Complete Hematology for Medical Student, Nurses and Lab Techs

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HEMATOLOGY

• IMEC Inc.

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Blood Cell Formation
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Promyeloblast
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Erythrocytes

• Anucleate, Biconcave?large surface area
• Easy Gas exchange
• Energy Source-Glucose
• (90 Anaerobic,10 HMP shunt)
• Membrane has chloride/bicarbonate antiport shift
  which enhances CO2 Transport
• Erythrocytosis/polycythemia?increased of cells
• Anisocytosis? varying sizes
• Poikilocytosis?varying shape

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Normal RBCs
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Rouleaux of Erythrocytes
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Blood Gases

• NORMAL VALUES
• PH---7.35-7.45
• pCo2 35-45 mmHg
• pO2 80-100 mmHg

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Formula

• H2O CO2 lt gt H2CO3 lt gt H HCO3
• Lungs
  Kidneys
• NOTE- If Bicarb follows Ph is is a Metabolic
  problem
• If Not more than likely Respiratory in Nature

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Troponin

• Normally, cardiac troponin levels are so low that
  they cannot be measured. Even slight elevations
  may indicate some degree of damage to the heart.
  When a patient has significantly elevated
  troponin concentrations, then it is likely that
  the patient has had a heart attack or some other
  form of damage to the heart. When a patient with
  chest pain and/or known stable angina has normal
  troponin values, then it is likely that their
  heart has not been injured.
• Troponin values can remain high for 12 weeks
  after a heart attack. The test is not affected by
  damage to other muscles, so injections,
  accidents, and drugs that can damage muscle do
  not affect troponin levels.

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D-Dimer

• D-dimer may be ordered when someone has symptoms
  of DVT, such as
• Leg pain or tenderness, usually in one leg
• Leg swelling,
• Discoloration of the leg
• It may be ordered when someone has symptoms of
  pulmonary embolism such as
• D-dimer is especially useful when the doctor
  thinks that something other than DVT or PE is
  causing the symptoms. It is also present when a
  person has symptoms of (DIC)

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INR

• The International Normalized Ratio (INR) is used
  to monitor the effectiveness of anticoagulants
  such as warfarin (COUMADIN). These drugs help
  inhibit the formation of blood clots. They are
  prescribed on a long-term basis to patients who
  have experienced recurrent inappropriate blood
  clotting. This includes those who have had heart
  attacks, strokes and deep vein thrombosis (DVT)..
  The anti-coagulant drugs must be carefully
  monitored to maintain a balance between
  preventing clots and causing excessive bleeding.

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Leukocytes

• Responsible for defense system
• 4000-10,000 per microliter
• Granulocytes
• Basophils
• Eosinophils
• Neutrophils
• Mononuclear
• Lymphocytes
• Monocytes

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BASOPHILS

• Mediate Allergic Reaction
• lt 1 of all leukocytes
• Bilobate Nucleus
• Basophilic Granules contain
• Heparin
• Histamine
• SRS-A

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Basophil
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Mast Cells

• Mediates Allergic Reaction
• Degranulation releases histamine, heparin and
  Eosinophilic Chemotactic Factors
• Can bind IgE to membrane
• Mast Cell structurally similar to basophils
• TYPE I Hypersensivity
• Cromilyn Sodium prevent degranulation

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MAST CELL RELEASE TO IgE SITE
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MAST CELL IN ELASTIC TISSUE
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IMMUNO-RESPONSE
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Eosinophils

• 1-6 of leukocytes
• Bilobate nucleus
• Large eosinophilic granules
• Defends against heminthic and protazoan
• Produces histaminase
• NAACP
• Neoplasm, Asthma, Allergic, Collagen (vascular),
  Parasite
• Usually responds after day 1

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Eosinophil
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Neutrophils

• ACUTE INFLAMATORY RESPONSE40-75 of WBCs
• Multilobed with hydrolytic enzymes called AZO
  granules
• Lysozyme, myeloperoxidase
• Hypersegmented polys are associated with Vit
  B12/Folate deficiency

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Neutrophils Oxidative Imaging
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Oxidative Burst
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Neutrophil
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TYPE 1 Pneumocyte
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Monocytes

• 2-10 of leukocytes
• Kidney shaped nucleus
• DIFFERENTIATE IN MACROPHAGES IN TISSUE

