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Phys 76

front 1

The pituitary gland is also called the:
A. Thalamus
B. Hypophysis
C. Pineal body
D. Hypothalamus

back 1

Hypophysis

front 2

The pituitary gland lies in the:
A. Foramen magnum
B. Sella turcica
C. Cribriform plate
D. Jugular foramen

back 2

B. Sella turcica

front 3

The structure connecting pituitary to hypothalamus is the:
A. Infundibulum stalk
B. Corpus callosum
C. Pineal stalk
D. Optic chiasm

back 3

A. Infundibulum stalk

front 4

The avascular zone between anterior and posterior pituitary is the:
A. Pars distalis
B. Median eminence
C. Pars intermedia
D. Zona reticularis

back 4

C. Pars intermedia

front 5

The embryologic origin of the anterior pituitary is:
A. Neural tube floor
B. Rathke’s pouch
C. Neural crest
D. Foregut endoderm

back 5

B. Rathke’s pouch

front 6

The embryologic origin of the posterior pituitary is:
A. Rathke’s pouch
B. Surface ectoderm
C. Neural tissue outgrowth
D. Foregut endoderm

back 6

C. Neural tissue outgrowth

front 7

Which hormone promotes whole-body growth via protein formation, cell multiplication, differentiation?
A. Thyroxine
B. Growth hormone
C. Prolactin
D. ACTH

back 7

B. Growth hormone

front 8

A patient has low cortisol output from adrenal cortex with impaired macronutrient metabolism control. Which pituitary hormone is deficient?
A. ACTH
B. TSH
C. Prolactin
D. Oxytocin

back 8

A. ACTH

front 9

A patient has low T3/T4 and slowed intracellular reactions due to lack of pituitary stimulation. Which hormone is deficient?
A. LH
B. FSH
C. TSH
D. ADH

back 9

C. TSH

front 10

A postpartum patient has poor mammary development and low milk production. Which hormone is deficient?
A. Oxytocin
B. Prolactin
C. ADH
D. Growth hormone

back 10

B. Prolactin

front 11

A patient has infertility with impaired ovarian/testicular growth and reproductive activity. Which hormones are deficient?
A. TSH and ACTH
B. ADH and oxytocin
C. GH and prolactin
D. FSH and LH

back 11

D. FSH and LH

front 12

A patient has polyuria with inability to concentrate body fluids due to loss of pituitary control of water excretion. Which hormone is deficient?
A. Prolactin
B. ADH
C. LH
D. ACTH

back 12

B. ADH

front 13

During lactation, milk production is normal but milk ejection is impaired; uterine contractions at term are weak. Which hormone is deficient?
A. ADH
B. Oxytocin
C. Prolactin
D. TSH

back 13

B. Oxytocin

front 14

Which is an anterior pituitary cell type?
A. Chromaffin cell
B. Lactotrope
C. Follicular cell
D. Juxtaglomerular cell

back 14

B. Lactotrope

front 15

Somatotropes primarily produce:
A. ACTH
B. PRL
C. hGH
D. TSH

back 15

C. hGH

front 16

Corticotropes primarily produce:
A. ACTH
B. TSH
C. LH
D. ADH

back 16

A. ACTH

front 17

Thyrotropes primarily produce:
A. FSH
B. Oxytocin
C. PRL
D. TSH

back 17

D. TSH

front 18

Gonadotropes primarily produce:
A. TSH and GH
B. LH and FSH
C. ACTH and PRL
D. ADH and oxytocin

back 18

B. LH and FSH

front 19

Lactotropes primarily produce:
A. Prolactin
B. Oxytocin
C. ADH
D. ACTH

back 19

A. Prolactin

front 20

Approximately 30–40% of anterior pituitary cells are:
A. Corticotropes
B. Thyrotropes
C. Somatotropes
D. Lactotropes

back 20

C. Somatotropes

front 21

Approximately 20% of anterior pituitary cells are:
A. Gonadotropes
B. Lactotropes
C. Somatotropes
D. Corticotropes

back 21

D. Corticotropes

front 22

Somatotropes stain strongly with acid dyes and are called:
A. Basophils
B. Chromophobes
C. Acidophils
D. Reticulocytes

back 22

C. Acidophils

front 23

Which set lists hormones of the anterior pituitary as given?
A. GH, ACTH, TSH, PRL
B. ADH, oxytocin, cortisol, T3
C. Calcitonin, PTH, insulin, GH
D. Renin, ANP, EPO, cortisol

back 23

A. GH, ACTH, TSH, PRL

front 24

The pituitary stalk is also called the:
A. Corpus luteum stalk
B. Hypophysial stalk
C. Adrenal stalk
D. Thyroglossal stalk

