DR FARISA

ASSOC PROFF
Dr S.Bashir 2
 Definition :

Blood is a mixture of cellular components suspended

in a fluid called plasma. It is the specialized fluid tissue
of the transport system.

• Total Blood Volume : 5 – 6 liters (7% of body weight or

70ml/kg body weight)

• Specific Gravity : 1050 – 1060

• Viscosity : 4 – 5 times that of water

• pH : 7.4 ± 0.05; alkaline

 Whole Blood has 2 main
components:
-Formed elements (36 - 50%).
-Plasma (50-64%)

 The formed elements consist of:

 Red blood cells (99.9%)
 White blood cells (>0.1%)
 Platelets (>0.1%).

Dr S.Bashir 4
Composition :

91% Water
Plasma Proteins

8% Organic Non-protein Nitrogenous (NPN)

55% Plasma substances, sugars, fats, amino acids,
9% enzymes and hormones
Solids Na+, Ca2+, Cl¯, HCO3¯ ( mainly extracellular)
1%
K+, Mg2+, Cu2+, PO4 3¯ (mainly intracellular)
Inorganic
Minerals like Iron, Iodine, Copper, Zinc…
 In a adult person,
Constituent )%(
total volume of about
2.5-3.0 L Water 90.O%
 Consists of:
 Water Proteins 08.0%
 Plasma proteins
Inorganic
 Other solutes? 0.9%
ions
Organic
01.1%
substances

Dr S.Bashir 6
 When blood is allowed
to clot then centrifuged
we get serum instead
of plasma.

 Serum=
Plasma – fibrinogen &
clotting factors.

Dr S.Bashir 7
Serum :

When blood is allowed to clot in a test tube, then

the clot retracts and give out serum.

Serum = Plasma – Fibrinogen and clotting factors

(II, V and VIII)
Composition :

55% Plasma

4,000 to 11,000

45% Cellular
Components

1.5 - 4 lacs
Red blood
cells

White blood
cells

Platelets

Dr S.Bashir 10
Dr S.Bashir 11
Functions of blood :

• Respiratory Function
• Nutritive Function
• Excretory Function
• Homeostasis
• Regulation of Body Temperature
• Body Defense
• Plasma Proteins Functions
• Transport Function
 Transport of ?
 Regulation of the pH and electrolyte
composition of interstitial fluids throughout
the body.
 Restriction of fluid losses (in event of injury).
 Defense against ?
 Regulation of body temp.?

Dr S.Bashir 13
 Increasing water or sodium reabsorption  High blood pressure

 Hormonal regulation of blood pressure

 Regulation of muscle tension in the artery walls
 Angiotensin
 Muscle contraction  increasing blood pressure
 Atrial natriuretic hormone (ANH)
 Relaxation of muscle  decreasing blood pressure
 Regulation of salt and water balance
 Aldosterone
 Increasing retention of salt  increase blood volume and pressure
 Antidiuretic hormone (ADH)
 Increasing retention of water
The Renin-Angiotensin Cascade
 Plasma Proteins

• Origin
• Types
• Functions
• Applied Importance
 Plasma Proteins

Origin :

In Embryo : Mesenchymal Cells

In Adults : Mainly liver

 Transport media:
Transport of dissolved gases, nutrients, hormones, and
metabolic wastes.
 Homeostatic function through:
1-Regulation of the pH and electrolyte composition of
interstitial fluids throughout the body.
2-Regulation of heat.
 Defensive function :- Defense against toxins and
pathogens
 Restriction of fluid losses (in event of injury).

Dr S.Bashir 19
 Types :
Normal total plasma protein concentration : 6.4 – 8.3 gm/100 ml of blood

1. Albumin : 3 – 5 gm% ( Average : 4.8 gm% )

2. Globulin : 2 – 3 gm% ( Average : 2.3 gm% )

- globulin
- globulin
- globulin

3. Fibrinogen : 0.3 gm%

4. Prothrombin : 40 mg%

Albumin : Globulin = 1.7 : 1 (A/G ratio)

Functions :
1. Role in Blood Coagulation
2. Maintenance of Colloidal Osmotic Pressure
3. Maintenance of viscosity of blood
4. Maintenance of systemic arterial blood pressure
5. Maintenance of Acid-Base balance
6. Provides stability to blood
7. Immune function
8. Transport function
9. Reservoir Function
10.Nutritive Function
Methods of separation of Plasma proteins :
•Precipitation by salts.
•Fractional precipitation.
•Sedimentation in ultracentrifugate.
•Electrophoresis.
•Immunoelectrophoretic technique.
•ELISA
•RIA.
Plasmapheresis or Whipple’s experiment
Relation of diet to plasma proteins.
Variations in plasma protein concentration :

