2/26 UWORLD test # 25 Flashcards
Q 2. Duodenal atresia
- pathphysiology
- presentation
- x-ray finding
- other associated medical condition
- failure of recanulation (makes duodenum lumen hollow during 9 weeks of gestation)
- bilious or non-bilious vomiting
- double bubble on x-ray (due to dilation of stomach and duodenum), polyhydramnios
- Associated with Down syndrome
Q 2. Jejunum/ ileum atresia
- pathophysiology
- presentation
- clinical finding
- vasocclusion leading to ischemia
- bilious vomiting
- spiral configuration of distal ileum around blood vessel- apple peeling
Q 2. Pathophysiology of tracheoesophageal fistula?
- Failure of tracheoesophageal septum to PARTITION the forgut into esophagus and trachea
partition: devision
Q 4. Somatic mosaicism vs. Germline mosaicism
somatic mosaicism: somatic mutation from parents can not pass affected gene (mosaicism needs to be in germ cells to pass next generation)
germline mosaicism: multiple siblings with variable disease manifestation from NORMAL parents. Germline mutation from normal parents can pass mutant.
Q 5. What is H. influenzae B vaccine made of? when should it be given?
- polysacchride capsule antigen conjugated to diptheria toxoid (inactivated toxin)
- 2-18 months
Q 5. Describe immune response to encapsulated bacteria vaccines
exogenous antigen presented to CD4 T cells
- > Th cell activation
- > B cell activation/ plasma cell
- > antibody production
It is antibody mediated immune response
Q 6. Describe the timeline regarding HBV serologic markers. Which one peaks disappears first? which one appears next? How can this time line explains window period?
- HBsAg
- HBeAg
- anti-HBsAg
- anti-HBeAg
- Anti-HBc IgG
- Anti-HBc IgM
- Both HBsAg and HBeAg arises, but HBeAg disappears first, followed by Anti-HBeAg productin
- HBsAg then disappear later, follwed by Anti-HBsAg production
- These processes above are still considered as acute infection, thus Anti-HBc IgM
- In window period, only Anti-HBeAg is positive (because it is synthesized earlier). Anti-HBc IgM will be detected
Q 8. Describe pathophysiology of secondary hyperparathyroidism/ renal osteodystrophy in CKD
CKD -> impaired 1-alpha hydroxylase
- > impaired (1.25)-OH vitamin D production
- > impaired gut Ca2+ absorption -> increased PTH
- > increased bone resorption, osteodystrophy
Q 9. Explain the mechanism in which opioid cause RUQ abdominal pain
opioid constricts oddi sphincter of bile duct, causing increased bile duct pressure
-> biliary colic like symptom
Q 10. Which cancer is associated with chronic postmastectomy lymphedema?
Angiosarcoma
Q 11. Which cell releases cholecystokinin? How does total parenteral nutrition (say after bowel surgery) results in gallstone?
I cells in duodenum and jejunum
parenteral nutrition will deplete enteral stimulation, causing less cholecystokinin release
- > less gallbladder emptying
- > stasis -> gall stone
Amitryptiline
- drug class, mechanism of action
- side effects (what is special about this drug compared to to other drugs in same class)
- TCA, block reuptake of serotonin and NE
- tertiary amine: more anti-muscarinic effect than secondary amine, like nortriptyline
- also QT prolongation, and cardiotoxicity by Na+ channel blocker. Cardiotoxicity can be reversed by NaHCO3
Q 13. Which complex mediates mRNA intron splicing? where in the cell does it occur?
snRNP
intron splicing occurs in nucleus
Q 13. What is P bodies? where is it located?
mRNA quality control (turnover)
cytoplasm
Q 14. sproatic colorectal cancer vs. colitis associated colorectal cancer
- From which cell does it arise?
- grade: which one is more aggressive?
- molecular pathogenesis
- distribution
Sporatic CRC
- arise from polyps
- less aggressive, lower grade
- APC mutation -> KRAS mutation -> COX-2 overexpression -> p53 mutation
- focal
Ulcerative colitis associated CRC
- arise from flat lesion
- more aggressive, higher grade
- early p53 mutation, followed by APC mutation
- multi-focal
