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223 Cards in this Set
- Front
- Back
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Reed-Sternberg (RS) cells are characteristic of what disease?
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Hodgkin's disease
Note: ↓ RS cells and ↑ lymphocytes = good prognosis |
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Describe the appearance of Reed-Sternberg cells.
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Owl's eyes: binucleate or bilobed with the 2 halves as mirror images
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What are the general characteristics of Hodgkin's lymphoma?
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Presence of Reed-Sternberg cells
Localized, single group of nodes (rarely extranodal) Contiguous spread B signs/sx (fever, night sweats, weight loss) Mediastinal lymphadenopathy Bimodal age distribution (young & old), mostly men |
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What are the general characteristics of Non-Hodgkin's lymphoma?
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Multiple peripheral nodes, commonly extranodal
Noncontiguous spread No hypergammaglobulinemia Few B signs/sx (fever, night sweats, weight loss) Peak incidence: 20-40 years of age Majority are of B-cell origin |
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Which type of lymphoma is associated with HIV and immunosuppression?
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Non-Hodgkin's
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Which type of lymphoma is associated with EBV?
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Hodgkin's (50% of mixed cellularity Hodgkin's cases)
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What is the most common type of Hodgkin's lymphoma and who is it seen in?
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Nodular sclerosing; seen in young adults, women more than men (excellent prognosis)
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What type of Hodgkin's lymphoma is associated with the greatest number of RS cells?
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Mixed cellularity
Note: seen in older men; strongly associated with EBV |
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Which type of Hodgkin's lymphoma has few RS cells, occurs in men <35 years old, and has an excellent prognosis?
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Lymphocyte predominant
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Which type of Hodgkin's lymphoma has a poor prognosis?
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Lymphocyte depleted
Note: this is rare and is seen in older men with disseminated disease |
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This disease is characterized by a monoclonal immunoglobulin spike on serum protein electrophoresis and Ig light chains in urine.
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Multiple myeloma
Monoclonal immunoglobulin spike = M protein Ig light chains in urine = Bence Jones Protein |
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What are the clinical features related to multiple myeloma?
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Lytic bone lesions (bone pain, pathologic fractures, hypercalcemia); Renal insufficiency (anemia); Immunosuppression (recurrent infections, death)
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This is a monoclonal plasma cell cancer that arises in the marrow and produces large amounts of IgG or IgA.
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Multiple myeloma
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Name 3 types of B-cell Non-Hodgkin's lymphoma that are seen in adults.
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Small lymphocytic lymphoma; Follicular lymphoma; Mantle cell lymphoma
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This type of T-cell Non-Hodgkin's lymphoma is most often seen in children.
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Lymphoblastic lymphoma
Note: commonly presents with ALL and mediastinal mass; very aggressive |
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Which type of Non-Hodgkin's lymphoma is decribed as having a Starry-sky appearance?
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Burkitt's lymphoma (starry-sky represents sheets of lymphocytes with interspersed macrophages)
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What is the difference between the endemic and sporadic forms of Burkitt's lymphoma?
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Endemic (African) form presents as a jaw lesion while the sporadic form presents in the pelvis or abdomen
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This is the most common form of adult non-Hodgkin's lymphoma.
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Diffuse large cell lymphoma
Note: majority are B cell (80%); 20% occur in kids; aggressive, but 50% are curable |
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What disorder is associated with t(9;22)?
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CML; this is the Philadelphia chromosome which produces a bcr-abl hybrid gene
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What disorder is associated with t(8;14)?
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Burkitt's lymphoma (c-myc becomes activated by moving nect to the heavy-chain Ig gene)
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What disorder is associated with t(14;18)?
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Follicular lymphoma (bcl-2 activation)
Note: bcl-2 inhibits apoptosis |
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What disorder is associated with t(15;17)?
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M3 type of AML (acute promyelocytic leukemia)
Note: this disorder is responsive to all-trans retinoic acid |
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What disorder is associated with t(11;22)?
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Ewing's sarcoma
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What disorder is associated with t(11;14)?
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Mantle cell lymphoma
Note: this lymphoma is CD5+ and has a poor prognosis |
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What is the leukemoid reaction?