back 24

B. Hypophysial stalk

front 25

Pituitary tumors that secrete large amounts of growth hormone are called:
A. Basophilic tumors
B. Chromophobic tumors
C. Acidophilic tumors
D. Gonadotrophic tumors

back 25

C. Acidophilic tumors

front 26

The cell bodies that secrete posterior pituitary hormones are located in the:
A. Arcuate nucleus
B. Supraoptic and paraventricular nuclei
C. Ventromedial nucleus
D. Mammillary bodies

back 26

B. Supraoptic and paraventricular nuclei

front 27

The posterior pituitary hormone–secreting neurons are best described as:
A. Parvocellular neurons
B. Pyramidal neurons
C. Bipolar neurons
D. Magnocellular neurons

back 27

D. Magnocellular neurons

front 28

Posterior pituitary secretion is controlled by nerve signals that originate in the:
A. Hypothalamus
B. Pituitary stalk
C. Anterior pituitary
D. Posterior pituitary

back 28

A. Hypothalamus

front 29

Secretion by the anterior pituitary is controlled by:
A. Thyroid hormones only
B. Adrenal steroids only
C. Hypothalamic releasing and inhibitory hormones
D. Posterior pituitary nerve endings

back 29

C. Hypothalamic releasing and inhibitory hormones

front 30

Hypothalamic hormones reach the anterior pituitary mainly via:
A. Lymphatics
B. Hypothalamic-hypophysial portal vessels
C. CSF flow
D. Jugular venous drainage

back 30

B. Hypothalamic-hypophysial portal vessels

front 31

The lowermost portion of the hypothalamus is the:
A. Medial eminence
B. Pineal recess
C. Tectum
D. Area postrema

back 31

A. Medial eminence

front 32

The extension of hypothalamic tissue into the pituitary stalk is the:
A. Pars intermedia
B. Tuber cinereum
C. Rathke’s pouch
D. Infundibular cleft

back 32

B. Tuber cinereum

front 33

Growth hormone consists of:
A. 84 amino acids
B. 100 amino acids
C. 191 amino acids
D. 200 amino acids

back 33

C. 191 amino acids

front 34

Which is a major metabolic effect of growth hormone?
A. Decreased protein synthesis
B. Increased protein synthesis
C. Decreased fatty acid mobilization
D. Increased glucose utilization

back 34

B. Increased protein synthesis

front 35

Which is a major metabolic effect of growth hormone?
A. Increased FFA mobilization and use
B. Decreased FFA levels in blood
C. Increased triglyceride storage only
D. Decreased fat use for energy

back 35

A. Increased FFA mobilization and use

front 36

Which is a major metabolic effect of growth hormone?
A. Increased glucose utilization
B. Decreased glucose utilization
C. No change in glucose uptake
D. Increased glycolysis in all tissues

back 36

B. Decreased glucose utilization

front 37

In the long run, the most important GH function is:
A. Acute glucose lowering
B. Promotion of protein synthesis and growth
C. Rapid fat mobilization only
D. Immediate ketone formation

back 37

B. Promotion of protein synthesis and growth

front 38

GH-induced fat mobilization requires several ___, whereas protein synthesis can begin in minutes:
A. Seconds
B. Minutes
C. Hours
D. Days

back 38

C. Hours

front 39

GH decreases carbohydrate utilization by:
A. Increasing tissue glucose uptake
B. Decreasing tissue glucose uptake
C. Decreasing hepatic glucose production
D. Decreasing insulin secretion

back 39

B. Decreasing tissue glucose uptake

front 40

GH decreases carbohydrate utilization by:
A. Increasing hepatic glucose production
B. Decreasing hepatic glucose production
C. Increasing muscle glucose uptake
D. Increasing insulin sensitivity

back 40

A. Increasing hepatic glucose production

front 41

GH decreases carbohydrate utilization by:
A. Decreasing insulin secretion
B. No change in insulin secretion
C. Increasing insulin secretion
D. Eliminating insulin release

back 41

C. Increasing insulin secretion

front 42

GH’s metabolic effects are termed ___, and excess GH can mimic type 2 diabetes disturbances:
A. Thyrogenic
B. Diabetogenic
C. Ketogenic
D. Lipogenic

back 42

B. Diabetogenic

front 43

GH fails to cause growth in animals if they:
A. Lack a thyroid gland
B. Lack a pancreas
C. Lack adrenal cortex
D. Lack posterior pituitary

