1. VAGAI - Physiology Notes.pdf

UNDER GRADUATE MATERIALS
PHYSIOLOGY

Sl.No. Chapter Page number
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
CONTENTS
Sl.No. Chapter Page number
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
44

1.CELL
2.NERVE MUSCLE PHYSIOLOGY
3.BLOOD AND BODY FLUIDS
4.GASTRO INTESTINAL SYSTEM
5.RENAL SYSTEM
6.MALE REPRODUCTIVE SYSTEM
7.FEMALE REPRODUCTIVE SYSTEM
8.ENDOCRINE SYSTEM
PHYSIOLOGY PAPER 1
CHAPTER NAME PAGE NUMBER
4
5
6 - 54
55 - 113
114 - 144
145 - 151
152 - 167
168 - 241
VᾹGAI (வாகை) INSTITUTE OF MEDICAL SCIENCES
NO.27, 1ST CROSS, 1ST MAIN ROAD, MOOGAMBIGAI NAGAR,
NAINARMANDAPAM, PUDUCHERRY – 605 004.
Phone number : 09566999802,9787100885, email id : vimspondy
@gmail.com, website : www.vimspondy.com

1.RESPIRATORY SYSTEM
2.CARDIO VASCULAR SYSTEM
3.NERVOUS SYSTEM
4.SPECIAL SENSES
PHYSIOLOGY PAPER 2
4
CHAPTER NAME PAGE NUMBER
242 - 304
305 - 364
365
366 - 148

1.CELL
5
Phone number : 09566999802 ,9787100885, email id : vimspondy

2.NERVE MUSCLE
PHYSIOLOGY
6

3.BLOOD AND BODY
FLUIDS
7

A.BODY FLUIDS
Total water in the body is about 40 liters.
1. Intracellular fluid (ICF) - 55%
2. Extracellular fluid (ECF)- 45%
i. Interstitial fluid and lymph
ii. Plasma
iii. Fluid in bones
iv. Fluid in dense connective tissues like cartilage
v. Transcellular fluid
a. Cerebrospinal fluid
b. Intraocular fluid
c. Digestive juices
d. Serous fluid
-intrapleural fluid,
-pericardial fluid,
-peritoneal fluid.
e. Synovial fluid in joints
f. Fluid in urinary tract
BODY FLUIDS AND BLOOD
B.BLOOD
I. INTRODUCTION
Connective tissue in fluid form.
II. PROSPERTIES OF BLOOD
a.Colour : Red in colour. (Arterial blood – scarlet red,
venous blood – purple red).
b.Volume : 5 liters in normal adult.
c. Reaction & pH : Alkaline
d. Specific gravity :
Total blood : 1.052 to 1.061
Total cells : 1.092 to 1.101
Plasma : 1.022 to 1.026
e. Viscosity : more viscous than water (due to red blood cells and plasma proteins). 8

III. FUNCTIONS OF BLOOD
a.Nutrient Function :Glucose, amino acids, lipids, vitamins are absorbed from gastrointestinal tract and carried by blood to different parts of the body for growth.
b.Respiratory Function
Transport of respiratory gases is done by the blood.
It carries oxygen from alveoli to different tissues
Carbon dioxide from tissues to alveoli.
c.Excretory Function : Waste products are removed by blood and carried to the excretory organs like kidney, skin, liver, etc.
d.Transport of hormones and enzymes :The hormones and enzymes are carried to different parts of the body.
e.Regulatory function
Regulation of water balance
Regulation of acid base balance
Regulation of body temperature
f.Storage function
Water and some important substances like proteins, glucose, sodium and potassium are constantly required by the tissues.
Blood serves as a readymade source for these substances.
g.Defensive function
Neutrophils and monocytes engulf the bacteria by phagocytosis.
Lymphocytes are involved in immunity.
Eosinophils are responsible for detoxification, disintegration and removal of foreign proteins
IV.COMPOSITION OF BLOOD,PLASMA AND SERUM
9

BLOOD CELLS
RED BLOOD CELLS
a. introduction and normal value
b. morphology of red blood cells
c. properties of red blood cells.
d. formation of rbc(erythropoiesis)
e. variations in red blood cells
f. lifespan and fate of red blood cells
g. determination of lifespan of RBC
h. functions of red blood cells
i. erythrocyte sedimentation rate
WHITE BLOOD CELLS
b. morphology of white blood cells
c. properties of white blood cells.
d. formation of white blood cells.(Leucopoiesis)
e. variations in white blood cells.
f. lifespan and fate of white blood cells.
g. determination of lifespan of WBC.
h. functions of white blood cells.
PLATELETS
b. morphology of platelets
c. properties of platelets.
d. formation of platelets.(megakaryopoisis)
e. variations in platelets.
f. lifespan and fate of platelets.
g. determination of lifespan of platelets.
h. functions of platelets.
A.INTRODUCTION AND NORMAL VALUE : Red blood cells (RBC) are the non-nucleated formed elements in the blood. The red colour of these
cells is due to the presence of the colouring matter-hemoglobin. Normal count ranges between 4 and 5.5 millions per cubic millimeter of blood.
B.MORPHOLOGY OF RED BLOOD CELLS
1.Size :
Diameter (7.2µ (6.9 – 7.4 µ))
Thickness (Periphery it is thicker center it is thinner)
2.Shape: Disc shaped and biconcave (dumb-bell shaped). Biconcave contour of red blood cells has the following mechanical advantages
1. It helps rapid diffusion of oxygen and other substances
2. Large surface area is provided for absorption or removal of different substances
3. Minimal tension is offered on the membrane when the volume of cell alters.
4. While passing through the capillaries very easily.
C.PROPERTIES OF RED BLOOD CELLS
1. Rouleaux Formation :When blood is taken out of the blood vessel, the red blood cells pile up one above another like the pile of coins.Property of the red blood
cells is called rouleaux
2. Specific Gravity :1.092 to 1.1101
3. Packed Cell Volume Variations in number of red blood cells :When the blood is collected in a centrifuge tube along with proper
anticoagulant and centrifuged for a period of 30 minutes at a speed of 3000 rpm (revolutions per minute), the red blood cells settle at
the bottom of the tube leaving the clear plasma at the top.
4. Suspension Stability : During circulation, the red blood cells remain suspended uniformly in the blood.
RED BLOOD CELLS
10

I. DEFINITION
Origin, Development and maturation
of erythrocytes.
II. SITE OF ERYTHROPOIESIS
a. In Fetal(intrauterine life-IUL) Life
1.Mesoblastic stage :
In first two months of IUL from Yolk
sac
2.Hepatic stage :
From third month of IUL from Liver,
Spleen, Lymphoid organs
3.Myeloid stage :
Last three months form Red bone
marrow, Liver
D.FORMATION OF RBC(ERYTHROPOIESIS)
I. DEFINITION
II. SITE OF ERYTHROPOIESIS
III.STAGES OF ERYTHROPOISIS
IV. FACTORS NECCESSORY FOR ERYTHROPOISIS
b. In postnatal life and in adults
1.Up to the age of 5 to 6 years: From
Red bone marrow of all bones
2.During 6th year to 20th year: From Red
bone marrow of long bones and all the
membranous (flat) bones.
After the age of 20 years: From All
membranous bones like vertebra, Sternum, ribs,
scapula, iliac bones, Skull bones and from the
ends of long bones.
Bone marrow
Red bone marrow
Pluripotent stem cells(haemocytoblast)
Myeloid stem cells
Burst forming unit - erythrocyte(BFU-E)
colony forming unit - erythrocyte(CFU-E)
III.STAGES OF ERYTHROPOIESIS
Pronormoblast(proerythroblast)
Early normoblast(basophilic)
Intermediate normoblast(polychromatic)
late normoblast(orthochromatic)
ejection of nucleus
reticulocyte
Matured erythrocyte(RBC)
Enter the circulations
11

Proerythroblast
(Megaloblast)
Early normoblast
(basophilic
erythro blast)
Intermediate
normoblast
(Polychromophilic
erythro blast)
Late normoblast
Orthochromic
erythroblast)
Reticulocyte (immature red
blood cell)
Matured erythrocyte
Size Larger in size Slightly smaller Smaller Smaller Larger than RBC Biconcave and smaller in size
Nucleus Occupies the cell
completely
Condensed
chromatin
Chromatin further
condensed
Very much
condensed
chromatin (Ink spot
nucleus), Nucleus
disintegrates and
disappears
(pyknosis)
Not present Not present
Nucleolus Two or more with
reticular network
disappears Not present Not present Not present Not present
Hb no hemoglobin no hemoglobin Starts appearing Hemoglobin
increases
Present Present
Cystoplasm Basophilic Basophilic Polychromophilic
(both acidic and
basic)
Acidophilic The cytoplasm contains the
reticular network or
reticulum formed by
remnants of disintegrated
organelles.
Reticular network disappears
Matured into Early normoblast intermeiatenorm
oblast
Late normoblast Reticulocyte Matured erythrocyte
The reticulum of reticulocyte
is stained by supravital stain.
It can enter the capillaries
through the capillary
membrane from source of
production (diapedesis).
It requires seven days for the
development of matured red
blood cell from
proerythroblast.
It takes five days for the
development of reticulocyte.
12
III. Features of cells in erythropoisis

A. GENERAL FACTORS
1. Erythropoietin
Chemistry – It is a glycoprotein
Secretion – peritubular capillaries of kidneys
Stimulant – hypoxia
Action - Production of proerythroblasts from the stem cells in CFU-E of the bone marrow, Development of proerythroblasts into matured red blood cells through the
normoblastic stages, Release of matured erythrocytes into blood through the capillary membrane from bone marrow.
2. Thyroxine
3. Hemopoietic growth factors (interleukin)
Induce the proliferation of pluripotent stemcells.
The interleukins (IL) involved in erythropoiesis are IL-3, IL-6.
4. Colony stimulating factors (CSF)
It forms the colony forming blastocytes.
5.Vitamins (B, C & D)
B. MATURATION FACTORS
1. Vitamin B12 (Cyanocobalamin)
 Vitamin B12 us essential for synthesis of DNA
 Deficiency Leads to failure in maturation of the cell and reduction in the cell division.
 So, the cells are larger with fragile and weak cell membrane
2. Intrinsic factor of castle
 This is produced in gastric mucosa.
 This is essential for the absorption of Vitamin B12 from intestine.
 In its absence vitamin B12 is not absorbed so causes pernicious anemia.
 The extrinsic and intrinsic factors are together called hematinic principle.
3. Folic acid
 Essential for maturation
 Required for the synthesis of DNA
 Anemia due to the folic acid deficiency is called megaloblastic anemia
C. FACTORS NECESSARY FOR HEMOGLOBIN FORMATION
 First class proteins and amino acids : Amino acids derived from these proteins are
required for the synthesis of protein part of hemoglobin, the globin.
 Iron : Iron is necessary for the formation of heme part of the hemoglobin
 Copper : This is necessary for the absorption of iron from the gastrointestinal tract
 Cobalt and nickel : Cobalt and nickel are essential for the utilization of iron during
hemoglobin formation.
 Vitamins : Vitamin C, riboflavin, nicotinic acid and pyridoxine are also essential for the
formation of hemoglobin.
13
IV.FACTORS NECESSARY FOR ERYTHROPOIESIS

