Insulin is a major ____ hormone.
A. Catabolic
B. Anabolic
C. Permissive
D. Contrainsular

B. Anabolic

After a mixed meal, which hormone promotes glycogen storage in liver and muscle?
A. Glucagon
B. Epinephrine
C. Cortisol
D. Insulin

D. Insulin

In adipocytes after eating, which hormone promotes nutrient storage as triacylglycerols?
A. Insulin
B. Glucagon
C. Cortisol
D. Growth hormone

A. Insulin

A resistance-trained patient uses post-workout nutrients for myofibrils. Insulin promotes synthesis of:
A. Glycogen
B. Ketone bodies
C. Proteins
D. Cholesterol

C. Proteins

Relative to fasting hormones, insulin antagonizes which process?
A. Fuel mobilization
B. Ketone oxidation
C. Cholesterol synthesis
D. Urea production

A. Fuel mobilization

A “counterregulatory” hormone to insulin is also called:
A. Autocrine
B. Endocrine
C. Paracrine
D. Contrainsular

D. Contrainsular

The major action of glucagon is fuel mobilization by stimulating:
A. Glycogenesis and lipogenesis
B. Glycolysis and lipogenesis
C. Glycogenolysis and gluconeogenesis
D. Protein synthesis and uptake

C. Glycogenolysis and gluconeogenesis

Which is NOT a contrainsular hormone?
A. Cortisol
B. Insulin
C. Epinephrine
D. Growth hormone

B. Insulin

Thyroid hormone is insulin-counterregulatory because it:
A. Decreases fuel use and sensitivity
B. Increases fuel use, lowers sensitivity
C. Increases fuel use and sensitivity
D. Decreases fuel use, raises sensitivity

B. Increases fuel use, lowers sensitivity

A hormone changes metabolism within minutes–hours mainly by:
A. Catalytic activity changes
B. Enzyme gene induction
C. Organelle biogenesis changes
D. DNA methylation changes

A. Catalytic activity changes

A hormone changes metabolism over hours–days mainly by:
A. Ion channel gating
B. Second messenger spikes
C. Allosteric binding only
D. Transcription and translation changes

D. Transcription and translation changes

Insulin’s growth effects are hard to separate from:
A. Kinins
B. Somatomedin
C. Interleukins
D. Prostanoids

B. Somatomedin

Within islets, β-cell insulin suppresses α-cell glucagon via:
A. Paracrine signaling
B. Endocrine signaling
C. Autocrine signaling
D. Neurocrine signaling

A. Paracrine signaling

A 37–amino acid peptide co-secreted with insulin when glucose rises is:
A. Glucagon
B. Somatostatin
C. Amylin
D. C-peptide

C. Amylin

Amylin most directly:
A. Increases fasting glucagon
B. Increases postprandial glucagon
C. Suppresses fasting glucagon
D. Suppresses postprandial glucagon

D. Suppresses postprandial glucagon

A patient on an amylin-mimetic has improved postprandial glucose partly by slowing:
A. Hepatic glycogenolysis
B. Gastric emptying
C. Renal glucose filtration
D. Muscle proteolysis

B. Gastric emptying

The shared physiologic goal of amylin’s actions is:
A. Reduces blood glucose
B. Raises blood glucose
C. Raises ketone production
D. Increases lipolysis

A. Reduces blood glucose

In type 1 diabetes, β-cell destruction removes secretion of:
A. Glucagon and insulin
B. Amylin and glucagon
C. Insulin and amylin
D. Somatostatin and amylin

C. Insulin and amylin

A patient with T1D wants an adjunct replacing a missing β-cell peptide. Best drug:
A. Metformin
B. Acarbose
C. Sitagliptin
D. Pramlintide

D. Pramlintide

The adverse effect most limiting pramlintide use is:
A. Hemolytic anemia
B. Nausea or vomiting
C. Nephrolithiasis
D. Bronchospasm

B. Nausea or vomiting

Glucagon is synthesized as part of the precursor:
A. Proglucagon
B. Proinsulin
C. Proalbumin
D. Proopiomelanocortin

A. Proglucagon

Proglucagon is produced primarily in:
A. β-cells and δ-cells
B. Liver and kidney cortex
C. α-cells and intestinal L-cells
D. Adrenal cortex and medulla

C. α-cells and intestinal L-cells

Pancreatic cleavage yields glucagon that is about what fraction of immunoreactive blood glucagon?
A. 5–10%
B. 10–20%
C. 60–80%
D. 30–40%

