B4.041 Hypertension Flashcards

1
Q

what are some factors that contribute to abnormal lipid values?

A

high saturated fat and trans fat intake
high simple carb intake
genetic factors
overweight and inadequate exercise

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2
Q

EKG findings consistent with hypertension

A

LAD, high QRS voltage, left ventricular hypertrophy

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3
Q

interaction between high salt diet and hydrochlorothiazide

A

increased excretion of potassium

can lead to development of hypokalemia

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4
Q

interaction between caffeine and hydrochlorothiazide

A

augmented diuretic effect leading to dehydration

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5
Q

discuss the dose dependent effects of hydrochlorothiazide

A

effects n HTN level off around 12.5 mg

any dose above 12.5 mg furthers K+ excretion effects but doesn’t help HTN anymore

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6
Q

what is the “cornerstone of management” in HTN

A

therapeutic lifestyle change

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7
Q

categories of BP measurements

A

normal
elevated
stage 1 HTN
stage 2 HTN

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8
Q

how many measurements do you need to make a diagnosis of HTN?

A

> 2 readings on >2 occasions
out of office and self monitoring measurements are recommended to confirm diagnosis and for medication titration purposes

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9
Q

old HTN definition

A

diastolic > 90

systolic > 140

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10
Q

summarize epidemiology of HTN in the US

A

1 in 3 adults have high BP, only 54% have it under control
1 in 3 have prehypertension
$46 billion in health care costs per year

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11
Q

new HTN definition

A

diastolic > 80

systolic > 130

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12
Q

what is prehypertension under the new definition

A

120-129/<80

increased risk of developing HTN and cardiovascular complications, but benefits of treatment undertain

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13
Q

what is malignant HTN

A

extremely high BP that develops rapidly and causes some type of organ damage
typical BP above 180/120
treated as a medical emergency

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14
Q

risk factors and prevalence of malignant HTN

A

rare, 1% of people with history of high BP

greater risk if man, black, lower economic status, or poor access to health care

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15
Q

causes of malignant HTN

A
collagen vascular disease (scleroderma)
kidney disease
spinal cord injuries
adrenal gland tumors
use of birth control pills or MAOIs
use of illegal drugs, such as cocaine, amphetamines
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16
Q

for an adults 45 years old without HTN, what is the 40 year risk of developing HTN

A

93%, African American
92% Hispanic
86% white
84% chinese

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17
Q

association between CVD and BP

A

20 mm Hg higher SBP and 10 mm Hg higher DBP are each associated with a doubling in the risk of death from stroke, heart disease, or other vascular disease

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18
Q

medical diagnoses which have higher risks that are associated with higher SBP and DBP

A
CVD
angina
MI
heart failure
stroke
peripheral arterial disease
abdominal aortic aneurysm
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19
Q

other CVD risk factors to screen for in adults with HTN

A
smoking
diabetes
dyslipidemia
excessive weight
poor fitness
unhealthy diet
psychosocial stress
sleep apnea
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20
Q

basic testing for primary HTN

A
fasting blood glucose
CBC
lipids
BMP (electrolytes and creatinine)
TSH
urinalysis
EKG w/ optional echo
uric acid
urinary albumin to creatinine ratio
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21
Q

cause of HTN

A
underlying mechanism(s) responsible for the increase in CO, TPR, or both that results in high BP
knowing that CO, TPR or both are elevated does not define the cause of HTN
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22
Q

factors which contribute to the development of HTN

A
aging
genetics
obesity
smoking
salt sensitivity
high, frequent alcohol consumption
high fat diet
low fiber diet
lifestyle/environmental influences
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23
Q

primary HTN

A

underlying cause is unknown
likely an interaction of multiple defects in BP regulation w environmental stressors
may be genetic predisposition
more than 95% of cases

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24
Q

secondary HTN

A

underlying cause is known

5% of cases

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25
Q

2 possibilities of primary HTN causes

A
  1. abnormal function of the Na/K ATPase resulting in elevated cytosolic Ca2+ level
  2. microvascular dysfunction: decreased levels of NO and increased endothelin-1
26
Q

result of decreased NO or increased endothelin 1

A

arteriolar constriction
increased TPR
increased MAP

27
Q

discuss the trends in essential HTN and aging

A

at younger age, CO contributes most to HTN and decreases as patient ages
at old age, TPR contributes most to HTN and decreases as patients are younger

28
Q

why does TPR contribute more to HTN as people age

A

heart and vessels adapt to chronically high pressure

  • arterioles hypertrophy which reduced lumen diameter and increase contractile force (progressive increase in TPR over time)
  • decreased ventricular compliance due to ventricular hypertrophy, impairs diastolic filling of the heart
29
Q

examples of conditions causing secondary HTN

A
renal parenchymal disease
renovascular disease
pheochromocytoma
primary hyperaldosteronism
hypothyroidism
hyperthyroidism
30
Q

discuss the pathophys of HTN in renal parenchymal disease

A

nephron damage leads to impaired renal excretion of sodium and thus water
increased blood volume > increased venous pressure > increased venous return > increased preload > increased SV > increased CO > increased MAP

31
Q

discuss the pathophys of HTN in renovascular HTN

A

atherosclerotic plaques in renal arteries > impaired renal blood flow > activation of renin-angiotensin system

32
Q

what are the effects of increased renin and thus angiotensin II formation?

