Hema/Onco 3 Flashcards
What do the lab results for Hemolytic uremic syndrome look like? (Hgb, haptoglobin, BT, PT, aPTT)
HUS is usually due to Shigella-like toxins entering the circulation and inducing capillary endothelial damage, resulting in microthrombi formation, leading to thrombocytopenia and hemolytic damage.
>dec. Hgb, dec. haptoglobin.
>Inc. BT, normal PT and aPTT.
What is the Virchow triad for venous thromboembolism?
> endothelial injury, venous stasis, hypercoagulable state.
>RFs: immobility after surgery, cancer, HTN, hyperlipidemia.
Why are patients w/ hemolytic anemias (ex. SCD) prone to developing megaloblastic anemia?
Pts w/ SCD or other hemolytic anemias are prone to folic acid deficiency due to inc. erythrocyte turnover. Low folic acid levels impair DNA synthesis and pts will produce macrocytes.
What is the gene that allows for tumor cells to become resistant to chemotherapy?
The MDR1 gene codes for for P-glycoprotein, a transmembrane ATP-dependent efflux pump found on the endothelium of the BBB where it prevents substances from entering the CNS. It’s also on intestinal and renal tubular cells to eliminate foreign compounds. In tumor cells, this pump actively removes chemotherapeutic agents.
How do you treat cyanide toxicity?
Cyanide binds to Fe3+, inhibiting cytochrome c oxidase in the mitochondria and preventing oxidative phosphorylation. Nitrates oxidize Fe2+ to Fe3+ in hgb, forming Methemoglobin, w/c can bind and sequester cyanide int he blood, thus limiting its toxic effects.
What is a major side effect of Vincristine?
Vincristine binds to B-tubulin and interferes w/ microtubule formation. As such, it can cause neurotoxicity due to interference w/ microtubule formation in nerve axons (peripheral neuropathy).
What is the genetic mutation and presentation associated w/ follicular lymphoma?
> t(14;18) translocation, overexpression of Bcl-2 oncogene.
Waxing and waning painless lymphadenopathy
Cleaved nuclei in follicle center cells.
