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HemeOnc Q's
| Question | Answer |
|---|---|
| What does "Neutrophils Like Making Everything Better" stand for? | WBC diff highest to lowest: neutrophils, lymphocytes, monocytes, eosinophils, basophils |
| What does the large SA:volume ratio in RBCs help facilitate? | easy gas exchange |
| what is the main source of energy in RBCs | 90% anearobically from glucose to lactate, 10% from HMP shunt |
| What causes the physiologic chloride shift and what does the chloride shift do? | chloride bicarb antiport system,, allows transport of C02 from periph to lungs |
| anisocytosis | varying sizes |
| poikilocytosis | varying shapes |
| What is the life span of a normal RBC | 120 days |
| From what cells are platelets derived from | megakaryocytes |
| what do platelets interact with to form a hemostatic plug | fibrinogen |
| What do the dense granules contain in platelets | ADP and Ca |
| What the alpha granules contain in platelets? | vWF and fibrinogen |
| Where are 1/3 of platelets stored | spleen |
| What is the life spance of a platelet? | 8-10 days |
| What is the result of thrombocytopenia or platelet dysfunction? | petechiae |
| What is the receptor for vWF | Gp1b |
| What is the receptor for fibrinogen? | GpIIb/IIIa |
| what are the azuraphilic granules in PMNs | lysosomes |
| What is contained within the azurophilic granules of PMNs | hydrolytic enzymes, lysozyme, myeloperoxidase, lactoferrin |
| Where do you see hypersegmented polys? | B12/folate def |
| What percentage if WBCs are polys? | 40 to 75 |
| What percentage of WBCs are monocytes? | 2 to 10 |
| Where are monocytes typically found, where do they go, and what do the differentiate into? | blod, tissue, MACS |
| What signal activates MACS | IFN gama |
| What percentage of WBCs are eosinophils? | 1 to 6 |
| What do eosinophils defend against and what do they use to do it? | helminth infections major basic protein |
| Eosinophils are highly phagocytic for what kind of complex? | antigen-antibody |
| what are the two substances produced by eosinophils help limit the reaction following mast cell degranulation? | histaminase and arylsulfatase |
| What does NAACP stand for, in regards to the causes of eosinophiia? | neoplastic, asthma, allergic processes, collagen vacsular disease, parasites |
| What percentage of WBCs are basophils, and what is found in their basophilic granules? | < 1%, heparin, histamine, LTD-4, other vasoactive amines |
| What substances are released in mast cell degranulation | histamine, heparin, and eosinohil chemotactic factors |
| What portion of IgE can mast cells bind | Fc |
| Where are mast cells found | tissue |
| Where are basophils found? | blood |
| What substance prevents mast cells degranulation? | cromolyn sodium |
| Who are the professional APCs? | dendritic cells? |
| What are dendritic cells called in the skin? | langerhans cells |
| What do they express on their surface? | MHC II and Fc receptors |
| What is their role? | inducers of primary antibody response |
| How are the nucleus and the cytoplasm characterized for lymphocytes | round densly staining nucleus with a small amount of pale cytoplasm |
| Where do B cells arise from, mature, and migrate to | marrow, marrow, follicles of lymph nodes, white pulp of spleen (unencapsulated lymphoid tissue) |
| Can B cells function as APCs? | Yes, via MHC II |
| How are plasma cells characterized? | Off center nuclues, clock face chromatin |
| Plasma cell neoplasm | multiple myeloma |
| What do plasma cells do | produce antibody, lots of RER and golgi |
| Where to T cells arise and mature, and migrate to | bone marrow, thymus, blood (80% of circulating lymphos are T) |
