Heme
What byproduct(s) would you expect to be increased if you are dealing with a B12 deficiency? Hint: think about RBC lifecycle
Increased homocysteine and methionine (vs folate deficiency is just increased homocysteine).
What type of necrosis is characteristic of myocardial infarction?
Coagulative necrosis
What markers are positive in Reed-Sternberg cells?
CD15, CD30, PAX5
What type of hypersensitivity reaction is Goodpasture?
Type II hypersensitivity
Which pneumoconiosis is typically found in the lower lung?
Asbestos
Give expected lab values for anemia of chronic disease vs iron deficient anemia (100 points for ACD and 100 points for IDA)
Iron deficiency anemia:
Anemia of chronic disease:
Which cell type mediates clearance of infected myocytes during viral myocarditis?
Cytotoxic T-cells (CD8+, NK cells)
What is the main difference between latent vs lytic EBV?
What does IgG attack on type IV collagen in Goodpasture?
NC1 on alpha3 chain of type IV collagen
Name 4 drugs that can cause drug-induced pulmonary diseases (50 points each).
What drug inhibits the ATP-binding site of BCR-ABL?
Imatinib
Should beta blockers be given before or after vasodilation in acute aortic dissection? Why? (150 points each)
Beta blockers should be given before vasodilators; B-blockers lower shear stress. If you give vasodilators before or without B-blockers, the shear stress increased and worsens the dissection.
How do malignant follicles differ from reactive follicles?
Loss of polarization; packed follicles; absent tangible bodies
Which two IHC stains are positive in mesothelioma?
Calretinin, CK5/6
DOUBLE OR NOTHING: How does Hep B infection contribute to PAN pathogenesis?
HPV infection leads to circulating HBsAg that forms immune complexes w/ anti-HBs antibodies. The complexes deposit in medium sized arteries, activating complement and recruiting neutrophils. This produces a transmural inflammation and fibrinoid necrosis that is characteristic of PAN.
How does a c-KIT mutation worsen the prognosis of AML w/ t(8;21)?
C-Kit mutations provides a stronger proliferative and survival signal that overrides the (normally favorable) t(8;21) AML. This leads to increased blast expansion, chemo resistance, and higher relapse rate.
DOUBLE OR NOTHING: Give the risk of rupture stats/percentages related to size for aortic dissection. (Frazier said we will need to know this).
How does mediastinal mass formation relate to T-cell origin?
Thymic tumor --> mediastinal mass formation
Fill in the blank - Small cell lung cancer works on the (anterior/posterior) pituitary system to release (ADH/ACTH) causing (SIADH/Cushing syndrome).
Small cell lung cancer works on the anterior pituitary system to release ACTH causing Cushing syndrome.
How does damage to type II pneumocytes worsen ARDS? Can you give a basic pathogenesis of ARDS? (200 points each)
Pathophys of ARDS:
A patient with MPO+ blasts has t(15;17). Explain PML-RARA fusion --> blocked differentiation --> DIC risk --> ATRA mechanism restoring maturation
TLDR:
t(15;17) creates the PML-RARA fusion protein --> inhibits transcription needed for myeloid differentiation --> promyelocytes accumulate --> granule release triggers DIC.
ATRA binds RARA --> releases transcription block --> forces differentiation --> reduces promyelocytes --> resolves DIC risk
Given the timeline of MI healing, what histologic findings would you expect 10-14 days post-MI, and how do they correlate w/ wall stability?
Histologic findings:
How does t(14;18) alter germinal center biology and why does this lymphoma transform into DLBCL?
BCL2 overexpression blocks apoptosis --> germinal center escape --> risk of transformation to DLBCL.
A woman has a peripheral lung nodule that stains TTF-1+. Explain the oncogenic pathway of EGFR mutations --> tumor growth --> response to TKIs and why KRAS mutations prevent response.
TLDR: EGFR stuck on and don’t die -->activates MAPK + PI3K pathways. TKIs work well on tumors that depend on EGFR. If KRAS is mutated, KRAS is stuck on and don’t die downstream. This process does not require EGFR so blocking it with TKIs fails.
A 58 y/o M presents w/ progressive fatigue and bone pain. Labs show anemia, hypercalcemia, and elevated creatinine. Serum protein electrophoresis reveals an M-spike, and bone marrow biopsy shows 30% plasma cells. Renal biopsy demonstrates fractured eosinophilic casts obstructing distal tubules, surrounded by multinucleated giant cells. What is the mechanism that best explains this patient’s renal failure?
Multiple myeloma produces excess free light chains that precipitate in tubules, forming toxic casts. This causes tubular obstruction and renal injury (cast nephropathy).