3/18 UWORLD test # 50 Flashcards
Q 4. Gram negative bacteria mediates septic shock by LPS. What is it composed of? (3) Which one mediates toxic effect?
O antigen
core polysaccharide
lipid A
- lipid A is toxic component
Q 5. Abnormal heart sound right before S1. what is this heart sound? what is underlying cause of this heart sound?
S4: PRESYSTOLIC
Atrial kicking due to increased stiffness of ventricular wall
Q 5. When does S3 heart sound heard? right before S1? S2? after S2? between S1 & S2?
Right after S2: POSTSYSTOLIC
Q 6. Renal cell carcinoma: describe histologic finding
clear cytoplasm enriched with lipid & glycogen
Q 7. Why surgeons need to preserve prostatic fascia during prostatectomy?
(Hint: think about nerve)
to prevent erectile dysfunction by disrupting cavernous nerves.
prostatic fascia contains inferior hypogastric plexus. Cavernous nerve, which mediates erection, is continuation of inferior hypogastric plexus
Q 10. What is anergy? Does it lead to apoptosis of T cell?
PROLONGED UNRESPONSIVENESS of T cell as immune tolerance when BOTH MHC/TCR and B7/CD28 interactions are formed.
anergy does NOT lead to apoptosis of T cell. It is just prolonged unresponsive state
Q 10. What is activation induced T lymphocyte death? What disease may develop if this process is impaired?
activated T cells undergo apoptosis via Fas-FasR mediated pathway when it gets continuously stimulated by self-antigen. This is developed to prevent development of over-active T cells that attack self tissue.
Impaired activation induced T cell death will lead to autoimmune disease
Q 11. Central DI may be due to direct to damage to what structure? hypothalamus? or posterior pituitary gland? or both?
hypothalamus: this is where ADH is synthesized.
Posterior pituitary serves as exit route where ADH gets released. Damage may lead to TRANSIENT DI, but if hypothalamus is intact, axonal regeneration and hypertrophy can allow adequate ADH sercretion into blood stream
Q 12. Buspirone
- MOA
- indication
- pharmacokinetics to note
- 5HT1A agonist
- 2nd line for generalized anxiety disorder
( 1st line is SSRI/SNRI) - slow onset: takes 1-2 weeks to take effect
Q 15. lead poisoning
- peripheral blood smear
- bone marrow blood smear
- peripheral blood smear: basophilic stippling
- bone marrow blood smear: sideroblastic ring
sideroblastic ring: defect in heme synthesis
where synthesis occurs? bone marrow
Q 17. Cerebral amyloid angiopathy
- what patient history suggest it?
- what amyloid is deposited?
- common site in brain for amyloid deposition
- recurrent history of cerebral hemorrhage
- beta amyloid (same as Alzheimer’s)
- commonly deposits in occipital and parietal lobes
Q 18. Triad of hemochromatosis? Does this happens all the time? what about other manifestations (3)
triad: bronze diabetes
- skin pigmentation
- diabetes
- hepatomegally (cirrhosis)
- These triads may happen in the late course of disease, so all of them may not be presented in question
- other manifestations
1. cardiomyopathy (arrythmia, dilated cardiomyopathy)
2. arthralgia
3. hypoganadism
Q 21. Concentration of anesthetic drug shows slow increase over time in what type of tissue?
poorly vascularized tissues (muscle, fat, bone).
site of action of anesthetic drug is CNS.
Recovery from anesthesia indicates drug is REDISTRIBUTED to poorly vascularized tissues from
well vascularized structures (CNS, kidney, lungs)
Q 22. How does HUS/TTP change serum indirect bilirubin level?
increased indirect bilirubin
Intravascular hemolysis -> heme -> indirect bilirubin
Q 22. What is heptoglobin? How does intravascular hemolysis changes haptoglobin level?
heptoglobin is hemoglobin scavenger molecule. That is it binds to free hemoglobin and take it back to spleen for recycle