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MONOCYTE
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LYMPHOCYTES

• SMALL, ROUND, DENSE NUCLEUS
• B-lymphocytes produce antibodies
• BONE
• T-lymphocytes cellular immune response
• Thymus
• THINK VIRAL

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Large Lymphocyte
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B-LYMPHOCYTES

• Humoral Immune Response
• Arise from stem cells in Bone Marrow
• Migrate to peripheral lymph
• White Pulp of Spleen, Follicles of lymph nodes
• When Antigen is encountered, B-cells
  differentiate into Plasma Cells
• Produce Antibodies
• Has Memory
• Can function as APC cells via MHC class II

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T-LYMPHOCYTES

• Mediates Cellular IMMUNE Response
• Maturation is in Thymus
• MHC 2 X CD 4 8 helper
• MHC 1 X CD 8 8 suppressor
• CD-Cluster of differentation
• Unlike Mast cell-?T-cell (delayed
  hypersensitivity)

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ANTIGEN PROCESSING
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PLASMA CELLS

• Off Center Nucleus
• CLOCK SHAPED CHROMATIN DISTRUBUTION
• Abundant RER, well developed Golgi
• Come from B-Cells
• Produce large amounts of antibody specific to
  antigen
• Multiple Myeloma is Plasma Cell Neoplasm

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PLASMA CELLS
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Macrophages

• Phagocytize Bacteria, cell debris
• SCAVENGER CELLS
• Macrophages from Monocytes
• Activated from y-IFN
• Can Function as APC

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APCs

• APCs fall into two categories professional or
  non-professional. There are three main types of
  professional antigen-presenting cells
• Dendritic Cells
• Macrophages
• B-cells
• These APCs are very efficient at phagocytosis,
  which allows them to present exogenous as well as
  internal antigens. For the purpose of effectively
  stimulating naive T cells, APCs possess
  co-stimulatory molecules cell-surface molecules
  that deliver essential signals to T cells,
  allowing the T cells to become activated and
  mature into fully-functional forms.

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MACROPHAGES AND PLASMA CELLS
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PLATELETS
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ABO BLOOD GROUPS

• Antigens A B are found on erythrocytic surfaces
• Type A
• Type B
• Type AB
• Type O

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Type A

• Has antigen A on erythrocyte
• Has anti-B in plasma
• Agglutinates when mixed with anti-A antibodies,
  found in plasma of type B whole blood

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Type B

• Has antigen B on erythrocyte
• Has anti-A antibodies in plasma
• Agglutinates when mixed with anti-B antibodies,
  found in plasma of type A whole blood

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TYPE AB (universal recipient)

• Has both antigen A and antigen B on erythrocyte
• Does not contain either anti-A or anti-B antibody
  in plasma
• Agglutinates when mixed with anti-A or anti-B
  antibodies
• But can receive

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TYPE 0 (universal donor)

• Has neither antigen A or B on erythrocyte
• Has both anti-A and anti-B antibodies in plasma
• Does not agglutinate with either anti-A or anti-B
  antibodies

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Rh Blood group

• Several antigens are involved, but consider Rh
  if it contains any one of the antigens
• Anti-Rh antibodies are only made after a
  transfusion of Rh- blood with Rh donor blood
• Or after an Rh- mother gives birth to an Rh child

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Erythroblastosis Fetalis
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Fibrin Clot
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PTT

• Partial Thromboplastin Time
• INTRINSIC
• All except VII and VIII

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PT

• Prothrombin Time
• EXTRINSIC
• Factors 1972
• (10, 9, 7, 2)

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COAGULATION CASCADE
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Protein C

• Protein C is an anticoagulant whose exact
  mechanism is unknown
• Deficiency has been associated with DIC

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ANEMIA

• Microcytic
• Macrocytic
• Normocytic

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MCV

• Mean Corpuscular Volume

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COOMBS TEST

• Direct Coombs Test is used to distinguish
  between immune and non-immune mediated hemolysis

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Microcytic

• HYPOCHROMATIC
• (MCV lt 80)
• Causes
• IRON DEFICIENCY
• Decreased Ferritin
• INCREASED TIBC
• THALESSEMIAS
• LEAD POISONING