C. 60–80%

Glucagon’s key second messenger in many target cells is:
A. IP3
B. cAMP
C. cGMP
D. Ca2+

B. cAMP

Portal vein glucagon can reach approximately:
A. 50 pg/mL
B. 100 pg/mL
C. 500 pg/mL
D. 5,000 pg/mL

C. 500 pg/mL

Adenylate cyclase activation by glucagon directly increases:
A. cAMP
B. DAG
C. IP3
D. Ca2+

A. cAMP

In the pancreas, glucagon is cleaved from proglucagon mainly in:
A. Intestinal L cells
B. β-cells
C. δ-cells
D. α-cells

D. α-cells

Thyroid hormone strengthens counterregulation partly by increasing sensitivity to:
A. Insulin only
B. Counterregulatory hormones
C. Glucose transporters
D. Leptin signaling

B. Counterregulatory hormones

A genetics question asks where the peptide precursor for somatostatin is encoded. Which locus fits the provided description?
A. Chromosome 17q
B. Chromosome 3q
C. Chromosome 11p
D. Chromosome Xp

B. Chromosome 3q

A cyclic peptide was named for inhibiting GH release from the anterior pituitary. Which peptide is this?
A. Somatostatin SS-14
B. Prosomatostatin SS-28
C. IGF-1
D. GHRH

A. Somatostatin SS-14

During a mixed-meal study, Somatostatin is released from two main sites. Which pairing is correct?
A. Hypothalamus and α cells
B. Liver and intestinal crypts
C. Hypothalamus and D cells
D. Pituitary and β cells

C. Hypothalamus and D cells

Compared with SS-14, prosomatostatin (SS-28) is structurally defined by:
A. Fourteen extra amino acids
B. Fourteen fewer amino acids
C. Twenty-eight extra amino acids
D. Loss of cyclic structure

A. Fourteen extra amino acids

A pharmacology stem compares biologic potency of SS-28 vs SS-14 on GH and insulin release. Which magnitude is correct?
A. 2–3 times more potent
B. 4–6 times more potent
C. 7–10 times more potent
D. 15–20 times more potent

C. 7–10 times more potent

A patient starts tolbutamide and has increased insulin secretion. Which additional pancreatic hormone secretion also rises?
A. Glucagon secretion rises
B. Somatostatin secretion rises
C. TRH secretion rises
D. IGF-1 secretion rises

B. Somatostatin secretion rises

An octreotide analog binds somatostatin receptors on target cells. What is the canonical effect on adenylate cyclase?
A. Strong activation
B. Weak activation
C. No change
D. Inactivation

D. Inactivation

A signaling question asks which pathway is directly regulated by somatostatin receptors besides adenylate cyclase.
A. Phosphotyrosine phosphatases
B. DNA polymerases
C. HMG-CoA reductase
D. Cyclooxygenases

A. Phosphotyrosine phosphatases

Somatostatin receptor signaling is also linked to modulation of:
A. Urea cycle enzymes
B. Ribosomal subunits
C. MAP kinases
D. Microtubule dynein

C. MAP kinases

Somatostatin receptors can alter intracellular ion concentrations, especially:
A. Na and Cl
B. Ca and K
C. Mg and PO4
D. Fe and Cu

B. Ca and K

Somatostatin reduces:
A. Nutrient absorption
B. Chloride secretion
C. Bile acid synthesis
D. Colonic water uptake

A. Nutrient absorption

A patient on octreotide develops fat malabsorption. Which mechanism best matches the provided notes?
A. Increased brush-border enzymes
B. Increased intestinal motility
C. Diminished pancreatic exocrine secretion
D. Increased visceral blood flow

C. Diminished pancreatic exocrine secretion

A patient with episodic flushing and diarrhea has elevated serotonin. Somatostatin analogs can suppress GH increases seen in:
A. Pheochromocytoma
B. Insulinoma
C. Medullary thyroid cancer
D. Carcinoid tumor syndrome

D. Carcinoid tumor syndrome

Somatostatin suppresses basal secretion of several hormones. Which is included?
A. CRH
B. TRH
C. GnRH
D. GHRH

B. TRH

Many growth-hormone effects in tissues are mediated by:
A. IGFs
B. Catecholamines
C. Cortisol
D. Thyroxine

A. IGFs

A patient with acromegaly needs a drug that blocks GH signaling at its receptor. Best choice?
A. Octreotide
B. Cabergoline
C. Bromide salts
D. Pegvisomant