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Very high leukocyte count with a left shift (80% bands) and ↑ leukocyte alkaline phosphatase
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Name 3 consequences of leukemia due to bone marrow failure.
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Anemia (↓ RBCs), infections (↓ mature WBCs), hemorrhage (↓ platelets)
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This type of leukemia is TdT+, has many lymphoblasts, and may spread to the CNS and testes.
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ALL
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What is a characteristic histological finding of AML?
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Auer rods (peroxidase-positive cytoplasmic inclusions in granulocytes and myeloblasts)
Note: Treatment of AML can release auer rods → DIC |
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This type of leukemia presents in older adults with lymphadenopathy and hepatosplenomegaly, but has few symptoms and an indolent course.
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CLL
Note: CLL may also present with warm antibody autoimmune hemolytic anemia |
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What specialized type of cells are seen in the peripheral blood smear of a patient with CLL?
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Smudge cells (small lymphocytes that are disrupted)
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This disorder is defined by a myeloid stem cell proliferation and the Philadelphia chromosome.
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CML
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Describe the appearance of the cells in Hairy cell leukemia, and name the characteristic stain used.
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The cells have filamentous, hair-like projections and stain positive for TRAP (tartrate-resistant acid phosphatase)
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List the age profile for ALL, AML, CML, and CLL.
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ALL: <15
AML: 15-40 CML: 30-60 CLL: >60 |
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What is Histiocytosis X?
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An infiltrate in the lung of Langerhans cells from the monocyte lineage. Primarily occurs in young adults who smoke. Birbeck granules are seen on EM.
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What is the mechanism of heparin?
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Catalyzes the activation of antithrombin III, ↓ thrombin (IIa) and Xa.
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Name the drug used to reverse the actions of heparin and describe its mechanism.
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Protamine sulfate is used. It is a positively charged molecule that acts by binding negatively charged heparin.
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What is heparin used for?
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Immediate anticoagulation for pulmonay embolism, stroke, angina, MI, DVT. Can be used during pregnancy (doesn't cross placenta)
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What are the side effects/toxicity of heparin?
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Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions
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How do the low-molecular-weight heparins (enoxaparin) differ from heparin?
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LMW heparins act more on Xa, have better bioavailability and longer half-life, and can be given subcutaneously
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What is the mechanism of heparin-induced thrombocytopenia (HIT)?
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Heparin binds to platelets, causing autoantibody production that destroys platelets and overactivates the remaining ones, resulting in a thrombocytopenic, hypercoagulable state.
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What test is used to monitor Heparin?
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Partial thromboplastin time (PTT); intrinsic pathway
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What are the mechanism and use of Lepirudin and Bivalirudin?
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These drugs directly inhibit thrombin. They are used as an alternative to heparin for patients with HIT.
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What is the mechanism of Warfarin?
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Interferes with normal synthesis and γ-carboxylation of vit. K-dependent factors (2, 7, 9, 10, protein C and S)
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What is Warfarin used for?
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Chronic anticoagulation. Not used in pregnancy (crosses placenta).
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What test is used to monitor Warfarin?
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Prothrombin time (PT) or INR; extrinsic pathway
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What are the side effects/toxicity of Warfarin?
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Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions (metabolized by CYP450 system)
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How do you treat an acute overdose of Warfarin?
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Give IV vitamin K and fresh frozen plasma
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Compare heparin and warfarin in terms of route of administration.
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Heparin is given parenterally (IV, SC)
Warfarin is given orally |
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Compare heparin and warfarin in terms of site and duration of action.
|
Heparin works in the blood acutely (hours), warfarin works in the liver chronically (days)
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Compare heparin and warfarin in terms of on-set of action.
|
Heparin is rapid (seconds), warfarin is slow (limited by the half-lives of normal clotting factors)
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What are the thrombolytic drugs?
|
Streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)
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What is the mechanism of the thrombolytic drugs?
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aid in conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots
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What is the effect of the thrombolytics on PT, PTT, & platelet count?
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Increased PT, Increased PTT, No change in platelet count
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How do you treat toxicity with thrombolytics?
