Ck hematology

ismailalmokyad's version from 2018-01-21 19:02


Question Answer
wt is the only microcytic anemia that has high reticulocyte count alpha thalassemia with 3 gene deletion
wt are the blood transfusion reaction associated with hypotension1-anaphylaxis
2- transfusion related acute lung injury
3- primary hypotension reaction
4- bacterial sepsis
wt is transfusion related acute lung injury resp distress and non cardiogenic pulmonary edema within 6 hours post blood transfusion ( caused by donor anti leukocyte antibody
wt is the most common blood transfusion reactionfebrile non hemolytic transfusion reaction within 1-6 hours of transfusion. present as transients fever , chill, malaise with no resp distress or shock symptom
wt is the only microcytic anemia that has high level of circulating iron sidroplastic anemia
wt cause megaloplastic macrocytic anemia megaloplastic mean hypersgmented neutophil only b12, folic acid and antimetabolite medication as methotrexate can cause that
wt should be screened in pernicious anemia hypo parathyroid, gastic atrophy and carcinoma and carcinoid
wt is pernicious anemia is auto immune anti intrinsic factor antibody which destroy parital cell that will give macrocytic anemia, glossitis and gastric atrophy
wt is fanconi anemiaAR, progressive pancytopenia, macrocytic anemia, average age 8 year, short, microcephaly, cafe lati spots microphthalmia, horseshoe kidney, absent thumb ,
wt is transient erythroblastopenia of children present after one year of age , no congenital anomaly and not macrocytic anemia
wt is diamond blackfan $AD or AR disease with low reticulocytes, macrocytic anemia( but no hypersignented neutrophils) , congenital anomaly and avreage age is 3 months
wt electrolyte abnormality can happen after replacing B12 and folic acid hypo K , BM produce cell so rapid (packing all the k inside the cells )
wt is the mutation of sickle cell anemia Hb beta chain at position 6 the valin will replace the glutamic acid
wt is most accurate test and ttt for B19 as a cause of drop in hct in sickle cellMost accurate test to confirm is PCR for the virus DNA, ttt is IVIG
how u ttt autoimmune warm igG anemiastart with corticosteroids, if sever acute and no response to steroid give IVIG, if recurrent spleenectomy, if steroid and spleenectomy didnt control it give rituximab
wt medication and diseases can cause TTPHIV,SLE,cyclosporin,ticlopidin, clopidogrel
wt is ttt for TTP and HUSplasmapherisis or plasma exchange if no response or rapid recurrence give cyclophosphamid
wt is most common cause of death In Rheumatic Arthritis corenary artery disease
wt is most common cause of death in paroxysmal nocturnal hemoglobinuriathrombosis
wt is the ttt of paroxysmal nocturnal hemoglobinuriafor hemolysis give steroid , Eculizumab (inactivate c5 which mean it is complement inhibitor ). the only cure is BM transplant. dont forget to give him folic and trasfuse patient if needed
wt is ttt of aplastic anemia-if young <50 BM transplant
-if > 50 give anti T lymphocyte globulin and cyclosporin or tacrolimus ( to inhibit t cell from attacking BM)
wt is the ttt of essential thrombocytosisif <60 year old with no symptom and the platelet count <1.5 million then no ttt , if not meeting the criteria for no ttt then start ttt with hydroxyuria ( if caused BM supprestion give anagrelide), for erythromelagia (painful swelled hand ) give aspirin
wt is myelofibrosis and wt is the ttt pancytopenia in old person with HSM and tear drop in smear and necleated RBCs( NL TRAP vs hairy cell) . ttt is thalidomide and lenalidomide (TNF inhibitors that increase cell production) if <55 BM transplant
wt is special about AML the M3 associated with DIC, it has esinophilic inclusion ( myeloperoxidase) called auer rods . in the ttt you add All trans reticulonic acid (ATRA)
wt special about ALL ttt add intrathecal methotrexate
wt conditions associated with increase of leukocyte alkaline phosphateaseleukemoid reaction , hypo phosphatemia, paroxysmal necurnal hemoglobinuria