VARIATIONS IN RBC
I.NUMBER II.SIZE III.SHAPE IV.STRUCTURE
V.VARIATIONS IN RED BLOOD CELLS
II. variations in size of red
blood cells
 Microcytes
– Small size
– Seen in Iron
deficiency anemia
– increased osmotic
pressure in blood
 Macrocytes
– Red blood cells with
larger size
– Seen in
Megaloblastic
anemia
– Decreased osmotic
pressure in blood.
III. variations in shape of
red blood cells
Crenation : Shrinkage as in
hypertonic solution
Spherocytosis : Globular
form as in hypotonic
solution
Elliptocytosis : Elliptical
shape as in certain types of
anemia
Sickle cell : Creascentic
shape as in sickle cell
anemia
Poikilocytosis : Unequal
shapes due to deformed
cell membrane.The shape
will be of flask, hammer or
any other unusual shape.
IV. variations in structure of red
blood cells
 Punctate Basophilism:
Dots of basophilic
materials appear in the
red blood cells occurs in
conditions like lead
poisoning
 Rin: Ring or twisted
strands of basophilic
material appear in the
periphery of the red
blood cells.
 Howell Jolly Bodies :
Nuclear fragments are
present in the ectoplasm
of the red blood cells
A.INCREASE IN
NUMBER
B.DECREASE IN
NUMBER
1.PHYSIOLOGICAL
2.PATHOLOGICAL
1.PHYSIOLOGICAL
2.PATHOLOGICAL
14

1.Increase in the red blood cell count 2. Decrease in red blood cell count
A. Physiological Variations  Age: Infants and growing children cell count is
higher than the value in adults.
 Sex: During reproductive period of females, the
count is less than in males
 High Altitude : During hypoxia, the erythropoietin
is released from the kidneys. The erythropoietin
in turn stimulates the bone marrow to produced
more red blood cells.
 Muscular Exercise : Temporary increase in red
blood cell count after exercise. Because of mild
hypoxia and contraction of spleen
 Emotional Conditions: Red blood cell count is
increased during the emotional conditions like
anxiety, because of sympathetic stimulation
 Increased Environmental Temperature : Increase
red blood cell count
 After Meals: Slight increase in the red blood cell
High Barometric Pressures: In deep sea,
when the oxygen tension of
blood is higher, the red blood
cell count decreases
After Sleep: Red blood cell count decreases
slightly after sleep.
Pregnancy: Red blood cell count decreases.
This is because of increase in
extra cellular fluid volume
(haemodilution).
B. Pathological Variations polycythemia
1.Primary polycythemia (polycythemia Vera):
Count above 14 millions/cu mm of blood Due to
myeloproliferative disorders (malignancy of red bone
marrow. )
2.Secondary polycythemia (Secondary to pathological
condition):
Congenital heart disease
Chronic carbon monoxide poisoning
Poisoning by chemicals like phosphorus and arsenic
Repeated mild hemorrhages.
Anemia - Abnormal reduction in the red
blood cell
1.Decreased production (aplastic anemia)
2.Decreased formation(nutritional anemia)
3.Increased destruction(lysis) –(hemolytic
anemia)
4.Increased loss (hemorrhagic anemia)
15
I.Variations in number of red blood cells

ANEMIA
a.MORPHOLOGIC b.ETIOLOGIC
microcytic
hypochromic
anemia
macrocytic
normochromic
macrocytic
hypochromic
Normocytic
normochromic
1.Aplastic
anemia
(decreased
production)
2.Nutritional anemia
(decreased formation)
-Iron deficiency and
vit B12 deficiency
3.Hemolytic anemia
(increased lysis)
4.Hemorrhagic
anemia
(increased blood
loss)
A. Definition
Anemia refers to abnormal reduction in
- Red blood cell
- Hemoglobin content and
- Packed cell volume
B. Classification of anemia
A. Definition
B. Classification of anemia
C. signs & symptoms
ANEMIA
Microcytic
hypochromi
c anemia
Macrocytic
normochromi
c anemia
Macrocytic
hypochromic
anemia
Normocytic
normochromic
anemia
Size of
RBC
Smaller size Larger in size Larger in size normal.
Hemoglo
bin
contents
reduced. normal. reduced. normal.
RBC
count
reduced. reduced. reduced. reduced.
Example
(etiology
)
iron
deficiency
anemia
megaloblastic
anemia
megaloblastic
anemia
haemorhagic
anemia
16

1.Aplastic Anemia
(decreased production due to bone marrow depression)
2. Nutrition DeficiencyAnemia(decreased RBC formation due to nutritional deficiency
Iron deficiency anemia Megaloblastic anemia
1.definition Anemia due to decreased production of RBC Decrease RBC formation due to iron
deficiency
Decrease RBC formation due to vit B 12
deficiency
2.Etiology The red bone marrow is reduced and replaced by fatty tissues in
conditions like repeated exposure to X-ray or gamma ray
radiation and by bacterial toxins, quinine, gold salts, benzene,
radium.It is common in tuberculosis and viral infections like
hepatitis and HIV infections.Normocytic
-Decreased intake of iron
-Poor absorption of iron from intestine
-Increased demand for iron i
-Decreased intake of vit B12
-Poor absorption of vit B12 from intestine
-Increased demand for vit B12
-atrophy of the gastric mucosa resulting in
reduced production of intrinsic factor and
poor
absorption vitamin B12 cause pernicious
anemia
Etiologic Classification of anemia
4.Clinical features( See in next page
5.investigation 1. Reduced RBC count
2. Bone marrow replaced by fibrous tissue
1. Reduced RBC count
2. red blood cells are microcytic and
hypochromic.
1. Reduced RBC count
2. red blood cells are Macrocytic and
hypochromic
6.treatment 1.Treat the cause
2.Blood transfusion
3.Bone marrow transplantation
1.Treat the cause
2.Blood transfusion
3.Iron supplementation
1.Treat the cause
2.Blood transfusion
3.Vit B12 and folic acid supplementation
Radiation.drugs,virus
bone marrow Depression
Decreased stem cells
leukopenia
Decreased production of blood cells
Decreased PLATELET
Decreased RBC Decreased WBC
thrombocytopenia
pancytopenia
anemia
Decreased Intake of iron rich food, decreased
absorbtion, increased demand, increased
loss
↓
Decreased serum iron
↓
Decreased haem synthesis
↓
Decreased Hb formation
↓
Defect in the cytoplasm formation
↓
Decreased haemocytoblast
↓
Decreased RBC
↓
anemia
Decreased Intake of VIT B12 and folic acid rich
food, decreased absorption, increased
demand,
increased loss
↓
Decreased serum VIT B12
↓
Decreased DNA synthesis in erythroblast
↓
Decreased nucleus formation
↓
Defect in the nuclear maturation
↓
formation of Megaloblast and Decreased RBC
↓
Megaloblastic anemia
3.pathogenesis
17

3. Hemolytic anemia (increased lysis of RBC) 4. Hemorrhagic anemia(increased blood loss)
1.definition Anemia due to excessive lysis of RBC Anemia due to excessive loss of blood
2.Etiology Chemical poisoning by substances like lead, coal and tar .Infections like malaria
damage RBC.destruction DESTRUCTION RBC by formation of abnormal
haemoglobin S (sickle cell anemia)
Acute hemorrhage : Accident,surgery, excessive uterine bleeding, purpura
and hemophilia.Reduction in total red blood cell count .Plasma portion of
blood is replaced within 24 hours.but Replacement of red blood cells takes
some time.
Chronic hemorrhage :Continuous loss of blood as in hook worm
infestation, a lot of iron is lost from the body.
Etiologic Classification of anemia - cont
4.Clinical features a.Clinical features common to all anemia
1. Skin - Skin becomes pale. The paleness is more constant in buccal and pharyngeal mucus membrane, conjunctivae, lips, ear lobes, palm and nail bed
2. Cardiovascular system - Increase in heart rate and cardiac output. Cardiac murmurs are common.
3. Respiration - Increase in rate and force of respiration. Breathlessness.
4. Digestion - Anorexia, nausea, vomiting, abdominal discomfort, constipation.
5. Metabolism - Basal metabolic rate is increased in severe anemia.
6. Kidney - Renal function is disturbed.
7. Reproductive system - Menstrual cycle is disturbed. There may be oligomenorrhea or amenorrhea.
8. Neuromuscular system - headache, lack of concentration, restlessness, irritability, drowsiness, dizziness or vertigo especially when standing.
b.In addition to above Clinical features ,the other features present in related to the type of anemia are
1.Aplastic anemia – infection ,bleeding
2. iron deficiency anemia - brittle nails, spoon shaped nails, brittle hair, trophy of papilla in tongue and dysphagia
3. megaloblastic anemia(vitamin B12 deficiency) - Neurological disorders such as paresthesia, progressive weakness and ataxia
4.Hemolytic anemia - jaundice
5.investigation 1.Reduced RBC count
2.Abnormal RBC - Sickle shaped RBC
1.Reduced RBC count
2.Normocytic normochromic anemia .
6.treatment 1.Treat the cause
2.Blood transfusion
1.Treat the cause
2.Blood transfusion
Normal production of RBC
↓
enter the circulations
↓
Trauma or surgery
↓
Increased loss of blood including RBC
↓
Decreased RBC count
↓
Anemia
Normal production of RBC
↓
enter the circulations
↓
Defect in the RBC structures
↓
Lysis of RBC
↓
Decreased RBC count
↓
Anemia
3.pathogenesis
18

E. LIFESPAN AND FATE OF RED BLOOD CELLS
F. FUNCTIONS OF RED BLOOD CELLS
 Erythrocytes transport oxygen from the lungs to the tissues.
 Red blood cells transport carbon dioxide from the tissues to the lungs.
 Hemoglobin in red blood cell also functions as a good buffer takes part in the
maintenance of acid base balance.
 Red blood cells carry the blood group antigens like a agglutinogen, B
agglutinogen and RH factor.
This helps in determination of blood group and blood transfusion .
Life span of red blood cell is about 120 days,senile red blood cells are destroyed in reticuloendothelial system

