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Step 1 11.29.12

Hematology IX

QuestionAnswer
What is the mechanism of leukemias? unregulated growth of leukocytes in BM--> incr or decr circulating leukocytes and marrow failure-->anemia, infections, hemmorhage. can see infiltrates in liver, spleen, LN
What are 5 types of lymphoid neoplasms? acute lympohblastic leukemia, AL lymphoma, small lymphocytic lymphoma (SLL), chronic lymphocytic leukemia (CLL), hairy cell leukemia
What is the onse and and presentation of Acute lymphoblastic leukemia/lymphoma (ALL)? < 15 y/o. may present with bone marrow invovlement in childhood and mediastinal mass in adolescent males
What happens to the BM in ALL and what biomarkers are useful? BM replaced by highly increased lymphoblasts. TdT+ (marker of pre-T and pre-B), CALLA+
What is the prognosis for ALL and what mutation gives a better prognosis? most respons. t(12;21) = better prognosis
What is the danger spread of Acute lymphoblastic leukemia/lymphoma (ALL)? CNS and testes
When and how does Small lymphocytic lymphoma (ALL)/chronic lymphocytic leukemia (CLL) present? age > 60 y/o. often Asx. warm Ab autoimmune hemolytic anemia
What is seen in PBS of Small lymphocytic lymphoma (ALL)/chronic lymphocytic leukemia (CLL) ? smudge cells
What is the difference between Small lymphocytic lymphoma (ALL) and chronic lymphocytic leukemia (CLL) ? CLL has peripheral blood plymphocytosis
When and how does hairy cell leukemia present? Adults. mature B cell tumor in the elderly
What is seen on PBS in hairy cell leukemia? filametous, hairlike projections
What is a key staining in hairy cell leukemia? stains TRAP (tartrate-resistant acid phosphatase) positive
What are 2 myeloid neoplasms?. acute myelogenous leukemia (AML), and Chronic myelongenous leukemia (CML)
What is the age and onset and what is seen in PBS in acute myelogenous leukemia (AML)? media onset at 60 y/o. auer rods and incr circulating myeloblasts on peripheral smear
What is significant about the t(15;17)---> M3 subtype of acute myelogenous leukemia (AML)? responds to all-trans retinoic acid (vit A) inducing differentiation of myeloblasts
What is a common presentation of acute myelogenous leukemia (AML)? disseminated intravenous coagulation (DIC)
What is the age of onset and what is a defining characteristic of Chronic myelongenous leukemia (CML)? Age 30-60 years. Defined by Philadelphia Chromosome (t 9;22, bcr-abl). myeloid stem cell proliferation
What is the philadelphia chromosome and what is it associated with? t9;22, bcr-abl. associated with Chronic myelongenous leukemia (CML)
How does chronic myelongenous leukemia (CML) present and what can it progress to? incr neutrophils, metamyelocytes, basophils; splenomegaly. can accelerate and tranform to AML or ALL
What is an importnant enzymatic characterisitc ofr chronic myelongenous leukemia (CML)? low leukocyte alkaline phosphatase due to immature granulocytes
What is the tx for chronic myelongenous leukemia (CML) and what is the mech of the drug? give imantinib ( small molecule inhibitor of bcr-abl tyrosine kinase)
What are Auer rods, when are they seen? peroxidase positive cytoplasmic inclusion in granulocytes and myeloblasts. commonly seen in promyelocytic leukenia M3 (AML)
What is a danger of treating AML M3? can cause release of auer rods which leads to disseminated intrvascular coagulation (DIC)
What is t 8;14 and what is it associated with? c myc activation in Burkitt's lymphoma
What is t (14;18) and what is it associated with? bcl-2 activation in Follicular lymphomas
What is t(15;17) associated with and does it mean? M3 type of AML mean its responsive to all-trans retinoic acid
What is t(11;22) associated with? Ewing's sarcoma
What is t (11;14) associated with? Mantle cell lymphoma
What is the pathogenesis of Langerhans cell histiocytosis (LCH)? proliferative disorder of dendritic cells from monocyte lineage. cell are functionally immature and cant stimulate T lymphocytes via Ag presentation
