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ENDO > Other > Flashcards

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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
Q

highest predicative value for cushing

A

proximal muscle weakness
osteoporosis
spontaneous bruising
hypokalemia

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25
Q

\false positives in dex test

A

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

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26
Q

if surgery isnt possible with cushings, block adrenal with

A

ketoconazole
aminogluteimide
metyrapone
opddd

27
Q

effects of hydrocortisone

A

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

28
Q

increased calcium..

A

increases TPR

29
Q

hy;er and hypothyroid in blood pressure

A

hyper–>increase CO–>increase RAAS

hypo–>increase TPR

30
Q

dx pheo

A

free meta (product of epinephrine degradation by comt)

31
Q

if decreased metanephrine + high nometanephrine to metanephrine ration

A

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

32
Q

nonoperative management pheos

A

alpha blockade- phenoxybenzamine, phentolamine

bblocker after ablocker

33
Q

whipple’s triad

A

symptoms
low sugar
relief by eating

34
Q

Main cause of hypoglycemia in kids

A

alcohol

35
Q

persistent hyperinsulinemic hypoglycemia of indancy

A

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

36
Q

three genetic mutations in hypoglycemia

A

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
Q

ddx of adult hypoglycemia

A 
drug/toxin induced hypogly
post meal (does not equal reactive)
fasting=pathological
38
Q

post meal hypoglyc in kids

A

hyperinsulinism-hyperammonia syndrome

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

39
Q

post meal hypo glyc in children

A

roux en y procedure
NIHPS
insulinomas

40
Q

fasting hypoglyc ddx

A

inapp insulin secretion-nesidioblastosis, insulinoma, pancreatogenous hyperinsulinism

hepatic dysfunction

autoimmune (lupus)

tumoral hypogly: IGF2 mediated

hormone deficiencies - adrenal insufficiency, +- GH def

41
Q

treatment of reactive hypoglycemia

A

arcarbose–>blocks disaccharides which slows starch absorption

42
Q

rule of 10 for insulinoma

A

10% multifocal
10% malignant
10% islet hyperplasia

43
Q

adenylate cyclase needs ___ to fx, so

A

mg

so decrease in Mg leads to refractive hypocalcemia

44
Q

albright’s osteodytsrophy

A

short staturemetacarpals, mental retard, obesity

due to hypocalcemia due to pth resistance from pth signaling

45
Q

other reasons for hypocal

A

pancreatitis
osteoblastic meta
drugs-plicamycin, citrated blood

46
Q

signs of hypocalcemia

A

excitability vague gi cataracts teef hypoplasia

47
Q

causes hypercalc

A

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

48
Q

humoral malignancy

A 
PTHrP mediates --only osteoclasts
urinary camp up
renal ca reabs inc
125 levels low
pth levels low
49
Q

local osteolytic

A 
MM, breast, lymphoma
yes bone mets
osteoclasts
multiple mediators: RANKL, tnfa, il6, mips, PTHrp in braest
pth low
50
Q

calcimimetics

A

bind casr

51
Q

ostetitis fibrosa cystica

A

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
Q

osteopenia

A

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

53
Q

two calsses of osteopenia

A

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
Q

how is osteomalacia demonstrated

A

tetracycline testing

55
Q

ostesclerosis

A

incrfease in bone mass

56
Q

MCSF deficiency

A

super dense bones (osteopetrosis)

57
Q

RANK

A

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

58
Q

osteoprotegerin

A

blocks oC recruitment by binding to RANKL on OB

59
Q

OPG def

A

osteopenia

60
Q

role of estrogen on bone turnover

A

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

–>increase osteoblast

61
Q

biochem markesr of bone turnover

A

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

OB bone formation: serume alkaline phosphatase, serum osteocalcin

62
Q

OP1

A

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

63
Q

OP2

A

increase bone loss that;s age-related

64
Q

secondary causes of OP

A

heritable: marfaans, morquios, homocystinuria, osteogenesis, imperfecta, werners
acquired: hyperthyroidism, cushings, immobilization, chronic heparin

65
Q

2x risk for every

A

10-15 bone loss

66
Q

ddx osteomalacia

A

decrease in vit d

hypophosphatemia- renaal tubular po4 leak, gi ingestion of phos binders, hypophatemic rickets

ENDO (5 decks)

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