TRU BIOL 1693: Anatomy and Physiology II
Cumulative Final Practice Exam — 2026/2027.
Total Questions: EXACTLY 100.
DOMAIN 1: ENDOCRINE SYSTEM (15 Questions)
HPT Axis & Negative Feedback (4 Questions)
Question 1 (MC) Which of the following correctly describes the negative feedback loop of the hypothalamic-
pituitary-thyroid (HPT) axis when circulating T3/T4 levels are elevated?
A) T3/T4 stimulate the hypothalamus to increase TRH secretion
B) T3/T4 inhibit both TRH release from the hypothalamus and TSH release from the anterior pituitary
C) T3/T4 stimulate the anterior pituitary to increase TSH secretion
D) TRH inhibits TSH, which then stimulates T3/T4 production
Answer: B [CORRECT]
Rationale: When circulating thyroid hormones (T3/T4) reach sufficient levels, they exert negative feedback
inhibition on both the hypothalamus (reducing TRH secretion) and the anterior pituitary (reducing TSH
secretion). This dual-site inhibition prevents overproduction and maintains metabolic homeostasis. The
hypothalamic-pituitary portal system transports TRH directly to the anterior pituitary, but T3/T4 in systemic
circulation can cross the blood-brain barrier to act on both regulatory centers.
Question 2 (SATA) Select ALL that apply regarding the hypothalamic-pituitary-thyroid axis negative feedback
mechanism:
A) Elevated T3/T4 inhibit TRH secretion from the hypothalamus
B) Elevated T3/T4 inhibit TSH secretion from the anterior pituitary
C) The hypothalamic-pituitary portal system carries TSH to the thyroid gland
D) TRH stimulates the anterior pituitary to release TSH
E) T3/T4 stimulate the hypothalamus to increase TRH when levels are high
Answers: A, B, D [CORRECT]
Rationale: The HPT axis operates through hypothalamic TRH → anterior pituitary TSH → thyroid T3/T4
production. The hypothalamic-pituitary portal system is a direct vascular link that transports releasing
hormones (like TRH) to the anterior pituitary, circumventing general systemic circulation. Elevated T3/T4
inhibit both TRH and TSH (negative feedback). TSH travels via systemic circulation, not the portal system, to
reach the thyroid. T3/T4 do NOT stimulate increased TRH when elevated—that would be positive feedback,
which does not occur in this axis.
,Question 3 (MC) A patient presents with elevated TSH but normal T3/T4 levels. Which component of the HPT
axis is most likely dysfunctional?
A) Hypothalamus (TRH deficiency)
B) Anterior pituitary (TSH resistance)
C) Thyroid gland (primary hypothyroidism)
D) Posterior pituitary (oxytocin excess)
Answer: B [CORRECT]
Rationale: Elevated TSH with normal T3/T4 indicates the thyroid is responding appropriately to TSH
stimulation, but the negative feedback signal from T3/T4 is not being recognized by the anterior pituitary. In
primary hypothyroidism (C), TSH would be elevated but T3/T4 would be low. TRH deficiency (A) would cause
low TSH. The posterior pituitary (D) is not involved in thyroid regulation. The anterior pituitary thyrotrophs
normally reduce TSH output when T3/T4 binds to nuclear receptors; resistance to this signal causes
inappropriate TSH elevation.
Question 4 (MC) The hypothalamic-pituitary portal system is functionally significant because it:
A) Allows T3/T4 to bypass the liver and reach target tissues faster
B) Provides a direct vascular connection that delivers hypothalamic releasing hormones to the anterior
pituitary without systemic dilution
C) Carries hormones from the posterior pituitary to the hypothalamus
D) Connects the thyroid gland directly to the parathyroid glands
Answer: B [CORRECT]
Rationale: The hypothalamic-pituitary portal system is a specialized capillary network that originates in the
median eminence of the hypothalamus and drains into the anterior pituitary. This direct vascular link ensures
that releasing hormones (TRH, CRH, GnRH, GHRH) reach the anterior pituitary in high concentration without
being diluted by systemic circulation. This anatomical arrangement is critical for precise endocrine regulation,
as hypothalamic hormones would otherwise be rapidly degraded in the general bloodstream before reaching
the pituitary.
