A tumor compresses the master control center for metabolism, growth, and reproduction. Which paired structures mediate this control?
A. Thalamus and pineal gland
B. Hypothalamus and pituitary gland
C. Medulla and adrenal medulla
D. Hippocampus and amygdala

B. Hypothalamus and pituitary gland

TRH must reach the anterior pituitary efficiently. What carries small hypothalamic hormones there?
A. Systemic arterial blood
B. Neurosecretory axons
C. Lymphatic channels
D. Portal venous system

D. Portal venous system

A patient lacks posterior pituitary hormones after hypothalamic injury. Where are posterior-lobe hormones synthesized?
A. Hypothalamus
B. Posterior pituitary
C. Anterior pituitary
D. Median eminence

A. Hypothalamus

After synthesis, posterior-lobe hormones reach the posterior pituitary via which pathway?
A. Portal capillaries
B. CSF bulk flow
C. Neurosecretory fibers
D. Hepatic sinusoids

C. Neurosecretory fibers

A child with hormone deficiency receives exogenous pituitary hormones. This drug use best fits:
A. Replacement therapy
B. Immunosuppression
C. Antimicrobial prophylaxis
D. Antiarrhythmic suppression

A. Replacement therapy

A patient with acromegaly is treated with a pituitary-hormone–blocking drug. This primary use is:
A. Diagnostic screening
B. Antagonism of hormone excess
C. Replacement for deficiency
D. Enhancing hormone secretion

B. Antagonism of hormone excess

A resident orders a stimulation test using hypothalamic hormones. This primary use is:
A. Replacement therapy
B. Symptomatic palliation
C. Toxicity mitigation
D. Diagnostic tool

D. Diagnostic tool

Two pituitary hormones share significant homology and are single-chain proteins. Which pair fits?
A. TSH and LH
B. ACTH and TSH
C. GH and prolactin
D. FSH and LH

C. GH and prolactin

A signaling inhibitor blocks the pathway used by both GH and prolactin receptors. Which pathway is it?
A. cGMP–PKG signaling
B. JAK/STAT signaling
C. IP3–DAG signaling
D. Nuclear receptor signaling

B. JAK/STAT signaling

A lab panel focuses on pituitary dimeric hormones with shared structure. Which set is dimeric?
A. TSH FSH LH
B. GH PRL ACTH
C. TRH CRH GnRH
D. IGF-1 cortisol T3

A. TSH FSH LH

Which receptor type do TSH, FSH, and LH activate?
A. Ion channel receptor
B. JAK/STAT receptor
C. Nuclear receptor
D. GPCR

D. GPCR

A mutation affects a subunit shared by TSH, FSH, and LH. Which subunit is shared?
A. Beta subunit
B. Alpha subunit
C. Gamma subunit
D. Delta subunit

B. Alpha subunit

A patient’s ACTH is abnormal; the hormone is derived from a larger precursor. ACTH is:
A. Steroid from cholesterol
B. Dimeric glycoprotein
C. Peptide from POMC
D. Catecholamine derivative

C. Peptide from POMC

Excess POMC processing increases other peptides besides ACTH. Which pair can result?
A. Alpha-MSH and beta-endorphin
B. T3 and thyroxine
C. Estrogen and progesterone
D. GHRH and somatostatin

A. Alpha-MSH and beta-endorphin

An ACTH analog is given; its receptor signals through which class?
A. Nuclear receptor
B. JAK/STAT receptor
C. Ligand-gated channel
D. GPCR

D. GPCR

A patient has ACTH resistance due to receptor defects. The ACTH receptor is also called:
A. Melanocortin 1 receptor
B. Melanocortin 2 receptor
C. Melanocortin 3 receptor
D. Melanocortin 4 receptor

B. Melanocortin 2 receptor

Despite normal ACTH receptor sequence, signaling fails due to defective trafficking. What is required for normal ACTH signaling?
A. MRAP accessory protein
B. Thyroid-binding globulin
C. Albumin carrier protein
D. SHBG cofactor

A. MRAP accessory protein

A patient’s low TSH is traced to impaired hypothalamic stimulation. TSH release is regulated by:
A. GnRH
B. CRH
C. TRH
D. Dopamine

C. TRH

Pulsatile hypothalamic output is needed for normal gonadotropin secretion. Which hormone must be pulsatile?
A. TRH
B. Somatostatin
C. Dopamine
D. GnRH

D. GnRH

A patient with adrenal insufficiency has low ACTH due to low hypothalamic drive. ACTH release is stimulated by:
A. CRH
B. Thyroxine
C. Estrogen
D. IGF-1

A. CRH

A hyperthyroid patient has suppressed TRH and TSH. Which feedback signal inhibits both?
A. Cortisol
B. T3 and T4
C. Testosterone
D. Dopamine

B. T3 and T4

A woman using high-dose hormones has suppressed GnRH and gonadotropins. Which hormones mediate this inhibition?
A. Thyroxine and T3
B. Cortisol and CRH
C. Estrogen and progesterone
D. GH and IGF-1

