UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
UT Tyler FNP NURS 5350 — Advanced
Pathophysiology
Comprehensive Examination 1 — 100 Questions with Verified Answers and Mechanistic Rationales
The University of Texas at Tyler | Family Nurse Practitioner Program | 2026/2027 — AGRADE
Verified
Aligned with current NURS 5350 Exam 1 learning objectives and advanced pathophysiology competencies
Instructions to Candidate: This examination consists of 100 multiple-choice items distributed across seven content areas. Each
item has exactly one best answer. Cognitive level distribution: approximately 30% recall (mechanisms, definitions), 50% application
(clinical scenarios requiring pathophysiological reasoning), and 20% analysis (integration of multiple mechanisms and diagnostic
interpretation). Mark the single best answer for each question. The correct answer and a pathophysiology-grounded rationale are
provided immediately beneath each item to support self-assessment and remediation.
Section 1: Cellular Biology and Homeostasis (Q1-Q15)
Cell Structure, Function, Transport, & Adaptation
Q1: A 48-year-old patient receiving chemotherapy develops severe mucositis. The oncology NP explains that the
rapidly dividing gastrointestinal epithelial cells are most vulnerable because of which organelle's central role in
ribosome synthesis and protein translation, which is required for cell renewal?
A. The Golgi apparatus, which packages digestive enzymes for mucosal defense
B. The nucleolus, which transcribes ribosomal RNA and assembles ribosomal subunits essential for protein
synthesis in dividing cells [CORRECT]
C. The smooth endoplasmic reticulum, which detoxifies chemotherapy agents
D. The lysosome, which hydrolyzes damaged intracellular proteins
Correct Answer: B
Rationale:
The nucleolus is the site of rRNA transcription and ribosomal subunit assembly. Rapidly dividing cells (mucosal epithelium,
hematopoietic precursors, hair follicles) are highly dependent on ribosome biogenesis for protein synthesis, making them exquisitely
sensitive to cell-cycle-specific chemotherapy. The Golgi packages proteins, the smooth ER detoxifies, and lysosomes degrade debris
- none of these directly limit renewal.
Q2: A patient with a suspected mitochondrial disorder presents with progressive external ophthalmoplegia and
lactic acidosis. The NP recognizes that impaired oxidative phosphorylation in mitochondria primarily affects
which step of cellular metabolism?
A. Glycolysis in the cytosol, producing lactate as the end product
B. The electron transport chain and ATP synthesis via chemiosmosis at the inner mitochondrial
membrane [CORRECT]
C. Fatty acid beta-oxidation in peroxisomes
D. Glycogenolysis in the cytosol
Correct Answer: B
Rationale:
Mitochondria generate ATP through oxidative phosphorylation at the inner mitochondrial membrane: the electron transport chain
(complexes I-IV) pumps protons to generate an electrochemical gradient, and ATP synthase (complex V) uses that gradient to
Page 1 | The University of Texas at Tyler
,UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
phosphorylate ADP. Impaired OXPHOS shunts pyruvate to lactate (explaining lactic acidosis). Glycolysis occurs in the cytosol,
beta-oxidation mostly in mitochondria but peroxisomes handle very long-chain fatty acids.
Q3: A 62-year-old patient with chronic alcohol use disorder exhibits hepatic steatosis. The NP explains that
impaired very-low-density lipoprotein assembly reflects dysfunction of which organelle?
A. The rough endoplasmic reticulum, where ribosomes synthesize apoproteins
B. The Golgi apparatus, which modifies and packages VLDL for secretion
C. The smooth endoplasmic reticulum, which is the site of lipid synthesis and is overwhelmed by ethanol
metabolism [CORRECT]
D. The mitochondrion, which beta-oxidizes fatty acids
Correct Answer: C
Rationale:
Hepatic steatosis in chronic alcohol use occurs because ethanol metabolism via MEOS (microsomal ethanol oxidizing system) in the
smooth ER generates NADH and acetate, increasing fatty acid synthesis while the increased NADH/NAD+ ratio inhibits fatty acid
beta-oxidation. Additionally, the SER proliferates under chronic induction, but its lipid-synthesis capacity outstrips VLDL export
capacity. The Golgi and rough ER are downstream of lipid handling.
Q4: A 7-month-old infant of Ashkenazi Jewish heritage presents with progressive loss of motor skills,
exaggerated startle response, and a cherry-red macula. The NP suspects Tay-Sachs disease, which results from
deficient activity of which organelle?
