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Hematology, Terminologies, TESTS, Chronic Lymphocytic/lymphatic Leukemia …

- - - - Dameshek Method
      - Modified Indirect Platelet Count
      - Fonio’s Method
  - - - Rees-Ecker
      - Phase Microscopy Method/
        Brecher-Cronkite
      - Guy’s and Leake Method
      - Unopette Method
- - - - DENSE granule deficiencies
        
        Thrombocytopenia with absent radii syndrome (TAR)
        
        RBM8A; 1q21.1
        
        🌟 Wiskott-Aldrich syndrome (WAS)
        
        🌟 Chediak-Higashi syndrome
        
        🌟 Hermansky-Pudlak syndrome
      - ALPHA granule deficiencies
        
        🌟 Gray platelet syndrome
  - - - MYH9
  - - - Chronic liver disease
      - Cardiopulmonary bypass surgery
      - Anti-platelet antibodies
      - Myeloproliferative & Lymphoproliferative disorders
      - Drug-induced membrane modification
  - - - Acquired uremia
      - Acquired VWB disease
- - - - Not responsive to TPO
      - Conditions
        
        ET
        
        Uncontrolled proliferation of marrow megakaryocytes
        1-3 or 2-4 megakaryocytes/LPF
        
        JAK2
        MPL
        CALR
        
        ↑ platelets, dysfunctional
        
        Thrombotic
        
        Overwhelming number of platelets = thrombotic risk
        
        Hemorrhagic
        
        Hindi responsive magform clot = risk of bleeding
        
        PM/MMM
        
        PCV
        
        CML
    - - Normal megakaryocyte & platelet function
        = responsive to TPO
      - Problem is only in the number of platelets
      - Conditions
        
        Post-splenectomy
        
        IDA
        
        Iron regulates thrombopoiesis
        
        Lactating mother
        
        Deficient in iron-rich food
        
        Infant/ Newborn
        
        Inflammation & Disease
        
        Exercise-induced
        
        Hemorrhage or surgery
        
        Rebound
        
        After therapy/ alcohol madecrease, BM
        will adjust = > megakaryocytes
  - - - Neonatal allo/autoimmune thrombocytopenia
      - Drug-induced thrombocytopenia
      - HDN/HTR
      - Post-transfusion
      - Immune Thrombocytopenic Purpura
        ITP
      - Pregnancy & Preeclampsia
    - - Hypersplenism
        
        Big Spleen Syndromes
      - Hypothermia
    - - Wiskott-Aldrich Anomaly
      - May-Hegglin Anomaly
        
        MYH9
        
        Misshapen & Giant Platelets
        ‘May Hanggod” na platelets
        
        Dohle bodies in segmented neutrophil
        
        Conditions
        
        Sebastian syndrome
        
        Fechtner syndrome
        
        Epstein syndrome
      - Bernard Soulier
      - Megaloblastic anemia
        
        Decrease of DNA synthesis/impaired DNA synthesis
        
        ↓ DNA synthesis = ↓ mega lobules = ↓ PLT
      - Replacement of normal marrow
      - Thrombocytopenia with Absent Radius
        TAR Syndrome
        
        RBM8A, 1q21-1 (long arm of chromosome 1)
        
        Defect in TPO/TPO-R signaling pathway resulting to hypoplasia of megakaryocyte lineage
        
        Congenital absence/ hypoplasia or the radius
        Absent, short, malformed ulna
      - Aplastic anemia
      - Chemotherapy, Drug/ Alcohol abuse
        
        Anagrelide
        
        Ethanol
        
        Interferon therapy
      - Congenital Amegakryocytic Thrombocytopenia
        
        MPL gene on chromosome 1 (1p34.1)
      - X-linked Thrombocytopenia
        
        WAS gene on the X chromosome (Xp11.23)
        
        GATA1 gene on the X chromosome at Xp11
      - Autosomal Dominant Thrombocytopenia
        
        ANKRD26 gene on the short arm of chromosome 10 (10p12.1)
    - - MicroAngiopathic Hemolytic Anemia
        MAHA
        
        Thrombotic Thrombocytopenic Purpura
        TTP
        
        Absence or dysfunction of ADAMTS13
        = UL-vWF multimers to remain in the circulation
        = Platelet-rich Thrombi
        
        ADAMTS13
        (A Disintegrin and Metalloprotease with a Thrombospondin with a Thrombospondin Type 1 Motif, Member 13) 😠
        
        Hemolytic Uremic Syndrome
        HUS
        
        DIsseminated Intravascular Coagulation
        DIC
- - - - need CYTOCHEMICAL STAIN
        why?
        
        lymphoblasts indistinguishable from myeloblasts
        
        WBC ct. = ⬆️ 20x10^9
    - - caused by virus EBV🦠
        
        AFRICAN
        
        AMERICAN
        
        WBC ct. = ↔️ normal/ mildly elevated
    - - BM must have 50% lymphocyte
        but 30% of 50 must be BLASTS
        