back 43

B. Lack a pancreas

front 44

GH fails to cause growth in animals if:
A. Protein is excluded
B. Carbohydrates are excluded
C. Fat is excluded
D. Vitamins are excluded

back 44

B. Carbohydrates are excluded

front 45

Growth hormone strongly stimulates:
A. Osteoclasts
B. Osteoblasts
C. Chondroclasts
D. Fibroclasts

back 45

B. Osteoblasts

front 46

Much of GH’s effect is mediated through intermediates called:
A. Calmodulins
B. Somatomedins
C. Corticotropins
D. Catecholamines

back 46

B. Somatomedins

front 47

GH causes the liver to form several small proteins called:
A. Somatomedins
B. Albumins
C. Globulins
D. Kinins

back 47

A. Somatomedins

front 48

Somatomedins are also called:
A. Thyroxine-binding globulins
B. Angiotensin-related factors
C. Insulin-like growth factors
D. Natriuretic peptides

back 48

C. Insulin-like growth factors

front 49

The most important somatomedin is:
A. Somatomedin A (IGF-1)
B. Somatomedin B (IGF-1)
C. Somatomedin C (IGF-1)
D. Somatomedin D (IGF-1)

back 49

C. Somatomedin C (IGF-1)

front 50

GH levels are highest with:
A. Exercise and midnight sleep
B. Fasting and late afternoon
C. Meals and early evening
D. Pain and sunrise

back 50

A. Exercise and midnight sleep

front 51

Growth hormone binds to plasma proteins:
A. Strongly
B. Weakly
C. Covalently
D. Irreversibly

back 51

B. Weakly

front 52

Somatomedin C (IGF-1) binds to a carrier protein in blood:
A. Weakly
B. Not at all
C. Strongly
D. Transiently

back 52

C. Strongly

front 53

A marathon runner has a physiologic surge in growth hormone (GH). Which factor most directly stimulates GH secretion?
A. Hyperglycemia
B. High plasma fatty acids
C. Exercise
D. Hyperinsulinemia

back 53

C. Exercise

front 54

A fasting patient has rising GH partly due to a stomach-derived signal. Which factor stimulates GH secretion?
A. Ghrelin
B. Secretin
C. Leptin
D. Gastrin

back 54

A. Ghrelin

front 55

A sleep-lab study measures GH pulses during deep sleep. GH rises most during the first:
A. Four hours of deep sleep
B. Six hours of deep sleep
C. One hour of deep sleep
D. Two hours of deep sleep

back 55

D. Two hours of deep sleep

front 56

A healthy adult’s baseline GH level is typically around:
A. 6 ng/mL
B. 1.6–3 ng/mL
C. 20–100 ng/mL
D. 0.1–0.5 ng/mL

back 56

B. 1.6–3 ng/mL

front 57

A healthy child’s baseline GH level is typically around:
A. 6 ng/mL
B. 1.6–3 ng/mL
C. 20–100 ng/mL
D. 0.1–0.5 ng/mL

back 57

A. 6 ng/mL

front 58

A child with edema and severe protein deficiency has markedly altered endocrine patterns. This malnutrition syndrome is:
A. Marasmus
B. Pellagra
C. Kwashiorkor
D. Scurvy

back 58

C. Kwashiorkor

front 59

The hypothalamic nucleus that drives GHRH secretion is the:
A. Supraoptic nucleus
B. Ventromedial nucleus
C. Paraventricular nucleus
D. Arcuate nucleus

back 59

D. Arcuate nucleus

front 60

“Panhypopituitarism” refers to:
A. Excess posterior pituitary secretion
B. Isolated GH deficiency
C. Excess anterior pituitary secretion
D. Decreased all anterior pituitary hormones

back 60

D. Decreased all anterior pituitary hormones

front 61

An adult develops panhypopituitarism from a suprasellar mass compressing pituitary structures. Most likely cause listed is:
A. Pituitary adenoma, lactotrope
B. Sheehan infarction
C. Craniopharyngioma
D. Thyroid carcinoma metastasis

back 61

C. Craniopharyngioma

front 62

An adult with panhypopituitarism has a pituitary mass composed of chromophobe cells. Diagnosis best matches:
A. Acidophilic tumor
B. Chromophobe tumor
C. Craniopharyngioma
D. Pheochromocytoma

back 62

B. Chromophobe tumor

front 63

An adult suddenly loses multiple anterior pituitary hormones after vascular injury. A listed mechanism is:
A. Pituitary vessel thrombosis
B. Ventromedial nucleus lesion
C. Neurophysin deficiency
D. Tuber cinereum overgrowth

