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M2 Cardiology > 6. Hypertension > Flashcards

6. Hypertension Flashcards

1
Q

the morbidity/mortality of HTN is more based on systolic or diastolic pressure?

A

systolic

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2
Q

what happens to the risk of CV disease each time systolic pressure rises by 20 mmHg?

A

doubles

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3
Q

systolic BP of 120-139 or diastolic of 80-89 = labeled how?

A

prehypertensive

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4
Q

normal systolic and diastolic values?

A

<80

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5
Q

HTN is the major health problem of what group of americans?

A

African Americans

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6
Q

what is the formula for BP? BP = what?

A

CO x TPR

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7
Q

control of BP is function of what 2 major systems?

A

sympathetic, and RAAS

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8
Q

juxtaglomerular cells produce renin under what 3 circumstances?

A
  1. decr stretch in wall due to decr systemic pressure or renal artery stenosis
  2. reduced Na concentration in distal tubule (sign of hypovolemia)
  3. Beta receptor stimulation
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9
Q

what constricts the efferent arterioles?

A

Angiotensin II

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10
Q

Angiotensin II stimulates the adrenal gland to release what?

A

aldosterone (contributes to hypertension through sodium retention)

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11
Q

what are the 3 general hemodynamic patterns causing hypertension?

A
  1. overall increased BV
  2. incr CO
  3. incr peripheral vascular tone
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12
Q

incr total blood vol is associated with high or low renin?

A

low

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13
Q

appropriate therapy for HTN due to incr BV?

A

diuretics

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14
Q

possible specific causes of HTN due to incr blood volume?

A
  • primary hyperaldosteronism
  • excessive salt intake
  • renal disease with salt retention
  • Cushing’s disease
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15
Q

possible specific causes of HTN due to incr CO?

A
  • hyperthyroid (cardiac B1 stimulation)

- hyperkinetic heart syndrome?

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16
Q

appropriate therapy for HTN due to incr CO?

A

beta-blockers

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17
Q

possible specific causes of HTN due to incr peripheral resistance?

A
  • renovascular HTN
  • hyperthyroid (catecholamine excess)
  • hypothyroid (decr Beta2 receptors in arterioles)
  • malignant HTN (late phase of essential HTN)
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18
Q

incr peripheral resistance is associated with high or low renin?

A

high

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19
Q

appropriate therapy for HTN due to incr TPR?

A

vasodilators

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20
Q

what needs to be done in order to diagnose essential/primary hypertension?

A

rule OUT secondary HTN.

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21
Q

3 causes of secondary HTN?

A
  1. primary hyperaldosteronism
  2. pheochromocytoma
  3. renal artery stenosis (renovascular HTN)
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22
Q

what is the cause of primary hyperaldosteronism?

A

hyperplasia or adenoma of adrenal cortex/zona glomerulosa

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23
Q

how is primary hyperaldosteronism diagnosed?

A

low renin and incr aldosterone, along with low K (aldosterone is K wasting and Na sparing)

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24
Q

what does hyperaldosteronism cause (at the level of the kidney)?

A

incr sodium retention, incr potassium excretion. –> hypokalemia and metabolic acidosis

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25
Q

Pheochromocytoma: where do the tumors occur?

A

tumors can be found in a variety of locations but the main site is adrenal medulla.

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26
Q

what are we currently using as pressures to define a disease state of HTN?

A

140/90

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27
Q

the prevalance of HTN increases with what three things?

A
  1. age
  2. Af-Americans
  3. reduced education levels (HTN lowers with education level)
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28
Q

what is the characteristic pathology of pheochromocytoma?

A

pts will have intermittent spells of HTN with symptoms associated with incr catecholamines which they are excreting. they may secrete NE or Epi or both.

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29
Q

WTF are catecholamines?

A

dopamine, Norepi, epinephrine. sympathetic response neurotransmitters released by the adrenal glands

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30
Q

appropriate therapy for HTN due to pheochromocytoma?

A

surgery. will locate tumor via CT after finding metabolites in urine or serum.

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31
Q

Etiology of renal artery stenosis, and what popn they are most common in?

