19 Growth Hormone Flashcards

1
Q

In somatotropic axis, GH secretion is stimulated by _____________ and _____________ from the hypothalamus.

A

GHRH; Ghrelin

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2
Q

In somatotropic axis, GH secretion is inhibited by _____________ from the hypothalamus, __________ and _________ from short loop and long loop feedback respectively.

A

GHIH/ Somatostatin;
GH (pituitary);
IGF-1 (liver

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3
Q

Which of the followings are stimulatory to GH secretion?

A. Puberty
B. Sleep
C. Hyperglycemia
D. Exercise
E. Stress
F. Amino acids 
G. Free fatty acids
A

All except C and G
C: should be hypoglycemia (stimulatory test for GH)
G: should be inhibit GH secretion

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4
Q

Which of the followings are inhibitory to GH secretion?
A. Glucocorticoid excess
B. Hyperthyroidism
C. Ageing
D. Obesity, thus a lot of free fatty acids
E. Hyperglycemia

A

All except B
Should be hypothyroidism

A: Glucocorticoid suppresses GH as it stimulates somatostatin and supresses GHRH, thus glucocorticoid treatment may affect children’s growth

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5
Q

Stimulation of GH secretion is consistent with the role of GH/IGF-1 in?

A
  1. Stimulating growth/ protein anabolism (GH/IGF-1 effects)

2. Promoting the use of fat, raising blood glucose as energy sources > spare protein from being metabolized (GH effect)

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6
Q

What test is used when there is GH deficiency?

A

Glucagon stimulation test.
○ Will initiate hyperglycemia, thus insulin will be released
○ Reactive hypoglycemia will occur, and hence the stimulation of GH/ACTH secretion
○ Safer test than insulin stress test as the reactive hypoglycemia is less severe

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7
Q

What test is used when there is GH excess?

A

Inhibitory test for GH: OGTT
Normally, GH secretion is inhibited by high blood glucose levels (hyperglycemia)

Patients with GH-secreting pituitary tumour (acromegalic patients), GH secretion fails to be suppressed/ shows paradoxical increase

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8
Q

What is the secretion pattern of GH?

A
  • Peak levels of GH secretion occur after the onset of slow-wave sleep (non-rapid eye movement or deep sleep)
  • 75% in night time, 25% day time
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9
Q

Which of the following statement(s) is/are false?

A. We can test GH levels in blood with a single blood test
B. Patients with acromegaly does not have sleep bursts of GH
C. GH pulse is higher at the time of puberty and it declines with age
D. GH pulse is higher in female

A

A

A: A single blood test of GH is unreliable as it has a short half life (20 mins), so IGF-1 is measured (with 15-20 hours half life)
B: because of GH excess (always at a high level)
D: estrogen enhances GH response to GHRH

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10
Q

What are the 3 differences between GH secretagogues (GHS) and GHRH?

  • Location of receptors
  • Endogenous ligand
  • G-protein?
A
  1. GSH-receptors are found on somatotrophs and GHRH-secreting neurons;
    GHRH-R are located on somatotrophs
  2. Endogenous ligand for GHS is ghrelin; while that of GHRH is GHRH
  3. GHS: Gq protein > PLC > IP3; GHRH: Gs protein > AC > cAMP
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11
Q

Ghrelin is produced by the stomach and the hypothalamus. What is its main function on GH?

A

Overall: GH releasing protein
1. synergize with GHRH to stimulate GH secretion; also stimulates GHRH

  1. inhibits somatostatin secretion
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12
Q

What are the direct and indirect action of GH respectively?

A

Direct: metabolic effect of liver, muscle and adipose tissue

Indirect: growth-promoting effect, mediated via local production of IGF-1 (insulin-like growth factor)

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13
Q

Which of the following about IGF-1 is false?

A. It has insulin-like activity
B. It mediates a lot of mitogenic, anabolic and growth promoting actions of GH
C. IGF-1 injection can cause hypoglycemia through binding to IGF-1 receptor stimulates glucose uptake in liver
D. High levels of IGF-1 can enhance insulin sensitivity through suppression of GH

A

C: should be in skeletal muscle

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14
Q

What is Mecasermin? What is it used for?

List a side effect of this drug.

A

Synthetic human IGF-1.
For the long-term treatment of growth failure in children with severe primary IGF-1 deficiency.

Hypoglycemia

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15
Q

Which of the following is/are true about IGFBPs?

A. They prolong the half life of IGF-1
B. At least 95% of total IGF are GH-dependent IGFBP complex consisting of IGFBP-3
C. They range from IGFBP-1 to IGFBP-6
D. IGFBP protease is important for releasing making the IGFBP bind to IGF

A

D. IGFBP proteases present in the circulation may play an important role in proteolytic cleavage of IGFBPs to release IGF-1 close to the target cells (for replenishment)

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16
Q

Can GH be completely replaced by IGF-1?

Give examples.

A

Part of the GH effect on target tissues cannot be fully replaced by IGF.
Examples are differentiation of prechondrocytes into early chondrocytes, local production of IGF-1 for autocrine and paracrine action.

17
Q

_________ is the principle source of IGF-1 in blood.

A

Liver

18
Q

What is the effect of GH on protein metabolism?

A
Protein anabolism.
○ Increase amino acid uptake
○ Increase protein synthesis
○ Increase muscle mass
Positive nitrogen balance
19
Q

What is the effect of GH on lipid metabolism?

A
  1. Stimulate lipolysis
  2. Antagonize insulin action (induce insulin resistance, lower glucose uptake, so as to raise plasma glucose)
  3. Protein sparing effect
20
Q

During protein intake:

A. GH increases/ decreases/ no significant change
B. IGF increases/ decreases/ no significant change
C. insulin increases/ decreases/ no significant change

A

A. increases
B. increases
C: increases

21
Q

During carbohydrate intake:

A. GH increases/ decreases/ no significant change
B. IGF increases/ decreases/ no significant change
C. insulin increases/ decreases/ no significant change

A

A: decreases
B: no significant change
C: increases

22
Q

During fasting:

A. GH increases/ decreases/ no significant change
B. IGF increases/ decreases/ no significant change
C. insulin increases/ decreases/ no significant change

A

A: increases
B: decreases
C: decreases

23
Q

________________occurs early in life before pubertal development (proliferation of epiphyseal plate) (such that the development hasn’t ended) causes closure of epiphyseal plate and cessation of linear growth.

The opposite (GH/IGF-1 deficiency or GH receptor defect) leads to: _____________.

A

Gigantism (GH excess);

Dwarfism

24
Q

_____________ is also a disease due to GH excess but happens in adults after the closure of epiphyseal plate.

A

Acromegaly.

§ Physical signs: increase in soft tissue (frontal bossing, supraorbital bulging, enlargement of nose)
§ Mandible overgrowth resulting in interdental separation (diastema) and prognathism (underbite)
§ Increase in skin thickness, enlargement of hands and tongue, increase in ring size
Thickening of bones (skull, thus frontal bossing…) (appositional growth)