C. Estrogen and progesterone

A male on anabolic steroids develops low LH/FSH and low GnRH. Which signal best explains this?
A. Estrogen and progesterone
B. Thyroxine and T3
C. Dopamine and TRH
D. Testosterone and androgens

D. Testosterone and androgens

A patient on chronic glucocorticoids has low ACTH and low CRH. Which mediator inhibits both?
A. IGF-1
B. Cortisol
C. Thyroxine
D. Estrogen

B. Cortisol

Which pairing correctly describes GH regulators?
A. GHRH stimulates; somatostatin inhibits
B. TRH stimulates; cortisol inhibits
C. GnRH stimulates; dopamine inhibits
D. CRH stimulates; IGF-1 inhibits

A. GHRH stimulates; somatostatin inhibits

GH release is limited by peripheral feedback from its main mediator. Which mediator provides that feedback?
A. Thyroxine
B. Cortisol
C. Estrogen
D. IGF-1

D. IGF-1

A patient with hyperprolactinemia improves on a D2 agonist. Prolactin production is inhibited by:
A. TRH
B. CRH
C. Dopamine
D. Thyroxine

C. Dopamine

A patient with primary hypothyroidism develops galactorrhea. Which hypothalamic hormone can raise prolactin when levels are high?
A. GnRH
B. CRH
C. TRH
D. Somatostatin

C. TRH

IGF-I is also known as:
A. Somatomedin C
B. Somatomedin A
C. Somatomedin B
D. Somatomedin D

A. Somatomedin C

Growth hormone is best described as:
A. Steroid, cholesterol-derived
B. Dimeric glycoprotein
C. Catecholamine derivative
D. 191-aa peptide hormone

D. 191-aa peptide hormone

A structural feature of GH includes:
A. Three disulfide bridges
B. Two sulfhydryl bridges
C. One transmembrane helix
D. Four alpha subunits

B. Two sulfhydryl bridges

Somatropin is:
A. Recombinant GH, native sequence
B. Pituitary extract GH mix
C. IGF-I analog therapy
D. GHRH antagonist drug

A. Recombinant GH, native sequence

Endogenous GH is predominantly cleared by the:
A. Kidney
B. Liver
C. Lung
D. Spleen

B. Liver

Recombinant human GH is typically administered:
A. Orally daily
B. Intravenous infusion
C. Subcutaneously
D. Intranasally

C. Subcutaneously

A standard rhGH schedule is:
A. Once monthly
B. Twice yearly
C. Weekly injections
D. 6–7 times weekly

D. 6–7 times weekly

After subcutaneous rhGH, peak levels occur:
A. 2–4 hours
B. 10–20 minutes
C. 12–24 hours
D. 36–48 hours

A. 2–4 hours

After rhGH dosing, active blood levels persist about:
A. 4 hours
B. 36 hours
C. 20 minutes
D. 7 days

B. 36 hours

Most circulating IGF-I is produced by the:
A. Bone
B. Kidney
C. Liver
D. Muscle

C. Liver

GH stimulates IGF-I production in tissues mainly for:
A. Autocrine/paracrine actions
B. Portal venous transport
C. Neurosecretory release
D. Renal tubular secretion

A. Autocrine/paracrine actions

In adults, GH shifts body composition by:
A. Catabolic muscle, anabolic fat
B. Anabolic fat, catabolic muscle
C. Anabolic both muscle and fat
D. Anabolic muscle, catabolic fat

D. Anabolic muscle, catabolic fat

GH and IGF-I have opposite effects on:
A. Thyroid hormone synthesis
B. Insulin sensitivity
C. ACTH release
D. Renal blood flow

B. Insulin sensitivity

GH reduces insulin sensitivity, causing mild:
A. Hypoglycemia
B. Ketoacidosis
C. Hyperinsulinemia
D. Insulinopenia

C. Hyperinsulinemia

IGF-I’s insulin-like action most directly:
A. Increases glucose transport
B. Decreases GH secretion
C. Inhibits TRH release
D. Blocks dopamine receptors

A. Increases glucose transport

Neonates with isolated GH deficiency are normal size because:
A. Postnatal growth is GH-free
B. Thyroid hormone replaces GH
C. Lactation supplies GH
D. Prenatal growth is GH-independent

D. Prenatal growth is GH-independent

An early sign of GH deficiency in young children is:
A. Hyperglycemia
B. Hypoglycemia
C. Bradycardia
D. Hyperkalemia

B. Hypoglycemia

A diagnostic criterion for GH deficiency includes reduced:
A. Appetite for age
B. Bone density for age
C. Serum TSH response
D. Height velocity for age

D. Height velocity for age

Which agent increases GHRH levels via dopaminergic action?
A. Somatostatin
B. TRH
C. Levodopa
D. Estrogen

C. Levodopa

Which physiologic factor increases GHRH levels?
A. High-fat meals
B. Sleep deprivation
C. Exercise
D. Hyperkalemia

C. Exercise

Arginine increases GH release primarily by reducing:
A. Somatostatin tone
B. Dopamine tone
C. TRH release
D. CRH release

A. Somatostatin tone

Insulin-induced hypoglycemia increases GH by reducing:
A. GHRH secretion
B. IGF-I secretion
C. Somatostatin tone
D. TRH secretion

