Hypothalamic-Pituitary Pharmacology

Question 1

Somatropin properties

Answer 1

• Recombinant GH
• Can be given IM
• Circulating t1/2of 25 min; peak levels in 2-4 hrs, active levels persist 36 hrs

Question 2

Somatropin uses

Answer 2

-GH deficiency - replacement therapy in children
-Children w/ idiopathic short stature (costly)
-Poor growth due to Turner’s, Prader-Willi, renal insufficiency
-AoGHD
-AIDS wasting/cachxia
-pt w/ short bowel syndrom dependent on TPN
all of the above FDA aproved

Question 3

Laron Dwarf Receptor mutation Tx

Answer 3

Recombinant IGF-1, mecasermin (take carbs with injections to avoid hypoglycemia.

Question 4

Somatostatin analogs

Answer 4

Octreotide

Lanreotide

Question 5

Somatostatin analogs effects

Answer 5

Inhibits GH release

Decreases GI motility

Question 6

Somatostatin analogs & somatropin admin

Answer 6

parenteral, none are oral

Question 7

Somatostatin non-pit uses

Answer 7

Control of bleeding from varices and GI hemorrhage (octreotide)

Question 8

Somatostatin adverse reactions

Answer 8

Hyperglycemia

Question 9

Tx for hypoprolactinemia

Answer 9

none exists, mainly expermently

Question 10

Tx for hyperprolactinemia

Answer 10

Bromocriptine (frequent dies effects)

Cabergoline (preferred agen, more effective, better tolerated)

Question 11

Desmopressin (DDAVP)

Answer 11

ADH analog that is more stable to degradation, t1/21.5-2.5 hrs

Question 12

Action of ADH

Answer 12

•Renal actionsare mediated by V2receptors(GPCRs coupled to Gs)
-Increasethe rate of insertion of (aquaporins) into luminal membrane
-increase water permeability leading to an antidiuretic effect
-Also activates urea transporters and increases Na+ transport in distal nephron
•Non-renal V2actions: release of coagulation factor VIII and von Willebrand’s factor (Pressor responsesoccur only at much higher Cp)

Question 13

Neurogenic(Central) Diabetes Insipidus

Answer 13

• Inadequate ADH secretion from posterior pituitary
• Desmopressinis treatment of choice (2nd line is ADH)
• Chlorpropamide( sulfonylurea potentiates ADH release and used in DDAVP intolrent patients)

Question 14

Nephrogenic Diabetes Insipidus

Answer 14

Inadequate ADH actions (congenital or drug-induced)

• Congenital: Diverse receptor and aquaporin mutations
• Drug-induced: Lithium( reduces V2-receptor stimulation of adenylyl cyclase& Demeclocyline(tetracycline antibiotic

Question 15

Nephrogenic Diabetes Insipidus Tx

Answer 15

• Low salt, low protein diet
• Thiazide diuretics: Paradoxically reduces polyuria
• NSAIDs(Indomethacin): PGs attenuate ADH-induced antidiuresis -inhibitionof PG synthesis may relate to the antidiuretic response seen
• Thiazides and indomethacin also used in combination

Question 16

SIADH

Answer 16

Incomplete suppressionof ADH secretionunder hypoosmolar conditions–>hyponatremia

Question 17

Drugs inducing SIADH

Answer 17

• Psychotropic agents: SSRIs, haloperidol, tricyclic antidepressant
• Sulfonylureas(chlorpropamide) 
• Vinca alkaloidschemotherapy
• Methylenedioxymethamphetamine(MDMA)

Question 18

SIADH Tx

Answer 18

• Demeclocycline: inhibits ADH on distal tuble

- V2 receptor Antagonists (Tolvaptan & Conivapta):V2 receptor anatgonist, this inhibits ADH effects