Shit - Endo UWorld Flashcards
(30 cards)
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
