BIOD 152 FINAL EXAM
ESSENTIAL HUMAN ANATOMY AND PHYSIOLOGY II WITH LAB
2026/2027 Edition
120 Questions with Verified Correct Answers • 10 Sections • Lab-Based & Clinical Application
Examination Overview: This comprehensive 120-question final examination assesses mastery of BIOD 152 Essential
Human Anatomy and Physiology II with Lab, covering the endocrine, blood, cardiovascular, lymphatic/immune,
respiratory, digestive, urinary, and reproductive systems, plus lab-based practical applications and clinical case studies. The
cognitive level distribution targets 20% recall, 50% application, and 30% analysis. Approximately 70% of items are
scenario-based (clinical cases, physiological processes, lab interpretations); 30% are direct knowledge. Each question
includes the correct answer marked with *[CORRECT]* and a rationale referencing BIOD 152 curriculum standards and
anatomical/physiological principles.
Section 1: Endocrine System
Q1: A patient presents with elevated blood glucose, and lab results show elevated TSH with low T3/T4.
The physician suspects a pituitary disorder. Which of the following best explains how the
hypothalamus-pituitary-thyroid axis is regulated?
A. The hypothalamus secretes thyroid-stimulating hormone (TSH), which directly stimulates the thyroid gland to
release T3 and T4
B. The hypothalamus secretes thyrotropin-releasing hormone (TRH), which stimulates the anterior
pituitary to release TSH, which then stimulates the thyroid to release T3 and T4; T3/T4 exert negative
feedback on both the hypothalamus and anterior pituitary *[CORRECT]*
C. The posterior pituitary releases TSH directly into the bloodstream, where it activates thyroid follicular cells
D. The thyroid gland secretes TRH, which inhibits the hypothalamus in a positive feedback loop
Correct Answer: B
Rationale: The hypothalamus secretes TRH, which stimulates the anterior pituitary to release TSH, which then stimulates
the thyroid follicular cells to synthesize and release T3 and T4. T3 and T4 exert negative feedback on both the
hypothalamus (decreasing TRH) and anterior pituitary (decreasing TSH) to maintain homeostasis. Options A and C
incorrectly localize TSH secretion; the anterior pituitary, not the hypothalamus or posterior pituitary, releases TSH. Option
D reverses the regulatory direction and incorrectly identifies positive feedback.
,Q2: A 45-year-old patient presents with weight gain, moon face, central obesity, and elevated blood
pressure. Lab tests reveal elevated cortisol levels. Which endocrine disorder is most consistent with these
findings, and what is the underlying mechanism?
A. Addison's disease, due to adrenal cortex hypofunction
B. Cushing's syndrome, due to hypersecretion of cortisol from the adrenal cortex (often from an adrenal
adenoma or pituitary ACTH-secreting adenoma) *[CORRECT]*
C. Cushing's disease, due to hypersecretion of aldosterone from the adrenal medulla
D. Pheochromocytoma, due to epinephrine hypersecretion from the adrenal cortex
Correct Answer: B
Rationale: Cushing's syndrome results from chronic hypercortisolism, commonly caused by an adrenal adenoma or
pituitary ACTH-secreting adenoma (Cushing's disease when pituitary in origin). Symptoms include moon face, buffalo
hump, central obesity, hypertension, hyperglycemia, and striae. Addison's disease (A) is adrenal insufficiency causing
hypocortisolism with fatigue, weight loss, and hyperpigmentation. Aldosterone (C) is from the adrenal cortex (not medulla)
and Cushing's is cortisol, not aldosterone. Pheochromocytoma (D) arises from adrenal medulla catecholamine
hypersecretion, causing episential hypertension.
Q3: Which hormone is released from the posterior pituitary and plays a key role in water reabsorption in
the kidneys?