Decrease in albumin :
PHYSIOLOGICAL PATHOLOGICAL
• Infancy and new borns • Impaired Protein Synthesis
• Pregnancy eg.. Hepatitis, Cirrhosis of
liver, malnutrition etc…
• Excessive loss
eg.. Burns, Nephrosis
 Erythrocytes (or)
Red Blood Corpuscles

• Morphology
• Erythropoiesis
• Functions
• Fate of RBC
 Morphology :

Shape : RBC is a circular, biconcave, non-nucleated disc

Composition : Water, Hemoglobin and others
Diameter : 6.5 – 8.8 m ( Average 7.2 m )
Thickness : at periphery 2 – 2.4 m; at the centre 1.2 – 1.5 m
Surface area : 140 m2
Volume : 78 – 94 m3
Normal count :

At birth : 6 – 7 million/ cu mm of blood

Adults :
Males :- 5 – 6 million/ cu mm of blood
(Average : 5.5 million/cu mm)

Females :- 4.5 – 5.5 million/ cu mm of blood

(Average : 4.8 million/cu mm)

Life span of RBC is 120 days

 ERYTHROPOIESIS

• Definition
• Site of production
• Stages
• Regulation
• Maturation Factors
Definition :

Production and maturation of RBC from the

stem cell is called Erythropoiesis.
Site :
A. During intrauterine life – 3 stages
1. Mesoblastic stage
2. Hepatic stage
3. Myeloid stage
B. In Children
C. In Adults
Stages : Haemocytoblast
Stem Cell

Proerythroblast

Early Normoblast

Intermediate Normoblast

Late Normoblast

Reticulocyte

RBC
 Changes during Erythropoiesis
Cytoplasm
Cell Size
Terminology Nucleus Mitosis
(µm) Staining Haemoglobin

Very big - occupies almost

whole of the cell with open
Haemocytoblast chromatin, containing 4-5
Deep Basophilic Absent Present
(Stem cell) 19 - 23 nucleoli
Occupies 3/4th of cell
Proerythroblast volume; 2-3 nucleoli; open Deep Basophilic Absent
Active
Mitosis
(Megaloblast) 15 - 20 chromatin
Size decrease; no nucleoli; Active
Less Basophilic Absent
Early Normoblast 14 - 16 condensation of chromatin Mitosis
Nucleus size further
Intermediate decreases; chromatin Polychromatophilic
Starts Active
appearing Mitosis
Normoblast 10 - 14 further condenses

Late Normoblast : 
Nucleus very small with
chromatin dot 'cart wheel Further
( a ) Early 8 - 10 appearance' Orthochromatic
increases
No Mitosis

Nucleus degenerates,
becomes uniformly deeply
( b ) Late 7-8 stained 'pyknotic'
No nucleus; remnants of Further
Acidophilic No Mitosis
Reticulocyte 7-8 RNA present increases
Further No
Acidophilic
Erythrocyte 7.2 - 7.4 No Nucleus increases Mitosis
 Reduction in cell size

 Staining reaction changes

 Reduction in nucleus size

Regulation :

1. General Factors
• Hypoxia

2. Special Maturation Factors

• Dietary factors
• Castle’s Intrinsic factor (I.F.)
• Extrinsic factor
1. General Factors
• Hypoxia
Hypoxia :
Factors affecting erythropoietin production :

1. Increase
( i ) Hypoxia due to :
a. Haemorrhage
b. High altitude
c. Cardio-respiratory disturbances
d. Methaemoglobin excess
( ii ) Vasoconstrictor agents due to renal hypoxia
( iii ) Products of RBC destruction, called hemosylates

2. Decrease
( i ) Chronic Renal Diseases
( ii ) Protein deficiency
( iii ) Cirrohosis of the liver
( iv ) Chronic inflammatory diseases
2. Special Maturation Factors
• Dietary factors
• Castle’s Intrinsic factor (I.F.)
• Extrinsic factor
Dietary Factors :

1. Proteins

2. Minerals
- Iron
- Copper
- Cobalt
- Mangaese
- Calcium
Dietary Factors :
3. Vitamins
- Vitamin B12 ( 2 µgm )
- Folic Acid ( 100-200 µgm )