Steroid vs. Peptide Hormones (3 Questions)
Question 5 (MC) A steroid hormone such as cortisol exerts its cellular effects by which mechanism?
A) Binding to a G-protein coupled receptor on the cell membrane and activating adenylyl cyclase
B) Diffusing through the plasma membrane and binding to an intracellular nuclear receptor to alter gene
transcription
C) Binding to a receptor tyrosine kinase that phosphorylates intracellular proteins
D) Activating phospholipase C to produce IP3 and DAG as second messengers
Answer: B [CORRECT]
Rationale: Steroid hormones are lipophilic (derived from cholesterol) and can freely diffuse through the
,plasma membrane. They bind to specific intracellular nuclear receptors (e.g., glucocorticoid receptor for
cortisol), forming hormone-receptor complexes that act as transcription factors. These complexes bind to
hormone response elements (HREs) on DNA, altering gene transcription and protein synthesis. This
mechanism explains the slower onset but longer duration of steroid hormone action compared to peptide
hormones, which act via membrane receptors and second messengers.
Question 6 (MC) Epinephrine binds to β-adrenergic receptors on cardiac muscle cells, resulting in increased
contractility. Which second messenger pathway is activated?
A) cGMP pathway
B) cAMP pathway via Gs-protein activation of adenylyl cyclase
C) IP3/DAG pathway via Gq-protein activation of phospholipase C
D) Direct opening of ligand-gated ion channels
Answer: B [CORRECT]
Rationale: Epinephrine is a catecholamine (peptide-like) hormone that binds to β-adrenergic receptors,
which are G-protein coupled receptors (GPCRs) associated with Gs proteins. Gs activation stimulates adenylyl
cyclase to convert ATP to cyclic AMP (cAMP). cAMP activates protein kinase A (PKA), which phosphorylates
various target proteins, including calcium channels and contractile proteins in cardiac muscle, increasing
heart rate and contractility. This is the classic second-messenger cascade for peptide/amino acid-derived
hormones that cannot cross the plasma membrane.
Question 7 (SATA) Select ALL characteristics that distinguish steroid hormones from peptide hormones:
A) Steroid hormones bind to intracellular nuclear receptors
B) Peptide hormones typically activate second-messenger systems like cAMP
C) Steroid hormones require gene transcription and protein synthesis for their effects
D) Peptide hormones can freely diffuse through the plasma membrane
E) Steroid hormones have a slower onset of action but longer duration
Answers: A, B, C, E [CORRECT]
Rationale: Steroid hormones (cortisol, aldosterone, estrogen, testosterone) diffuse through membranes and
bind nuclear receptors, requiring DNA transcription and protein synthesis—resulting in slow onset (hours)
but prolonged effects. Peptide hormones (insulin, glucagon, TSH) bind membrane receptors and activate
second-messenger cascades (cAMP, IP3/DAG) with rapid onset (seconds to minutes). Peptide hormones are
hydrophilic and CANNOT diffuse through membranes (D is incorrect); they require membrane receptors.
Pancreatic Islets & Glucose Regulation (4 Questions)
Question 8 (MC) After a carbohydrate-rich meal, which pancreatic islet cell secretes insulin to lower blood
glucose, and what is its mechanism of action on skeletal muscle?
, A) Alpha cells; insulin stimulates glycogenolysis
B) Beta cells; insulin promotes GLUT-4 translocation to the sarcolemma for glucose uptake
C) Delta cells; insulin inhibits glucagon secretion
D) Beta cells; insulin stimulates gluconeogenesis in muscle
Answer: B [CORRECT]
Rationale: Beta (β) cells of the pancreatic islets secrete insulin in response to elevated blood glucose. In
resting skeletal muscle, glucose uptake is insulin-dependent via the GLUT-4 transporter. Insulin binding to its
receptor activates a signaling cascade that causes GLUT-4 vesicles to translocate to the sarcolemma, allowing
glucose entry. This lowers blood glucose by promoting glycogenesis (not glycogenolysis, which raises glucose)
and glycolysis. Alpha cells secrete glucagon; delta cells secrete somatostatin.
