Hema 2 MTAP

Hematology 1

• Covers:
  • Scientific and Technical Components of Laboratory Testing
  • Blood Cell Production, Structure, Metabolism and Function
  • Routine Laboratory Evaluation of Blood Cells
  • Blood Disorders
  • Coagulation
  • Quality Assurance and Laboratory Communication

Blood Disorders

• Divided into:
  • Erythrocyte Disorders
  • Leukocyte Disorders
  • Thrombocyte Disorders

Coagulation

• Covers:
  • Hemostasis
  • Tests
  • Disorders

Quality Assurance and Laboratory Communication

• Encompasses:
  • Quality Assurance
  • Laboratory Communication

Erythrocyte Disorders

• Includes RBC Anomalies like Anisocytosis, Anisochromia, Poikilocytosis, and RBC Inclusion Bodies
• Anemia is also a key component

Red Blood Cell Anomaly

• Anisocytosis: Increased number of RBCs with variation in size
• Anisochromia: Variation in the normal coloration of RBCs
• Poikilocytosis: Increased number of RBCs with variation in shape
• Inclusion Bodies: Abnormal structures inside the RBC

Anisocytosis

• Macrocytes: Large RBCs greater than 8.0um, are observed when MCV is greater than 100fL, and linked to impaired DNA synthesis
• Microcytes: Small RBCs less than 6.0um, are observed when MCV is less than 80fL, and associated with defective Hgb formation

RBC Histogram

• A visual display of cell size and cell frequency
• Two parameters are computed: MCV (Mean Corpuscular Volume) and RDW (Red Cell Distribution Width)
• Volume sizes between 36fL and 360fL are counted as RBCs
• Volumes of 24-36fL are not counted as RBCs

RDW

• RDW is calculated to identify anisocytosis.
• The reference value is between 11.5% to 14.5%
• It's dependent on the width of the distribution curve and MCV.
• RDW CV (Coefficient of Variation):
  • Reference value: 39-46fL
  • The width of the curve is measured at a point 20% above the baseline level.
  • Not influenced by MCV
  • A more reliable measure of erythrocyte variability than standard deviation.

RBC Histogram Examples

• Normal RBC Histogram: Normocytic RBC population with MCV of 89fL and RDW (CV) is 13%
• Shift to the Left: Microcytic RBC Population: MCV is 75fL and RDW is 14.2%
• Shift to the Right: Macrocytic RBC Population: MCV is 125fL and RDW is 13.8%.
• Shift to the Left: Microcytic RBC Population: MCV is 64fL and RDW is 25.1%.
  • The lower discriminator includes WBC fragments, large platelets, microcytic RBCs, and platelet clumps.
  • The higher discriminator includes RBC agglutination, cold agglutination, nucleated RBCs, and small lymphocytes.
• Bimodal Curve: 2 greater population of RBC
  • Automatic anisocytosis
  • May be present due to recent blood transfusion, presence of cold agglutination, Hemolytic Anemia, and Schistocytes

Conditions with MCV and RDW

• Normal RDW (little to no anisocytosis):
  • Decreased MCV: Anemia of Chronic Inflammation
  • Normal MCV: G6PD Deficiency
  • Increased MCV: Liver disease
• Increased RDW (Anisocytosis):
  • Decreased MCV: Iron Deficiency Anemia
  • Normal MCV: Sickle Cell Anemia
  • Increased MCV: Megaloblastic Anemia

Anisochromia

• The "Variation in the normal color (Salmon-pink) of RBC"
• Central pallor: approximately 1/3 of diameter

Hypochromic Cells

• Typically microcytic
• Grading of Hypochromia
  • 1+: ½ Central pallor
  • 2+: 2/3 central pallor
  • 3+: 3/4 central pallor
  • 4+: Thin Rim of Hgb
• Anulocyte: aka Pessary cell, Ghost cell
  • Occurs with IDA

