McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1
Reference
Ch. 22 — Alterations of Hormonal Regulation — Disorders of
the Adrenal Cortex (Addison Disease)
Stem
A 42-year-old woman presents with 3 weeks of increasing
fatigue, weight loss, dizziness on standing, and new
hyperpigmentation of palmar creases. BP 88/56 mmHg, HR 96,
serum sodium 126 mEq/L, potassium 5.6 mEq/L, morning
cortisol low, ACTH markedly elevated. Which interpretation best
explains her presentation?
Options
A. Secondary adrenal insufficiency due to pituitary failure
causing low ACTH and low cortisol.
B. Primary adrenal insufficiency (Addison disease) with loss of
aldosterone causing hyponatremia and hyperkalemia.
C. Exogenous steroid withdrawal causing transient ACTH
elevation with preserved aldosterone.
,D. Pheochromocytoma causing episodic hypotension and
hyperkalemia.
Correct answer
B
Rationales
Correct (B): Primary adrenal cortex destruction (Addison
disease) causes decreased cortisol and aldosterone. Loss of
aldosterone → renal sodium wasting (hyponatremia),
potassium retention (hyperkalemia), and orthostatic
hypotension. Elevated ACTH reflects lack of negative feedback;
hyperpigmentation occurs from increased POMC/ACTH-derived
melanocyte stimulation. This aligns with McCance’s description
of primary adrenal insufficiency mechanisms and early red-
flags.
A (incorrect): Secondary adrenal insufficiency shows low ACTH
(not elevated) and usually spares aldosterone, so hyperkalemia
and hyperpigmentation are unlikely.
C (incorrect): Exogenous steroid withdrawal typically
suppresses ACTH (low) initially; aldosterone is less affected and
hyperkalemia is not a primary feature.
D (incorrect): Pheochromocytoma causes episodic hypertension
and catecholamine excess signs, not chronic hyponatremia with
hyperkalemia and high ACTH.
Teaching point
Primary adrenal failure → low cortisol + low aldosterone →
hyponatremia, hyperkalemia, hypotension, ↑ACTH.
,Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 22.
2
Reference
Ch. 22 — Alterations of Hormonal Regulation — Disorders of
the Adrenal Cortex (Cushing Syndrome)
Stem
A 55-year-old man with progressive central obesity, proximal
muscle weakness, poorly controlled hypertension, and fasting
glucose 180 mg/dL is noted to have easy bruising and purple
abdominal striae. Random cortisol elevated; 24-hr urinary free
cortisol elevated. Which pathophysiologic mechanism best
accounts for his hyperglycemia and muscle weakness?
Options
A. Excess cortisol increases insulin sensitivity, causing
hyperinsulinemia and muscle catabolism.
B. Cortisol promotes gluconeogenesis and protein catabolism,
causing insulin resistance and proximal muscle wasting.
C. Aldosterone excess causes hypokalemia that triggers
proteolysis and hyperglycemia.
D. ACTH deficiency reduces adrenal androgen production
leading to hyperglycemia and weakness.
, Correct answer
B
Rationales
Correct (B): Chronic glucocorticoid excess increases hepatic
gluconeogenesis and peripheral insulin resistance, raising blood
glucose. Cortisol stimulates protein catabolism in muscle
(proximal weakness) and redistributes fat centrally—classic
mechanisms in Cushing syndrome as described in McCance.
A (incorrect): Cortisol decreases, not increases, insulin
sensitivity. Hyperinsulinemia may result secondarily but is not
the primary mechanism.
C (incorrect): Aldosterone excess leads to hypokalemia and
hypertension but does not explain cortisol-driven
gluconeogenesis and muscle wasting.
D (incorrect): ACTH deficiency would lower cortisol (not raise
it); symptoms would differ.
Teaching point
Cortisol → ↑gluconeogenesis + ↓insulin sensitivity + ↑protein
catabolism → hyperglycemia and proximal weakness.
Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 22.
