Clarkson College
Course Number: NRS 205
Course Title: Pathophysiology
Exam: Final Exam
Date:2026
A 58-year-old male presents with crushing substernal chest pain radiating to his left arm,
diaphoresis, and nausea. His 12-lead ECG shows ST-segment elevation in leads II, III, and aVF.
Which coronary artery is most likely occluded?
A) Left anterior descending artery
B) Right coronary artery
C) Left circumflex artery
D) Left main coronary artery
CORRECT ANSWER: B) Right coronary artery
Rationale: ST elevation in leads II, III, and aVF corresponds to the inferior wall of the left
ventricle, which is perfused primarily by the right coronary artery (RCA) in approximately 85% of
individuals with right-dominant circulation. The left anterior descending artery (LAD) supplies the
anterior wall, reflected in leads V1 to V4. The left circumflex supplies the lateral wall, seen in
leads I, aVL, V5, and V6. Left main occlusion produces extensive, multi-territory ST changes and
is usually rapidly fatal. Understanding coronary territory mapping is critical for nurses during
cardiac monitoring and during rapid triage decisions.
1
,---
RESPIRATORY | Acute Respiratory Distress Syndrome
A 42-year-old woman is admitted to the ICU following septic shock from a ruptured appendix. She
is mechanically ventilated with an FiO2 of 0.80 and PEEP of 12 cmH2O. Her PaO2 is 68 mmHg.
What is her PaO2/FiO2 ratio, and how does this classify her condition according to the Berlin
Definition?
A) PaO2/FiO2 = 85; severe ARDS
B) PaO2/FiO2 = 85; moderate ARDS
C) PaO2/FiO2 = 68; moderate ARDS
D) PaO2/FiO2 = 54; severe ARDS
CORRECT ANSWER: A) PaO2/FiO2 = 85; severe ARDS
Rationale: PaO2/FiO2 = 68 divided by 0.80 = 85 mmHg. Per the Berlin Definition of ARDS: mild
is 200 to 300 mmHg, moderate is 100 to 200 mmHg, and severe is below 100 mmHg. A ratio of 85
classifies this as severe ARDS. The condition arises from diffuse alveolar damage, increased
vascular permeability, non-cardiogenic pulmonary edema, surfactant dysfunction, and resultant
refractory hypoxemia. Nurses must understand lung-protective ventilation strategies, including low
tidal volume (6 mL/kg ideal body weight) and permissive hypercapnia, which are the cornerstones
of ARDS management.
---
RENAL | Acute Kidney Injury
A 72-year-old man with chronic hypertension and type 2 diabetes was started on an ACE inhibitor
two weeks ago. He now presents with a serum creatinine of 3.2 mg/dL (baseline 1.1 mg/dL),
2
,hyperkalemia of 6.2 mEq/L, and bilateral flank tenderness. Renal ultrasound reveals bilaterally
small, echogenic kidneys. What is the most likely etiology of his acute kidney injury?
A) Intrinsic renal injury from contrast nephropathy
B) Pre-renal azotemia from volume depletion
C) Bilateral renal artery stenosis unmasked by ACE inhibitor therapy
D) Post-renal obstruction from benign prostatic hyperplasia
CORRECT ANSWER: C) Bilateral renal artery stenosis unmasked by ACE inhibitor therapy
Rationale: In bilateral renal artery stenosis, or unilateral stenosis in a solitary functioning kidney,
the glomerular filtration rate is critically dependent on angiotensin II-mediated efferent arteriolar
vasoconstriction to maintain glomerular capillary pressure. ACE inhibitors block angiotensin II
synthesis, causing efferent arteriolar dilation, a sudden drop in GFR, and acute creatinine rise.
Small echogenic kidneys suggest chronic renovascular disease. This is a classic contraindication
for ACE inhibitor use that nurses must recognize. A rise in creatinine of more than 30% above
baseline within two weeks of starting an ACE inhibitor or ARB warrants immediate reassessment.
---
NEUROLOGY | Ischemic Stroke and Penumbra
A 67-year-old woman with atrial fibrillation presents with sudden-onset expressive aphasia, right
facial droop, and right arm weakness. CT head excludes hemorrhage. She was last seen well 2
hours ago. Which pathophysiological mechanism is primarily responsible for the progression of her
ischemic penumbra to infarcted tissue if reperfusion does not occur promptly?