| Blood type A | A antigen and B antibodies |
| Blood type B | B antigena and A antibodes |
| universal recipient | AB, no antibodies |
| universal donor | no antigen, both antibodies |
| In a Rh- mother who has developed anti Rh antibodies, who is at risk of hemolytic disease? | her next Rh+ fetus |
| What is the treatment to prevent a woman from forming anti Rh antibody? | Rhogam, Rh antigen immunoglobulin |
| Which maternal antibodies cross the placenta, anti A/B or anti Rh | anti Rh |
| What begins the extrinsic pathway? | tissue factor converst the VII and VIIa |
| What activates the intrinsic pathway? | collagen, BM, activated platelets |
| What activates the fibrinolytic pathway? | XIIa activates kallikrein, which activates plasmin (and converts HMWK to bradykinin |
| What does plasmin do? | degrades fibrin mesh and converts C3 to C3a |
| What does bradykinin do? | inc vasodiltion, inc perm, inc pain |
| What is hemophiliia A | deficiency in factor VIII |
| What is hemophilia B? | def in factor IX |
| What does Vit K deficiency cause? | dec synthesis of factors 1972, protein C/S |
| What does antithrombin do and what activates it? | inhibits thrombin, ixa, xa, xiia, and activated by heparin |
| What is the purpose of the fibrin mesh | acts to stabilize platelet plug |
| What is the effect of ACE on bradykinin | inactivates it |
| Which enzyme converts vit k to activated vit k, and what substance inhibits this enzyme | epoxide reductase, warfarin inhibits |
| Which factor does vWF carry/protect | VIII |
| What role does antithrombin play? | incactivates II, VII, IX, X, XI, XII |
| What activates protein C and what does activated protein C do? | protein S, cleaves and invactivates Va and VIIIa |
| What is factor V leidin? | factor V resistant to activated protein C's inhibition |
| What converts plasminogen to plasm and what does plasmin do? | tPA, cleavage of fibrin mesh |
| After an injury, what does vWF bind to begin platelet plug formation? | exposed collagen upon endothelial damage |
| What do the platelets bind? What is the step called | they bind vWF via GpIb |
| What do platelets release necessary for coagulation cascaed? | ADP and Ca |
| What does ADP do? | helps platelts adhere to endothelium |
| What is the activation stage of platelet plug formation? | ADP binding to receptors causes upregulation of GpIIb/IIIa expression at platelet surface |
| What is the aggregation phase of ppf? | fibrinogen bind GpIIb/IIIa and links platelts |
| What are the pro aggregation factors? | TXA2, dec blood flow, inc platelet aggregation |
| what are the anti aggregation factors? | PGI2, NO inc blood flow, dec platelet aggregation |
| Deficiency in GpIb | bernard soulier |
| Deficiency in vWF | von Willebrand's disease |
| Deficiency in GpIIb/IIIa | Glanzmann's throbmasthenia |
| Drug that inhibits COX and therefore TXA2 synthesis | aspirin |
| drug that inhibits ADP induced expression of GpIIb/IIIa | ticlopidine/clopidogrel |
| Drug that inhbits the GpIIb/IIIa directly | abciximab |
| Acanthocyte (spur cell) | liver disease, abetalipoproteinemia, acntho |
| Basophilica stippling | TAIL, thalassemias, anemia of chronic disease, iron def, lead poisoning |
| Bite cell | G6PD |
| Elliptocyte | hereditary elloptocytosis |
| Macro-ovalocyte | megaloblastic anemia (also hypersegmented PMNs, marrow failure) |
| Ringed sideroblasts | Sideroblastic anemia |
| Schisotcyte, helmet cell | DIC, TTP/HUS, traumatic hemolysis |
| Sickle cell | Sickle cell anemia |
| Spherocyte | hereditary spherocytosis, autoimmune hemolysis |
| Teardrop cell | Bone marrow infiltration, myelofibrosis |
| Target cell | HbC disease, Asplenia, Liver disease, thalassemia, "HALT the hunter said to his target" |