4. Hormones
- Erythropoietin
- Thyroid hormone
- Adrenal hormone
- Sex hormones
- Growth hormone

5. Other factors
- Cyclic AMP
- NAD, NADP
- Angiotensin
• Castle’s Intrinsic factor

(I.F.)
• Extrinsic factor
Anisocytosis

Poikilocytosis

Spherocytosis
 Haemoglobin

• Structure
• Types
• Functions
• Derivatives of Hb
• Abnormal Hemoglobin
Structure :

• Haem is an iron containing porphyrin

• It is a tetrapyrrole i.e. it consists of 4 pyrrole rings
• It consists of iron in the form of ferrous (Fe2+)
• It consists globin - 4 polypeptide chains
Types :

• Adult Haemoglobin ( HbA ) - 22

• Adult Haemoglobin ( HbA2 ) - 22

• Foetal Haemoglobin ( HbF ) - 22

Normal Values :
• At Birth – 18 to 23 gm%

• Adult Males - 14 to 18 gm%

(Average : 16 gm%)

• Adult Females – 12 to 16 gm%

(Average : 14 gm%)
Functions :

• Transport of O2 from lungs to tissues

• Transport of CO2 from tissue to lungs

• Acts as buffer
• Transports the nitric oxide (NO) from lungs
to tissues
Derivatives of Hb :
• Oxyhaemoglobin
• Reduced (Deoxygenated) Haemoglobin
• Carbaminohaemoglobin
• Carboxyhaemoglobin
• Methaemoglobin
Abnormal Haemoglobins :
• Thalassaemia
• Haemoglobin S ( HbS)
FATE OF RBC :

HAEMOGLOBIN

GLOBIN HAEM TISSUE

MACROPHAGE
SYSTEM
PORPHYRIN RING
Fe2+

BILIVERDIN + CO

BILIRUBIN FERRITIN
 Anemia
Qualitative or quantitative decrease
In RBC or Hb is called Anemia

Decrease in oxygen carrying

capacity of blood
Grading of Anemia :

Haemoglobin Concentration

Mild Anemia : 8 – 12 gm%

Moderate Anemia : 5 – 8 gm%
Severe Anemia : less than 5 gm%
 Classification :
Anemia

Etiological (or) Morphological (or)

Whitby’s Wintrobe’s

1. Decreased production of RBC 1. Based on size and Hb%

2. Increased destruction of RBC
3. Excess loss of blood
Etiological (or) Whitby’s Classification -

Based on the cause -

1. Decreased production of RBC :

A. Nutritional Factors – Iron, Vitamin B12 & Folic Acid
B. Dyshemopoiesis
C. Hypothyroidism
1. Decreased Production of RBC

A . NUTRITIONAL FACTORS

Iron Deficiency Anemia :

Cause : - Decreased Intake

- Increased demand : less supply
- Due excess blood loss
- Defective absorption
Iron Deficiency Anemia :

Features : - Microcytic Hypochromic

- Normoblastic Hyperplasia
- Investigations
- Nails
- Tongue
- Cardio vascular/Respiratory system
- Nervous System
Megaloblastic Anemia /
Pernicious Anemia (or) Addison’s Anemia:

Cause : - Decreased Intake of Vitamin B12

- Increased demand : less supply
- Defective absorption
Megaloblastic Anemia /
Pernicious Anemia (or) Addison’s Anemia:
Megaloblastic Anemia /
Pernicious Anemia (or) Addison’s Anemia:
Megaloblastic Anemia / Folic Acid Deficiency :

Cause : - Decreased Intake of Folic Acid

- Increased demand : less supply
- Defective absorption
- Anti folate drugs ( eg. Methotrexate )
B . Dyshaemopoiesis

C. Hypothyroidism
2. Increase Destruction of RBC – Hemolytic Anemia

- Intrinsic (intra-corpuscular defects) - hereditary

- Congenital Spherocytosis
- Haemoglobinopathies
- Erythroblastosis Foetalis
- Glucose-6-phosphatase deficiency
2. Increase Destruction of RBC – Hemolytic Anemia

- Intrinsic (intra-corpuscular defects) - hereditary

2. Increase Destruction of RBC – Hemolytic Anemia

- Intrinsic (intra-corpuscular defects) - hereditary

2. Increase Destruction of RBC – Hemolytic Anemia

- Extrinsic (Extra-corpuscular defects) – Acquired

- Antigen-Antibody Reaction
- Infection e.g. malaria
- Drugs / Poisons e.g. quinine,snake venom
- Hypersplenism
3. Excess loss of blood

- Acute i.e. sudden loss of blood

- Chronic – slow loss of blood
e.g. Menorrhagia
Piles
Hookworm Infestation
Peptic Ulcer etc..
 Jaundice
• Definition
• Chemistry of Bilirubin Formation
• Fate of Bilirubin
• Type of Jaundice
• Physiological Jaundice
Definition :

Jaundice is a yellowish discoloration of the skin,

eyes, mucous membrane and other body tissues due to
the presence of excessive bilirubin in the plasma and tissue
fluids.

