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Pharm 37

front 1

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

back 1

B. Hypothalamus and pituitary gland

front 2

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

back 2

D. Portal venous system

front 3

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

back 3

A. Hypothalamus

front 4

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

back 4

C. Neurosecretory fibers

front 5

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

back 5

A. Replacement therapy

front 6

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

back 6

B. Antagonism of hormone excess

front 7

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

back 7

D. Diagnostic tool

front 8

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

back 8

C. GH and prolactin

front 9

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

back 9

B. JAK/STAT signaling

front 10

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

back 10

A. TSH FSH LH

front 11

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

back 11

D. GPCR

front 12

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

back 12

B. Alpha subunit

front 13

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

back 13

C. Peptide from POMC

front 14

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

back 14

A. Alpha-MSH and beta-endorphin

front 15

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

back 15

D. GPCR

front 16

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

back 16

B. Melanocortin 2 receptor

front 17

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

back 17

A. MRAP accessory protein

front 18

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

back 18

C. TRH

front 19

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

back 19

D. GnRH

front 20

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

back 20

A. CRH

front 21

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

back 21

B. T3 and T4

front 22

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

back 22

C. Estrogen and progesterone

front 23

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

back 23

D. Testosterone and androgens

front 24

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

back 24

B. Cortisol

front 25

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

back 25

A. GHRH stimulates; somatostatin inhibits

front 26

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

back 26

D. IGF-1

front 27

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

back 27

C. Dopamine

front 28

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

back 28

C. TRH

front 29

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

back 29

A. Somatomedin C

front 30

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

back 30

D. 191-aa peptide hormone

front 31

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

back 31

B. Two sulfhydryl bridges

front 32

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

back 32

A. Recombinant GH, native sequence

front 33

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

back 33

B. Liver

front 34

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

back 34

C. Subcutaneously

front 35

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

back 35

D. 6–7 times weekly

front 36

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

back 36

A. 2–4 hours

front 37

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

back 37

B. 36 hours

front 38

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

back 38

C. Liver

front 39

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

back 39

A. Autocrine/paracrine actions

front 40

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

back 40

D. Anabolic muscle, catabolic fat

front 41

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

back 41

B. Insulin sensitivity

front 42

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

back 42

C. Hyperinsulinemia

front 43

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

back 43

A. Increases glucose transport

front 44

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

back 44

D. Prenatal growth is GH-independent

front 45

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

back 45

B. Hypoglycemia

front 46

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

back 46

D. Height velocity for age

front 47

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

back 47

C. Levodopa

front 48

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

back 48

C. Exercise

front 49

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

back 49

A. Somatostatin tone

front 50

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

back 50

C. Somatostatin tone

front 51

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

back 51

A. Turner syndrome

front 52

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

back 52

D. Gonadal steroids

front 53

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

back 53

B. Idiopathic short stature

front 54

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

back 54

C. Increasing CYP isoforms

front 55

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

back 55

B. Contraindicated with active malignancy

front 56

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

back 56

C. Recombinant human IGF-I

front 57

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

back 57

B. Mecasermin, mecasermin rinfabate

front 58

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

back 58

A. Recombinant IGFBP-3

front 59

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

back 59

C. Hypoglycemia

front 60

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

back 60

D. Eat carbs near dosing

front 61

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

back 61

B. 20 minutes before or after

front 62

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

back 62

C. Adults

front 63

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

back 63

A. Gigantism

front 64

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

back 64

A. Cartilage, bone, many organs

front 65

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

back 65

C. Gigantism

front 66

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

back 66

A. Endoscopic transsphenoidal surgery

front 67

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

back 67

B. GH antagonist medical therapy

front 68

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

back 68

B. Somatostatin analogs, D2 agonists

front 69

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

back 69

C. Pegvisomant

front 70

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

back 70

A. 14–amino-acid peptide

front 71

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

back 71

B. Pancreas and GI tract

front 72

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

back 72

C. Inhibitory paracrine factor

front 73

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

back 73

A. GH, TSH, insulin, gastrin

front 74

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

back 74

C. Kidney

front 75

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

back 75

B. Short action, multiple effects

front 76

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

back 76

C. 45 times more potent

front 77

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

back 77

B. Twice as potent

front 78

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

back 78

B. SC every 8 hours

front 79

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

back 79

A. Insulinoma, VIPoma, carcinoid

front 80

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

back 80

B. Variceal bleeding

front 81

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

back 81

C. Steatorrhea

front 82

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

back 82

B. Sinus bradycardia

front 83

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

back 83

D. Vitamin B12

front 84

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

back 84

A. Lanreotide

front 85

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

back 85

C. Acromegaly

front 86

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

back 86

B. Pulsatile GnRH secretion

front 87

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

back 87

C. Hypogonadotropic hypogonadism

front 88

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

back 88

D. Synthetic GnRH acetate salt

front 89

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

back 89

D. More potent, longer-lasting

front 90

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

back 90

C. IV or subcutaneous

front 91

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

back 91

C. Nasal spray

front 92

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

back 92

B. Subcutaneous implant

front 93

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

back 93

D. Age two until puberty

front 94

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

back 94

B. Higher frequency and amplitude

front 95

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

back 95

C. Gonadal steroids

front 96

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

back 96

C. Luteal phase

front 97

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

back 97

B. Late follicular phase

front 98

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

back 98

A. FSH

front 99

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

back 99

C. LH

front 100

