ADVANCED PATHOPHYSIOLOGY
CERTIFICATION EVALUATION TEST 2026
QUESTIONS AND SOLUTIONS GUARANTEED
TO PASS
◉ 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
◉ coronary artery injury r/t chronic HTN. Answer: MOI - accelerated
atherosclerois, CAD
, effect:
-Myocardial ischemia
-myocardial infarction
-sudden death
◉ kidney injury r/t chronic HTN. Answer: MOI - reduced blood flow,
increased arteriolar pressure, RAAS and SNS stim, inflammation
effect:
-glomerulosclerosis
-decreased glomerular flow
-ESRF
-creatinine>1.5, proteinuria 1+, microalbuminuria
◉ brain injury r/t chronic HTN. Answer: MOI - reduced blood flow
and oxygen supply, weakened vessel walls, accelerated sclerosis
effects:
-transient ischemic attack
-cerebral thrombosis
-aneurysm
-hemorrhage
-acute brain infarction
CERTIFICATION EVALUATION TEST 2026
QUESTIONS AND SOLUTIONS GUARANTEED
TO PASS
◉ 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
◉ coronary artery injury r/t chronic HTN. Answer: MOI - accelerated
atherosclerois, CAD
, effect:
-Myocardial ischemia
-myocardial infarction
-sudden death
◉ kidney injury r/t chronic HTN. Answer: MOI - reduced blood flow,
increased arteriolar pressure, RAAS and SNS stim, inflammation
effect:
-glomerulosclerosis
-decreased glomerular flow
-ESRF
-creatinine>1.5, proteinuria 1+, microalbuminuria
◉ brain injury r/t chronic HTN. Answer: MOI - reduced blood flow
and oxygen supply, weakened vessel walls, accelerated sclerosis
effects:
-transient ischemic attack
-cerebral thrombosis
-aneurysm
-hemorrhage
-acute brain infarction