| Oxidation of iron, denatured hemoglobin preceipitation damage to RBC membrane, formation of bite cells | Heinz bodies, seen in alpha thal and G6PD |
| Basophilic nuclear remnants fonud in RBCs | Howell-Jolly bodies, hypo/asplenia |
| Ddx for microcytic anemia | fe def, thal, pb poison, sideroblastic anemia |
| iron deficiency anemia, esophageal web, atrophic glossitis | plummer-vinson syndrome |
| Causes of iron def? | bleeding, malnutrition/absorption, inc demand pregs |
| defect in alpha globin gene, dec alpha globin synth, disease and populations? | alpha thal, asian and african american |
| What are the four levels of alpha thal? | defect in 4, not compatible with life, defect in 3, HbH disease, defect in 1/2 not associated with sig anemia |
| What causes hydrops fetalis | Hb Barts, gamma4 in defect in all 4 alpha genes |
| What is HbH | beta 4 |
| What is the defect in beta thal? | splicing sites and promotor sequences |
| What happens in betal thal minor? | beta chain underproduced, asymptomatic, heterozygote |
| How is beta thal minor dx | inc HbA2 on electrophoresis |
| What happens in beta thal major? | beta chain absent, homozgote, severe anemia requiring blood transfusion, secondary hemochromatosis |
| Marrow expansion, "crew cut" on skull x ray, skeletal deformaties, and chipmunk faces | beta thal |
| inc HbF on electrophoresis | both alpha and beta thal |
| inhibition of ferrochelatase and ALA dehydrogenase leading to dec heme synthesis, also inhibition of rRNA degradation | lead poisoning, rRNA causes aggregration of ribosomes and basophilic stippling |
| X linked defect in delta aminolevulinic acid synthase gene causes a defect in hemesynthesis | sideroblastic anemia |
| What is the treatment for sideroblastic anemia | B6 therapy (pyrodixine) |
| What reveresible things can a sideroblastic anemia | lead, and EtOH |
| What do you see on peripheral smear with sideroblastic anemia, | ringed sideronblasts with iron laden mitochondria |
| What do the iron studies show in sideroblastic anemia | inc serum iron, normal TIBC, inc ferratin |
| What does LEAD stand for in lead poisoning? | Lead lines on gingivae and epiphyses of long bones on xray, Encephalopathy and Erythrocyte basophilic stippling, Abdominal colic and Anemia, Drops -wrist and foot drop, |
| What is the treatment for lead poising? | Dimercaprol and EDTA 1st line of treatment, succimer for kids - it sucks to be a kid who eats lead |
| What is the Ddx for for a macrocytic anemia | Folate/B12, nonmegaoblastic anemias, liver dz, EtOH (non folate/B12) reticulocytosis, metabolic disorder, drugs |
| What is a metabolic disorder tht can cause macrocytic anemia? | orotic aciduria |
| Which drugs can cause macrocytic anemia? | 5-FU, AZT, hydroxyurea |
| What is the general pathology of a macrocytic anemia? | DNA synth impaired, maturation of nucleus delayed relative to maturation of cytoplasm |
| hypersegmented PMNs, glossitis, dec folate, inc homocysteine, nl methylmalonic acid | folate def |
| What are the etiologies of folate def | malnutrition, malabsoprtion, impaired metabolism, inc requirement as in an hemolytic anemia or pregnancy |
| hypersegmented PMNs, glossitis, dec B12, inc homocysteine, inc methymalonic acid | B12 def |
| What are the etiologies of B12 def | insufficient intake as with strict vegans, malabsorption as in crohns, pernicious anemia, diphyllobothrium |
| Why does B12 def cause neuro sx? | B12 in fatty acid pathways leads to subacute combined degeneration |
| What are the neuro sx of B12 def? | Peripheral neuropathy, posterior columns (vibration/proprioception), lateral corticospinal (spasticity), dementia |
| What is the Ddx for a normocytic, normochromic anemia? | Hemolytic or non hemolytic, and then for the hemolytiuc, intravascular hemolysis or extravascular hemolysis |