I. Definition
Normally, the red blood cells remain suspended uniformly in circulation.
If blood is mixed with an anticoagulant and allowed to stand on a vertical tube, the red cells settle down due to gravity with a
supernatant layer of clear plasma.
The rate at which the cells settle down is called Erythrocyte Sedimentation Rate (ESR).
II. Determination of ESR
By Westergren’s Method
By Wintrobe’s Method
III.Normal values of ESR
In males 3 to 7 mm in one hour
In females 5 to 9 mm in one hour
IV. Variations of ESR
a.physiological variation
Age : ESR is less in children and infants.
Sex : It is more in females than in males.
Menstruation : The ESR is increased during menstruation.
Pregnancy : From 3rd month to parturition, ESR is increased up to 35mm in one hour.
b.pathological variation
1.ESR increases in the following diseases :
 Tuberculosis
 In all type of anemia except the sickle cell anemia
 Malignant tumors
 Rheumaoid arthitis
 Rheumatic fever and
 Liver diseases
2.ESR decreases in the following diseases :
 Allergic conditions
 Sickle cell anemia
 septic shock
 Polycythemia and
 Extreme leukocytosis
V.Significance of Determining ESR
 Helps in diagnosis as well as prognosis.
 Determination of ESR is especially helpful in assessing the progress of patients treated for chronic disorders like pulmonary
tuberculosis and
rheumatoid arthritis.
VI.Factors affecting ESR
 Specific gravity of red blood cells : ESR is increased.
 Rouleaux formation : increases the ESR.
 Increased size of red blood cells : ESR is increased.
 Viscosity of blood : ESR is decreased.
 Number of red blood corpuscles : ESR is decreased. VᾹGAI (வாகை) INSTITUTE OF MEDICAL SCIENCES
Erythrocyte sedimentation rate

C. PROPERTIES OF WHITE BLOOD CELLS
1. Diapedesia : Process by which the leukocytes squeeze through the narrow blood vessels.
2. Ameboid Movement : Neutrophils, monocytes and lymphocytes show amebic movement.
3. Chemotaxis : Chemical substances in the tissues causes the leukocytes to move towards tissues is called
chemotaxis.
4. Phagocytosis : Neutrophils and monocytes swallow foreign bodies by means of pseudopodia.
A. INTRODUCTION AND NORMAL VALUE
INTRODUCTION : leukocytes Protect body against microorganisms and
remove dead cells and debris
NORMAL VALUE : 4000 to 11000 /cmm
WHITE BLOOD CELLS
AGRANULOCYTE
NEUTROPHILS
GRANULOCYTE
BASOPHILS
EOSINOPHILS
MONOCYTE
LYMPHOCYTE
SMALL LYMPHOCYTE
LARGE LYMPHOCYTE
B.MORPHOLOGY AND CLASSIFICATION OF WHITE BLOOD CELLS
21
A.INTRODUCTION AND NORMAL VALUE
B.MORPHOLOGY AND CLASSIFICATION OF WHITE BLOOD CELLS
C.PROPERTIES OF WHITE BLOOD CELLS.
D. FORMATION OF WBC(LEUCOPOIESIS)
E. VARIATIONS IN WHITE BLOOD CELLS
F. LIFESPAN AND FATE OF WHITE BLOOD CELLS
G.DETERMINATION OF LIFESPAN OF WHITE BLOOD CELL
H.FUNCTIONS OF WHITE BLOOD CELLS

D.CHARACTERISTICS OF WHITE BLOOD CELLS
Sl. No. Cell Size Nucleus Cytoplasm Lifespan
(days)
Functions
Granulocytes
1. Neutrophils
(50-70%)
(3000 to 6000)
10-14 µ Vary from 1 to 5 lobes Neutrophilic fine
granules/purple colour
granules
2 – 5 -Front line soliders
-Engulf bacteria in the ECF by phagocytosis
-Help in opsonisation
2. Eosinophils
(2%-4%)
(150 to 450)
10-14 µ Bilobed / spectach shaped Eosinophilic (Brick red),
Coarse granules
7 – 12 -Clot lysis (produces prefibrinolysins)
-Prevents hypersensitivity by antigen antibody
complexes (Anti allergy)
-Destroys parasites
-Detoxifies foreign bodies
3. Basophils
(0-1%)
(0 to 100)
10-12 µ Bilobed, covered by thick
brush granules
Thick bluish/violet
granules, making the
Nucleus and cell
border is not clear
12 – 15 -- prevents intravascular clotting by the relesae
of heparin
-Removes fat particles from blood after a fatty
meal (LIPID metabolism)
-Taken part in allergy reactions along with mast
cells.
Agranulocytes
1. Lymphocytes (20%-40%) (1500 to 2700)
(a) Small 8-10 µ Single -Basophilic cytoplasm,
(little)
-No granules
½ - 1 -Form tissue macrophages and acts as Scavenger
(b) Large 12-16 µ Large lobe
Centrally placed chromatin
-Basophilic cytoplasm,
(abundant)
-No granules
½ - 1 -Phogocytoze several bacteria
2. Monocyte
(2-6%)
(200 to 600)
15-20 µ Large single lobed kidney
shaped eccentrically placed
- Basophilic, abundant
-Frost glass appearance
-No granules
2 – 5 -Along with B and T lymphocytes they help in
humoral & cellular mediated immunity
22

Bone marrow
↓
Red bone marrow
↓
Pluripotent stem cells
↓
Myeloid stem cells
↓
colony forming unit –Gm
↓
E. FORMATION OF WBC(LEUKOPOIESIS)
Myeloblast
↓
Promyelocyte
↓
Myelocyte
↓
Metamyelocyte
↓
band cells
↓
mature WBC
(STAGES OF LEUCOPOIESIS FOR DIFFERENT CELL)
• Neutrophils
• Myeloblast
• Promyelocyte
• Neutrophilic myelocyte
• Neutrophilic
metamyelocyte
• Band cell
• Neutrophil
• Basophils
• Myeloblast
• Promyelocyte
• Basophilic myelocyte
• Metamyelocyte
• Band cells
• Basophil
 Eosinophils
• Myeloblast
• Promyelocyte
• Eosinophilic myelocyte
• Metamyelocyte
• Band cell
• Eosinophil
 Monocytes
• Monoblast
• Promonocyte
• Monocyte
• Macrophage
23

A.Leucocytosis
(Increase in total leucocyte count (TLC) Above 11,000/mm3)
B. Leucopenia
(Decrease in TLC beyond 4000/mm3 of blood (cells mainly affected Are
neutrophils))
1.Physiological At birth
Exercise
Diurnal variatio (evening)
After meals
Stress
Pregnancy,
Lactation. Menstruation
Starvation or prolonged fasting
2. Pathological Pyogenic infections
Following an injection of epinephrine or norepinephrine
Administration of steroids
 Leukemia
It is a cancerous condition in which there is a marked increase in
immature WBCs in the peripheral blood.
Viral infections
Typhoid fever
Bone marrowdeperssion
Drug induced
X-ray irradiation
F.VARIATIONS IN WHITE BLOOD CELLS
24
1. Neutrophils 2. Eosinophils 3. Basophil 4.Lymphocytes 5. Monocytes
(a) Increase
in count
Neutrophilia
Pyogenic
infection
Tissue
destruction,
(myocardial
infarction,
postoperative)
Eosinophilia
Allergic conditions
Parasitic infections
Skin infections
Basophilia
During healing
and
repair
Smallpox and
chickenpox (viral
infections)
Lymphocytosis
In chronic infections,
e.g. tuberculosis
Viral infections
In infancy (50% cells are
lymphocytes)
Monocytosis
Chronic infections,
e.g. tuberculosis, syphilis
Malaria
(a) Decrease
in count
Neutropenia
Infancy
Viral infection
Typhoid fever
Bone marrow depression
Eosinopenia
Due to an injection of
ACTH or steroids
because of increased
sequestration in lungs and spleen.
Basopenia
Drug induced
Administration of
glucocorticoids
Lymphopenia
AIDS
Bone marrow
depression
Monocytopenia
Bone marrow depression
G.VARIATIONS IN DIFFERENTIAL WHITE BLOOD COUNT

CELL LIFESPAN(DAYS)
Neutrophils 2 – 5
Eosinophils 7 – 12
Basophils 12 – 15
Small lymphocyte ½ - 1
Large lymphocyte ½ - 1
Monocyte 2 – 5
H. LIFESPAN AND FATE OF WHITE BLOOD CELLS
CELL FUNCTION
Neutrophils Front line soliders
Engulf bacteria in the ECF by phagocytosis
Help in opsonisation
Eosinophils Clot lysis (produces prefibrinolysins)
Prevents hypersensitivity by antigen antibody complexes (Anti allergy)
Destroys parasites
Detoxifies foreign bodies
Basophils - prevents intravascular clotting by the relesae of heparin
Removes fat particles from blood after a fatty meal (LIPID metabolism)
Taken part in allergy reactions along with mast cells.
Small lymphocyte Form tissue macrophages and acts as Scavenger
Large lymphocyte Phogocytoze several bacteria
Monocyte Along with B and T lymphocytes they help in humoral & cellular mediated immunity
J.FUNCTIONS OF WHITE BLOOD CELLS
25
I.DETERMINATION OF LIFESPAN OF WHITE BLOOD CELL- Radiosotope method

PLATELETS (OR) THROMBOCYTES(OR) MEGAKARYOCYTES
A.INTRODUCTION AND NORMAL VALUE
B. MORPHOLOGY OF PLATELETS
C. PROPERTIES OF PLATELETS.
D. FORMATION OF PLATELETS
E. VARIATIONS IN PLATELETS
F. LIFESPAN AND FATE OF PLATELETS
G.DETERMINATION OF LIFESPAN OF PLATELETS
H.FUNCTIONS OF PLATELETS
A .INTRODUCTION AND NORMAL VALUE
Introduction:
 Small colourless, nonnucleated and moderately
refractive bodies.
 Platelets are spherical or rod shaped and become
oval or disc shaped when inactivated
Normal count:
 2,50,000 (2,00,000 to 4,00,000) cu mm of blood.
B. MORPHOLOGY OF PLATELETS
1. Cell membrane
Contains ,Lipids,Carbohydrates,Glycoproteins.
2. Microtubules
Maintain the disc like shape.
3. Cytoplasm
Has Golgi apparatus, endoplasmic reticulum, mitochondria,
microtubule, micro vessels, filaments and different types of
granules.
a. Proteins : Contractile proteins (Actin and myosin for contraction of platelet and thrombosthenin for clot retraction)
Other proteins 1.Von willebrand factor – responsible for adherence of platelets
2.Fibrin stabilizing factor – a clotting factor
3.Platelet derived growth factor (PDGF) – involved in repair of damaged blood vessels. This also regulates the plasma level of factor
VIII
4.Platelet activating factor (PAF) – causes aggregation of platelets during the injury of blood vessels.
b. Enzymes (Adenosine triphosphatase)
c. Hormonal substances (Adrenaline, 5HT Serotonin, Histamine).
d. Other chemical substances
1.Glycogen substances like blood group antigens.
2.Inorganic substances – calcium, copper, magnesium and iron. 26

C. PROPERTIES OF PLATELETS.
1. Adheesiveness
The factors, which cause adhesiveness, are collagen, thrombin, ADP, Thromboxane A2,
calcium ions and von Willebrand factor.
2. Aggregation (grouping of platelets)
The stickiness is due to ADP and thromboxane A2.
3. Agglutination
Clumping together of platelets.
Agglutination of platelets occurs due to the actions of some platelet agglutinins.
Bone marrow
↓
Red bone marrow
↓
↓
Myeloid stem cells
↓
colony forming unit –MEG
↓
megakaryoblast
↓
promegakaryocyte
↓
megakaryocyte
↓
Platelets
↓
Enter the circulation
D. FORMATION OF PLATELETS
27

