NSG 530 CERTIFICATION EVALUATION
2026 EXAM QUESTIONS AND SOLUTIONS
◉ 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
◉ eyes (retinas) injury r/t chronic HTN.
Answer: MOI - retinal vascular sclerosis, increased retinal artery
pressure
effects:
-hypertensive retinopathy
-retinal exudates and hemorrhages
◉ aorta injury r/t chronic HTN.
Answer: MOI - weakened vessel wall
effects:
-dissecting aneurysm
◉ arteries of lower extremities injury r/t chronic HTN.
2026 EXAM QUESTIONS AND SOLUTIONS
◉ 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
◉ eyes (retinas) injury r/t chronic HTN.
Answer: MOI - retinal vascular sclerosis, increased retinal artery
pressure
effects:
-hypertensive retinopathy
-retinal exudates and hemorrhages
◉ aorta injury r/t chronic HTN.
Answer: MOI - weakened vessel wall
effects:
-dissecting aneurysm
◉ arteries of lower extremities injury r/t chronic HTN.