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Macrocytic

• MEGALOBLASTIC
• (MCV gt 100)
• B12 is associated with Neurological Problems
• Associated with Folate and B12---Hypersegmented
• Drugs that block DNA synthesis
• Sulfa
• AZT
• Marked Reticulocytosis

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Normocytic

• NORMOCHROMIC
• CAUSES
• Hemorrhage
• Enzyme deficiency (G6PD, PK)
• RBC membrane defect (H. Spherocytosis)
• Bone Marrow disorders ( Aplastic Anemia,
  Leukemia)
• Hemoglobinopathies (sickle cell anemia)
• Auto Immune anemaia
• Anenemia of chronic disease (decreases TIBC,
  Increased Ferritin, decreased serum iron,
  increased iron storage)

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APLASTIC ANEMIA

• Pancytopenia/ destruction of myeloid cells
• Causes
• Radiation, benzene, alkalating agents, (virals,
  cholamphenicol, antimetabolytes)
• Symptoms
• Fatigue, malaise, mucosal bleeding, petachiae
• Treatment
• Withdraw agents, bone transplant, TRANSFUSION

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Hereditary Spherocytosis

• INTRINSIC
• SPECTRIN DEFECT of Membrane
• RBC are small and round
• Less membrane (INCREASED MCHC)
• COOMBS Negative

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Sickle Cell

• HbS mutation
• Substitution of Glutamic Acid for Valine
• Heterozygotic (sickle cell trait)
• Homozygote (B19 parvovirus)
• 8 of African Americans Affected
• Salmonella Osteomylitis

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_at_-Thalessemia

• There are 4-alpha globin genes
• The alpha globin chain is under produced
• No compensation in any other chain
• HbH (B4 tetramer lacks 3 _at_ chains)
• Hb Barts (y4 tetramer lacks all 4 _at_ chains)

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B-Thalessemia

• Heterozygotic-(B-minor) is underproduced
• Homozygotic-(B-major) it is abscent
• In both cases there is compensation on the
  hemoglobin chain, yet is inadaquate
• HbS/B-thalassemia has mild to moderate disease

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DIC

• Activation of Coagulation Cascade that leads to
  micro thrombi and global consumption of
  platelets, fibrin, and coagulation factors.
• Causes-Obstetric, Gram (-) sepsis, trauma,
  transfusion, end stage AIDS
• LABS- Increase PT, PTTDecrease Platelets

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Bleeding Disorders

• Platelet Abnormalities
• (Micro-hemmorhage)
• Mucous Membrane Bleeding
• Petachia
• Purpura
• Prolonged Bleeding Time
• Include ITP (antiplatelet antibodies and
  increased Megakaryocytes). TTP, (schistocytes),
  drugs, and DIC (increased fibrin split products)

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Bleeding Disorders

• Coagulation Factors Defects
• ( Macro-Hemmorhage)
• Hemathrosis-bleeding in joints
• Prolonged PT, and or PTT
• Coagulopathies include
• HEMOPHILIA A (FACTOR VIII DEFECIENCY)
• HEMOPHILIA B (FACTOR IX DEFECIENCY)
• VON WILLEBRANDS VW ANTIGEN
• The most common bleeding disorder

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HEMORRHAGIC DISORDERS

• QUALITATIVE PLATELET DEFECT
• Bernard-Soulier disease
• Defect in Platelet Adhesion
• Glanzmanns Thombobastenia
• Defect in Platelet Aggregation
• INCREASED BLEEDING TIME ONLY !!!

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HEMORRHAGIC DISORDERS

• VASCULAR BLEEDING
• Increased Bleeding Time ONLY!!!

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HEMORRHAGIC DISORDERS

• THROMBOCYTOPENIA
• DECREASED PLATLETS
• INCREASED BLEEDING TIME

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HEMORRHAGIC DISORDERS

• Hemophilia A
• FACTOR VIII Deficiency
• INCREASED PTT

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HEMORRHAGIC DISORDERS

• Hemophilia B
• FACTOR XI Deficiency
• INCREASED PTT

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HEMORRHAGIC DISORDERS

• Von Willebrands Disease
• Antigenic defect
• INCREASED PTT- and Bleeding time

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Von Willebrands Antigen
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HEMORRHAGIC DISORDERS

• DIC
• Decreased Platelets
• Increased Bleeding time
• Increased Prothrombin Time (PT)
• Increased Partial Thomboplastin Time (PTT)