D. Pegvisomant

A patient with acromegaly cannot undergo surgery. Which listed dopamine agonist inhibits GH secretion?
A. Metoclopramide
B. Haloperidol
C. Cabergoline
D. Ondansetron

C. Cabergoline

A stem asks where the growth hormone gene is located. Which chromosome is correct?
A. Chromosome 3
B. Chromosome 17
C. Chromosome 11
D. Chromosome 7

B. Chromosome 17

Growth hormone is secreted by which anterior pituitary cell type?
A. Thyrotroph
B. Corticotroph
C. Lactotroph
D. Somatotroph

D. Somatotroph

A patient suspected of acromegaly drinks 100 g glucose. Which abnormal result supports the diagnosis?
A. GH remains high
B. GH becomes undetectable
C. IGF-1 falls immediately
D. Glucose fails to rise

A. GH remains high

GH increases expression of which gene in liver and extrahepatic tissues?
A. GLUT4
B. IGF-1
C. POMC
D. ACTH

B. IGF-1

IGF-1 from hepatocytes limits GH secretion by negative feedback on:
A. Thyrotrophs
B. Corticotrophs
C. Somatotrophs
D. Gonadotrophs

C. Somatotrophs

A physiologic question: rising blood glucose normally does what to GH release?
A. Suppresses GH release
B. Triggers GH bursts
C. Has no effect
D. Inverts GH feedback

A. Suppresses GH release

During an insulin overdose, which change in GH secretion is expected in normal physiology?
A. No change
B. Decreased secretion
C. Absent secretion
D. Increased secretion

D. Increased secretion

In a provocative endocrine test, which substrate can stimulate GH release when levels rise?
A. Glucose
B. Arginine
C. Lactate
D. Palmitate

B. Arginine

A subject receives arginine to stimulate GH. Rising free fatty acids would most likely:
A. Enhance the GH rise
B. Prolong the GH rise
C. Blunt the GH rise
D. Reverse the GH rise

C. Blunt the GH rise

GH shifts adipocyte metabolism by changing responsiveness to other hormones. GH increases adipocyte:
A. Sensitivity to catecholamine lipolysis
B. Sensitivity to insulin lipogenesis
C. Resistance to catecholamine lipolysis
D. Sensitivity to glucose uptake

A. Sensitivity to catecholamine lipolysis

Shortly after a GH pulse, which circulating substrates rise due to adipose effects?
A. Lactate and pyruvate
B. Ketones and glucose
C. Cholesterol and HDL
D. FFA and glycerol

D. FFA and glycerol

GH can reduce glucose uptake in fat and muscle by postreceptor inhibition of:
A. Glucagon action
B. Thyroid action
C. Insulin action
D. Cortisol action

C. Insulin action

A somatostatin receptor agonist decreases adenylate cyclase activity. Which second messenger falls in hepatocytes?
A. IP3
B. cAMP
C. DAG
D. cGMP

B. cAMP

IGF-2 is also called somatomedin:
A. Somatomedin C
B. Somatomedin A
C. Somatomedin B
D. Somatomedin D

B. Somatomedin A

IGFs exert effects through which mechanisms?
A. Endocrine mechanism only
B. Paracrine mechanism only
C. Autocrine mechanism only
D. Endocrine or paracrine or autocrine

D. Endocrine or paracrine or autocrine

Most cells express IGF mRNA, but the highest message concentration is in the:
A. Liver
B. Heart
C. Kidney
D. Skeletal muscle

A. Liver

After liver, the next-highest IGF mRNA concentration is in the:
A. Brain
B. Lung
C. Kidney
D. Pancreas

C. Kidney

Catecholamines are best classified as:
A. Bioamines
B. Steroids
C. Peptides
D. Eicosanoids

A. Bioamines

A patient with an adrenal mass has excess epinephrine. Epinephrine is synthesized in the:
A. Adrenal cortex
B. Sympathetic ganglia
C. Adrenal medulla
D. Thyroid follicles

C. Adrenal medulla

A catecholamine that is stored in the adrenal medulla is also stored in:
A. Pancreatic β cells
B. Hepatocytes
C. Thyroid follicles
D. Adrenergic nerve endings

D. Adrenergic nerve endings

The major precursor for catecholamine synthesis is:
A. Tryptophan
B. Histidine
C. Tyrosine
D. Glycine

C. Tyrosine

Episodic headaches, palpitations, diaphoresis, and elevated urine catecholamines most strongly suggest:
A. Pheochromocytoma
B. Insulinoma
C. Carcinoid tumor
D. Pituitary adenoma