A. Oxytocin
B. Antidiuretic hormone (ADH, vasopressin) *[CORRECT]*
C. Aldosterone
D. Atrial natriuretic peptide (ANP)
Correct Answer: B
Rationale: Antidiuretic hormone (ADH, also called vasopressin) is synthesized in the hypothalamus and released from the
posterior pituitary; it increases water reabsorption in the collecting ducts of the kidney by inserting aquaporin-2 channels.
Oxytocin (A) is also released from the posterior pituitary but stimulates uterine contractions and milk ejection. Aldosterone
(C) is from the adrenal cortex and regulates sodium reabsorption. ANP (D) is from the heart atria and promotes sodium
excretion.
Q4: A patient with Type 1 diabetes mellitus asks why they must take insulin injections. Which
explanation best describes the underlying pathophysiology?
A. The alpha cells of the pancreatic islets are destroyed, preventing glucagon secretion
B. The beta cells of the pancreatic islets of Langerhans are destroyed by autoimmune processes,
preventing insulin production; without insulin, glucose cannot enter most cells (muscle, adipose), leading
to hyperglycemia *[CORRECT]*
C. The delta cells of the pancreas oversecrete somatostatin, inhibiting insulin release
D. Insulin receptors in the liver are downregulated, causing insulin resistance
Correct Answer: B
Rationale: Type 1 diabetes mellitus is caused by autoimmune destruction of beta cells in the pancreatic islets of
Langerhans, eliminating insulin production. Without insulin, glucose transporter (GLUT4) translocation in muscle and
adipose cells fails, causing hyperglycemia, polyuria, polydipsia, and polyphagia. Alpha cells (A) secrete glucagon and are
spared. Delta cells (C) secrete somatostatin. Insulin resistance (D) characterizes Type 2 diabetes, not Type 1. Exogenous
insulin is required for survival in Type 1 diabetes.
,Q5: A patient presents with muscle cramps, tingling in the fingers, and a positive Chvostek sign (facial
muscle spasm with facial nerve tapping). Lab tests show low serum calcium. Which endocrine disorder is
most likely, and what is the mechanism?
A. Hyperparathyroidism, due to excessive PTH causing calcium release from bone
B. Hypoparathyroidism, due to insufficient PTH secretion leading to decreased blood calcium and
increased neuromuscular excitability *[CORRECT]*
C. Hyperthyroidism, due to excessive T4 causing calcium loss in urine
D. Cushing's syndrome, due to cortisol excess causing bone resorption
Correct Answer: B
Rationale: Hypoparathyroidism (low PTH) decreases blood calcium by reducing bone resorption, renal calcium
reabsorption, and vitamin D activation. Low calcium increases neuromuscular excitability, causing tetany, paresthesias,
and positive Chvostek/Trousseau signs. Hyperparathyroidism (A) causes hypercalcemia with "stones, bones, groans, and
psychiatric overtones." Hyperthyroidism (C) does not typically cause hypocalcemia. Cushing's (D) causes cortisol excess but
not the tetany of hypocalcemia. PTH is the master regulator of blood calcium.
Q6: Which endocrine gland is both an endocrine and exocrine gland, and what are its respective
hormone and enzyme products?
A. The liver, which produces bile (exocrine) and insulin-like growth factors (endocrine)
B. The pancreas, which secretes digestive enzymes (exocrine, via acinar cells into the duodenum) and
hormones insulin, glucagon, somatostatin (endocrine, via islets of Langerhans into blood)
*[CORRECT]*
C. The thyroid gland, which produces thyroid hormones (endocrine) and digestive enzymes (exocrine)
D. The adrenal gland, which produces cortisol (endocrine) and adrenaline (exocrine)
Correct Answer: B
Rationale: The pancreas is a dual gland. The exocrine portion (acinar cells and ducts) secretes digestive enzymes (amylase,
lipase, proteases) into the duodenum via the pancreatic duct. The endocrine portion (islets of Langerhans) secretes
hormones directly into the bloodstream: insulin (beta cells), glucagon (alpha cells), somatostatin (delta cells), and
pancreatic polypeptide (PP/F cells). The liver (A) is primarily exocrine (bile). The thyroid (C) is purely endocrine. The
adrenal (D) is purely endocrine.