Question 9 (MC) During prolonged fasting, alpha cells of the pancreatic islets secrete glucagon. What is the
primary target organ and mechanism?
A) Skeletal muscle; stimulation of glycogenolysis
B) Liver; activation of glycogenolysis and gluconeogenesis to raise blood glucose
C) Adipose tissue; inhibition of lipolysis
D) Brain; stimulation of glucose uptake via GLUT-4
Answer: B [CORRECT]
Rationale: Alpha (α) cells secrete glucagon when blood glucose falls (e.g., during fasting). The primary target
is the liver, where glucagon binds GPCRs that activate adenylyl cyclase → cAMP → PKA pathway. This
stimulates glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (synthesis of glucose from
amino acids and glycerol), releasing glucose into the bloodstream. Glucagon does not significantly affect
skeletal muscle glycogen (muscle lacks glucagon receptors) and promotes (not inhibits) lipolysis in adipose
tissue.
Question 10 (SATA) Select ALL correct statements about pancreatic islet cell function:
A) Beta cells secrete insulin in response to elevated blood glucose
B) Alpha cells secrete glucagon in response to decreased blood glucose
C) Insulin promotes glucose uptake in all tissues via GLUT-4 transporters
D) Glucagon stimulates glycogenolysis in the liver to raise blood sugar
E) Insulin inhibits glucagon secretion from alpha cells
Answers: A, B, D, E [CORRECT]
Rationale: Beta cells release insulin when glucose is high; alpha cells release glucagon when glucose is low.
Glucagon targets the liver to stimulate glycogenolysis and raise blood sugar. Insulin suppresses glucagon
secretion (paracrine inhibition within the islets). However, insulin promotes GLUT-4 translocation primarily in
muscle and adipose tissue, NOT all tissues—the brain and liver use different glucose transporters (GLUT-1,
GLUT-2) that are insulin-independent.
Cumulative Final Practice Exam — 2026/2027.
Total Questions: EXACTLY 100.
DOMAIN 1: ENDOCRINE SYSTEM (15 Questions)
HPT Axis & Negative Feedback (4 Questions)
Question 1 (MC) Which of the following correctly describes the negative feedback loop of the hypothalamic-
pituitary-thyroid (HPT) axis when circulating T3/T4 levels are elevated?
A) T3/T4 stimulate the hypothalamus to increase TRH secretion
B) T3/T4 inhibit both TRH release from the hypothalamus and TSH release from the anterior pituitary
C) T3/T4 stimulate the anterior pituitary to increase TSH secretion
D) TRH inhibits TSH, which then stimulates T3/T4 production
Answer: B [CORRECT]
Rationale: When circulating thyroid hormones (T3/T4) reach sufficient levels, they exert negative feedback
inhibition on both the hypothalamus (reducing TRH secretion) and the anterior pituitary (reducing TSH
secretion). This dual-site inhibition prevents overproduction and maintains metabolic homeostasis. The
hypothalamic-pituitary portal system transports TRH directly to the anterior pituitary, but T3/T4 in systemic
circulation can cross the blood-brain barrier to act on both regulatory centers.
Question 2 (SATA) Select ALL that apply regarding the hypothalamic-pituitary-thyroid axis negative feedback
mechanism:
A) Elevated T3/T4 inhibit TRH secretion from the hypothalamus
B) Elevated T3/T4 inhibit TSH secretion from the anterior pituitary
C) The hypothalamic-pituitary portal system carries TSH to the thyroid gland
D) TRH stimulates the anterior pituitary to release TSH
E) T3/T4 stimulate the hypothalamus to increase TRH when levels are high
Answers: A, B, D [CORRECT]
Rationale: The HPT axis operates through hypothalamic TRH → anterior pituitary TSH → thyroid T3/T4
production. The hypothalamic-pituitary portal system is a direct vascular link that transports releasing
hormones (like TRH) to the anterior pituitary, circumventing general systemic circulation. Elevated T3/T4
inhibit both TRH and TSH (negative feedback). TSH travels via systemic circulation, not the portal system, to
reach the thyroid. T3/T4 do NOT stimulate increased TRH when elevated—that would be positive feedback,
which does not occur in this axis.
