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Biochem 41

front 1

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

back 1

B. Anabolic

front 2

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

back 2

D. Insulin

front 3

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

back 3

A. Insulin

front 4

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

back 4

C. Proteins

front 5

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

back 5

A. Fuel mobilization

front 6

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

back 6

D. Contrainsular

front 7

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

back 7

C. Glycogenolysis and gluconeogenesis

front 8

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

back 8

B. Insulin

front 9

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

back 9

B. Increases fuel use, lowers sensitivity

front 10

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

back 10

A. Catalytic activity changes

front 11

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

back 11

D. Transcription and translation changes

front 12

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

back 12

B. Somatomedin

front 13

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

back 13

A. Paracrine signaling

front 14

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

back 14

C. Amylin

front 15

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

back 15

D. Suppresses postprandial glucagon

front 16

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

back 16

B. Gastric emptying

front 17

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

back 17

A. Reduces blood glucose

front 18

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

back 18

C. Insulin and amylin

front 19

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

back 19

D. Pramlintide

front 20

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

back 20

B. Nausea or vomiting

front 21

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

back 21

A. Proglucagon

front 22

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

back 22

C. α-cells and intestinal L-cells

front 23

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%

back 23

C. 60–80%

front 24

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

back 24

B. cAMP

front 25

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

back 25

C. 500 pg/mL

front 26

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

back 26

A. cAMP

front 27

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

back 27

D. α-cells

front 28

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

back 28

B. Counterregulatory hormones

front 29

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

back 29

B. Chromosome 3q

front 30

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

back 30

A. Somatostatin SS-14

front 31

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

back 31

C. Hypothalamus and D cells

front 32

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

back 32

A. Fourteen extra amino acids

front 33

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

back 33

C. 7–10 times more potent

front 34

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

back 34

B. Somatostatin secretion rises

front 35

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

back 35

D. Inactivation

front 36

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

back 36

A. Phosphotyrosine phosphatases

front 37

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

back 37

C. MAP kinases

front 38

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

back 38

B. Ca and K

front 39

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

back 39

A. Nutrient absorption

front 40

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

back 40

C. Diminished pancreatic exocrine secretion

front 41

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

back 41

D. Carcinoid tumor syndrome

front 42

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

back 42

B. TRH

front 43

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

back 43

A. IGFs

front 44

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

back 44

D. Pegvisomant

front 45

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

back 45

C. Cabergoline

front 46

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

back 46

B. Chromosome 17

front 47

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

back 47

D. Somatotroph

front 48

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

back 48

A. GH remains high

front 49

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

back 49

B. IGF-1

front 50

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

back 50

C. Somatotrophs

front 51

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

back 51

A. Suppresses GH release

front 52

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

back 52

D. Increased secretion

front 53

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

back 53

B. Arginine

front 54

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

back 54

C. Blunt the GH rise

front 55

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

back 55

A. Sensitivity to catecholamine lipolysis

front 56

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

back 56

D. FFA and glycerol

front 57

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

back 57

C. Insulin action

front 58

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

back 58

B. cAMP

front 59

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

back 59

B. Somatomedin A

front 60

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

back 60

D. Endocrine or paracrine or autocrine

front 61

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

back 61

A. Liver

front 62

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

back 62

C. Kidney

front 63

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

back 63

A. Bioamines

front 64

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

back 64

C. Adrenal medulla

front 65

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

back 65

D. Adrenergic nerve endings

front 66

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

back 66

C. Tyrosine

front 67

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

back 67

A. Pheochromocytoma

front 68

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

back 68

D. Alpha and beta receptors

front 69

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

back 69

B. Short half-life

front 70

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

back 70

A. Low receptor affinity

front 71

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

back 71

C. Acetylcholine and serotonin

front 72

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

back 72

D. Portal vessels

front 73

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

back 73

B. Cholesterol to pregnenolone

front 74

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

back 74

C. Adrenal cortex

front 75

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

back 75

A. CRH and ACTH

front 76

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

back 76

D. Cushing disease

front 77

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

back 77

B. Cushing syndrome

front 78

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

back 78

C. DNA and RNA protein synthesis

front 79

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

back 79

A. DNA and RNA protein degradation

front 80

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

back 80

B. T4 and T3

front 81

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

back 81

D. Iodide trapping into cell

front 82

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

back 82

A. Iodinating species

front 83

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

back 83

B. MIT and DIT

front 84

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

back 84

D. Proteolysis of thyroglobulin

front 85

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

back 85

C. Heart

front 86

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

back 86

A. CNS regions

front 87

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

back 87

D. Sympathoadrenal system

front 88

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

back 88

B. Plasma membrane

front 89

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

back 89

B. S cells

front 90

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

back 90

A. Amylin and GLP-1

front 91

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

back 91

C. Amylin

front 92

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

back 92

D. Somatostatin

front 93

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

back 93

C. Glucose arginine leucine

front 94

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

back 94

B. Glucagon VIP CCK

front 95

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

back 95

D. Ornithine decarboxylase

front 96

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

back 96

A. GHRH

front 97

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

back 97

B. IGF-1

front 98

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

back 98

D. Growth hormone

front 99

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

back 99

C. ↑FA oxidation, ↓glucose oxidation

front 100

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

back 100

A. ↓Insulin, ↑glucagon

front 101

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

back 101

D. Adrenal medulla chromaffin cells

front 102

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

back 102

B. Pheochromocytoma

front 103

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

back 103

A. Overridden

front 104

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

back 104

C. JAK/STAT

front 105

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

back 105

D. Somatostatin

front 106

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

back 106

A. Cortisol

front 107

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

back 107

B. Alpha-2 macroglobulin

front 108

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

back 108

A. Adipose lipolysis, muscle protein synthesis

front 109

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

back 109

D. IGF-1

front 110

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

back 110

C. Acetylcholine and serotonin

front 111

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

back 111

B. Motilin

front 112

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

back 112

D. S cells

front 113

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

back 113

A. Pancreatic polypeptide

front 114

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

back 114

B. Peptide YY

front 115

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

back 115

A. Motilin

front 116

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

back 116

D. Secretin

front 117

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

back 117

C. GLP-1

front 118

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

back 118

A. GLP-1

front 119

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

back 119

B. GIP

front 120

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

back 120

C. DPP-4

front 121

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

back 121

A. Alanine

front 122

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

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C. AMPK

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

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D. Neuropeptide Y

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

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B. Tolbutamide

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

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C. Octreotide

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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

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B. Adrenal medulla neoplasm

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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

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A. Hyperthyroidism

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

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B. Insulin clearance

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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

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A. GLP-1

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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

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D. Insulin and amylin