University of Hargeisa

Department: BSc in Laboratory Science

Introduction Of Hematology

Dr.Abdishakur A. Mohamed MD

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Blood is a circulating tissue composed of
fluid plasma and cells

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 Artery

White blood cells

Platelets

Red blood cells

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• Deliver O2
• Remove metabolic wastes
• Maintain temperature, pH, and fluid volume
• Protection from blood loss- platelets
• Prevent infection- antibodies and WBC
• Transport hormones

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 Amount: 7-9% of total body weight 79ml/kg
 Blood Volume: 5-6litter
 Viscosity: (3.5-5.5) times more than water
 Specific Gravity: 0.45-1.065
 PH:3-7.4(slightly alkaline)
 Venous blood had slow more CO
 Arterial has fast more Oxygen
 Temperature: 38c
 Osmotic pressure: 25 mmHg
 Color: Red due Haemoglobin
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 Plasma-55%

Buffy coat-<1%

Formed
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 90% Water
8% Solutes:
• Proteins
– Albumin (60 %)
– Alpha and Beta Globulins
– Gamma Globulins
– fibrinogens
• Gas
• Electrolytes
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 • Organic Nutrients
• Carbohydrates
• Amino Acids
• Lipids
• Vitamins
• Hormones
• Metabolic waste
• CO2
• Urea

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 • Platelets
• Leukocytes

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• Erythrocytes (red blood cells)
• Leukocytes (white blood cells)
• Platelets (thrombocytes)

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 Erythrocytes

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Erythrocyte7.5m in dia
   Anucleate
   Hematopoiesis- production of RBC
   Function- transport respiratory gases
   Hemoglobin- quaternary structure, 2  chains
and 2  chains
   Lack mitochondria. Why?
  1 RBC contains 280 million hemoglobin
molecules
   Men- 5 million cells/mm3
   Women- 4.5 million cells/mm3
   Life span 100-120 days and then destroyed in
spleen (RBC graveyard)
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 Hemoglobin

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 Hematopoiesis
• Hematopoiesis (hemopoiesis):
blood cell formation
– Occurs in red bone marrow of
axial skeleton, girdles and
proximal epiphyses of humerus
and femur

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 Erythropoiesis
• Erythropoiesis: red blood cell
production

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 Erythropoiesis

– Phases in development
1. Ribosome synthesis
2. Hemoglobin accumulation
3. Ejection of the nucleus and
formation of reticulocytes
– Reticulocytes then become
mature erythrocytes
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 Stem cell Committed Developmental pathway
cell Phase 1 Phase 2 Phase 3
Ribosome Hemoglobin Ejection of
synthesis accumulation nucleus

Proerythro- Early Late Reticulo- Erythro-

Hemocytoblast blast erythroblast erythroblast Normoblast cyte cyte

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Figure 17.5
Regulation of Erythropoiesis
• Too few RBCs leads to tissue hypoxia
• Too many RBCs increases blood
viscosity
• Balance between RBC production and
destruction depends on
– Hormonal controls
– Adequate supplies of iron, amino acids,
and B vitamins

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 Hormonal Control of
Erythropoiesis

• Erythropoietin (EPO)
– Direct stimulus for erythropoiesis
– Released by the kidneys in
response to hypoxia

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 Hormonal Control of
Erythropoiesis

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 Hormonal Control of
Erythropoiesis
• Causes of hypoxia
– Hemorrhage or increased RBC
destruction reduces RBC numbers
– Insufficient hemoglobin (e.g., iron
deficiency)
– Reduced availability of O2 (e.g., high
altitudes)
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 Hormonal Control of
Erythropoiesis
• Effects of EPO
– More rapid maturation of committed bone
marrow cells
– Increased circulating reticulocyte count in
1–2 days
• Testosterone also enhances EPO
production, resulting in higher RBC
counts in males
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 Blood Cell Production

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 Formation & Destruction of RBCs

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 RBC Diseases
Anemia- when blood has low O2 carrying
capacity; insufficient RBC or iron deficiency.
Factors that can cause anemia- exercise,
B12 deficiency

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 RBC Diseases
Sickle-cell anemia-
•HbS results from a change in just one of the 287
amino acids in the  chain in the globin molecule.
•Found in 1 out of 400 African Americans.
•Homozygous for sickle-cell is deadly, but in malaria
infested countries, the heterozygous condition is
beneficial.

