Shit - Endo Flashcards
MSH
from intermediate lobe of AP
AP vs PP origins
AP = oral ectoderm PP = neuroectoderm
Increase C-peptide via
Insulinoma
Sulfonyluras (chlorpromazine, tolbutamide, Glimeperide, glipizide, glyburide)
insulin effects on the kidney:
increase Na+ resorption
Insulin-independent glucose transporters:
1 = brain, RBC, cornea 2 = liver, panc, kidney, GIT 3 = brain, placenta, neurons 5 = fructose @ spermatocytes, GIT
Adrenergics on insulin release
a2 = decrease insulin release (stronger) (b2 = increase insulin release)
Effect of drugs that open K+ channels (diazoxide) or cause decreased EC K+ (thiazides)
Can;t close b-cell K+ channels .: can’t release insulin .: hyperglycaemia
CRH effects
ACTH, MSH, b-endorphins
Tesamorelin
GHRH analog to treat lipodystrophy in HIV
GnRH regulated by:
prolactin (i.e. breastfeeding stops GnRH release; prolactinoma causes infertility, OP, galactorhea)
delta cells in pancreas secrete + function
somatostatin; inhibits GH and TSH release in HPA (also many GIT actions).
Somatostatin role in HPA
inhibit GH and TSH release
Somatostatin role in GIT
INHIBITS RELEASE OF: Gastrin Cholecystokinin (CCK) Secretin Motilin Vasoactive intestinal peptide (VIP) Gastric inhibitory polypeptide (GIP) Enteroglucagon Decrease rate of GE
Panc:
Insulin
GCG
Exocrine function
TRH effects
increases TSH and prolactin release.
[so 1’ or 2’ hypothyroidism would cause hyperprolactinemia]
How is prolactin regulated
Increase: TRH
Decrease: DA, Prolactin (increases DA synthesis)
Somatomedin C =
IGF-1 (muscle mass, linear growth) [GH = InsResistance]
GH: increased and decreased by:
Increased:
GHRH
Sleep
Exercise
Decreased:
somatostatin
glucose
somatomedin negative feedback
Ghrelin function:
induce hunger
cause HG release
Conditions that increase ghrelin release
Sleep deprivation
Prader-willi
Regulation of AHD
1' = osmo-Rs in hypothalamus (most important job is osmolarity) 2' = hypovolemia
desmolase: other name, job, regulated by
= side chain cleavage enzyme
Turns cholesterol to pregnenolone
Increased by ACTH
Inhibited by Ketoconazole
renin levels in CAHs
21 = high 17 = low 11 = low
Hormone in 11-CAH that causes HTN
11-deoxycorticosterone
17-CAH presentation wrt sexes
XX = lack secondary sex characteristics XY = pseudohermaphroditism, cryptorchidism
Rx CAH
Exogenous cortisol to inhibit ACTH release
Other supplements i.e. aldosterone
Functions of cortisol:
BP: upregulates a1-Rs, acts as aldosterone at high conc
Insulin resistance
Gluconeo, lipolysis, proteolysis
Decrease fibroblast activity (striae)
Decrease immune system (incl. IL-2 production –> candidiasis and reactivation of TB). Neutrophilia
Decreased OBL activity
Ca and pH
40% Ca bound by albumin (45% ionized = free)
Increase pH = less H+ = albumin binds more Ca++ = hypocalcemia (tetany, cramps, spasms, paresthesias)
Vit D2 vs D3
D2 = plant foods D3 = skin
Vit D regulation
Increased by: low Ca, low PO4, high PTH
Decreased by: high Vit D (inhibits itself and PTH)
Ca++ regulation cells
Chief = parathyroid (bone, kidney, vitD) C-cell = calcitonin (bone)
PTH in kidney
PO4 - decrease resorption in PCT
Ca - increase resorption in DCT
Vit D - increase a-1-OHase in PCT
PTH in bone
increase Macrophage-CSF and OBL to secrete RANK-L
PTH secretion and Mg levels
Low Mg = increased PTH release
VERY low Mg = decreased PTH release
*get low Mg via diarrhea, loops, aminoglycosides, alcohol abuse
Increase SHBG via:
pregnancy and OCPs
.: more T bound up .: feminizing