March 28 - Heme/onc Flashcards Preview

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Flashcards in March 28 - Heme/onc Deck (19):

Azathioprine/ 6-mercaptopurine pathway

Azathioprine is prodrug activated to 6-mercaptopurine

6-mercaptopruine can be converted to active metabolites by HGPRT

Can be converted to inactive metabolites by xanthine oxidase or TPMT


Factor Xa vs thrombin inhibitors

Direct factor Xa inhibitors: rivaroxaban and apixaban (X in name)

Direct thrombin inhibitors: Argatroban, bivalirudin, dabigatran. Drugs of choice in HIT


Factors made in endothelial cells

vWF and VIII


Tumor basement membrane penetration

1. Detach from surrounding cells by decreasing adhesion molecule expression (e-cadherin)
2. Adhere to BM by increaseing laminin and other adheion molecules
3. Invade BM by secreting proteolytic enzymes like metalloproteinases


Proteosome inhibitors

Used in multiple myeloma, Causes accumulation of toxic intracellular proteins which leads to apoptosis of malignant plasma cells


Burkitt lymphoma translocation

t(14;18). c myc and Ig heavy chain. Associated with EBV



Anorexia, malaise, anemia, weight loss, and wasting seen in cancer. Mediated by TNF-alpha which is produced by some neoplastic cells



In ifection, produced by macropahges and increases acute phase reactants.

In cancer, produced by neoplastic cells and causes chachexia


Pure red cell aplasia

Hypoplasia of marrow erythroid elements with normal granulopoiesis and thrombopoiesis. Caused by inhibition of erythrocytic precursors and progenitors by autoantibodies and T cells. Associated with thymoma, parvovirus B19 infection


Fanconi anemia

Inherited aplastic anemia + short stature + absent thumbs



Caused by VEGF and fibroblast growth factor


Warfarin-induced skin necrosis pathophys

Not an allergic reaction to drug. Seen due to deficiency of protein C or S when starting warfarin leading to transient hypercoagulability and thrombotic occlusion of the micrvasculature, causing skin necrosis


Paroxysmal nocturnal hemoglobinuria: pathophysiology and presentation

Pathophysiology: Complement-mediated hemolysis. Caused by mutation in PIGA gene which helps to synthesize GPI anchor. GPI needed to attach CD55 and CD59 which inactivate complement. Thus, in their absence, get complement-mediated hemolysis.

Presentation: Hemolytic anemia. Thrombosis at atypical sites because lysed cells release prothrombotic factors. Pancytopenia due to stem cell injury. Hemosiderosis of kidney due to break down of iron-containing red cells and dposition in kidney


vWF function

1. Promotes platelet adhesion by crosslinking platelet glycoproteins (GpIb) with exposed collagen on damaged endothelium

2. Carries factor VIII, increasing its half life



Inhibits platelet aggregation


CML vs leukemoid reaction

both increase WBCs and increase precursor forms

CML causes decreased leukocyte alk phos as cells are cytogenetically abnormal
Leukemoid reaction has normal to increased leukocyte alk phos


Uremic platelet dysfunction

Seen in those with severe renal dysfunction. Accumulation of uremic toxins in circulation leads to decreased platelet aggregation and adhesion. This increases bleeding time but wiht normal platelet count.


T-ALL presentation

Can present with large anterior mediastinal mass (where thymus is(. Can compress great vessels leading to superior SVC syndrome, compress esophagus leading to dysphagia, and compress trachea leading to dyspnea and stridor


Thrombotic thrombocytopenic purpora pathogenesis

Decreased ADAMTS13 activity, either due to autoantibody or inerited defect. ADAMTS13 is a protease that normally vleaves vWF. Deficiency results in large vWF multimers that cause diffuse microvascular thrombi