1
NUR 600 Module 5 Exam – Questions and Answers | 2026
Update
St. Thomas University | Advanced Pathophysiology & Clinical
Pharmacology.
Question 1 (Multiple Choice)
A 14-year-old patient is admitted with new-onset diabetes mellitus. Laboratory studies reveal:
fasting glucose 342 mg/dL, A1c 10.2%, C-peptide 0.3 ng/mL (normal 1.1-4.4 ng/mL), and
positive glutamic acid decarboxylase (GAD-65) antibodies. The patient has no family history of
diabetes and has lost 12 pounds over the past month. Which pathophysiologic mechanism
best explains this patient's condition?
A) Progressive beta-cell dysfunction secondary to insulin resistance and glucotoxicity
B) Autoimmune-mediated destruction of pancreatic beta cells resulting in absolute insulin
deficiency
C) Insulin receptor post-receptor signaling defects causing peripheral insulin resistance
D) Amyloid deposition in pancreatic islets disrupting beta-cell function
[CORRECT: B]
Rationale: This patient presents with classic Type 1 diabetes mellitus (T1DM). The key
diagnostic clues include: age of onset in adolescence, low C-peptide level (indicating minimal
endogenous insulin production), positive GAD-65 antibodies (a marker of autoimmune beta-
cell destruction), and significant weight loss despite hyperglycemia. The pathophysiology of
T1DM involves autoimmune-mediated destruction of pancreatic beta cells, typically by T-
lymphocytes, resulting in absolute insulin deficiency. This absolute deficiency explains why
the patient requires exogenous insulin for survival and is prone to diabetic ketoacidosis (DKA).
C-peptide is cleaved from proinsulin in a 1:1 ratio with insulin, so a low level confirms minimal
endogenous insulin secretion. The absence of family history and the acute presentation
further support T1DM over Type 2 diabetes mellitus (T2DM), which typically presents in older
adults with obesity, family history, and relative insulin deficiency with preserved (though
impaired) beta-cell function.
, 2
Question 2 (Multiple Choice)
A 52-year-old male with a BMI of 34 kg/m² presents for routine screening. His father and two
siblings have Type 2 diabetes. Laboratory studies show: fasting glucose 138 mg/dL, A1c 7.1%,
fasting insulin 28 µIU/mL (elevated). He reports feeling fatigued but has no polyuria or weight
loss. Which statement best describes the underlying pathophysiology of this patient's
condition?
A) Autoimmune destruction of beta cells with complete loss of insulin secretion
B) Severe insulin deficiency requiring immediate initiation of basal insulin therapy
C) Insulin resistance with compensatory hyperinsulinemia and progressive beta-cell
dysfunction
D) Genetic defect in insulin receptor structure causing extreme insulin resistance
[CORRECT: C]
Rationale: This patient has Type 2 diabetes mellitus (T2DM), which accounts for 90-95% of all
diabetes cases. The pathophysiology is characterized by insulin resistance in peripheral tissues
(muscle, liver, adipose) combined with progressive beta-cell dysfunction. The elevated fasting
insulin level (28 µIU/mL) demonstrates compensatory hyperinsulinemia—the pancreas is
working harder to overcome peripheral insulin resistance. Over time, beta cells cannot
maintain this compensatory response, leading to relative insulin deficiency and
hyperglycemia. Key risk factors present include obesity (BMI 34 kg/m²), family history (father
and siblings with T2DM), and age >45 years. Unlike T1DM, this patient retains some beta-cell
function, does not have autoimmune markers, and typically does not present with DKA. The
"twin cycle hypothesis" suggests that ectopic fat accumulation in the liver and pancreas drives
both insulin resistance and beta-cell dysfunction.