Q7: A patient has elevated TSH, low T3/T4, fatigue, cold intolerance, weight gain, and bradycardia.
What is the most likely diagnosis and the level of dysfunction?
A. Primary hyperthyroidism (thyroid origin)
B. Primary hypothyroidism (thyroid gland dysfunction, such as Hashimoto's thyroiditis); elevated TSH
reflects loss of negative feedback from low T3/T4 *[CORRECT]*
C. Secondary hypothyroidism (pituitary dysfunction with low TSH)
D. Tertiary hypothyroidism (hypothalamic dysfunction with low TRH)
Correct Answer: B
Rationale: Primary hypothyroidism (e.g., Hashimoto's thyroiditis) features low T3/T4 due to thyroid gland failure. The
pituitary responds with elevated TSH (loss of negative feedback). Symptoms include fatigue, cold intolerance, weight gain,
bradycardia, dry skin, and constipation. Hyperthyroidism (A) would show low TSH with elevated T3/T4. Secondary (C)
and tertiary (D) hypothyroidism show low/normal TSH because the pituitary/hypothalamus is the problem. The elevated
TSH confirms primary thyroid dysfunction.
, Q8: Which hormone counteracts insulin by promoting glycogenolysis, gluconeogenesis, and lipolysis,
especially during fasting or hypoglycemia?
A. Glucagon, secreted by alpha cells of the pancreatic islets *[CORRECT]*
B. Insulin, secreted by beta cells of the pancreatic islets
C. Somatostatin, secreted by delta cells of the pancreatic islets
D. Aldosterone, secreted by the adrenal cortex
Correct Answer: A
Rationale: Glucagon, secreted by alpha cells of the pancreatic islets, raises blood glucose during fasting by stimulating
glycogenolysis (liver), gluconeogenesis, and lipolysis. It is the primary counter-regulatory hormone to insulin. Insulin (B)
lowers blood glucose. Somatostatin (C) inhibits both insulin and glucagon. Aldosterone (D) regulates sodium and water
balance, not glucose. Glucagon and insulin work in opposition to maintain blood glucose homeostasis.
Q9: A patient presents with hypertension, hypokalemia, and muscle weakness. Labs reveal elevated
aldosterone with low renin. Which endocrine disorder is most likely?
A. Addison's disease (adrenal insufficiency)
B. Conn's syndrome (primary hyperaldosteronism), typically from an adrenal adenoma *[CORRECT]*
C. Cushing's syndrome (cortisol excess)
D. Pheochromocytoma (catecholamine-secreting tumor)
Correct Answer: B
Rationale: Conn's syndrome (primary hyperaldosteronism) is characterized by autonomous aldosterone secretion (typically
adrenal adenoma), causing sodium retention (hypertension), potassium excretion (hypokalemia and muscle weakness), and
suppressed renin. Addison's (A) is adrenal insufficiency with hypoaldosteronism. Cushing's (C) is cortisol excess.
Pheochromocytoma (D) causes episodic hypertension from catecholamines. Low renin distinguishes primary from
secondary hyperaldosteronism.
Q10: The adrenal medulla secretes epinephrine and norepinephrine in response to sympathetic
stimulation. Which physiological response is NOT typical of these hormones?
A. Increased heart rate and contractility
B. Bronchodilation and increased respiratory rate
C. Increased digestive activity and gastrointestinal motility *[CORRECT]*
D. Glycogenolysis and lipolysis to provide energy
Correct Answer: C
Rationale: Epinephrine and norepinephrine mediate the "fight-or-flight" response, increasing heart rate and contractility
(A), bronchodilation (B), and mobilizing energy via glycogenolysis and lipolysis (D). They inhibit digestive activity and GI
motility (opposite of C), redirecting blood flow away from the digestive tract to skeletal muscle. The sympathetic system
generally inhibits digestion; the parasympathetic system stimulates it. Option C is the parasympathetic response, not the
sympathetic.
