BIOL 2402 Anatomy & Physiology II
Final Exam // Latest Edition {2026/2027}.
DOMAIN 1: ENDOCRINE SYSTEM (12 Questions)
1.1 Hypothalamic-Pituitary Axis and Target Organ Feedback Loops (3 Questions)
Question 1 (Multiple-Choice)
A 34-year-old patient presents with fatigue, weight gain, cold intolerance, and a goiter.
Laboratory studies reveal elevated TSH, low free T4, and low free T3. Which structure is the
primary site of dysfunction in this condition?
A) Anterior pituitary thyrotrophs
B) Hypothalamic paraventricular nucleus
C) Thyroid follicular cells [CORRECT]
D) Posterior pituitary
Rationale: The patient has primary hypothyroidism. The key distinguishing feature is the inverse
relationship between TSH and thyroid hormones: elevated TSH with low T3/T4 indicates the
thyroid gland itself (follicular cells) is failing to produce hormones, causing loss of negative
feedback on the anterior pituitary. In secondary hypothyroidism (pituitary dysfunction), TSH
would be low or inappropriately normal with low T3/T4. In tertiary hypothyroidism
(hypothalamic dysfunction), TRH would be deficient.
Question 2 (Select-All-That-Apply)
Which of the following hormones are synthesized in the hypothalamus and released from the
posterior pituitary? (Select all that apply)
A) Growth hormone (GH)
B) Antidiuretic hormone (ADH) [CORRECT]
C) Oxytocin [CORRECT]
D) Thyroid-stimulating hormone (TSH)
E) Prolactin (PRL)
,Rationale: ADH (vasopressin) and oxytocin are synthesized by hypothalamic neurons in the
supraoptic and paraventricular nuclei, respectively, and transported down axons through the
infundibulum to be released from the posterior pituitary (neurohypophysis). This distinguishes
them from anterior pituitary hormones (GH, TSH, PRL, ACTH, FSH, LH), which are synthesized
and released by anterior pituitary cells under hypothalamic releasing/inhibiting hormone
control.
Question 3 (Multiple-Choice)
A patient with Cushing's disease has a pituitary adenoma secreting excess ACTH. Which of the
following feedback relationships is disrupted in this condition?
A) Cortisol normally exerts negative feedback on hypothalamic CRH and anterior pituitary ACTH
secretion [CORRECT]
B) Cortisol normally exerts positive feedback on hypothalamic CRH secretion
C) ACTH normally exerts negative feedback on the adrenal cortex
D) CRH normally exerts negative feedback on the anterior pituitary
Rationale: In the HPA axis, cortisol (the end-product glucocorticoid) exerts long-loop negative
feedback on both the hypothalamus (decreasing CRH release) and the anterior pituitary
(decreasing ACTH release). In Cushing's disease, the pituitary adenoma autonomously secretes
ACTH, overriding this negative feedback. The key distinguishing feature from Cushing's
syndrome (adrenal adenoma) is that ACTH levels are elevated in Cushing's disease but
suppressed in adrenal Cushing's syndrome.
1.2 Hormone Classes and Mechanisms of Action (3 Questions)
Question 4 (Multiple-Choice)
A researcher is studying a newly discovered hormone that binds to a cell surface receptor,
activates Gs protein, and increases intracellular cAMP. Which hormone class does this molecule
most likely belong to?
A) Steroid hormone
B) Thyroid hormone
C) Peptide hormone [CORRECT]
D) Nitric oxide
,Rationale: Peptide hormones (and catecholamines) are hydrophilic and cannot cross the plasma
membrane, so they bind to cell surface receptors and use second messenger systems. The Gs
protein → adenylyl cyclase → cAMP pathway is characteristic of peptide hormones like
glucagon, ACTH, TSH, and LH. Steroid hormones (cortisol, aldosterone, sex hormones) and
thyroid hormones are lipophilic, cross the membrane, and bind to intracellular receptors that
alter gene transcription.
Question 5 (Select-All-That-Apply)
Which of the following statements correctly describe differences between steroid and peptide
hormone mechanisms of action? (Select all that apply)
A) Steroid hormones bind intracellular receptors and alter gene transcription [CORRECT]
B) Peptide hormones typically act within seconds to minutes via second messengers [CORRECT]
C) Steroid hormones require protein synthesis for their effects, resulting in slower onset (hours
to days) [CORRECT]
D) Peptide hormones can freely cross the plasma membrane to reach intracellular receptors
E) Steroid hormones use cAMP as their primary second messenger system
Rationale: The fundamental distinction is membrane permeability: steroid hormones are
lipophilic (derived from cholesterol) and diffuse through the plasma membrane to bind
intracellular receptors, forming hormone-receptor complexes that act as transcription factors.
Peptide hormones are hydrophilic, bind membrane receptors, and use second messengers
(cAMP, IP3/DAG, Ca2+) for rapid responses. D is incorrect because peptide hormones cannot
cross membranes. E is incorrect because steroid hormones do not use second messengers.
Question 6 (Multiple-Choice)
Epinephrine binds to β1-adrenergic receptors on cardiac myocytes, increasing heart rate and
contractility. Which second messenger system mediates this response?