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aminocaproic acid (an inhibitor of fibrinolysis)
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Which platelet receptor binds to exposed collagen on an injured vascular endothelium?
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GP Ia
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Which platelet receptor forms fibrinogen bridges between platelets?
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GP IIb/IIIa
|
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Which platelet receptor binds vWF bound to collagen?
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GP Ib
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What is the mechanism of Aspirin?
|
irreversibly acetylates COX1 and COX2 preventing conversion of arachidonic acid to TXA2
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What is the effect of aspirin on bleeding time, PT, & PTT?
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Aspirin increases bleeding time with no effect on PT or PTT
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What are toxicities associated with aspirin?
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gastric ulceration, bleeding, hyperventilation, Reye's syndrome, tinnitus (CNVIII)
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What is the mechanism of Clopidogrel & Ticlopidine?
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inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa expression
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What toxicity is associated with Clopidogrel & Ticlopidine?
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neutropenia
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What is the mechanism of Abciximab?
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monoclonal antibody that binds GP IIb/IIIa on activated platelets preventing aggregation
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What phase of the cell cycle do vinca alkaloids inhibit?
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M phase
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What phase of the cell cycle do taxols inhibit?
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M phase
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What phase of the cell cycle do the antimetabolites inhibit?
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S phase
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What phases of the cell cycle does Etoposide inhibit?
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S phase and G2 phase
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What phase of the cell cycle does Bleomycin inhibit?
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G2 phase
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What is the mechanism of methotrexate?
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S phase antimetabolite. Folic acid analog that inhibits DHFR causing a decrease in dTMP and therefore decreased DNA & protein synthesis
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What are the clinical indications of methotrexate?
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leukemias, lymphomas, choriocarcinoma, sarcomas, abortion, ectopic pregnancy, RA, psoriasis
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What is a toxicity of methotrexate?
|
myelosuppression
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How can you reverse myelosuppression due to methotrexate?
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leucovorin (folinic acid)
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What is the mechanism of 5-fluorouracil?
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S phase antimetabolite. Pyrimidine analog bioactivated to 5F-dUMP which covalently complexes folic acid & thus inhibits thymidylate synthase. This causes a decrease in dTMP and therefore a decrease in DNA and protein synthesis.
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What are the clinical indications of 5-fluorouracil?
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colon cancer & other solid tumors & basal cell carcinoma
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What is a toxicity of 5-fluorouracil?
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myelosuppression
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How can you reverse myelosuppression due to 5-fluorouracil?
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thymidine (NOT leucovorin)
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What is the mechanism & clinical indication of Cytarabine (ara-C)?
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Inhibits DNA polymerase used to treat AML
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What is the mechanism of Cyclophosphamide, ifosfamide?
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alkylating agents which covalently cross link DNA at guanine N-7
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What is the clinical use of Cyclophosphamide, ifosfamide?
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Non-Hodgkin's lymphoma, breast & ovarian carcinomas, immunosuppressant
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What is the mechanism of the nitrosureas (carmustine, lomustine, semustine, streptozocin)?
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alkylate DNA (can cross BBB)
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What is the clinical use of the nitrosureas?
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brain tumors including glioblastoma multiforme
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What is the mechanism of cisplatin & carboplatin?
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alkylating agents which covalently cross link DNA at guanine N-7
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What is the clinical use of cisplatin & carboplatin?
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testicular, bladder, ovary, & lung carcinomas
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What are the toxicities associated with cisplatin & carboplatin?
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nephrotoxicity and acoustic nerve damage
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What is the mechanism of Busulfan?
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alkylates DNA
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What is the clinical indication of Busulfan?
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CML
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What are the toxicities associated with Busulfan?
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pulmonary fibrosis & hyperpigmentation
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What is the mechanism of Doxorubicin (adriamycin) & daunorubicin?
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generates free radicals & noncovalently intercalates in DNA causing strand breaks
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What are the toxicities of Doxorubicin (adriamycin) & daunorubicin?
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cardiotoxicity, myelosuppression, marked alopecia, toxic extravasation
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What is the mechanism of Dactinomycin (actinomycin D)?
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intercalated in DNA
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What is the clinical use of Dactinomycin?