back 63

A. Pituitary vessel thrombosis

front 64

A patient with panhypopituitarism develops fatigue, cold intolerance, and low T3/T4 from loss of pituitary drive. This effect is:
A. Hyperthyroidism
B. Hyperaldosteronism
C. Hypercortisolism
D. Hypothyroidism

back 64

D. Hypothyroidism

front 65

A patient with panhypopituitarism has poor stress tolerance due to reduced adrenal glucocorticoid output. This is best described as:
A. Increased catecholamine synthesis
B. Depressed glucocorticoid production
C. Increased thyroid hormone secretion
D. Elevated mineralocorticoid output

back 65

B. Depressed glucocorticoid production

front 66

A patient with panhypopituitarism has infertility due to low LH/FSH output. This effect is:
A. Increased prolactin secretion
B. Increased gonadotropin secretion
C. Increased adrenal androgens
D. Suppressed gonadotropin secretion

back 66

D. Suppressed gonadotropin secretion

front 67

Panhypopituitary dwarfism characteristically:
A. Does not enter puberty
B. Enters puberty early
C. Has normal gonadotropins
D. Has excess gonadotropins

back 67

A. Does not enter puberty

front 68

Recombinant human growth hormone can be synthesized using:
A. Saccharomyces cerevisiae
B. Mycobacterium tuberculosis
C. Escherichia coli
D. Human fibroblast culture

back 68

C. Escherichia coli

front 69

A patient with gigantism develops a metabolic complication classically linked to excess GH. Most likely is:
A. Severe hypoglycemia
B. Addison disease
C. Hyperthyroidism
D. Hyperglycemia and diabetes mellitus

back 69

D. Hyperglycemia and diabetes mellitus

front 70

A patient with acromegaly most characteristically shows:
A. Thick long bones, soft growth
B. Short long bones only
C. Pure fat loss without growth
D. Only decreased bone density

back 70

A. Thick long bones, soft growth

front 71

In acromegaly, most bony enlargement occurs in the:
A. Vertebral bodies and ribs
B. Skull base foramina
C. Hands, feet, membranous bones
D. Femoral shafts only

back 71

C. Hands, feet, membranous bones

front 72

In patients who lose the ability to secrete GH, some aging features will:
A. Reverse rapidly
B. Accelerate
C. Remain unchanged
D. Stop entirely

back 72

B. Accelerate

front 73

GH-deficiency–related “accelerated aging” is mainly due to:
A. Increased protein deposition only
B. Decreased fat deposition only
C. Decreased protein, increased fat
D. Increased protein, decreased fat

back 73

C. Decreased protein, increased fat

front 74

The posterior pituitary gland is mostly composed of:
A. Chromaffin cells
B. Somatotropes
C. Lactotropes
D. Pituicytes

back 74

D. Pituicytes

front 75

Pituicytes primarily do NOT:
A. Produce hormones
B. Support nerve terminals
C. Maintain posterior structure
D. Surround axon endings

back 75

A. Produce hormones

front 76

Pituicytes function mainly as support for many:
A. Secretory vesicles
B. Terminal nerve fibers
C. Parathyroid chief cells
D. Thyroid follicular cells

back 76

B. Terminal nerve fibers

front 77

If the pituitary stalk is cut above the gland but the hypothalamus remains intact, the posterior pituitary will:
A. Stop secreting permanently
B. Secrete only oxytocin
C. Secrete only ADH
D. Still secrete hormones

back 77

D. Still secrete hormones

front 78

Carrier proteins that run along posterior pituitary nerve endings are called:
A. Albumins
B. Thyroglobulins
C. Neurophysins
D. Globulins

back 78

C. Neurophysins

front 79

ADH is formed primarily in the:
A. Paraventricular nuclei
B. Supraoptic nuclei
C. Ventromedial nucleus
D. Arcuate nucleus

back 79

B. Supraoptic nuclei

front 80

Oxytocin is formed primarily in the:
A. Paraventricular nuclei
B. Supraoptic nuclei
C. Ventromedial nucleus
D. Arcuate nucleus

back 80

A. Paraventricular nuclei

front 81

Which physiologic state is a listed stimulus for GH secretion?
A. Postprandial hyperglycemia
B. High plasma fatty acids
C. Starvation
D. Hyperlipidemia

back 81

C. Starvation

front 82

A trauma patient has increased GH secretion as part of the stress response. Which is a listed stimulus?
A. Hypocalcemia
B. Hypernatremia
C. Hyperthyroidism
D. Trauma

back 82

D. Trauma

front 83

A patient’s GH rises during an acute emotional surge. Which is a listed stimulus?
A. Hypoventilation
B. Excitement
C. Hyperkalemia
D. Bradycardia