| dec haptoglobin, inc LDH, hemoglobin in urine (paroxysmal nocturnal hemoglobinuria, mechanical destruction as in aortic stenosis or a prosthetic valve | intravascular hemolysis |
| inc LDH, jaundice, | extravascular hemolysis |
| What causes the jaundice in extravascular hemolysis | inc UCB |
| What are some classic examples of extravascular hemolysis | hereditary spherocytosis, G6PD, sickle cell |
| What is the Ddx for nonhemolytic normocytic anemia | Anemia of chronic disease, Aplastic anemia, kidney disease |
| What is the pathogenesis of ACD? | inflammation leads to inc hepcidin causing a dec in release from iron from macs: dec serum fe, dec TIBC, inc ferritin |
| hypocellular bone marrown tih fatty infiltration | aplastic anemia, pancytopenia |
| What is the ddx for aplastic anemia | radiation/drugs, viral agents, fanconi's anemia, idiopathic may follow acute hepatitis |
| fatigue, malaise, pallor, purpura, mucosal bleeding, petechiae, infection | signs and sx of aplastic anemia |
| what is the tx for aplastic anemia | allogenic bone marrow transplant, RBC/platelet transfusion, C-GSF, or GM-CSF |
| What is the pathogenesis of aplastic anemia with kidney disease | decrease EPO |
| Defect in proteins interacting with RBC membrane skeleton and plasma membrane | hereditary spherocytosis |
| Is HS extravascular or intravascular? | extravascular |
| what proteins can be defective in HS? | ankryin, band 4.1 or spectrin |
| What virus can cause an aplastic crisis in pts with HS? | parvovirus |
| What finding you do you see in patients after splenectomy | Howell Jolly bodies |
| What are the labs and tx for HS? | positive osmootic fragility test and splenectomy |
| X linked, dec glutathione inc RBC susceptibility to oxidative stress | G6PD |
| Fava beans, sufla drugs, infectinos, | examples of oxidative stress |
| Back pain, hemoglobinuria | common a few days after oxidative stress in a pt with G6PD |
| What do you see in peripheral smear in a pt with G6PD? | bite cells and Heinz bodies |
| Is G6PD intravascular or extravascular | intravascular |
| hemolytic in a newborn, dec ATP and rigid RBCs | pyruvate kinase def, extravascular |
| Crew cut on skull xray due to marrow supression, 8% of AA population, single amino acid replacement in beta chain at position 6, after a DNA point mutation | Sickle cell |
| Why can newborns with sickle cell be asymptomatic | inc HbF and dec HbS |
| What is the pathogenesis of sickle cell | deoxygenated HbS polymerizes, low O2 or dehydration precipiates sickling, anemia and veno-occlusive disease |
| Aplastic crisis after parvovirus, autosplenectomy, salmonella osteomyelitis, painful crisis, renal papillary necrosis, splenic sequestration | complications of sickle cell anemia |
| What causes renal papillary necrosis in sickle cell | low O2 in papilla; can also get microhematuria from medullary infarcts |
| What is the tx for sickle cell | hydroxyurea, bone marrow transplant |
| What is the mutation in HbS | valine for glutamate |
| What is the mutation in HbC | lysine for glutamate at position 6 |
| Who has more severe disease, HbSS or HbSC | HbSS |
| Impaired synthesis of DAF leading to inc complement mediated desctruction of RBCs via the GPI ancho | paroxysmal nocturnal hemoglobinuria |
| What are the extrinsic hemolytic normocytic anemias? | ... |
| What are some causes of warm agglutinin autoimmune hemolytic anemia? | SLE, CLL, alpha methyldopa |
| Which immunoglobulin is involved in warm agglutination? | IgG, Warm is GREAT |
| What are some causes of cold agglutinin anemia | Cold, seen in CLL, mycoplasma pneumoniae infections or infectious mononucleosis |