A. Lysosomes, due to deficiency of hexosaminidase A causing GM2 ganglioside accumulation in
neurons [CORRECT]
B. Peroxisomes, due to defective very long-chain fatty acid oxidation
C. Mitochondria, due to defective oxidative phosphorylation
D. The Golgi apparatus, due to defective protein glycosylation
Correct Answer: A
Rationale:
Tay-Sachs disease is an autosomal recessive lysosomal storage disorder caused by deficiency of hexosaminidase A, leading to
accumulation of GM2 ganglioside in neuronal lysosomes. The progressive neuronal dysfunction causes loss of motor skills,
exaggerated startle (hyperacusis), and the cherry-red macula (the ganglion cells surrounding the fovea accumulate lipid, making the
underlying choroidal vasculature appear prominent). Peroxisomal, mitochondrial, and Golgi defects cause other phenotypes.
Q5: A graduate nursing student asks why intracellular fluid (ICF) and extracellular fluid (ECF) electrolyte
compositions differ. The NP correctly explains that the sodium-potassium ATPase pump maintains these
gradients by:
A. Passively allowing Na+ to enter the cell down its concentration gradient
B. Hydrolyzing ATP to export 3 Na+ and import 2 K+ per cycle, maintaining high intracellular K+ and high
extracellular Na+ [CORRECT]
C. Exchanging 2 Na+ for 2 K+ in an electroneutral manner
D. Using GTP to move Na+ and K+ against their gradients in equal molar amounts
Correct Answer: B
Rationale:
The Na+/K+-ATPase is a P-type ATPase that hydrolyzes one ATP to export 3 Na+ and import 2 K+, creating both concentration
gradients (high intracellular K+, high extracellular Na+) and an electrogenic effect (net outflow of one positive charge per cycle,
contributing to the resting membrane potential). The pump establishes the gradients that secondary active transport (e.g.,
Na+/glucose cotransport) exploits.
Page 2 | The University of Texas at Tyler
,UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
Q6: A patient with cystic fibrosis has a G551D mutation in the CFTR gene. The NP understands that this
mutation produces a CFTR protein that reaches the cell surface but fails to open properly in response to ATP.
This represents dysfunction of which class of membrane protein?
A. A ligand-gated ion channel opened by acetylcholine binding
B. An ATP-binding cassette (ABC) transporter that functions as a chloride channel gated by ATP
hydrolysis [CORRECT]
C. A voltage-gated sodium channel in neuronal tissue
D. A gap junction connexin
Correct Answer: B
Rationale:
CFTR is an ATP-binding cassette (ABC) transporter family member that functions as a cAMP-regulated chloride channel. The
G551D mutation is a class III (gating) mutation: the protein is processed and reaches the membrane but the ATP-binding
nucleotide-binding domain 1 fails to hydrolyze ATP properly, so the channel opens rarely. Ivacaftor potentiates channel opening in
patients with G551D. This is distinct from the F508del class II trafficking mutation.
Q7: A patient in diabetic ketoacidosis has a serum glucose of 720 mg/dL and a serum sodium of 128 mEq/L. The
NP recognizes that the hyponatremia is primarily caused by which mechanism?
A. True sodium depletion from renal wasting due to osmotic diuresis
B. Dilutional hyponatremia from hyperglycemia drawing intracellular water into the extracellular space;
corrected sodium = measured Na + 1.6 × (glucose − 100)/100 [CORRECT]
C. Syndrome of inappropriate antidiuretic hormone secretion from cerebral edema
D. Pseudohyponatremia from hyperlipidemia
Correct Answer: B
Rationale:
In hyperglycemia, the high serum osmolality from glucose draws water from the intracellular space into the extracellular space,
diluting serum sodium - this is translocational (dilutional) hyponatremia. The corrected sodium formula adds 1.6 mEq/L for every
100 mg/dL glucose above 100. The true total body sodium may be normal or low (osmotic diuresis also causes sodium loss), but the
immediate dilutional effect explains the measured hyponatremia. SIADH and pseudohyponatremia are different mechanisms.
Q8: A patient has familial hypercholesterolemia due to an LDL receptor mutation. The NP understands that
LDL particles are taken into hepatocytes by which transport mechanism?
