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Clin Med - Cardio I > Hypertension - Washington > Flashcards

Hypertension - Washington Flashcards

1
Q

how often does preHTN develop into Stage I HTN

A

50% of people within 4 years therefore monitored closely!

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2
Q 
what are BP readings for the following:
Normal
PreHTN
Stage I HTN
Stage II HTN
Isolated systolic HTN
A
  1. Normal: sys /= 160 OR dias >/= 100

5. isolated systolic HTN: >/= 140 AND dias

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2
Q

what type of monitoring best correlates with target organ damage

A

home BP monitoring

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4
Q

what is more common diastolic or systolic HTN

A

in pts under 50 = combined sys and dias HTN

in pts over 50 = usually systolic HTN

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5
Q

most common dx in primary care

A

HTN

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6
Q

HTN in more common in what ethnicities

A

blacks more than whites

  • appears earlier
  • more severe
  • higher rates of morbidity and mortality
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7
Q

what does HTN do to the risk of CV dz

A

HTN doubles the risk for CV dz

-including CHD

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8
Q

what is likely to happen to the number of patients with HTN

A

likely will rise due to aging population and rising obesity

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9
Q

after age 60 who is more likely to have a higher SBP, males or females?

A

females

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10
Q

what happens to SBP as we age?

A

increases

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11
Q

definition of HTN

A

systolic >140
diastolic >90
over 2+ occasions over one to several weeks to dx HTN

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12
Q

what happens to pulse pressure as we age?

A

greater widening of pulse pressure after 55

pulse pressure is difference bw systolic and diastolic = systolic is increasing, diastolic is decreasing

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13
Q

which BP is a better predictor of morbid events in older patients, SBP or DBP?

A

SBP

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14
Q

which BP is more helpful for CV risk in younger population without comorbidities, SBP or DBP?

A

DBP

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15
Q

why is there such a low rate of control of HTN?

A

poor access to health care and meds
lack of adherence with long term therapy
“silent dz”

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16
Q

4 major complications of HTN

A
  1. HTN CardioV Dz
  2. HTN CerebroV Dz and dementia
  3. HTN kidney Dz
  4. atherosclerotic complications
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17
Q

HTN Cardiovascular Dz

  • morality?
  • progression of dz?
A

most common cause of death in HTN pts

results in LVH -> CHF ->ventricular arrhythmias ->myocardial ischemia ->sudden death

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18
Q

occurrence of CHF can be reduced by how much with antiHTN therapy in HTN cardiovascular DZ?

A

50%

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19
Q

what happens to LVH with antiHTN therapy?

A

regresses therefore preventable dz

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20
Q

HTN cerebrovascular DZ and dementia

  • mortality?
  • what is the most common risk factor for ischemic and hemorrhagic stroke?
  • what risk is associated with higher incidence of both vascular and Alzheimer types of dementia?
  • correlates with SBP or DBP?
A
  • 2nd most common cause of death in world
  • HTN
  • HTN
  • SBP
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21
Q

what happens to the risk of stroke when treated with pharmacologic therapy

A

risk decreases - preventable

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22
Q

HTN kidney Dz

  • kidney is a target or a cause of HTN?
  • what is the most common etiology of secondary HTN?
  • effect of HTN on kidney?
  • more common in which race?
  • what is a reliable marker of severity of kidney disease
  • what can slow progression of kidney dz
  • correlates to SBP or DBP?
A
  • kidney is both a target and a cause of HTN
  • primary renal dz
  • renal injury and end stage renal dz
  • blacks more than whites
  • proteinuria
  • aggressive control of BP =130/80
  • SBP
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23
Q

atherosclerotic complications of HTN

  • what is a target of these complications
  • mortality?
  • effect of antiHTN therapy
  • how to control?
  • what conditions can this cause?
A
  • blood vessels may be a target organ for this secondary to long standing elevated BP
  • most pts with HTN die of complications of atherosclerosis
  • antiHTN therapy has little effect
  • reduction of atherosclerosis requires control of multiple risk factors
  • aortic aneurysms/dissections
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24
Q