A.THROMBOCYTOSIS
(increase in total
platelet count)
B. THROMB0
CYTOPENIA
(Decrease in total
platelet count).
Thrombocythemia (persistent and abnormal
increase in platelet count)
Physiological  High altitude ,
 After meals.
 Age : less in infants
 Sex : no difference in males and females.
---
Pathological  Allergic conditions
 Asphyxia
 Hemorrhage
 Bone fractures
 Surgical operations
 Splenectomy
 Rehumatic fever and
 Trauma (wound or
injury or damage
produced by external
force).
 Acute infections
 Acute leukemia
 Aplastic and pernicious anemia
 Chickenpox
 Smallpox
 Splenomegaly
 Scarlet fever
 Typhoid and
 Tuberculosis
 Carcinoma
 Chronic leukemia and
 Hodgkin’s disease
E.VARIATIONS IN PLATELETS
G.DETERMINATION OF LIFESPAN OF PLATELETS : Radiosotope method
H.FUNCTIONS OF PLATELETS
1. Role in blood clotting
a. Responsible for the formation of intrinsic prothrombin activator.
b. This substance is responsible for the onset of blood clotting.
2. Role in clot retraction
c. In the blood clot, the blood cells including platelets are entrapped in between the fibrin
threads.
3. Role in prevention of blood loss (Hemostasis)
a. Platelets secrete 5HT, which causes the constriction of blood vessels.
b. It seal the damaged blood vessels by adhesive property.
c. It seal the damaged blood vessels by forming temporary plug
4. Role in repair of ruptured blood vessel
The platelet derived growth factor (PDGF) of platelets is useful for the repair of the
endothelium and other structures of the ruptured blood vessels.
5. Role in defense mechanism
By the property of agglutination, platelets encircle the foreign bodies and kill them by the
process of phagocytosis.
28
F. LIFESPAN AND FATE OF PLATELETS : 10 days after that destroyed in spleen.

I. DEFINITION
Arrest of bleeding or stoppage of bleeding is called hemostasis.
II. STAGES OF HEMOSTASIS
1. Vasoconstriction 2. Platelet plug formation 3. Coagulation of blood
HAEMOSTASIS
29

COAGULATION OF BLOOD
I. DEFINITION
Blood is becomes a jelly like mass after few minutes out of the blood
vessels clotting of blood.
II. FACTORS INVOLVED IN BLOOD CLOTTING
Sl. No. Factor Name
1. Factor I Fibrinogen
2. Factor II Prothrombin
3. Factor III Tissue thromboplastin (TPL)
4. Factor IV Calcium Ions
5. Factor V Proaccelerin (accelerator globulin)
6. Factor VI No such factor exists
7. Factor VII Pro Convertin
8. Factor VIII Antihaemophilic globulin (Anti haemophilic factor A)
9. Factor IX Christmas factor (anti-hemophilic factor B)
10. Factor X Stuart – Prower factor
11. Factor XI Plasma thromboplastin antecedent (antihemophilic factor C)
12. Factor XII Hageman factor (glass contact factor)
13. Factor XIII Fibrin Stabilising Factor (Loki-Lorand factor)
III. SEQUENCE OF CLOTTING MECHANISM
Stage 1: Formation of prothrombin activator
a. Extrinsic pathway for the formation of
prothrombin activator – by tissue thromboplastin
b. Intrinsic pathway for the formation of
prothrombin activator- by platelet
Stage 3 : conversion of fibrinogen into fibrin
Stage 2 : Conversion of Prothrombin into Thrombin
30

Stage 1: Formation of prothrombin activator
a.Extrinsic pathway for the formation of prothrombin activator – by tissue
thromboplastin
1.After injury, the damaged tissues release tissue thromboplastin act as proteolytic.
2.The glycorprotein and phospholipid components of thromboplastin convert factor X
into activated factor X, in the presence of factor VII.
3.The activated factor X reacts with factor V and phospholipid component of tissue
thromboplastin to form prothrombin activator, requires the presence of
calcium ions.
4.Factor V is activated by thrombin, which is formed from prothrombin. This factor V
now accelerates processes of blood clot.
b.Intrinsic pathway for the formation of prothrombin activator by platelet
1. Blood vessel is ruptured, endothelium is damaged and collagen
exposed.
2.When factor XII (Hegman factor) comes in contact with collagen, it is
converted into activated factor XII.
3.The activated factor XII converts factor XI into activated factor XI in the
presence of Kinogen and Prekallikrein.
4.The activated factor XI activates factor IX in the presence of factor IV
(calcium)
Activated factor IX activates factor X in the presence of factor VIII and
calcium.
5. When platelet comes in contact with collagen of damged blood vessel,
it releases phospholipids.
6. Now the activated factor X reacts with platelet phospholipid and factor
V to form prothrombin activator. This needs presence of calcium ions.
7. Factor V is also activated by positive feedback effect of thrombin.
b.Intrinsic pathway for the formation of prothrombin activator
by platelet
a.Extrinsic pathway for the formation of prothrombin activator
31

Stage 2 : Conversion of Prothrombin into Thrombin
= Prothrombin activator converts prothrombin into thrombin in the presence of
calcium.
Stage 3 : conversion of fibrinogen into fibrin
= Soluble fibrinogen is converted into insoluble fibrin by thrombin.
= The activated fibrinogen is called fibrin monomer. This polymerizes with other
monomer molecules to form fibrin.
= First formed fibrin contains loosely arranged strands. This is modified later into
a dense tight aggregate by fibrin stabilizing factor (factor XIII) and this reaction
requires the persence of calcium ions.
32

33

IV. CHEMICAL AGENTS TO PREVENT BLOOD CLOTTING – ANTICOAGULANTS
The substances, which prevent or postpone coagulation of blood used to prevent clotting inside the body, i.e. in vivo . used to prevent clotting outside the body, i.e. in vitro,
used both in vivo and in vitro.
1. Heparin, 2. Coumarin Derivatives ,3. EDTA ,4. Oxalate Compounds ,5. Citrates
1. Heparin
Heparin is produced in mast cells -Wandering cells are abundant in liver and lungs naturally produce anticoagulatnt.
a.Mechanism of Action of Heparin
- Direct action on thrombin by suppressing its activity. Removes thrombin from circulation.
- It inactivates the active form of other clotting factors ,also activates antithrombin III.
b.Uses of Heparin
Is used vivo and vitro.
Clinical Use
- To prevnet intravascular blood clotting during surgery.
- It is used during dialysis
- Heparin is used during cardiac surgery, which involves passing the blood thorugh heart lung machine.
- Heparin is used as anticoagulant to preserve the blood before transfusion.
Uses in the Laboratory
- Heparin is also used as anticoagulant in vitro while collecting blood for various investigations.
2. Coumarin Derivatives
- Dicoumoral and warfarin are derivatives of coumarin.
a. Mechanism of Action
- Inhibiting the action of vitamin K. Vitamin K is essential for the formation of various clotting factors namely, II, VII, IX and X.
b.Uses
- Oral anticoagulants.
3. EDTA - Ethylenediaminetetraacetic acid
a.Mechanism of Action
- Prevent blood clotting by removing calcium from blood.
b.Uses
- Lead poisoning, anticoagulant in the laboratory.
4. Oxalate Compounds
- Oxalate compounds prevent coagulation is calcium oxalate, reduce the blood calcium level in vitro.
5. Citrates
- Sodium, ammonium or potassium citrate can be used as anticoagulants in laboratory (in vitro). Citrate combines with calcium in blood to form calcium
citrate and the reduction in calcium level prevents coagulation.
- Citrate is also used in blood bank as acid citrate dextrose (ACD) or citrate phosphate dextrose (CPD).
34

V. TESTS FOR CLOTTING
1. Bleeding Time
- Time interval from oozing of blood after a cut (injury) to arrest of
bleeding.
- Normal duration of 3 to 6 minutes.
- It is prolonged in purpura.
2. Clotting Time
- Time interval form oozing of blood after a cut (injury) to the formation of
clot is called clotting time.
- Normal duration of the clotting time is 3 to 8 minutes.
- Prolonged in hemophilia.
3. Prothrombin Time
- Blood is collected and oxalated so that, the calcium is precipitated and prothrombin is not converted into thrombin. Thus, the blood clotting is
prevented. Then a large quantity of tissue thromboplastin with calcium is added to this blood. Calcium nullifies the effect of oxalate. And, the tissue
thromboplastin activates prothrombin and blood clotting occurs. During this procedure, the time taken by blood to clot after adding tissue
thromboplastin is called prothrombin time. Prothrombin time indicates the total quantity of prothrombin present in the blood.
- The normal duration of prothrombin time is about 12 seconds.
- The prothrombin time is prolonged in deficiency of prothrombin and other factors like factors I, V, VII and X.
VI. BLEEDING DISORDERS
The diseases in which there is prolonged bleeding time or the clotting time are called the bleeding disorders.
1. Hemophilia
2. Purpura
3. von Willebrand Disease
1. Hemophilia
- Sex Linked Inherited Disease
- Affecting Males,
- Females Being The Carriers.
- Prolonged Clotting time
- Mild Trauma Can Cause Excessive Bleeding Which Can Lead To Death.
Causes of Hemophilia
- Lack of formation of prothrombin activator
. - Bleeding time and prothrombin time are normal clotting time is prolonged due to the deficiency of factor VIII or IX.
Types Of Hemophilia
Hemophilia A : classic hemophilia due to the deficiency of factor VIII.
Hemophilia B : christmas disease. Deficiency of factor IX.
Treatment for Hemophilia
Injection of pure factor VIII. 35

