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0
Q

IG2 made by
binds
job

A

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

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1
Q

IGF1 made by

binds

A

liver

IGF 1 R

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2
Q

jobs of GH

A

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

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3
Q

IGFBP3

A

GH dependent, therefore used to monitor GH levels clinically

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4
Q

laron dwarfism

A

defective GH receptor

presents as IGF1 def

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5
Q

eunuchoid body status

A

disproportionately long arms and legs

seen with hypogonadism

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6
Q

basophil

A

acth

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7
Q

acidophiles

A

make prolactin and growth hormone

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8
Q

sheehan’s syndrome

A

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

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9
Q

drugs that cause hypothyroidism

A

amioradarone
PTU
methimazole
lithium

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10
Q

main cause of hypothy resistance

A

mutation in B1 subtype of nuclear T3 receptor

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11
Q

the B1 mutation is a

A

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

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12
Q

how do you treat hypothyroidism in rpegnancy

A

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

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13
Q

why treat hypoadrenalism before hypothyroid

A

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

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14
Q

drug induced hyperthyroidism

A

iodine or iodinated contrast

thyroiditis (release stored T)–amiodarone, ifn, radiotherapy

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15
Q

free thyroxine index

A

T4 x T3 RU

= active T4

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16
Q

HLA for hyperthyrodisim

A

DRW3 and HLABA

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17
Q

graves triad

A

diffuse thyroid hyperplasia
infiltrative opthalmopathy
infiltrative dermopathy

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18
Q

mechanism of GD opthalmopathy

A

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

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19
Q

how do androgen secreting tumors present

A

clitormegaly and menstraul change

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20
Q

ddx hirsutism

A 
polycystic kidney disease- acanthosis nigricans
idiopathic
congenital adrenal hyperplasia
rare neoplasm- ovarian, adrenal
cushing syndrome
exogenous andr0gen use
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21
Q

how to differentiate between adrenal adn ovarian

A

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

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22
Q

pseudogene + 21 hydroxylase block

A

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

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23
Q

dx CAH

A

measure urinary 17OHP

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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

ENDO (5 decks)

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