<130/80

69
Q

HTN target

CKD

A

<130/80 `

70
Q

lifestyle modifications in HTN

A
weight loss
DASH diet
reduced salt intake 
exercise
alcohol
71
Q

tx goal of essential HTN

A

lifestyle and if insufficient, drug tx

reduction in CV and renal morbidity and mortality

72
Q

HTN tx and drug chosen

A

mortality benefit for HTN related to AMOUNT lowering, not drug chosen

SO look at compelling indications and try to reduce # of pills

73
Q

compelling indications (def + 6)

A

specific classes of drugs that should be initiated where evidence based survival benefit

  1. heart failure
  2. high CAD risk
  3. CKD
  4. Post Myocardial Infarction
  5. Diabetes Mellitus
  6. Recurrent Stroke Prevention