What are some key biomarkers and characterisitcs in Langerhans cell histiocytosis (LCH)? S-100 and CD1a expressed. see birbeck granules (tennis rackets) on EM
What are the levels of RBCs, WBCs, platelets seen in polycythemia vera? incr RBCs, incr WBCs, incr platelets
Does polycythemia vera have Philadelphia chromosomes or JAK2 mutations? YES to JAK2, not to philadelphia
What are the RBCs, WBCs and platelet levels seen in essential thrombocytosis? normal RBCs, normal WBCs, incr platelets
Does essential thrombocytosis have philadelphia chromosome or JAK2 mutations? 30-50% hav JAK2, no philadelphia
What RBC, WBC, and platelet leves are seen in myelofibrosis? decr RBCs, variable WBCs, variable platelets
Does myelofibrosis have JAK2 mutation of philadelphia chromisome? 30-50% have JAK2, none have philadelphia chromosome
What are the RBC, WBC, and platelet levels seen in CML? decr RBC, incr WBC, incr platelets
Does CML have a JAK2 mutation or philadelphia chrmosome? no JAK2, yes to philadelphia chromosome
What are the classic findings in polycythemia vera? abnormal clone of hematopoetic stem cells are increasingly sensitive to growth factors
What are the classic findings in essential thrombocytosis? similar to polycythemia vera, but specfic for megakaryocytes
What are the classic findings in myelofibrosis? fibrotic obliteration of bone marrow. tear drop cell. "Bone marrow is crying"
What are the classic findings in CML? bcr-abl tr4ansformation leads to incr cell division and apoptosis. DO NOT see JAK2 mutations
What plasma volume, RBC mass and O2 sat is seen in relative polycythemia? decr plasma volume, no change in RBCs, no O2 sat
What plasma volume, RBC mass and O2 sat is seen in appropriate absolute polycythemia? no change in plasma volume, incr in RBC mass, decr O2 sat
What disease is appropriate absolute polycythemia seen in? lung disease, CHD, high altidtude
What plasma volume, RBC mass and O2 sat is seen in inappropriate absolute polycythemia? no change in plasma volume, incr RBC mass, no change in O2 sat
What diseases is inappropriate absolute polycythemia? What is it due to? RCC, Wilm's tumor, cyst, HCC, hydronephrosis, due to ectopic eryhtropoetin
What plasma volume, RBC mass and O2 sat is seen in polycythemia vera? incr plasma volume, very incr RBCs, no change in O 2 sat
What is the mechanism of heparin? cofactor for activation of antithrombin. decr thrombin and Xa. short half life
What is the clinical use of heparin? Can it be used during pregnancy immediate anticoagulation for PE, stroke, acute coronary sndrome, MI, DVT. can used during pregnancy
What lab value should be followed on a pt on heparin? PTT
What are the major SE of heparin? thrombocytopenia (HIT), osteoporosis
What can be used for rapid reversal of heparin SE? How does it work? use protamine sulfate (positively charged that binds negatively charged heparin)
What is the advantages and disadvantages of low molecular weight heparins? act more on Xa, better bioavailability. can be given subQ. dont lead to monitor labs buts its less reversible
How does heparin induce thrombocytopenia? heparin binds platelet factor IV, causing Ab production that binds to and activates platelets leading to their clearance
What are lepirudin, bivalirudin? hirudin derivatives, directly inhibit thrombin. used as alternative to heparin for anticoagulating patients with HIT
What is the mechanism of warfarin (coumadin)? intereferes with normal synth and carboxylation of K dependent clotting factors II,VII,IX,X, protein C and S
What metabolizes warfarin (coumadin) and what lab values should be followeD? metabolized by cyt p450. affects EXtrinsic pathay, and incr PT. Follow PT/INR
What is used for warfarin overdose? vitamin K for slow reversal. for rapid reversal in a sever OD give fresh frozen plasma
What is the clinical use of warfarin? chronic anticoagulation (post STEMI, venous thrombosis prophylaxis)
IS warfarin used in pregnancy? NO
What are the major SE of warfarin (coumadin)? bleeding, teratogenic, skin/tissue necrosis,