Normal Serum Bilirubin : 0.2 – 0.8 mg%

Clinical Jaundice Bilirubin is > 2 mg%
Chemistry of Bilirubin Formation :

HAEMOGLOBIN

GLOBIN HAEM TISSUE

MACROPHAGE
SYSTEM
PORPHYRIN RING
Fe2+

BILIVERDIN + CO

BILIRUBIN FERRITIN
Fate of Bilirubin :

1. Uptake
2. Conjugation
3. Excretion
4. Degradation
5. Reexcretion
Fate of Bilirubin :

1. Uptake
2. Conjugation
3. Excretion
4. Degradation
5. Reexcretion
 Pre-Hepatic Hepatic Jaundice Post-Hepatic
Jaundice Jaundice
Cause Increase Infective or toxic Obstruction of bile
breakdown of RBC damage to liver, ducts 
 increased unable to conjugate & conjugated bilirubin
serum excrete the conjugated
unconjugated bilirubin :
bilirubin Increase in conjugate
& unconjugated
bilirubin
Van Den Bergh Indirect Positive ‘Biphasic’ Reaction Direct Positive
Test
Blood Anaemia, Normal Normal
Examination Reticulocytes
Plasma Normal Decrease in albumin, Normal
Albumin, A/G ratio decreases
Globulin levels
and A/G ratio
Thymol- Nil Markedly increased Usually slight
turbidity
 Pre-Hepatic Hepatic Jaundice Post-Hepatic
Jaundice Jaundice
Serum Alkaline Normal Increase Markedly increases
Phosphatase
Urine Bilirubin Absent ( Acholuric Present Absent
Jaundice )
Urine Increases Decreases Absent
Urobilinogen
Faecal Markedly Increased Reduced Absent
Stercobilinogen
Faecal Fat Normal Increase upto 40-50% Increase upto 40-
(Steatorrhoea) 50%
Liver Function Normal Impaired Normally (or) Mildly
Tests Impaired
Physiological Jaundice
 LEUCOCYTES (OR)
WHITE BLOOD CELLS
 Introduction
 Classification
 Normal Values
 Leucopoiesis
 Structure & Functions
 Phagocytosis
 Introduction

Total Leucocyte Count : 4,000 to 11,000 / cubic mm of blood

Ratio between RBC & WBC = 600 : 1

 Classification :

LEUCOCYTES

GRANULOCYTES AGRANULOCYTES
 Neutrophils  Lymphocytes
 Eosinophils  Monocytes
 Basophils
 Normal Values :
Absolute Count
Percentage
( per cumm)
GRANULOCYTES
 Neutrophils 50 – 70 % 3000-6000

 Eosinophils 1–4% 150-300

 Basophils < 1% 10-100

AGRANULOCYTES
 Lymphocytes 20 – 40 % 1500-2700

 Monocytes 2–8% 300-600

 Leucopoiesis : Primitive WBC
(Stem Cell)

Myeloblast

Pre-myelocyte
( Myelocyte – A )

Myelocyte Proper
( Myelocyte – B )

Metamyelocyte
( Myelocyte – C )

Mature WBC
( Neutrophiol, Eosinophil,
Basophil )
Changes :

1. Reduction in size
2. Differentiation into three types
3. Appearance of specific granules
4. Loss of divisibility
5. Appearance of nuclear lobes
6. Development functional ability
(Phagocytosis)
 Structure & Functions :
Neutrophils

 Size
 Nucleus
 Cytoplasm
 Granules
 Functions
 Lifespan of about 6hrs to a
few days.
 Their % increases in cases of:
 Acute inflammation e.g.
Acute bacterial
infections: tonsillitis,
pneumonia & wound infections.

