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IGF1 made by
binds

liver
IGF 1 R

1

IG2 made by
binds
job

made by mesenchymla tissue
binds IGF1 R and insulin R
important for fetal development

2

jobs of GH

increase lipolysis (ILGF1 doesnt)
acts like glucagon (increases glucose)
decreases urinary PO4, increases urinary Ca
retains Na, K, Cl, Mg

3

IGFBP3

GH dependent, therefore used to monitor GH levels clinically

4

laron dwarfism

defective GH receptor
presents as IGF1 def

5

eunuchoid body status

disproportionately long arms and legs
seen with hypogonadism

6

basophil

acth

7

acidophiles

make prolactin and growth hormone

8

sheehan's syndrome

spectrum of symptoms starting with failure of lactation that are representative of pituitary failure by hemorrhage and infarct

P is more sensitive during pregnancy because it undergoes hyperplasia an dneeds more blood

9

drugs that cause hypothyroidism

amioradarone
PTU
methimazole
lithium

10

main cause of hypothy resistance

mutation in B1 subtype of nuclear T3 receptor

11

the B1 mutation is a

dominant negative (one bad subunit ruins the heterodimer) mutation-->heterodimer can no longer bind DNA

12

how do you treat hypothyroidism in rpegnancy

increase dosage of medication because of increase in T3 degradation by placenta

13

why treat hypoadrenalism before hypothyroid

tx with thyroxine with increase cortisol clearance further decreasing cortisol leevels- cortisol crisis

14

drug induced hyperthyroidism

iodine or iodinated contrast
thyroiditis (release stored T)--amiodarone, ifn, radiotherapy

15

free thyroxine index

T4 x T3 RU
= active T4

16

HLA for hyperthyrodisim

DRW3 and HLABA

17

graves triad

diffuse thyroid hyperplasia
infiltrative opthalmopathy
infiltrative dermopathy

18

mechanism of GD opthalmopathy

activated t cells invade tissue-->local accum of glycoasminoglycans and edema

19

how do androgen secreting tumors present

clitormegaly and menstraul change

20

ddx hirsutism

polycystic kidney disease- acanthosis nigricans
idiopathic
congenital adrenal hyperplasia
rare neoplasm- ovarian, adrenal
cushing syndrome
exogenous andr0gen use

21

how to differentiate between adrenal adn ovarian

PE and increase DHEAS--DHEA is produced by both, but only adrenals can maek DHEAS

22

pseudogene + 21 hydroxylase block

pseudogene cxover with real gene-->now pseudogene has a promoter-->can accumulate mutations that are tolerated and keep goign

23

dx CAH

measure urinary 17OHP

24

highest predicative value for cushing

proximal muscle weakness
osteoporosis
spontaneous bruising
hypokalemia

25

\false positives in dex test

stress
mising dex dose
estrogen, pregnancy, obesity-->increases transcortin
phenytoin (increases dexA METAB)

26

if surgery isnt possible with cushings, block adrenal with

ketoconazole
aminogluteimide
metyrapone
opddd

27

effects of hydrocortisone

increase gluconeogenesis
decrease protein and fa synthesis
decrease intestinal absorption, decrease osteoblast activity
immune anti-inflam

28

increased calcium..

increases TPR

29

hy;er and hypothyroid in blood pressure

hyper-->increase CO-->increase RAAS
hypo-->increase TPR

30

dx pheo

free meta (product of epinephrine degradation by comt)

31

if decreased metanephrine + high nometanephrine to metanephrine ration

suspect paragangliomas because they lack NE to E enxyme or massive adrenal pheos

32

nonoperative management pheos

alpha blockade- phenoxybenzamine, phentolamine
bblocker after ablocker

33

whipple's triad

symptoms
low sugar
relief by eating

34

Main cause of hypoglycemia in kids

alcohol

35

persistent hyperinsulinemic hypoglycemia of indancy

islet cells hyperplasia secondary to over-activation of the insulin sensor mechanism