        PEAK - 3 yrs. old
        
        < 10 yrs old - good prognosis
        
        10 yrs old - bad prognosis
        
        WBC ct. = ⬇️ 20x10^9
    - - B cell ALL
        
        poor prognosis
      - T cell ALL
        
        best prognosis
        
        blasts forms rosette
      - non B non T ALL
        e.g. NK cell
        
        common ALL
        
        cell reacts to anti-ALL non t non B serum
        
        null cell ALL
        
        don't react with serum
        
        Pre - B ALL
        
        mu heavy chain demonstrated in cytoplasm
  - - - M2
        
        M1
        
        Acute myeloblastic leukemia
        without maturation
        
        ● >30% blasts
        ● <10% granulocytic cells
        
        Acute myeloblastic leukemia
        with maturation
        
        ● >30% blasts
        ● >10% granulocytic cells
      - Acute hypergranular promyelocytic leukemia (APL)
        
        ● leukocytosis
        ● Involves chromosomal translocation = (t: 15,17)
        ● With Faggot Cells (mass of Auer tods)
        ● Associated with DIC
        
        ● >30% blasts
        ● >10% granulocytic cells
        ● >50% promyelocytes
      - Acute microgranular promyelocytic leukemia
        
        ● Leukopenia
        ● Less faggot cells
        ● With abnormal eosinophils
    - - M6
        
        M7
        
        Megakaroblastic Leukemia
        
        , >30% blast
        , >30% megakaryocytic cells
        
        Erythroleukemia (EL)
        
        Aka Di Guglielmo's Syndrome/Eythremic leukemia
        
        , >30% blast
        , >50% erythroid precursors
        
        M6b
        
        Di Guglielmo's
        
        M6c
        
        behaves differently
        requires differential therapy
        
        M6a
        
        Acute erythroleukemia
        , >50 yrs old
      - Acute monocytic leukemia (AMoL)
        
        M5a
        AMoL without differentiation
        
        AKA Schilling
        
        , >80% monocytic
        , >80% monoblastic
        
        M5b
        AMoL with differentiation
        
        , >80% monocytic
        , <80%monoblastic
    - - ● 5% eosinophils in BM
    - - ● Aka NAEGELI’s
        
        ● 20 to <80% monocytic cells
- - - - Immunophenotyping
        
        Uses CD markers
        
        Table - Check me out!
        
        CD45 Common leukocyte antigen, expressed on lymphoid and myeloid cells
        
        CD3 T-lymphocytes
        
        CD45RO T-lymphocytes but less specific than CD3
        
        CD20 B- lymphocytes
        
        CD79a B-lymphocytes & plasma cells
        
        CD57 Natural Killer (NK) cells
        
        Neutrophil Elastase Granulocytic series
        
        CD15 Granulocytic & Monocytic series,
        Reed-Sternberg & Hodgkin’s cells
        
        CD68 Monocytic series, Mast cells, more
        weakly on granulocytic series
        
        Glycophorin Erythroid
        
        CD61 Megakaryocytes & Platelets
        
        CD30 Reed-Sternberg & Hodgkin’s cells,
        Anaplastic large cell lymphoma
      - Know what type of mutation na natabo
        
        Cytogenetic
        
        Types of mutation
        
        Deletion
        
        Duplication
        
        Inversion
        
        Insertion
        
        Translocation
        
        Know the products formed due to mutation
        
        Molecular genetic
- - - - MPO
        
        MPO is present in myeloid cells
        
        Napthol ASD Chloroacetate Esterase
        
        detect neutrophilic & Monocytic esterases
        
        Sudan Black B (SBB)
        
        same sa MPO but it stains the granules
- - - - hematocrit is aka?
        
        is it measured directly or indirectly?
        derived from what parameters?
        (if lipat, GURIPAT use commonsense no.1)
    - - uses direct current or?
      - METHODS OF DIFFERENTIAL COUNT
        
        Aperture - impedance
        
        RF - frequency
        
        Light Scatter Flow cyto - shape
        
        Cytochemistry - enzyme
        
        Fluorescence - immunological
        
        give keywords on each methods
        like size, granularity, volume etc.
        remember same2 si RF and light scatter
        difference is frequency can MEASURE
        internal characteristics of cell
        
        Next topic🎉
        
        USUAL na gina measure regarding RBCs
        RBC INDICES
        pg.2 lower right
        
        4 ni sila but give 5
        because ang isa is also measure by automated analyzers
        
        give units, why muna unit ya?
        
        give formula
        
        ano gina measure ka indices mentioned?
        