back 83

B. Excitement

front 84

A patient’s GH rises when plasma substrates signal low energy availability. Which stimulus matches?
A. Hypoglycemia or low fatty acids
B. Hyperglycemia with high fatty acids
C. High insulin with high glucose
D. High cortisol with high glucose

back 84

A. Hypoglycemia or low fatty acids

front 85

Vasopressin differs from oxytocin at position 3. Which residue is vasopressin’s 3rd amino acid?
A. Isoleucine
B. Leucine
C. Phenylalanine
D. Arginine

back 85

C. Phenylalanine

front 86

Vasopressin differs from oxytocin at position 8 as well. Which residue is vasopressin’s 8th amino acid?
A. Leucine
B. Arginine
C. Phenylalanine
D. Isoleucine

back 86

B. Arginine

front 87

In complete absence of ADH, collecting tubules/ducts become almost ____ to water.
A. Freely permeable
B. Highly permeable
C. Moderately permeable
D. Impermeable

back 87

D. Impermeable

front 88

When ECF becomes hypertonic, osmoreceptor cells:
A. Swell and hyperpolarize
B. Shrink and trigger hypothalamus
C. Lyse and stop signaling
D. Depolarize from water influx

back 88

B. Shrink and trigger hypothalamus

front 89

The highly vascular structure in the anteroventral wall of the third ventricle is the:
A. Organum vasculosum
B. Pars intermedia
C. Median eminence
D. Tuber cinereum

back 89

A. Organum vasculosum

front 90

Hemorrhage with low blood pressure most directly increases:
A. Oxytocin secretion
B. Prolactin secretion
C. ADH secretion
D. TSH secretion

back 90

C. ADH secretion

front 91

At high concentrations, ADH most potently:
A. Dilates arterioles widely
B. Constricts arterioles bodywide
C. Blocks portal blood flow
D. Inhibits renin release

back 91

B. Constricts arterioles bodywide

front 92

ADH and oxytocin are both composed of ____ amino acids.
A. Seven
B. Eight
C. Ten
D. Nine

back 92

D. Nine

front 93

The anterior pituitary is also called the:
A. Adenohypophysis
B. Neurohypophysis
C. Pars nervosa
D. Infundibulum

back 93

A. Adenohypophysis

front 94

The posterior pituitary is also called the:
A. Adenohypophysis
B. Pars distalis
C. Neurohypophysis
D. Rathke pouch

back 94

C. Neurohypophysis

front 95

All listed hypothalamic hormones are peptides except:
A. TRH
B. GHRH
C. Somatostatin
D. Dopamine

back 95

D. Dopamine

front 96

Growth hormone’s net effect on protein is:
A. Decreases protein deposition
B. No net protein change
C. Increases protein deposition
D. Increases protein catabolism

back 96

C. Increases protein deposition

front 97

GH promotes protein deposition partly by:
A. Enhancing amino acid transport
B. Blocking amino acid entry
C. Inhibiting ribosomes
D. Degrading mRNA rapidly

back 97

A. Enhancing amino acid transport

front 98

GH increases protein synthesis by increasing:
A. DNA methylation only
B. RNA translation rate
C. Ion-channel opening
D. cGMP production

back 98

B. RNA translation rate

front 99

GH increases protein synthesis by stimulating:
A. GTP hydrolysis
B. Lysosomal activation
C. Protein phosphorylation only
D. Gene transcription

back 99

D. Gene transcription

front 100

GH promotes net protein gain by:
A. Decreasing protein breakdown
B. Increasing protein breakdown
C. Increasing renal protein loss
D. Blocking peptide secretion

back 100

A. Decreasing protein breakdown

front 101

Which finding is NOT a GH protein mechanism?
A. Enhanced amino acid transport
B. Increased RNA translation
C. Increased protein catabolism
D. Increased gene transcription

back 101

C. Increased protein catabolism

front 102

Posterior pituitary secretion is controlled by nerve signals originating in the:
A. Anterior pituitary
B. Posterior pituitary
C. Median eminence
D. Hypothalamus

back 102

D. Hypothalamus

front 103

Growth hormone’s overall effect on fat metabolism is to:
A. Decrease fatty acid mobilization
B. Decrease fat use for energy
C. Increase fatty acid mobilization/use
D. Increase triglyceride storage

back 103

C. Increase fatty acid mobilization/use

front 104

Growth hormone is considered “protein-sparing” mainly because it:
A. Promotes protein deposition/synthesis
B. Increases protein catabolism
C. Inhibits amino acid uptake
D. Blocks RNA translation