Hyperchromic Cells

• Lack of central pallor
• True hypochromia occurs with high MCHC
• Hereditary Spherocytosis: only disease with high MCHC
  • 3 key clinical manifestation (Splenomegaly, Anemia and Jaundice)
• Autohemolysis test: greatly increased
• OFT: not diagnostic for HS
• EMA binding test (eosin 5 maleimide test): decreased fluorescence

Polychromatophilic Erythrocytes

• Aka diffusely basophilic erythrocytes (Reticulocytes in Wright stain)
• Results in a Bluish tinge, caused by residual RNA
• Grading Polychromasia
  • Slight: 1%
  • 1+: 3%
  • 2+: 5%
  • 3+: 10%
  • 4+: >11%

Poikilocytosis

• Stomatocyte are also known as Mouth cells: Elongated RBC with slit-like central pallor
  • Associated with Rh Deficiency Syndrome, alcoholism, Electrolyte imbalance, Severe liver disease, and Overhydrated HS
  • Dehydrated HS: aka Hereditary Xerocytosis -*Xerocytes: dehydrated form of stomatocyte, half dark and half light
• Acanthocyte are also known as Thorn cell/ Spur cell
  • Associated with Abetalipoproteinemia
  • aka Hereditary Acanthocytosis, Bassen Kornzweig Syndrome
  • absent Lipoproteins (VLDL, LDL and chylomicron)
  • Associated McLeod Syndrome (associated with Kell blood group system), and Pyruvate Kinase Deficiency
• Ovalocyte
  • Oval shaped RBCs
  • Related to Hereditary Ovalocytosis
  • aka South East Asian ovalocytosis
• Elliptocyte
  • Elliptical/Cigar shaped RBCs
  • Hereditary Elliptocytosis
  • Thalassemia
  • aka Mediterranean Anemia
• Schistocyte
  • Aka Schizocyte: Fragmented RBCs
  • MAHA (MicroAngiopathic Hemolytic Anemia
  • Helmet cells: schistocyte in MAHA
  • TTP (Thrombotic thrombocytopenic purpura)
  • HELLP (Hemolysis, Elevated Liver enzymes, low platelet count)
  • HUS (Hemolytic Uremic Syndrome): associated with E.coli serotype 0157:H7
  • DIC: Disseminated Intrravascular Coagulation
• Drepanocyte
  • Aka meniscocyte: sickle or crescent shaped RBCs
  • Sickle cell anemia and Hemoglobin SC disease
  • There are 2 forms of Drepanocytes
  • 1. ISC (Irreversible Sickle cells): Crescent shaped and Fragment when reoxygenated
  • 2. Oat shaped sickle cells*: less pronounced projections and return to original when reoxygenated

Inclusion Bodies

• Basophilic Stippling
  • is also known as Punctate Basophilia
  • Irregular dark blue to purple granules evenly distributed
  • Aggregated RNA with Wright stain and Supravital stain
  • Found in Lead Poisoning
    • aka Plumbism/ Saturnism
  • May be due to Megaloblastic Anemia
• Siderotic Granules
  • Aka Siderocytic Granules/ Pappenheimer bodies
  • Multiple dark blue irregular granules (Prussian blue iron stain) OR Pale blue cluster (Wright stain)
  • Intra-erythrocytic collections of Iron
  • Iron Stains (Perl's reagent through Prussian blue reaction) or NMB and Wright Stain: Pappenheimer bodies
  • Sideroblastic anemia
  • Dimorphic blood: both normochromic and hypochromic RBCs
• Heinz bodies
  • Large and round, blue to purple material eccentrically located along the inner membrane
  • Content: denatured and precipitated hgb
  • Stain: Supravital stains (BCB, NMB, Crystal violet, Methyl violet)
  • Dissolves in Wright stain
  • Occur with G6PD Deficiency or DIHA (Drug Induced Hemolytic anemia)
  • and Unstable Hgb dse (Hb Casper, Hb Genova Hb Bristol, Hb Torino, etc)
• Howell-Jolly bodies
  • Usually round, blue to purple and frequently appears singly
  • mistaken as Heinz bodies
  • denatured and precipitated hgb
  • Stain: Wright stain, NMB, and Feulgen reaction (+): Histochem, reaction for DNA
  • Megaloblastic Anemia, Refractory anemia and Lead posoning