What is the structure of heparin vs warfarin? heparin: large anionic, acidic polymer warfarinL small lipid soluble
What is the route of administration of heaprin vs warfarin? heparin: parenteral (IV,SC). warfarin: oral
What is the site of action of heparin vs warfarin? heparin: blood warfarin: liver
What is the onset of heparin vs warfarin? heparin: seconds warfarin: slow, limited by half lives of normal clotting factors
What is the duration of action of heparin vs warfarin? heparin: hours warfarin: days
Does heparin or warfarin inhibit coagulation in vitro? heparin, not warfarin
What is the class of streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)? thrombolytics
What is the mech of streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)? directly or indirectly aid in conversion of plasminogen to plasmin which cleaves thrombin and fibrin clots
What is the effect of streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase) on lab vaules? incr PT, PTT
what is the clinical use of streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)? early MI, early ischemic stroke
What are the major SE of streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)? bleeding. contraI in pt with active bleeding, hx of intracranial bleed, surgery, sever HTN
How do you tx the SE of streptokinase, urokinase, tPA (alteplase), APSAC (antistreplase)? aminocaprioic acid, an inhibitor of fibrinolyisis
What is the mech of aspirin? acetylates and irreversibly inhibts COX1 and COX2 to prevent conversion of arachidonic acid to TXA2
What is the effect of aspirin on BT and PT, PTT? incr bleeding time no effect on PT and PTT
What is the clinical sue of aspirin? antipyretic, analgesic, anti-inflammatory, antiplatelet drug
What are the major SE of aspirin? gastric ulceration, bleeding, hyperventialtion, Reye's syndrome, tinnitus (CNVIII)
What is the mech of clopidogrel, ticlopidine? inhibit platelet aggregation by irreversibly blocking ADP receptors. inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa expression
What is the clinical use of clopidogrel, ticlopidine? acute coronary sndrome, coronary stenting, decr incidence of recurrence of thrombotic stroke
What are the major SE of clopidogrel, ticlopidine? netropenia (esp ticlopidine)
What is the mech of cilostazol, dipyridamole? phosphodiesterase III inhibitor, incr cAMP in platelets thus inhibiting platelet aggregation; vasodilators
What is the clinical use of cilostazol, dipyridamole? intermittent claudication, coronary vasodilation, prevention of stroke or TIAs (combined w aspirin), angina prophylaxis
What are the major SE of cilostazol, dipyridamole? nausea, HA, facial flushing, hypotension, abdominal pain
What is the mech of abciximab? monoclonal ab that binds to IIb/IIIa on platelets, preventing aggregations
What is the clinical use of abciximab? acute coronary syndrome, percutaneous translumina coronary angioplasty
What are the major toxicities of abciximab? bleeding, thrombocytopenia
What part of the cell cycle do antimetabolites interfere with? S. DNA synthesis
What part of the cell cycle does etopodside interefere with? S DNA synth, and G2 synthesis of mitosis components
What part of the cell cycle does bleomycin interfere with? G2, synthesis of components for mitosis
What part of the cell cycle do vinca alkaloids and taxols interfere with? M
What 3 antineoplastics inhibit nucleotide synth? methotrexate, 5-FU (thymidine) and 6-MP (purines)
How do alkylating agents and cisplatin interfere with DNA? cross link the DNA
How do dactinomycin, doxorubicin interfere with DNA? DNA intercalators
How does etoposide interfere with DNA? inhibits topoisomerase II
How do Vinca alkaloids inhibit cellular division? inhibit microtubule assembly
How does Paclitaxel interfere with cellular division? inhibits microtubule disassembly
What is the class of methotrexate, 5-FU, 6-MP, 6-TG, and ara-c? antimetabolite neoplastics
What is the mechanism of methotrexate? folic acid analog that inhibits DHF reductase= decr dTMP= decr DNA and protein synth
What is the clinical use of methotrexate for cancers? leukemias, lymphomas, choriocarcinomas, sarcomas