A) Mitochondrial autophagy and programmed apoptosis
B) Glutamate-mediated excitotoxicity and cytotoxic edema
C) Immunoglobulin deposition and complement system activation
3
, D) Demyelination of corticospinal tracts
CORRECT ANSWER: B) Glutamate-mediated excitotoxicity and cytotoxic edema
Rationale: During cerebral ischemia, ATP depletion causes failure of the Na/K-ATPase pump,
membrane depolarization, and massive glutamate release from presynaptic terminals. Excess
glutamate overstimulates NMDA and AMPA receptors, triggering an uncontrolled influx of
calcium ions. Intracellular calcium overload activates proteases, lipases, and endonucleases,
culminating in neuronal death. Sodium and water follow intracellularly, causing cytotoxic edema.
The ischemic penumbra, the zone of potentially salvageable tissue surrounding the infarct core, is
the therapeutic target of thrombolytic therapy (IV alteplase within 4.5 hours) and mechanical
thrombectomy. Nurses play a critical role in rapid stroke identification, documentation of last-
known-well time, and minimizing door-to-needle time.
---
ENDOCRINE | Diabetic Ketoacidosis
A 19-year-old male with type 1 diabetes presents with Kussmaul respirations, fruity breath odor,
nausea, and vomiting. Labs: glucose 520 mg/dL, pH 7.18, bicarbonate 10 mEq/L, anion gap 28,
serum ketones positive, serum potassium 5.8 mEq/L. After confirming DKA, intravenous insulin is
initiated. Which of the following best explains the life-threatening fall in serum potassium expected
during treatment?
A) Insulin causes renal potassium excretion through aldosterone stimulation
B) Insulin drives potassium intracellularly by activating Na/K-ATPase
C) Correction of acidosis causes potassium-hydrogen exchange across cell membranes
D) Both B and C contribute to a transcellular potassium shift
CORRECT ANSWER: D) Both B and C contribute to a transcellular potassium shift
4
Course Number: NRS 205
Course Title: Pathophysiology
Exam: Final Exam
Date:2026
A 58-year-old male presents with crushing substernal chest pain radiating to his left arm,
diaphoresis, and nausea. His 12-lead ECG shows ST-segment elevation in leads II, III, and aVF.
Which coronary artery is most likely occluded?
A) Left anterior descending artery
B) Right coronary artery
C) Left circumflex artery
D) Left main coronary artery
CORRECT ANSWER: B) Right coronary artery
Rationale: ST elevation in leads II, III, and aVF corresponds to the inferior wall of the left
ventricle, which is perfused primarily by the right coronary artery (RCA) in approximately 85% of
individuals with right-dominant circulation. The left anterior descending artery (LAD) supplies the
anterior wall, reflected in leads V1 to V4. The left circumflex supplies the lateral wall, seen in
leads I, aVL, V5, and V6. Left main occlusion produces extensive, multi-territory ST changes and
is usually rapidly fatal. Understanding coronary territory mapping is critical for nurses during
cardiac monitoring and during rapid triage decisions.
1
,---
RESPIRATORY | Acute Respiratory Distress Syndrome
A 42-year-old woman is admitted to the ICU following septic shock from a ruptured appendix. She
is mechanically ventilated with an FiO2 of 0.80 and PEEP of 12 cmH2O. Her PaO2 is 68 mmHg.
What is her PaO2/FiO2 ratio, and how does this classify her condition according to the Berlin
Definition?
A) PaO2/FiO2 = 85; severe ARDS
B) PaO2/FiO2 = 85; moderate ARDS
C) PaO2/FiO2 = 68; moderate ARDS
D) PaO2/FiO2 = 54; severe ARDS
CORRECT ANSWER: A) PaO2/FiO2 = 85; severe ARDS
Rationale: PaO2/FiO2 = 68 divided by 0.80 = 85 mmHg. Per the Berlin Definition of ARDS: mild
is 200 to 300 mmHg, moderate is 100 to 200 mmHg, and severe is below 100 mmHg. A ratio of 85
classifies this as severe ARDS. The condition arises from diffuse alveolar damage, increased
vascular permeability, non-cardiogenic pulmonary edema, surfactant dysfunction, and resultant
refractory hypoxemia. Nurses must understand lung-protective ventilation strategies, including low
tidal volume (6 mL/kg ideal body weight) and permissive hypercapnia, which are the cornerstones
of ARDS management.