C. Somatostatin tone

GH therapy improves final height in girls with:
A. Turner syndrome
B. Klinefelter syndrome
C. Cushing syndrome
D. Addison disease

A. Turner syndrome

In Turner syndrome, GH should be combined with:
A. Thyroid hormones
B. Cortisol analogs
C. Dopamine agonists
D. Gonadal steroids

D. Gonadal steroids

A controversial but approved GH indication is:
A. Congenital adrenal hyperplasia
B. Idiopathic short stature
C. Primary hypothyroidism
D. Central diabetes insipidus

B. Idiopathic short stature

GH therapy can reduce levels of some drugs by:
A. Decreasing renal filtration
B. Inhibiting CYP isoforms
C. Increasing CYP isoforms
D. Blocking gut absorption

C. Increasing CYP isoforms

A child with short stature has a newly diagnosed leukemia. Which statement about GH therapy is correct?
A. Safe if monitored closely
B. Contraindicated with active malignancy
C. Contraindicated only in adults
D. Increases malignancy incidence

B. Contraindicated with active malignancy

A patient has severe IGF-I deficiency unresponsive to GH. Which therapy is FDA-approved for this scenario?
A. Octreotide
B. Pegvisomant
C. Recombinant human IGF-I
D. Dopamine agonist

C. Recombinant human IGF-I

Which pair are FDA-approved forms of rhIGF-I?
A. Pegvisomant, lanreotide
B. Mecasermin, mecasermin rinfabate
C. Somatostatin, octreotide
D. Levodopa, clonidine

B. Mecasermin, mecasermin rinfabate

Mecasermin rinfabate contains rhIGF-I plus:
A. Recombinant IGFBP-3
B. Recombinant GH
C. Dopamine agonist
D. Somatostatin analog

A. Recombinant IGFBP-3

A child starts mecasermin and becomes diaphoretic and confused. Most important adverse effect?
A. Bradycardia
B. Steatorrhea
C. Hypoglycemia
D. Hyperglycemia

C. Hypoglycemia

To reduce mecasermin hypoglycemia risk, the patient should:
A. Fast before injection
B. Avoid carbohydrates that day
C. Take dose at bedtime
D. Eat carbs near dosing

D. Eat carbs near dosing

The meal/snack timing recommended with mecasermin is:
A. 2 hours before dose
B. 20 minutes before or after
C. Only after symptoms occur
D. Exactly 6 hours after

B. 20 minutes before or after

Hormone-secreting pituitary adenomas occur most commonly in:
A. Neonates
B. Children
C. Adults
D. Adolescents

C. Adults

An adult with GH-secreting adenoma develops coarse facial features and organ enlargement. Diagnosis?
A. Gigantism
B. Acromegaly
C. Cushing disease
D. Hypopituitarism

A. Gigantism

Acromegaly reflects abnormal growth of:
A. Cartilage, bone, many organs
B. Only long bones
C. Only skeletal muscle
D. Only adipose tissue

A. Cartilage, bone, many organs

A GH-secreting tumor arises before epiphyseal closure. Most likely outcome?
A. Acromegaly
B. Dwarfism
C. Gigantism
D. Hyperprolactinemia

C. Gigantism

Initial therapy of choice for GH-secreting adenoma is:
A. Endoscopic transsphenoidal surgery
B. High-dose octreotide first
C. Pegvisomant monotherapy first
D. Dopamine agonist monotherapy

A. Endoscopic transsphenoidal surgery

GH hypersecretion persists after surgery. Next step typically adds:
A. Levothyroxine
B. GH antagonist medical therapy
C. Insulin infusion
D. Glucocorticoid taper

B. GH antagonist medical therapy

Which agents reduce GH production post-op?
A. Pegvisomant only
B. Somatostatin analogs, D2 agonists
C. IGF-I analogs only
D. TRH analogs, CRH analogs

B. Somatostatin analogs, D2 agonists

Which drug prevents GH receptor signaling?
A. Octreotide
B. Lanreotide
C. Pegvisomant
D. Mecasermin

C. Pegvisomant

Somatostatin is best described as:
A. 14–amino-acid peptide
B. 191–amino-acid peptide
C. Steroid hormone
D. Dimeric glycoprotein

A. 14–amino-acid peptide

Somatostatin is found in hypothalamus and also:
A. Thyroid follicles
B. Pancreas and GI tract
C. Adrenal cortex
D. Gonadal stroma

B. Pancreas and GI tract

Somatostatin functions primarily as:
A. Excitatory neurotransmitter
B. Stimulatory endocrine hormone
C. Inhibitory paracrine factor
D. Growth factor mediator

C. Inhibitory paracrine factor

Somatostatin inhibits release of which set?
A. GH, TSH, insulin, gastrin
B. GH, ACTH, estrogen, cortisol
C. FSH, LH, prolactin, ADH
D. T3, T4, cortisol, aldosterone

A. GH, TSH, insulin, gastrin

Key organ for somatostatin metabolism/excretion:
A. Liver
B. Lung
C. Kidney
D. Skin