What are the non neoplastic uses of methotrexate? abortion, ectopic pregnancy, rheumatoid arthritis, psoriasis
What are the major SE of methotrexate? What can be done to reverse some of them? 1. myelosurpression (reversible with leucovorin (folinic acid) 2. macrovesicular fatty change in liver 3. mucositis 4. teratogenic
What is the mechanism of 5-fluorouracil (5-FU)? pyrimadine analog which covalently complexes folic acid. this complex inhibits thymidylate synthase= decr TMP, decr DNa and protein synth
What is the clinical use of 5-fluorouracil (5-FU)? What other anti neoplastic is it syngergisitc with? colon cancer and other solid tumors, basal cell carcinoma. synergisitic with MTX
What are the major SE of 5-fluorouracil (5-FU) and how can an OD be rescued? 1, myelosurpression that is reversible with thymidine 2. photosensitivity
What is the mechanism of 6-mercaptopurine (6-MP)? What activates it? purine (thiol) analog which decr de novo purine synth, activated by HGPRTase
What is the clinical use of 6-mercaptopurine (6-MP)? leukemias, lymphomas (not CLL or Hodgkin's)
What are the major SE of 6-mercaptopurine (6-MP)? What other drug can increase these and why? bone marrow, GI, liver. metabolized by xanthine oxidase so toxicity will increase with allopurinol
What is the mech of 6-thioguanine (6-TG)? What activates it? purine (thiol) analog which decr de novo purine synth, activated by HGPRTase
What is the clinical use of 6-thioguanine (6-TG)? acute lymphoid leukemia
What are the major SE of 6-thioguanine (6-TG)? bone marrow depression, liver toxicity. can be given with allopurinol unlike 6-MP
What is the mechanism of Cytarabine (ara-c)? pyrimidine analog--> inhibits DNApol
What is the clinical use of Cytarabine (ara-c)? AML,ALL, high grade non hodgkin's lymphoma
What are the major SE of Cytarabine (ara-c)? leukopenia, thrombocytopenia, megaloblastic anemia
5-FU would cause a build up of what substrate? dUMP
MTX would cause a build up of what substrate? DHF
What is the class of dactinomycin, doxorubicin, daunorubicin, bleomycin, etoposide, teniposide? anti tumor abtx
What is the mechanism of dactinomycin, (actinomycin D)? intercalates in DNA
What is the clinical use of dactinomycin, (actinomycin D)? Wilm's tumor, Ewing's sarcoma, rhabdomyosarcoma. used for child hood tumors
What are the major SE of dactinomycin, (actinomycin D)? myelosurpression
What is the mech of Doxorubicin (adriamycin), daunorubicin? generate free radicals which noncovalently intercalate in DNa causing breaks and decr replication
What is the clinical use of Doxorubicin (adriamycin), daunorubicin? Hodgkin;s lymphomas, also myelomas, sarcomas, solid tumors of breast ovary lung
What are the major SE of Doxorubicin (adriamycin), daunorubicin? What can be given to help prevent some of them? cardiotoxicity (DCM), myelosurpression, alopecia. toxic to tissues with extravasation. Dexrazoxane (iron chelating agent) used to prevent cardiotoxicity
What is the mechanism of bleomycin? induces free radical formation, which causes breaks in DNA strands
What is the clinical use of bleomycin? testicular cancer, Hodkin's lymphoma
What are the major SE of bleomycin? pulmonary fibrosis, skin changes. minimal myelosupression
What is the mechanism of Etoposide (VP-16), teniposide? inhibits topoisomerase II--> incr DNA degradation
What is the clinical use of Etoposide (VP-16), teniposide? small cell carcinoma of the lung and prostate, testicular carcinoma
What is the major SE of Etoposide (VP-16), teniposide? myelosurpression, GI irritation, alopecia
What is the class of cyclophosphamide, ifofamine, mitrosureas ( carmustine, lomustine, semustine, streptozocin), busulfan? Alkylating agent anti neoplastics
What is the mech of Cyclophosphamide, ifosfamide? What activates them? covalently X link (interstrand) DNA at guanine N-7. Requires bioactivation by liver
What is the clinical use of Cyclophosphamide, ifosfamide? Non hodgkin's lymphoma, breast and ovarian carcinoma. also immunosurpressants.