2. Purpura
Prolonged bleeding time and clotting time is normal.
Spontaneous bleeding from large number of capillaries causes, tini
hemorrhagic spots under the skin are called purpuric spots.
Causes and type of Purpura
a. Thrombocytopenic Purpura
Bone marrow disease decrease the platelet production leads to purpura.
b. Thromboesthenic Purpura
due to the abnormal platelets in circulation leads to Purpura .
c. Idiopathic Thrombocytopenic Purpura
platelet count is reduced due to development of antibodies against platelets, occur due to
autoimmunity leads to purpura.
3. von Willebrand Disease
Excessive bleeding due to inherited deficiency of von Wilebrand factor secreted by endothelium
of damaged blood vessels and platelets. This factors Responsible for adherence of platelets to
endothelium of blood vessels during hemostasis.
BLOOD GROUPS
I. Introduction
Blood groups are determined by protein molecules present on the surface of red blood cells.
II. Landsteiner’s Law
If a particular antigen is present in the red blood corresponding antibody must be absent in the serum.
If the particular antigen is absent in the red blood cells, the corresponding antibody must be present in the serum
III. Blood Group Systems
More than 20 genetically determined blood group systems are known today. But, Landsteiner discovered two blood group systems called
1.ABO system and
2.Rh system.
These are most important to considered in blood transfusions.
1. ABO SYSTEM
a. Types -based on the presence or absence of antigen A and antigen B, blood is divided into four groups, A, B, AB and O groups.
“A” group has two subgroups namely “A1” and “A2”. Similarly “AB” group has two subgroups namely
“A1B” and “A2B”.
36

b. Determination of the ABO group
Determination of the ABO group is also called blood grouping, blood typing or blood matching.
1. Principle of Blood Typing
Done on the basis of agglutination. Agglutination occurs if an antigen is mixed with its corresponding anitbody, which is called isoagglutinin.
2. Requisites for blood typing
Suspension of red blood cell, testing antisera.
The test sera are :
1.Antiserum A, containing alpha antibody and
2.Antiserum B, containing beta antibody.
3.Procedures :
- One drop of antiserum A is placed on one end of a glass slide (or a tile) and one drop of
antiserum B on the other end.
- One drop of red blood cell suspension is mixed with each antiserum.
- The slide is slightly rocked for 2 minutes.
- The presence or absence of agglutination is observed by naked eyes or under microscope.
Presence of clumping :Thick masses of red
blood cells are seen.
Absence of clumping : The mixture is clear with
separate cells.
4.Results :
If agglutination occurs with antiserum A : The antiserum A contains alpha antibody. The
agglutination occurs if the red cell contains A antigen. So, the blood group is A.
If agglutination occurs with antiserum B : The antiserum B contains beta antibody. The
agglutination occurs if the red cell contains B antigen. So, the blood group is B.
If agglutination occurs with both antisera A and B : The red cell contains both A and B
antigen to cause agglutination. And, the blood group is AB.
If agglutination does not occur either with antiserum A or antiserum B : The agglutination
does not occur if the red blood cell does not contain any antigen. The blood group is O.
c. Importance of ABO groups in blood transfusion
• Who gives blood is called the donor
• Who Receives The Blood Is Called Recipient.
• While transfusing the blood antigen of the donor and the antibody of the recipient are considered.
• Red blood cell of “O” group blood has no antigen and so agglutination does not occur with any other
group of blood. So called universal donors.
• The plasma of AB group blood has no antibody. This does not cause agglutination of red blood cell
from any other group of blood called universal recipients.
d. Cross Matching
• For blood typing, red blood cell of the individual (recipient) and test sera are used.
• Cross matching is done by mixing the serum of the recipient and the red blood cells of donor. In
clinics, cross matching is always done before blood transfusion. If agglutination of red blood cells from
a donor occurs during cross matching, the blood from that person is not used for transfusion.
37

e. Transfusion Reactions due to ABO Incompatibility
 Mismatched blood is transfused to a person, tranfusion reactions occur. If the donor’s plasma contains antibody against red blood cell, agglutination does not occur. Because, these
antibodies are diluted in recipient’s blood.
 But, if recipient’s plasma contains antibodies against donor’s red blood cells, the donor red blood cells are agglutinated and destroyed. More amount of free hemoglobin is liberated.
1.Jaundice
2.Cardiac Shock
Increases the viscosity of blood. Increases the work load on the heart leading to heart failure. The toxic substances released from hemolyzed cells also reduce the arterial blood pressure
and develop circulatory shock.
3.Renal Shut Down
Toxic substances from hemolyzed cells cause constriction of blood vessels in kidney. The toxic substances along with free hemoglobin are filtered through glomerular membrane and
enter the renal tubules. Because of poor rate of reabsorption from renal tubules, all these substances precipitate and obstruct the renal tubule. This suddenly stops the formation of
urine and the condition is called renal shut down.
2. Rh SYSTEM (Rh SYSTEM)
a.Introduction
• Rh factor is an antigen present in red blood cell. Discovered by landsteiner and Wiener. It was first discovered in rhesus monkey, it was named as Rh factor. There are
many Rh antigens but only the D is more antigenic.
• The persons having D antigen are called Rh positive and those without D antigen are called Rh negative.
b.Rh Incompatibility (Hemolytic disease of newborn)
1.mechanism of rh incompatibility
- Rh negative mother carries a Rh positive fetus, usually the first child escapes the complications of Rh incompatibility. This is because, the Rh
antigen cannot pass from fetal blood into the mother’s blood through the placental barrier.
- However, at the time of delivery, the Rh antigen from fetal blood leaks into mother’s blood because of severance of umbilical cord, within a month
after delivery, the mother develops Rh antibody in her blood
- When the mother conceives for the second time and if the fetus happens to be Rh positive again, the Rh antibody from mother’s blood crosses the
placental barrier and enters the fetal blood.
-The Rh agglutinins(antibody), which enter the fetus, cause agglutination of fetal red blood cells and hemolysis.
2.Clinical features of rh incomptibility
a. Erythroblastosis Fetalis
• The severe hemolysis in the fetus causes jaundice and anemia. To compensate the hemolysis there is rapid production of red blood cells, not
only from bone marrow, but also from spleen and liver. Now, many large and immature cells in proerythroblastic stage are released into
circulation.
• Because of this, the disease is called erythroblastosis fetalis.
• Infant dies because of severe anemia.
b. Hydrops Fetalis - If hemolysis is very severe, it leads to intrauterine death.The death occurs mainly because of the development of
edema.enlargement of liver and spleen and cardiac failure.
c. Kernicterus - During the hemolysis, more amount of bilirubin is formed. The blood-brain barrier is not well developed in infants as in the adults. So,
the bilirubin enters the brain and causes permanent brain damage. The bilirubin mostly affects basal ganglia and the motor activities are severely
disturbed. If the condition is mild it may lead to deafness, choreoathetosis and spasticity, kernicterus.
3.Prevention and Treatment for Erythroblstosis Fetalis
1.If mother is found to be Rh negative and the fetus is Rh positive, anti D should be administered to the mother at 28th and 34th weeks of gestations as prophylactic
measure. If the mother with rh negative blood delivers Rh positive baby, then anti D should be administered to the mother within 48 hours of delivery.
2.If the baby is born with erythroblastosis fetalis, the treatment is given by means of exchange transfusion. Rh negative blood is transfused into the infant replacing the infant’s own
Rh positive blood
3.Premarital counseling .4.Proper matching of blood particularly in women before childbearing. .5.Blood grouping must for every woman, before 1st pregnancy.
38

Mechanism in previously non sensitized mother
Rh Negative Women married with Rh positive Man
↓
Rh negative mother become pregnant
↓
Rh negative mother carries Rh positive Fetus
↓
Mother is Non sensitized (no previous exposure to Rh antigen)
↓
Fetus unaffected ( 1st Baby usually escapes.)
↓
Rh+ve R.B.C.s enter Maternal circulation during delivery of 1st baby
↓
Mother gets sensitised (exposure to Rh antigen)
↓
antibody (IgG) produced by mother
↓
antibody (IgG) crosses placenta during 2nd pregnancy
↓
Enter Fetus
↓
Haemolysis of rh +ve RBC’s in fetus
↓
Decreased RBC Increased bilirubin Cardiac failure due to
hypoxia of heart
Increased erythropoitin secretion due to hypoxia of kidney
caused increased erythropoisis
More Erythoblast in fetus blood(erythroblasto fetalis)
Oedema(hydrops fetalis)
Hemolytic jaundice(kernicterus
when bilirubin deposit in basal
ganglia)
Hemolytic anemia
39

Rh Negative Women married with Rh positive Man
↓
Rh negative mother become pregnant
↓
Rh negative mother carries Rh positive Fetus
↓
Mother is previously sensitized (previous exposure to Rh antigen during abortion,version,amniocentesis or chorionic villi
biopsy,previous delivery)
↓
antibody (IgG) produced by mother during previous sensitization circulates in mother blood
↓
antibody (IgG) crosses placenta
↓
Enter Fetus
↓
Haemolysis of rh +ve RBC’s in fetus
↓
Decreased RBC Increased bilirubin Cardiac failure due to
hypoxia of heart
Increased erythropoitin secretion due to hypoxia of
kidney caused increased erythropoisis
More Erythoblast in fetus blood(erythroblasto fetalis)
Oedema(hydrops fetalis)
Hemolytic jaundice(kernicterus
when bilirubin deposit in basal
ganglia)
Hemolytic anemia
Mechanism in previously sensitized mother
40

41

BLOOD TRANSFUSION
I. Indication
Hemorrhage
Trauma
Burns
Anemia
II. Precautions
1. Precautions to be taken before the transfusion of blood
- Donor must be healthy without any diseases like
- Only compatible blood must be transfused
- Both matching and cross matching of recipient blood
and donor blood must be done
- Rh compatibility must be confirmed.
2. Precautions to be taken while transfusing blood
- Apparatus for transfusion must be sterile
- The temperature of blood to be transfused must be same as body
temperature
- The transfusion of blood must be slow. The sudden rapid infusion
of blood into the body increases the load on the heart resulting in
many complications.
III. Transfusion reactions
1.Transfusion Reactions due to ABO Incompatibility
a.mechanism
 Mismatched blood is transfused to a person, tranfusion reactions occur. If the donor’s plasma contains antibody against red blood cell,
agglutination does not occur. Because, these antibodies are diluted in recipient’s blood.
 But, if recipient’s plasma contains antibodies against donor’s red blood cells, the donor red blood cells are agglutinated and destroyed. More
amount of free hemoglobin is liberated.
b.Clinical features
- Jaundice
destroyed rbc releases hemoglobin so increased level of bilirubin
level in the blood
- Cardiac Shock
Increases the viscosity of blood. Increases the work load on the heart leading to heart failure. The toxic substances released from hemolyzed
cells also reduce the arterial blood pressure and develop circulatory shock.
- Renal Shut Down
Toxic substances from hemolyzed cells cause constriction of blood vessels in kidney. The toxic substances along with free hemoglobin
are filtered through glomerular membrane and enter the renal tubules. Because of poor rate of reabsorption from renal tubules, all
these substances precipitate and obstruct the renal tubule. This suddenly stops the formation of urine and the condition is called renal
shut down.
2. Transfusion Reactions due to Rh incompatability
42

RETICULOENDOTHELIAL SYSTEM
I. Definition
• Play an important role in the defense mechanism of the body.
II. Distribution
• The endothelial lining of vascular and lymph channels and
• Connective tissue and some organs like spleen, liver, lungs,
lymph nodes, bone marrow.
III. Classification of reticuloendothelial cells
a. Fixed reticuloendothelial cells (tissue macrophages)
1. Connective Tissue
• Omentum and mesentery
2. Endothelium of Blood Sinusoid
• The endothelium of the blood sinusoid in bone marrow, liver, spleen,
lymph nodes, adrenal glands and pituitary glands.
Kupffer’s cells present in liver.
3. Reticulum
• The reticulum of spleen, lymph node, and bone marrow contain fixed
reticuloendothelial cells.
4. Central Nervous system
• Meningiocytes of meninges, microglia from the tissue.
5. Lungs
• Alveolar macrophage of lungs.
6. Subcutaneous Tissue
b.Circulaing reticuloendothelial cells(wandering macrophages)
1. monocyte
43

IMMUNITY
Bone marrow
↓
Red bone marrow
↓
↓
lymphoid stem cells
↓
colony forming unit
↓
lymphoblast
↓
pro lymphocyte
↓
lymphocyte
thymus liver & bone marrow
T lymphocyte B Lymphocyte
cell mediated immunity plasma cells
antibody(ig)
humeral immunity(antibody mediated)
Resistance of the body against the pathogenic agents is known as immunity.
A.DEFINITION
B.DEVELOPMENT OF IMMUNITY
44

