CHAPTER

BLOOD
2
Q. Platelets. Oct. 2008

ANSWER:

Platelets are small colorless, nonnucleated and refractive

bodies.
Size2- 4u; Volume : 7-8 cu.u
Shape: Spherical or rod shaped.
Structure:
1. Cell membrane: 6nm thick, contains
phospholipids (accel-
erate the clotting reaction), cholesterol, glycolipids, carbo-
hydratesglycoproteins (prevent adherence to normal en-
dothelium) and proteins.
2. Microtubules: They form a ring around cytoplasm below
the cell membrane. It maintains the shape for the cell.
3. Cytoplasm: It contains various organelles and some chem-
icals.
Chemicals are of various types as
Proteins: Actin, myosin, platelet activating factor, platelet
derived growth factor, von willebrand factor.
Enzymes: ATPase
Hormones: Adrenaline, histamine
Others: Glycogen,.calcium.copper
Granules: Contain clotting factors, serotonin etc.
Normal count : 2,00,000 - 4,00,000/cumm of blood.

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 6 BLOOD
Variations in count:
(a) Physiological
-

age (|), sex(no change ), high altitude

(t), after meals(1)
(b) Pathological
Properties:
1. Adhesiveness -sticking to rough surface
2. Aggregation-grouping
3. Agglutination clumping together
Functions
1. Role in blood clotting
2. Clot retraction
3. Prevention of blood loss
4. Repair of ruptured blood vessels
5. Defence mechanism act as phagocytes
Activators of platelets
1. Collagen which is exposed during damage of blood vessels
2. Thromboxane
3. Platelet activating factor
4. Thrombin
5. ADP
6. Calcium ions
7. Cell adhesion molecule
Inhibitors of platelets:
1. Nitric oxide
2. Clotting factors 2,9,11,12
3. Prostacyclin
4. Nucleotidases
Life span 8-11
-

days
PHYSIOLOGY
 BLOOD7-
Applied physiology
1. Thrombocytopenia decrease in count in
-

typhoid,acute in-
fections, leukemia,TB etc.
2. Thrombocytosis -

increase in the count in

allergic disor-
ders, asphyxia,splenectomy etc.
3. Trombocythemia -

persistent and abnormal increase in

platelet count in carcinoma etc.
4. Glanzmann thrombasthenia- inherited hemorrhagic disor-
der.
Q. Blood group systems and their importance and
describe about A.B.O. Blood Groups and mention
the effects of mismatched blood transfusion.
May. 2008, April 2007, Nov. 2003, Dec. 2000
ANSWER:
Blood groups are determined by the presence of antigen in
RBC membrane .
Landsteiner's laws:
Ifa particular antigen is present in the RBC's correspond-
ing antibody must be absent in the seum.
Ifa particular antigen is absent in the RBC's the corre-
sponding antibody must be present in the serum.
Blood group systems:
ABO SYSTEM:
Group Antigen in Antibody in Percentage of
RBC serum people
A Anti B
A 25
B B Anti A 25

AB A and BB No antibody 5
O No antigen Anti A and Anti 45
B

PHYSIOLOGY=
 8 BLOOD
Rh System:
D is one of that antigen
Rh factor is antigen in the RBC.
The person having D antigen are called Rh positive and
those with out are called Rh negative.

Lewis Blood Group:

formed in the tissues are released in the body and
Antigens
are absorbed by the RBC's. They are also called secretory

antigens.
Others:
MNS blood groups
Bombay groups
I group

Importance of bood groups:

During blood transfusion
.Forblood donation
For couples to prevent complications
I n medicolegal cases

Transfusion reactions due in ABO incompatibility:

The severity depends on the amount of blood transfused,
general health of the patient. Symptoms are
Nonhemolytic reaction - develop in few minutes to hours
It includes fever, difficulty in breathing, itching.
Hemolytic transfusion reaction acute reactions include
chills, increased heart rate, low blood pressure, shortness
of breath, nausea, vomiting, chest pain, back ache, rigor.
Delayed reations occur in 1-5 days which include jaundice
cardiac shock, renal shut down.