,Question 3 (MC) A patient presents with elevated TSH but normal T3/T4 levels. Which component of the HPT
axis is most likely dysfunctional?
A) Hypothalamus (TRH deficiency)
B) Anterior pituitary (TSH resistance)
C) Thyroid gland (primary hypothyroidism)
D) Posterior pituitary (oxytocin excess)
Answer: B [CORRECT]
Rationale: Elevated TSH with normal T3/T4 indicates the thyroid is responding appropriately to TSH
stimulation, but the negative feedback signal from T3/T4 is not being recognized by the anterior pituitary. In
primary hypothyroidism (C), TSH would be elevated but T3/T4 would be low. TRH deficiency (A) would cause
low TSH. The posterior pituitary (D) is not involved in thyroid regulation. The anterior pituitary thyrotrophs
normally reduce TSH output when T3/T4 binds to nuclear receptors; resistance to this signal causes
inappropriate TSH elevation.
Question 4 (MC) The hypothalamic-pituitary portal system is functionally significant because it:
A) Allows T3/T4 to bypass the liver and reach target tissues faster
B) Provides a direct vascular connection that delivers hypothalamic releasing hormones to the anterior
pituitary without systemic dilution
C) Carries hormones from the posterior pituitary to the hypothalamus
D) Connects the thyroid gland directly to the parathyroid glands
Answer: B [CORRECT]
Rationale: The hypothalamic-pituitary portal system is a specialized capillary network that originates in the
median eminence of the hypothalamus and drains into the anterior pituitary. This direct vascular link ensures
that releasing hormones (TRH, CRH, GnRH, GHRH) reach the anterior pituitary in high concentration without
being diluted by systemic circulation. This anatomical arrangement is critical for precise endocrine regulation,
as hypothalamic hormones would otherwise be rapidly degraded in the general bloodstream before reaching
the pituitary.
Steroid vs. Peptide Hormones (3 Questions)
Question 5 (MC) A steroid hormone such as cortisol exerts its cellular effects by which mechanism?
A) Binding to a G-protein coupled receptor on the cell membrane and activating adenylyl cyclase
B) Diffusing through the plasma membrane and binding to an intracellular nuclear receptor to alter gene
transcription
C) Binding to a receptor tyrosine kinase that phosphorylates intracellular proteins
D) Activating phospholipase C to produce IP3 and DAG as second messengers
Answer: B [CORRECT]
Rationale: Steroid hormones are lipophilic (derived from cholesterol) and can freely diffuse through the
,plasma membrane. They bind to specific intracellular nuclear receptors (e.g., glucocorticoid receptor for
cortisol), forming hormone-receptor complexes that act as transcription factors. These complexes bind to
hormone response elements (HREs) on DNA, altering gene transcription and protein synthesis. This
mechanism explains the slower onset but longer duration of steroid hormone action compared to peptide
hormones, which act via membrane receptors and second messengers.
Question 6 (MC) Epinephrine binds to β-adrenergic receptors on cardiac muscle cells, resulting in increased
contractility. Which second messenger pathway is activated?
A) cGMP pathway
B) cAMP pathway via Gs-protein activation of adenylyl cyclase
C) IP3/DAG pathway via Gq-protein activation of phospholipase C
D) Direct opening of ligand-gated ion channels
Answer: B [CORRECT]
Rationale: Epinephrine is a catecholamine (peptide-like) hormone that binds to β-adrenergic receptors,
which are G-protein coupled receptors (GPCRs) associated with Gs proteins. Gs activation stimulates adenylyl
cyclase to convert ATP to cyclic AMP (cAMP). cAMP activates protein kinase A (PKA), which phosphorylates
various target proteins, including calcium channels and contractile proteins in cardiac muscle, increasing
heart rate and contractility. This is the classic second-messenger cascade for peptide/amino acid-derived
hormones that cannot cross the plasma membrane.