ESSENTIAL HUMAN ANATOMY AND PHYSIOLOGY II WITH LAB
2026/2027 Edition
120 Questions with Verified Correct Answers • 10 Sections • Lab-Based & Clinical Application
Examination Overview: This comprehensive 120-question final examination assesses mastery of BIOD 152 Essential
Human Anatomy and Physiology II with Lab, covering the endocrine, blood, cardiovascular, lymphatic/immune,
respiratory, digestive, urinary, and reproductive systems, plus lab-based practical applications and clinical case studies. The
cognitive level distribution targets 20% recall, 50% application, and 30% analysis. Approximately 70% of items are
scenario-based (clinical cases, physiological processes, lab interpretations); 30% are direct knowledge. Each question
includes the correct answer marked with *[CORRECT]* and a rationale referencing BIOD 152 curriculum standards and
anatomical/physiological principles.
Section 1: Endocrine System
Q1: A patient presents with elevated blood glucose, and lab results show elevated TSH with low T3/T4.
The physician suspects a pituitary disorder. Which of the following best explains how the
hypothalamus-pituitary-thyroid axis is regulated?
A. The hypothalamus secretes thyroid-stimulating hormone (TSH), which directly stimulates the thyroid gland to
release T3 and T4
B. The hypothalamus secretes thyrotropin-releasing hormone (TRH), which stimulates the anterior
pituitary to release TSH, which then stimulates the thyroid to release T3 and T4; T3/T4 exert negative
feedback on both the hypothalamus and anterior pituitary *[CORRECT]*
C. The posterior pituitary releases TSH directly into the bloodstream, where it activates thyroid follicular cells
D. The thyroid gland secretes TRH, which inhibits the hypothalamus in a positive feedback loop
Correct Answer: B
Rationale: The hypothalamus secretes TRH, which stimulates the anterior pituitary to release TSH, which then stimulates
the thyroid follicular cells to synthesize and release T3 and T4. T3 and T4 exert negative feedback on both the
hypothalamus (decreasing TRH) and anterior pituitary (decreasing TSH) to maintain homeostasis. Options A and C
incorrectly localize TSH secretion; the anterior pituitary, not the hypothalamus or posterior pituitary, releases TSH. Option
D reverses the regulatory direction and incorrectly identifies positive feedback.
,Q2: A 45-year-old patient presents with weight gain, moon face, central obesity, and elevated blood
pressure. Lab tests reveal elevated cortisol levels. Which endocrine disorder is most consistent with these
findings, and what is the underlying mechanism?
A. Addison's disease, due to adrenal cortex hypofunction
B. Cushing's syndrome, due to hypersecretion of cortisol from the adrenal cortex (often from an adrenal
adenoma or pituitary ACTH-secreting adenoma) *[CORRECT]*
C. Cushing's disease, due to hypersecretion of aldosterone from the adrenal medulla
D. Pheochromocytoma, due to epinephrine hypersecretion from the adrenal cortex
Correct Answer: B
Rationale: Cushing's syndrome results from chronic hypercortisolism, commonly caused by an adrenal adenoma or
pituitary ACTH-secreting adenoma (Cushing's disease when pituitary in origin). Symptoms include moon face, buffalo
hump, central obesity, hypertension, hyperglycemia, and striae. Addison's disease (A) is adrenal insufficiency causing
hypocortisolism with fatigue, weight loss, and hyperpigmentation. Aldosterone (C) is from the adrenal cortex (not medulla)
and Cushing's is cortisol, not aldosterone. Pheochromocytoma (D) arises from adrenal medulla catecholamine
hypersecretion, causing episential hypertension.
Q3: Which hormone is released from the posterior pituitary and plays a key role in water reabsorption in
the kidneys?
A. Oxytocin
B. Antidiuretic hormone (ADH, vasopressin) *[CORRECT]*
C. Aldosterone
D. Atrial natriuretic peptide (ANP)
Correct Answer: B
Rationale: Antidiuretic hormone (ADH, also called vasopressin) is synthesized in the hypothalamus and released from the
posterior pituitary; it increases water reabsorption in the collecting ducts of the kidney by inserting aquaporin-2 channels.
