Shit - Endo UWorld Flashcards
Gastrinoma presentation
Refractory ulcers, especially in jejunum (abnormal)
Also abd. pain and diarrhea
MEN 2A+B gene and what that means for lineage
RET oncogene
ALL NEURAL CREST CELLS!
Reverse T3: role and synthesis
Inactive form of T3 to down regulate the response
Formed via peripheral T4
Aromatase inhibitors
anastrozole, letrozole, exemestane
Papillary vs Follicular thyroid cancer
Papillary = Orphan annie, nuclear grooves, psammoma, RET/BRAF, childhood irradiation
Follicular = invade capsule, HEMATOGENOUS mets
Esrtogen and TH
increases TBG by decreasing catabolism; increased total T4 pool and free T4, but normal T3 .: EUthyroid
Down Syndrome levels
1st timester: low PAPP-A, high b-hCG; nuchal translucency and hypo plastic nasal bone
2nd timester: high b-hCG, LOW AFP, low estriol, high inhibin A
MCC of high AFP readings
Underestimation of gestational age
(if correct age, then body wall defect or multiple gestations
T2DM MCCD
MI
Levels of stuff in Kleinfelters
LH and FSH: high
Inhibin and T: low
Sperm count: zero
Estrogen: high [E:T ratio determines extent of feminization/disease]
GH vs IGF-1 effects
GH form AP causes increased liver IGF-1 production
GH:
- insulin resistance
- lipolysis
- protein synthesis
IGF-1:
- growth and development of bones, cartilage, soft tissue (muscles)
Excess Iodine effects
1) wolf-Chaikoff: inhibition of TPO .: decreased oxidation, iodination (organification), and coupling [.: production]
2) competitive inhibition @ NIS (outcompete smaller amounts of radioactive Iodine in chemical exposures)
3) decrease amount of T3/T4 released
Iodine uptake in DeQuervain subacute thyroiditis
Initial thyrotoxicosis via release of stored T3/T4, then hypothyroidism with pain.
NEVER increase iodine uptake! initial thyrotoxicosis via increased release, not increased production.
Ransom receptors that increase or decrease insulin release
Increase: M3 (Gq) GCG (Gs/Gq) B2 (Gs) GLP-1 (Gs) Hist (H2)
Decrease:
a2 (Gi)
Somatostatin-2 (Gi)
Winters formula and what it means
PaCO2 = [HCO3- * 1.5] + 8 +/- 2
If PaCO2 differs from this predicted PaCO2, then there is a mixed acid-base disorder
i.e. severe DKA, expect low PaCO2 to compensate for metabolic acidosis, but PaCO2 is high indicating respiratory failure (pull. deem or altered mental status) adding a respiratory acidosis on top
DOC for hyperthyroidism
Methimazole
Pregnancy = PTU
Thyroid storm = PTU (because also blocks T4 to T3 peripherally)
Iodine uptake blockers vs. peripheral conversion blockers
Block I- uptake:
- Perchlorate
- Pertechnetate
- Thiocyabate
Block peripheral T4 to T3 conversion:
- PTU
- beta blockers
- ipodate (contrast agent)
Cushing disease results in what cellular changes in the adrenals
HyperPLASIA of fasiculata and reticularis
also some hyperTROPHY of fasiculata
XX with ambiguous genetalia and maternal virilization: enzyme deficient?
Aromatase
Male-pattern baldness rx
finasteride (5a-reductase inhibitor)
Minoxidil
What drug to co-administer with flutamide
continuous GnRH agonist i.e. leuprolide
[flutamide = non-steroid androgen-R blocker, so will cause feedback up regulation of Testosterone which would nullify the drugs effects]
Mechanism of drugs to decrease proptosis/opthamology problems in graves
Decrease inflammatory infiltration
[i.e. glucocorticoids; also decrease peripheral T4 to T3]
drugs that inhibits DHF
Trimethoprim (bacteria)
methotrexate (human)
pyrimethamine (toxo/plasmodia)
PCOS DOC and mechanism
OCP
Suppress LH, decreasing total androgen production
Increase SHBG - more T bound, less free for virualization
Orthostatic HYPERtension =
hyperaldosteronism
When to use OGTT
Gestational DM
CF
When other tests are equivocal
bHCG shot for infertility used to mimic what hormone?
LH surge (LH, FSH, bHCG all look similar)
Best marker for menopause
FSH
Drugs causing lipodystrophy and lipoatrophy
Lipodystrophy = protease inhibitors Lipoatrophy = NRTI (stavudine and zidovudine)
SGLT-2 inhibitors - check for what
BUN + creatinine
