Hematology

Mohamad H Qari, MD, FRCPA

 Hematology
Cellular Components
Components of Blood
 Red Blood Cells
 White Blood Cells
 Inflammatory process
 Coagulation

Blood Typing
Clotting disorders
 Hematology
Spleen
Spleen

Blood
Blood Kidneys
Kidneys
Hematopoietic
Hematopoietic
System
System

Bone
Bone Liver
Liver
Marrow
Marrow
 Hematopoeisis
Three developmental periods
 Mesoblastic
 Blood islands of yolk sac
 Primarily RBC production
 Embryonic hemoglobin produced
 Hepatic
 At 6 weeks cell production in liver
 Fetal hemoglobin produced
 Spleen, thymus, lymph nodes also active prod.
 Myeloid
 At 5th month Bone Marrow becomes site of prod.
 Liver & spleen now Extramedullary
 Hemoglobin A (22)
 Requirements For
Hematopoiesis
Stem Cells
Growth Factors
Microenviroment
 Stem Cell theory
 Pluripotent stem cell originator of all cells
 Gives rise to cells committed to specific
development
 Research supporting the theory
 PHSC has self-maintaining ability
 Committed cells differentiate continuously/ No
Reverse Flow
 Stem cells in Research
Pluripotent cells derived from:
 Cell mass of embryos at blastocyst stage (IVF)
 Fetal tissue from terminated pregnancy
Application
 Identification of factors of cellular decision-making
 Development and testing of drugs
 Generation of cells and tissue for therapy
 Cytokines & Growth Factors
 Cytokines stimulate or inhibit
 Prevent apoptosis
 Colony-Stimulating Factors produced by
many different cells
 Interleukins numbered according to discovery
 Components of Blood
Plasma Components
Plasma
 Transport mechanism Water
90%
 90-92% water.
 6-7% proteins
 2-3%
 Fats
 Carbohydrates
(glucose)
 Electrolytes
 Gases (O2, CO2)
 Chemical messengers

Other Protein
3% 7%
 Cellular Components
Pluripotent Stem Cell

Myeloid Multipotent Common Lymphoid

Stem Cells Stem Cells

Unipotent Lymphocytes
Progenitors

WBC’s
Basophils
RBC’s
Eosinophils
Thrombocytes Erythrocytes
Neutrophils
Monocytes Platelet Erythropoietin
s
 Components of Blood
Red Blood Cells
 Erythrocyte
 Hemoglobin – O2
bearing molecule
 Comprised of 4
subunits:
• Globin (binds to
1 O2 molecule)
• Heme (iron)
 100% saturation = 4
globin subunits
carrying O2
• Each gram of Cellsalive.com
hemoglobin =
1.34 ml O2
Blood Products and Blood Typing

Blood Types
 Antigens
 A, B, AB, O
 Rh factor
 Rh+ = ~85%
 Rh- = ~15%

Blood transfusion
 Components of Blood
Red Blood Cells
(cont.)
 Oxygen Transport
 Oxy-hemoglobin
dissociation curve
 2,3-DPG
 Components of Blood
White Blood Cells (Leukocytes)

 Margination

 Phagocytosis

The macrophage is using its internal

cytoskeleton to envelop cells of the fungus
Candida albicans.
 Components of Blood
Leukocytes (cont.)
 White Blood Cell Count
 Leukopoiesis
 Granulocytes
 Neutrophil
 Basophil
 Eosinophil
 Monocytes
Human Neutrophil:
 Lymphocytes Phagocytosis of Strep pyogenes
 Components of Blood
Leukocytes (cont.)
 Immunity
 Subpopulation of lymphocytes known as T cells and B cells
 T cells develop cellular immunity.
 B cells produce humoral immunity
 Components of Blood
Inflammatory Process
 MAST CELLS.
 Immunoglobulin E antibody
IgE,  
 Antigens
 Antigens stick to the mast cell IgE
antibodies, causing granules in the
mast cell to fire their contents into
the surrounding tissue.
 This releases a host of inflammatory
materials - leukotrienes, tumor
necrosis factor, interleukin-4 and
other cytokines that turn on other
inflammatory cells.
 These materials cause fluid to leak
from the capillaries and white cells
including neutrophils, T cells and
eosinophils to leave the circulation.
The end result is a "local
inflammatory response", a red, itchy
welt.

