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Hem-Onc: Answer

This document provides a summary of hematology concepts including: 1) The normal order of cells in a white blood cell differential and causes of eosinophilia. 2) Components of the coagulation cascade including vitamin K dependent and activated protein C factors. 3) Causes and treatments of anemias including microcytic, normocytic, macrocytic, and aplastic anemia as well as sickle cell disease and thalassemia. 4) Translocation genetics involved in various cancers and their associations such as t(9;22) with chronic myeloid leukemia.

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0% found this document useful (0 votes)
256 views3 pages

Hem-Onc: Answer

This document provides a summary of hematology concepts including: 1) The normal order of cells in a white blood cell differential and causes of eosinophilia. 2) Components of the coagulation cascade including vitamin K dependent and activated protein C factors. 3) Causes and treatments of anemias including microcytic, normocytic, macrocytic, and aplastic anemia as well as sickle cell disease and thalassemia. 4) Translocation genetics involved in various cancers and their associations such as t(9;22) with chronic myeloid leukemia.

Uploaded by

Aman Raj K
Copyright
© Attribution Non-Commercial (BY-NC)
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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Hem-Onc

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

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