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IDT Spring > Endocrine System (Growth Hormone) > Flashcards

Endocrine System (Growth Hormone) Flashcards

1
Q

The major functions of the body are regulated by the nervous and endocrine system which are linked by?

A

Hypothalamus/pituitary and adrenal medulla

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2
Q

Define endocrinology

A

Analyzes formation of hormones, site of production and mechanisms of action

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3
Q

What are the two classes that hormones are typically divided into?
What do they do? Examples?

A

Hormones that act via nuclear receptors to modulate transcription (steroid, thyroid, vitamin D and vitamin A, and via membrane receptors to exert rapid effects on signal transduction pathways (peptide and amino acid hormones)

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4
Q

Three classes of hypothalamus hormones?

A
  1. Produced in hypothalamus and released in the pars nervosa
  2. Stimulating or inhibiting hormones produced by hypothalamus
  3. Hormones produced in the pars distalis
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5
Q

anterior pituitary (AP) hormone:
Growth Hormone:
hypothalamic releasing factor(s)?
AP cell type?
systemic effects?

A

growth hormone releasing hormone (GHRH) (+) and somatostatin (-)
somatotropes
growth promotion, gluconeogenesis

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6
Q

anterior pituitary (AP) hormone:
Prolactin:
hypothalamic releasing factor(s)?
AP cell type?
systemic effects?

A

Suckling (+) and Dopamine (-)
Lactotropes
stimulate lactation, induce milk proteins

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7
Q

anterior pituitary (AP) hormone:
Thyroid-stimulating hormone:
hypothalamic releasing factor(s)?
AP cell type?
systemic effects?

A

thyrotropin-releasing hormone (TRH)
thyrotropes
stimulate thyroid gland to synthesize T4 and T3. increase size and secretion of thyroid gland

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8
Q

anterior pituitary (AP) hormone:
Adrenocorticotropic hormone:
hypothalamic releasing factor(s)?
AP cell type?
systemic effects?

A

corticotropin-releasing hormone (CRH)
corticotropes
cortisol secretion (to adrenal cortex)

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9
Q

Which AP hormone is a POMC-derived hormone?
a. Corticotropin
b. Follicle-stimulating hormone
c. Prolactin
d. TSH

A

a. Corticotropin

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10
Q

Which AP hormone is a POMC-derived hormone?
a. hCG
b. LH
c. a-Melanocyte SH
d. EGF

A

c

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11
Q

Which AP hormone is a somatotropic hormone?
a. a-Melanocyte SH
b. EGF
c. HGF
d. Prolactin

A

d

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12
Q

Which AP hormone is a human chorionic somatomammotropin (HCS) hormone?
a. TSH
b. Placental lactogen
c. HCG
d. FSH

A

b

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13
Q

From the list: Identify the Glycoprotein hormones:
1. Luteinizing hormone
2. Corticotropin
3. EGF
4. FSH
5. TSH
6. Lactogen
7. Prolactin
8. hCG
9. HGH
10. EGFR

A

1, 4,5,8

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14
Q

T/F GH and PRL can stimulate each other’s corresponding receptor

A

False: GH can activate PRL-R, but PRL cannot activated GH-R

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15
Q

what is the relationship between GH and insulin-like growth factors (IGF)?

A

GH stimulates release of IGF-1 and -2 from liver which help with several of the growth-promoting effects of GH

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16
Q

GHRH release from hypothalamus is __________
Somatostatin release from hypothalamus is ______
Growth hormone release is _________

A

constant, pulsatile, pulsatile

17
Q

Ghrelin’s effect on:
growth hormone?
somatostatin?
GHRH?

A

stimulate
inhibit
stimulate

18
Q

somatostatin’s effect on:
GH?
GHRH?

A

inhibit
inhibit

19
Q

IGF-1’s effect on:
GH?
GHRH?

A

inhibit
inhibit

20
Q

GH is secreted as a heterogeneous mixture of peptides; the principal form is a single polypeptide chain of _________.
Alternative splicing produces a smaller form of ______ (~20) with equal bioactivity that makes up 5-10% of _________.
_____ consists of the ______ form only, providing a way to detect ___________.
In the circulation, a ______ protein, which is derived from the extracellular domain of the _________________, binds and transports GH
Bound GH has a biological t1/2 about __ times that of unbound GH.
Bound GH may provide a __________ that dampens acute fluctuations in GH levels associated with its pulsatile secretion

A

22 kDa
kDa, circulating GH
rGH, 22 kDa, GH abuse
55 kDa, proteolytically cleaved GH receptor
10
GH reservoir

21
Q

Which of the following does NOT promote tissue growth?
a. IGF-1
b. IGF-2
c. Ghrelin
d. GH

A

c

22
Q

Insulin receptor a2b2 tetramer has what what important activity?
GH receptor does/does not have the same activity?

A

intrinsic tyrosine kinase activity
does not

23
Q

Binding of GH to GHR results in the activation of JAKs, what does JAKs do?