Anemia

• Anemia is a Decrease of one or more of the following: Red blood cell count, Hemoglobin, and Hematocrit
• Classification of Anemia based on morphologic and pathophysiologic factors
• Morphologic:
• Normocytic, Normochromic Anemia
• Microcytic, Hypochromic Anemia
• Macrocytic, Normochromic Anemia
• Pathophysiologic:
  • Anemia caused by decreased production
  • Anemia caused by increased destruction
  • Blood loss

Normocytic, Normochromic Anemia

• MCV and MCHC will read as Normal
  • If there is Normal or Decreased Reticulocyte Count it will be Aplastic Anemia, Kidney Disease, and or Acute Blood Loss
  • Aplastic Anemia
  • Rare but potentially deadly bone marrow failure syndrome
  • Pancytopenia, Reticulocytopenia, BM hypocellularity and depletion of HSC
  • Acquired: Idiopathic or Secondary to chemicals, viruses, drugs
  • (Chloramphenicol: most frequently implicated in acquired aplastic anemia)
  • Inherited: Dyskeratosis congenita, Shwachman-Bodian Diamond Syndrome,
  • Fanconi Anemia (most common Inherited aplastic anemia
  • If there is Increased Reticulocyte Count it will be:
  • Paroxysmal Nocturnal Hemoglobinuria (PNH)
  • PCH (Donath Landsteiner Hemolytic Anemia)
  • Sickle Cell Disease
  • Porphyria
  • Enzyme deficiency (G6PD Def, PK def)
  • Other Hemolytic Anemia
  • Paroxysmal Nocturnal Hemoglobinuria (PNH)
  • Aka Marchiafava- Micheli Syndrome
  • Deficiency of Complement Regulator Proteins
  • DAF (Decay-accelerating factor/ CD55)
  • MIRL (Membrane inhibitor of reactive lysis/ CD59)
  • Ham's Acidified Serum Test, Sugar water/ Sucrose Hemolysis Test
  • Flow Cytometry (using FLAER- Fluorescein labeled proaerolysin): confirmatory

Microcytic, Hypochromic Anemia

• MCV and MCHC will read as Low
• Also Iron level insufficient to maintain normal erythropoiesis
• Associated conditions (CTAILS)
• Chronic blood loss
• Thalassemia
• Anemia of Chronic Infection
• Iron Deficiency Anemia
• Lead Poisoning
• Sideroblastic Anemia

Anemia of Chronic inflammation (ACI)

• Is previously called: Anemia of Chronic Disease (ACD)
• The Most common anemia among hospitalized patients
• Associated with chronic infections: TB, RA, and Tumors
• Central feature of ACI: sideropenia (decreased serum iron) despite abundant stores
  • Early stage: Normocytic, Normochromic
  • Advanced stage: Microcytic, hypochromic
• Acute phase reactants (APRs) that contribute to ACI
• Hepcidin (master regularoty hormone for systemic iron metabolism, inactivates Ferroportin
• Ferritin
• Lactoferrin

Sideroblastic Anemia

• Is the Defective incorporation of iron into protoporphyrin which causes iron to be trapped inside of the mitochondria
• Sideroblast: nucleated RBC precursor with cytoplasmic iron granules
• "Rings: mitochondria loaded with iron
• Rings Sideroblast: Hallmark of Sideroblastic anemias
• Results in a Dimorphic blood picture: normochromic and hypochromic