Question 3 (Select-All-That-Apply)
Which of the following clinical features are more characteristic of Type 1 diabetes mellitus
than Type 2 diabetes mellitus? (Select all that apply)
A) Presence of anti-islet cell antibodies
B) Ketoacidosis as a common presenting complication
C) Gradual onset over months to years with minimal symptoms
, 3
D) Association with other autoimmune disorders (e.g., Hashimoto's thyroiditis, celiac disease)
E) Requirement for exogenous insulin from time of diagnosis
[CORRECT: A, B, D, E]
Rationale: Type 1 diabetes mellitus (T1DM) is distinguished from Type 2 diabetes mellitus
(T2DM) by several key clinical and pathophysiologic features. T1DM is an autoimmune
disorder characterized by the presence of autoantibodies including anti-islet cell antibodies
(ICA), anti-glutamic acid decarboxylase (GAD-65) antibodies, anti-insulin autoantibodies (IAA),
and anti-zinc transporter 8 (ZnT8) antibodies—these markers support answer A. Because
T1DM involves absolute insulin deficiency, patients are unable to suppress lipolysis and
ketogenesis, making diabetic ketoacidosis (DKA) a common presenting complication—
supporting answer B. T1DM demonstrates strong associations with other autoimmune
conditions due to shared genetic susceptibility (HLA-DR3/DR4 haplotypes), including
Hashimoto's thyroiditis, celiac disease, Addison's disease, and pernicious anemia—supporting
answer D. Due to complete or near-complete beta-cell destruction, patients with T1DM
require exogenous insulin for survival from the time of diagnosis—supporting answer E.
Answer C is incorrect because gradual onset with minimal symptoms is characteristic of
T2DM, not T1DM; T1DM typically presents acutely over days to weeks with classic symptoms
of polyuria, polydipsia, polyphagia, and weight loss.
Question 4 (Case Study/Scenario-Based)
A 28-year-old female presents with polyuria, polydipsia, and 15-pound weight loss over 3
weeks. Physical exam reveals dry mucous membranes and tachycardia (HR 112 bpm).
Laboratory studies: glucose 486 mg/dL, bicarbonate 18 mEq/L, anion gap 22, pH 7.28, ketones
positive in urine and serum. She has no family history of diabetes.
Which combination of pathophysiologic events is primarily responsible for this patient's
metabolic derangement?
A) Severe insulin deficiency → uncontrolled lipolysis → increased hepatic ketogenesis →
metabolic acidosis
B) Insulin resistance → compensatory hyperinsulinemia → hepatic gluconeogenesis →
hyperosmolar state
C) Autoimmune beta-cell destruction → amylin deficiency → delayed gastric emptying →
, 4
hyperglycemia
D) Peripheral insulin resistance → decreased GLUT4 translocation → muscle glycogen
accumulation → lactic acidosis
[CORRECT: A]
Rationale: This patient presents with diabetic ketoacidosis (DKA), a life-threatening
complication most commonly associated with Type 1 diabetes mellitus. The clinical picture—
acute onset in a young adult, significant weight loss, no family history of diabetes, and
metabolic acidosis with ketosis—strongly suggests T1DM with DKA. The pathophysiologic
cascade is: absolute insulin deficiency (from autoimmune beta-cell destruction) leads to
uncontrolled lipolysis in adipose tissue, releasing free fatty acids into circulation. These free
fatty acids are transported to the liver where they undergo beta-oxidation and are converted
into ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone). The accumulation of
ketone bodies overwhelms the body's buffering capacity, resulting in metabolic acidosis (pH
7.28, bicarbonate 18 mEq/L, elevated anion gap of 22). Simultaneously, insulin deficiency
promotes hepatic gluconeogenesis and glycogenolysis, causing severe hyperglycemia (486
mg/dL). The hyperglycemia drives an osmotic diuresis, causing dehydration (dry mucous
membranes, tachycardia) and electrolyte losses. This differs from Hyperglycemic
Hyperosmolar State (HHS), which occurs in T2DM with sufficient insulin to prevent
ketogenesis but not hyperglycemia.
Sub-Topic 1B: Diabetic Ketoacidosis (DKA) vs. Hyperglycemic Hyperosmolar State (HHS) (3
Questions)
Question 5 (Multiple Choice)
A 68-year-old male with Type 2 diabetes is brought to the emergency department with
confusion and lethargy. His family reports decreased oral intake and increased urination over
the past week. Vital signs: BP 92/58 mmHg, HR 118 bpm, RR 22/min, Temp 37.2°C. Laboratory
studies: glucose 920 mg/dL, sodium 152 mEq/L, potassium 3.2 mEq/L, chloride 118 mEq/L,
bicarbonate 24 mEq/L, BUN 48 mg/dL, creatinine 2.1 mg/dL, serum osmolality 358 mOsm/kg,
pH 7.35, urine ketones negative, serum ketones trace. Which diagnosis best fits this clinical
presentation?
