HPH- Khan

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Explain GH signaling by JAK-STAT Pathway. Which other hormone uses this pathway?

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1

Explain GH signaling by JAK-STAT Pathway. Which other hormone uses this pathway?

GH binds to JAK-STAT receptor extracellularly. Then the intracellular domain phosphorylates multiple times. After phosphorylation, the STAT molecule dimerizes and activates transcription.

Prolactin also uses this pathway.

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2

GH has structural resemblance to which other hormone?

Prolactin

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3

What is JAK? What is STAT?

JAK- Janus Kinase, the enzyme that phosphorylates

STAT- signal transducer and activator of transcription

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4

What is the Role of IGF?

  • anabolic and growth promoting effects

    • increase bone growth, mineral density, muscle mass, and differentiation of fat cells

    • decreases BG

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5

What are the adverse effects of Recombinant Growth Hormone?

  • CANCER (neoplasms)

  • DECREASE INSULIN SENSITIVITY

  • others: peripheral edema, myalgia, arthralgia, carpal tunnel

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6

What are the long-term complications of acromegaly?

CVD, respiratory disease, cancer

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7

What 3 classes of agents can be used to treat acromegaly?

  1. somatostatin analogues

  2. dopamine agonists

  3. GH receptor antagonists

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8

What is the MOA of Somatostatin Analogs?

inhibit GH release from the pituitary gland

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9

What is the MOA of Dopamine Agonists?

inhibits GH paradoxically by activating D2 receptor to inhibit prolactin release

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10

What is the MOA of Pegvisomant?

GH receptor antagonist… AKA won’t let GH bind to target cells

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11

What are the ADRs of Pegvisomant?

(i don’t think this is very important)

elevated LFTs, lipohypertrophy at injection site

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12

What are the ADRs of Dopamine Agonists?

n/v, HA, postural hypotension

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13

What is the role of dopamine in prolactin secretion?

dopamine is the molecule responsible for inhibiting the release of prolactin secretion

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14

What are the causes of hyperprolactinemia?

  • ANTIPSYCHOTIC DRUGs- D2 receptor antagonists

  • tumors (pituitary, HT)

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15

How would you treat hyperprolactinemia?

Dopamine agonists

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16

What are the CNS adverse effects of Bromocriptine?

hallucinations, mood swings, psychosis, nightmare, insomnia

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17

How does the half-life of cabergoline compare to bromocriptine?

cabergoline has longer half-live

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18

Why is cabergoline preferred over bromocriptine?

greater efficacy, longer half life, less ADRs

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19

Oxytocin and vasopressin are made up of a _______ amino acid peptide.

9 amino acid peptide

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20

What causes the release of vasopressin?

  • low bp

  • high plasma osmolarity

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21

Where are the V1a receptors located? What is their function?

  • located- vascular smooth muscle

  • function- vasoconstriction

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22

Where are the V2 receptors located? What is their function?

  • located- kidneys

  • function- water reabsorption

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23

True or False: V1a and V2 receptors use Tyrosine Kinase receptors.

FALSE—> use GCPRs

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24

What are the indications for vasopressin use?

  • DIABETES INSIPIDUS

  • nocturnal enuresis

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25

What is desmopressin?

long-acting analogue of vasopressin (ADH) with minimal V1a activity

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26

What is an ADR of desmopressin?

hyponatremic convulsions

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27

How is vasopressin different from desmopressin?

desmopressin does NOT cause vasoconstriction like vasopressin

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28

What are the names of the 2 vasopressin antagonists?

  • conivaptan

  • tolvaptan

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29

What are the MOA of each vasopressin antagonist?

conivaptan- V1a and V2 receptor antagonist

tolvaptan- V2 receptor antagonist

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30

What is the major ADR of vasopressin antagonists?

osmotic demyelination syndrome

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31

WHAT IS THE BOXED WARNING OF VASOPRESSIN ANTAGONISTS?

FATAL LIVER INJURY

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