Anterior Pituitary Drugs Flashcards

1
Q

GH/IGF-1 promotes

A

lipolysis, glycogenolysis, detents against hypoglycemia

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2
Q

Laron’s Dwarfism

A

mutations in GH receptor - completely resistant to GH but respond to IGF-1
GH>GHR>JAK2 kinase>STAT5>IGF-1

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3
Q

GH release inhibited by

A

somatostatin, glucose load, FA’s, B-adrenergics

Stim. by sleep, protein, a-adrenergics, exercise

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4
Q

Provocative testing for GH

A

stimulate GH with arginine, clonidine, or insulin (hypoglycemia); oral glucose load should suppress GH

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5
Q

Somatotropin

A

recombinant hGH to treat GH deficiency (Turner’s, chronic renal disease)

  • C/I: any active malignancy, ICU
  • S/E: HA, HTN, increased cranial P, arthralgias, carpal tunnel
  • SQ injection
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6
Q

Mecasermin

A

IGF-1 therapy, SQ injection

  • For GH deficiency, Laron’s dwarfism, STAT56 mutations
  • C/I: active neoplasm, hypoglycemia conditions
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7
Q

Octreotide

A

Somatostatin analog inhibits GH secretion; SQ

  • Treats acromegaly, decreases portal HTN, inhibits insulin release
  • S/E: gallstones or gallbladder sludge
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8
Q

Pegvisomant

A

GH receptor antagonist, SQ, PEGylated

  • Treat acromegaly not responding to other drug/surgery
  • S/E: hepatitis, tumor growth (can get adenoma)
  • IGF-1 used to assess dosing, not GH
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9
Q

Bromocriptine, Cabergoline

A

Dopamine agonists - stimulate GH secretion but can inhibit it in adenomas of mixed somatotropes/lactotropes (GH/PRL)

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10
Q

PRL regulation

A
  • mainly inhibition through dopamine

- stimulated by estrogen, breast manipulation, high TRH

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11
Q

Hyperprolactinemia causes

A

amenorrhea, galactorrhea, ED, libido loss
- caused by pituitary adenoma, D2 antagonists, polycystic ovarian syndrome, primary hypothyroidism (TRH hormone spillover)*

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12
Q

Treat PRL excess with

A

Bromocriptine, Carbegoline (higher affinity, better tolerated)
- S/E: GI complaints, orthostasis, syncope

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13
Q

Gonadotropins

A

FSH, LH, hCG (placenta) - all have same alpha unit; Beta unit confers specificity (LH and hCG similar and activate LH receptor)
- activate GPCRs>AC>cAMP

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14
Q

FSH

A
  • Sertoli cells/granulosa cells

> spermatogenesis, inhibin secretion/supports follicle growth and estrogen synthesis

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15
Q

LH

A

Leydig cells/Theca cells, CL

- promotes testosterone synthesis/estrogen and progesterone

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16
Q

hCG

A
  • corpus luteum

- stimulates progesterone production

17
Q

Inhibin

A

increased by FSH; feeds back to suppress gonadotropes and inhibit FSH secretion

18
Q

GnRH stimulates

A

FSH/LH release; very pulsatile

  • receptors down-regulated if constant delivery of GnRH
  • Inhibited by testosterone, estrogen, progesterone
19
Q

Follicular Phase

A

Gonadotropins stimulate follicle growth and estrogen - stimulates endometrium

20
Q

Ovulation

A

Estrogen increases and does positive feedback on gonadotropes and causes LH surge > ovulation
- residual follicle becomes corp. luteum producing estrogen and progesterone

21
Q

Luteal phase

A

increasing progesterone stimulates endometrium to vascularize and secrete mucus
- feedback to pituitary increases amplitude and longer frequency of gonadotropin pulses

22
Q

Menstruation

A

If unfertilized, CL regresses, endometrium no longer supported

23
Q

Fertilization

A

trophoblast synth. hCG - supports estro/prog. synthesis by CL until week 9 when placenta takes over

24
Q

Cryptorchidism

A

failure of testes descent - requires hCG

25
Q

GnRH agonists

A

Leuprolide (IM)
Synarel (nasal)
Zolodex (SC)
Supprelin (implant)

26
Q

Leuprolide, Synarel, Zolodex, Supprelin

A

GnRH agonists used to treat hormone dependent cancers, fibroids, central precocious puberty because persistent stimulation of normally pulsatile GnRH receptor leads to receptor down regulation and ‘chemical castration’
- short term for fertility treatment

27
Q

Dx central precocious puberty by

A

leuprolide > FSH/LH increase if gonadotropes have been exposed to GnRH (true puberty)

28
Q

Ganirelix

A

GnRH antagonist to treat hormone-responsive cancers

Fertilization treatment to shorten time b/w IVF cycles