A. Pheochromocytoma

Catecholamines act mainly via which receptor classes?
A. Insulin and IGF receptors
B. Nuclear steroid receptors
C. TSH and ACTH receptors
D. Alpha and beta receptors

D. Alpha and beta receptors

Epinephrine blood half-life is:
A. Long half-life
B. Short half-life
C. Protein-bound, prolonged
D. Renally retained, prolonged

B. Short half-life

Catecholamines often require high local concentrations because they have:
A. Low receptor affinity
B. High receptor affinity
C. Covalent receptor binding
D. Irreversible receptor activation

A. Low receptor affinity

Hypothalamic CRH synthesis/release is driven in part by:
A. Dopamine and GABA
B. Glutamate and glycine
C. Acetylcholine and serotonin
D. Norepinephrine and histamine

C. Acetylcholine and serotonin

CRH reaches anterior pituitary targets primarily through:
A. Systemic arterial blood
B. CSF diffusion
C. Axonal transport
D. Portal vessels

D. Portal vessels

ACTH’s major trophic influence on cortisol synthesis is at the step:
A. Pregnenolone to progesterone
B. Cholesterol to pregnenolone
C. Cortisol to cortisone
D. Cholesterol to bile acids

B. Cholesterol to pregnenolone

Cortisol is secreted from the ____ in response to ACTH.
A. Adrenal medulla
B. Thyroid gland
C. Adrenal cortex
D. Pancreatic islets

C. Adrenal cortex

High circulating cortisol suppresses secretion of:
A. CRH and ACTH
B. TRH and TSH
C. GnRH and LH
D. GHRH and GH

A. CRH and ACTH

Excess cortisol due to excess ACTH secretion is termed:
A. Cushing syndrome
B. Addison disease
C. Ectopic ACTH
D. Cushing disease

D. Cushing disease

Primary cortisol excess from an adrenocortical tumor (for example) is termed:
A. Cushing disease
C. Nelson syndrome
D. Sheehan syndrome

B. Cushing syndrome

A key genomic effect of glucocorticoids is inhibition of:
A. Glycogen breakdown
B. Lipolysis
C. DNA and RNA protein synthesis
D. Catecholamine synthesis

C. DNA and RNA protein synthesis

In addition to synthesis inhibition, glucocorticoids stimulate:
A. DNA and RNA protein degradation
B. Cholesterol uptake
C. Iodide trapping
D. Ribosomal biogenesis

A. DNA and RNA protein degradation

Thyroid acinar (follicular) cells secrete primarily:
A. Calcitonin only
B. T4 and T3
C. Aldosterone and cortisol
D. Epinephrine and norepinephrine

B. T4 and T3

The first listed step in thyroid T3/T4 synthesis is:
A. Coupling MIT DIT
B. Proteolysis thyroglobulin
C. Iodination of residues
D. Iodide trapping into cell

D. Iodide trapping into cell

After iodide trapping, iodide is oxidized to form an:
A. Iodinating species
B. Iodotyrosines
C. Thyroxine directly
D. Iodide gradient

A. Iodinating species

Formation of T3/T4 within thyroglobulin requires coupling of:
A. Iodide to cholesterol
B. MIT and DIT
C. T4 to T3
D. Tyrosine to phenylalanine

B. MIT and DIT

The step that releases free thyroid hormone into blood is:
A. Iodide trapping
B. Oxidation of iodide
C. Coupling MIT DIT
D. Proteolysis of thyroglobulin

D. Proteolysis of thyroglobulin

After liver and kidney, the next-highest IGF mRNA concentration is in the:
A. Lung
B. Spleen
C. Heart
D. Skin

C. Heart

Norepinephrine is synthesized/stored in adrenal medulla and also in:
A. CNS regions
B. Pancreatic acini
C. Thyroid follicles
D. Renal tubules

A. CNS regions

Catecholamines are secretory products of the:
A. HPA axis
B. HPT axis
C. Renin-angiotensin system
D. Sympathoadrenal system

D. Sympathoadrenal system

Catecholamine receptors (alpha/beta) are located on the:
A. Nucleus
B. Plasma membrane
C. Mitochondria
D. Golgi membrane

B. Plasma membrane

Acidic chyme entering the proximal small bowel triggers a hormone from which enteroendocrine cell?
A. I cells
B. S cells
C. G cells
D. K cells

B. S cells

Type 2 diabetes improves after gastric bypass before weight loss mainly due to sustained increases in:
A. Amylin and GLP-1
B. Insulin and cortisol
C. Somatostatin and TSH
D. Glucagon and epinephrine