A

phosphorylates STAT proteins which go into nucleus and regulate gene expression

24
Q

although GH does not have intrinsic tyrosine kinase activity, how does it indirectly activate tyrosine kinase?

A

when GH binds to GHR, JAK2 can bind to GHR which is a cytoplasmic tyrosine kinase of the Janus kinase family

25
Q

JAK2 binds to GFR and causes tyrosine phosphorylation to mediate downstream signaling such as ______ which activates expression of _____
Negative feedback: GH, through ______, induces expression of a family of _______________ proteins and a group of tyrosine phosphatases that disrupt the communication of the activated ______ with _____

A

STAT5, IGF-1
STAT5, suppressor of cytokine signaling (SOCS), GHR, JAK2

26
Q

Growth hormone:
longitudinal growth of ______ is most striking physiological effect.
increases ____________ after the epiphyses have closed.
increases __________, _________ and ___________.

has potent anti-_____ actions in both the liver and peripheral tissues that decrease _______ utilization and increase _________.
most of the anabolic and growth-promoting effects of GH are mediated indirectly through the induction of ______ and ______.

______ and _____ belong to the cytokine and receptor tyrosine kinase superfamily, respectively.
loss-of-function mutations in both alleles of the ______ gene results in severe intrauterine and postnatal _________ that is unresponsive to GH, but responsive to _____

A

bones
bone mineral density
muscle mass, kidney size, GFR of kidney

insulin, glucose, lipolysis
IGF-1, IGF-2

GHRs, IGF-1Rs
IGF1, growth retardation, IGF1

27
Q

Pegvisomant, a variant of GH, causes GHR internalization but cannot trigger the conformational change that stimulates _______________

A

downstream events

28
Q

Excess production of GH:
syndromes of excess secretion of GH typically are caused by _______ that oversecrete GH.

Clinical Manifestations of Excess GH:
if the epiphyses are unfused, GH excess causes increased longitudinal growth, resulting in _______.
GH excess in adults causes _______ (describe it).
Mortality is _______.
Tumor also causes compression of and injury to __________, ____________ and ______________.
Other problems may include ____, ____ and increased risk of ________

A

somatotrope adenomas
gigantism
acromegaly: flat-bone growth, causes enlargement of the face, hands, and feet.
increased
pituitary gland, optic nerves, optic chasm
HTN, DM, colon cancer

29
Q

Diagnosis of Growth Hormone Excess:
Gigantism/acromegaly should be suspected in pts with the appropriate signs/symptoms, diagnostic confirmation requires demonstration of increased circulating ________ or ____.
Another diagnostic test for both conditions is the _________ (describe test)

A

GH, IGF-1
oral glucose tolerance test: normal ppl suppress GH level to less than 1 ng/mL

30
Q

Treatment of GH Excess:
initial treatment of gigantism/acromegaly is selective _____ of the _______.
radiation and drugs that _____________ are given if surgery does not cure.
Pituitary irradiation may be associated with long-term complications, including ______________ and __________. Thus, increases attention has been given to pharm management of acromegaly

A

removal, adenoma
inhibit GH secretion
visual deterioration, pituitary dysfunction

31
Q

We use somatostatin analogues (usually for acromegaly). The goal of treatment is to decrease GH levels to less than _______ after an ____________ and to bring ____ levels to within normal range
Synthetic SST agonist analogues are selective for which SST receptors?

A

2.5 ng/mL, oral glucose tolerance test, IGF1
SST2 and SST5

32
Q

SST Analogue:
Ocreotide (Sandostatin):
Administration?
Effect?

A

Ocreotide: subQ TID
Ocreotide LARIM: once every 4 weeks
decreases tumor size while pt stays on med

33
Q

SST Analogue:
Lanreotide (Somatuline):
Administration?
Effect?

A

subQ every 4 weeks
prolonged suppression of GH secretion

34
Q

SST Analogue:
Pasireotide LAR (Signafor):
Use?

A

Cushing disease

35
Q

SST Analogue:
Vapreotide (Sanvar):
Use?

A

treating esophageal variceal hemorrhage pts with portal hypertension

36
Q

Adverse effect of SST analogs:
GI:
CV:
Endocrine:

A

GI: diarrhea, nausea, and abdominal pain: very common, lessen over time. May develop tiny gallstones\
CV: bradycardia and QT prolongation
Endocrine: -inhibit TSH secretion
-Pasireotide can cause hypocortisolism
-decrease insulin secretion, but reduce insulin resistance

37
Q

GH deficiency:
Children with GH deficiency present with _____, ______, and a __________.
GH deficiency in adults is associated with increased _______, decreased ___________ and _______ with reduced _______ and ______, with an increased mortality from _______________

A

short stature, delayed bone age, low age-adjusted growth velocity
body fat, muscle, bone mass, strength, endurance, CV causes

38
Q

GH is listed as a prohibited class ____ substance

A

E

IDT Spring (22 decks)

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