What are the major SE of Cyclophosphamide, ifosfamide? how can some of them be prevented? myelosupression; hemorragic cystitis can be partially prevented with mesna
What is the mech of Nitrosureas (carmustine, lomustine, semustine, streptozocin)? require bioactivation, cross blood-brain barrier-->CNS
What is the clinical use of Nitrosureas (carmustine, lomustine, semustine, streptozocin)? brain tumors (including glioblastoma multiforme)
What are the major SE of Nitrosureas (carmustine, lomustine, semustine, streptozocin)? CNS toxicity ( dizziness, ataxia)
What is the mechanism of busulfan? alkylates DNA
What is the clinical use of busulfan? CML, also used to ablate patients bone marrow before BMT
What are the major SE of Busulfan? pulmonary fibrosis, hyperpigmentation
What is the class of vincristine, vinblastine, paclitaxel and the taxols? microtubule inhibitors
What is the mechanism of vincristine, vinblastine? alkaloids bind to tubulin in M phase and block polymerization of microtubules so that mitotis spindle cant form. microtubules are the VINES of the cell
What is the clinical use of vincristine, vinblastine? Hodgkin's lymphoma, Wilm's tumor, choriocarcinoma, ALL
What is the major SE of vincristine? neurotoxic (areflexia, peripheral neuritis), parylactic ileus
What is the major SE of vinblastine? Bone marroe surpression
What is the mech of paclitaxel and the taxols? hyperstabilize polymerized microtubules in M phase so the mitotic spindle cant break down (no anaphase)
What is the clinical use of paclitaxel and the taxols? ovarian and breast carcinomas
What is the major SE of paclitaxel and the taxols? myelosurpression and hypersensitivity
What is the mech of cisplatin, carboplatin? cross link DNa
What is the clinical use of cisplatin, carboplatin? testicular, bladder, ovarian, lung carcinomas
What is the major SE of cisplatin, carboplatin? how can these be prevented? nephrotoxicity and acoustic nerve damage. prevent nephrotoxicity with amifostine (free radical scavenger), chloride diuresis
What is the mechanism of hydroxyurea? inhbits ribonucelotide reductase--> decr DNA synthesis (S phase)
What is the clinical use of hydroxyureas? melanoma, CML, Sickle cell disease (incr HbF)
What is the mech of prednisone? may trigger apoptosis, might work on nondividing cells
What is the clinical use of prednisone? used in CLL, Hodgkin's lymphoma (part of MOPP). also immunosurpressant used in AID
What are the major SE of prednisone? Cushing-like syndrome, immunosupression, cataracts, acne, osteoprosis, HTN, peptic ulcers, hyperglycemia, psychosis
What is the mech of tamoxifen, raloxifene? SERMs- receptor antagonists in breast and agonists in bones. block binding of estrogen to estrogen receptor + cells
What is the clinical use of tamoxifen, raloxifene? breast cancer, also useful to prevent osteoporosis
What is the major SE of tamoxifen? incr risk of endometrial carcninamo via partial agonist effects, hot flashes
what is the major SE of raloxifene compared to tamoxifen? no incr in endometrial carcinoma because it is an endometrial antagonist
What is the mech of trastuzumab (herceptin)? monoclonal ab against HER-2 (erbB2), tyrosine kinase. heps kill breast cancer cells which overexpress HER-2
What is the clinical use of trastuzumab (herceptin)? metastatic breast cancer
What is the major SE of trastuzumab? cardiotoxicity
What is the mechanism of imantinib (gleevec)? philadelphia chromosome bcr-abl tyrosine kinase inhibitor
What is the clinical use of imantinib (gleevec)? CML, GI stromal tumors
What is the major SE of imantinib (gleevec)? fluid retention
What is the mechanism of rituximab? monoclonal Ab against CD 20 which is found on most B cell neoplasms
What is the clinical use of rituximab? non-Hodgkin's lymphoma, rheumatoid arthritis (with methotrexate)
What antineoplastics commonly cause nephrotoxicity and acoustic nerve damage? cisplatin/carboplatin
What antineoplastic commonly causes peripheral neuropathy? vincristine
What antineoplastic commonly causes pulmonary fibrosis? bleomycin
What antineoplastic commonly causes cardiotoxicity? doxorubicin
What antineoplastic commonly causes hemorrhagic cystitis? cyclophosphamide
What antineoplastics commonly causes myelosurpression? 5-FU, 6-MP, methotrexate
Created by: tjs2123