96
 Structure & Functions :
 Variations
1. Neutropenia :
- Typhoid/Paratyphoid fever
- Viral infection
- Bone Marrow Depression

2. Neutrophilia
- Acute Pyogenic Infections
- Tissue Distruction like
burns, hemorrhage,
myocardial infarction
 Structure & Functions :
 Eosinophil

 Size
 Nucleus
 Cytoplasm
 Granules
 Functions
 1-4% of circulating WBC.
 Reddish-orange staining granules.
 Bi-lobed nucleus
 Functions:
 Phagocytose antibody-coated
bacteria & protozoa
 Exocytose toxic compounds onto
the surface of large multi-cellular
parasites such as flukes or
parasitic worms that are too big
to be phagocytosed

Dr. S.Bashir 99
 Typical lifespan of 8-12d

 Their % increase during?

-Parasitic infections.
-Also  during allergic
reactions, (asthma, hay
fever), because their
secretions may induce
allergic reactions.

100
 Less than 1% of WBC
 Have large deep blue cytoplasmic
granules which cover the nucleus.
 Migrate to injury sites and discharge
the contents of their granules:
 Histamine
(Vasodilator and increaser of capillary
permeability.)
 Heparin
(An anticoagulant.)
 These 2 chemicals enhance the
local inflammation

Dr. S.Bashir 101

 Structure & Functions :
 Basophil

 Size
 Nucleus
 Cytoplasm
 Granules
 Functions
 Structure & Functions :
 Variations
1. Basopenia :
- Injection of Glucocorticoids
- Drug induced reactions

2. Basophilia
- Chickenpox
- Smallpox
- Tuberculosis
- Influenza
 They leave blood and
enter tissues
 mast cells.
-Function? Release
inflammatory
chemicals 
chemotaxis.

 They are
non-phagocytic.

Dr. S.Bashir 104

 Structure & Functions :
 Lymphocyte

 Size
 Nucleus
 Cytoplasm
 Granules
 Functions
 Structure & Functions :

 Variations
1. Lymphocytopenia :
- Hypoplastic Bone Marrow
- AIDS

2. Lymphocytosis
- Chronic Infections
- Lymphatic Leukaemia
- Viral Infections
 Structure & Functions :
 Monocyte

 Size
 Nucleus
 Cytoplasm
 Granules
 Functions
 2-8% of WBC in blood.
 Their nuclei deeply indented or
U-shaped, with reticular-appearing
chromatin
 The cytoplasm contains lysosomal
granules .
 Have more phagocytic power than
neutrophils & longer life span.
 Leave the bloodstream to become
large phagocytic cells called tissue
macrophages .

108
 Structure & Functions :

 Variations
1. Monocytopenia :
- Hypoplastic Bone Marrow

2. Monocytosis
- Tuberculosis
- Syphilis
- Some leukaemias
 Fixed macrophages derived from monocytes
include the
 Langerhans cells within the Skin
 Histiocytes within connective tissues.
 Kupffer cells of the liver
 Sinus lining cells of the spleen and lymph nodes
 Pulmonary alveolar macrophages
 Life span : days - years.

110
 PHAGOCYTOSIS :
Disorders :
1. Agranulocytosis
2. Myeloid Leukaemia
3. Neutrophil Hypomotility
4. Chronic Granulomatous disease
of childhood
5. Congenital Neutropenia
6. Congenital Myeloperoxidase Deficiency
PLATELETS
 PLATELETS
 Structure
 Normal Count & Variation
 Thrombopoiesis
 Functions
 Structure :

 Platelet Membrane
 Cytoplasm
 Normal Count

Normal Count : 1.5 to 4 lacs / cumm of blood

Life Span : 8 to 12 days

 Thrombopoiesis
BONE MARROW
Polyploid Precursor Cell
(Stem Cell)

Megakaryoblast
(Stage I)

Pro-megakaryocyte
( Stage II )

Granular Megakaryocyte
( Stage III)

Platelets
 Functions :

 Hemostasis
 Blood Coagulation
 Clot Retraction
 Phagocytic Function
 Storage and Transport Function
 COAGULATION OF BLOOD

 Hemostasis
 Physiology of Hemostasis
 Physiology of Clotting Mechanism
 Invivo – Blood in liquid form ?
 Fibrinolytic System
 Anticoagulents
 Haemorrhagic Disorders
 Injury to vessel wall

Release of 5-HT and Release of tissue

Endothelium is
other vasoconstrictors thromboplastin
disrupted
from platelets

Exposure of collagen
Constriction of injured via via
blood vessel ‘ Platelet Adhesion’ Intrinsic System Extrinsic System

‘ Platelet Activation’ Activation of coagulation

Loose platelet Formation of Fibrin

aggregation

Formation of Formation of
Temporary Haemostatic Definitive Haemostatic
Plug of platelets Plug
 Physiology of Clotting Mechanism