Oxytocin (A) is also released from the posterior pituitary but stimulates uterine contractions and milk ejection. Aldosterone
(C) is from the adrenal cortex and regulates sodium reabsorption. ANP (D) is from the heart atria and promotes sodium
excretion.
Q4: A patient with Type 1 diabetes mellitus asks why they must take insulin injections. Which
explanation best describes the underlying pathophysiology?
A. The alpha cells of the pancreatic islets are destroyed, preventing glucagon secretion
B. The beta cells of the pancreatic islets of Langerhans are destroyed by autoimmune processes,
preventing insulin production; without insulin, glucose cannot enter most cells (muscle, adipose), leading
to hyperglycemia *[CORRECT]*
C. The delta cells of the pancreas oversecrete somatostatin, inhibiting insulin release
D. Insulin receptors in the liver are downregulated, causing insulin resistance
Correct Answer: B
Rationale: Type 1 diabetes mellitus is caused by autoimmune destruction of beta cells in the pancreatic islets of
Langerhans, eliminating insulin production. Without insulin, glucose transporter (GLUT4) translocation in muscle and
adipose cells fails, causing hyperglycemia, polyuria, polydipsia, and polyphagia. Alpha cells (A) secrete glucagon and are
spared. Delta cells (C) secrete somatostatin. Insulin resistance (D) characterizes Type 2 diabetes, not Type 1. Exogenous
insulin is required for survival in Type 1 diabetes.
,Q5: A patient presents with muscle cramps, tingling in the fingers, and a positive Chvostek sign (facial
muscle spasm with facial nerve tapping). Lab tests show low serum calcium. Which endocrine disorder is
most likely, and what is the mechanism?
A. Hyperparathyroidism, due to excessive PTH causing calcium release from bone
B. Hypoparathyroidism, due to insufficient PTH secretion leading to decreased blood calcium and
increased neuromuscular excitability *[CORRECT]*
C. Hyperthyroidism, due to excessive T4 causing calcium loss in urine
D. Cushing's syndrome, due to cortisol excess causing bone resorption
Correct Answer: B
Rationale: Hypoparathyroidism (low PTH) decreases blood calcium by reducing bone resorption, renal calcium
reabsorption, and vitamin D activation. Low calcium increases neuromuscular excitability, causing tetany, paresthesias,
and positive Chvostek/Trousseau signs. Hyperparathyroidism (A) causes hypercalcemia with "stones, bones, groans, and
psychiatric overtones." Hyperthyroidism (C) does not typically cause hypocalcemia. Cushing's (D) causes cortisol excess but
not the tetany of hypocalcemia. PTH is the master regulator of blood calcium.
Q6: Which endocrine gland is both an endocrine and exocrine gland, and what are its respective
hormone and enzyme products?
A. The liver, which produces bile (exocrine) and insulin-like growth factors (endocrine)
B. The pancreas, which secretes digestive enzymes (exocrine, via acinar cells into the duodenum) and
hormones insulin, glucagon, somatostatin (endocrine, via islets of Langerhans into blood)
*[CORRECT]*
C. The thyroid gland, which produces thyroid hormones (endocrine) and digestive enzymes (exocrine)
D. The adrenal gland, which produces cortisol (endocrine) and adrenaline (exocrine)
Correct Answer: B
Rationale: The pancreas is a dual gland. The exocrine portion (acinar cells and ducts) secretes digestive enzymes (amylase,
lipase, proteases) into the duodenum via the pancreatic duct. The endocrine portion (islets of Langerhans) secretes
hormones directly into the bloodstream: insulin (beta cells), glucagon (alpha cells), somatostatin (delta cells), and
pancreatic polypeptide (PP/F cells). The liver (A) is primarily exocrine (bile). The thyroid (C) is purely endocrine. The
adrenal (D) is purely endocrine.