Question 7 (SATA) Select ALL characteristics that distinguish steroid hormones from peptide hormones:
A) Steroid hormones bind to intracellular nuclear receptors
B) Peptide hormones typically activate second-messenger systems like cAMP
C) Steroid hormones require gene transcription and protein synthesis for their effects
D) Peptide hormones can freely diffuse through the plasma membrane
E) Steroid hormones have a slower onset of action but longer duration
Answers: A, B, C, E [CORRECT]
Rationale: Steroid hormones (cortisol, aldosterone, estrogen, testosterone) diffuse through membranes and
bind nuclear receptors, requiring DNA transcription and protein synthesis—resulting in slow onset (hours)
but prolonged effects. Peptide hormones (insulin, glucagon, TSH) bind membrane receptors and activate
second-messenger cascades (cAMP, IP3/DAG) with rapid onset (seconds to minutes). Peptide hormones are
hydrophilic and CANNOT diffuse through membranes (D is incorrect); they require membrane receptors.
Pancreatic Islets & Glucose Regulation (4 Questions)
Question 8 (MC) After a carbohydrate-rich meal, which pancreatic islet cell secretes insulin to lower blood
glucose, and what is its mechanism of action on skeletal muscle?
, A) Alpha cells; insulin stimulates glycogenolysis
B) Beta cells; insulin promotes GLUT-4 translocation to the sarcolemma for glucose uptake
C) Delta cells; insulin inhibits glucagon secretion
D) Beta cells; insulin stimulates gluconeogenesis in muscle
Answer: B [CORRECT]
Rationale: Beta (β) cells of the pancreatic islets secrete insulin in response to elevated blood glucose. In
resting skeletal muscle, glucose uptake is insulin-dependent via the GLUT-4 transporter. Insulin binding to its
receptor activates a signaling cascade that causes GLUT-4 vesicles to translocate to the sarcolemma, allowing
glucose entry. This lowers blood glucose by promoting glycogenesis (not glycogenolysis, which raises glucose)
and glycolysis. Alpha cells secrete glucagon; delta cells secrete somatostatin.
Question 9 (MC) During prolonged fasting, alpha cells of the pancreatic islets secrete glucagon. What is the
primary target organ and mechanism?
A) Skeletal muscle; stimulation of glycogenolysis
B) Liver; activation of glycogenolysis and gluconeogenesis to raise blood glucose
C) Adipose tissue; inhibition of lipolysis
D) Brain; stimulation of glucose uptake via GLUT-4
Answer: B [CORRECT]
Rationale: Alpha (α) cells secrete glucagon when blood glucose falls (e.g., during fasting). The primary target
is the liver, where glucagon binds GPCRs that activate adenylyl cyclase → cAMP → PKA pathway. This
stimulates glycogenolysis (breakdown of glycogen to glucose) and gluconeogenesis (synthesis of glucose from
amino acids and glycerol), releasing glucose into the bloodstream. Glucagon does not significantly affect
skeletal muscle glycogen (muscle lacks glucagon receptors) and promotes (not inhibits) lipolysis in adipose
tissue.
Question 10 (SATA) Select ALL correct statements about pancreatic islet cell function:
A) Beta cells secrete insulin in response to elevated blood glucose
B) Alpha cells secrete glucagon in response to decreased blood glucose
C) Insulin promotes glucose uptake in all tissues via GLUT-4 transporters
D) Glucagon stimulates glycogenolysis in the liver to raise blood sugar
E) Insulin inhibits glucagon secretion from alpha cells
Answers: A, B, D, E [CORRECT]
Rationale: Beta cells release insulin when glucose is high; alpha cells release glucagon when glucose is low.
Glucagon targets the liver to stimulate glycogenolysis and raise blood sugar. Insulin suppresses glucagon
secretion (paracrine inhibition within the islets). However, insulin promotes GLUT-4 translocation primarily in
muscle and adipose tissue, NOT all tissues—the brain and liver use different glucose transporters (GLUT-1,
GLUT-2) that are insulin-independent.