| mother's antibodies attack fetal RBCs | erythroblastosis fetalis, Rh or other blood antigen incompatibility |
| What is the coombs test results in AIHA? | pos |
| anti-Ig antibody added to patients RBCs; | direct coombs, agglutinate if RBCs are coated with Ig |
| normal RBCs added to patient's serum | indirect coombs, agglutinate if serum anti RBC surface Ig |
| RBCs damagaed from passing through obstructed, narrowed vessel lumina | MAHA |
| When do you see MAHA? | DIC, TTP-HUS, SLE malignant HTN, prostethic heart valves, aortic stenosis |
| What is the characteristic finding for MAHA on peripheral smear? | schistocytes, helmet cells |
| Which infections can cause MAHA? | malaria, Babesia |
| Serum iron, transferrin, ferritin lab values for iron def anemia | down, up, down |
| Serum iron, transferrin, ferritin lab values for anemia of chronic disease | down, down, up |
| Serum iron, transferrin, ferritin lab values for hemochromatosis | up, down, up |
| Serum iron, transferrin, ferritin lab values for pregs, OCP use | nl, up, nl |
| Serum iron, transferrin, ferritin lab values for lead poisoning anemia | up, down, nl |
| Conditions of defective heme synthesis leading to accumulation of heme precurors | porphyrias |
| What is the affected enzyme in lead poisoning | ferrocheletase and ALA dehydrogenase |
| What is the accumulated substance in lead poisoning | protoporphyrin (blood) |
| What is the are the presenting symptoms of lead poisoning in kids and adults | Kidney, Gi, microcytic anemai in both, kids |
| What are the likely exposures of kids and adults for lead poisoning | kids |
| What is the effected enzyme in acute intermittment porphyria? | porphobilinogen deaminase aka uroporphyrinogen I synthase |
| What is the affected enzyme in acute intermittment porphyria | porphobilinogen, delta ALA, uroporphyrin |
| What are the presenting symptoms of acute intermittent porphyria | painful abdomen (also in lead poisoning), red wine colored urine, polyneuropathy, psychological distrubances, precipated by drugs, |
| What is the treatment for acute intermittent porphyria | glucose and heme, which inhibit ALA synthase |
| What is the enzyme defect in Porphyria cutanea tarda | uroporphyrinogen decarboxylase |
| What substance accumulates in porphyria cutanea | uroporphyrin (tea colored urine) |
| What are the presenting symptoms of porphyria cutanea tarda | blistering cutaneous photosens, most common porphyria |
| what does decreasing heme do to ALA synthase activity? | inc |
| What does increasing heme do to ALA synthase activity | dec |
| Which substrates begin the heme synthesis pathway | glycine and succinyl-coa |
| What vitamin is a cofactor for the first step of heme synthesis | B6 |
| What substance is Fe added to to yield heme | protoporphyrin |
| Which pathway and factorrs are tested by the PT coag test | extrinsic, I, II, V, VII and X |
| Which pathway and factors are tested in the PTT test | intrinsic, all factors except, VII, XIII |
| In hemophilia A or B what do you see in the coag tests | nl PT, elevated PTT - intrinsic pathway defect |
| What do you see in vit K def | eleveated PT, PTT |
| What is the clinical picture of hemophilia A or B | macrohemorrhage, hemarthroses, easy bruising |
| How do platelet disorders present? | inc bleeding time, microhemorrhage: mucuous membrane bleeding, epitaxis, petechiae, purpura, possible thrombocytopenia |
| Defect in platelet to collagen adhesion, receptor, disorder, platelet count and BT | Gp1b, bernard-soulier, dec platelets (giant platelets not counted), inc BT |
| Defect in platelet to platelet adhesion, receptor, disorder, platelet count and bleeding time | Glanzmann's throbmasthenia, GpIIb/IIIa, nl platelets, inc BT |