A

atherosclerosis: older men

fibromuscular hyperplasia: younger women

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32
Q

why does BP increase as a result of Renal artery stenosis?

A

fall in afferent arteriola pressure, jux apparatus releases renin, initiating response by renan-antiogensin system. BP rises are a result of increased AtII and aldosterone.

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33
Q

why might a pt have hypokalemia due to excess aldosterone secr?

A

aldosterone is K wasting

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34
Q

how might you dx renal artery stenosis?

A

sample blood from each renal vein and see which one is excreting more renin

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35
Q

what is coarctation of the aorta?

A

rare congenital lesion in which the proximal aorta is narrowed, resulting in diminished perfusion of the lower half of the body.

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36
Q

what BP pattern can you expect to see in coarctation of the aorta?

A

BP low in the legs and high in the arms.

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37
Q

why does coarctation of the aorta lead to HTN?

A

kidneys see diminished blood flow, act as if there is hypovolemia and secrete renin –> HTN.

38
Q

what is the leading theory as to why alcoholism can cause HTN?

A

stimulation of the sympathetic NS. though withdrawal from alcohol can also cause hypertension (it is another hyper-adrenergic state)

39
Q

what are some causes of essential hypertension (90-95% of pts)?

A

-genetic predisposition
-hyperactive SANS
-hyperactive RAAS
-increased intracellular sodium (maybe due to incr Na absorption or decr Na excretion)
vascular hypertrophy

40
Q

what are the 2 hemodynamic phases that pts tend to progress through in essential HTN?

A
  1. hyperkinetic. excessive CO and inc BV. BP is ‘labile’ ie sometimes high, sometimes low. renin tends to be low.
  2. established/late HTN. high peripheral vasc resistance. renin tends to be high.
41
Q

list a few consequences of HTN

A
  • risk factor for atherosclerosis
  • coronary disease
  • hypertensive heart disease
  • cerebrovascular atherosclerosis
  • aneurysms and cerebral hemorrhage
  • kidney problems
  • aortic dissection
  • hypertensive retinopathy
  • malignant HTN
42
Q

what are the most impt causes of morbidity and mortality in hypertensive patietns?

A
  • renal disease
  • MIs
  • strokes
43
Q

how does HTN lead to atherosclerosis?

A

mech presumable involves injury of arterial endothelium by arterial stretching. (this is why systolic pressure is most impt factor to consider)

44
Q

how does HTN lead to coronary disease?

A

via atherosclerosis which then causes CD.

45
Q

how does HTN lead to hypertensive heart disease?

A

leads to dev of concentric LV hypertrophy, which can lead to LV failure associated with diastolic dysfunction. LV can function ok but requires incr LA and pulmonary artery pressures in order to fill it up before contracting.

46
Q

what would be the presentation of severe LV hypertension (over years of hypertensive heart disease)?

A

dyspnea, pulm congestion S4 gallop

47
Q

arteriolar stenosis causes what in the kidney?

A

nephrosclerosis: thickening of the cap basement membrane, some hyalinazation, atrophy. hyalinazation due to inc pressure in the glomerular capillaries.

48
Q

describe aortic dissection

A

life threatening. blood-filled channel divides the medial layers of the heart, splitting the intima from the adventitia. HTN is usually the cause, but this is not related to atherosclerosis.

49
Q

describe the findings with hypertensive retinopathy

A

may have hemorrhage, exudate, cotton wool spots.

50
Q

describe malignant hypertension

A

viscous cycle where HTN leads to renal arteriolar sclerosis, which leads to inc renin release, which leads to more HTN. etc.

51
Q

what are 3 lifestyle changes that can act as non-drug HTN therapy?

A
  1. diet
  2. exercise
  3. relaxation therapy
52
Q

what dietary changes should someone with HTN make?

A

decr salt, decr alcohol intake. also, reduce obesity.

salt intake does not increase the incidence of HTN, but decr salt in already established HTN will help.

53
Q

what are the 8 categories of anti-HTN drugs?

A
  1. diuretics
  2. beta blockers
  3. central alpha-agonists
  4. Ca channel blockers
  5. direct vasodilators
  6. alpha blocking agents
  7. ACE inhibitors
  8. Angiotensin II blockers
54
Q

Diuretics: mechanism?

