ADVANCED PATHOPHYSIOLOGY EXAM 3
ACTUAL TEST PAPER COMPLETE
QUESTIONS AND SOLUTIONS TESTED
ANSWERS
◉ heart disease structure differences for women
Answer: -smaller size, increased stiffness (fibrosis, remodeling, etc.)
-more diffuse disease
-more plaque erosion versus rupture
-microemboli, rarefaction (drop out), disarray
◉ heart disease functional differences for women
Answer: -endothelial dysfunction
-smooth muscle dysfunction (raynauds, migraine, coronary artery
spasm)
-inflammation: plasma markers and vasculitis (takayasu's,
rheumatoid, SLE, CNSV, giant cell)
◉ symptomatic differences for women in heart disease
Answer: women rate angina pain as more intense, more often
described pain as throbbing, sharp, hot/burning, fearful, pressing
,more often reported pain/discomfort in neck area
◉ primary (essential; idiopathic) HTN
Answer: -90-95% of people with HTN, unknown cause
-results from complicated interaction btwn genetics and the
environment that increases vascular tone (increase peripheral
resistance) and blood volume, thus causing sustained increase in BP
◉ factors associated with primary HTN
Answer: family hx
advanced age
gender (men <50yo, women>50yo)
AA race
high dietary Na intake
glucose intolerance
sedinatry lifestyle
tobacco use
poor diet
◉ secondary HTN
Answer: 50-10% caused by underlying disease process that raises
peripheral vascular resistance or CO
,-renal parenchymal disease, renovascular disease, primary
aldosteronism, obstructive sleep apnea, drug or alcohol induced
◉ Isolated Systolic HTN
Answer: can be due to age-related aortic stiffening
◉ HTN in racial/ethnic minorities
Answer: prevalence in AA is higher
AA does not respond well to ACE inhibitors d/t decrease in renin
respond better to CCB and diuretic
◉ Stages of HTN
Answer: Normal: < 120/<80
Elevated: 120-129/<80
HTN stage 1: 130-139/80-89
Stage 2: >140/>90
HTN crisis: >180/>120
◉ hyperkinetic circulatory state
Answer: -revved up circulation
-increased cardiac output
-elevated blood pressure and elevated resting HR
, -increase in resting HR is thought to be a predictor of the
development of HTN even thought they may not clinically have it yet
◉ cardiac hypertrophy
Answer: enlargement of the heart
-associated with increased CO
-long standing uncontrolled HTN tend to develop LV hypertrophy,
and this was thought to be a compensatory mechanism
-hypertrophy may reflect a primary response to repeated neural
stim. So it could be an initiating mechanism of HTN
◉ t/f increased peripheral resistance is the hallmark of established
HTN
Answer: true
◉ heart myocardium injury r/t chronic HTN
Answer: MOI - increased workload combined with dimihnished
blood flow through coronary arteries
Effect:
-congestive heart failure
-LV hypertrophy
-LV dysfunction
-heart failure
ACTUAL TEST PAPER COMPLETE
QUESTIONS AND SOLUTIONS TESTED
ANSWERS
◉ heart disease structure differences for women
Answer: -smaller size, increased stiffness (fibrosis, remodeling, etc.)
-more diffuse disease
-more plaque erosion versus rupture
-microemboli, rarefaction (drop out), disarray
◉ heart disease functional differences for women
Answer: -endothelial dysfunction
-smooth muscle dysfunction (raynauds, migraine, coronary artery
spasm)
-inflammation: plasma markers and vasculitis (takayasu's,
rheumatoid, SLE, CNSV, giant cell)
◉ symptomatic differences for women in heart disease
Answer: women rate angina pain as more intense, more often
described pain as throbbing, sharp, hot/burning, fearful, pressing
,more often reported pain/discomfort in neck area
◉ primary (essential; idiopathic) HTN
Answer: -90-95% of people with HTN, unknown cause
-results from complicated interaction btwn genetics and the
environment that increases vascular tone (increase peripheral
resistance) and blood volume, thus causing sustained increase in BP
◉ factors associated with primary HTN
Answer: family hx
advanced age
gender (men <50yo, women>50yo)
AA race
high dietary Na intake
glucose intolerance
sedinatry lifestyle
tobacco use
poor diet
◉ secondary HTN
Answer: 50-10% caused by underlying disease process that raises
peripheral vascular resistance or CO
,-renal parenchymal disease, renovascular disease, primary
aldosteronism, obstructive sleep apnea, drug or alcohol induced
◉ Isolated Systolic HTN
Answer: can be due to age-related aortic stiffening
◉ HTN in racial/ethnic minorities
Answer: prevalence in AA is higher
AA does not respond well to ACE inhibitors d/t decrease in renin
respond better to CCB and diuretic
◉ Stages of HTN
Answer: Normal: < 120/<80
Elevated: 120-129/<80
HTN stage 1: 130-139/80-89
Stage 2: >140/>90
HTN crisis: >180/>120
◉ hyperkinetic circulatory state
Answer: -revved up circulation
-increased cardiac output
-elevated blood pressure and elevated resting HR
, -increase in resting HR is thought to be a predictor of the
development of HTN even thought they may not clinically have it yet
◉ cardiac hypertrophy
Answer: enlargement of the heart
-associated with increased CO
-long standing uncontrolled HTN tend to develop LV hypertrophy,
and this was thought to be a compensatory mechanism
-hypertrophy may reflect a primary response to repeated neural
stim. So it could be an initiating mechanism of HTN
◉ t/f increased peripheral resistance is the hallmark of established
HTN
Answer: true
◉ heart myocardium injury r/t chronic HTN
Answer: MOI - increased workload combined with dimihnished
blood flow through coronary arteries
Effect:
-congestive heart failure
-LV hypertrophy
-LV dysfunction
-heart failure