| What does the blood smear show in glanzmann's? | no platelet clumping |
| anti-GpIIb/IIIa antibodies leading to peripheral platelet destruction | Idiopathic thrombocytopenia (ITP) |
| What do labs show in ITP? | dec platelet survival and inc megakaryocytes, thrombocytopenia and inc BT |
| deficiency in ADAMTS13 leading to dec degradation of vWF | thrombotic thrombocytopenic purpura |
| What is the presenting scenario for TTP? | PENTAD: neurologic sx, renal sx, fever, thrombocytopenia, MAHA |
| What is the pathogenesis of TTP? | inc large vWF multimers, inc platelet aggregation and thrombosis |
| What do the labs show for TTP? | schistocytes and inc LDH |
| Intrinsic pathway coagulation defect and defect in platelet plug formation, most common inherited bleeding disorder, AD | vWD |
| How does vWD cause elevated PTT? | vWF carries/protects factor VIII |
| What is the tx for vWD | DDAVP (desmopressin) which releases stored vWF stored in endothelium |
| Widespread activation of clotting to a deficiency in clotting factors which causes a bleeding states | DIC |
| What does STOP Making New Thrombi stand for | Causes of DIC: Sepsis (gram neg), Trauma, Obstetric complications, acute Pancreatitis, Malignancy, Nephrotic syndrome, Tranfusion |
| What do labs show in DIC? | schistocytes, inc fibrin split products (D-dimers), dec fibrinogen, dec factors V and VIII |
| Production of mutant factor V that cannot by degraded by protein C, most common cause of inherited hypercoaguability | Factor V Leiden |
| Mutation in 3' untranslated region associated with venous clots | prothrombin gene mutation |
| Inherited deficiency of antithrombin; reduced inc in PTT after administration of heparin | ATIII def |
| dec ability to activate factors V and VIII, inc risk of thrombotic skin necrosis with hemorrhage following administration of warfarin | Protein C or S deficiency |
| lymphoid neoplasms with widespread involvement of bone marrow, tumor cells usually foind in peripheral blood | Leukemia |
| discrete tumor masses arising from lymph nodes | lymphoma |
| inc WBC count with left shift, inc leukocyte alkaline phosphatase, often due to infection | leukemoid reaction |
| What is the characteristic histologic finding in Hodgkin Lymphoma | Reed-sternberg cells |
| What is the characteristic spread of Hodgkin Lymphoma | contiguous |
| What symptoms are associated with Hodgkin lymphoma | B symptoms - fever night sweats, weight loss |
| Which lymphoma is characterized by localized involvement with a single group of nodes and mediastinal lymphadenopathy | Hodgkin |
| What virus is associated with 50% of Hodgkin lymphoma | EBV |
| What is the age breakdown for hodgkins | bimodal, men>women, except for nodular sclerosing type |
| What indicated a good prognosis in Hodgkin lymphoma? | inc lymphoctes, and less RS cells |
| When is the peak incidence for nonHod lymphoma | 20 to 40 |
| What cell is primarily involved in non Hod lymph | B cells |
| What is the pattern of involvement and spread for nonHod lympho | multiple, peripheral nodes, extranodal involvement, noncontiguous spread |
| What state is commonly associated with nonHod lymphoma | HIV or immunosupression |
| What are the variants of the RS cells | lacunar in nodular sclerosing variant |
| What CD molecules are on RS cells | CD15 and CD30 pos |
| What is the most common hodgkin lymphoma | nodular sclerosing |
| t(8;14) c-myc gene | Burkitt lymphoma |
| What virus is associated with Burkitt lymphoma | EBV |
| What is the difference of presentation of Burkitt in Africa vs the United States | Africa |
| What do you see a starry sky appearance in Burkitt | sheets of lymphocytes interspersed with macs |
| What is the most common nonhodgkin lymphoma | Diffuse Large b cell lymphoma |