PHYSIOLOGY
 BLOOD9
Q. Classify W.B.C.and the functions of W.B.C.'s in detail.
Oct. 2009, April 2004, Nov. 2003, May 1999, Nov. 1999
ANSWER
Leukocytes are classified into 2 groups:
1. Granulocytes -

with granules
(a) Neutrophils: 10-12 4, nucleus has 2-5 lobes,granules
areboth acidic and basic types.
(6) Eosinophils :have coarse granules and stain eosin,
nucleus is bilobed, 10-144.
(c)Basophils : coarse granules stain with blue, nucleus
isbilobed, 8-10
Agranulocytes with out granules
(a) Monocytes: nucleusis round, 14-18
(b) Lymphocytes: nucleus is oval - large (10-12u), small

(7-10 )
Functions
Neutrophils help in defence mechanism of the body
against the invading microorganisms.
Eosinophils fight against the parasites
Basophils play a role in healing processes.They play
a role in allergy or acute hypersensitivity reactions.
Monocy tes are phagocytic
Lymphocytes help in providing immunity.

Q. Lymphocytes. c t . 2006

ANSWER:
They are divided into 2 types:
1. TLymphocytes - concerned with cellular immunity

2. BLymphocytes- concerned with humoral immunity

PHYSIOLOGY
 10 BLOOD
T Lymphocytes:
TLymphocytes are processed in thymus. It plays an
an
important role in immunity.

Types of T Lymphocytes
During the processing T lymphocy tes are trans
formed into four types;
1. Helper T cells or inducer T'cells
2. Cytotoxic T cells or killer T cells
3. Suppressor T cells
4. Memory T cells
After the transformation,all the of T
types
leave the thymus and are stored in lymphoid tissues of
lymphocytes
lymph nodes, spleen,bone marrow and the Gl tract.
B Lymphocytes:
The processing of B lymphocytes takes place in bone
marrow and liver.
Types of B Lymphocytes
After processing, the B lymphocytes are transformed
into two types;
1. Plasma cells
2. Memory cells.
Blymphocytes are stored in the lymphoid tissues o
lymph nodes,spleen,bone marrow and the Gl ract.
Q. Stages of erythropoiesis and the
morphologico
changes and factors influencing erythropoiesis.
Add a brief note on Anaemias. Oct. 2005, May 199

ANSWER:
Erythropoiesis is the process of origin, development "and
maturation of erythrocytes.

PHYSIOLOGY
 BLOOD 11
Site
Infetal life -3 stages:
Mesoblastic stage : during first two months from
mesenchyme of yolk sac.
Hepatic stage : From third month of intrauterine life
in liver.
Myeloid stage: During last months from bone mar-
row, liver.
In new born Babies, Children and Adults:
Upto 201yrs: from bone marrow of all long bone.
After 20 yrs: from membranous bones like vertebra,
sternumribs.
Process
Hemopoietic stem cells are primitive in the bone marrow
which give rise to blood cells.
Pluripotent hemopoietic stem cells

Colony forming blastocyte

CFU E

Proerythroblast(20u,basophilic cytoplasm,large nucleus)

Early normoblast(15u,basophilic cytoplasm, no nucleoli)

Intermediate normoblast(124, both acidophilic and basophilic

cytoplasmn)
Late normoblast(8u, ink spot
nucleus,acidophilic cytoplasm)
Reticulocyte(immature RBC)
Erythrocyte(No reticular network,biconcave shape)
Duration :7 days
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1212 BLOOD
Factors necessary:
1. General factors:
(a) Erythropoietin: It is a glycoprotein produced
kidney,liver.Secreted duringhypoxia and stimulrom
the production of RBC'S.
stimulats
(b) Thyroxine: It accelerates the process
(c) Hemopoietic growth factors: Interleukins, stemocell
factors
(d) Vitamins: B,C,D,E
2. Maturation factors
(a) Vitamin B 12/Extrinsicfactor: Helps in synthesis ot
DNA in RBC'S, obtained from diet.
(b) Intrinsicfactor of castle: Produced from gastric mu
cosa, helps in absorption of extrinsic factor.
(c) Folic acid: Essential for maturation for synthesis d
DNA.
3. Factors necessary for hemoglobin formation:
(a) First class proteins and amino acids
(b) Iron
()Copper
(d) Cobalt and nickel
(e) Vitamin C,
riboflavin,pyridoxine.
ANEMIA: It is charecterised by ount
reduction in RBC Co
hemoglobin content, packed cell volume.
Classification:
1.
Morphological: Depends on color and size.
(a) Normocytic
normochromic anemia
(b) Macrocytic
normochromic anemia
(c) Macrocytic
(d) Microcytic hypochromic anemia
hypochromic anemia
PHYSIOLoGY
 BLOOD 13
2. Etiological:
(a) Hemorrhagic -due to loss of blood
(b) Hemolytic destruction of cells due to liver
failure,renal disorder, burns,infection,poisoning,hy-
persplenism etc.