Cellsalive.com
 Components of Blood
Hemostasis-
3 mechanisms
 Vascular spasm
 Contraction of
tunica media
 Platelet plug
 Platelet aggregation
 Coagulation
 Formation of fibrin
clot
 Components of Blood
Hemostasis (cont.)
 Fibrinolysis
 Lysis of clot (plasmin)
 Thrombosis
 Thrombolytics
 Medications affecting clot formation
 Alter the enzyme
on the platelet.
 Affect the coagulation cascade.
 Enhance clotting.
Coagulation Cascade -
Synopsis
This scanning electron micrograph shows the fine structure of
a blood clot. Platelets released from the circulation and
exposed to the air use fibrinogen from the blood plasma to
spin a mesh of fibrin.
 General Assessment -
Management
Focused History and
Physical Exam
 SAMPLE history
 Hematological
disorders are rarely
the chief complaint.
 Physical exam
 Evaluate nervous
system function.
 Skin signs
General Assessment - Management
Physical Exam (cont.)
 Lymphatic signs
 Gastrointestinal signs
 Epistaxis
 Atraumatic bleeding gums
 Thrush
 Atraumatic splenic/hepatic pain
 Musculoskeletal signs
 Arthralgia (rheumatoid arthritis)
 Hemarthrosis
 Cardiorespiratory signs
 Tachycardia, cx pn, dyspnea - CHF
 Genitourinary signs
 Hematuria
 Menorrhagia
 Infection
Blood Products and Blood Typing

Blood Typing - ABO

Blood type Antigen present Antibody
on erythrocyte present in
serum
O None Anti-A, Anti-B
AB A and B None
B B Anti-A
A A Anti-B
Blood Products and Blood Typing
Compatibility Among ABO Blood Groups
Reaction with serum of Recipient
Donor Cells AB B A O
AB - + + +
B - - + +
A - + - +
O - - - -
-= no reaction
+ = reaction
Blood Products and Blood Typing

Brady; Paramedic Care Principles and Practice

 Diseases of Erythrocytes
Anemias
 Anemia is a sign, not a separate disease process.
 Signs and symptoms may not be present until the body
is stressed.
 Differentiate chronic anemia from acute episode.
 Treat signs and symptoms.
 Maximize oxygenation and limit blood loss.
 Establish IV therapy if indicated.
Diseases of Erythrocytes

Brady; Paramedic Care Principles and Practice

 Diseases of Erythrocytes
Sickle Cell Disease
 Normal red cells maintain
their shape as they pass
through the capillaries and
release oxygen to the
peripheral tissues (upper
panel). Hemoglobin
polymers form in the sickle
rell cells with oxygen
release, causing them to
deform. The deformed cells
block the flow of cells and
interrupt the delivery of
oxygen to the tissues
(lower panel).
 Diseases of Erythrocytes
Sickle Cell Disease (cont.)
 Sickle cell crises
 Vaso-occlusive
 Musculoskeletal/abdominal pain
 Priapism
 Renal/cerebral infarctions
 Hematological
 Lowered hemoglobin
 Splenic sequestration
 Infectious
 Management
 Follow general treatment guidelines prn.
 Consider analgesics.
 Diseases of Erythrocytes
Polycythemia
 Overproduction of erythrocytes.
 Occurs in patients > 50 years old or with
secondary dehydration.
 Most deaths due to thrombosis

 Results in bleeding abnormalities:

 Epistaxis, spontaneous bruising, GI bleeding.
 Management:
 Follow general treatment guidelines.
 Diseases of Leukocytes
Leukopenia/Neutropenia
 Too few white blood cells or neutrophils.
 Follow general treatment guidelines and
provide supportive care.
Leukocytosis
 An increase in the number of circulating
white blood cells, often due to infection.
 Leukemoid reaction
 Diseases of Leukocytes
Leukemia
 Cancer of hematopoietic cells
 Initial presentation
 Acutely ill, fatigued, febrile and weak, anemic.
 Thrombocytopenia

 Often have a secondary infection.

