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 — Addison
Disease
Stem
A 42-year-old woman presents with progressive fatigue,
dizziness when standing, salt craving, and new diffuse skin
hyperpigmentation. Vital signs: BP 92/60 mmHg, HR 96 bpm.
Labs: Na⁺ 124 mEq/L, K⁺ 5.6 mEq/L, morning serum cortisol
low, ACTH markedly elevated. Which interpretation best
explains these findings?
Options
A. Primary adrenal insufficiency (autoimmune destruction)
causing decreased cortisol and aldosterone with
compensatory elevated ACTH.
B. Secondary adrenal insufficiency due to pituitary failure
causing low ACTH and low cortisol.
C. Chronic exogenous glucocorticoid use causing adrenal
,suppression with low ACTH.
D. Pseudohyperkalemia from hemolysis causing spurious
potassium elevation and adrenal function is normal.
Correct answer
A
Rationales
Correct (A): Elevated ACTH with low cortisol and
hyponatremia/hyperkalemia indicates primary adrenal
(Addison) disease. Loss of cortisol and aldosterone
(mineralocorticoid) explains hypotension, salt craving,
hyponatremia, and hyperkalemia; increased ACTH produces
hyperpigmentation. Mechanistically, autoimmune destruction
of the adrenal cortex reduces glucocorticoid and
mineralocorticoid synthesis, consistent with McCance’s
description of primary adrenal insufficiency. This is the safest
interpretation and guides urgent replacement therapy.
Incorrect (B): Secondary (pituitary) failure causes low ACTH
with low cortisol but normal aldosterone (renin–angiotensin
driven), so hyperkalemia and hyperpigmentation are unlikely.
Incorrect (C): Exogenous steroids produce low ACTH and low
endogenous cortisol; they do not cause hyperpigmentation or
hyperkalemia.
Incorrect (D): Pseudohyperkalemia would not explain
hyponatremia, hypotension, low cortisol, or elevated ACTH.
,Teaching point
Primary adrenal failure → low cortisol/aldosterone, ↑ACTH,
hyponatremia, hyperkalemia, hyperpigmentation.
Citation
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 — Addisonian
(Acute) Crisis
Stem
A 58-year-old man with known primary adrenal insufficiency is
brought from home confused and vomiting after a febrile
gastroenteritis. BP 74/48 mmHg, HR 120 bpm, temperature
38.9°C. He has tacky mucous membranes. Lab: Na⁺ 118 mEq/L,
K⁺ 6.2 mEq/L, glucose 52 mg/dL. What is the immediate
pathophysiologic priority in management?
Options
A. IV hydrocortisone and aggressive IV fluids to restore
vascular tone and correct electrolyte shifts.
B. IV broad-spectrum antibiotics first, as hypotension is most
likely septic shock.
C. IV insulin and glucose infusion to correct hyperkalemia by
driving K⁺ into cells.
, D. Immediate administration of oral fludrocortisone at home
dosing to restore mineralocorticoid activity.
Correct answer
A
Rationales
Correct (A): In acute adrenal crisis extreme cortisol and
aldosterone deficiency cause vasodilation, decreased vascular
responsiveness to catecholamines, hypovolemia,
hyponatremia, and hyperkalemia. IV hydrocortisone restores
cortisol (rapid hemodynamic effects) and glucocorticoid-
mediated vascular responsiveness while IV fluids correct
hypovolemia — immediate, life-saving measures per
McCance.
Incorrect (B): While infection may precipitate crisis, empiric
antibiotics without steroid/fluid resuscitation delays
correction of life-threatening hypotension and metabolic
derangements.
Incorrect (C): Insulin-dextrose temporarily shifts K⁺
intracellularly but does not reverse cortisol/aldosterone
deficiency causing hemodynamic collapse; treat cortisol deficit
first.
Incorrect (D): Oral fludrocortisone is too slow and insufficient
in the acute setting; IV glucocorticoid is indicated immediately.
Teaching point
Acute adrenal crisis: IV glucocorticoid + fluids first — restores
vascular tone and corrects electrolytes.
