NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
NSG530 / NSG 530 EXAM 4 (LATEST )
Advanced Pathophysiology | Questions and Verified Answers | 100% Correct — Wilkes
Course: NSG 530 — Advanced Pathophysiology (Wilkes University) | Examination: Exam 4 — Comprehensive | Edition: 2026
/ 2027 | Format: 100 single-best-answer MCQs | Cognitive levels: 20% recall, 50% application, 30% analysis
Section 1: Endocrine Pathophysiology (Q1–Q20) | Section 2: Reproductive Pathophysiology (Q21–Q35) | Section 3: Renal &
Urologic Pathophysiology (Q36–Q50)
Section 4: Gastrointestinal & Hepatic Pathophysiology (Q51–Q65) | Section 5: Multisystem & Integrative Pathophysiology
(Q66–Q80)
Section 6: Pediatric & Geriatric Pathophysiology (Q81–Q90) | Section 7: Emerging & Special Topics in Pathophysiology
(Q91–Q100)
Section 1: Endocrine Pathophysiology
Q1: A 14-year-old girl with type 1 diabetes mellitus presents to the emergency department with deep,
rapid respirations (Kussmaul), a fruity breath odor, vomiting, and lethargy. Laboratory studies reveal
glucose 480 mg/dL, arterial pH 7.18, serum bicarbonate 9 mEq/L, and moderate serum ketones. Urine
is positive for ketones. Which pathophysiologic mechanism is the PRIMARY driver of the metabolic
acidosis observed in this patient?
A. Hypoinsulinemia increases hepatic gluconeogenesis and lipolysis, generating acetoacetate and
beta-hydroxybutyrate that dissociate and consume bicarbonate, producing a high-anion-gap metabolic
acidosis. [CORRECT]
B. Hyperglycemia directly suppresses renal bicarbonate reabsorption in the proximal tubule, causing bicarbonate
wasting and metabolic acidosis with a normal anion gap.
C. Lactic acid accumulates from tissue hypoperfusion and anaerobic glycolysis, producing a predominantly
lactate-driven metabolic acidosis with mild ketonuria.
D. Renal failure from acute tubular necrosis impairs hydrogen ion secretion, causing retention of inorganic acids
and a uremic metabolic acidosis.
Correct Answer: A
Rationale: Diabetic ketoacidosis (DKA) is defined by absolute insulin deficiency, which disinhibits hormone-sensitive lipase
and hepatic gluconeogenesis; free fatty acids are converted in hepatic mitochondria to ketone bodies (acetoacetate and
beta-hydroxybutyrate), which dissociate and consume bicarbonate, producing a high-anion-gap metabolic acidosis with
compensatory Kussmaul respirations. Option B describes proximal renal tubular acidosis, not DKA. Option C describes lactic
acidosis, which can coexist but is not the primary mechanism. Option D describes uremic acidosis from renal failure, which
is not present here.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 1
,NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
Q2: An elderly patient with type 2 diabetes presents with profound hyperglycemia (glucose 920
mg/dL), serum osmolality 360 mOsm/kg, minimal ketones, pH 7.34, and bicarbonate 22 mEq/L. The
patient is somnolent but responsive. Which combination of pathophysiologic mechanisms best
characterizes this hyperosmolar hyperglycemic state (HHS) versus DKA?
A. Markedly reduced insulin action with residual insulin secretion sufficient to suppress lipolysis and ketogenesis
but insufficient to promote peripheral glucose uptake; profound dehydration from osmotic diuresis dominates
the clinical picture. [CORRECT]
B. Complete insulin absence with full activation of lipolysis and ketogenesis; severe ketoacidosis dominates the
clinical picture with dehydration playing a secondary role.
C. Primary renal tubular defect in glucose handling leading to massive glycosuria and dehydration without insulin
resistance playing any role in pathogenesis.
D. Autoimmune beta-cell destruction causing acute insulin deficiency that triggers both profound hyperglycemia
and ketoacidosis identical to classical DKA in younger patients.