Iron Deficiency Anemia

• Most common Anemia
• Possible causes
  • Blood loss (especially menstruating women)
  • Nutritional deficiency (infants)
  • Inrease in iron demand (Pregnancy, lactation, adolescence)
  • Malignancies of gastrointestinal tract
  • Hookworm infections
• Clinical features
  • *Koilonychia (spooning of fingernails)
  • *Glossitis (inflammation of tongue)
  • *Angular cheilosis -*Pica: craving for non-food items like dirt, clay, hair or ICE (most common-pagophagia)
• Lab results for:
  • Stage 1 presents as normal
  • Stage 2 and 3: gradual decrease of Hgb, Serum, and Ferritin results

Macrocytic, Normochromic Anemia

• MCV will read as High and MCHC will read as Normal
• Differentiated by Megaloblastic and NonMegaloblastic -Megaloblastic Anemia occurs when There is B12 Deficiency or Folate Deficiency
  • oval macrocytes and present hypersegmented Neutrophils and Megaloblasts in BM
• NonMegaloblastic Anemia related to Liver Disease, Alcoholism or BM failure
• round macrocytes and there is Absent hypersegmented Neutrophils and Megaloblasts in BM
• Vit B12 Deficiency
• Causes from Inadequate intake
• Increased need (pregnancy, lactation, growth)
• Competition (e3x. D. latum infection)
• Lack of Intrinsic Factor (IF)
• Ex. Gastrectomy, H. pylori infection, Pernicious Anemia
• Pernicious Anemia
• Presence of: Antibodies against Parietal cells and Antibodies against IF
• Folate Deficiency
• Causes from Inadequate intake
• Increased need
• Renal Dialysis

Anemia by Cause

• Decreased production can be caused by:
  • Aplastic Anemia
  • Megaloblastic Anemia
  • Iron Deficiency Anemia
  • Thalassemia
  • Anemia of Chronic Renal failure
  • Anemia of Chronic disorders
  • Anemia of Chronic Inflammation
  • Anemia associated with marrow infiltration
  • Sideroblastic Anemia
• Increased destruction can be caused by:
  • Intracorpuscular abnormality
  • Membrane defect: HS, HE, Pyropoikilocytosis
  • Enzyme deficiency: G6PD, Pyruvate Kinase def, Porphyria
  • Globin abnormality (Hemoglobinopathies)
  • PNH
  • Extracorpuscular abnormality
  • Mechanical: microangiopathic Hemolytic anemia, etc.
  • Infection: Malaria, Bartonella, Ehrlichia, Babesia
  • Chemical and Physical agents: Drugs, toxins, burns
  • ,Antibody mediated: WAIHA

Porphyria, Hemoglobinopathies and Thalassemia

• Abnormal hemoglobin
• Mitochondria = Heme = Porphyria
• Ribosome = Globin = Hemoglobinopathy (Qualitative) and Thalassemia (Quantitative)

Porphyria

• Disorders characterized by impaired Heme synthesis and can be as acute and serious as Lead Poisoning
• Lead will inhibit enzymes, Ferrochelastase and pyramidine 5' nucleotidase
• Pyramidine 5' nucleotidase removes RNA from reticulocytes
• no enzyme- leads to Basophilic stippling
• Enzymes involved in ALA Deficient Porphyria Succinyl CoA +Glycine = ALA synthase ALA= ALA dehydrase PBG= PBG deaminase Hydroxymethylbilane Uroporphyrinogen =Uroporphyrinogen III synthase Coproporphyrinogen =Uroporphyrinogen decarboxylase Protoporphyrinogen =Coproporphyrinogen oxidase Protoporphyrin IX (Porphyrin) = Protoporphyrinogen oxidase Heme = Ferrochelatase

Hemoglobinopathies

• The differences in the arrangement of amino acids in the polypeptide chain
• There are Four Major Groups of Hemoglobinopathies
• Alpha hemoglobinopathies: 2nd most common
• Beta hemoglobinopathies: Most common
• Gamma hemoglobinopathies
• Delta hemoglobinopathies
• Α1/Α: 2α2β
• Α2: 2α2δ
• F: 2α2γ

