NR283 / NR 283
Exam 3 Pathophysiology Review
Latest
Pathophysiology: Mechanisms of Disease for Nursing Practice
Chamberlain University
50 Questions with Verified Answers
5 Domains | Multiple Choice | A+ Graded Rationales
Total Questions 50
Question Format Multiple Choice (A-D)
Domains 5
Cognitive Levels 25% Recall | 55% Application | 20% Analysis
Content Style 70% Scenario-Based | 20% Direct Recall | 10% Analysis
, Domain 1: Endocrine Disorders (Q1–Q15)
Q1: A nurse reviews Type 1 DM pathophysiology. Which describes the mechanism?
A. Insulin resistance with relative insulin deficiency.
B. Autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency.
[CORRECT]
C. Excessive glucagon suppressing insulin release.
D. Beta-cell exhaustion from chronic hyperglycemia.
Correct Answer: B
Rationale: Type 1 DM results from autoimmune destruction of beta cells by T-lymphocytes and autoantibodies, causing absolute
insulin deficiency. Genetic susceptibility plus environmental triggers initiate the process. Autoantibodies (anti-GAD, anti-IA-2) and
low/absent C-peptide confirm diagnosis. Option A describes Type 2. Option C misattributes to alpha cells. Option D describes Type
2 beta-cell burnout.
Q2: A Type 1 DM patient has Kussmaul respirations, fruity breath, glucose 450. What explains the metabolic
acidosis?
A. Lactic acid from anaerobic metabolism.
B. Lipolysis and ketogenesis produce beta-hydroxybutyrate and acetoacetate, creating anion gap
metabolic acidosis. [CORRECT]
C. Renal H+ retention from AKI.
D. Impaired hepatic fatty acid metabolism.
Correct Answer: B
Rationale: In DKA, insulin deficiency plus counter-regulatory hormones drive lipolysis. The liver converts free fatty acids to
ketone bodies (beta-hydroxybutyrate, acetoacetate), strong organic acids depleting bicarbonate and creating high anion gap acidosis.
Kussmaul respirations are compensatory. Fruity breath reflects acetone. Option A is lactic acidosis. Option C is renal tubular
acidosis.
Q3: Caring for a DKA patient. Which lab is priority to prevent cardiac complications?
A. Serum sodium.
B. Serum potassium; total body K+ is depleted but initially normal/elevated; insulin and correction
cause dangerous hypokalemia. [CORRECT]
C. Serum calcium.
D. Serum magnesium.
Correct Answer: B
Rationale: DKA patients have significant total-body K+ deficit from osmotic diuresis, but initial serum K+ may be normal or high
because acidosis shifts K+ out of cells. As insulin and fluids correct acidosis and drive K+ back into cells, serum K+ drops rapidly,
causing life-threatening hypokalemia and arrhythmias. Potassium must be monitored and replaced before and during insulin
therapy.
Q4: A 72-year-old Type 2 DM patient has dehydration, glucose 680, altered mental status. Ketones negative.
Condition?
A. DKA with atypical presentation.
B. HHS: severe hyperglycemia, hyperosmolality, minimal ketosis because residual insulin
prevents lipolysis. [CORRECT]
C. Hypoglycemic coma.
D. Glucocorticoid-induced hyperglycemia.
Correct Answer: B
Exam 3 Pathophysiology Review
Latest
Pathophysiology: Mechanisms of Disease for Nursing Practice
Chamberlain University
50 Questions with Verified Answers
5 Domains | Multiple Choice | A+ Graded Rationales
Total Questions 50
Question Format Multiple Choice (A-D)
Domains 5
Cognitive Levels 25% Recall | 55% Application | 20% Analysis
Content Style 70% Scenario-Based | 20% Direct Recall | 10% Analysis
, Domain 1: Endocrine Disorders (Q1–Q15)
Q1: A nurse reviews Type 1 DM pathophysiology. Which describes the mechanism?
A. Insulin resistance with relative insulin deficiency.
B. Autoimmune destruction of pancreatic beta cells causing absolute insulin deficiency.
[CORRECT]
C. Excessive glucagon suppressing insulin release.
D. Beta-cell exhaustion from chronic hyperglycemia.
Correct Answer: B
Rationale: Type 1 DM results from autoimmune destruction of beta cells by T-lymphocytes and autoantibodies, causing absolute
insulin deficiency. Genetic susceptibility plus environmental triggers initiate the process. Autoantibodies (anti-GAD, anti-IA-2) and
low/absent C-peptide confirm diagnosis. Option A describes Type 2. Option C misattributes to alpha cells. Option D describes Type
2 beta-cell burnout.
Q2: A Type 1 DM patient has Kussmaul respirations, fruity breath, glucose 450. What explains the metabolic
acidosis?
A. Lactic acid from anaerobic metabolism.
B. Lipolysis and ketogenesis produce beta-hydroxybutyrate and acetoacetate, creating anion gap
metabolic acidosis. [CORRECT]
C. Renal H+ retention from AKI.
D. Impaired hepatic fatty acid metabolism.
Correct Answer: B
Rationale: In DKA, insulin deficiency plus counter-regulatory hormones drive lipolysis. The liver converts free fatty acids to
ketone bodies (beta-hydroxybutyrate, acetoacetate), strong organic acids depleting bicarbonate and creating high anion gap acidosis.
Kussmaul respirations are compensatory. Fruity breath reflects acetone. Option A is lactic acidosis. Option C is renal tubular
acidosis.
Q3: Caring for a DKA patient. Which lab is priority to prevent cardiac complications?
A. Serum sodium.
B. Serum potassium; total body K+ is depleted but initially normal/elevated; insulin and correction
cause dangerous hypokalemia. [CORRECT]
C. Serum calcium.
D. Serum magnesium.
Correct Answer: B
Rationale: DKA patients have significant total-body K+ deficit from osmotic diuresis, but initial serum K+ may be normal or high
because acidosis shifts K+ out of cells. As insulin and fluids correct acidosis and drive K+ back into cells, serum K+ drops rapidly,
causing life-threatening hypokalemia and arrhythmias. Potassium must be monitored and replaced before and during insulin
therapy.
Q4: A 72-year-old Type 2 DM patient has dehydration, glucose 680, altered mental status. Ketones negative.
Condition?
A. DKA with atypical presentation.
B. HHS: severe hyperglycemia, hyperosmolality, minimal ketosis because residual insulin
prevents lipolysis. [CORRECT]
C. Hypoglycemic coma.
D. Glucocorticoid-induced hyperglycemia.
Correct Answer: B