IMMUNITY
ACQUIRED(ADAPTIVE)
INNATE(NATIVE) IMMUNITY
NON SPECIFIC SPECIFIC PASSIVE
ACTIVE
SPECIES
RACIAL
INDIVIDUAL
ARTIFICIAL-
vaccine
NATURAL-
infection
SPECIES
RACIAL
INDIVIDUAL
ARTIFICIA-
antiserum
NATURAL-
Breast milk
Present from birth and it is the inborn capacity of the body to resist
the entry of microorganisms into the body
The resistance that an individual acquires during life
C.TYPES

CELL MEDIATED IMMUNITY
I. Introduction
The cell mediated immunity is carried by the T lymphocytes. It develops when an antigen or the antigenic material from the invading microbial or nonmicrobial
cells is exposed to the T lymphocytes.
II. Antigen presenting cells
1. Macrophages
Large phagocytic cells, which digest the invading organisms to release the antigen. The macrophages are present along with lymphocytes in almost all the
lymphoid tissues.
2. Dendritic Cells (Nonphagocytic in nature)
Dendritic cells in spleen, which trap the antigen in blood
Follicular dendritic cells in lymph nodes which trap the antigen in the lymph and
Langerhans’ dendritic cells in skin, which trap the organisms coming in contact with body surface.
III. Function of immune cells in CMI
1.Role of Antigen Presenting Cells
When foreign organisms invade the body, the macrophages or other antigen presenting cells kill them mostly by means of phagocytosis. Later, the antigen from
the organisms is digested into polypeptides. The polypeptide products are presented to T lymphocytes along with human leukocyte antigens.
The antigenic products activate the helper T cells and B lymphocytes.
2.Role of helper T cells
Helper T cells stimulate the other T cells and the B cells.
3.Role of cytotoxic T cells
Cytotoxic T cells circulate though blood, lymph and lympahtic tissues and destory the invading organism by attacking them directly.
The cytotic T cells also destroy cancer cells, transplanted cells.
4.Role of suppressor T cells
The suppressor T cells are called regulatory T cells. These T cells suppress the activities of the killer T cells. The suppressor T cells play an important role in
preventing destroying the body’s own tissues along with invaded organisms. The suppressor cells suppress the activities of helper T cell also.
5.Role of memory T cells
Some of the T cells activated by an antigen remain in lymphoid tissue instead of entering circulation. These T cells are called memory T cells.
In later periods, the memory cells migrate to various lymphoid tissues throughout the body. When the body is exposed to the same organism for
the second time, the memory cells identify the organism and immediately activate the other T cells.
46

HUMORAL IMMUNITY
1. Introduction
Humoral immunity is developed by the antibodies, which are circulating in the blood. The antibodies are the gamma globulins produced by B lymphocytes. These
antibodies fight against the invading organisms.
2.Role of cells in humeral immunity
a.Role of antigen presenting cells
When foreign bodies or organisms invade, macrophages and other antigen presenting cells destroy them mostly by phagocytosis. Then, the antigen from the
organisms is digested into polypeptides. The polypeptide products are presented to B lymphocytes along with human leukocyte.
Now, the antigenic products activate the B lymphocytes and also the helper T cells. The macrophages also secrete some substance called interleukin1. this causes
b.Role of plasma cells
B lymphocytes are proliferated and transformed into two types of cells namely, plasma cells, memory cells. Plasma cells produce the antibodies, which are globulin in
nature. The antibodies are called immunoglobulins.
c.Role of memory B cells
Some of the B lymphocytes activated by the antigen are transformed into memory B cells. The memory cells are in inactive condition until the body is exposed to the
same organism for the second time.
During the second exposure, the memory cells are stimulated by the antigen and produce more quantity of antibodies at a faster rate, than in the first exposure. The
antibodies produced during the second exposure to the foreign antigen are also more potent than those produced during first exposure.
d.Role of helper T cells
Activated helper T cells secrete two substances called interleukin 2 and B cell growth factor.
Activation of more number of B lymphocytes
Proliferation of plasma cells and
Production of antibodies
e.Role Of Antibodies
Antibodies or immunoglobulins (Ig) are produced by plasma cells in response to the presence of antigens.
activation and proliferation of lymphocytes.
47

CELL MEDIATED IMMUNITY ANTIBODY MEDIATED(HUMERAL) IMMUNITY
MECHANISMIMMUNITY
48

Bone marrow
↓
Red bone marrow
↓
↓
lymphoid stem cells
↓
colony forming unit
↓
lymphoblast
↓
pro lymphocyte
↓
lymphocyte
↓
liver & bone marrow
↓
B Lymphocyte
↓
plasma cells
↓
antibody(ig)
INTRODUCTION:
IMMUNOGLOBULINS
FORMATION:
TYPES:
IgG
IgM
IgA
IgE
IgD
Antibodies or immunoglobulins (Ig) are produced by plasma cells in response to the presence of antigens.
49

HEAVY & LIGHT CHAIN:
STRUCTURES:
FUNCTIONS:
Class Heavy chain Light chain
Igg Gamma Kappa & lamda
Igm Miu Kappa & lamda
Iga Alpha Kappa & lamda
Ige Epsilon Kappa & lamda
Igd Delta Kappa & lamda
50

Characteristics IgG IgA IgM IgD IgE
Structure Monomer Pentamer Dimer Monomer Monomer
Percentage of total serum 80% 5-10% 10-15% 0.2% 0.002%
Location Blood, lymph intestine Blood, lymph, B cell
surface
Secretions B cell surface, blood, lymph Bound to mast and basophil
cell
Sedimentation coefficient 7 7 19 7 8
Molecular weight (kDa) 150 160 900 180 190
Carbohydrate (%) 3 8 12 13 12
Serum concentration
(mg/ml)
12 2 1.2 0.03 0.00004
Half-life (days) 23 6-8 5 2-3 1-5
Heavy chain γ1, γ2, γ3, γ4 α1, α2 µ Δ Ε
Light chain ᴋor δ ᴋor δ ᴋor δ ᴋor δ ᴋor δ
Complement binding Classical pathway Alternate pathway Classical pathway None None
Placental transport + - - - -
Present in milk + + - - -
Seromucous secretion - + - - -
Heat stability (560 C) + + + + -
Binding to tissue Heterologous None None None Homologous
51
COMPARISON OF VARIOUS PROPERTIES OF IMMUNOGLOBULINS

BODY FLUIDS
I. Composition of body fluids
Water and solids. Solids are organic and inorganic substances.
1. Organic substances
2. Inorganic substances
Sodium, potassium, calcium, magnesium, chloride, bicarbonate, phosphate and sulfate.
II. Measurement of volume of body fluids
Indicator dilution method
a. Principle
A known quantity of a substance such as a dye is administered into a specific body fluid compartment. These substances are called the marker substances or indicators.
After administration into the fluid, the substance is allowed to mix thoroughly with the fluid compartment. Then, a sample of fluid is drawn and the concentration of
the marker substance is determined. The substances whose concentration can be determined by using colorimeter or radioactive substances are generally used as
marker substances.
b. Formula to measure the volume of fluid by indicator dilution method
The quantity of fluid in the compartment is measured by using the formula.
V = the volume of fluid in the compartment
M = mass or total quantity of marker substance injected
C = concentration of the marker substance in the sample of fluid
c. Correction factor : some amount of marker substance is lost through urine during distribution. So, the formula is corrected as follows
d. Uses of indicator dilution method : Used to measure extracellular fluid volume, plasma volume and the volume of total body water.
Amount of substance injected – Amount of substance excreted
Volume = Concentration of substance in sample of fluid
M
V = C
Marker substances
I. Characteristics of marker substances : The dye or any substance used as a marker substance should have the following qualities :
1. It must be nontoxic
2. It must mix with the fluid compartment within reasonable time.
3. It should not be excreted rapidly
4. It should be excreted from the body completely within reasonable time.
5. It should not change the colour of the body fluid.
II. Marker substances used to measure total body water
1. Deuterium oxide
2. Tritium oxide
3. Antipyrine
III. Marker substances used to measure extracellular fluid
1. Radioactive sodium, chloride, bromide, sulfate and thiosulfate.
2. Nonmetabolizable saccharides like inulin, mannitol, raffinose and sucrose.
IV. Marker substances used to measure plasma volume
1. Radioactive iodine
2. Evan’s blue
6. It should not alter the volume of body fluid.
52

PLASMA PROTEINS
I. INTRODUCTION
Proteins in the plasma are
a. Serum albumin
b. Serum globulin and
c. Fibrinogen
II. NORMAL VALUES
Total proteins (7.3 gm% (6.4 to 8.3 gm%))
serum albumin (4.7 gm%)
Serum globulin (2.3 gm%)
Fibrinogen (0.3 gm%)
III. SEPARATION OF PLASMA PROTEINS
a. Precipitation Method - Protein in the serum are separated into albumin and globulin. This is done by precipitating globulin with 22% sodium sulfate
solution. The albumin remains in solution.
b. Salting out Method :Serum globulin is separated into two fractions called euglobulin and pseudoglobulin by salting out with different solutions.
Euglobulin is salted out by full saturation with sodium chloride solution; half saturation with magnesium sulfate solution; and one third saturation with
ammonium sulfate solution. It is insoluble in water. Pseudoglobulin is salted out by full saturation with magnesium sulfate; half saturation with
ammonium sulfate. It is soluble in water but it cannot be salted out by sodium chloride solution.
c. Electrophoretic Method
d. Cochn’s Fractional Precipitation Method
e. Ultra Centrifugation Method
f. immunoelectrophoretic Method
IV. PROPERTIES OF PLASMA PROTEINS
a. Molecular Weight
Albumin (69,000)
Globulin (1,56,000)
Fibranogen (4,00,000)
b. Oncotic Pressure
The plasma proteins are responsible for the oncotic or osmotic pressure in the blood.
c. Specific Gravity
1.026.
d. Buffer Action
Acceptance of hydrogen ions is called buffer action.
V. ORIGIN OF PLASMA PROTEINS
1. In Embryo
Synthesized by the mesenchyme cells. Albumin is synthesized first and other proteins are synthesized later
2. In Adults
Synthesized mostly from reticuloendothelial cells of liver. Also synthesized from spleen, bone marrow
53