NUR 600 Module 5 Exam – Questions and Answers | 2026
Update
St. Thomas University | Advanced Pathophysiology & Clinical
Pharmacology.
Question 1 (Multiple Choice)
A 14-year-old patient is admitted with new-onset diabetes mellitus. Laboratory studies reveal:
fasting glucose 342 mg/dL, A1c 10.2%, C-peptide 0.3 ng/mL (normal 1.1-4.4 ng/mL), and
positive glutamic acid decarboxylase (GAD-65) antibodies. The patient has no family history of
diabetes and has lost 12 pounds over the past month. Which pathophysiologic mechanism
best explains this patient's condition?
A) Progressive beta-cell dysfunction secondary to insulin resistance and glucotoxicity
B) Autoimmune-mediated destruction of pancreatic beta cells resulting in absolute insulin
deficiency
C) Insulin receptor post-receptor signaling defects causing peripheral insulin resistance
D) Amyloid deposition in pancreatic islets disrupting beta-cell function
[CORRECT: B]
Rationale: This patient presents with classic Type 1 diabetes mellitus (T1DM). The key
diagnostic clues include: age of onset in adolescence, low C-peptide level (indicating minimal
endogenous insulin production), positive GAD-65 antibodies (a marker of autoimmune beta-
cell destruction), and significant weight loss despite hyperglycemia. The pathophysiology of
T1DM involves autoimmune-mediated destruction of pancreatic beta cells, typically by T-
lymphocytes, resulting in absolute insulin deficiency. This absolute deficiency explains why
the patient requires exogenous insulin for survival and is prone to diabetic ketoacidosis (DKA).
C-peptide is cleaved from proinsulin in a 1:1 ratio with insulin, so a low level confirms minimal
endogenous insulin secretion. The absence of family history and the acute presentation
further support T1DM over Type 2 diabetes mellitus (T2DM), which typically presents in older
adults with obesity, family history, and relative insulin deficiency with preserved (though
impaired) beta-cell function.
, 2
Question 2 (Multiple Choice)
A 52-year-old male with a BMI of 34 kg/m² presents for routine screening. His father and two
siblings have Type 2 diabetes. Laboratory studies show: fasting glucose 138 mg/dL, A1c 7.1%,
fasting insulin 28 µIU/mL (elevated). He reports feeling fatigued but has no polyuria or weight
loss. Which statement best describes the underlying pathophysiology of this patient's
condition?
A) Autoimmune destruction of beta cells with complete loss of insulin secretion
B) Severe insulin deficiency requiring immediate initiation of basal insulin therapy
C) Insulin resistance with compensatory hyperinsulinemia and progressive beta-cell
dysfunction
D) Genetic defect in insulin receptor structure causing extreme insulin resistance
[CORRECT: C]
Rationale: This patient has Type 2 diabetes mellitus (T2DM), which accounts for 90-95% of all
diabetes cases. The pathophysiology is characterized by insulin resistance in peripheral tissues
(muscle, liver, adipose) combined with progressive beta-cell dysfunction. The elevated fasting
insulin level (28 µIU/mL) demonstrates compensatory hyperinsulinemia—the pancreas is
working harder to overcome peripheral insulin resistance. Over time, beta cells cannot
maintain this compensatory response, leading to relative insulin deficiency and
hyperglycemia. Key risk factors present include obesity (BMI 34 kg/m²), family history (father
and siblings with T2DM), and age >45 years. Unlike T1DM, this patient retains some beta-cell
function, does not have autoimmune markers, and typically does not present with DKA. The
"twin cycle hypothesis" suggests that ectopic fat accumulation in the liver and pancreas drives
both insulin resistance and beta-cell dysfunction.
