McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
Great — I’ll create the 20 advanced NCLEX-style MCQs based
only on the Endocrine Guidelines topics you provided. Each
item follows your required structure exactly. Because you asked
for many detailed, high-quality items, here are the 20 questions
(Ch. 20 — Endocrine Guidelines) you requested.
1)
Reference
Ch. 20 — Endocrine Guidelines — Addison Disease (Primary
adrenal insufficiency)
Stem
A 42-year-old woman presents with fatigue, dizziness when
standing, weight loss, and new tanning of her palmar creases.
Vital signs: BP 86/52 mmHg supine, HR 98; labs: Na⁺ 128 mEq/L,
K⁺ 5.6 mEq/L, glucose 62 mg/dL, ACTH markedly elevated.
Which pathophysiologic process best explains her presentation?
,A. Autoimmune destruction of the adrenal cortex causing loss
of cortisol and aldosterone synthesis.
B. Pituitary ACTH deficiency leading to inadequate cortisol
production but preserved aldosterone.
C. Ectopic ACTH production from a distant tumor causing
cortisol excess and mineralocorticoid suppression.
D. Primary hyperaldosteronism producing potassium wasting
and hypertension.
Correct answer
A
Rationales
Correct (A): Autoimmune adrenal destruction (common in
primary Addison disease) destroys adrenal cortical cells,
decreasing cortisol and aldosterone. Loss of aldosterone leads
to hyponatremia, hyperkalemia, hypotension from salt wasting,
and orthostatic symptoms; loss of cortisol contributes to
hypoglycemia and hyperpigmentation via elevated ACTH. This
aligns with McCance’s description of primary adrenal cortical
failure causing combined glucocorticoid and mineralocorticoid
deficiency. Clinically, recognizing the electrolyte pattern and
high ACTH prioritizes treatment.
Incorrect (B): Pituitary (secondary) insufficiency reduces ACTH
and cortisol but usually preserves aldosterone (regulated by
RAAS), so hyperkalemia and marked hypotension from
aldosterone loss would be unlikely.
Incorrect (C): Ectopic ACTH causes cortisol excess (Cushingoid
,features), not hyponatremia with hyperkalemia and not low
cortisol. Elevated ACTH with hypercortisolism would produce
hyperglycemia and hypertension, not the findings here.
Incorrect (D): Primary hyperaldosteronism causes hypertension
and hypokalemia — the opposite of this patient’s hypotension
and hyperkalemia.
Teaching point
Primary adrenal failure → low cortisol + low aldosterone →
hypotension, hyponatremia, hyperkalemia.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 20.
2)
Reference
Ch. 20 — Endocrine Guidelines — Addison Disease (Secondary
adrenal insufficiency / abrupt steroid withdrawal)
Stem
A 55-year-old man with rheumatoid arthritis abruptly stopped
long-term high-dose prednisone 3 days ago. He now reports
severe weakness, nausea, and lightheadedness. BP 92/60
mmHg; labs show Na⁺ 132 mEq/L, K⁺ 4.3 mEq/L, morning
cortisol low, ACTH low. Which pathophysiologic explanation is
most consistent?
, A. Secondary adrenal insufficiency due to chronic suppression
of hypothalamic–pituitary ACTH secretion, causing cortisol
deficiency but intact aldosterone.
B. Primary adrenal destruction causing both aldosterone and
cortisol loss.
C. Acute adrenal hemorrhage causing sudden loss of all adrenal
hormones and hyperkalemia.
D. Exogenous steroid pharmacologic action producing
continued mineralocorticoid excess.
Correct answer
A
Rationales
Correct (A): Chronic exogenous glucocorticoids suppress
CRH/ACTH via negative feedback; abrupt withdrawal causes
secondary adrenal insufficiency with low ACTH and low cortisol.
Aldosterone synthesis is primarily driven by RAAS, so
mineralocorticoid function is typically preserved — explaining
normal potassium. McCance emphasizes that secondary
insufficiency presents with hypotension and hypoglycemia
without the hyperkalemia of primary adrenal failure.
Incorrect (B): Primary adrenal destruction would show elevated
ACTH and hyperkalemia due to aldosterone loss; that’s not
present.
Incorrect (C): Adrenal hemorrhage is uncommon and would
produce low cortisol and aldosterone with hyperkalemia —
inconsistent with near-normal K⁺ and low ACTH.