Correct Answer: A
Rationale: HHS occurs in type 2 diabetes when residual insulin secretion is sufficient to suppress lipolysis and ketogenesis
(preventing significant ketoacidosis) but inadequate to facilitate peripheral glucose uptake, resulting in profound
hyperglycemia, hyperosmolality, and dehydration from osmotic diuresis. The pH is typically >7.30 and bicarbonate >18
mEq/L. Option B describes DKA. Option C is incorrect because insulin resistance and relative insulin deficiency are central to
HHS pathogenesis. Option D describes type 1 diabetes DKA, which would feature prominent ketones and acidosis.
Q3: A patient receiving IV insulin for DKA experiences tremor, diaphoresis, tachycardia, confusion, and
a fingerstick glucose of 38 mg/dL. Which neuroendocrine counterregulatory response is MOST
responsible for the patient's adrenergic symptoms?
A. Activation of the sympathoadrenal system with epinephrine release, producing tremor, palpitations, and
diaphoresis, alongside glucagon-mediated hepatic glucose production. [CORRECT]
B. Cortisol-mediated gluconeogenesis occurring over hours, producing delayed reactive hyperglycemia without
acute adrenergic symptoms.
C. ADH release from the posterior pituitary causing water retention that dilutes serum sodium without producing
adrenergic symptoms.
D. Aldosterone-mediated sodium retention that increases intravascular volume and produces reflex bradycardia
rather than tachycardia.
Correct Answer: A
Rationale: Hypoglycemia triggers a hierarchical counterregulatory response: glucagon and epinephrine act within minutes
to increase hepatic glucose output and produce classic adrenergic symptoms (tremor, diaphoresis, tachycardia). Cortisol
and growth hormone are slower-acting and support later recovery. Option B describes cortisol's delayed effect. Options C
and D describe posterior pituitary and adrenal mineralocorticoid responses that do not mediate hypoglycemic symptoms.
AACN Essentials master's-level preparation emphasizes recognition of iatrogenic hypoglycemia during insulin therapy.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 2
,NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
Q4: A 42-year-old man with a 12-year history of type 2 diabetes, BMI 34, hemoglobin A1c 9.2%,
hypertension, and triglycerides 320 mg/dL has fasting C-peptide of 4.5 ng/mL (reference 0.8-3.1) and
negative autoantibodies. Which pathophysiologic mechanism is the PRIMARY driver of his
hyperglycemia?
A. Peripheral insulin resistance in skeletal muscle and adipose tissue, combined with a progressive defect in
beta-cell insulin secretion that develops as beta-cell mass declines over time, producing relative insulin
deficiency despite hyperinsulinemia early in disease. [CORRECT]
B. Autoimmune destruction of pancreatic beta cells producing absolute insulin deficiency and undetectable
C-peptide levels, identical to the pathophysiology of type 1 diabetes mellitus.
C. Primary defect in renal glucose reabsorption causing glycosuria-induced hypoglycemia and compensatory
hepatic glucose overproduction.
D. Excess glucagon secretion from pancreatic alpha cells that overrides normal insulin action and produces
hyperglycemia without any contribution from insulin resistance.
Correct Answer: A
Rationale: Type 2 diabetes pathophysiology is defined by insulin resistance in peripheral tissues (skeletal muscle, adipose,
liver) and a progressive defect in beta-cell insulin secretion. Early disease is characterized by hyperinsulinemia (elevated
C-peptide) as beta cells compensate; later disease features beta-cell exhaustion and relative insulin deficiency. Option B
describes type 1 diabetes (autoimmune beta-cell destruction with low/absent C-peptide). Options C and D describe
mechanisms that are not the primary drivers of type 2 diabetes.
Q5: A pregnant patient at 26 weeks' gestation has a 50-g oral glucose challenge result of 168 mg/dL,
confirmed by a 3-hour 100-g oral glucose tolerance test with two elevated values. Which
pathophysiologic mechanism is the PRIMARY cause of gestational diabetes mellitus (GDM)?
A. Placental secretion of diabetogenic hormones (human placental lactogen, progesterone, cortisol, prolactin,
tumor necrosis factor-alpha) induces maternal insulin resistance, which exceeds the maternal beta-cell
capacity for compensatory insulin secretion. [CORRECT]
B. Autoimmune destruction of maternal pancreatic beta cells during pregnancy causing acute-onset type 1
diabetes that resolves after delivery of the placenta.
C. Transient pituitary-dependent hypercortisolism from placental ACTH that suppresses endogenous insulin
secretion without peripheral insulin resistance.