A

arteriolar constriction > increased TPR
venous constriction > increased CO
aldosterone secretion > increased blood volume > increased CO

33
Q

discuss the pathophys of HTN in pheochromocytoma

A

catecholamine secreting tumor in the adrenal medulla > increased epi and NE in the blood

34
Q

what are the effects of increased epi and NE in the blood?

A

arteriolar constriction > increased TPR
venous constriction > increased CO
increased inotropic state> increased CO
increased HR > increased CO

35
Q

what is primary hyperaldosteronism?

A

Conn’s syndrome
66% of cases due to enlargement of both adrenal glands
33% of cases due to an adrenal adenoma that produces aldosterone

36
Q

discuss the different layers of the adrenal glands and their function

A

outermost > innermost
zona glomerulosa (cortex) - mineralcorticoids - aldosterone
zona fasiculata (cortex) - glucocorticoids - cortisol, corticosterone, cortisone
zona reticularis (cortex) - androgens - dehydroepiandrosterone
adrenal medulla - stress hormones - epi, NE

37
Q

what are 2 causes of primary hyperaldosteronism and how do treatments differ

A

adrenal gland tumor- gland is removed

adrenal hyperplasia- aldosterone antagonist given

38
Q

discuss the pathophys of HTN in primary hyperaldosteornism

A

increased aldosterone > increased sodium and water reabsorption from kidneys > increased blood volume > increased CO

increased aldosterone> increased potassium excretion > hypokalemia > skeletal muscle weakness

39
Q

discuss the pathophys of HTN in hypothyroidism

A

decreased metabolic rate > decreased production of metabolic vasodilators in systemic organs > increased TPR

40
Q

discuss the pathophys of HTN in hyperthyroidism

A

increased metabolic rate > increased O2 demand by systemic organs > increased CO

41
Q

discuss the baroreflex

A

homeostatic mechanism that helps to maintain BP at nearly constant levels
elevated BP > causes decrease in HR and thus BP
decreased BP > causes HR to increase and restore BP

42
Q

how does baroreceptor desensitivity occur

A

cause is unknown
after chronic increases in arterial pressure, baroreceptor sensitivity to changes in arterial pressure is decreased compared to a normotensive person

43
Q

physiologic dysfunction of the heart in development of HTN

A

high CO due to abnormal neuronal or hormonal stimulation may contribute to HTN

44
Q

physiologic dysfunction of blood vessels in development of HTN

A
  1. greater than normal sym vasoconstrictor responses
  2. abnormal reg of vascular tone by local metabolic vasodilators
  3. ion channel defects in vascular SM
  4. endothelial dysfunction
  5. increased circulating levels of vasoconstrictors
45
Q

physiologic dysfunction of kidney in development of HTN

A
  1. impaired renal blood flow
  2. inappropriate hormone regulation (increased aldosterone release)
  3. ion channel defects causing sodium retention
  4. increased renin resulting in higher circulating angiotensin II
46
Q

physiologic dysfunction of baroreceptor in development of HTN

A

in a person with HTN, MAP will be maintained at a pressure higher than normal

47
Q

physiologic dysfunction of adrenal gland in development of HTN

A
  1. increased release of aldosterone will raise blood volume and CO
  2. in pheochromocytoma, excessive NE and epi will increased TPR and CO
48
Q

heart damage from HTN

A

workload is increased and oxygen delivery is compromised
ventricular hypertrophy and higher arterial pressure significantly increases myocardial O2 consumption, reduced ventricular compliance, increases filling pressures, and can lead to systolic or diastolic dysfunction and ultimately heart failure

49
Q

arterial damage from HTN

A

combined effects of elevated pressure and accelerated atherosclerosis
high pressure may cause endothelial dysfunction
endothelial damage will promote plaque and thrombus formation
physical rupture of an artery (aneurysm) can also occur due to high arterial pressures

50
Q

lifestyle changes to reduce HTN risk factors

A
decrease body weight
reduced salt intake
exercise
reduced alcohol consumption and smoking
reduce chronic stress
biofeedback interventions
51
Q

first line therapy for stage 1 HTN

A

thiazide diuretics
CCBs
ACE inhibs or ARBs

52
Q

therapy for stage 2 HTN

A

2 first line drugs of different classes

53
Q

how can improved adherence to therapy be obtained

A

once daily dosing

combination therapy

54
Q

preferred diuretic

A

chlorthalidone

long half life and proven reduction of CVD risk

55
Q

what should not be used in combo

A

ACE inhib, ARBs, and direct renin inhib

56
Q

which drugs increase risk of hyperkalemia in CKD or with supplemental K+ or K+ sparing drugs

A

ACE inhib and ARBs

57
Q

which drugs should be discontinued during pregnancy

A

ACE inhib and ARBs

58
Q

which drugs cause edema

A

CCBs and dihydropyrodines

59
Q

side effects of non-dihydropyridine CCBs

A

bradycardia and heart block

avoid in HFrEF

60
Q

when are loop diuretics preferred

A

in HF and when GFR is < 30