3
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1
Reference
Ch. 22 — Alterations of Hormonal Regulation — Disorders of
the Adrenal Cortex (Addison Disease)
Stem
A 42-year-old woman presents with 3 weeks of increasing
fatigue, weight loss, dizziness on standing, and new
hyperpigmentation of palmar creases. BP 88/56 mmHg, HR 96,
serum sodium 126 mEq/L, potassium 5.6 mEq/L, morning
cortisol low, ACTH markedly elevated. Which interpretation best
explains her presentation?
Options
A. Secondary adrenal insufficiency due to pituitary failure
causing low ACTH and low cortisol.
B. Primary adrenal insufficiency (Addison disease) with loss of
aldosterone causing hyponatremia and hyperkalemia.
C. Exogenous steroid withdrawal causing transient ACTH
elevation with preserved aldosterone.
,D. Pheochromocytoma causing episodic hypotension and
hyperkalemia.
Correct answer
B
Rationales
Correct (B): Primary adrenal cortex destruction (Addison
disease) causes decreased cortisol and aldosterone. Loss of
aldosterone → renal sodium wasting (hyponatremia),
potassium retention (hyperkalemia), and orthostatic
hypotension. Elevated ACTH reflects lack of negative feedback;
hyperpigmentation occurs from increased POMC/ACTH-derived
melanocyte stimulation. This aligns with McCance’s description
of primary adrenal insufficiency mechanisms and early red-
flags.
A (incorrect): Secondary adrenal insufficiency shows low ACTH
(not elevated) and usually spares aldosterone, so hyperkalemia
and hyperpigmentation are unlikely.
C (incorrect): Exogenous steroid withdrawal typically
suppresses ACTH (low) initially; aldosterone is less affected and
hyperkalemia is not a primary feature.
D (incorrect): Pheochromocytoma causes episodic hypertension
and catecholamine excess signs, not chronic hyponatremia with
hyperkalemia and high ACTH.
Teaching point
Primary adrenal failure → low cortisol + low aldosterone →
hyponatremia, hyperkalemia, hypotension, ↑ACTH.
,Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 22.
2
Reference
Ch. 22 — Alterations of Hormonal Regulation — Disorders of
the Adrenal Cortex (Cushing Syndrome)
Stem
A 55-year-old man with progressive central obesity, proximal
muscle weakness, poorly controlled hypertension, and fasting
glucose 180 mg/dL is noted to have easy bruising and purple
abdominal striae. Random cortisol elevated; 24-hr urinary free
cortisol elevated. Which pathophysiologic mechanism best
accounts for his hyperglycemia and muscle weakness?
Options
A. Excess cortisol increases insulin sensitivity, causing
hyperinsulinemia and muscle catabolism.
B. Cortisol promotes gluconeogenesis and protein catabolism,
causing insulin resistance and proximal muscle wasting.
C. Aldosterone excess causes hypokalemia that triggers
proteolysis and hyperglycemia.
D. ACTH deficiency reduces adrenal androgen production
leading to hyperglycemia and weakness.
, Correct answer
B
Rationales
Correct (B): Chronic glucocorticoid excess increases hepatic
gluconeogenesis and peripheral insulin resistance, raising blood
glucose. Cortisol stimulates protein catabolism in muscle
(proximal weakness) and redistributes fat centrally—classic
mechanisms in Cushing syndrome as described in McCance.
A (incorrect): Cortisol decreases, not increases, insulin
sensitivity. Hyperinsulinemia may result secondarily but is not
the primary mechanism.
C (incorrect): Aldosterone excess leads to hypokalemia and
hypertension but does not explain cortisol-driven
gluconeogenesis and muscle wasting.
D (incorrect): ACTH deficiency would lower cortisol (not raise
it); symptoms would differ.
Teaching point
Cortisol → ↑gluconeogenesis + ↓insulin sensitivity + ↑protein
catabolism → hyperglycemia and proximal weakness.
Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 22.
3