A. Passive diffusion through the plasma membrane
B. Receptor-mediated endocytosis via clathrin-coated pits, requiring the LDL receptor and
apoB-100 [CORRECT]
C. Facilitated diffusion through a channel protein
D. Active transport against the concentration gradient using ATP
Correct Answer: B
Rationale:
LDL is internalized by receptor-mediated endocytosis: apoB-100 on the LDL particle binds the LDL receptor on hepatocyte
membranes, the receptor-LDL complex clusters in clathrin-coated pits, the pit invaginates and forms an endosome, the receptor
recycles, and the LDL is delivered to lysosomes for cholesterol release. Familial hypercholesterolemia (FH) results from mutations
in the LDL receptor (or apoB-100 or PCSK9), impairing this clearance and causing elevated serum LDL.
Q9: A researcher is studying cell signaling. Which of the following describes a paracrine signaling mechanism?
A. A hormone released into the bloodstream acts on distant target cells
B. A neurotransmitter released at a synaptic cleft acts on the postsynaptic membrane of an adjacent
neuron [CORRECT]
Page 3 | The University of Texas at Tyler
, UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
C. A signaling molecule acts on the same cell that secreted it
D. A signaling molecule acts on a gap-junction-connected neighboring cell
Correct Answer: B
Rationale:
Paracrine signaling refers to a cell releasing signaling molecules that act on nearby cells of a different type - the classic example is a
neurotransmitter (e.g., acetylcholine) released at a synapse acting on an adjacent postsynaptic cell. Endocrine signaling uses the
bloodstream to reach distant targets (e.g., thyroid hormone). Autocrine signaling involves a cell responding to its own secreted signal
(e.g., tumor growth factors). Gap junctions transfer ions and small molecules directly between adjacent cells - not true signaling.
Q10: A patient receives a beta-1 adrenergic agonist (dobutamine) for acute heart failure. The NP understands
that this drug acts through which second messenger system?
A. The phospholipase C pathway, generating IP3 and DAG
B. The Gs protein - adenylyl cyclase - cAMP - protein kinase A pathway, increasing intracellular
cAMP [CORRECT]
C. The Gi protein pathway, decreasing cAMP
D. Receptor tyrosine kinase activation leading to Ras-MAPK signaling
Correct Answer: B
Rationale:
Beta-1 adrenergic receptors are G protein-coupled receptors (GPCRs) linked to the Gs alpha subunit. Agonist binding activates
adenylyl cyclase, which converts ATP to cAMP. cAMP activates protein kinase A (PKA), which phosphorylates L-type calcium
channels (increasing calcium influx) and phospholamban (relieving inhibition of the SERCA pump, increasing calcium reuptake into
the sarcoplasmic reticulum). The net effect is increased cardiac contractility and heart rate.
Q11: A 38-year-old patient with type 2 diabetes mellitus is prescribed a GLP-1 receptor agonist (semaglutide).
The NP recognizes that the GLP-1 receptor signals through which mechanism?
A. Receptor tyrosine kinase autophosphorylation, activating the Ras-MAPK pathway
B. G protein-coupled receptor activation of adenylyl cyclase, increasing cAMP and protein kinase A in
pancreatic beta cells [CORRECT]
C. Janus kinase (JAK) activation leading to STAT phosphorylation
D. Direct ligand-gated ion channel opening
Correct Answer: B
Rationale:
The GLP-1 receptor is a Gs-coupled GPCR on pancreatic beta cells. Agonist binding activates adenylyl cyclase, increasing cAMP
and activating PKA, which potentiates glucose-stimulated insulin secretion. GLP-1 also slows gastric emptying, reduces glucagon,
and promotes satiety. Unlike insulin (which acts through a receptor tyrosine kinase and IRS-1 signaling), GLP-1 acts through cAMP.
Q12: Insulin binds its receptor on skeletal muscle cells. The NP correctly identifies that this receptor's
mechanism of action involves:
A. A G protein-coupled receptor that activates adenylyl cyclase
B. A receptor tyrosine kinase that autophosphorylates and recruits IRS-1, leading to PI3K-Akt pathway
activation and GLUT4 translocation [CORRECT]
C. A ligand-gated ion channel that allows sodium influx
D. An intracellular receptor that translocates to the nucleus as a transcription factor
Correct Answer: B
Rationale:
The insulin receptor is a receptor tyrosine kinase (RTK). Insulin binding causes autophosphorylation of the beta subunit, which then
phosphorylates insulin receptor substrate-1 (IRS-1). IRS-1 activates PI3K, generating PIP3, which activates PDK1 and Akt. Akt
Page 4 | The University of Texas at Tyler
UT Tyler FNP NURS 5350 — Advanced
Pathophysiology
Comprehensive Examination 1 — 100 Questions with Verified Answers and Mechanistic Rationales
The University of Texas at Tyler | Family Nurse Practitioner Program | 2026/2027 — AGRADE
Verified
Aligned with current NURS 5350 Exam 1 learning objectives and advanced pathophysiology competencies
Instructions to Candidate: This examination consists of 100 multiple-choice items distributed across seven content areas. Each
item has exactly one best answer. Cognitive level distribution: approximately 30% recall (mechanisms, definitions), 50% application
(clinical scenarios requiring pathophysiological reasoning), and 20% analysis (integration of multiple mechanisms and diagnostic
interpretation). Mark the single best answer for each question. The correct answer and a pathophysiology-grounded rationale are
provided immediately beneath each item to support self-assessment and remediation.
