Hyp-Pit Flashcards

1
Q

GH deficiency is treated with?

A

Somatotropin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Laron syndrome is treated with?

A

Mecasermin (IGF-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Treatment for acromegaly?

A

Octreotide (IR-ER), Lanreotide (ER), Cabergoline, Pegvisomant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatment for neurogenic diabetes insipidus?

A

Desmopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment for nephrogenic diabetes insipidus?

A

Fluids, thiazides, and NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Treatment for SAIDH?

A

Restrict free H2O, NaCl, Tolvaptan, Canivaptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Thy hypothalamus releases ______ to stimulate GH release from the ant. pituitary.

A

GHRF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What hormone released by the hypothalamus causes negative feedback for GH release?

A

Somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

GH is metabolized to what in the liver?

A

IGF-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

IGF-1 preforms positive feedback where?

A

On somatostatin release from the hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

IGF-1 preforms negative feedback where?

A

GH release from ant. pituitary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

GH preforms negative feedback where?

A

GHRH release from hypothalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Function of both GH and IGF-1 is?

A

Growth of peripheral tissue.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Growth hormone is also called?

A

Somatotropin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List some things that increase release of GH.

A

GHRH, exercise, hypoglycemia, dopamine, arginine, ghrelin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

List some things that decrease GH release.

A

somatostatin, dopamine agonists.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the route of administration for somatotropin?

A

SC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How long after injection do somatotropin levels peak? How long is it active after injection?

A

Peak 2-4 hours

Active levels persist 36 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the treatment for a child with GH deficiency?

A

SC injection of somatotropin daily at bedtime.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

List some of the brand names for somatotropin injections.

A

Humatrope, serostim, genotropin, nutropin, norditripin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is more common, GH deficiency or GH insensitive deficiency?

A

GH deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

GH insensitive deficiency is also known as?

A

Laron syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Treatment for Laron syndrome?

A

Recombinant IGF-1 (mecasermin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What side effect of mecasermin is concerning?

What can you do to minimize this side effect?

A

Hypoglycemia

Increase carb intake prior to SC injection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Uses of GH in adults?

A

Pituitary tumor, turner’s syndrome, prader willi syndrome, chronic renal insufficiency, wasting or cachexia in AIDS patients, short bowel syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

T/F? Off label use of GH is illegal.

A

True

27
Q

Adverse reactions to GH?

A

Insulin resistance, idiopathic intracranial hypertension, pancreatitis, gynecomastia, nevus growth.

28
Q

GH misuse in athletes can cause?

A

Acromegaly, arthropathy, extremity enlargement, visceromegaly.

29
Q

Somatostatin is also known as?

A

SST, SRIH (somatotropin releaseing inhibiting hormone)

30
Q

What medication are somatostatin analogs?

A

Octreotide and Lanreotide

31
Q

Routes of administration for somatostatin analogs?

A

Octreotide - SQ every 6-12 hours
Lanreotide - SQ every 4 weeks
Octreotide LAR - IM every 4 weeks

32
Q

Preferred treatment for excess of growth hormone?

A

Surgical resection when possible.

33
Q

When surgical resection is not possible, what is the preferred therapy for excess growth hormone?

A

Lanreotide is preferred after response seen to SC octreotide

34
Q

Second line treatment for excess GH?

A

Dopamine agonists - Cabergoline
OR
GH receptor antagonist - Pegvisomant

35
Q

What are non-pituitary uses of somatostatin analogs?

A

Constriction of vascular smooth muscle for treatment of esophageal varices and GI hemorrhage

36
Q

Adverse reactions to somatostatin analogs?

A

Hyperglycemia, abd cramps, loose stools, sinus brady, and conduction disturbances

37
Q

Prolactin is released from?

A

Ant pituitary

38
Q

Prolactin release is inhibited by?

A

Dopamine

39
Q

Main stimulus for prolactin release?

A

Suckling - causes 10-100 fold increase within 30 minutes

40
Q

Prolactin release is under inhibitory control by hypothalamic dopamine at ___ receptors.

A

D2

41
Q

Prolactin stimulates?

A

Milk production

42
Q

Prolactin inhibits?

A

Gonadotropin (FSH/LH) release and ovarian response to those hormones.
Results in lack of ovulation during breastfeeding

43
Q

Treatment for hypoprolactinemia?

A

No commercially available preperation

44
Q

Treatment for hyperprolactinemia?

A

Dopamine agonists

45
Q

Preferred dopamine agonist for hyperprolactinemia?

A

Cabergoline - More selective for D2 receptor and more effective in reducing prolactin secretion.

46
Q

Second line dopamine agonist for hyperprolactinemia?

A

Bromocriptine

47
Q

ADH is also known as?

A

Vasopressin

48
Q

ADH is released from?

A

Post pituitary

49
Q

The main stimulus for release of ADH is?

A

Rising blood osmolarity

50
Q

ADH release is inhibited by?

A

Ethanol

51
Q

Renal actions of ADH are mediated by?

A

V2 receptors (GCPRs)

52
Q

Mechanism of action of ADH to decrease water excretion?

A

Increase rate of insertion of aquaporins into luminal membrane

53
Q

What are non-renal V2 actions?

A

Increased release of coagulation factor VIII and von Willebrand’s factor

54
Q

Treatment of choice for neurogenic diabetes insipidus?

A

Desmopressin

55
Q

Routes of administration for desmopressin?

A

SC, IV, Nasally, Orally

56
Q

Nephrogenic diabetes insipidus can be congenital due to aquaporin mutations, or caused by drugs. Name 2 drugs that can cause nephrogenic diabetes insipidus.

A

Lithium

Demeclocycline

57
Q

Treatment of nephrogenic diabetes insipidus?

A

Fluids
Thiazide diuretics
NSAIDs (indomethacin)

58
Q

Diabetes insipidus is post. pituitary _____ (hypo/hyperfunction).
SAIDH is post. pituitary ______(hypo/hyperfunction).

A

hypofunction

hyperfunction

59
Q

What drug classes are most commonly implicated in SAIDH?

A

SSRIs, haldoperidol, TCAs
Sunfonylureas (chlorporpamide)
Vinca alkaloids (chemo)
Methylenedioxymethamphetamine (MDMA)

60
Q

Treatment of SAIDH?

A

Restriction of free water intake
NaCl administration
Demeclocyline or lithium

61
Q

SAIDH causes hyponatremia. How is this treated?

A

V2 receptor antagonists - Tolvaptan (oral), Conivaptan (IV)

62
Q

Rapid correction of hyponatremia should be avoided to reduce risk of?

A

Cerebellar pontine myelinolysis

63
Q

Vasopressin is used for treatment of?

A

Severe septic shock