D. Placental production of insulinase and proteolytic enzymes that directly degrade circulating maternal insulin
without altering insulin sensitivity.
Correct Answer: A
Rationale: GDM results from placental hormones (human placental lactogen, progesterone, prolactin, cortisol, TNF-alpha)
inducing maternal insulin resistance; the disorder arises when maternal beta cells cannot mount sufficient compensatory
hyperinsulinemia. Autoimmune beta-cell destruction (Option B) is type 1 diabetes, which would not resolve postpartum.
Options C and D do not represent the established mechanism. Symptoms typically resolve after delivery, but women with
GDM have a 35-60% lifetime risk of type 2 diabetes.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 3
, NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
Q6: A 32-year-old woman presents with weight loss of 15 lb, heat intolerance, palpitations, anxiety,
and a diffuse goiter. Laboratory studies show TSH <0.05 mIU/L, free T4 3.2 ng/dL, free T3 580 pg/dL,
and positive thyroid-stimulating immunoglobulins. Which pathophysiologic mechanism best explains
her hyperthyroidism?
A. Autoantibodies that activate the TSH receptor (thyroid-stimulating immunoglobulins, TSI) mimic TSH, driving
follicular hyperplasia, iodine uptake, and unregulated synthesis and release of T3 and T4, with loss of
hypothalamic-pituitary feedback suppression of TSH. [CORRECT]
B. Autoantibodies that destroy thyroid follicular cells, releasing pre-formed T3 and T4 in a transient surge
followed by permanent hypothyroidism, with elevated TSH throughout.
C. Autonomous hyperfunctioning thyroid adenoma secreting T3 and T4 independent of TSH, with a single hot
nodule on radioactive iodine uptake scan and suppressed TSH.
D. Pituitary TSH-secreting adenoma causing bilateral thyroid hyperplasia with elevated TSH, elevated free T4, and
absent thyroid autoantibodies.
Correct Answer: A
Rationale: Graves' disease is caused by thyroid-stimulating immunoglobulins (TSI) that bind and activate the TSH receptor,
driving unregulated thyroid hormone synthesis and diffuse goiter; TSH is suppressed by negative feedback from elevated
T4/T3. Option B describes Hashimoto's thyroiditis with hashitoxicosis. Option C describes toxic multinodular goiter or
solitary toxic adenoma. Option D describes a TSH-secreting pituitary adenoma, which is rare and would have elevated (not
suppressed) TSH.
Q7: A 58-year-old woman with a 20-year history of Hashimoto's thyroiditis is brought to the emergency
department in winter with hypothermia 32°C (89.6°F), bradycardia 38 bpm, hypoventilation,
hyponatremia 122 mEq/L, and obtundation. Which pathophysiologic mechanism best explains the
multisystem decompensation of myxedema coma?
A. Long-standing severe hypothyroidism causes generalized interstitial accumulation of glycosaminoglycans,
depressed cardiovascular and respiratory function, impaired renal free-water clearance with inappropriate
ADH activity, and decreased cerebral metabolism, culminating in hypothermia, hypoventilation,
hyponatremia, and coma. [CORRECT]
B. Acute autoimmune destruction of thyroid follicles releasing massive T4 and T3, producing thyroid storm with
hyperthermia, tachycardia, hypertension, and agitation, but not hypothermia.
C. Acute central pituitary failure causing sudden loss of TSH secretion and secondary hypothyroidism with normal
adrenal function, mild hypothermia, and preserved consciousness.
D. Sepsis-induced thyroid suppression (non-thyroidal illness syndrome) producing transient low T3 without TSH
elevation, hypothermia, or coma in the absence of preexisting thyroid disease.
Correct Answer: A
Rationale: Myxedema coma is a life-threatening decompensation of long-standing hypothyroidism characterized by
interstitial glycosaminoglycan accumulation, decreased cardiac output and ventilation, impaired renal water excretion with
hyponatremia, hypothermia, and altered mental status. Triggers include cold exposure, infection, sedatives, and trauma.