C. Kidney

Native somatostatin has limited usefulness because:
A. Slow onset, narrow window
B. Short action, multiple effects
C. Poor oral absorption only
D. High malignancy risk

B. Short action, multiple effects

Octreotide potency compared with somatostatin for GH inhibition:
A. 2 times more potent
B. 10 times more potent
C. 45 times more potent
D. 100 times more potent

C. 45 times more potent

Octreotide potency for insulin suppression is about:
A. Same as somatostatin
B. Twice as potent
C. 45 times as potent
D. Not clinically relevant

B. Twice as potent

Typical octreotide regimen for tumors is:
A. Oral daily tablets
B. SC every 8 hours
C. IM monthly injections
D. IV continuous infusion

B. SC every 8 hours

Octreotide reduces symptoms from many tumors, including:
A. Insulinoma, VIPoma, carcinoid
B. AML, ALL, CLL
C. Medullary thyroid carcinoma
D. Renal cell carcinoma

A. Insulinoma, VIPoma, carcinoid

Octreotide is also useful for acute control of:
A. GI reflux
B. Variceal bleeding
C. Asthma exacerbation
D. Migraine aura

B. Variceal bleeding

A patient on octreotide reports bulky oily stools. This adverse effect is:
A. Constipation
B. Diarrhea from lactose
C. Steatorrhea
D. GI bleeding

C. Steatorrhea

A patient on octreotide develops HR 48. This cardiac adverse effect is:
A. Atrial flutter
B. Sinus bradycardia
C. Ventricular tachycardia
D. Complete AV block

B. Sinus bradycardia

Long-term octreotide therapy may cause deficiency of:
A. Folate
B. Vitamin B6
C. Vitamin A
D. Vitamin B12

D. Vitamin B12

Another approved somatostatin analog for acromegaly is:
A. Lanreotide
B. Mecasermin
C. Pegvisomant
D. Clonidine

A. Lanreotide

Pegvisomant is used to treat:
A. Primary hypothyroidism
B. Gigantism only
C. Acromegaly
D. Prolactinoma

C. Acromegaly

A patient with hypothalamic infertility needs GnRH to stimulate pituitary gonadotrophs. What pattern is required?
A. Continuous GnRH infusion
B. Pulsatile GnRH secretion
C. Single monthly GnRH bolus
D. Rectal GnRH delivery

B. Pulsatile GnRH secretion

A man receives sustained leuprolide (nonpulsatile). What pituitary outcome results in both sexes?
A. Hypergonadotropic hypogonadism
B. Hyperthyroid flare
C. Hypogonadotropic hypogonadism
D. Acromegaly

C. Hypogonadotropic hypogonadism

Gonadorelin is best described as:
A. Recombinant LH preparation
B. Pituitary extract hMG
C. Somatostatin analog peptide
D. Synthetic GnRH acetate salt

D. Synthetic GnRH acetate salt

Compared with native GnRH, GnRH agonist analogs are generally:
A. Shorter-acting, less potent
B. Same potency, same duration
C. Less potent, longer-acting
D. More potent, longer-lasting

D. More potent, longer-lasting

Gonadorelin can be administered by:
A. Oral tablet
B. Intranasal spray
C. IV or subcutaneous
D. Transdermal patch

C. IV or subcutaneous

A patient is prescribed nafarelin (GnRH agonist). Which route matches this agonist?
A. Intravenous infusion
B. Intramuscular depot
C. Nasal spray
D. Oral capsule

C. Nasal spray

Histrelin (a GnRH agonist) may be delivered as a:
A. Rectal suppository
B. Subcutaneous implant
C. Sublingual tablet
D. Inhaled aerosol

B. Subcutaneous implant

Between which ages does GnRH secretion fall off with very low pituitary sensitivity?
A. Birth until age two
B. Puberty through adulthood
C. Late follicular phase
D. Age two until puberty

D. Age two until puberty

Just before puberty, GnRH release typically shows:
A. Lower frequency, lower amplitude
B. Higher frequency and amplitude
C. Higher amplitude only
D. Higher frequency only

B. Higher frequency and amplitude

In early puberty, pituitary sensitivity rises partly due to increasing:
A. Thyroid hormones
B. Cortisol levels
C. Gonadal steroids
D. IGF-1 levels

C. Gonadal steroids

Highest GnRH pulse amplitudes occur during the:
A. Early follicular phase
B. Late follicular phase
C. Luteal phase
D. Ovulatory phase

C. Luteal phase

Highest GnRH pulse frequency occurs late in the:
A. Early follicular phase
B. Late follicular phase
C. Luteal phase
D. Early pregnancy

B. Late follicular phase

Lower GnRH pulse frequencies preferentially favor secretion of:
A. FSH
B. LH
C. ACTH
D. Prolactin

A. FSH

Higher GnRH pulse frequencies preferentially favor secretion of:
A. FSH
B. TSH
C. LH
D. ACTH

C. LH

Continuous gonadorelin (or analog) produces a:
A. Monophasic stimulatory response
B. Triphasic stimulatory response
C. Nonresponsive state
D. Biphasic response