| CD5+, poor prognosis, t(11;14) | Mantle cell, older males |
| bcl-2 t(14;18) adults | follicular lymphoma, indolent course |
| HTLV-1 | adult T cell lymphoma, presents with cutaneous lesions |
| Adults present with cutaneous patches/nodules, indolent CD4+ | mycosis fundgoides/Sezary syndrome |
| Bone pain plus anemia | Multiple myeloma |
| What does CRAB stand for in multiple myeloma | hyperCalcemia, Renal insuff, Anemia, Bone lytic lesions/Back pain |
| What is the age group most commonly affected by multiple myeloma | 40 to 50 |
| What is the characteristic lab finding on electrophoresis | paraprotein spike, monoclonal protein |
| What are the main associations with multiple myeloma? | inc suscept to infxn, primary amyloidosis, punched out lytic bone lesions, M spike, Ig light chains in urine, Rouleaud formations (stacked RBCs) |
| What distinguishes multiple myeloma fromk Waldenstroms macroglobulinemia? | no lytic bone lesions in WM |
| Which cell is neoplastic in multiple myeloma | plasma cell |
| What is monoclonal expansion without symptoms associated with multiple myeloma? | MGUS - monoclonal gammopathy of undetermined significance |
| Upregulated growth of leukocytes in bone marro | leukemia |
| Tdt+, CALLA+, kids in the marrow, adolescent males with mediastinal mass | ALL |
| Where does ALL spread | CNS and testis |
| What chromosomal translocation is associated with a better prognosis in ALL | t(12;21) |
| can be asymptomatic, often in older adults, peripheral blood lymphcytosis with smudge cells and warm antibody autoimmune hemolytic anemia | CLL (SLL without the peripheral lymphocytosis |
| Elderly, mature b cell tumor with filamentous, hairlike projections | Hairy cell leukemia |
| What does hairy cell leukemia stain with | TRAP (tartrate resistant acid phosphatase |
| adults, auer rods, inc circulating myeblasts on peripheral smear | AML |
| What is the therapy for the M3 variant? | all trans retinoic acid |
| How does the therapy for M3 vairant work? | induces differentiation of myeloblasts |
| philadelphia chromosome, blood looks like marrow | CML |
| What is the philadelphia chromosome | t(9;22) bcr abl |
| what is a blast crisis | CML to AML or ALL |
| What level of leukocyte alkaline phosphatase is expected in CML versus leukemoid reaction | low in CML |
| What is the therapy for CML (philly chrom) | imatinib, anti bcr abl |
| What are the age ranges for the various leukemias | ALL < 15, AML |
| What is makes a leukemia acute | blasts > 5% |
| What do auer rods stain with | peroxidase |
| What condition can result from treating AML M3 from the release of the Auer rods | DIC |
| t(15;17) | M3 AML (acute promyelocytic leukemia) |
| t(11:22) | Ewing sarcoma |
| t(11;14) | Mantle cell lymphoma |
| tennis rackets on EM | Birbeck granules |
| S-100 and CD1a with birbeck granules | Langerhans cell histiocytosis |
| abnormal clone of hematopoetic stem cells are increasingly sensitive to growth factors, inc RBC, JAK2 mut | Polycythemia vera |
| Megakaryocytosis | Essential thrombocytosis |
| Fibrotic obliteration of bone marow with teardrop cells | Myelofibrosis (marow is crying being its fibrosed" |
| Does CML have a JAK2 mut | no |
| What is relative polycythemia | dec plasma volume |
| What is appropriate absolute polycythemia | inc RBC, dec O2 sat, inc EPO |
| What is appropriate absolyte polycythemia associated with | lung disease, congenital heart diseaes, and high altitude |
| What does ectopic EPO produce | inappropriate absolute with inc RBCs and EPO |
| Wilm's tumor, RCC, HCC, hydronephrosis | Polycythemia vera with inc plasma volume, inc RBCs, inc EPO |
Created by:
ykirti
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