back 104

A. Promotes protein deposition/synthesis

front 105

A patient given excess GH has elevated free fatty acids. The most direct mechanism is:
A. Decreased hepatic gluconeogenesis
B. Decreased adipose lipolysis
C. Increased muscle glucose uptake
D. Increased fatty acid release adipose

back 105

D. Increased fatty acid release adipose

front 106

GH enhances conversion of fatty acids into:
A. Lactate
B. Acetyl-CoA
C. Pyruvate
D. Glycogen

back 106

B. Acetyl-CoA

front 107

Excess GH increases ketogenesis mainly by increasing hepatic production of:
A. Acetoacetic acid
B. Lactic acid
C. Carbonic acid
D. Uric acid

back 107

A. Acetoacetic acid

front 108

Massive GH-driven fat mobilization can lead to:
A. Hepatitis
B. Cirrhosis
C. Fatty liver
D. Fibrotic liver

back 108

C. Fatty liver

front 109

Excess GH is described as diabetogenic mainly because it:
A. Causes autoimmune beta-cell loss
B. Increases insulin sensitivity
C. Lowers hepatic glucose output
D. Causes insulin resistance

back 109

D. Causes insulin resistance

front 110

GH-driven insulin resistance is best explained by:
A. ↑ uptake, ↓ gluconeogenesis
B. ↓ uptake, ↑ gluconeogenesis
C. ↑ uptake, ↑ glycogen storage
D. ↓ uptake, ↓ insulin secretion

back 110

B. ↓ uptake, ↑ gluconeogenesis

front 111

Part of GH-related insulin resistance may be due to increased:
A. Free fatty acids
B. Calcium ions
C. Plasma amino acids
D. Thyroxine levels

back 111

A. Free fatty acids

front 112

GH stimulates cartilage/bone growth partly by increasing protein deposition by:
A. Hepatocytes
B. Parietal cells
C. Chondrocytic/osteogenic cells
D. Juxtaglomerular cells

back 112

C. Chondrocytic/osteogenic cells

front 113

GH promotes bone growth partly by increasing:
A. Osteoblast apoptosis
B. Cartilage matrix breakdown
C. Osteoclast differentiation only
D. Reproduction of growth cells

back 113

D. Reproduction of growth cells

front 114

GH promotes bone deposition partly by:
A. Osteoblasts become chondrocytes
B. Chondrocytes become osteogenic cells
C. Fibroblasts become adipocytes
D. Osteoclasts become osteocytes

back 114

B. Chondrocytes become osteogenic cells

front 115

Gigantism occurs because GH acts at:
A. Epiphyseal cartilages
B. Skull sutures
C. Vertebral bodies
D. Metaphyseal periosteum

back 115

A. Epiphyseal cartilages

front 116

With closed epiphyseal plates, excess GH mainly makes bones:
A. Longer
B. Shorter
C. Thicker
D. Thinner

back 116

C. Thicker

front 117

Small stature here is linked to inability to synthesize:
A. Growth hormone
B. Cortisol
C. Somatomedin C (IGF-1)
D. Thyroxine

back 117

C. Somatomedin C (IGF-1)

front 118

GH secretion pattern is best described as:
A. Pulsatile
B. Tonic continuous
C. One-time burst
D. Random chaotic

back 118

A. Pulsatile

front 119

Starvation stimulates GH especially with severe:
A. Sodium deficiency
B. Water excess
C. Protein deficiency
D. Fat overload

back 119

C. Protein deficiency

front 120

Ghrelin is best described as:
A. Adipocyte hormone after meals
B. Posterior pituitary hormone
C. Thyroid peptide hormone
D. Stomach hormone before meals

back 120

D. Stomach hormone before meals

front 121

More potent acute GH stimulus is:
A. Acute protein deficiency
B. Acute hypoglycemia
C. Acute hyperglycemia
D. Acute high fatty acids

back 121

B. Acute hypoglycemia

front 122

More potent chronic GH stimulus is:
A. Chronic protein deficiency
B. Chronic hyperglycemia
C. Chronic high fatty acids
D. Chronic high insulin

back 122

A. Chronic protein deficiency

front 123

GHRH is best described as a:
A. 9-AA neuropeptide
B. Catecholamine transmitter
C. 191-AA pituitary protein
D. 44-AA polypeptide

back 123

D. 44-AA polypeptide

front 124

GHRH secretion is controlled by the hypothalamic:
A. Paraventricular nucleus
B. Ventromedial nucleus
C. Supraoptic nucleus
D. Arcuate nucleus