1. Formation of Prothrombin Activator

2. Conversion of Prothrombin to Thrombin

3. Conversion of Fibrinogen to Insoluble Fibrin

4. Clot Retraction

5. Prevention of Intravascular Thrombosis

Clotting Factor Factor Name
I Fibrinogen
II Prothrombin
III Thromboplastin
IV Ionic Calcium
V Labile Factor
VI ----
VII Proconvertin
VIII Antihemophilic Factor
IX Christmas Factor
X Stuart Prower Factor
XI Plasma Thromboplastin Antecedent
XII Hageman Factor
XIII Fibrin Stabilizing Factor
 1. Formation of Prothrombin Activator :
a. Intrinsic Mechanism

b. Extrinsic Mechanism

2. Converstion of Prothrombin to Thrombin

Intrinsic Pathway Extrinsic Pathway
Vessel damage Vessel damage
(collagen exposed)
Subendothelial cells
Exposed to blood
XII XIIa Tissue factor

VIIa VII
XI XIa

IX IXa IX
VIII VIIIa Activated
Platelets

X Xa X

V Va Activated
Platelets

Prothrombin Thrombin
3. Conversion of Fibrinogen to Fibrin

a. Proteolysis

b. Polymerisation

c. Stabilisation
 Fibrinogen

Proteolysis

Fibrin
Monomer

Polymerisation

Soluble
Fibrin Polymer
Stabilisation
Factor III & XIII
Ca2+

Insoluble
Fibrin Clot
4. Clot Retraction

5. Prevention of Intravascular Thrombosis

6. Role of Calcium
Why blood does not clot in circulation……
………..………….?

• Endothelial Factors
• Velocity of Circulation
• Natural Anticoagulents
• Fibrinolytic System
• Role of liver
Why blood does not clot in circulation……
………..………….?

Applied Aspect : Thrombosis

• Sluggish Blood Flow
• Damage to Tunica Intima
• Mutation of gene for factor V
• Mutation in antithrombin III & protein S
Fibrinolytic System :

Thrombin
Fibrinolytic System :

Promoted by :

- Stress and Strains (Physical or Mental)

- Administration of Epinephrine, Corticosteroids & Phenformin
- Tissue Activators e.g. urokinase

Inhibited by :

- E-amino caproic acid (EACA)

- Aprotinin or Trasylol (Trypsin inhibitor)
 Anticoagulents

Natural Synthetic

1. Heparin 1. Vitamin K Antagonists like

dicoumarol, warfarin, phenindione,
2. Anti-Thrombin
nicoumalone
3. Protein C
2. Ca2+ chelating agents like
EDTA, Sodium Citrate, Sodium Oxalate

3. Malayan (Malaysian) Pit Viper

4. Arvin (Ancord)
Haemorrhagic Disorders
 Classification :

BLEEDING DISORDERS

DEFECTIVE DEFECTIVE
BLOOD CLOTTING CAPPILARY CONTRACTILITY

Deficiency of clotting PURPURA

factors
Deficiency of Vit. K
Anticoagulent overdose
 Deficiency of Clotting Factors
Causes :

1. Deficiency of clotting factors

2. Vitamin K deficiency

3. Anticoagulent Overdose
Deficiency Clinical syndrome Cause
of factor
I Afibrinogenemia (or) Premature separation of
Fibrinogenopenia placenta, Congenital,
Snake Venom
II Hypoprothrombinemia Liver Disease
Vitamin K Deficiencty
V Parahaemophilia Congenital
VIII Hemophilia A Congenital
(Classical Hemophilia) Abnormal gene on X-chro.
IX Hemophilia B Congenital
(Christmas Disease)
X Stuart-Prower Factor Congenital

Von- Von-Willebrand’s Congenital

Willebrand’s disease
Factor
Hemophilia A (Classical Hemophilia) :

 Cause
 Diagnosis
 Treatment
Intrinsic Pathway Extrinsic Pathway
Vessel damage Vessel damage
(collagen exposed)
Subendothelial cells
Exposed to blood
XII XIIa Tissue factor

VIIa VII
XI XIa

IX IXa IX
VIII VIIIa Activated
Platelets

X Xa X

V Va Activated
Platelets

Prothrombin Thrombin
Vitamin K Deficiency :

 Causes
- Obstructive Jaundice
- Chronic Diarrhoeas
- Liver Diseases
- Hemorrhagic states in infants
 Diagnosis
 Treatment
 Defective Capillary Contractility