A. Amylin and GLP-1

A patient has rapid gastric emptying and large post-meal nutrient spikes. Which β-cell peptide dysfunction best fits?
A. Glucagon
B. Somatostatin
C. Amylin
D. Secretin

C. Amylin

A hormone that inhibits GH, TSH, insulin, glucagon, gastrin, and TRH is:
A. GLP-1
B. Insulin
C. GHRH
D. Somatostatin

D. Somatostatin

Which metabolite trio increases somatostatin release?
A. Lactate alanine glycerol
B. Palmitate acetate ketones
C. Glucose arginine leucine
D. Cholesterol bilirubin urea

C. Glucose arginine leucine

Which hormone trio increases somatostatin release?
A. ACTH CRH cortisol
B. Glucagon VIP CCK
C. TSH TRH prolactin
D. ADH renin angiotensin

B. Glucagon VIP CCK

After GH administration, hepatocytes increase expression of:
A. PEP carboxykinase
B. HMG-CoA reductase
C. Glycogen phosphorylase
D. Ornithine decarboxylase

D. Ornithine decarboxylase

A hypothalamic hormone encoded on chromosome 20 and released from the arcuate nucleus to stimulate somatotrophs is:
A. GHRH
B. Somatostatin
C. CRH
D. GnRH

A. GHRH

Rising levels of which growth factor provide negative feedback that inhibits GHRH?
A. T3
B. IGF-1
C. Insulin
D. Cortisol

B. IGF-1

During low plasma insulin (fasting), which hormone enhances fatty acid oxidation supporting hepatic gluconeogenesis?
A. Insulin
B. Amylin
C. Secretin
D. Growth hormone

D. Growth hormone

Which oxidation pattern best matches GH “sparing” effects?
A. ↓FA oxidation, ↑glucose oxidation
B. ↑protein oxidation, ↑glucose oxidation
C. ↑FA oxidation, ↓glucose oxidation
D. ↓FA oxidation, ↓ketone oxidation

C. ↑FA oxidation, ↓glucose oxidation

In acute stress, increased NE/E causes which pancreatic secretion pattern?
A. ↓Insulin, ↑glucagon
B. ↑Insulin, ↓glucagon
C. ↑Insulin, ↑glucagon
D. ↓Insulin, ↓glucagon

A. ↓Insulin, ↑glucagon

Elevated urinary metanephrines (VMA) most strongly implicate a tumor arising from:
A. Zona fasciculata cells
B. Thyroid follicular cells
C. Pituitary corticotrophs
D. Adrenal medulla chromaffin cells

D. Adrenal medulla chromaffin cells

A patient with consistently high catecholamines in blood/urine should be evaluated for:
A. Medullary thyroid carcinoma
B. Pheochromocytoma
C. Addison disease
D. SIADH

B. Pheochromocytoma

During severe stress, cortisol negative feedback on CRH/ACTH is typically:
A. Overridden
B. Amplified
C. Irreversibly fixed
D. Absent at baseline

A. Overridden

The GH receptor is classically linked to which signaling pathway?
A. Gs–cAMP
B. Gi–cAMP
C. JAK/STAT
D. IP3–DAG

C. JAK/STAT

The hormone in this set that signals via Gi-protein receptors is:
A. Insulin
B. Glucagon
C. Secretin
D. Somatostatin

D. Somatostatin

Which hormone is classified as contra-insular in these notes?
A. Cortisol
B. Insulin
C. Amylin
D. Secretin

A. Cortisol

A hepatic protein induced by GH (besides IGF-1) in these notes is:
A. Albumin
B. Alpha-2 macroglobulin
C. Transferrin
D. Ceruloplasmin

B. Alpha-2 macroglobulin

Which GH tissue-effect pairing best matches these notes?
A. Adipose lipolysis, muscle protein synthesis
B. Adipose lipogenesis, muscle glycogenolysis
C. Adipose glycogenesis, muscle ketogenesis
D. Adipose gluconeogenesis, muscle glycolysis

A. Adipose lipolysis, muscle protein synthesis

In hepatocytes, GH most directly increases expression of:
A. GLUT4
B. Hexokinase
C. TRH
D. IGF-1

D. IGF-1

Stressors like pain, hemorrhage, exercise, and hypoglycemia increase hypothalamic drive partly via:
A. Dopamine and GABA
B. Norepinephrine and histamine
C. Acetylcholine and serotonin
D. Glycine and glutamate