how imatinib ttt CMLBCR-ABL 9:22t (phladelphia )give abnormal tyrosin kinase activite that can be inhibited by imatinib or any medication end with tinib
wt is the cure for CMLBM transplant
wt is most accurate test for CMLpcr or FISH( fluorescent in situ hybridization) to catch phladelphia chro, done in perephral smeae
wt is myelodysplastic syndromit is slowly progressive pre leukemic disease , present as old patient with pancytopenia despite hyper cellular BM, with high MCV , low reticulocyte, with very special 2 nucleated neutophil called pelger huet cell and nl B12
how you ttt myelodysplastic syndromtransfusion and erythropiotien , lenalidomide and azecitidine can decrease transfusion need
wt can happen in untreated CML and CLLCML can go into blast crisis (AML) where CLL can go into high grad lymphoma
how you ttt CLL depend on the stage. stage 0 ( elevated WBCs) and 1(LAD() no ttt, stage 2 (HSM), stage3(anemia) and stage 4 (thrombocytopenia) ttt with fludarabine and rituximab. for mild disease or for ppl who can't tolerate fludarabine use alemtuzumab or chlorambucil
how you Dx CLL BI is smuged cell . MA is flow cytometry
wt is hairy cell leuckemia and how you Dx it and tttpancytopenia with HSM and dry tap (hypocellular BM) , BI test is hair cell in smear , MA test is cytometry that show tarteat resistant acid phosphate . ttt cladribin or pentostatin
wt is used do assess sevirity of NHLLDH level
how to ttt NHLstage 1 (one LAD) or 2 ( 2 LAD in same side of diaphragm) ttt with local radiation and small does of chemo. stage 3 ( 2 or more LAD in both side of diaphragm) or stage 4 ( metastasis) ttt with cyclophosphamide, Adriamycin(doxorubicin), vincristine, prednisone and rituximab (CHOP +rituximab)
wt is ttt of hodgkin lymphomastage 1 and 2 ttt with local radiation and low does chemo . stage 3 and 4 ttt with Adriamycin, Belomycin, vinblastin and Dacarbazin(ABVD)
wt are the difference between NHL and HLHL present almost always in stage 1 or 2 where NHL present almost always stage 3 or 4 . HL has reed sternberg cell .
wt is the SE of doxorubicincadiotoxic
wt is the SE of bleomycinlung fibrosis
wt is the SE of vincristineneuropathy
wt is the SE of cisplatinrenal and ototoxic
wt is the ttt of multiple myelomadexamethason with lenalidomide or bortezmib or both ( remember melphalan is used in older patient who can't tolerate the SE). the most effective ttt for < 70 is BM transplant after induction with steroid and lenalidomide
wt is the most common cause of death in multiple myloma renal failure and infections
wt correspond with severity of multiple myelomabeta 2 microglobulin level
how u ttt symptoms of multiple myeloma1-hyper Ca use bisphosphonate,
2-RF use hydration,
3-anemia use erythropiotien,
4- vaccination aginst pneumoccous and tetanus
wt is monoclonal gammopathy of unknown significant and how we manage itit is increase in igG or igA but with no bone metastasis and low plasma cell in bone marrow. to manage it first do BM biopsy to exclude MM then follow the amount of immunoglobulin( correlate with who gonna develop MM), no ttt .
wt is waldenstrom macroglobulinemia and how u manage itits malignant plasma cell that secrets igm given viscosity symptom and ryanoid phenomenon but no renal or bone . ttt start with plasmapherisis then for long term ttt give rituximab or prednisone and cyclophosphamid . u can also decrease the production usind lenalidomid or bortezomib
wt is romiplostim and elrombopag ? wt we use them for they are synthetic thrombopietin used for ITP
how u dx ITPonly low platelet with anti platelet antibody( if -ve exclude if +mean nothing ), Nl size spleen on ct and magakaryocytosis ( exclude production problem )
how u manage ITPif child with skin only observe if child with bleeding give IVIG or glucocorticoid. if adult no bleeding and count >30000 no ttt, mild bleeding or count <30000 prednisone. sever bleeding (git or cns) or count <20000 ivig or ant D also called rhogam. if recurrent spleenectomy if not enough romiplostim or eltroboag or rituximab

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