Section 1: Cellular Biology and Homeostasis (Q1-Q15)
Cell Structure, Function, Transport, & Adaptation
Q1: A 48-year-old patient receiving chemotherapy develops severe mucositis. The oncology NP explains that the
rapidly dividing gastrointestinal epithelial cells are most vulnerable because of which organelle's central role in
ribosome synthesis and protein translation, which is required for cell renewal?
A. The Golgi apparatus, which packages digestive enzymes for mucosal defense
B. The nucleolus, which transcribes ribosomal RNA and assembles ribosomal subunits essential for protein
synthesis in dividing cells [CORRECT]
C. The smooth endoplasmic reticulum, which detoxifies chemotherapy agents
D. The lysosome, which hydrolyzes damaged intracellular proteins
Correct Answer: B
Rationale:
The nucleolus is the site of rRNA transcription and ribosomal subunit assembly. Rapidly dividing cells (mucosal epithelium,
hematopoietic precursors, hair follicles) are highly dependent on ribosome biogenesis for protein synthesis, making them exquisitely
sensitive to cell-cycle-specific chemotherapy. The Golgi packages proteins, the smooth ER detoxifies, and lysosomes degrade debris
- none of these directly limit renewal.
Q2: A patient with a suspected mitochondrial disorder presents with progressive external ophthalmoplegia and
lactic acidosis. The NP recognizes that impaired oxidative phosphorylation in mitochondria primarily affects
which step of cellular metabolism?
A. Glycolysis in the cytosol, producing lactate as the end product
B. The electron transport chain and ATP synthesis via chemiosmosis at the inner mitochondrial
membrane [CORRECT]
C. Fatty acid beta-oxidation in peroxisomes
D. Glycogenolysis in the cytosol
Correct Answer: B
Rationale:
Mitochondria generate ATP through oxidative phosphorylation at the inner mitochondrial membrane: the electron transport chain
(complexes I-IV) pumps protons to generate an electrochemical gradient, and ATP synthase (complex V) uses that gradient to
Page 1 | The University of Texas at Tyler
,UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
phosphorylate ADP. Impaired OXPHOS shunts pyruvate to lactate (explaining lactic acidosis). Glycolysis occurs in the cytosol,
beta-oxidation mostly in mitochondria but peroxisomes handle very long-chain fatty acids.
Q3: A 62-year-old patient with chronic alcohol use disorder exhibits hepatic steatosis. The NP explains that
impaired very-low-density lipoprotein assembly reflects dysfunction of which organelle?
A. The rough endoplasmic reticulum, where ribosomes synthesize apoproteins
B. The Golgi apparatus, which modifies and packages VLDL for secretion
C. The smooth endoplasmic reticulum, which is the site of lipid synthesis and is overwhelmed by ethanol
metabolism [CORRECT]
D. The mitochondrion, which beta-oxidizes fatty acids
Correct Answer: C
Rationale:
Hepatic steatosis in chronic alcohol use occurs because ethanol metabolism via MEOS (microsomal ethanol oxidizing system) in the
smooth ER generates NADH and acetate, increasing fatty acid synthesis while the increased NADH/NAD+ ratio inhibits fatty acid
beta-oxidation. Additionally, the SER proliferates under chronic induction, but its lipid-synthesis capacity outstrips VLDL export
capacity. The Golgi and rough ER are downstream of lipid handling.
Q4: A 7-month-old infant of Ashkenazi Jewish heritage presents with progressive loss of motor skills,
exaggerated startle response, and a cherry-red macula. The NP suspects Tay-Sachs disease, which results from
deficient activity of which organelle?