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 — Addison
Disease
Stem
A 42-year-old woman presents with progressive fatigue,
dizziness when standing, salt craving, and new diffuse skin
hyperpigmentation. Vital signs: BP 92/60 mmHg, HR 96 bpm.
Labs: Na⁺ 124 mEq/L, K⁺ 5.6 mEq/L, morning serum cortisol
low, ACTH markedly elevated. Which interpretation best
explains these findings?
Options
A. Primary adrenal insufficiency (autoimmune destruction)
causing decreased cortisol and aldosterone with
compensatory elevated ACTH.
B. Secondary adrenal insufficiency due to pituitary failure
causing low ACTH and low cortisol.
C. Chronic exogenous glucocorticoid use causing adrenal
,suppression with low ACTH.
D. Pseudohyperkalemia from hemolysis causing spurious
potassium elevation and adrenal function is normal.
Correct answer
A
Rationales
Correct (A): Elevated ACTH with low cortisol and
hyponatremia/hyperkalemia indicates primary adrenal
(Addison) disease. Loss of cortisol and aldosterone
(mineralocorticoid) explains hypotension, salt craving,
hyponatremia, and hyperkalemia; increased ACTH produces
hyperpigmentation. Mechanistically, autoimmune destruction
of the adrenal cortex reduces glucocorticoid and
mineralocorticoid synthesis, consistent with McCance’s
description of primary adrenal insufficiency. This is the safest
interpretation and guides urgent replacement therapy.
Incorrect (B): Secondary (pituitary) failure causes low ACTH
with low cortisol but normal aldosterone (renin–angiotensin
driven), so hyperkalemia and hyperpigmentation are unlikely.
Incorrect (C): Exogenous steroids produce low ACTH and low
endogenous cortisol; they do not cause hyperpigmentation or
hyperkalemia.
Incorrect (D): Pseudohyperkalemia would not explain
hyponatremia, hypotension, low cortisol, or elevated ACTH.
,Teaching point
Primary adrenal failure → low cortisol/aldosterone, ↑ACTH,
hyponatremia, hyperkalemia, hyperpigmentation.
Citation
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 — Addisonian
(Acute) Crisis
Stem
A 58-year-old man with known primary adrenal insufficiency is
brought from home confused and vomiting after a febrile
gastroenteritis. BP 74/48 mmHg, HR 120 bpm, temperature
38.9°C. He has tacky mucous membranes. Lab: Na⁺ 118 mEq/L,
K⁺ 6.2 mEq/L, glucose 52 mg/dL. What is the immediate
pathophysiologic priority in management?
Options
A. IV hydrocortisone and aggressive IV fluids to restore
vascular tone and correct electrolyte shifts.
B. IV broad-spectrum antibiotics first, as hypotension is most
likely septic shock.
C. IV insulin and glucose infusion to correct hyperkalemia by
driving K⁺ into cells.
, D. Immediate administration of oral fludrocortisone at home
dosing to restore mineralocorticoid activity.
Correct answer
A
Rationales
Correct (A): In acute adrenal crisis extreme cortisol and
aldosterone deficiency cause vasodilation, decreased vascular
responsiveness to catecholamines, hypovolemia,
hyponatremia, and hyperkalemia. IV hydrocortisone restores
cortisol (rapid hemodynamic effects) and glucocorticoid-
mediated vascular responsiveness while IV fluids correct
hypovolemia — immediate, life-saving measures per
McCance.
Incorrect (B): While infection may precipitate crisis, empiric
antibiotics without steroid/fluid resuscitation delays
correction of life-threatening hypotension and metabolic
derangements.
Incorrect (C): Insulin-dextrose temporarily shifts K⁺
intracellularly but does not reverse cortisol/aldosterone
deficiency causing hemodynamic collapse; treat cortisol deficit
first.
Incorrect (D): Oral fludrocortisone is too slow and insufficient
in the acute setting; IV glucocorticoid is indicated immediately.
Teaching point
Acute adrenal crisis: IV glucocorticoid + fluids first — restores
vascular tone and corrects electrolytes.