A) cGMP
B) IP3/DAG
C) cAMP [CORRECT]
D) Tyrosine kinase receptor autophosphorylation
Rationale: β-adrenergic receptors (β1, β2, β3) are Gs-coupled receptors that activate adenylyl
cyclase, increasing cAMP, which then activates protein kinase A (PKA). PKA phosphorylates L-
type Ca2+ channels and phospholamban, increasing Ca2+ influx and sarcoplasmic reticulum
, Ca2+ release, enhancing contractility. This is a classic example of a catecholamine (amine class
hormone) using the cAMP second messenger system. The key distinction: α1 receptors use
IP3/DAG; insulin uses tyrosine kinase receptors; NO uses cGMP.
1.3 Endocrine Pancreas and Diabetes Mellitus (2 Questions)
Question 7 (Multiple-Choice)
A patient with Type 1 diabetes mellitus develops diabetic ketoacidosis (DKA). Which hormonal
imbalance is primarily responsible for the metabolic derangements in DKA?
A) Excess insulin and deficient glucagon
B) Deficient insulin with relative excess of glucagon [CORRECT]
C) Excess somatostatin and deficient insulin
D) Deficient glucagon with relative excess of insulin
Rationale: In DKA, absolute insulin deficiency (characteristic of Type 1 DM) removes the
suppressive effect of insulin on glucagon secretion and hepatic glucose production. The
resulting relative glucagon excess promotes hepatic ketogenesis (via increased fatty acid
oxidation and HMG-CoA pathway) and gluconeogenesis. Insulin normally inhibits glucagon
secretion from α-cells; without insulin, glucagon is inappropriately elevated for the
hyperglycemic state. Somatostatin deficiency is not a feature of DKA.
Question 8 (Select-All-That-Apply)
Which of the following statements about pancreatic islet hormones are correct? (Select all that
apply)
A) Insulin is secreted by β-cells in response to elevated blood glucose [CORRECT]
B) Glucagon is secreted by α-cells and raises blood glucose by promoting glycogenolysis and
gluconeogenesis [CORRECT]
C) Somatostatin is secreted by δ-cells and inhibits both insulin and glucagon secretion
[CORRECT]
D) Insulin promotes glycogen synthesis in the liver and muscle [CORRECT]
E) Glucagon promotes glycogen synthesis in the liver
Rationale: The endocrine pancreas contains three main cell types: α-cells (glucagon, 20%), β-
cells (insulin, 70%), and δ-cells (somatostatin, 5%). Insulin is anabolic, promoting glucose uptake
Final Exam // Latest Edition {2026/2027}.
DOMAIN 1: ENDOCRINE SYSTEM (12 Questions)
1.1 Hypothalamic-Pituitary Axis and Target Organ Feedback Loops (3 Questions)
Question 1 (Multiple-Choice)
A 34-year-old patient presents with fatigue, weight gain, cold intolerance, and a goiter.
Laboratory studies reveal elevated TSH, low free T4, and low free T3. Which structure is the
primary site of dysfunction in this condition?
A) Anterior pituitary thyrotrophs
B) Hypothalamic paraventricular nucleus
C) Thyroid follicular cells [CORRECT]
D) Posterior pituitary
Rationale: The patient has primary hypothyroidism. The key distinguishing feature is the inverse
relationship between TSH and thyroid hormones: elevated TSH with low T3/T4 indicates the
thyroid gland itself (follicular cells) is failing to produce hormones, causing loss of negative
feedback on the anterior pituitary. In secondary hypothyroidism (pituitary dysfunction), TSH
would be low or inappropriately normal with low T3/T4. In tertiary hypothyroidism
(hypothalamic dysfunction), TRH would be deficient.
Question 2 (Select-All-That-Apply)
Which of the following hormones are synthesized in the hypothalamus and released from the
posterior pituitary? (Select all that apply)
A) Growth hormone (GH)
B) Antidiuretic hormone (ADH) [CORRECT]
C) Oxytocin [CORRECT]
D) Thyroid-stimulating hormone (TSH)
E) Prolactin (PRL)
,Rationale: ADH (vasopressin) and oxytocin are synthesized by hypothalamic neurons in the
supraoptic and paraventricular nuclei, respectively, and transported down axons through the
infundibulum to be released from the posterior pituitary (neurohypophysis). This distinguishes
them from anterior pituitary hormones (GH, TSH, PRL, ACTH, FSH, LH), which are synthesized
and released by anterior pituitary cells under hypothalamic releasing/inhibiting hormone
control.
Question 3 (Multiple-Choice)
A patient with Cushing's disease has a pituitary adenoma secreting excess ACTH. Which of the
following feedback relationships is disrupted in this condition?