back 124

A. Paraventricular nucleus

front 125

GHRH receptor signaling in somatotrophs activates:
A. Adenylyl cyclase
B. Phospholipase C
C. Guanylyl cyclase
D. Tyrosine kinase

back 125

A. Adenylyl cyclase

front 126

Short-term GHRH signaling increases GH release mainly by:
A. Decreased Ca2+ entry
B. Decreased cAMP
C. Increased Ca2+ entry and fusion
D. Blocked vesicle formation

back 126

C. Increased Ca2+ entry and fusion

front 127

Long-term GHRH signaling increases GH synthesis mainly by:
A. Decreased gene transcription
B. Increased renal clearance
C. Decreased mRNA production
D. Increased nuclear gene transcription

back 127

D. Increased nuclear gene transcription

front 128

Major long-term controller of GH secretion is:
A. Daily exercise duration
B. Tissue nutrition state
C. Pain perception state
D. Thyroid status only

back 128

B. Tissue nutrition state

front 129

A major effect of panhypopituitarism is:
A. Hyperthyroidism
B. Hyperaldosteronism
C. Hyperprolactinemia
D. Hypothyroidism

back 129

D. Hypothyroidism

front 130

A major effect of panhypopituitarism is decreased:
A. Catecholamines from adrenal
B. Glucocorticoids from adrenal
C. Thyroxine-binding globulin
D. Gastrin from stomach

back 130

B. Glucocorticoids from adrenal

front 131

A major effect of panhypopituitarism is decreased:
A. Gonadotropic hormone secretion
B. Calcitonin secretion
C. Erythropoietin secretion
D. ADH secretion

back 131

A. Gonadotropic hormone secretion

front 132

Treatment listed for panhypopituitarism includes:
A. Leptin and insulin
B. ADH and oxytocin
C. ACTH and thyroid hormone
D. Gastrin and secretin

back 132

C. ACTH and thyroid hormone

front 133

An adult with proportional dwarfism from generalized panhypopituitarism during childhood asks about fertility. Most accurate answer?
A. Yes, normal fertility expected
B. Yes, after GH therapy
C. No, usually cannot reproduce
D. No, due to high prolactin

back 133

C. No, usually cannot reproduce

front 134

The fertility limitation in generalized panhypopituitary dwarfism is mainly from:
A. Insufficient gonadotropins
B. Excess gonadotropins
C. Excess thyroid hormone
D. Insulin deficiency

back 134

A. Insufficient gonadotropins

front 135

Which dwarfism variant commonly does allow sexual maturation?
A. Isolated GH insufficiency
B. Isolated ACTH insufficiency
C. Isolated TSH insufficiency
D. Isolated ADH insufficiency

back 135

A. Isolated GH insufficiency

front 136

Gigantism most commonly results from excessively active:
A. Thyrotropes
B. Corticotropes
C. Lactotropes
D. Somatotrophs

back 136

D. Somatotrophs

front 137

In gigantism, pancreatic β cells are prone to:
A. Hypertrophy only
B. Degeneration
C. Neoplasia
D. Hyperplasia only

back 137

B. Degeneration

front 138

Later in life, many gigantism patients develop panhypopituitarism because:
A. Hypothalamus stops signaling
B. Tumor grows, destroys gland
C. Thyroid feedback shuts pituitary
D. Portal vessels dilate permanently

back 138

B. Tumor grows, destroys gland

front 139

A key treatment principle for gigantism is:
A. Dopamine agonist therapy only
B. Late surgery after adulthood
C. Early surgery/irradiation pituitary
D. Thyroidectomy first-line

back 139

C. Early surgery/irradiation pituitary

front 140

Acromegaly is most consistent with:
A. Acidophilic tumor after adolescence
B. Chromophobe tumor in infancy
C. Basophilic tumor before puberty
D. Craniopharyngioma in adults

back 140

A. Acidophilic tumor after adolescence

front 141

In acromegaly, long bones primarily:
A. Grow longer
B. Become thinner
C. Stop remodeling entirely
D. Become thicker

back 141

D. Become thicker

front 142

In acromegaly, enlargement is marked in hands/feet and:
A. Long-bone epiphyses
B. Membranous bones
C. Bone marrow only
D. Costal cartilages only

back 142

B. Membranous bones

front 143

Which structure is a membranous bone site listed for acromegaly enlargement?
A. Femur shaft
B. Supraorbital ridge
C. Tibial plateau
D. Humeral head

back 143

B. Supraorbital ridge

front 144

A patient with acromegaly has protruding lower jaw. This reflects enlargement of the:
A. Mandible
B. Maxilla
C. Clavicle
D. Scapula

