NSG 3280 Pathophysiology for Nurses -
Exam 3 Review (2026/2027 Update)
Pathophysiology for Nurses I Review
Questions and Answers Grade A 100%
NSG 3280 Pathophysiology for Nurses - Exam | Comprehensive
Examination
NSG 3280 Pathophysiology for Nurses - Exam 3 Review
(2026/2027 Update) Pathophysiology for Nurses I Review
Questions and Answers Grade A 100% Correct (Verified
INTRODUCTION
This document is an important and very helpful preparation
resource for NSG 3280 Pathophysiology for Nurses - Exam 3
Review (2026/2027 Update) Pathophysiology for Nurses I
Review Questions and Answers Grade A 100% Correct
(Verified Solutions) Instant pdf - Galen. Every item uses a
focused exam stem, four response options, a keyed response,
and a clear rationale, making it easier to understand the
subject, spot distractors, and build real exam confidence.
Page 1
, Question 1
A patient with severe sepsis develops hypotension unresponsive to fluids.
Which pathophysiologic mechanism best explains the persistent vasodilation?
A. Increased systemic vascular resistance due to sympathetic overdrive
B. Excessive nitric oxide production and ATP-sensitive potassium
channel activation
C. Enhanced baroreceptor sensitivity causing vagal withdrawal
D. Upregulation of alpha-1 adrenergic receptors on vascular smooth
muscle
Correct Answer: B - Excessive nitric oxide production and
ATP-sensitive potassium channel activation
RATIONALE
In septic shock, inflammatory mediators induce nitric oxide synthase,
leading to excessive NO and activation of ATP-sensitive potassium
channels, causing profound vasodilation and hyporesponsiveness to
catecholamines. The other options describe mechanisms that would
increase vascular tone or are not primary in sepsis.
Question 2
Which statement accurately distinguishes apoptosis from necrosis in the
context of ischemic injury?
A. Apoptosis is energy-dependent and involves caspase activation,
whereas necrosis is characterized by cellular swelling and inflammation.
B. Necrosis is programmed and mediated by Bcl-2 proteins, while
apoptosis triggers an inflammatory response.
C. Apoptosis results in loss of membrane integrity and release of
damage-associated molecular patterns.
D. Necrosis is a regulated process requiring ATP, whereas apoptosis is
always accidental and passive.
Correct Answer: A - Apoptosis is energy-dependent and involves
Page 2
,caspase activation, whereas necrosis is characterized by cellular
swelling and inflammation.
RATIONALE
Apoptosis is an active, energy-requiring process mediated by caspases
and regulated by Bcl-2 family proteins, typically without
inflammation. Necrosis involves ATP depletion, cell swelling,
membrane rupture, and inflammation. The other options reverse these
characteristics.
Question 3
In a patient with chronic kidney disease, which laboratory finding best
indicates the transition from reduced renal reserve to renal insufficiency?
A. Serum creatinine increase from 1.0 to 1.5 mg/dL
B. Glomerular filtration rate (GFR) declining from 90 to 60 mL/min/1.73
m²
C. Activation of the renin-angiotensin-aldosterone system with
hypertension
D. Development of anemia due to erythropoietin deficiency
Correct Answer: B - Glomerular filtration rate (GFR) declining
from 90 to 60 mL/min/1.73 m²
RATIONALE
Renal insufficiency is defined by a GFR between 60 and 89
mL/min/1.73 m² with evidence of kidney damage, often
asymptomatic. A GFR of 90 or above is normal; below 60 indicates
failure. The other options may occur but are not the defining
transition.
Question 4
Which pathophysiologic alteration is most directly responsible for the
development of hyperkalemia in metabolic acidosis?
Page 3
, A. Increased renal potassium excretion due to aldosterone stimulation
B. Shift of potassium from intracellular to extracellular fluid in exchange
for hydrogen ions
C. Enhanced insulin-mediated cellular uptake of potassium
D. Decreased gastrointestinal potassium absorption
Correct Answer: B - Shift of potassium from intracellular to
extracellular fluid in exchange for hydrogen ions
RATIONALE
In metabolic acidosis, excess hydrogen ions move into cells and
potassium shifts out to maintain electroneutrality, causing
hyperkalemia. Aldosterone and insulin would lower potassium, and GI
absorption is not a major acute regulator.
Question 5
A patient with heart failure has elevated B-type natriuretic peptide (BNP).
Which mechanism explains this finding?
A. Increased ventricular stretch due to volume overload
B. Reduced renal clearance of BNP
C. Systemic vasoconstriction from angiotensin II
D. Decreased sympathetic nervous system activity
Correct Answer: A - Increased ventricular stretch due to volume
overload
RATIONALE
BNP is released from ventricular myocytes in response to increased
wall stretch from volume or pressure overload. Renal clearance and
angiotensin II do not directly stimulate BNP release; sympathetic
activity would increase, not decrease, in heart failure.