A. Lysosomes, due to deficiency of hexosaminidase A causing GM2 ganglioside accumulation in
neurons [CORRECT]
B. Peroxisomes, due to defective very long-chain fatty acid oxidation
C. Mitochondria, due to defective oxidative phosphorylation
D. The Golgi apparatus, due to defective protein glycosylation
Correct Answer: A
Rationale:
Tay-Sachs disease is an autosomal recessive lysosomal storage disorder caused by deficiency of hexosaminidase A, leading to
accumulation of GM2 ganglioside in neuronal lysosomes. The progressive neuronal dysfunction causes loss of motor skills,
exaggerated startle (hyperacusis), and the cherry-red macula (the ganglion cells surrounding the fovea accumulate lipid, making the
underlying choroidal vasculature appear prominent). Peroxisomal, mitochondrial, and Golgi defects cause other phenotypes.
Q5: A graduate nursing student asks why intracellular fluid (ICF) and extracellular fluid (ECF) electrolyte
compositions differ. The NP correctly explains that the sodium-potassium ATPase pump maintains these
gradients by:
A. Passively allowing Na+ to enter the cell down its concentration gradient
B. Hydrolyzing ATP to export 3 Na+ and import 2 K+ per cycle, maintaining high intracellular K+ and high
extracellular Na+ [CORRECT]
C. Exchanging 2 Na+ for 2 K+ in an electroneutral manner
D. Using GTP to move Na+ and K+ against their gradients in equal molar amounts
Correct Answer: B
Rationale:
The Na+/K+-ATPase is a P-type ATPase that hydrolyzes one ATP to export 3 Na+ and import 2 K+, creating both concentration
gradients (high intracellular K+, high extracellular Na+) and an electrogenic effect (net outflow of one positive charge per cycle,
contributing to the resting membrane potential). The pump establishes the gradients that secondary active transport (e.g.,
Na+/glucose cotransport) exploits.
Page 2 | The University of Texas at Tyler
,UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
Q6: A patient with cystic fibrosis has a G551D mutation in the CFTR gene. The NP understands that this
mutation produces a CFTR protein that reaches the cell surface but fails to open properly in response to ATP.
This represents dysfunction of which class of membrane protein?
A. A ligand-gated ion channel opened by acetylcholine binding
B. An ATP-binding cassette (ABC) transporter that functions as a chloride channel gated by ATP
hydrolysis [CORRECT]
C. A voltage-gated sodium channel in neuronal tissue
D. A gap junction connexin
Correct Answer: B
Rationale:
CFTR is an ATP-binding cassette (ABC) transporter family member that functions as a cAMP-regulated chloride channel. The
G551D mutation is a class III (gating) mutation: the protein is processed and reaches the membrane but the ATP-binding
nucleotide-binding domain 1 fails to hydrolyze ATP properly, so the channel opens rarely. Ivacaftor potentiates channel opening in
patients with G551D. This is distinct from the F508del class II trafficking mutation.
Q7: A patient in diabetic ketoacidosis has a serum glucose of 720 mg/dL and a serum sodium of 128 mEq/L. The
NP recognizes that the hyponatremia is primarily caused by which mechanism?
A. True sodium depletion from renal wasting due to osmotic diuresis
B. Dilutional hyponatremia from hyperglycemia drawing intracellular water into the extracellular space;
corrected sodium = measured Na + 1.6 × (glucose − 100)/100 [CORRECT]
C. Syndrome of inappropriate antidiuretic hormone secretion from cerebral edema
D. Pseudohyponatremia from hyperlipidemia
Correct Answer: B
Rationale:
In hyperglycemia, the high serum osmolality from glucose draws water from the intracellular space into the extracellular space,
diluting serum sodium - this is translocational (dilutional) hyponatremia. The corrected sodium formula adds 1.6 mEq/L for every
100 mg/dL glucose above 100. The true total body sodium may be normal or low (osmotic diuresis also causes sodium loss), but the
immediate dilutional effect explains the measured hyponatremia. SIADH and pseudohyponatremia are different mechanisms.
Q8: A patient has familial hypercholesterolemia due to an LDL receptor mutation. The NP understands that
LDL particles are taken into hepatocytes by which transport mechanism?