VI.FUNCTION OF PLASMA PROTEINS
a. Role in Coagulation of Blood
Fibrinogen is essential for the coagulation of blood
b. Role in Defense Mechanism of Body
The gamma globulins play an important role antibodies (immunglobin).
The antibodies react with antigens of various microorganisms,
c. Role in Transport Mechanism
Albumin, alpha globulin and beta globulin are responsible for the
transport of the hormones enzymes and respiratory gases, particularly
dioxide. The alpha and beta globulins play in important role in the
transport of metals in the blood.
d. Role in Maintenance of Oncotic Pressure in Blood
Because of their large size, the plasma protein cannot pass through the
capillary membrane easily and remain int eh blood. In the blood these
proteins exert the colloidal oncotic pressure
e. Role in Regulation of Acid Base Balance
Plasma proteins, particularly the albumin, regulating the acid base
balance by their buffering action.
f. Role in Erythrocyte Sedimentation Rate (ESR)
Globulin and fibrinogen of the plasma accelerate the tendency of
rouleaux formation by the red blood cells. Rouleaux formation is
responsible for ESR.
g. Role in Suspension Stability or Red Blood Cells
During circulation, the red blood cells remain suspended uniformly in
the blood. This property of the red blood cells is called the suspension
stability. Globulin and fibrinogen help in the suspension stability of the
red blood cells.
h. Role in Production of Trephone Substances
Trephone substances are necessary for nourishment of tissue cells in
culture. These substances are produced by leukocytes from the plasma
proteins.
i. Role as Reserve Proteins
During fasting, inadequate food intake plasma proteins are utilized by
the body tissues.
j. Role in viscosity of blood
It provide viscosity to the blood to maintain the blood pressure.
54

VII. PLASMAPHERESIS
a. Definition
• plasmapheresis is an experimental procedure in animals to demonstrate the importance of plasma proteins.
b. Procedure
• Demonstrated in dog
• blood is removed completely from the body of the dog.
• Red blood cells of the blood are separated from plasma and are washed in saline and re-infused into the body of the same dog along with a
physiological solution called Locke’s solution.
• Due to sudden lack of proteins, the animal undergoes a state of shock.
• If the animal is fed with diet containing sufficiently high quantity of proteins, the normal level of plasma proteins is restored within seven days
and the animal survives.
• The new plasma proteins are synthesized by the liver of the dog.
• If the experiment is done in animals after removal of liver and if the diet does not contain adequate quantity of proteins, the state of shock
leads to death.
c. Significance
• To demonstrate the importance of plasma proteins for survival of the life.
• To demonstrate the synthesis of plasma proteins by the liver.
VIII. VARIATIONS IN PLASMA PROTEIN LEVEL
a. Decrease in All Fractions of Proteins (Hypoproteinemia)
 Hemorrhage
 Extensive burns
 Pregnancy
 Malnutrition
 Prolonged starvation
 Cirrhosis of liver and
 Chronic infections like chronic hepatitis or chronic nephritis.
b. Increase in all Fractions (Hyperproteinemia)
 Dehydration and
 Acute infections like acute hepatitis or acute nephritis.
55

4.GASTRO
INTESTINAL SYSTEM
56

SALIVA
A.PROPERTIES OF SALIVA
1.Volume: 1000 to 1500 ml/day
70% - submaxillary glands
25% - parotid glands
05% - sublingual glands
2.Reaction: Acidic with pH of 6.35 to 6.85.
3.Specific gravity: 1.002 & 1.012.
4.Tonicity: Hypotonic to plasma.
B.COMPOSITION OF SALIVA
1.Water 99.5%
2.Solids 0.5% (a.organic ,b. inorganic and c.gases)
a.Organic Substances:
• Salivary proteins – mucin and
albumin
• Salivary enzymes – amylase,
maltase, lingual lipase,
lysozyme, phosphatase
carbonic anhydrase
• Kallikrein,
• Blood group components –
antigens
• Free amino acids
• Nonprotein nitrogenous
substances like urea, uric acid,
creatinine, xanthine and
hypoxanthine.
b.Inorganic Substances:
• Sodium Bromide
• Calcium Chloride
• Potassium Fluoride
• Bicarbonate
Phosphate
c.Gases:
• Oxygen
• Carbon
dioxide
• Nitrogen
• Phosphat
e
GASTRO INTESTINAL SYSTEM
57

C. FUNCTIONS OF SALIVA
1.Preparation of Food for Swallowing
- Saliva moistens and dissolves food.
- Saliva lubricates the bolus and facilitates the swallowing.
2.Appreciation of Taste
- The dissolved food substances by saliva can stimulate the taste buds.
3.Digestive Function
- Salivary amylase converts cooked or boiled starch into maltose.
- Lingual Lipase
- converts triglycerides into fatty acids.
4.Cleansing and protective Function
- Mouth and teeth kept free from food debris by constant secretion of saliva so
prevents growth of bacteria
- Lysozyme of saliva kills bacteria
5.Role in Speech
- Helps in speech by moistening parts of mouth .
6.Excretory Function
- Organic and inorganic substances are excreted.
- It excretes some viruses (rabies and mumps).
7.Regulation of Body Temperature
- In dogs and cattle, excessive dripping of saliva during panting helps in loss of
heat.
8.Regulation of water balance
- reduced body water content  ↓ salivary secretion  dryness of the mouth 
thirst  water is taken  restores the body water content.
58

REGULATION OF SALIVARY SECRETION
REGULATION OF SALIVARY SECRETION IN
SUBMANDIBULAR AND SUBLINGUAL GLAND
REGULATION OF SALIVARY SECRETION IN PAROTID
GLAND
Conditioned reflex
UnConditioned reflex
Conditioned reflex
E.REGULATION OF SALIVARY SECRETION
D.NERVE SUPPLY TO SALIVARY GLANDS
Submandibular & Sublingual Gland Parotid Gland
a. Sympathetic T1 &T2 (Superior cervical ganglion) T1 &T2 (Superior cervical ganglion)
b. Parasympathetic Facial. N (VII) Glosso phargngeal. N (IX)
c.
c. Sensory Mandibular division (V) Mandibular division (V)
59

Chordae tympani branch through lingual nerve
Superior salivatory nucleus
facial nerve(parasympathetic fibres)
Relay in Submandibular ganglion
Stimulation of Submandibular gland
Secretion of saliva
1.CONDITIONED REFLEX
sight
Appetite center in amygdala and hypothalamus.
Olfactory nerve Optic nerve Vestibulocochlear nerve
Cerebral cortex and hypothalamus
smell hearing
Olfactory receptors Rods & cones Inner & outer hair cells
AFFERENT
EFFERENT
STIMULUS
RECEPTOR
CENTER
ACTION
thought of food
A.REGULATION OF SALIVARY SECRETION IN SUBMANDIBULAR AND SUBLINGUAL GLAND
60

2.UNCONDITIONED REFLEX
Chordae tympani branch through lingual nerve
facial nerve(parasympathetic fibres)
Relay in Submandibular ganglion
Stimulation of Submandibular gland
Secretion of saliva
Food is placed in the mouth
Stimulate Taste buds(taste receptor) in the tongue
Vagus nerve
Anterior 2/3 of the tongue posterior 1/3 of the tongue posterior most of the tongue
Chordae tympani branch of facial nerve Glossopharyngeal nerve
Nucleus of tractus salitorius in the brain stem
Taste area in the cerebral cortex
Superior salivatory nucleus
AFFERENT
EFFERENT
STIMULUS
RECEPTOR
CENTER
ACTION
61
VᾹGAI
(வாகை)
INSTITUTE
OF
MEDICAL
SCIENCES
NO.27,
1
ST
CROSS,
1
ST
MAIN
ROAD,
MOOGAMBIGAI
NAGAR,
NAINARMANDAPAM,
PUDUCHERRY
–
605
004.
Phone
number
:
09566999802
,9787100885,
email
id
:
vimspondy
@gmail.com,
website
:
www.vimspondy.com

Tympanic branch (jacobson nerve)
sight
inferior salivatory nucleus
Glossopharyngeal nerve(parasympathetic fibres)
Tympanic plexus
Lesser petrosal nerve
Relay in otic ganglion
smell hearing thought of food
Auriculotemporal nerve
Stimulation of parotid gland
Secretion of saliva
AFFERENT
EFFERENT
STIMULUS
RECEPTOR
CENTER
ACTION
B.REGULATION OF SALIVARY SECRETION IN PAROTID GLAND
62
VᾹGAI
(வாகை)
INSTITUTE
OF
MEDICAL
SCIENCES
NO.27,
1
ST
CROSS,
1
ST
MAIN
ROAD,
MOOGAMBIGAI
NAGAR,
NAINARMANDAPAM,
PUDUCHERRY
–
605
004.
Phone
number
:
09566999802
,9787100885,
email
id
:
vimspondy
@gmail.com,
website
:
www.vimspondy.com

Vagus nerve
AFFERENT
EFFERENT
STIMULUS
RECEPTOR
CENTER
ACTION
Tympanic branch (jacobson nerve)
inferior salivatory nucleus
Glossopharyngeal nerve(parasympathetic fibres)
Tympanic plexus
Lesser petrosal nerve
Relay in otic ganglion
Auriculotemporal nerve
Stimulation of parotid gland
Secretion of saliva
63
VᾹGAI
(வாகை)
INSTITUTE
OF
MEDICAL
SCIENCES
NO.27,
1
ST
CROSS,
1
ST
MAIN
ROAD,
MOOGAMBIGAI
NAGAR,
NAINARMANDAPAM,
PUDUCHERRY
–
605
004.
Phone
number
:
09566999802
,9787100885,
email
id
:
vimspondy
@gmail.com,
website
:
www.vimspondy.com

STRUCTURE AND FUNCTIONS OF GASTRIC
GLANDS
• .
Fundic glands Pyloric glands Cardiac Glands
Situation Body and fundus
of stomach.
Pyloric part of the
stomach
Cardiac region
of the stomach.
Shape Long and tubular
glands ,Has body, neck
and isthmus
Short and
tortuous.
Short and
tortuous.
Secretion a.Chief cells
Secrete
pepsinogen
b.Parietal cells
or
oxyntic cells
Secrete
Hydrochloric
acid,
intrinsic factor of
castle.
c.Mucus neck
cell secrete
mucin
Columnar
epithelial cells -
secrete mucin
G cells -
secrete gastrin.
secrete more
mucus &
pepsinogen.
64

FUNCTIONS OF STOMACH
1.Storage function
-The food is stored in the stomach for a long period.
-The slow emptying of stomach provides enough time for the intestine for proper
digestion and absorption of food substances.
2.Mechanical function
-Peristaltic movements of stomach mix the bolus with gastric juice and convert in
into the semisolid material known as chyme.
3.Digestive function
-Gastric juice secreted by the glands of the stomach contains mostly the enzymes
acting on proteins.
4.Protective function
-The hydrochloric acid present in the gastric juice destroys many types of bacteria
entering the body along with food.
5.Hemopoietic function
-Intrinsic factor of castle, present in gastric juice is necessary for the absorption of
vitamin B12, which is called extrinsic factor.
6.Excretory function
-Toxins, alkaloids and metals are excreted through gastric juice.
65

GASTRIC JUICE
A.PROPERTIES OF SALIVA
Volume : 1200 to 1500ml/day
Reaction : highly acidic with pH of 0.9 to 1.2.
Specific gravity : 1.002 to 1.004
B.COMPOSITION OF SALIVA
1.Water 99.5%
2.Solids 0.5% (a.organic ,b. inorganic and )
a.Organic Substances:
i.Gastric Enzymes
Pepsin : Protein splitting enzyme
in the gastric juice.
Rennin : Is a milk curdling
enzyme.
Gastric lipase : Lipid splitting
enzyme
Other gastric
enzymes : gelatinase, urase.
ii.Gastric Mucus
iii.Intrinsic Factor
b.Inorganic Substances:
• Hydrochloric acid
• Sodium
• Calcium
• PotassiumChloride
• Bicarbonate
• Phosphate
• Sulfate.
66