Question 3 (Select-All-That-Apply)
Which of the following clinical features are more characteristic of Type 1 diabetes mellitus
than Type 2 diabetes mellitus? (Select all that apply)
A) Presence of anti-islet cell antibodies
B) Ketoacidosis as a common presenting complication
C) Gradual onset over months to years with minimal symptoms
, 3
D) Association with other autoimmune disorders (e.g., Hashimoto's thyroiditis, celiac disease)
E) Requirement for exogenous insulin from time of diagnosis
[CORRECT: A, B, D, E]
Rationale: Type 1 diabetes mellitus (T1DM) is distinguished from Type 2 diabetes mellitus
(T2DM) by several key clinical and pathophysiologic features. T1DM is an autoimmune
disorder characterized by the presence of autoantibodies including anti-islet cell antibodies
(ICA), anti-glutamic acid decarboxylase (GAD-65) antibodies, anti-insulin autoantibodies (IAA),
and anti-zinc transporter 8 (ZnT8) antibodies—these markers support answer A. Because
T1DM involves absolute insulin deficiency, patients are unable to suppress lipolysis and
ketogenesis, making diabetic ketoacidosis (DKA) a common presenting complication—
supporting answer B. T1DM demonstrates strong associations with other autoimmune
conditions due to shared genetic susceptibility (HLA-DR3/DR4 haplotypes), including
Hashimoto's thyroiditis, celiac disease, Addison's disease, and pernicious anemia—supporting
answer D. Due to complete or near-complete beta-cell destruction, patients with T1DM
require exogenous insulin for survival from the time of diagnosis—supporting answer E.
Answer C is incorrect because gradual onset with minimal symptoms is characteristic of
T2DM, not T1DM; T1DM typically presents acutely over days to weeks with classic symptoms
of polyuria, polydipsia, polyphagia, and weight loss.
Question 4 (Case Study/Scenario-Based)
A 28-year-old female presents with polyuria, polydipsia, and 15-pound weight loss over 3
weeks. Physical exam reveals dry mucous membranes and tachycardia (HR 112 bpm).
Laboratory studies: glucose 486 mg/dL, bicarbonate 18 mEq/L, anion gap 22, pH 7.28, ketones
positive in urine and serum. She has no family history of diabetes.
Which combination of pathophysiologic events is primarily responsible for this patient's
metabolic derangement?
A) Severe insulin deficiency → uncontrolled lipolysis → increased hepatic ketogenesis →
metabolic acidosis
B) Insulin resistance → compensatory hyperinsulinemia → hepatic gluconeogenesis →
hyperosmolar state
C) Autoimmune beta-cell destruction → amylin deficiency → delayed gastric emptying →
, 4
hyperglycemia
D) Peripheral insulin resistance → decreased GLUT4 translocation → muscle glycogen
accumulation → lactic acidosis
[CORRECT: A]
Rationale: This patient presents with diabetic ketoacidosis (DKA), a life-threatening
complication most commonly associated with Type 1 diabetes mellitus. The clinical picture—
acute onset in a young adult, significant weight loss, no family history of diabetes, and
metabolic acidosis with ketosis—strongly suggests T1DM with DKA. The pathophysiologic
cascade is: absolute insulin deficiency (from autoimmune beta-cell destruction) leads to
uncontrolled lipolysis in adipose tissue, releasing free fatty acids into circulation. These free
fatty acids are transported to the liver where they undergo beta-oxidation and are converted
into ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone). The accumulation of
ketone bodies overwhelms the body's buffering capacity, resulting in metabolic acidosis (pH
7.28, bicarbonate 18 mEq/L, elevated anion gap of 22). Simultaneously, insulin deficiency
promotes hepatic gluconeogenesis and glycogenolysis, causing severe hyperglycemia (486
mg/dL). The hyperglycemia drives an osmotic diuresis, causing dehydration (dry mucous
membranes, tachycardia) and electrolyte losses. This differs from Hyperglycemic
Hyperosmolar State (HHS), which occurs in T2DM with sufficient insulin to prevent
ketogenesis but not hyperglycemia.
Sub-Topic 1B: Diabetic Ketoacidosis (DKA) vs. Hyperglycemic Hyperosmolar State (HHS) (3
Questions)
Question 5 (Multiple Choice)
A 68-year-old male with Type 2 diabetes is brought to the emergency department with
confusion and lethargy. His family reports decreased oral intake and increased urination over
the past week. Vital signs: BP 92/58 mmHg, HR 118 bpm, RR 22/min, Temp 37.2°C. Laboratory
studies: glucose 920 mg/dL, sodium 152 mEq/L, potassium 3.2 mEq/L, chloride 118 mEq/L,
bicarbonate 24 mEq/L, BUN 48 mg/dL, creatinine 2.1 mg/dL, serum osmolality 358 mOsm/kg,
pH 7.35, urine ketones negative, serum ketones trace. Which diagnosis best fits this clinical
presentation?