D. Biphasic response

The first 7–10 days of continuous GnRH agonist therapy is the:
A. Flare phase
B. Downregulation phase
C. Withdrawal phase
D. Escape phase

A. Flare phase

During the flare phase, gonadal hormone concentrations:
A. Fall immediately
B. Increase transiently
C. Remain unchanged
D. Oscillate randomly

B. Increase transiently

After the flare, continued agonist presence causes:
A. Increased gonadotropins persist
B. Decreased gonadotropins and steroids
C. Increased progesterone surge
D. Increased GnRH secretion

B. Decreased gonadotropins and steroids

A major barrier to pulsatile GnRH therapy is:
A. IV pump use, cost, access
B. Requires daily oral tablets
C. Always causes OHSS
D. Only works after menopause

A. IV pump use, cost, access

In women undergoing gonadotropin ovulation induction, gonadorelin (or an agonist analog) can be used to:
A. Suppress estradiol production
B. Treat endometriosis pain
C. Induce androgen deprivation
D. Trigger LH surge, ovulation

D. Trigger LH surge, ovulation

GnRH testing can help evaluate delayed puberty by assessing:
A. Thyroid hormone reserve
B. Adrenal cortisol reserve
C. Pituitary LH response
D. Placental hCG response

C. Pituitary LH response

An impaired LH response to GnRH most strongly suggests:
A. Rules out constitutional delay
B. Confirms constitutional delay
C. Proves pituitary tumor
D. Hypogonadotropic hypogonadism likely

D. Hypogonadotropic hypogonadism likely

In controlled ovarian stimulation for IVF, a critical goal is to:
A. Trigger early ovulation
B. Raise endogenous LH surge
C. Increase prolactin secretion
D. Suppress endogenous LH surge

D. Suppress endogenous LH surge

The most common LH suppression approach uses:
A. Daily oral clomiphene
B. IM hCG weekly
C. SC leuprolide or nasal nafarelin
D. IV gonadorelin bolus

C. SC leuprolide or nasal nafarelin

Continuous GnRH agonist therapy reduces endometriosis pain primarily because it:
A. Increases ovarian estrogen cycling
B. Suppresses estrogen and progesterone
C. Stimulates LH surge daily
D. Blocks androgen receptors

B. Suppresses estrogen and progesterone

Preferred GnRH agonist treatment duration for endometriosis is limited to ~6 months because of:
A. Bone mineral density loss
B. Severe hypoglycemia risk
C. Acute renal failure
D. Higher malignancy incidence

A. Bone mineral density loss

Uterine leiomyomata are:
A. Malignant smooth muscle tumors
B. Benign uterine smooth muscle tumors
C. Pituitary lactotroph tumors
D. Estrogen-resistant endometrial cysts

B. Benign uterine smooth muscle tumors

A patient with leiomyomata most classically presents with:
A. Menorrhagia anemia pelvic pain
B. Amenorrhea galactorrhea headache
C. Hirsutism acne virilization
D. Hot flashes sleep disturbance

A. Menorrhagia anemia pelvic pain

Treating leiomyomata for 3–6 months with a GnRH agonist plus iron most directly:
A. Shrinks fibroids, improves anemia
B. Raises fibroid size rapidly
C. Worsens anemia without iron
D. Has no effect on size

A. Shrinks fibroids, improves anemia

Primary medical therapy for prostate cancer is:
A. Surgery is primary therapy
B. Chemotherapy is primary therapy
C. Androgen deprivation therapy
D. Radiation is primary therapy

C. Androgen deprivation therapy

Negative feedback inhibition of GH is mediated by which pair?
A. GH and IGF-1
B. TRH and TSH
C. LH and hCG
D. Dopamine and prolactin

A. GH and IGF-1

Prolactin release is primarily inhibited by:
A. Dopamine via D2
B. TRH via TRH-R
C. Somatostatin via SSTR
D. GnRH via GnRH-R

A. Dopamine via D2

TRH stimulates release of which set?
A. ACTH and cortisol
B. FSH and LH
C. TSH and prolactin
D. GH and IGF-1

C. TSH and prolactin

Growth-promoting effects of GH are mediated mainly through:
A. Cortisol
B. Somatomedin C
C. Dopamine
D. Progesterone

B. Somatomedin C

Most circulating IGF-1 is synthesized in the:
A. Kidney
B. Liver
C. Bone
D. Pancreas

B. Liver

Reduced GH levels would most likely lead to:
A. Hyperglycemia
B. Hypoglycemia
C. Ketoacidosis
D. No glucose change

B. Hypoglycemia

Clonidine, levodopa, and exercise have what effect on GHRH?
A. Decrease GHRH levels
B. No effect on GHRH
C. Increase GHRH levels
D. Block GHRH receptors

C. Increase GHRH levels

In provocative testing, clonidine acts primarily as:
A. Alpha2-adrenergic agonist
B. Beta1-adrenergic agonist
C. Dopaminergic antagonist
D. Muscarinic agonist

A. Alpha2-adrenergic agonist

In provocative testing, levodopa acts primarily as:
A. D2 antagonist
B. Dopaminergic agonist
C. Alpha2 antagonist
D. Serotonin agonist