back 144

A. Mandible

front 145

Vertebral changes in acromegaly can cause:
A. Lordosis only
B. Scoliosis only
C. Kyphosis
D. No posture changes

back 145

C. Kyphosis

front 146

Which soft-tissue organ enlargement is consistent with acromegaly?
A. Pancreas only
B. Tongue enlargement
C. Spleen shrinkage
D. Thymus loss

back 146

B. Tongue enlargement

front 147

GH is not used to prevent aging mainly because adverse effects include:
A. Insulin resistance and edema
B. Severe anemia and rash
C. Hyperthyroidism and fever
D. Bronchospasm and cough

back 147

A. Insulin resistance and edema

front 148

GH therapy adverse effects listed include:
A. Carpal tunnel syndrome
B. Nephrolithiasis
C. Cataracts
D. Hearing loss

back 148

A. Carpal tunnel syndrome

front 149

ADH and oxytocin are:
A. 191-AA proteins
B. 44-AA peptides
C. 9-AA polypeptides
D. 3-AA peptides

back 149

C. 9-AA polypeptides

front 150

ADH and oxytocin are identical except that in ADH:
A. Ile and Leu replace Phe, Arg
B. Phe and Arg replace Ile, Leu
C. Phe and Leu replace Ile, Arg
D. Ile and Arg replace Phe, Leu

back 150

B. Phe and Arg replace Ile, Leu

front 151

Without ADH, collecting ducts become almost:
A. Impermeable to water
B. More permeable to water
C. Permeable to urea only
D. Permeable to glucose only

back 151

A. Impermeable to water

front 152

ADH’s general effect is to:
A. Increase water excretion
B. Decrease water excretion
C. Increase sodium excretion only
D. Decrease potassium secretion only

back 152

B. Decrease water excretion

front 153

ADH increases collecting duct permeability mainly by:
A. Closing aquaporin pores
B. Removing membrane vesicles
C. Forming water-permeable pores
D. Blocking cAMP production

back 153

C. Forming water-permeable pores

front 154

When ADH binds its membrane receptor, the key second messenger is:
A. IP3
B. cAMP
C. cGMP
D. DAG

back 154

B. cAMP

front 155

In kidney tubule cells, ADH increases water permeability by causing vesicles to:
A. Leave membrane into cytosol
B. Insert into cell membrane
C. Fuse with nucleus
D. Bind mitochondria

back 155

B. Insert into cell membrane

front 156

ADH effects occur rapidly in about:
A. 30–60 minutes
B. 1–2 hours
C. 5–10 minutes
D. 1–2 days

back 156

C. 5–10 minutes

front 157

In absence of ADH, reversal of its effects occurs in:
A. 5–10 minutes
B. 30–60 minutes
C. 6–12 hours
D. 1–2 days

back 157

A. 5–10 minutes

front 158

Increased ECF osmolarity causes ADH secretion because osmoreceptor cells:
A. Swell from water influx
B. Shrink from water efflux
C. Lyse in hypertonic ECF
D. Stop firing entirely

back 158

B. Shrink from water efflux

front 159

Decreased ECF osmolarity inhibits ADH because osmoreceptor cells:
A. Shrink from water efflux
B. Swell from water influx
C. Lose membrane receptors
D. Increase cAMP synthesis

back 159

B. Swell from water influx

front 160

ECF osmolarity is detected mainly by:
A. Kidney macula densa
B. Hepatic stellate cells
C. Hypothalamic osmoreceptors
D. Pancreatic beta cells

back 160

C. Hypothalamic osmoreceptors

front 161

High ADH can raise blood pressure by:
A. Vasodilating arterioles
B. Constricting arterioles
C. Increasing venous compliance
D. Blocking sympathetic tone

back 161

B. Constricting arterioles

front 162

Oxytocin’s role in pregnancy is mainly to:
A. Inhibit uterine contractions
B. Cause uterine contraction
C. Increase renal water reabsorption
D. Increase cortisol secretion

back 162

B. Cause uterine contraction

front 163

After pregnancy, oxytocin mainly aids:
A. Milk production in alveoli
B. Milk ejection from breast
C. Follicle maturation in ovary
D. Progesterone secretion

back 163

B. Milk ejection from breast

front 164

Milk ejection reflex pathway is best:
A. Suckling→sensory→hypothalamus→oxytocin
B. Suckling→vagus→stomach→ghrelin
C. Suckling→pituitary→TRH release
D. Suckling→kidney→renin release

back 164

A. Suckling→sensory→hypothalamus→oxytocin