C.FUNCTIONS OF GASTRIC JUICE
1.Digestive function Through enzymes
Pepsin – Major proteolytic enzyme secreted as inactive epsinogen, formed in
zymogen granules of chief cells.
– It digest protein into proteoses, peptones & polypeptides.
– curdling & digestion milk.
Rennin – milk curdling enzyme.
Gastric Lipase
1.Gelatinase : acts on gelatin
2.Urase : acts on urea and produces ammonia.
2.Hemopoietic function Through Intrinsic factor
Intrinsic factor necessary for absorption of the extrinsic factor (Vitamin B12) from
gastrointestinal tract into the blood. Absence of intrinsic factor in gastric juice causes
deficiency of vitamin B12 leads to pernicious anemia.
3.Protective function Through Mucus
The mucus membrane of the stomach is lined by a thick coat of mucus. The mucus
lubricates the gastric mucosa and protects it from irritation or mechanical injury.
It prevents the digestive action of pepsin on the wall of the stomach particularly gastric
mucosa.Mucus protects the gastric mucosa from hydrochloric acid of gastric juice.
4.Function of Hydrochloric Acid
It activates pepsinogen into pepsin
Bacteriolytic action.
Acidity of the chyme causes release of hormones – secretin and cholecystokinin.
Provides acid medium for the action of enzymes.
67

MECHANISM OF SECRETION OF GASTRIC JUICE
1.SECRETION OF HYDROCHLORIC ACID
• In the parietal cells, carbon dioxide combines with water to form carbonic acid.
• The carbonic acid is formed in the presence of the enzyme carbonic anhydrase.
Co2 + H2O H2Co3
• Carbonic acid is the most unstable compound, immediately it splits into hydrogen ion and bicarbonate ion.
H2Co3  H +HCo3
• The hydrogen ion is actively pumped into the canaliculus of parietal cell.
• Simultaneously the chloride ion is also pumped into canaliculus actively.
• Chloride is derived from sodium chloride in the blood.
• Now the hydrogen ion combines with chloride ion to from hydrochloric acid.
H + Cl  Hcl
• To compensate the loss of chloride ion, the bicarbonate ion from parietal cell enters the blood and combines with
sodium to form sodium bicarbonate.
HCO3 + Na  Na HCo3
Factors Regulating the Secretion of Hydrochloric Acid
• Gastrin : Stimulates acid secretion
• Histamine : Stimulates acid secretion
• Enterogastrone : Inhibits acid secretion
• Vagal stimulation : Increases acid secretion
2.SECRETION OF PEPSINOGEN
• Pepsinogen are secreted from the zymogen granules of chief cell
68

Control ; Nervous control.
Time ; Secretion of gastric juice starts even before food enters the
stomach.
Secretion ; Pepsinogen and hydrochloric acid are secreted.
Mechanism Procedure ;
Unconditioned Reflex ; This causes gastric secretion when food is placed in the mouth. Afferent impulses arise from
taste buds and other receptors in the mouth and reach the appetite center in amygdala and hypothalamus. From
here, the efferent impulses pass through dorsal nucleus of vagus and vagal fibers to the wall of the stomach.
Conditioned Reflex ; In this, the sight, smell, hearing or thought of food causes gastric secretion.
Experimental Evidence ; pavlov’s pouch, Sham feeding
REGULATION OF GASTRIC SECRETION
CEPHALIC PHASE
(NEURONAL)
GASTRIC PHASE
(NEURONAL &
HORMONAL)
INTESTINAL PHASE
(HORMONAL)
Conditioned reflex
A.CEPHALIC PHASE
69
VᾹGAI
(வாகை)
INSTITUTE
OF
MEDICAL
SCIENCES
NO.27,
1
ST
CROSS,
1
ST
MAIN
ROAD,
MOOGAMBIGAI
NAGAR,
NAINARMANDAPAM,
PUDUCHERRY
–
605
004.
Phone
number
:
09566999802
,9787100885,
email
id
:
vimspondy
@gmail.com,
website
:
www.vimspondy.com

Reach the Wall of the stomach.
Dorsal nucleus of vagus in the brain stem
Vagus nerve
Gives gastric glandular branch (Nerve of laterjet)
Stimulation of gastric gland
Secretion of gastric juice
EFFERENT
CENTER
ACTION
sight
smell hearing thought of food
AFFERENT
STIMULUS
RECEPTOR
REGULATION GASTRIC JUICE SECRETION
A.CEPHALIC PHASE(NEURONAL)
70
VᾹGAI
(வாகை)
INSTITUTE
OF
MEDICAL
SCIENCES
NO.27,
1
ST
CROSS,
1
ST
MAIN
ROAD,
MOOGAMBIGAI
NAGAR,
NAINARMANDAPAM,
PUDUCHERRY
–
605
004.
Phone
number
:
09566999802
,9787100885,
email
id
:
vimspondy
@gmail.com,
website
:
www.vimspondy.com

Reach the Wall of the stomach.
Dorsal nucleus of vagus in the brain stem
Vagus nerve
Gives gastric glandular branch (Nerve of laterjet)
Stimulation of gastric gland
Vagus nerve
AFFERENT
EFFERENT
STIMULUS
RECEPTOR
CENTER
ACTION
71
VᾹGAI
(வாகை)
INSTITUTE
OF
MEDICAL
SCIENCES
NO.27,
1
ST
CROSS,
1
ST
MAIN
ROAD,
MOOGAMBIGAI
NAGAR,
NAINARMANDAPAM,
PUDUCHERRY
–
605
004.
Phone
number
:
09566999802
,9787100885,
email
id
:
vimspondy
@gmail.com,
website
:
www.vimspondy.com

Control; Nervous and hormonal control.
Time ; Secretion of gastric juice when the food enters the stomach,
Secretion ;pepsinogen and hydrochloric acid
Mechanism;
Local myenteric reflex – nervous mechanism
When food enters the stomach, the food particles stimulate the nerve plexus in the wall of the
stomach. These nerves, in turn activate the glands of the stomach, and a large quantity of gastric.
Vagovagal reflex – nervous mechanism,
Presence of food in stomach stimulates the sensory nerve endings. Sensory impulses pass to the
brainstem via sensory fibers of vagus. The efferent impulses pass through the motor fibers of vagus
back to stomach and cause secretion.
Gastrin – hormonal mechanism
The neurotransmitter called gastrin releasing peptide is released at vagal nerve ending. This acts on
the G cells and causes release of the hormone.
Action of Gastrin
It stimulates the secretion of pepsinogen and hydrochloric acid by the gastric glands.
It increases the motility of stomach.
It promotes growth of gastric mucosa
It causes secretion of pancreatic juice, which is rich in enzymes.
It also stimulates the production of hormones by pancrease.
Experimental Evidence ; Palov’s , Heidenhain’s , Bickel’s ,farrel and ivy pouch
B. GASTRIC PHASE
72

B.GASTRIC PHASE(NEURONAL & HORMONAL)
NEURONAL MECHANISM HORMONAL MECHANISM
Local myenteric reflex Vagovagal reflex
food enters the stomach
Activation of local nerve
plexus in the wall of the
stomach
activate the glands of the
stomach
large quantity of gastric juice
secretion
Activation of sensory nerve
endings(receptors).
Sensory impulses enter
brainstem
Impuse passes via motor fibers
of vagus(efferent)
release of gastrin
releasing peptide
acts on the G cells
release of the gastrin hormone
Sensory impulses passes via
sensory fibers of vagus(afferent)
Stimulation of dorsal nucleus of
vagus(center)
Stimulation of gastric glands
Glandular branch
Stimulates vagal nerve
ending in the stomach
wall
Stimulates gastric glands
(hydrochloric acid)
Distention of the stomach
food enters the stomach
Distention of the stomach
Stimulation of the stretch
receptors
Food enters the stomach
Enter blood stream
Reach stomach
Food gets mixed up with the
gastric juice produced by
cephalic phase
Proteose and peptones
produced from the
Digested proteins
73

Control ; Hormonal Control
Time ; When chyme enters the intestine,
Secretion ; Gastrin
mechanism;
When chyme enters the intestine, immediately the gastrin is secreted by intestinal mucosa. This hormone is transported to stomach
by blood. Now, gastrin acts on glands of the stomach anc causes the secretion of the gastric juice.
Inhibition of Gastric Secretion
When chyme enters the intestine, after the initial increase in secretion of gastric juice, there is complete stoppage of secretion of
gastric juice. This is due to enterogastrone and some other hormonal substances like gastric inhibitory peptide and vasoactive
intestinal polypeptide secreted in small in testine.
Enterogastrone: Secreted in the mucosa of duodenum, inhibits gastric secretion &gastric motility.
Gastric Inhibitory Peptide (GIP): This is secreted in deodenum and in jejunum. Inhibits the secretion of gastric juice and the motility of stomach.
Vasoactive Intestinal Polypeptide (VIP): Secreted in intestine. This causes inhibition of secretion of hydrochloric acid in gastric juice.
Secretin, cholecystokinin and somatostain secreted from intestine are also responsible for inhibition of gastric secretion.
Experimental
Evidence ; Bickel’s pouch, Ivy pouch farrel and ivy pouch
C.INTESTINAL PHASE
74

C.INTESTINAL PHASE(HORMONAL)
Mechanism for initial increase in
secretion of gastric juice
Mechanism for complete stoppage of
secretion of gastric juice
chyme enters the intestine With a
pH less than 2 or containing fat
digestion products (lipids) or
hyperosmolar
Secretin, gastric inhibitory polypeptide, and
cholecystokinin reach the stomach
Inhibit the gastric glands secretion
Stoppage of gastric juice secretion
No Sensory impulses enter
brainstem
No Impuse passes via motor fibers of vagus
Stimulates the
intestinal G cells
release of the
gastrin hormone
Inhibition of Sensory impulses
passes via vagus
No Stimulation of dorsal nucleus
of vagus(center)
No Stimulation of gastric glands
No Secretion of gastric juice
Stimulates gastric glands
(oxyntic cells)
(hydrochloric acid)
cholecystokinin produced by the duodenum
cholecystokinin enter the circulation
chyme enters the
intestine
Enter blood stream
Reach stomach
Hormonal inhibitory mechanism Inhibition of motor input
chyme enters the intestine With a
pH less than 2 or containing fat
digestion products (lipids) or
hyperosmolar
Local reflexes
from the
Duodenum
inhibit
gastric secretion
75

1. VAGAI - Physiology Notes.pdf

1. VAGAI - Physiology Notes.pdf

Recommandé

Recommandé

Contenu connexe

Similaire à 1. VAGAI - Physiology Notes.pdf

Similaire à 1. VAGAI - Physiology Notes.pdf (20)

Plus de MonenusKedir

Plus de MonenusKedir (20)

Dernier

Dernier (20)

1. VAGAI - Physiology Notes.pdf