B. Dopaminergic agonist

Arginine and insulin-induced hypoglycemia increase GH mainly by:
A. Increasing TRH tone
B. Increasing cortisol feedback
C. Increasing IGF-1 production
D. Reducing somatostatin tone

D. Reducing somatostatin tone

A patient on GH develops swelling and muscle pains. Which adverse effect fits GH therapy?
A. Peripheral edema
B. Steatorrhea
C. Bradycardia
D. Hypoglycemia

A. Peripheral edema

Another adverse effect of GH therapy is:
A. Carpal tunnel syndrome
B. Nephrolithiasis
C. Variceal bleeding
D. Retinal detachment

A. Carpal tunnel syndrome

Mecasermin is:
A. Recombinant human IGF-1
B. Recombinant human GH
C. GH receptor antagonist
D. Somatostatin analog

A. Recombinant human IGF-1

Mecasermin rinfabate is best described as:
A. IGF-1 plus IGFBP-3
B. GH plus IGF-1 complex
C. IGF-1 plus albumin complex
D. IGF-1 plus insulin complex

A. IGF-1 plus IGFBP-3

Most important adverse effect of mecasermin is:
A. Bradycardia
B. Hyperglycemia
C. Hypoglycemia
D. Steatorrhea

C. Hypoglycemia

Somatostatin inhibits release of which set?
A. GH TSH glucagon insulin gastrin
B. GH LH estrogen progesterone
C. TSH ACTH cortisol aldosterone
D. Prolactin dopamine GH GHRH

A. GH TSH glucagon insulin gastrin

Somatostatin half-life is closest to:
A. 36 hours
B. 20 minutes
C. 80 minutes
D. 1–3 minutes

D. 1–3 minutes

Octreotide is best described as:
A. GH receptor antagonist
B. Widely used SST analog
C. Recombinant IGF-1 agent
D. GnRH agonist analog

B. Widely used SST analog

Octreotide half-life is closest to:
A. 1–3 minutes
B. 20 minutes
C. 80 minutes
D. 36 hours

C. 80 minutes

Lanreotide is:
A. Long-acting SST analog
B. Recombinant LH analog
C. Recombinant IGF-1 analog
D. TRH antagonist

A. Long-acting SST analog

Pegvisomant is:
A. Dopamine receptor agonist
B. Somatostatin analog
C. GH receptor antagonist
D. GnRH receptor antagonist

C. GH receptor antagonist

Pegvisomant can lead to increased GH levels because it:
A. Inhibits GH secretion
B. Blocks GH clearance
C. Does not inhibit secretion
D. Stimulates GHRH release

C. Does not inhibit secretion

In the ovary, LH stimulates androgen production by:
A. Granulosa cells
B. Theca cells
C. Leydig cells
D. Sertoli cells

B. Theca cells

In the ovary, FSH stimulates androgen→estrogen conversion in:
A. Theca cells
B. Granulosa cells
C. Leydig cells
D. Corpus luteum

B. Granulosa cells

In the luteal phase, estrogen/progesterone are controlled first by LH and then by:
A. FSH
B. IGF-1
C. hCG
D. TRH

C. hCG

FSH maintains local androgen by stimulating Sertoli production of:
A. Thyroxine-binding globulin
B. Androgen-binding protein
C. Sex hormone-binding globulin
D. Cortisol-binding globulin

B. Androgen-binding protein

FSH also stimulates Sertoli conversion of testosterone to:
A. DHT
B. Estradiol
C. Progesterone
D. Cortisol

B. Estradiol

LH and hCG are used interchangeably because their:
A. Alpha subunits differ
B. Clearance rates identical
C. Receptors are unrelated
D. Beta subunits nearly identical

D. Beta subunits nearly identical

In the first 8 weeks of pregnancy, the progesterone/estrogen that maintain pregnancy are produced primarily by the:
A. Placenta
B. Corpus luteum
C. Maternal adrenal cortex
D. Fetal liver

B. Corpus luteum

For the corpus luteum to persist beyond early luteal support, maternal LH must be taken over by:
A. FSH
B. Progesterone
C. Prolactin
D. hCG

D. hCG

Human chorionic gonadotropin (hCG) is produced by:
A. Placental syncytiotrophoblasts
B. Placental cytotrophoblasts
C. Ovarian granulosa cells
D. Testicular Leydig cells

A. Placental syncytiotrophoblasts

A patient undergoing ovulation induction asks about the two most common serious complications. Best answer:
A. Ectopic pregnancy and torsion
B. Infection and hemorrhage
C. Multiple pregnancies and OHSS
D. Prematurity and gestational diabetes

C. Multiple pregnancies and OHSS

A patient with hypothalamic infertility is placed on a GnRH pump. Which pattern is required to stimulate LH/FSH release?
A. Pulsatile GnRH secretion
B. Continuous GnRH infusion
C. Monthly depot GnRH
D. Single high-dose bolus