Beta Hemoglobinopathies

• Can be Homozygous where both genes are mutated
• There is HbA1 is not produced and is ABSENT
• Examples of Homozygous Beta Hemoglobinopathies Includes Sickle cell dse (HbSS) and Hgb C (HbCC)
• Can be Heterozygous where only one gene is mutated
• There is HbA1 production still present
• Examples of Heterozygous Beta Hemoglobinopathies Includes Sickle cell trait (HbAS) and Hgb C trait (HbAC)

Thalassemias

• Aka: Hereditary Leptocytosis and Mediterranean Anemia
• These are Quantitative: Reduction or total absence of one or more globin chains
• Alpha Thalassemia (α α / α α)
• Beta Thalassemia (β / β)
• Molecular Genetic tests are confirmatory

Alpha thalassemia (αα/αα)

• Is the Deletion of alpha globin genes
  • There are 4 forms of this genetic mutation
  • Silent carrier where 1 gene deleted and the individual will be Asymptomatic
  • Alpha Thalassemia Trait/ Minor where 2 genes deleted and the individual will have Mild microcytic hypochromic anemia
  • HgH Disease where 3 genes deleted and the individual will have Microcytic hypochromic anemia, are Found in adults, May co-exist with Hb Constant Spring
  • Hb Bart Hydrops Fetalis syndrome/ Alpha Thalassemia Major where 4 genes deleted and the individual will result with Most severe Fetus incompatible with life

Beta thalassemia (β / β)

• Is the Mutation of beta globin genes which produces lesser amount of Beta chains
• There are 4 forms of this genetic mutation
• Silent carrier (ẞsilent / β) and individual will be Asymptomatic and require Molecular Genetic testing
• Beta Thalassemia Trait/ Minor (β+ / β and or B° / β ) and individual will have Mild HA leading to Microcytic, Hypochromic
• Beta Thalassemia Intermedia (Bsilent / Bsilent and or β+ / silent and or B°/ slient) resulting with Moderate clinical symptoms and Transfusion-Independent
• Beta thalassemia major/ Cooley's Anemia/TDT (β+ / β+ and or β+ / B° and or B° / B°) resulting with Most severe Target cells, tear drop cells, elliptocytes, nRBCs, Polychromasia, Basophilic stippling, and HJ bodies, Pappenheimer bodies

Leukocyte Disorders

• Includes WBC Anomalies
• Leukemia

WBC Anomalies

• Niemann-Pick Disease (NPD)
  • Macrophage where cytoplasm is swollen by many small lipid droplets
  • Deficiency of sphingomyelinase (an enzyme needed to breakdown lipids)
  • Rare autosomal recessive disease; More commonly seen in Ashkenazi Jews
  • Symptoms begin in infancy and is Often fatal by 3yrs of age
• Gaucher cell (Gaucher Disease)
  • Large macrophage with small eccentric nucleus
  • Cytoplasm distended by glucocerebrosides ( "Crumpled tissue paper")
  • Defect in the catabolic enzyme ẞ-glucocerebrosidase)
  • Autosomal recessive; Most common of the lipidoses leading to Pseudo Gaucher cells
  • Is related to: Thalassemia, CML, ALL, NHL, and Plasma cell neoplasm
• Chediak Higashi Syndrome Description
  • Presence of large, abnormal cytoplasmic granules in phagocytes (sometimes lymphocytes) which lead to Abnormally large lysosomes with fused dysfunctional granules
  • Autosomal recessive disease of immune dysregulation resulting Abnormal granules in both Granulocytes Peroxidase + and Lymphocytes: Peroxidase -
• Wiskott Aldrich Syndrome (WAS)
  • Dysfunctional B cells, T cells, NK cells, Neutrophils and Monocytes which are Microthrombocytes
  • Mutation is X-linked recessive which gives a Thrombocytopenia, Eczema, and Recurrent Infection TRIAD.
  • Leads to Immune deficiency and is prone to bacterial, viral and fungal infections
• May Hegglin Anomaly
  • Presence of gray blue spindle shaped inclusions in granulocytes and monocytes caused from
  • Autosomal dominant genes. This lead to: Thrombocytopenia, Giant platelets with Dohle-like Inclusion bodies. In both Granulocytes: Peroxidase + and Lymphocytes: Peroxidase -
• Grape Cell/ Morula cell/ Mot cell, is also known as An abnormal plasma cell filled entirely with Russell bodies and are
• Found in Multiple Myeloma (Plasma Cell Myeloma)
  • Can be identified by Presence of Bence Jones Proteins
  • CRAB (Hypercalcemia, Reanl, Anemia, and Bone lesion)