PURPURA : It is of two types

1. Primary (Idiopathic) Purpura

2. Secondary (Symptomatic) Purpura
Different Forms of Purpura :

1. Thrombocytopenic Purpura
2. Athrombocytopenic Purpura
3. Thrombo-asthenic Purpura
4. Haemorrhagic Telangiectasis
 BLEEDING TIME
 CLOTTING TIME
 PROTHROMBIN TIME


 THROMBIN TIME
BLOOD GROUPS
 Introduction :
- Terminology
- What is the basis of blood grouping..?
- Land Stenier’s Law
 ABO Blood Groups

Group Agglutinogen Agglutinin

A A  (or) Anti B
B B  (or) Anti A
AB A and B No Agglutinins
O A and B Absent Anti A and Anti B
(or)
 and 
 ABO Blood Groups

Determination of ABO Blood Groups

Bombay phenotype
Gal
NAGA Gal
A antigen
H antigen Gal
NAGA Gal
Gal
NAGA Gal Fuc NAGA

Fuc
Gal
H substrate ( 0 group) NAGA Gal
Gal  Galactose
NAGA  N Acetyl Galactosamine Fuc Gal
FUC  Fucose B antigen
 ABO Blood Groups

Inheritance of
Classical ABO Blood Groups
 Rhesus (Rh) Group

Group Agglutinogen Agglutinin

Rh +ve D No Agglutinin
Rh –ve No Agglutinogen No Agglutinin
 Rhesus (Rh) Group

Inheritance of
Rhesus (Rh) Blood Group
 Rhesus (Rh) Group

Rh factor & Hemolytic Disease

 Rhesus (Rh) Group

Hemolytic Disease :
1. Hydrops Foetalis
2. Icterus Gravis Neonatorum
3. Erythroblastosis Foetalis
4. Kernicterus
5. Liver Damage
 Rhesus (Rh) Group

Treatment :

Exchange Transfusion
- Removes Rh +ve cells
- Removes Bilirubin
- Removes Anti-D
 Rhesus (Rh) Group

Prevention :
Administration of Rh-immuno globulins
(Anti-Rh Antibodies)
Uses of Blood Grouping :

 Blood Transfusion
 Rh incompatibility during pregnancy
 Paternity Dispute Cases
 Medicolegal Value
 Cell Recognition
 Anthropological Studies
Blood Transfusion :
Indications :
- Blood Loss
- Blood Disorders
- Blood Diseases
- Poisoning
- Acute Infections
- Pre (or) Post-operative cases
- Shocks
Blood Transfusion :

Rules :
- Blood Grouping
- Cross Matching
- No Rh –ve female with Rh +ve
 RBCs of Donor
Recipient
Blood Agglutinin
Group in serum AB A B O
AB
- - - -
Nil

A 
+ - + -
B 
+ + - -
O 
+ + + -
Blood Transfusion :
Hazards :
- Effect of Incompatible Blood
Inapparent Hemolysis
Post-transfusion Jaundice
Haemoglobinuria

- Mechanical Overloading of Circulation

- Chemical Risks
- Pyrogenic Reactions
- Allergic Reactions
- Transmission of Diseases
 SPLEEN
Functions :
1)Formation of RBC’s.
2)Contains lymphoid tissues which form lymphocytes
and plasma cells.
3)Reservoir of RBC’s.
4)Part of tissue macrophage system.
5)Participates in defence reations.
lymph
Formation :
•Capillary has 2 ends (arterial{A} and venous{V}
end).
•The Hydrostatic pressure (out driving force) at A end
is 35mmHg and 16mmHg at Venous end COP
(indriving force) is 25mmHg through out the length of
capillary tube.
•Since the outdriving force is greater at A end some
fluid goes out of capillary into tissue spaces. At V end
since the indriving force is greater, a major part of
fluid which had gone out will return back into
capillary. A small portion of fluid left behind is known
as tissue fluid and returns via lymphatic vessels.
Rate of formation :
1 – 1.5ml/min i.e 2-4L/day.
Factors influencing lymph formation:
Hydrostatic pressure.

Colloidal Osmotic Pressure.