A. Pulsatile GnRH secretion

A man receives sustained nonpulsatile GnRH agonist therapy. What pituitary-gonadal outcome occurs in both sexes?
A. Hypergonadotropic hypogonadism
B. Hypogonadotropic hypogonadism
C. Primary gonadal failure
D. Premature ovarian insufficiency

B. Hypogonadotropic hypogonadism

Which drug is a GnRH agonist analog?
A. Ganirelix
B. Octreotide
C. Leuprolide
D. Pegvisomant

C. Leuprolide

In this framework, lower GnRH pulse frequency favors which menstrual-cycle phase?
A. Follicular phase
B. Luteal phase
C. Ovulatory phase
D. Menstrual phase

A. Follicular phase

A patient starts continuous leuprolide. What is expected during the first 7–10 days?
A. Immediate LH/FSH suppression
B. Immediate ovarian shutdown
C. No gonadal hormone change
D. Increased gonadal hormone levels

D. Increased gonadal hormone levels

After the initial 7–10 day flare, continued GnRH agonist exposure causes:
A. Persistent estrogen elevation
B. Increased LH pulse frequency
C. Decreased LH and FSH
D. Increased ovarian androgen output

C. Decreased LH and FSH

A hypogonadotropic adolescent is given GnRH to assess LH responsiveness. A robust LH rise most suggests:
A. Primary gonadal failure
B. Early pubertal status
C. Pituitary apoplexy
D. Permanent infertility

B. Early pubertal status

A hypogonadotropic adolescent is given GnRH to assess LH responsiveness. The test shows a low/impaired LH response. This most strongly suggests:
A. Isolated ovarian failure
B. Androgen insensitivity syndrome
C. Thyroid hormone deficiency
D. Hypogonadotropic hypogonadism

D. Hypogonadotropic hypogonadism

A patient with fibroids has menorrhagia and anemia. A 3–6 month regimen most consistent with your notes is:
A. GnRH antagonist plus progesterone
B. GnRH agonist plus iron
C. Dopamine agonist plus iron
D. hCG injections plus iron

B. GnRH agonist plus iron

For advanced prostate cancer, the primary medical strategy in your notes is:
A. Aromatase inhibitor monotherapy
B. Estrogen receptor antagonist only
C. GnRH agonist plus antiandrogen
D. Continuous pulsatile GnRH pump

C. GnRH agonist plus antiandrogen

A 7-year-old girl develops breast development and pubic hair. Best treatment approach:
A. Continuous GnRH agonist
B. Pulsatile GnRH infusion
C. GnRH antagonist “flare” dosing
D. Recombinant FSH injections

A. Continuous GnRH agonist

A patient is prescribed a GnRH agonist for endometriosis. Which is a contraindication?
A. Past anemia from menorrhagia
B. Prior ovarian cyst history
C. Pregnant or breastfeeding
D. History of acne vulgaris

C. Pregnant or breastfeeding

One month after starting a GnRH agonist, a patient develops pelvic pain and an ovarian cyst. This is most associated with:
A. Immediate receptor blockade
B. Flare-related cyst formation
C. Placental hCG stimulation
D. Dopamine withdrawal effect

B. Flare-related cyst formation

GnRH receptor antagonists in this set are best described as:
A. Partial agonist heptapeptides
B. Competitive steroid receptor blockers
C. Noncompetitive ion-channel inhibitors
D. Competitive decapeptide antagonists

D. Competitive decapeptide antagonists

Which drug is a GnRH receptor antagonist?
A. Cetrorelix
B. Nafarelin
C. Triptorelin
D. Histrelin

A. Cetrorelix

During ovarian stimulation procedures, which GnRH antagonists are used (per your list)?
A. Degarelix and abarelix
B. Leuprolide and nafarelin
C. Goserelin and triptorelin
D. Ganirelix and cetrorelix

D. Ganirelix and cetrorelix

For advanced prostate cancer, which GnRH receptor antagonists are used (per your list)?
A. Ganirelix and cetrorelix
B. Nafarelin and leuprolide
C. Degarelix and abarelix
D. Triptorelin and goserelin

C. Degarelix and abarelix

Two advantages of GnRH antagonists over continuous GnRH agonist therapy are:
A. Immediate inhibition; less ovarian suppression
B. Stronger flare; longer depot duration
C. Higher multiple-gestation risk
D. Greater ovarian receptor downregulation

A. Immediate inhibition; less ovarian suppression

Which GnRH antagonist is associated with elevated liver enzymes (per your notes)?
A. Ganirelix
B. Cetrorelix
C. Degarelix
D. Abarelix

C. Degarelix

Which description best matches prolactin?
A. Placental glycoprotein heterodimer
B. 198-aa anterior pituitary peptide
C. Steroid from adrenal cortex
D. Hypothalamic catecholamine hormone

B. 198-aa anterior pituitary peptide

A nonfunctioning pituitary mass compresses the pituitary stalk. What happens to prolactin levels?
A. Increased prolactin levels
B. Decreased prolactin levels
C. No prolactin change
D. Biphasic prolactin change

A. Increased prolactin levels

A patient has hyperprolactinemia with low libido and infertility. Which mechanism-and-treatment pairing best fits?
A. Blocks LH; estrogen therapy
B. Low FSH; pulsatile GnRH
C. High GnRH; GnRH antagonist
D. Inhibits GnRH; dopamine agonist