Leukemia Overview

• Is Overproduction of various types of immature and mature cells in the bone marrow and/ or the peripheral blood
• If it is Myeloid Leukemia then Granulocytes, Monocytes and Platelets are produced
• If it is Lymphocytic Leukemia then B cells and T cells are produced

Leukemia Characterization

• By Timeline it can be Acute and or Chronic
• Results from Myeloid cells it will be characterize to AML
• If results from Lymphatic cells it will be characterize to ALL
• While, if the cell line is of Chronic Line results form the Myeloid cells can be characterize as CML
• And results form the Lymphatic cells can be characterize as to CLL
• Characteristics of those Results differs from Signs and Symptoms
• For Acute: Short duration, Numerous immature cell forms and Increase WBC count
• While For Chronic Long duration
• Mostly mature cell forms and WBC count: extremely elevated to lower than normal

Acute Lymphocytic Leukemia (ALL)

• It is characterized into L1, L2, and L3
• L1 is 70% ALL in childhood with Homogenous pop of small blasts, having +PAS and - Methyl Green Pyronine and V oil Red O (ORO) while L1 will produce a+ E-rosettes, -Surface Ig and Serum Anti-ALL
• L2 is 70% ALL in Adults with Heterogenous popup of large blasts, having +PAS and - Methyl Green Pyronine and V oil Red O (ORO) while L2 will produce a – E-rosettes, + Surface Ig and -Serum Anti-ALL
• L3 are Rare in both with Homogenous pop of large blasts (with nuclear and cytoplasmic vacuoles), having -PAS and + Methyl Green Pyronine and + oil Red O (ORO) while L3 will produce a – E-rosettes, - Surface Ig and + Serum Anti-ALL

Acute Myeloid Leukemia (AML)

• Is characterized into how differentiated is leukemia cell

   - MO results in Minimum differentiated
     results with – MPO (Myeloperoxidase) and SBB (Sudan Black B)

   - M1results in Without maturation results - MPO (Myeloperoxidase) and SBB

   - M2 results in With maturation
     results with Auer rods  with the most common subtype of Acute Myeloid Leukemia (AML)

   - M3 result in Acute Promyelocytic Leukemia
 is  Associated will Disseminated Intravascular Coagulation
    results with -Faggot cells (Auer rods in cells)-
	
   - M3V microangular variant with *Characteristic cells: butterfly, bowtie, coin-on- coin or apple core nuclei
	
   - M4 Acute MyeloMonocytic Leukemia  also known as Naegeli Monocytic Leukemia
     results in  the Second Most common  subtype and having Auer rods with -M4E: with increased eosinophils
		
	- M5 is Acute Monocytic Leukemiaalso known as  Schilling Leukemia characterized  as:
    - M5a: poorly differentiated 
      (>80% monoblast in Bone Marrow, mostly found in children)
   -  M5b: well differentiated
     (<80% monoblast in Bone Marrow also found in middle-aged adults)		

   - M6 Acute Erythroleukemia also known as DiGuglielmo's Syndrome and results in  -Auer rods, Macrocytic norrmochromic also PAS strongly positive

   - M7 is Acute Megakaryocytic Leukemia
     Factor VIII staining required other platelet immunochemical stains required

   - M8 is Acute Basophilic Leukemia
  and is not popular as of date
		

Characteristics of the M line

MPO and Specific Esterase  will render + in  ALL types from M1-M4

   - +/- is for  MPO and Specific Esterase result from   M6
      -/ the MPO result for  M5 and - M7