3 types of HTN

A
  1. primary or essential HTN
  2. white coat syndrome
  3. secondary HTN
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25
what is essential primary HTN - % of pts with HTN - etiology? what contributes to it? - onset ages - what happens to prevalence with age?
- 80-95% of pts with HTN - no single reversible cause - specific etiology unknown - genetic and environmental factors - onset bw 25-55 yo - prevalence increases with age
26
risk factors for HTN
``` race (blacks) age (>55 men, >65 women) - women menopause = decr estrogen = estrogen helps keep heart healthy first degree relative with HTN obesity/weight gain diet high in sodium excess ETOH metabolic syndrome smoking inactivity dislipidemia polycythemia vitD deficiency low K intake ```
27
what is white coat HTN - % of pts with stage I office HTN - how to rule out real HTN? - best type of monitoring for these pts?
-20-25% pts with stage I office HTN -repeated normal HTN at home work or ambulatory BP monitoring ps have an increased risk of developing sustained primary HTN -ambulatory BP monitoring is useful in these cases
28
causes of secondary HTN
``` primary renal dz drug induced renal artery stenosis adrenal dz other endocrine disorders obstructive sleep apnea coarctation of the aorta pregnancy rare genetic disorders ```
29
what is the most common cause of secondary HTN
renal parenchymal dz (CKD)
30
drugs that can induce secondary HTN
``` oral contraceptives NSAIDS antidepressants decongestants cocaine glucocorticosteroids ```
31
renal artery stenosis is secondary to what causing HTN
arteriosclerosis - older pts with obstructing plaque | fibromuscular dysplasia - young white women, unilateral or bilateral
32
definitive diagnostic test for renal artery stenosis
renal arteriography
33
how is renal artery stenosis treated
meds or surgery
34
renal artery stenosis should be suspected if:
1. onset of HTN before age 20 or after age 50 2. HTN is resistant to 3+ drugs 3. epigastric or renal bruits 4. atherosclerotic dz 5. abrupt increase in SCr after administrtion of ACE-I 6. episodes of pulmoary edema associated with abrupt surge in BP
35
how does a pheochromocytoma cause secondary HTN
catecholamine secreting tumor in adrenal gland
36
how does primary aldosteronism cause secondary HTN | -when should it be suspected?
- increased aldosterone production results in sodium retention, HTN, hypokalemia, and low plasma renin activity - should be suspected in in any pt with a triad of HTN unexplained hypokalemia and metabolic alkalosis
37
how does cushing's syndrome cause secondary HTN? | -HTN occurs in how many of these pts
- related to excess cortisol production d/t either excess ACTH secretion or to ACTH independent adrenal production of cortisol - HTN occurs in 75-80% of these pts
38
what other endocrine disorders can cause secondary HTN
hypothyroidism, hyperthyroidism, hyperparathyroidism
39
obstructive sleep apnea and HTN
occurs in >50% of pts | independent of obesity
40
what is the most common congenital cardiovascular cause of HTN
coarctation of the aorta
41
most common cause of maternal and fetal morbidity and mortality
pre eclampsia and eclampsia
42
when should blood pressure start being screened?
18 yo and older - to ID adults at increased risk of CV dz
43
how often should BP be monitored in pts with BP
every 2 years
44
how often should pts be checked if systolic BP is 120-139 or diastolic BP of 80-89?
yearly
45
proper way to take a blood pressure
sitting position with arm at level of heart after 5+ minutes of rest and 20-30 min after smoking/caffeine intake
46
how should the systolic pressures be in comparison of left to right arm
should be roughly equivalent
47
what if there is a discrepancy of >15mmHg bw left and right arms?
indicates subclavian stenosis --> peripheral artery dz
48
symptoms of HTN
1. silent dz - most pts do not have any symptoms 2. headache can occur in pts with severe HTN (morning and in occipital region) 3. nonspecific: dizzy, palpitations, easily fatigues and impotence
49
patient hx questions important for HTN