        HINT:
        volume, Hgb, distribution
        
        MCH VS MCHC
        answer...if lipat
        see commonsense no.2
        MCV VS RDW
        answer...if lipat
        see commonsense no.3
        
        Next topic🎉
        
        1 more item...
    - - give three common
        HGB method na gina use
        
        sino ang toxic sa ila?
        kay sino si DRABKIN'S soln?
        at what wavelength sila na read?
- - - - MDS 1
        Refractory Anemia (RA)
        
        <5% blasts
        
        Survival time: 47(4yr)
        
        AML progression: 10-13%
      - <5% blasts
        
        Survival time: 52 (4yr)
        
        AML progression: 13-15%
    - - MDS 5
        Refractory Anemia w/ excessive blast in Transformation (RAEB-T)
        
        21-30% blasts
        
        15-20 yr (6 months)
        
        Progression to AML: 60-100%
      - 5-20% blasts
        
        Survival time: variable (2yr)
        
        Progression to AML: 15-50%
- - - - red clot
        (fibrin clot)
- - - - white clot
        (platelet clot)
- - - - Thrombomodulin
        
        Heparan sulfate
        
        Tissue Plasminogen Activator
        TPA
        
        Smooth EC lining
        
        Protein C Receptor
        EPCR
        
        CD39
        
        Protein C control system
        
        Activates fibrinolysis
        
        Anticogulant that regulates
        thrombin generation
        
        Protein C control system activator
      - EXTRINSIC pathway regulator
- - - - VWF
        
        P-selectins
        
        iCAMS
        
        PECAMS
        
        ADAMS13
- - - - NORMAL
        aggregation with
        Ristocetin
      - Aggregation defect
        Glycoprotein IIb-IIIa
- - - - Basophilic normoblast
        
        Polychromatic normoblast
        
        Orthochromic normoblast
        
        Reticulocyte
        
        Erythrocyte
        
        Erythrocyte
        
        3 more items...
        
        Erythrokinetics
        
        2 more items...
  - - - Basophilic erythroblast
        
        Polychromatic erythroblast
        
        Orthochromic erythroblast
        
        Polychromatophillic erythrocyte
        
        Erythrocyte
  - - - Rubricyte
        
        Metarubricyte
        
        Polychromatic erythrocyte
        
        Erythrocyte
- - - - Primary Polycythemia Vera
        AKA ''cryptogenic polycythemia''
        ''Vasquez-Osler Disease''
        
        Mutation in JAK2 gene = activation of JAK2 kinase
        
        JAK2 exon 12
        
        Proliferation of pluripotential stem cell
        
        Bone Marrow
        
        increased all cell lines
        
        myelofibrosis in later stage
        
        Abnormal Megakaryocytes (blebs/clefts)
        
        decreased/absent iron stores (due to EPO activity)
        
        Chemistry relation
        
        ⬆️ UA
        
        ⬇️ EPO
        
        gadako: KIDNEY, LIVER
        
        Erythrocyte
        
        HGB >16g/dL
        
        HCT >55%
        
        ocassional nucleated RBC
        
        Granulocytes
        
        LAP >100
        
        absolute granulocyte >12x10^9/L
        
        Platelets
        
        Thrombocytosis (>400x10^9/L)
        
        abnormal& dysfunctional = bleeding
        
        IF TREATED w/ Chemotherapeutic drug
        muni makitan na cells:
        
        Oval macrocytes
        
        HJ bodies
        
        Agranular large platelets
        
        Hypersegmented neutrophil
        
        TREATMENT
        
        Therapeutic phlebotomy
        depletes iron stores
        
        Chemotherapy
        kills malignant stem cell
        
        Splenectomy
        relieve symptoms and blood pooling
        
        Radioactive Phosphate
        last 6 mo. to years
        
        Interferron Alpha
        for those who cannot tolerate hydroxyurea (a chemotherapy medication capsule)
      - Relative/Spurious Polycythemia
        
        ⬇️ Plasma volume = increase HCT ; increase RBCs
        
        Acute dehydrations
        Stress erythrocytosis
      - ⬆️ EPO Muna Ang reason Yaya sa increased RBCs
        
        Due to hypoxia
        Abnormal EPO production
        Hemoglobinopathies
        ⚠️ Chronic Mountain Sickness (Monges disease) - fail to adapt in high altitude home
- - - - < thickness & vascularity >
        
        < intercapillary pressure >
        
        < efficiency of tissue fluids in
        accelerating clotting process >
        
        prolonged
        
        shortened
        
        prolonged
        
        shortened
        
        shortened
        
        prolonged
      - prolonged
      - shortened
- - - - Fibrin-platelet plug formation
        
        Fibrin stabilization
        
        5
        
        Fibrin clot is stabilized by Factor XIII
        (Fibrin-Stabilizing factor)
        
        4
        
        Coagulation factors interact on platelet surface to produce fibrin; Fibrin-platelet plug then forms at the site of vessel injury
      - 3
      - Interaction and adhesion of platelets to one another to form initial platelet plug
- - - - Fibroblasts
      - Smooth Muscle Cell
      - Collagen