(c) Nutrition deficiency due to deficiency of iron

-

(microcytic),protein,vitamins(macrocytic),folic
acid(megablastic).
(d) Aplastic disorder of reb bone marrow.
Anemia of chronic disorder noninfectious inflam-
(e)
-

chronic renal
matory disorders, chronic infections,
failure, neoplastic disorders.

Signs and symptoms of anemia:

Pale skin
Tachycardia
Increase in rate of respiration
Anorexia, nausea, vomiting, abdominal discomfort
Increase in basal metabolism

Albuminuria
Disturbed menstrual cycle
Headache,irritability
April 2005
Q. Rh factor.

ANSWER:
Rh factor is antigen in the RBC. It was
discovered by Land-
one of that
steiner and Wiener in rhesus monkey. D is
a r e called Rh posi-
antigen. The person having D antigen
called Rh negative(15%).
tive(85%) and those with out
are
natural an-
The antigen D does not have corresponding
to Rh negative
tibody.IfRh positive blood is transfused Rh
then anti D is formed in that person. But if the
person
blood there is no risk.
positive person receives Rh negative
- PHYSIOLOGY
 14 | BLOoD
Inheritance of Rh antigen:It is an inherited dominantfac
tor. It may be homozygous DD or heterozygous Dd.
Transfusion reactions
The Rh antibodies develop in the receipt 's blood
.The
transfused RBC'S are agglutinated and are lysed by
mac
rophages. The antibodies develop in the receipt remain in
the body for ever.
Hemolytic disease of fetus and newborn - Erythroblastosis
fetalis
It is due to Rh
incompatibility due to difference between
Rh blood group of the mother and
baby.Hemolytic disease
leads to eryhroblastosis fetalis. Complications like
1. Severe anemia
2. Hydrops fetalis edema,
-

enlargement of liver and spleen

and cardiac failure.
3. Kernicterus -

brain damage in infants caused by severe

jaundice.The blood brain barrier is not well developed and
the bilirubin causes permanent damage of brain.
Treatment:
I f the mother is Rh negative and the fetus is Rh
posi-
tive antiD should be administered to the mother
at 28th
and 34th weeks of gestation. Anti D should be adminis-
tered to the mother with in 48 hrs of
delivery.
If the baby is born with erythroblastosis fetalis the
treatment is given by exchange transfusion.
Q. Coagulation of blood and the intrinsic mechanism of
coagulation of Blood. Add a note on haemophilia.
Oct. 2007, April 2003, Nov. 1998
ANSWER:
Coagulation is the process in which blood losses its fluidity
and becomes a jelly like mass few minutes after it is
out or collected in a container.The clot is a mesh of tn"
she
fibrils entangling the blood cells.
PHYSIOLOGY.
 BLOOD 15
Intrinsic mechanism:
Stage 1

Endothelial damage + collagen exposure .

Kallikren, HMW Kinogen

XII XIla Platelets
HMW Kinogen
XI Xla Phospholipid
Calcium
IX IXa
VIII Ca
X Xa+ Thrombin Prothrombin activator
Prothrombin
Stage 2 Thrombin

Stage 3 Fibrinogen-Fibrin
Polymerisation
Loose strands of fibrin
XII Ca
Fibrin tight blood clot

Hemophilia I t is a group linked inheritance fea-

of sex
tured by prolonged clotting time.lt usually affects males
and the females are usually carriers.
Causes: Lack of formation of prothrombin activator.

Types:
1. Hemophilia A - Deficiency of factor VIII

2. Hemophilia B - Deficiency of factor IX

3. Hemophilia C - Deficiency of factor XI

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16 BLOOD
Symptoms:
Spontaneus bleeding
Prolonged bleeding in cuts, injury

Hemorrhage in GIT, US
Bleeding in joints
Blood in urine
Treatment: Replacement of the missing factor.

PHYSIOLOGY.