C. Acetylcholine and serotonin

A patient has a GI hormone that stimulates gastric and pancreatic enzyme secretion to aid nutrient digestion. It is secreted by proximal small-bowel M cells. Which hormone?
A. Secretin
B. Motilin
C. Peptide YY
D. GLP-1

B. Motilin

A hormone that regulates pancreatic enzyme secretion and inhibits gastrin/acid is released from which proximal small-bowel cell type?
A. M cells
B. I cells
C. K cells
D. S cells

D. S cells

A post-op patient has reduced gastric emptying and slower upper-intestinal motility from a peptide secreted by pancreatic islets. Which hormone?
A. Pancreatic polypeptide
B. Secretin
C. Motilin
D. GLP-1

A. Pancreatic polypeptide

A peptide from pancreatic islet alpha cells inhibits gastric secretion. Which hormone?
A. Secretin
B. Peptide YY
C. Motilin
D. GIP

B. Peptide YY

A patient’s proximal small-bowel enteroendocrine dysfunction reduces a cyclic hormone that stimulates GI/pancreatic enzyme secretion. Which hormone is missing?
A. Motilin
B. Secretin
C. GLP-1
D. CCK

A. Motilin

A patient with refractory gastric acid hypersecretion improves with a proximal small-bowel hormone that inhibits gastrin and gastric acid and regulates pancreatic enzyme secretion. Which hormone?
A. Motilin
B. Pancreatic polypeptide
C. Peptide YY
D. Secretin

D. Secretin

A patient receives an incretin-based therapy that reduces postprandial glucagon and slows gastric emptying. Which hormone mediates this?
A. GIP
B. Amylin
C. GLP-1
D. Motilin

C. GLP-1

A peptide hormone improves glucose homeostasis by inhibiting alpha-cell glucagon release and slowing gastric emptying. Which hormone?
A. GLP-1
B. Secretin
C. Pancreatic polypeptide
D. Peptide YY

A. GLP-1

A patient’s adipocytes increase energy storage after meals via a peptide hormone acting on adipocyte receptors. Which hormone?
A. GLP-1
B. GIP
C. Motilin
D. Somatostatin

B. GIP

A surface protease rapidly limits incretin signaling by inactivating both GLP-1 and GIP. Which protease?
A. Renin
B. ACE
C. DPP-4
D. Trypsin

C. DPP-4

That protease cleaves GLP-1 into which amino acid (per provided note)?
A. Alanine
B. Glycine
C. Valine
D. Leucine

A. Alanine

A patient with hyperphagia has elevated ghrelin signaling. Ghrelin increases appetite by activating which hypothalamic kinase?
A. PKA
B. PKC
C. AMPK
D. mTOR

C. AMPK

Ghrelin-driven AMPK activation increases appetite by promoting release of:
A. POMC
B. CART
C. Somatostatin
D. Neuropeptide Y

D. Neuropeptide Y

A sulfonylurea increases insulin secretion and also increases somatostatin secretion. Which drug is most consistent?
A. Glipizide
B. Tolbutamide
C. Repaglinide
D. Sitagliptin

B. Tolbutamide

A long-acting analog used clinically for somatostatin has ~110-minute half-life. Which drug?
A. Pramlintide
B. Cabergoline
C. Octreotide
D. Pegvisomant

C. Octreotide

A patient with episodic headaches, palpitations, and elevated catecholamine metabolites is diagnosed with pheochromocytoma. Major cause?
A. Adrenal cortex hyperplasia
B. Adrenal medulla neoplasm
C. Pituitary adenoma
D. Thyroid follicular tumor

B. Adrenal medulla neoplasm

A patient has increased insulin degradation/clearance and variable glucose intolerance (“metathyroid diabetes mellitus”). Underlying disorder?
A. Hyperthyroidism
B. Addison disease
C. Hypothyroidism
D. Acromegaly

A. Hyperthyroidism

In hyperthyroidism, glucose intolerance is partly explained by increased:
A. Insulin secretion
B. Insulin clearance
C. Glucose absorption
D. Glucagon clearance

B. Insulin clearance

An obese patient with T2D has near-immediate glycemic improvement after gastric bypass, before weight loss. The key rapidly increased hormone is:
A. GLP-1
B. Peptide YY
C. Secretin
D. Motilin

A. GLP-1

Shortly after gastric bypass, improved glycemia is linked to increased release of:
A. Glucagon and somatostatin
B. GIP and secretin
C. Motilin and peptide YY
D. Insulin and amylin

D. Insulin and amylin