Page 4
Exam 3 Review (2026/2027 Update)
Pathophysiology for Nurses I Review
Questions and Answers Grade A 100%
NSG 3280 Pathophysiology for Nurses - Exam | Comprehensive
Examination
NSG 3280 Pathophysiology for Nurses - Exam 3 Review
(2026/2027 Update) Pathophysiology for Nurses I Review
Questions and Answers Grade A 100% Correct (Verified
INTRODUCTION
This document is an important and very helpful preparation
resource for NSG 3280 Pathophysiology for Nurses - Exam 3
Review (2026/2027 Update) Pathophysiology for Nurses I
Review Questions and Answers Grade A 100% Correct
(Verified Solutions) Instant pdf - Galen. Every item uses a
focused exam stem, four response options, a keyed response,
and a clear rationale, making it easier to understand the
subject, spot distractors, and build real exam confidence.
Page 1
, Question 1
A patient with severe sepsis develops hypotension unresponsive to fluids.
Which pathophysiologic mechanism best explains the persistent vasodilation?
A. Increased systemic vascular resistance due to sympathetic overdrive
B. Excessive nitric oxide production and ATP-sensitive potassium
channel activation
C. Enhanced baroreceptor sensitivity causing vagal withdrawal
D. Upregulation of alpha-1 adrenergic receptors on vascular smooth
muscle
Correct Answer: B - Excessive nitric oxide production and
ATP-sensitive potassium channel activation
RATIONALE
In septic shock, inflammatory mediators induce nitric oxide synthase,
leading to excessive NO and activation of ATP-sensitive potassium
channels, causing profound vasodilation and hyporesponsiveness to
catecholamines. The other options describe mechanisms that would
increase vascular tone or are not primary in sepsis.
Question 2
Which statement accurately distinguishes apoptosis from necrosis in the
context of ischemic injury?
A. Apoptosis is energy-dependent and involves caspase activation,
whereas necrosis is characterized by cellular swelling and inflammation.
B. Necrosis is programmed and mediated by Bcl-2 proteins, while
apoptosis triggers an inflammatory response.
C. Apoptosis results in loss of membrane integrity and release of
damage-associated molecular patterns.
D. Necrosis is a regulated process requiring ATP, whereas apoptosis is
always accidental and passive.
Correct Answer: A - Apoptosis is energy-dependent and involves
Page 2
,caspase activation, whereas necrosis is characterized by cellular
swelling and inflammation.
RATIONALE
Apoptosis is an active, energy-requiring process mediated by caspases
and regulated by Bcl-2 family proteins, typically without
inflammation. Necrosis involves ATP depletion, cell swelling,
membrane rupture, and inflammation. The other options reverse these
characteristics.
Question 3
In a patient with chronic kidney disease, which laboratory finding best
indicates the transition from reduced renal reserve to renal insufficiency?
A. Serum creatinine increase from 1.0 to 1.5 mg/dL
B. Glomerular filtration rate (GFR) declining from 90 to 60 mL/min/1.73
m²
C. Activation of the renin-angiotensin-aldosterone system with
hypertension
D. Development of anemia due to erythropoietin deficiency
Correct Answer: B - Glomerular filtration rate (GFR) declining
from 90 to 60 mL/min/1.73 m²
RATIONALE
Renal insufficiency is defined by a GFR between 60 and 89
mL/min/1.73 m² with evidence of kidney damage, often
asymptomatic. A GFR of 90 or above is normal; below 60 indicates
failure. The other options may occur but are not the defining
transition.
Question 4
Which pathophysiologic alteration is most directly responsible for the
development of hyperkalemia in metabolic acidosis?
Page 3
, A. Increased renal potassium excretion due to aldosterone stimulation
B. Shift of potassium from intracellular to extracellular fluid in exchange
for hydrogen ions
C. Enhanced insulin-mediated cellular uptake of potassium
D. Decreased gastrointestinal potassium absorption
Correct Answer: B - Shift of potassium from intracellular to
extracellular fluid in exchange for hydrogen ions
RATIONALE
In metabolic acidosis, excess hydrogen ions move into cells and
potassium shifts out to maintain electroneutrality, causing
hyperkalemia. Aldosterone and insulin would lower potassium, and GI
absorption is not a major acute regulator.
Question 5
A patient with heart failure has elevated B-type natriuretic peptide (BNP).
Which mechanism explains this finding?
A. Increased ventricular stretch due to volume overload
B. Reduced renal clearance of BNP
C. Systemic vasoconstriction from angiotensin II
D. Decreased sympathetic nervous system activity
Correct Answer: A - Increased ventricular stretch due to volume
overload
RATIONALE
BNP is released from ventricular myocytes in response to increased
wall stretch from volume or pressure overload. Renal clearance and
angiotensin II do not directly stimulate BNP release; sympathetic
activity would increase, not decrease, in heart failure.
Page 4
