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Heme Onc Step 1
| Question | Answer |
|---|---|
| What types of cells does a myeloblast give rise to? | neutrophils, basophils, eosinophils |
| What are two enzymes released from eosinophils? | histaminase and arylsulfatase, help limit reaction following mast cell degranulation |
| What effects does bradykinin have? | incr vasodilation, permeability, pain |
| What is the pathogenesis of Glanzmann's disease? | absent GpIIb/IIIa recepts - no platelet aggregation w/ fibrinogen |
| Which diseases have abnormal ristocetin cofactor assay? | Class vWD and Bernard-Soulier disease (absent GpIb receptors) |
| What causes Heinz bodies? | Oxidation of ferrous to ferric iron leads to denature Hgb precipitation and membrane damage |
| What are some causes of nonmegaloblastic macrocytic anemia? | liver disease, alcoholism, reticulocytosis, orotic aciduria, drugs: 5FU, AZT, Hydroxyurea |
| What is the pathogenesis of Anemia of Chronic Disease? | liver synthesis and release of hepicidin; prevents release of Iron to Transferrin; decr Fe, TIBC, incr ferritin |
| What enzyme defect results in Acute Intermittent Porphyria? | Porphobilinogen deaminase (uroporhyrinogen-I-synthase) |
| What causes ITP? | anti-GpIIb/IIIa Ab |
| What causes TTP? | deficiency of ADAMTS13 (vWFmetalloproteinase) decr degradation of vWF multimers |
| Where is EPO synthesized? | renal cortex by interstitial cells in the peritubular capillary bed |
| Why do men have higher Hgb levels? | testosterone stimulates erythropoiesis; also lack of cyclic bleeding |
| How do Heinz bodies form? | peroxide oxidized Hgb which precipitates |
| What activates factor VII in the extrinsic coagulation system? | tissue thromboplastin (factor III) which is released from injured tissue |
| What does the prothrombin complex consist of? | Factor Xa, factor V, PF3 (phospholipid), Ca |
| What causes post-transfusion purpura? | pt receives blood and has Ab against platelet specific antigens that are on the donor platelets |
| What are the clinical findings of TTP? | fever, thrombyocytopenia, renal failure, microangiopathic hemolytic anemia, CNS deficits |
| If a mixing study does not correct prolonged PT or PTT, what is the most likely cause of disease? | circulating antibodies causing immune destruction (most commonly anti-VIII post-partum) |
| What are the causes and clinical findings of primary fibrinolysis? | open heart surgery and diffuse liver disease (decr alpha2-antiplasmin), prostatectomy (release of urokinase); severe bleeding with (+) FDPs and (-) D-dimer assay |
| What is involved in a major crossmatch? | pt serum (check for Ab against foreign antigens on donor RBCs) added to donor RBCs |
| What type of blood products must an IgA deficient pt receive? | blood or blood products that lack IgA (to prevent severe anaphylactic reaction due to IgE Ab) |
| What can protect a mother from developing Rh sensitization? | ABO incompatibility (fetal RBCs will be destroyed immediately upon entering mother's circulation) |
Created by:
ash0403
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