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Hem-Onc

QuestionAnswer
WBC Differential Neutrophils > Lymphocytes > Monocytes > Eosinophils > Basophils
Anisocytosis Varying sizes
Poikilocytosis Varying shape
Eosinophilia Cause NAACP: Neoplasia, Asthma, Allergies, Collagen vascular diseases (Churg-Straus), Parasites
INF-Gamma Activates macrophages
Phospholipid & Ca++ Mediated Factor Activity Factors 5(10), 7, 9, 11
Vitamin-K Dependent Factors Factors 2, 7, 9, 10, Prot S, C.
Activated Protein C Targets Factor 8a, 5a (10a synthesis & effector co-factors)
Antithrombin III Targets Factor 9a, 10a, 11a (Intrinsic focus)
Kalikrein Function HMWK->Bradykinin & Plasminogen->Plasmin
Plasmin Function Cross-link Fibrin & C3->C3a
Platelet Aggregation Regulation Pro: TXA2, Anti:PGI (prostacyclin) & NO
Target Cell DDx HALT, said the hunter to his target: HbC, Asplenia, Liver disease, Thalasemia
Macrocytic Anemia MCV>100. High Retic Ct. Megaloblastic (DNA synthesis problem). 1)B12,Folate Def 2)Sulfa drugs, AZT, Phenytoin 3)Reticulocytosis(secondary)
Microcytic Anemia MCV<80. Etiology: 1)Iron Deficiency: Low Fe, High TIBC, Low Ferritin 2)Thalassemias Target cells 3)Lead poisoning:dimorphic,sideroblastic cells
Normocytic Anemia 1)Hemorrhage, AI hemolytic anemia 2)G6PD (X-linked),Pyruvate Kinase Def (AR) 3)Hereditary spherocytosis 4)Aplastic anemia/leukemia 5)Chronic Disease (reticuloendothelial macrophages hide iron from potential pathogens)
Transferrin FE/TIBC
TIBC Indicates the “need for iron”
Ferritin Indicates how much iron a person has
Aplastic Anemia Etiology 1)Radiation 2)Chemicals: Benzene, chloramphenicol, alkylating agents, antimetabolites 3)Viral:ParvoB19, EBV, HIV 4)Fanconi’s Anemia 5)Idiopathic.
Aplastic Anemia Tx Allogenic bone marrow xplant. RBC & platelet transfusion. G-CSF, GM-CSF: Granulocyte (+Macrophage) Colony Stimulating Factor
Sickle Cell Complications, Tx Low O2, H20-> Aplastic crisis (ParvoB19 infx), Spleen sequestration, Increased risk for encapsulated organism infx, Salmonella osteomyelitis, pain crisis (vaso-occlusion), renal papillary necrosis. Tx: Hydroxyurea increases HBF production.
Hb H Beta tetramers. Only 1 functional Alpha gene. Thalassemia
Hb Barts Gamma Tetramers. No functional alpha gene. Hydrops Fetalis- fetal death. Thalassemia.
Beta Thalassemia Major: Crazy hepatosplenomegaly. Crew cut skull. Frequent blood transfusions -> Hemachromatosis, heart failure. Minor: Meh.
Warm Agglutinin IgG-mediated Chronic Immune Anemia: SLE, CLL, methyldopa
Cold Agglutinin IgM-mediated Acute Immune Anemia: Mono, Mycoplasma Pneumoniae
Erythroblastosis Fetalis Rh negative mother’s serum antibodies attack newborn’s Rh+ RBCs 
Coombs Test Determines Autoimmune cause of hemolytic anemias. Direct: Anti-Ig antibodies agglutinate Ig-bound RBCs. Indirect: Pt’s anti-RBC Igs attack & agglutinate normal RBCs
Paroxysmal Nocturnal Hemoglobinuria Membrane defect(GP1 def)-> more susceptible to complement lysis. Elevated Urine Hemosiderin.
Microangiopathic Anemia “Fragmentation” hemolytic anemia. DIC, TTP, HUS, SLE, HTN-> schistocytes.
DIC Etiology STOP Making New Thrombi! Sepsis, Trauma, Obstetric complications, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion. Depletes coagulation cascade & platelets.
Idiopathic v. Thrombotic Thrombocytopenic Purpura Idiopathic: Antiplatelet antibodies, more megakaryocytes. Thrombotic: Vascular damage-> thrombosis. Elevated LDH, neuro & renal sx.
Hemophilia A vs B A:Factor 8 deficiency. B: Factor 9 Deficiency. Both X-linked.
Bleeding Time, PT, PTT Bleeding Time: Marker for platelets only, PT: Extrinsic PWY, PTT: Intrinsic PWY
Bernard-Soulier Low GP1b, low platelet ct.
Glanzmann’s Thrombasthenia Low GP IIb-IIIa. Poor aggregation
t(9;22) CML- Philadelphia Chromosome
t(8;14) Burkitt’s Lymphoma. C-myc
t(14,18) Follicular Lymphoma. bcl-2
t(15,17) Acute promyelocytic (M3-type) AML. Tx w/ all-trans retinoic acid
t(11;22) Ewing’s Sarcoma
t(11;14) Mantle Cell Lymphoma
Histiocytosis X Lagerhans macrophages w/ Birbeck Granules “Tennis rackets” ->-> Restrictive Pulm Dz
Extrinsic Pathway 7, 10, 5, 2, 1
Intrinsic Pathway 12, 11, 9, 8, 10, 5, 2, 1
vWF Disease Most common heritable coagulopathy-> prolonged bleeding time. Autosomal DOMINANT > Hemophilia A > B(XR). Normal bleeding time.
AT3 Deficiency 1) Estrogen use 2)congenital
Created by: Kyle Tiemeier
 

 



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