A) Cortisol normally exerts negative feedback on hypothalamic CRH and anterior pituitary ACTH
secretion [CORRECT]
B) Cortisol normally exerts positive feedback on hypothalamic CRH secretion
C) ACTH normally exerts negative feedback on the adrenal cortex
D) CRH normally exerts negative feedback on the anterior pituitary
Rationale: In the HPA axis, cortisol (the end-product glucocorticoid) exerts long-loop negative
feedback on both the hypothalamus (decreasing CRH release) and the anterior pituitary
(decreasing ACTH release). In Cushing's disease, the pituitary adenoma autonomously secretes
ACTH, overriding this negative feedback. The key distinguishing feature from Cushing's
syndrome (adrenal adenoma) is that ACTH levels are elevated in Cushing's disease but
suppressed in adrenal Cushing's syndrome.
1.2 Hormone Classes and Mechanisms of Action (3 Questions)
Question 4 (Multiple-Choice)
A researcher is studying a newly discovered hormone that binds to a cell surface receptor,
activates Gs protein, and increases intracellular cAMP. Which hormone class does this molecule
most likely belong to?
A) Steroid hormone
B) Thyroid hormone
C) Peptide hormone [CORRECT]
D) Nitric oxide
,Rationale: Peptide hormones (and catecholamines) are hydrophilic and cannot cross the plasma
membrane, so they bind to cell surface receptors and use second messenger systems. The Gs
protein → adenylyl cyclase → cAMP pathway is characteristic of peptide hormones like
glucagon, ACTH, TSH, and LH. Steroid hormones (cortisol, aldosterone, sex hormones) and
thyroid hormones are lipophilic, cross the membrane, and bind to intracellular receptors that
alter gene transcription.
Question 5 (Select-All-That-Apply)
Which of the following statements correctly describe differences between steroid and peptide
hormone mechanisms of action? (Select all that apply)
A) Steroid hormones bind intracellular receptors and alter gene transcription [CORRECT]
B) Peptide hormones typically act within seconds to minutes via second messengers [CORRECT]
C) Steroid hormones require protein synthesis for their effects, resulting in slower onset (hours
to days) [CORRECT]
D) Peptide hormones can freely cross the plasma membrane to reach intracellular receptors
E) Steroid hormones use cAMP as their primary second messenger system
Rationale: The fundamental distinction is membrane permeability: steroid hormones are
lipophilic (derived from cholesterol) and diffuse through the plasma membrane to bind
intracellular receptors, forming hormone-receptor complexes that act as transcription factors.
Peptide hormones are hydrophilic, bind membrane receptors, and use second messengers
(cAMP, IP3/DAG, Ca2+) for rapid responses. D is incorrect because peptide hormones cannot
cross membranes. E is incorrect because steroid hormones do not use second messengers.
Question 6 (Multiple-Choice)
Epinephrine binds to β1-adrenergic receptors on cardiac myocytes, increasing heart rate and
contractility. Which second messenger system mediates this response?
A) cGMP
B) IP3/DAG
C) cAMP [CORRECT]
D) Tyrosine kinase receptor autophosphorylation
Rationale: β-adrenergic receptors (β1, β2, β3) are Gs-coupled receptors that activate adenylyl
cyclase, increasing cAMP, which then activates protein kinase A (PKA). PKA phosphorylates L-
type Ca2+ channels and phospholamban, increasing Ca2+ influx and sarcoplasmic reticulum
, Ca2+ release, enhancing contractility. This is a classic example of a catecholamine (amine class
hormone) using the cAMP second messenger system. The key distinction: α1 receptors use
IP3/DAG; insulin uses tyrosine kinase receptors; NO uses cGMP.
1.3 Endocrine Pancreas and Diabetes Mellitus (2 Questions)
Question 7 (Multiple-Choice)
A patient with Type 1 diabetes mellitus develops diabetic ketoacidosis (DKA). Which hormonal
imbalance is primarily responsible for the metabolic derangements in DKA?
A) Excess insulin and deficient glucagon
B) Deficient insulin with relative excess of glucagon [CORRECT]
C) Excess somatostatin and deficient insulin
D) Deficient glucagon with relative excess of insulin
Rationale: In DKA, absolute insulin deficiency (characteristic of Type 1 DM) removes the
suppressive effect of insulin on glucagon secretion and hepatic glucose production. The
resulting relative glucagon excess promotes hepatic ketogenesis (via increased fatty acid
oxidation and HMG-CoA pathway) and gluconeogenesis. Insulin normally inhibits glucagon
secretion from α-cells; without insulin, glucagon is inappropriately elevated for the
hyperglycemic state. Somatostatin deficiency is not a feature of DKA.
Question 8 (Select-All-That-Apply)
Which of the following statements about pancreatic islet hormones are correct? (Select all that
apply)
A) Insulin is secreted by β-cells in response to elevated blood glucose [CORRECT]
B) Glucagon is secreted by α-cells and raises blood glucose by promoting glycogenolysis and
gluconeogenesis [CORRECT]
C) Somatostatin is secreted by δ-cells and inhibits both insulin and glucagon secretion
[CORRECT]
D) Insulin promotes glycogen synthesis in the liver and muscle [CORRECT]
E) Glucagon promotes glycogen synthesis in the liver
Rationale: The endocrine pancreas contains three main cell types: α-cells (glucagon, 20%), β-
cells (insulin, 70%), and δ-cells (somatostatin, 5%). Insulin is anabolic, promoting glucose uptake