Option B describes thyroid storm. Option C describes secondary hypothyroidism. Option D describes euthyroid sick
syndrome, which is mild and does not cause coma.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 4
NSG530 / NSG 530 EXAM 4 (LATEST )
Advanced Pathophysiology | Questions and Verified Answers | 100% Correct — Wilkes
Course: NSG 530 — Advanced Pathophysiology (Wilkes University) | Examination: Exam 4 — Comprehensive | Edition: 2026
/ 2027 | Format: 100 single-best-answer MCQs | Cognitive levels: 20% recall, 50% application, 30% analysis
Section 1: Endocrine Pathophysiology (Q1–Q20) | Section 2: Reproductive Pathophysiology (Q21–Q35) | Section 3: Renal &
Urologic Pathophysiology (Q36–Q50)
Section 4: Gastrointestinal & Hepatic Pathophysiology (Q51–Q65) | Section 5: Multisystem & Integrative Pathophysiology
(Q66–Q80)
Section 6: Pediatric & Geriatric Pathophysiology (Q81–Q90) | Section 7: Emerging & Special Topics in Pathophysiology
(Q91–Q100)
Section 1: Endocrine Pathophysiology
Q1: A 14-year-old girl with type 1 diabetes mellitus presents to the emergency department with deep,
rapid respirations (Kussmaul), a fruity breath odor, vomiting, and lethargy. Laboratory studies reveal
glucose 480 mg/dL, arterial pH 7.18, serum bicarbonate 9 mEq/L, and moderate serum ketones. Urine
is positive for ketones. Which pathophysiologic mechanism is the PRIMARY driver of the metabolic
acidosis observed in this patient?
A. Hypoinsulinemia increases hepatic gluconeogenesis and lipolysis, generating acetoacetate and
beta-hydroxybutyrate that dissociate and consume bicarbonate, producing a high-anion-gap metabolic
acidosis. [CORRECT]
B. Hyperglycemia directly suppresses renal bicarbonate reabsorption in the proximal tubule, causing bicarbonate
wasting and metabolic acidosis with a normal anion gap.
C. Lactic acid accumulates from tissue hypoperfusion and anaerobic glycolysis, producing a predominantly
lactate-driven metabolic acidosis with mild ketonuria.
D. Renal failure from acute tubular necrosis impairs hydrogen ion secretion, causing retention of inorganic acids
and a uremic metabolic acidosis.
Correct Answer: A
Rationale: Diabetic ketoacidosis (DKA) is defined by absolute insulin deficiency, which disinhibits hormone-sensitive lipase
and hepatic gluconeogenesis; free fatty acids are converted in hepatic mitochondria to ketone bodies (acetoacetate and
beta-hydroxybutyrate), which dissociate and consume bicarbonate, producing a high-anion-gap metabolic acidosis with
compensatory Kussmaul respirations. Option B describes proximal renal tubular acidosis, not DKA. Option C describes lactic
acidosis, which can coexist but is not the primary mechanism. Option D describes uremic acidosis from renal failure, which
is not present here.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 1
,NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
Q2: An elderly patient with type 2 diabetes presents with profound hyperglycemia (glucose 920
mg/dL), serum osmolality 360 mOsm/kg, minimal ketones, pH 7.34, and bicarbonate 22 mEq/L. The
patient is somnolent but responsive. Which combination of pathophysiologic mechanisms best
characterizes this hyperosmolar hyperglycemic state (HHS) versus DKA?
A. Markedly reduced insulin action with residual insulin secretion sufficient to suppress lipolysis and ketogenesis
but insufficient to promote peripheral glucose uptake; profound dehydration from osmotic diuresis dominates
the clinical picture. [CORRECT]
B. Complete insulin absence with full activation of lipolysis and ketogenesis; severe ketoacidosis dominates the
clinical picture with dehydration playing a secondary role.
C. Primary renal tubular defect in glucose handling leading to massive glycosuria and dehydration without insulin
resistance playing any role in pathogenesis.
D. Autoimmune beta-cell destruction causing acute insulin deficiency that triggers both profound hyperglycemia
and ketoacidosis identical to classical DKA in younger patients.
Correct Answer: A
Rationale: HHS occurs in type 2 diabetes when residual insulin secretion is sufficient to suppress lipolysis and ketogenesis
(preventing significant ketoacidosis) but inadequate to facilitate peripheral glucose uptake, resulting in profound
hyperglycemia, hyperosmolality, and dehydration from osmotic diuresis. The pH is typically >7.30 and bicarbonate >18
mEq/L. Option B describes DKA. Option C is incorrect because insulin resistance and relative insulin deficiency are central to
HHS pathogenesis. Option D describes type 1 diabetes DKA, which would feature prominent ketones and acidosis.