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 Transmission of Malaria

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 Sickle Cell Anemia
Sickle cell is prevalent in parts of all of
the following areas:
•Africa
•Mediterranean countries (such as Greece,
Turkey, and Italy)
•The Arabian peninsula
•India
•Spanish-speaking regions (South America,
Central America, and parts of the
Caribbean)
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Distribution of the sickle cell gene

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 RBC Diseases
Polycythemia- excess of erythrocytes, 
viscosity of blood;
8-11 million cells/mm3
Usually caused by cancer; however, naturally
occurs at high elevations
Blood doping- in athletesremove blood 2
days before event and then replace it- banned
by Olympics.

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 4,000-11,000 cells/mm 3

Never let monkeys eat bananas

Granulocytes
Neutrophils- 40-70%
Eosinophils- 1-4%
Basophils- <1%
Agranulocytes
Monocytes- 4-8%
Lymphocytes- 20-45%
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 Eosinophil Lymphocyte
Basophil

platelet

Neutrophil
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Leukocyte Squeezing Through Capillary Wall

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 Leukopenia
• Abnormally low WBC count—drug induced
Leukemias
• Cancerous conditions involving WBCs
• Named according to the abnormal WBC
clone involved

Mononucleosis
• highly contagious viral disease caused by
Epstein-Barr virus; excessive # of
agranulocytes; fatigue, sore throat, recover
in a few weeks
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 Platelets
• Small fragments of megakaryocytes
• Formation is regulated by
thrombopoietin
• Blue-staining outer region, purple
granules

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Stem cell Developmental pathway

Hemocyto- Promegakaryocyte
blast Megakaryoblast Megakaryocyte Platelets

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Figure 17.12
Hemostasis- stoppage of bleeding
Platelets: 250,000-500,000 cells/mm3

Tissue Damage

Platelet Plug

Clotting Factors
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Hemostasis:
1. Vessel injury

2. Vascular spasm

3. Platelet plug formation

4. Coagulation
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 Hemostasis
(+ feedback)

Clotting Factors
thromboplastin

Prothrombin Thrombin

Fibrinogen Fibrin
Traps RBC & platelets

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Platelets 39
release thromboplastin
Blood Clot
Platelet Fibrin thread

RBC

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 Disorders of Hemostasis
• Thromboembolytic disorders:
undesirable clot formation
• Bleeding disorders:
abnormalities that prevent
normal clot formation

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 Thromboembolytic Conditions
Prevented by
– Aspirin
• Antiprostaglandin that inhibits thromboxane
A2
– Heparin
• Anticoagulant used clinically for pre- and
postoperative cardiac care
– Warfarin
• Used for those prone to atrial fibrillation
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Thrombocytosis- too many platelets due to
inflammation, infection or cancer

Thrombocytopenia- too few platelets

• causes spontaneous bleeding
• due to suppression or destruction of bone
marrow (e.g., malignancy, radiation)
– Platelet count <50,000/mm3 is diagnostic
– Treated with transfusion of concentrated
platelets
 
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 Type A
Type B
Type AB
Type O
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Blood type is based on the presence of 2 major antigens in
RBC membranes-- A and B
Blood type Antigen Antibody
A A anti-B
B B anti-A
A&B AB no anti body
Neither A or B O anti-A and anti-B

Antigen- protein on the surface of a RBC membrane

Antibody- proteins made by lymphocytes in plasma which are

made in response to the presence of antigens.
They attack foreign antigens, which result in clumping
(agglutination)
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Type AB- universal recipients
Type O- universal donor
 
Rh factor:
Rh+ 85% dominant in pop
Rh- 15% recessive

Blood Type Clumping Antibody

A antigen A anti-A serum antibody anti-b
B antigen B anti-B serum antibody anti-a
AB antigen A & B anti A & B serum -
O 12/13/20
neither A or B no Dr.Abdishakur
clumping A. w/Mohamed
either MD
anti A or B anti-a,
46
anti-b
 Blood being tested Serum
Anti-A Anti-B
Type AB (contains
agglutinogens A and B;
agglutinates with both
sera)
RBCs

Type A (contains
agglutinogen A;
agglutinates with anti-A)

Type B (contains
agglutinogen B;
agglutinates with anti-B)

Type O (contains no
agglutinogens; does not
agglutinate with either
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Figure 17.16