SBB will render + in ALL types from M1-M4 and the +/- for  M6
  -/ will result in M5 and  - / for M7

The  nonspecific esterase will result in
     - will result to M1-M3
	
+/- for  M4
  + for M5
        +/- M6 types

Factor VIII result = in M7 and all types 0

Thrombocyte Disorders

• Grouped Using sizes
• Small Platelets can be due to WAS (Wiskott Aldrich Syndrome): X-linked, TORCH, Toxoplasma, Other agents, Rubella virus, Cytomegalovirus, Herpes virus
• Large/ Giant platelets can be due toBSS: Autosomal Recessive, GPS: Autosomal Recessive, MyH9 gene mutations: Autosomal Dominant, MHA, Fechtner, Sebastian, Epstein

Hemostasis

• Covers
  • Coagulation Factors and Cascade
  • Fibrinolytic Pathway

Coagulation Factors

(I): Fibrinogen
- <100mg/dL: Pt and aPTT prolonged
- Afibrinogenemia, Hypofibrinogenemia and Dysfibrinogenemia

(II): Prothrombin
- Half life: 60 hours
- Mean plasma: 10mg/dL

(III): Tissue Factor also known as Tissue Thrombplastin/ and or Thrombokinase of CFIII does not have condtion

(IV): Calcium Ions has a mean pamas of 8-10mg/dL

(V): Proaccelerin also  known as Lablabele factor/Thrombogen does has V Leiden to Parahaemphilia

VII: Proconvertin is A  Stable Factor and first affected by Warfarin and Shortest life of 6

VWF: von Willebrand Factor is  the largest molecule iche plasma and has  receptor for Platelets and Collageen to cause  Von Willebrand Disease

X: Stuart-Prower Factor half  life: 48-52 hours. 1mg/dL
    - Mean plasma concentration of 1mg/dL

VIII: Antihemophilic known as Antihemophilic AHG is
 Unstable I plasma and is   A/Classic Haemophillia

IX: Christmas Factor. Antihemophilic Plasma thromboplastic B- Hemophilliac Christmas disease

XI: Antihemophilic Plasma Thromboplast Antecedent C PTA
Hema C/ Rosental Ashkiniz

XII:  Hageman Factor known as glass/contact factor
No butbut is there
PKFactor of 8 - 35

XIIIFactor, 5 or 32mcg / M- Fletched

Proverties of Fibrinogen

• Thrombin sentenceresistant
• I, M, XI
• Absent in clot Pregnancy Stress Oral
• Vitamin Kdependent
• Age serum present
• Excepts
• Ivkab - absends

Fibrinolysis Proteins

• Plasminogen is produced by the liver and stored inside of Eosinophils. Is Converted to plasmind, and helps prevent Fiber from bounding, or digests it, factorV and 3 anti and factor V
  • Plasmitogen Activitator (PAI-I) TPA and UPA

1. and
2. Activated

Fibrinolsysis and Antifibroysis

• Priming liver
• Pryimin
• Min

Tests

• Lab assessment of hemmorrhargic disorder or a thrombotic

Lab assessments of a hemmerhargic dissodr

Play 
Functioning of

Pt extrinstic

AP  im trnsiuc - watazin

Measure and 06

Volwillibrand Lavel

Studding VS inhibitor

Characteristics of Propeties

Corrected

deficiency vs

in Hemophilia

I, II, XIII Hem A

Lab thrombod

Measure

ANT111

C and C

Prithrobin 02011

Disorders

Disorders of homeostasis prim
secondary homestatic ALY incorporated
in Lecture

F. Quality Assurance

• Diagnostic Diagnostic
• Quality Quality

Communication

• Labsresults

Measurment error a

• Rand

• Quality

Analytical

Utilization

Form

Information
Time

Transfer

Plate

Staff response

• Accurate
• Interbais
• Information
• Lab
• Critical
• Anomalous