Q3: A patient receiving IV insulin for DKA experiences tremor, diaphoresis, tachycardia, confusion, and
a fingerstick glucose of 38 mg/dL. Which neuroendocrine counterregulatory response is MOST
responsible for the patient's adrenergic symptoms?
A. Activation of the sympathoadrenal system with epinephrine release, producing tremor, palpitations, and
diaphoresis, alongside glucagon-mediated hepatic glucose production. [CORRECT]
B. Cortisol-mediated gluconeogenesis occurring over hours, producing delayed reactive hyperglycemia without
acute adrenergic symptoms.
C. ADH release from the posterior pituitary causing water retention that dilutes serum sodium without producing
adrenergic symptoms.
D. Aldosterone-mediated sodium retention that increases intravascular volume and produces reflex bradycardia
rather than tachycardia.
Correct Answer: A
Rationale: Hypoglycemia triggers a hierarchical counterregulatory response: glucagon and epinephrine act within minutes
to increase hepatic glucose output and produce classic adrenergic symptoms (tremor, diaphoresis, tachycardia). Cortisol
and growth hormone are slower-acting and support later recovery. Option B describes cortisol's delayed effect. Options C
and D describe posterior pituitary and adrenal mineralocorticoid responses that do not mediate hypoglycemic symptoms.
AACN Essentials master's-level preparation emphasizes recognition of iatrogenic hypoglycemia during insulin therapy.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 2
,NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
Q4: A 42-year-old man with a 12-year history of type 2 diabetes, BMI 34, hemoglobin A1c 9.2%,
hypertension, and triglycerides 320 mg/dL has fasting C-peptide of 4.5 ng/mL (reference 0.8-3.1) and
negative autoantibodies. Which pathophysiologic mechanism is the PRIMARY driver of his
hyperglycemia?
A. Peripheral insulin resistance in skeletal muscle and adipose tissue, combined with a progressive defect in
beta-cell insulin secretion that develops as beta-cell mass declines over time, producing relative insulin
deficiency despite hyperinsulinemia early in disease. [CORRECT]
B. Autoimmune destruction of pancreatic beta cells producing absolute insulin deficiency and undetectable
C-peptide levels, identical to the pathophysiology of type 1 diabetes mellitus.
C. Primary defect in renal glucose reabsorption causing glycosuria-induced hypoglycemia and compensatory
hepatic glucose overproduction.
D. Excess glucagon secretion from pancreatic alpha cells that overrides normal insulin action and produces
hyperglycemia without any contribution from insulin resistance.
Correct Answer: A
Rationale: Type 2 diabetes pathophysiology is defined by insulin resistance in peripheral tissues (skeletal muscle, adipose,
liver) and a progressive defect in beta-cell insulin secretion. Early disease is characterized by hyperinsulinemia (elevated
C-peptide) as beta cells compensate; later disease features beta-cell exhaustion and relative insulin deficiency. Option B
describes type 1 diabetes (autoimmune beta-cell destruction with low/absent C-peptide). Options C and D describe
mechanisms that are not the primary drivers of type 2 diabetes.
Q5: A pregnant patient at 26 weeks' gestation has a 50-g oral glucose challenge result of 168 mg/dL,
confirmed by a 3-hour 100-g oral glucose tolerance test with two elevated values. Which
pathophysiologic mechanism is the PRIMARY cause of gestational diabetes mellitus (GDM)?
A. Placental secretion of diabetogenic hormones (human placental lactogen, progesterone, cortisol, prolactin,
tumor necrosis factor-alpha) induces maternal insulin resistance, which exceeds the maternal beta-cell
capacity for compensatory insulin secretion. [CORRECT]
B. Autoimmune destruction of maternal pancreatic beta cells during pregnancy causing acute-onset type 1
diabetes that resolves after delivery of the placenta.
C. Transient pituitary-dependent hypercortisolism from placental ACTH that suppresses endogenous insulin
secretion without peripheral insulin resistance.