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
Great — I’ll create the 20 advanced NCLEX-style MCQs based
only on the Endocrine Guidelines topics you provided. Each
item follows your required structure exactly. Because you asked
for many detailed, high-quality items, here are the 20 questions
(Ch. 20 — Endocrine Guidelines) you requested.
1)
Reference
Ch. 20 — Endocrine Guidelines — Addison Disease (Primary
adrenal insufficiency)
Stem
A 42-year-old woman presents with fatigue, dizziness when
standing, weight loss, and new tanning of her palmar creases.
Vital signs: BP 86/52 mmHg supine, HR 98; labs: Na⁺ 128 mEq/L,
K⁺ 5.6 mEq/L, glucose 62 mg/dL, ACTH markedly elevated.
Which pathophysiologic process best explains her presentation?
,A. Autoimmune destruction of the adrenal cortex causing loss
of cortisol and aldosterone synthesis.
B. Pituitary ACTH deficiency leading to inadequate cortisol
production but preserved aldosterone.
C. Ectopic ACTH production from a distant tumor causing
cortisol excess and mineralocorticoid suppression.
D. Primary hyperaldosteronism producing potassium wasting
and hypertension.
Correct answer
A
Rationales
Correct (A): Autoimmune adrenal destruction (common in
primary Addison disease) destroys adrenal cortical cells,
decreasing cortisol and aldosterone. Loss of aldosterone leads
to hyponatremia, hyperkalemia, hypotension from salt wasting,
and orthostatic symptoms; loss of cortisol contributes to
hypoglycemia and hyperpigmentation via elevated ACTH. This
aligns with McCance’s description of primary adrenal cortical
failure causing combined glucocorticoid and mineralocorticoid
deficiency. Clinically, recognizing the electrolyte pattern and
high ACTH prioritizes treatment.
Incorrect (B): Pituitary (secondary) insufficiency reduces ACTH
and cortisol but usually preserves aldosterone (regulated by
RAAS), so hyperkalemia and marked hypotension from
aldosterone loss would be unlikely.
Incorrect (C): Ectopic ACTH causes cortisol excess (Cushingoid
,features), not hyponatremia with hyperkalemia and not low
cortisol. Elevated ACTH with hypercortisolism would produce
hyperglycemia and hypertension, not the findings here.
Incorrect (D): Primary hyperaldosteronism causes hypertension
and hypokalemia — the opposite of this patient’s hypotension
and hyperkalemia.
Teaching point
Primary adrenal failure → low cortisol + low aldosterone →
hypotension, hyponatremia, hyperkalemia.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 20.
2)
Reference
Ch. 20 — Endocrine Guidelines — Addison Disease (Secondary
adrenal insufficiency / abrupt steroid withdrawal)
Stem
A 55-year-old man with rheumatoid arthritis abruptly stopped
long-term high-dose prednisone 3 days ago. He now reports
severe weakness, nausea, and lightheadedness. BP 92/60
mmHg; labs show Na⁺ 132 mEq/L, K⁺ 4.3 mEq/L, morning
cortisol low, ACTH low. Which pathophysiologic explanation is
most consistent?
, A. Secondary adrenal insufficiency due to chronic suppression
of hypothalamic–pituitary ACTH secretion, causing cortisol
deficiency but intact aldosterone.
B. Primary adrenal destruction causing both aldosterone and
cortisol loss.
C. Acute adrenal hemorrhage causing sudden loss of all adrenal
hormones and hyperkalemia.
D. Exogenous steroid pharmacologic action producing
continued mineralocorticoid excess.
Correct answer
A
Rationales
Correct (A): Chronic exogenous glucocorticoids suppress
CRH/ACTH via negative feedback; abrupt withdrawal causes
secondary adrenal insufficiency with low ACTH and low cortisol.
Aldosterone synthesis is primarily driven by RAAS, so
mineralocorticoid function is typically preserved — explaining
normal potassium. McCance emphasizes that secondary
insufficiency presents with hypotension and hypoglycemia
without the hyperkalemia of primary adrenal failure.
Incorrect (B): Primary adrenal destruction would show elevated
ACTH and hyperkalemia due to aldosterone loss; that’s not
present.
Incorrect (C): Adrenal hemorrhage is uncommon and would
produce low cortisol and aldosterone with hyperkalemia —
inconsistent with near-normal K⁺ and low ACTH.