---
RENAL | Acute Kidney Injury
A 72-year-old man with chronic hypertension and type 2 diabetes was started on an ACE inhibitor
two weeks ago. He now presents with a serum creatinine of 3.2 mg/dL (baseline 1.1 mg/dL),
2
,hyperkalemia of 6.2 mEq/L, and bilateral flank tenderness. Renal ultrasound reveals bilaterally
small, echogenic kidneys. What is the most likely etiology of his acute kidney injury?
A) Intrinsic renal injury from contrast nephropathy
B) Pre-renal azotemia from volume depletion
C) Bilateral renal artery stenosis unmasked by ACE inhibitor therapy
D) Post-renal obstruction from benign prostatic hyperplasia
CORRECT ANSWER: C) Bilateral renal artery stenosis unmasked by ACE inhibitor therapy
Rationale: In bilateral renal artery stenosis, or unilateral stenosis in a solitary functioning kidney,
the glomerular filtration rate is critically dependent on angiotensin II-mediated efferent arteriolar
vasoconstriction to maintain glomerular capillary pressure. ACE inhibitors block angiotensin II
synthesis, causing efferent arteriolar dilation, a sudden drop in GFR, and acute creatinine rise.
Small echogenic kidneys suggest chronic renovascular disease. This is a classic contraindication
for ACE inhibitor use that nurses must recognize. A rise in creatinine of more than 30% above
baseline within two weeks of starting an ACE inhibitor or ARB warrants immediate reassessment.
---
NEUROLOGY | Ischemic Stroke and Penumbra
A 67-year-old woman with atrial fibrillation presents with sudden-onset expressive aphasia, right
facial droop, and right arm weakness. CT head excludes hemorrhage. She was last seen well 2
hours ago. Which pathophysiological mechanism is primarily responsible for the progression of her
ischemic penumbra to infarcted tissue if reperfusion does not occur promptly?
A) Mitochondrial autophagy and programmed apoptosis
B) Glutamate-mediated excitotoxicity and cytotoxic edema
C) Immunoglobulin deposition and complement system activation
3
, D) Demyelination of corticospinal tracts
CORRECT ANSWER: B) Glutamate-mediated excitotoxicity and cytotoxic edema
Rationale: During cerebral ischemia, ATP depletion causes failure of the Na/K-ATPase pump,
membrane depolarization, and massive glutamate release from presynaptic terminals. Excess
glutamate overstimulates NMDA and AMPA receptors, triggering an uncontrolled influx of
calcium ions. Intracellular calcium overload activates proteases, lipases, and endonucleases,
culminating in neuronal death. Sodium and water follow intracellularly, causing cytotoxic edema.
The ischemic penumbra, the zone of potentially salvageable tissue surrounding the infarct core, is
the therapeutic target of thrombolytic therapy (IV alteplase within 4.5 hours) and mechanical
thrombectomy. Nurses play a critical role in rapid stroke identification, documentation of last-
known-well time, and minimizing door-to-needle time.
---
ENDOCRINE | Diabetic Ketoacidosis
A 19-year-old male with type 1 diabetes presents with Kussmaul respirations, fruity breath odor,
nausea, and vomiting. Labs: glucose 520 mg/dL, pH 7.18, bicarbonate 10 mEq/L, anion gap 28,
serum ketones positive, serum potassium 5.8 mEq/L. After confirming DKA, intravenous insulin is
initiated. Which of the following best explains the life-threatening fall in serum potassium expected
during treatment?
A) Insulin causes renal potassium excretion through aldosterone stimulation
B) Insulin drives potassium intracellularly by activating Na/K-ATPase
C) Correction of acidosis causes potassium-hydrogen exchange across cell membranes
D) Both B and C contribute to a transcellular potassium shift
CORRECT ANSWER: D) Both B and C contribute to a transcellular potassium shift
4