 Management
 Follow general treatment guidelines.
 Utilize isolation techniques to limit risk of infection.
 Diseases of Leukocytes
Lymphomas
 Cancers of the lymphatic system
 Hodgkin's
 Non-Hodgkins
 Presentation
 Swelling of the lymph nodes
 Fever, night sweats, anorexia, weight loss, fatigue, and
pruritis
 Management
 Follow general treatment guidelines.
 Utilize isolation techniques to limit risk of infection.
 Clotting Disorders
Thrombocytosis and Thrombocytopenia
 Thrombocytosis
 An abnormal increase in the number of platelets
 Thrombocytopenia
 An abnormal decrease in the number of platelets
 Sequestration
 Destruction (ITP)
 Decreased production
 Management
 Provide supportive care and follow general treatment
guidelines.
 Clotting Disorders
Hemophilia
 Deficiency or absence of a blood clotting factor
 Deficiency of factor VIII causes hemophilia A.
 Deficiency of factor IX causes hemophilia B.
 Deficiency is a sex-linked, inherited disorder.
 Defective gene is carried on the X chromosome.
 Signs & Symptoms
 Numerous bruises, deep muscle bleeding, and joint
bleeding.
 Clotting Disorders
Hemophilia (cont.)
 Management
 Treat the patient similarly to others.
 Administer supplemental oxygen.
 Establish IV access.
 Be alert for recurrent or prolonged bleeding, and prevent
additional trauma.
Von Willebrand’s Disease
 Deficient component of factor VIII
 Generally results in excessive bleeding.
 Generally is not serious; provide supportive care.
 Clotting Disorders
Disseminated Intravascular Coagulation
 Components of Blood
Leukocytes (cont.)
 Autoimmune disease
 May be specific or general
 Alterations in the immune process
 Immunosuppression
 HIV
 Anti-rejection medication
 Chemotherapy/Cancer

 System activation of coagulation cascade.

 Results from sepsis, hypotension, OB complications, severe tissue or brain injury,
cancer, and major hemolytic reactions.
Multiple Myeloma
 Cancerous disorder of plasma cells.
 Pathologic fractures are common.
Anticoagulants/Antiplatelets
Classifying agents
 Anticoagulants
 Block synthesis and activation of clotting
factors
 Antiplatelets
 Interfere with platelet aggregation or activation
 Fibrinolytics
 Dissolve fibrin component of thrombi
Anticoagulants/Antiplatelets
Anticoagulants
 Warfarin
 Blocks activation of Vit K
 Interferes w/ coagulation factors II, VII, IX, and X
 Unfractionated Heparin
 Binds antithrombin III (AT-III)
 Inhibits coagulation factors IX and X and thrombin
 Hirudin (medicinal leech)
 Prevents thrombin binding
Anticoagulants/Antiplatelets
Antiplatelets
 Aspirin
 Prevents platelet activation through
cyclooxygenase blockade.
 Prevents production of thromboxane A2
 Allows prostacyclin synthesis
 Ticlodipine
 Deforms platelet membrane fibrinogen receptor
 Anticoagulants/Antiplatelets
Antiplatelets (cont.)
 Glycoprotein IIb-IIIa Receptor Inhibitors
 G IIb-IIIa = platelet membrane receptor of fibrinogen
 Abciximab
 Eptifibatide
 Tirofiban

Fibrinolytics
 Activate plasminogen to plasmin = fibrinolysis
 Streptokinase
 Anistreplase
 Tissue Plasminogen Activator
 Reteplase
 Urokinase
 Hemorrhage
Class I Class II Class III Class IV
Blood Loss (ml) Up to 750 750-1500 1500-2000 >2000
Blood Loss (% Up to 15% 15%-30% 30%-40% >40%
volume)
Pulse <100 >100 >120 >140
BP Normal Normal Decreased Decreased
Pulse Pressure Normal or Decreased Decreased Decreased
increased
Resp. Rate 14-20 20-30 30-40 >35
Urine Output (ml/hr) >30 20-30 5-15 Negligible
Mental Status Slightly Mildly Anxious, Confused,
anxious anxious confused lethargic
Fluid Replacement Crystalloid Crystalloid Crystalloid and Crystalloid and
(3:1) rule blood blood
 Transfusion Reactions
Hemolytic Reaction
 Signs & Symptoms
 Facial flushing, hyperventilation, tachycardia, hives,
chest pain, wheezing, fever, chills, and cyanosis
 Treatment
 Stop transfusion, change all IV tubing, and initiate IV
therapy with normal saline or lactated Ringer’s.
 Consider furosemide, dopamine, and diphenhydramine.
 Transfusion Reactions
Febrile Non-hemolytic Reactions
 Signs & Symptoms
 Headache, fever, and chills
 Treatment
 Stop transfusion, change all IV tubing, and
initiate IV therapy with normal saline or lactated
Ringer’s.
 Consider Diphenhydramine and an antipyretic.

 Observe closely to ensure reaction is non-

hemolytic.