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Wilm's Tumor, Ewing's Sarcoma, Rhabdomyosarcoma
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What is the mechanism of bleomycin?
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induces formation of free radicals which cause DNA strand breaks
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What is the mechanism of hydroxyurea?
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Inhibits ribonucleotide reductase which decrease DNA synthesis (S-phase specific)
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What are the clinical uses of hydroxyurea?
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Melanoma, CML, sickle cell disease
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What is the mechanism of Etoposide (VP-16)?
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G2 phase specific agent that inhibits topoisomerase II and increase DNA degradation
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What are the clinical uses of Etoposide (VP-16)?
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small cell carcinoma of the lung and prostate & testicular carcinoma
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What is the mechanism of Prednisone?
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may trigger apoptosis (may even work on nondividing cells)
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What are the side effects of Prednisone?
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cushing-like symptoms, immunosuppression, cataracts, acne, osteoporosis, hypertension, peptic ulcers, hyperglycemia, psychosis
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What is the mechanism of Tamoxifen & Raloxifene?
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Receptor antagonists in the breast and receptor agonists in bone; block the binding of estrogen to ER positive cells
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What are the clinical uses of Tamoxifen & Raloxifene?
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Breast Cancer & Osteoporosis Prevention
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What is the mechanism of Trastuzumab (Herceptin)?
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monoclonal antibody against HER-2 (erb-B2) which helps kill breast cancer cells that overexpress HER-2 (possibly through antibody mediated cytotoxicity)
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What is the use of Trastuzumab (Herceptin)?
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metastatic breast cancer
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What is the major toxicity of Trastuzumab (Herceptin)?
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cardiotoxicity
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What is the mechanism of Imatinib (Gleevec)?
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Philadelphia chromosome bcr-abl tyrosine kinase inhibitor
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What are the clinical indications for Imatinib (Gleevec)?
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CML & GI stromal tumors
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What is the side effect associated with Imatinib (Gleevec)?
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fluid retention
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What is the mechanism of vincristine & vinblastine?
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M-phase specific alkaloids that bind to tubulin & block the polymerization of microtubules so that the mitotic spindle cannot form
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What are the clinical indications for vincristine & vinblastine?
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lymphoma, Wilm's tumor, & choriocarcinoma
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What are the side effects of vincristine?
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neurotoxicity (areflexia, peripheral neuritis) & paralytic ileus
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What is the major side effect of vinblastine?
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bone marrow suppression
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What is the mechanism of the taxols including Paclitaxel?
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M phase specific agents that bind to tubulin & hyperstabilize polymerized microtubules so that the mitotic spindle cannot break down (anaphase cannot occur)
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What are the clinical indications of the taxols?
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ovarian and breast carcinomas
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What are the toxicities associated with the taxols?
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myelosuppression & hypersensitivity
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A antigens on RBCs, anti-B antibodies in plasma
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Blood Groups
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B antigens on RBCs, anti-A antibodies in plasma
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Blood Groups
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A and B antigens on RBCs, no anitbodies
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Blood Groups
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No antigens, A and B antibodies in plasma
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Blood Groups
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Type O
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Blood Groups
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Type AB
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Blood Groups
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Rh+ blood given to an Rh- recipient (massive IgG response)
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Blood Groups
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Biconcave
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RBC Forms
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Hereditary spherocytosis, autoimmune hemolysis
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RBC Forms
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herediatry elliptocytosis
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RBC Forms
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megaloblastic anemia, bone marrow failure
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RBC Forms
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DIC, traumatic hemolysis
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RBC Forms
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G-6-PD deficiency
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RBC Forms
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Spiny RBC seen in abetalipoproteinemia
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RBC Forms
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HbC disease, Asplenia, Liver disease, Thalassemias
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RBC Forms
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TTP/HUS, microvascular damage, DIC
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RBC Forms
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Thalassemias, Anemia of chronic disease, iron deficiency, lead poisoning
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RBC Forms
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Megaloblastic anemia
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RBC Forms
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Iron deficiency, Thalessemias, Lead poisoning
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Anemia
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Megaloblastic anemias (Vit B12/folate deficiency), DNA-synth inhibiting drugs,
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Anemia
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acute hemorrhage, enzyme defects (G6PD), RBC membrane defects, bon marrow disorders, autoimmune hemolysis, Anemia of chronic disease
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Anemia
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RBC hemolysis
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Lab Values in Anemia
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decr, incr, decr, very decreased
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Lab Values in Anemia
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decr, decr, incr, normal
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Lab Values in Anemia
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normal, incr, normal, decr
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Lab Values in Anemia
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incr, decr, incr, very increased