D. Inhibits GnRH; dopamine agonist

Bromocriptine and cabergoline are best classified as:
A. GnRH receptor antagonists
B. Oxytocin receptor antagonists
C. D2 dopamine receptor agonists
D. Somatostatin analog peptides

C. D2 dopamine receptor agonists

First-line pharmacotherapy for hyperprolactinemia is:
A. GnRH agonist therapy
B. Dopamine agonist therapy
C. Vasopressin antagonist therapy
D. Oxytocin infusion therapy

B. Dopamine agonist therapy

Dopamine agonists inhibit prolactin by activating:
A. D2 receptors
B. V2 receptors
C. GnRH receptors
D. Oxytocin receptors

A. D2 receptors

A patient with acromegaly needs an adjunct that partially inhibits GH. Which drug fits?
A. Nafarelin
B. Tolvaptan
C. Atosiban
D. Cabergoline

D. Cabergoline

Oxytocin is a peptide composed of:
A. 14 amino acids
B. 9 amino acids
C. 191 amino acids
D. 198 amino acids

B. 9 amino acids

Oxytocin contracts smooth muscle via:
A. Gi cAMP inhibition
B. Gs cAMP activation
C. Gq PLC Ca2 signaling
D. JAK STAT signaling

C. Gq PLC Ca2 signaling

For augmentation of labor, oxytocin is typically given by:
A. Intravenous infusion
B. Oral tablet
C. Nasal spray
D. Transdermal patch

A. Intravenous infusion

Milk letdown occurs when oxytocin contracts:
A. Leydig cells
B. Myoepithelial cells
C. Theca cells
D. Sertoli cells

B. Myoepithelial cells

An oxytocin antagonist for preterm labor outside the US is:
A. Leuprolide
B. Conivaptan
C. Atosiban
D. Bromocriptine

C. Atosiban

High-dose oxytocin can cause fluid retention by activating:
A. Vasopressin receptors
B. Dopamine receptors
C. Androgen receptors
D. Estrogen receptors

A. Vasopressin receptors

Which is a contraindication to oxytocin?
A. Postterm pregnancy
B. Premature rupture membranes
C. Postpartum hemorrhage
D. Placental abruption

D. Placental abruption

Another oxytocin contraindication is:
A. Postdates pregnancy
B. Fetal malpresentation
C. Prior cesarean history
D. Maternal hypothyroidism

B. Fetal malpresentation

Oxytocin should be avoided with:
A. Fetal distress
B. Mild edema only
C. Prior acne history
D. Low hemoglobin only

A. Fetal distress

Vasopressin release increases most with:
A. Decreased plasma tonicity
B. Increased blood pressure
C. Increased plasma tonicity
D. Decreased plasma glucose

C. Increased plasma tonicity

ADH V2 receptors are primarily located on:
A. Renal tubule cells
B. Vascular smooth muscle
C. Mammary alveolar ducts
D. Gonadotroph pituitary cells

A. Renal tubule cells

V2 receptor signaling decreases diuresis via:
A. Gi inhibition of cyclase
B. Gs adenylyl cyclase
C. Gq PLC activation
D. Nuclear receptor binding

B. Gs adenylyl cyclase

V1 receptors mediate vasoconstriction through:
A. Gs adenylyl cyclase
B. Gi cAMP inhibition
C. Gq PLC signaling
D. JAK STAT signaling

C. Gq PLC signaling

ADH-mediated release of factor VIII and vWF occurs via:
A. V1 receptors
B. Oxytocin receptors
C. V2 receptors
D. D2 receptors

C. V2 receptors

Per these notes, diabetes insipidus is treated with:
A. Vasopressin at bedtime
B. Tolvaptan at bedtime
C. Oxytocin at bedtime
D. Cabergoline at bedtime

A. Vasopressin at bedtime

Which agent does NOT cause vasoconstriction?
A. Vasopressin
B. Desmopressin
C. Oxytocin
D. Leuprolide

B. Desmopressin

Conivaptan and tolvaptan are:
A. Dopamine agonists
B. GnRH agonists
C. Vasopressin antagonists
D. Somatostatin analogs

C. Vasopressin antagonists

Conivaptan has high affinity for:
A. V2 receptors only
B. V1 receptors only
C. D2 receptors only
D. V1a and V2 receptors

D. V1a and V2 receptors

Tolvaptan’s receptor affinity is best described as:
A. V1a and V2 equal
B. V2 thirtyfold over V1
C. D2 over V2
D. Oxytocin over V1

B. V2 thirtyfold over V1

Tolvaptan duration is limited due to:
A. Risk of hepatotoxic liver failure
B. Risk of renal stone disease
C. Risk of severe neutropenia
D. Risk of adrenal suppression

A. Risk of hepatotoxic liver failure

A hyponatremic heart-failure patient receives a V1a/V2 blocker. Which drug is used?
A. Tolvaptan
B. Conivaptan
C. Cabergoline
D. Bromocriptine

B. Conivaptan