Q7: A patient has elevated TSH, low T3/T4, fatigue, cold intolerance, weight gain, and bradycardia.
What is the most likely diagnosis and the level of dysfunction?
A. Primary hyperthyroidism (thyroid origin)
B. Primary hypothyroidism (thyroid gland dysfunction, such as Hashimoto's thyroiditis); elevated TSH
reflects loss of negative feedback from low T3/T4 *[CORRECT]*
C. Secondary hypothyroidism (pituitary dysfunction with low TSH)
D. Tertiary hypothyroidism (hypothalamic dysfunction with low TRH)
Correct Answer: B
Rationale: Primary hypothyroidism (e.g., Hashimoto's thyroiditis) features low T3/T4 due to thyroid gland failure. The
pituitary responds with elevated TSH (loss of negative feedback). Symptoms include fatigue, cold intolerance, weight gain,
bradycardia, dry skin, and constipation. Hyperthyroidism (A) would show low TSH with elevated T3/T4. Secondary (C)
and tertiary (D) hypothyroidism show low/normal TSH because the pituitary/hypothalamus is the problem. The elevated
TSH confirms primary thyroid dysfunction.
, Q8: Which hormone counteracts insulin by promoting glycogenolysis, gluconeogenesis, and lipolysis,
especially during fasting or hypoglycemia?
A. Glucagon, secreted by alpha cells of the pancreatic islets *[CORRECT]*
B. Insulin, secreted by beta cells of the pancreatic islets
C. Somatostatin, secreted by delta cells of the pancreatic islets
D. Aldosterone, secreted by the adrenal cortex
Correct Answer: A
Rationale: Glucagon, secreted by alpha cells of the pancreatic islets, raises blood glucose during fasting by stimulating
glycogenolysis (liver), gluconeogenesis, and lipolysis. It is the primary counter-regulatory hormone to insulin. Insulin (B)
lowers blood glucose. Somatostatin (C) inhibits both insulin and glucagon. Aldosterone (D) regulates sodium and water
balance, not glucose. Glucagon and insulin work in opposition to maintain blood glucose homeostasis.
Q9: A patient presents with hypertension, hypokalemia, and muscle weakness. Labs reveal elevated
aldosterone with low renin. Which endocrine disorder is most likely?
A. Addison's disease (adrenal insufficiency)
B. Conn's syndrome (primary hyperaldosteronism), typically from an adrenal adenoma *[CORRECT]*
C. Cushing's syndrome (cortisol excess)
D. Pheochromocytoma (catecholamine-secreting tumor)
Correct Answer: B
Rationale: Conn's syndrome (primary hyperaldosteronism) is characterized by autonomous aldosterone secretion (typically
adrenal adenoma), causing sodium retention (hypertension), potassium excretion (hypokalemia and muscle weakness), and
suppressed renin. Addison's (A) is adrenal insufficiency with hypoaldosteronism. Cushing's (C) is cortisol excess.
Pheochromocytoma (D) causes episodic hypertension from catecholamines. Low renin distinguishes primary from
secondary hyperaldosteronism.
Q10: The adrenal medulla secretes epinephrine and norepinephrine in response to sympathetic
stimulation. Which physiological response is NOT typical of these hormones?
A. Increased heart rate and contractility
B. Bronchodilation and increased respiratory rate
C. Increased digestive activity and gastrointestinal motility *[CORRECT]*
D. Glycogenolysis and lipolysis to provide energy
Correct Answer: C
Rationale: Epinephrine and norepinephrine mediate the "fight-or-flight" response, increasing heart rate and contractility
(A), bronchodilation (B), and mobilizing energy via glycogenolysis and lipolysis (D). They inhibit digestive activity and GI
motility (opposite of C), redirecting blood flow away from the digestive tract to skeletal muscle. The sympathetic system
generally inhibits digestion; the parasympathetic system stimulates it. Option C is the parasympathetic response, not the
sympathetic.