1. duration of HTN (if ongoing) 2. previous therapies (if any) responses and side effects 3. FH of HTN or CVD 4. dietary and psychosocial Hx 5. other risk factors - weight change, dyslipidemia, smoking, diabetes, physical inactivity, habits 6. evidence of secondary HTN - renal dz, change in appearance, muscle weakness, spells of sweating, palpitations, tremor, snoring, erratic sleep, s/s of thyroid dz 7. evidence of target organ damage - TIA, stroke, MI, CHF, kidney dz
50
what happens to diastolic BP as we age
rises until age 55, then tends to decrease
52
physical exam for HTN
``` body habitus weight, height, BMI BP in both arms HR fundoscopic exam thyroid & systemic signs of thyroid dz displaced apical impulse/PMI/LVH distal pulses auscultate heart bruits - carotid and femoral and abdominal kidneys signs of CHF neuro exam ```
53
s/s suggesting secondary HTN: arm to leg SBP difference >20mmHg with delayed or absent femoral pulses & murmur - possible cause and workup?
coarctation of the aorta MRI for adults transthoracic echo in children
54
s/s suggesting secondary HTN: increase in SCr >0.5 to 1mg after starting ACE-I or ARB with renal artery bruit -workup and possible cause
-renal artery stenosis -renal CT angiography doppler, ultrasonography of renal arteries, MRI
55
s/s suggesting secondary HTN: brady/tachycardia, cold/hot intolerance, constipations/diarrhea, heavy irregular or absent menstrual cycle -possible cause and workup
- thyroid dz | - thyroid function panel
56
s/s suggesting secondary HTN : hypokalemia -possible cause and workup
- aldosteronism | - renin and aldosterone levels to calculate ratio
57
s/s suggesting secondary HTN: apneic events during sleep, daytime somnolence, loud snoring -workup and possible cause
obstructive sleep apnea | -polysomnography (sleep study)
58
s/s suggesting secondary HTN: flushing, HAs, labile BP, orthostatic hypotension, palpitations, sweating, syncope -possible cause and workup
pheochromocytoma | -24 hr urinary fractionated metanephrines
59
s/s suggesting secondary HTN: buffalo hump, central obesity, moon facies, striae -possible cause and workup?
- cushing's syndrome | - 24 hr urinary cortisol late night salivary cortisol, low dose dexamethasone suppression
60
Labs for HTN
``` urinalysis CBC BMP (fasting) fasting lipids TSH EKG echocardiogram to assess LVH ```
61
lab testing for kidneys in HTN
microscopic urinalysis, albumin excretion, serum BUN and/or creatinine
62
lab testing for endocrine with HTN
serum sodium, potassium, calcium, TSH/Thyroid function
63
lab testing for metabolic issues for HTN
fasting blood glucose, lipid profile
64
HTN treatment
non pharmacological - lifestyle modifications (essential in all pts) pharmacological - multiple classes of medications available
65
treatment goals for HTN >60 yo 60 with isolated systolic HTN
>/= 60yo: 60 with isolated systolic HTN: do not lower DBP
66
primary goal of HTN treatment
prevent end organ damage
67
secondary goals of HTN treatment
minimize SEs, minimize pt cost, increase pt adherence, treat comorbid conditions
68
what 3 things need to be done if we determine our pt has HTN?
1. assess presence or absence of target organ damage and CVD 2. assess lifestyle (diet, exercise, habits) and ID other CV risk factors or current disorders that may affect prognosis and guide treatment 3. rule out identifiable/secondary causes of high BP (often curable)
69
benefits of treatment of HTN
1. lowering SBP by 10-12 mmHg and DBP by 5-6mmHg confers relative risk reduction (35-40% for stroke, 12-16% for CHD w/i 5 years of initiation of tx, risk of heart failure reduced by >50%) 2. HTN control is the single most effective intervention for slowing the rate or preogression of HTN-related chronic kidney dz
70
most common symptom if HTN is symptomatic
H/A
71
lifestyle modification
1. dietary salt restriction 2. weight loss 3. DASH diet 4. exercise 5. decreased alcohol intake 6. adequate vitD and K intake 7. limit NSAID 8. smoking cessation

Clin Med - Cardio I (7 decks)

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