A. Passive diffusion through the plasma membrane
B. Receptor-mediated endocytosis via clathrin-coated pits, requiring the LDL receptor and
apoB-100 [CORRECT]
C. Facilitated diffusion through a channel protein
D. Active transport against the concentration gradient using ATP
Correct Answer: B
Rationale:
LDL is internalized by receptor-mediated endocytosis: apoB-100 on the LDL particle binds the LDL receptor on hepatocyte
membranes, the receptor-LDL complex clusters in clathrin-coated pits, the pit invaginates and forms an endosome, the receptor
recycles, and the LDL is delivered to lysosomes for cholesterol release. Familial hypercholesterolemia (FH) results from mutations
in the LDL receptor (or apoB-100 or PCSK9), impairing this clearance and causing elevated serum LDL.
Q9: A researcher is studying cell signaling. Which of the following describes a paracrine signaling mechanism?
A. A hormone released into the bloodstream acts on distant target cells
B. A neurotransmitter released at a synaptic cleft acts on the postsynaptic membrane of an adjacent
neuron [CORRECT]
Page 3 | The University of Texas at Tyler
, UT Tyler FNP NURS 5350 - Advanced Pathophysiology - Exam 1 100 Questions - AGRADE Verified 2026/2027
C. A signaling molecule acts on the same cell that secreted it
D. A signaling molecule acts on a gap-junction-connected neighboring cell
Correct Answer: B
Rationale:
Paracrine signaling refers to a cell releasing signaling molecules that act on nearby cells of a different type - the classic example is a
neurotransmitter (e.g., acetylcholine) released at a synapse acting on an adjacent postsynaptic cell. Endocrine signaling uses the
bloodstream to reach distant targets (e.g., thyroid hormone). Autocrine signaling involves a cell responding to its own secreted signal
(e.g., tumor growth factors). Gap junctions transfer ions and small molecules directly between adjacent cells - not true signaling.
Q10: A patient receives a beta-1 adrenergic agonist (dobutamine) for acute heart failure. The NP understands
that this drug acts through which second messenger system?
A. The phospholipase C pathway, generating IP3 and DAG
B. The Gs protein - adenylyl cyclase - cAMP - protein kinase A pathway, increasing intracellular
cAMP [CORRECT]
C. The Gi protein pathway, decreasing cAMP
D. Receptor tyrosine kinase activation leading to Ras-MAPK signaling
Correct Answer: B
Rationale:
Beta-1 adrenergic receptors are G protein-coupled receptors (GPCRs) linked to the Gs alpha subunit. Agonist binding activates
adenylyl cyclase, which converts ATP to cAMP. cAMP activates protein kinase A (PKA), which phosphorylates L-type calcium
channels (increasing calcium influx) and phospholamban (relieving inhibition of the SERCA pump, increasing calcium reuptake into
the sarcoplasmic reticulum). The net effect is increased cardiac contractility and heart rate.
Q11: A 38-year-old patient with type 2 diabetes mellitus is prescribed a GLP-1 receptor agonist (semaglutide).
The NP recognizes that the GLP-1 receptor signals through which mechanism?
A. Receptor tyrosine kinase autophosphorylation, activating the Ras-MAPK pathway
B. G protein-coupled receptor activation of adenylyl cyclase, increasing cAMP and protein kinase A in
pancreatic beta cells [CORRECT]
C. Janus kinase (JAK) activation leading to STAT phosphorylation
D. Direct ligand-gated ion channel opening
Correct Answer: B
Rationale:
The GLP-1 receptor is a Gs-coupled GPCR on pancreatic beta cells. Agonist binding activates adenylyl cyclase, increasing cAMP
and activating PKA, which potentiates glucose-stimulated insulin secretion. GLP-1 also slows gastric emptying, reduces glucagon,
and promotes satiety. Unlike insulin (which acts through a receptor tyrosine kinase and IRS-1 signaling), GLP-1 acts through cAMP.
Q12: Insulin binds its receptor on skeletal muscle cells. The NP correctly identifies that this receptor's
mechanism of action involves:
A. A G protein-coupled receptor that activates adenylyl cyclase
B. A receptor tyrosine kinase that autophosphorylates and recruits IRS-1, leading to PI3K-Akt pathway
activation and GLUT4 translocation [CORRECT]
C. A ligand-gated ion channel that allows sodium influx
D. An intracellular receptor that translocates to the nucleus as a transcription factor
Correct Answer: B
Rationale:
The insulin receptor is a receptor tyrosine kinase (RTK). Insulin binding causes autophosphorylation of the beta subunit, which then
phosphorylates insulin receptor substrate-1 (IRS-1). IRS-1 activates PI3K, generating PIP3, which activates PDK1 and Akt. Akt
Page 4 | The University of Texas at Tyler