D. Placental production of insulinase and proteolytic enzymes that directly degrade circulating maternal insulin
without altering insulin sensitivity.
Correct Answer: A
Rationale: GDM results from placental hormones (human placental lactogen, progesterone, prolactin, cortisol, TNF-alpha)
inducing maternal insulin resistance; the disorder arises when maternal beta cells cannot mount sufficient compensatory
hyperinsulinemia. Autoimmune beta-cell destruction (Option B) is type 1 diabetes, which would not resolve postpartum.
Options C and D do not represent the established mechanism. Symptoms typically resolve after delivery, but women with
GDM have a 35-60% lifetime risk of type 2 diabetes.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 3
, NSG 530 Exam 4 — Advanced Pathophysiology (2026/2027) Wilkes University
Q6: A 32-year-old woman presents with weight loss of 15 lb, heat intolerance, palpitations, anxiety,
and a diffuse goiter. Laboratory studies show TSH <0.05 mIU/L, free T4 3.2 ng/dL, free T3 580 pg/dL,
and positive thyroid-stimulating immunoglobulins. Which pathophysiologic mechanism best explains
her hyperthyroidism?
A. Autoantibodies that activate the TSH receptor (thyroid-stimulating immunoglobulins, TSI) mimic TSH, driving
follicular hyperplasia, iodine uptake, and unregulated synthesis and release of T3 and T4, with loss of
hypothalamic-pituitary feedback suppression of TSH. [CORRECT]
B. Autoantibodies that destroy thyroid follicular cells, releasing pre-formed T3 and T4 in a transient surge
followed by permanent hypothyroidism, with elevated TSH throughout.
C. Autonomous hyperfunctioning thyroid adenoma secreting T3 and T4 independent of TSH, with a single hot
nodule on radioactive iodine uptake scan and suppressed TSH.
D. Pituitary TSH-secreting adenoma causing bilateral thyroid hyperplasia with elevated TSH, elevated free T4, and
absent thyroid autoantibodies.
Correct Answer: A
Rationale: Graves' disease is caused by thyroid-stimulating immunoglobulins (TSI) that bind and activate the TSH receptor,
driving unregulated thyroid hormone synthesis and diffuse goiter; TSH is suppressed by negative feedback from elevated
T4/T3. Option B describes Hashimoto's thyroiditis with hashitoxicosis. Option C describes toxic multinodular goiter or
solitary toxic adenoma. Option D describes a TSH-secreting pituitary adenoma, which is rare and would have elevated (not
suppressed) TSH.
Q7: A 58-year-old woman with a 20-year history of Hashimoto's thyroiditis is brought to the emergency
department in winter with hypothermia 32°C (89.6°F), bradycardia 38 bpm, hypoventilation,
hyponatremia 122 mEq/L, and obtundation. Which pathophysiologic mechanism best explains the
multisystem decompensation of myxedema coma?
A. Long-standing severe hypothyroidism causes generalized interstitial accumulation of glycosaminoglycans,
depressed cardiovascular and respiratory function, impaired renal free-water clearance with inappropriate
ADH activity, and decreased cerebral metabolism, culminating in hypothermia, hypoventilation,
hyponatremia, and coma. [CORRECT]
B. Acute autoimmune destruction of thyroid follicles releasing massive T4 and T3, producing thyroid storm with
hyperthermia, tachycardia, hypertension, and agitation, but not hypothermia.
C. Acute central pituitary failure causing sudden loss of TSH secretion and secondary hypothyroidism with normal
adrenal function, mild hypothermia, and preserved consciousness.
D. Sepsis-induced thyroid suppression (non-thyroidal illness syndrome) producing transient low T3 without TSH
elevation, hypothermia, or coma in the absence of preexisting thyroid disease.
Correct Answer: A
Rationale: Myxedema coma is a life-threatening decompensation of long-standing hypothyroidism characterized by
interstitial glycosaminoglycan accumulation, decreased cardiac output and ventilation, impaired renal water excretion with
hyponatremia, hypothermia, and altered mental status. Triggers include cold exposure, infection, sedatives, and trauma.
Option B describes thyroid storm. Option C describes secondary hypothyroidism. Option D describes euthyroid sick
syndrome, which is mild and does not cause coma.
NSG530 / Exam 4 — 100 Questions — Verified Answers Page 4