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

back 100

D. Biphasic response

front 101

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

back 101

A. Flare phase

front 102

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

back 102

B. Increase transiently

front 103

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

back 103

B. Decreased gonadotropins and steroids

front 104

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

back 104

A. IV pump use, cost, access

front 105

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

back 105

D. Trigger LH surge, ovulation

front 106

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

back 106

C. Pituitary LH response

front 107

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

back 107

D. Hypogonadotropic hypogonadism likely

front 108

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

back 108

D. Suppress endogenous LH surge

front 109

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

back 109

C. SC leuprolide or nasal nafarelin

front 110

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

back 110

B. Suppresses estrogen and progesterone

front 111

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

back 111

A. Bone mineral density loss

front 112

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

back 112

B. Benign uterine smooth muscle tumors

front 113

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

back 113

A. Menorrhagia anemia pelvic pain

front 114

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

back 114

A. Shrinks fibroids, improves anemia

front 115

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

back 115

C. Androgen deprivation therapy

front 116

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

back 116

A. GH and IGF-1

front 117

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

back 117

A. Dopamine via D2

front 118

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

back 118

C. TSH and prolactin

front 119

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

back 119

B. Somatomedin C

front 120

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

back 120

B. Liver

front 121

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

back 121

B. Hypoglycemia

front 122

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

back 122

C. Increase GHRH levels

front 123

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

back 123

A. Alpha2-adrenergic agonist

front 124

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

back 124

B. Dopaminergic agonist

front 125

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

back 125

D. Reducing somatostatin tone

front 126

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

back 126

A. Peripheral edema

front 127

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

back 127

A. Carpal tunnel syndrome

front 128

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

back 128

A. Recombinant human IGF-1

front 129

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

back 129

A. IGF-1 plus IGFBP-3

front 130

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

back 130

C. Hypoglycemia

front 131

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

back 131

A. GH TSH glucagon insulin gastrin

front 132

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

back 132

D. 1–3 minutes

front 133

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

back 133

B. Widely used SST analog

front 134

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

back 134

C. 80 minutes

front 135

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

back 135

A. Long-acting SST analog

front 136

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

back 136

C. GH receptor antagonist

front 137

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

back 137

C. Does not inhibit secretion

front 138

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

back 138

B. Theca cells

front 139

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

back 139

B. Granulosa cells

front 140

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

back 140

C. hCG

front 141

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

back 141

B. Androgen-binding protein

front 142

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

back 142

B. Estradiol

front 143

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

back 143

D. Beta subunits nearly identical

front 144

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

back 144

B. Corpus luteum

front 145

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

back 145

D. hCG

front 146

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

back 146

A. Placental syncytiotrophoblasts

front 147

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

back 147

C. Multiple pregnancies and OHSS

front 148

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

back 148

A. Pulsatile GnRH secretion

front 149

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

back 149

B. Hypogonadotropic hypogonadism

front 150

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

back 150

C. Leuprolide

front 151

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

back 151

A. Follicular phase

front 152

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

back 152

D. Increased gonadal hormone levels

front 153

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

back 153

C. Decreased LH and FSH

front 154

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

back 154

B. Early pubertal status

front 155

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

back 155

D. Hypogonadotropic hypogonadism

front 156

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

back 156

B. GnRH agonist plus iron

front 157

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

back 157

C. GnRH agonist plus antiandrogen

front 158

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

back 158

A. Continuous GnRH agonist

front 159

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

back 159

C. Pregnant or breastfeeding

front 160

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

back 160

B. Flare-related cyst formation

front 161

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

back 161

D. Competitive decapeptide antagonists

front 162

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

back 162

A. Cetrorelix

front 163

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

back 163

D. Ganirelix and cetrorelix

front 164

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

back 164

C. Degarelix and abarelix

front 165

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

back 165

A. Immediate inhibition; less ovarian suppression

front 166

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

back 166

C. Degarelix

front 167

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

back 167

B. 198-aa anterior pituitary peptide

front 168

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

back 168

A. Increased prolactin levels

front 169

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

back 169

D. Inhibits GnRH; dopamine agonist

front 170

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

back 170

C. D2 dopamine receptor agonists

front 171

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

back 171

B. Dopamine agonist therapy

front 172

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

back 172

A. D2 receptors

front 173

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

back 173

D. Cabergoline

front 174

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

back 174

B. 9 amino acids

front 175

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

back 175

C. Gq PLC Ca2 signaling

front 176

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

back 176

A. Intravenous infusion

front 177

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

back 177

B. Myoepithelial cells

front 178

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

back 178

C. Atosiban

front 179

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

back 179

A. Vasopressin receptors

front 180

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

back 180

D. Placental abruption

front 181

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

back 181

B. Fetal malpresentation

front 182

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

back 182

A. Fetal distress

front 183

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

back 183

C. Increased plasma tonicity

front 184

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

back 184

A. Renal tubule cells

front 185

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

back 185

B. Gs adenylyl cyclase

front 186

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

back 186

C. Gq PLC signaling

front 187

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

back 187

C. V2 receptors

front 188

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

back 188

A. Vasopressin at bedtime

front 189

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

back 189

B. Desmopressin

front 190

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

back 190

C. Vasopressin antagonists

front 191

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

back 191

D. V1a and V2 receptors

front 192

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

back 192

B. V2 thirtyfold over V1

front 193

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

back 193

A. Risk of hepatotoxic liver failure

front 194

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

back 194

B. Conivaptan