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Lab Values in Anemia
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pancytopenia resulting from failure/destruction of myeloid multipotent stem cells
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Aplastic anemia
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radiation, drugs/chemicals (benzene, immunosuppressants), viral (B19, EBV, HIV, acute hepatitis), Fanconi's anemia, idiopathic
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Aplastic anemia
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fatigue/malaise, infections, abnormal bleeding/petechiae/purpura
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Aplastic anemia
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pancytopenia (but normal cell morphologies), Bone marrow: hypocellular, increase fat infiltration
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Aplastic anemia
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withdraw offending agent, BM transplant, transfusion, G-CSF or GM-CSF
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Aplastic anemia
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glutamic acid --> valine in Beta chain of HgB gene
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Blood Dyscrasias
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aplastic crisis (B19 infection), autosplenectomy (incr risk of encapsulated bacterial infections, Salmonella osteomyelitis), vaso-occlusive pain crises, renal papillary necrosis, splenic sequestration syndrome
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Blood Dyscrasias
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hydroxyurea (increase HbF); BM transplant
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Blood Dyscrasias
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african americans
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Blood Dyscrasias
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malaria
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Blood Dyscrasias
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Underproduction of one or more of the alpha HgB chains (there are 4)
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Blood Dyscrasias
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Absent Beta chain production (homozygote), severe anemia
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Blood Dyscrasias
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Bone marrow expansion/abnormatlity; seen in Sickle Cell and Beta-Thal major
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Blood Dyscrasias
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Incr serum bilirubin (jaundice, pigmented gallstones), incr reticulocytes (marrow compensation)
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Hemolytic Anemias
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Paroxysmal nocturnal hemoglobinuria, microangiopathic anemia
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Hemolytic Anemias
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|
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Autoimmune (most), hereditary spherocytosis
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Hemolytic Anemias
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|
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Coombs Test (anti-Ig Abs added to patients RBCs, positive if agglutination occurs)
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Hemolytic Anemias
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IgG
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Hemolytic Anemias
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SLE, CLL, drugs (methyldopa)
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Hemolytic Anemias
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IgM
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Hemolytic Anemias
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|
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infections (mycoplasma pneumoniae, infectious mononucleosis), triggered by cold
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Hemolytic Anemias
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Spectrin or ankyrin
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Hemolytic Anemias
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Incr MCHC and RDW
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Hemolytic Anemias
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Osmotic fragility test (increased in HS)
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Hemolytic Anemias
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|
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Impaired GP I anchor synthesis (membrane defect --> increased sensitivity to complement lysis)
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Hemolytic Anemias
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DIC, TTP/HUS, SLE, malignant hypertension
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Hemolytic Anemias
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Schistocytes (helmet cells)
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Hemolytic Anemias
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coaguation cascade activation, microthrombi production, consumption of platelets, coagulation factors, and fibrin
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DIC
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Gm- sepsis, Trauma, OB/GYN complications, acute Pancreatis, malignancy, nephrotic syndrome, transfusion
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DIC
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Incr PT, PTT, fibrin split products (d-dimers), decr platelet count. Schistocytes on blood smear
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DIC
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frequent nose bleeds (epistaxis), bleeding gums, petechiae/purpura; incr bleeding time
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Bleeding Disorders
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platelyet defects --> mucous membrane defects
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Bleeding Disorders
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ITP, TTP, DIC, aplastic anemia, drugs
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Bleeding Disorders
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hemoarthrosis (joint bleeding), easy brusing, incr PT and/or PTT
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Bleeding Disorders
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Coagulation factor defects
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Bleeding Disorders
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Hemophilia A/B, von Willenbrand disease
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Bleeding Disorders
|
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decr, incr, normal, normal
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Hemorrhagic disorders
|
|
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normal, normal, normal, incr
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Hemorrhagic disorders
|
|
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normal, incr, normal, incr
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Hemorrhagic disorders
|
|
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decr, incr, incr, incr
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Hemorrhagic disorders
|
|
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normal, normal, incr, incr
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Hemorrhagic disorders
|
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decr, incr, normal, normal
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Hemorrhagic disorders
|
|
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normal, incr, normal, normal
|
Hemorrhagic disorders
|
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platelet adhesion (GP Ib deficiency)
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Hemorrhagic disorders
|
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platelet aggregation (GP Iib-IIIa deficiency)
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Hemorrhagic disorders
|
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Extrinsic factors (II, V, VII, X)
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Hemorrhagic disorders
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|
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Intrinsic factors all except VII
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Hemorrhagic disorders
|
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Which types of lymphocytes are of lymphoid stem cell origin
|
B Cells (including plasma cells) and T cells
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|
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What is the WBC differential from highest to lowest?