Factors like hypoxia, ADP, H+,Bradykinin,

Histamine increases capillary permeability
Lymphatic circulation:

Tissue fluid  Lymph Lymph nodes

Lymphatics Right & Left collecting ducts
 Subclavian veins.
Lymph flow is aided by :
1)Presence of valves in lymphatic vessels.
2)Movement of muscles.
3)Respiratory pump during inspiration.
4)Pressure gradient.
composition of Lymph:
Water – 94% and solids – 6%.
Lymphocytes (1000 – 2000mm3) and plasma cells.
Electrolytes, urea, amino acids and creatine {same
as plasma}.
Protein content {less than plasma}
Chlorides and glucose {more than plasma}.
Clotting factors and antibodies.
Lipids.
Functions :
I. Returns proteins, electrolytes, and water
to blood from tissue spaces.
II. Helps in redistribution of body water,
III.Transports absorbed long chain fatty
acids & Cholesterol from intestines.
IV.Supplies nutrition and oxygen to those
parts where blood cannot reach.
V. Body defence by lymphocytes& antibodies.
Applied aspects :
1.Lymphadenopathy.
2.Elephantiasis.
3.Chyluria.
4.Chylo-Thorax.
BLOOD VOLUME DETERMINATION:
1.Direct method : in animals.
2.Indirect method: Calculated by
•Estimating RBC MassRadioactive methods.
•Estimating Plasma volume by dye dilution
principle.
Blood volume = 100 X Plasma volume
55{Hematocrit}
BLOOD VOLUME
REGULATION
Regulation of blood volume includes:
I. Regulation of volume.

II. Regulation of RBC mass.

III.Regulation of Plasma proteins.

IV.Regulation of Electrolytes.
1.Regulation of Volume :
a)Capillary fluid shift mechanism.
b)Osmoreceptor mechanism.
c)Volume receptors.
d)Baroreceptor mechanism.
e)Renin-Angiotensin system.
2.Regulation of RBC mass:
Low blood volume

Hypoxia

Liver Kidney

Erythropoietin

RBC production increased

RBC mass restored

3.Regulation of Plasma proteins:
•Shift of stored proteins
•Consuming food containing good quality
proteins.

4.Regulation of Electrolytes:
•Na+,K+,Cl- regulated by Aldosterone, ADH,
ANP.
•Ca++,PO4-,Mg++ are regulated by PTH,
Calcitonin and Vit-D.
 IMMUNITY
( THE IMMUNE SYSTEM )
 THE IMMUNE SYSTEM

Natural Acquired
( Innate or Non-specific ) (Specific )

Humoral Cell Mediated Humoral Cell Mediated

Responses Responses Responses Responses
e.g. Complement System ( Neutrophils, ( B-Lymphocytes ( T-Lymphocytes )
Interferon etc.. Monocytes and and
Macrophages ) Antibodies )
THE NATURAL IMMUNE SYSTEM
Humoral Responses :

1. The Complement System

2. C-reactive protein
3. Interferons
4. Natural Killer Cells
1. The Complement System
Classical Pathway Alternative (or Properdin) Pathway
( Initiated by antibody initiated by polysaccharides on
binding to antigen) bacterial cell walls
C1q, r, s Factor I, Properdin, Mg2+
C4, C2, Ca2+

C3
C3a
C5
C3b
C6 C5a

C7 Inflammatory Response
C8 activated ( Histamine release activity,
Opsonization and C5, 6, 7 promotes movement of
C9 macrophages towards
Phagocytosis
invasion site)

C5b to C9 cause pores to appear in the cell membrane

of the foreign invaders and results in its destruction
2. C-Reactive Protein :

3. Interferons :

4. Natural Killer Cells :

- No need of sensitization
- Against cancer tumours
- Attacks viruses
- Role of interleukin-2 ( IL-2 )
- First line of defense against viral infections
- Primitive Immune System
THE NATURAL IMMUNE SYSTEM
Cell Mediated Responses : PHAGOCYTOSIS
 THE ACQUIRED IMMUNE SYSTEM

Humoral Immunity Cellular/

( B-Lymphocytes Cell Mediated Immunity
and
( T-Lymphocytes )
Antibodies )
 Development of the Acquired Immune System :
Memory-T Cells

T-Lymphocytes Cytotoxic T-Cells

( T8 Cells )

During foetal
development Helper T Cells Suppressor T Cells
‘Lymphocyte (T4 cells) ( T8 Cells )
precursors’
from bone
marrow

Plasma Cells
B-Lymphocytes

Memory- B cells
Development of the Acquired Immune Responses
Body invasion by Cytotoxic-T Cells
ANTIGEN
T-Lymphocytes

Antigen peptide Suppressor-T Cells

+ MHC I

IL -2
MACROPHAGES
Antigen peptide
fragment + MHC II

secretes Helper-T cells

IL - 1
IL -2,
contact Plasma Cells
Systemic Effects
B-Lymphocytes

ANTIGEN Memory-B Cells

Primary and Secondary Antibody Responses