A

initial reduction in blood volume, followed by reduction of peripheral vascular resistance.

55
Q

diuretics: side effects?

A

hypovolemia, sodium and/or K depletion

56
Q

diuretics: drugs?

A

thiazides (HCTZ), loop diuretics (furosemide), K-sparing diuretics (spironolactone, triamterene)

57
Q

beta-blockers: mechanism?

A

reduction in CO and/or peripheral renin activity

58
Q

beta blockers: side effects?

A

precipitation of heart failure, depression, fatigue, bronchospasm

59
Q

beta blockers: drugs?

A

propanolol, metoprolol, atenolol

60
Q

central alpha-agonists: mechanism?

A

decr sympathetic outflow from the CNS –> decr cardiac output and or decr PVR.

61
Q

central alpha-agonists: side effects?

A

dry mouth, sedation, depr

62
Q

central alpha-agonists: drugs?

A

methyldopa, clonidine

63
Q

Ca channel blockers: mechanism?

A

reduction of CO and or PVR

64
Q

Ca channel blockers: side effects?

A

peripheral edema, heart failure

65
Q

Ca channel blockers: drugs?

A

diltiazem, verapamil, nifedipine

66
Q

direct vasodilators: mechanism?

A

reduction in PVR

67
Q

direct vasodilators: side effects?

A

reflex tachycardia (can precipitate angina), headache

68
Q

direct vasodilators: drugs?

A

hydralazine, minoxidil

69
Q

alpha blocking agents: mechanism?

A

reduction in PVR

70
Q

alpha blocking agents: side effects?

A

orthostatic hypotension

71
Q

alpha blocking agents: drugs?

A

prazosin

72
Q

converting enzyme inhibitors: mechanism?

A

ACH inh = inhibits conversion of angiotensin I to angiotensin II –> decr peripheral vascular resisgance, decr secretion of aldosterone.

73
Q

converting enzyme inhibitors: side effects?

A

cough, renal failure

74
Q

converting enzyme inhibitors: drugs?

A

captoprin, lisinopril

75
Q

Angiotensin II blockers: mechanism?

A

block Angiotensin II receptors

76
Q

Angiotensin II blockers: side effects?

A

none/no cough

77
Q

Angiotensin II blockers: drugs?

A

losartan

78
Q

Treatment of men with DBP > 115 reduces the combination of death and end organ damage from 30% per year to less than 3% per year - is effect of treatment in those with DBP between 90 and 115 as great?

A

no, substantially smaller.

79
Q

Pts with mile disease are more likely to experience what from treatment?

A

a net harm: because they have less opportunity to benefit.

80
Q

the degree of benefit from HTN treatment is related to what?

A

the level of BP prior to treatment, with clear benefits for severely HTN pts and less dramatic benefits for milder pts.

81
Q

what is the stepped care approach?

A

adding drugs in combinations, over a period of weeks/months in order to minimize side effects and allow for a gradual fall in BP

82
Q

what % of americans over 50 have HTN?

A

50%

83
Q

peripheral venous tone does what to systemic blood flow or location?

A

shifts blood from one compartment to another: affects distribution of blood volume between peripheral and pulmonary beds

84
Q

systemic venoconstriction does what to LV preload and CO?

A

increases left ventricular preload, thereby increasing cardiac output.

85
Q

increased peripheral arteriolar tone does what to BP

A

increases BP

86
Q

circulatory system is regulated by what two systems?

A

sympathetic nervous system and RAAS

87
Q

both angiotensin II and aldosterone do what to cardiac growth?

A

stimulate it by inc preload on LV.

88
Q

name three types of shock

A
  1. decr blood volume (hemorrhagic)
  2. decr peripheral venous tone (septic)
  3. decr CO (cardiogenic shock, due to MI)
89
Q

why would you have low renin with primary hyperaldosteronism?

A

feedback from the RAAS system

90
Q

Concentric hypertrophy is also called…

A

hypertensive heart disease

91
Q

what is a LV strain pattern on EKG?

A

Left Ventricular “Strain”: ST-depression & T-inversion in left ventricular leads: I, aVL, V5-6

M2 Cardiology (32 decks)

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