|
Neutrophils > Lymphocytes > Monocytes > Eosinophils > Basophils
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|
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Main energy source for RBCs
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Glucose
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Definition of anisocytosis
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Varying sizes of RBCs
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Definition of poikilocytosis
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Varying shapes of RBCs
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WBCs (2) that mediate allergic reaction
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Basophil, mast cell
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|
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Substances (4) found in basophil's granules
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Heparin, histamine, leukotrienes, other vasoactive amines
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|
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Which type of WBC does a mast cell resemble structurally and functionally?
|
Basophil
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|
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What type of hypersensitivity reactions are mast cells involved in?
|
Type I
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Which type of WBC defends against helminthic and protozoan infections?
|
Eosinophil
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|
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What are 5 causes of eosinophilia?
|
Neoplastic, Asthma, Allergic processes, Collagen vascular diseases, Parasites
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|
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Which type of WBC has a multilobed nucleus?
|
Neutrophil
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|
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In what disease states does one see hypersegmented neutrophils?
|
Vitamin B12/folate deficiency
|
|
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Which WBC has a kidney shaped nucleus and a frosted glass cytoplasm
|
Monocyte
|
|
|
What is the main function of macrophages?
|
Phagocytose bacteria, cell debris, and senescent RBCs and scavenges damaged cells and tissues
|
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What is a substance that activates macropages?
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IFN-gamma
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Macrophages use which MHC class to present antigens?
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Class II
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What cells are professional APCs?
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Dendritic cells
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Which WBCs have round, densely staining nucleus?
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Lymphocytes
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Where do B cells arise from?
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Stem cells in bone marrow
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When a B cell encounters antigen, what does a B cell differentiate to, and produce?
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Plasma cells, and they produce antibodies
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Which type ofWBC has an off-center nucleus and clock-face chromatin?
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Plasma cells, and they produce antibodies
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Multiple myeloma is a neoplasm of what cells?
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Multiple myeloma
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Where do T cells originate from?
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Stem cells in bone marrow, and mature in thymus
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The majority of circulating lymphocytes are what kind of cells?
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T cells
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Cytotoxic T cells are CD_____ and receive antigen presentation from MHC Class ______
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CD8, MHCI
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Helper T cells are CD ______ and receive antigen prenstation from MHC _____
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CD4, MHC II
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What factors are involved in the intrinsic clotting pathway (before convergence)
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XII, XI, IX, VIII, X
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What factors are involved in the extrinsic clotting pathway (before convergence)
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VII, tissue factor
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Factor Va converts what to what?
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Prothrombin to thromin
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Thrombin converts what to what?
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Fibrinogen to fibrin
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What are the vitamin K-dependent coagulation factors?
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II, VII, IX, X, protein C, protein S
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What does activated protein C do?
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Inactivates Factors Va and VIIIa
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What does antithrombin III do?
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Inactivates thrombin, IX a, X a, XI a
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What does tPA do?
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Genetrates plasmin from plasminogen, which cleaves fibrin clots
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Factor V Leiden mutation causes resistance to what?
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Activated Protein C
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Activation of the kinin cascade causes what three effects?
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Increased vasodilation, increased permeability, increased pain
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