36

three genetic mutations in hypoglycemia

gain of function in islet cell glucokinase

loss of function in B cells ATP dependent K channel-->overactivation

gain of function mutation of mito cutamate DH in b cells-->this makes GDH sensitive to leucine-->child sensitive to leucine induced hypoglycemia

37

ddx of adult hypoglycemia

drug/toxin induced hypogly
post meal (does not equal reactive)
fasting=pathological

38

post meal hypoglyc in kids

hyperinsulinism-hyperammonia syndrome
roux-en-y procedure (insulin released but food bypass GI)

39

post meal hypo glyc in children

roux en y procedure
NIHPS
insulinomas

40

fasting hypoglyc ddx

inapp insulin secretion-nesidioblastosis, insulinoma, pancreatogenous hyperinsulinism

hepatic dysfunction

autoimmune (lupus)

tumoral hypogly: IGF2 mediated

hormone deficiencies - adrenal insufficiency, +- GH def

41

treatment of reactive hypoglycemia

arcarbose-->blocks disaccharides which slows starch absorption

42

rule of 10 for insulinoma

10% multifocal
10% malignant
10% islet hyperplasia

43

adenylate cyclase needs ___ to fx, so

mg
so decrease in Mg leads to refractive hypocalcemia

44

albright's osteodytsrophy

short staturemetacarpals, mental retard, obesity

due to hypocalcemia due to pth resistance from pth signaling

45

other reasons for hypocal

pancreatitis
osteoblastic meta
drugs-plicamycin, citrated blood

46

signs of hypocalcemia

excitability vague gi cataracts teef hypoplasia

47

causes hypercalc

primary/malignancy
granulomatous disease: sarcoid, tb, fungal, lymphoma, berylliosis- ectopic 125
meds: thiazides, vitd vita, milk-alkali
endocrinopathies: thryotoxicosis, decrease adrenal
immobilization

48

humoral malignancy

PTHrP mediates --only osteoclasts
urinary camp up
renal ca reabs inc
125 levels low
pth levels low

49

local osteolytic

MM, breast, lymphoma
yes bone mets
osteoclasts
multiple mediators: RANKL, tnfa, il6, mips, PTHrp in braest
pth low

50

calcimimetics

bind casr

51

ostetitis fibrosa cystica

spotty decrease in bone density esp at subperiostel cortical bone
osteoclasts remove, osteoblasts replace with scar, angiogenesis

ultimately micro fx, intramed hemm-->influx hemosederin macrophages-->brown tumor

52

osteopenia

signfiicant decrease in mineralized bone content as assessed by varuous x ray techniques

53

two calsses of osteopenia

osteoporosis- loss of total bone volume (decrease mineralized bone mass because of increase in resorption relative to formation)
osteomalacia- increase unmin bine mass (osteoid) because of decreased mineralization usually due to vit d def

54

how is osteomalacia demonstrated

tetracycline testing

55

ostesclerosis

incrfease in bone mass

56

MCSF deficiency

super dense bones (osteopetrosis)

57

RANK

binds RANKL on mature OB and OC-->stimulates OB production of OC GFs-->prevents OC apoptosis

58

osteoprotegerin

blocks oC recruitment by binding to RANKL on OB

59

OPG def

osteopenia

60

role of estrogen on bone turnover

dec MCSF prod
decrease RANKL expression on OB
increase OPG secretion
increase local TGFB

-->increase osteoblast

61

biochem markesr of bone turnover

OC bone resorption-->urinary type I collagen breakdown products: ntelopeptide

OB bone formation: serume alkaline phosphatase, serum osteocalcin

62

OP1

rapid bone loss in 1st 10 years of post menopause, surgical oophorectomy, or change in gonadal axis

63

OP2

increase bone loss that;s age-related

64

secondary causes of OP

heritable: marfaans, morquios, homocystinuria, osteogenesis, imperfecta, werners

acquired: hyperthyroidism, cushings, immobilization, chronic heparin

65

2x risk for every

10-15 bone loss

66

ddx osteomalacia

decrease in vit d
hypophosphatemia- renaal tubular po4 leak, gi ingestion of phos binders, hypophatemic rickets