This PPT includes the information about blood, its components, types of blood grouping, deficiency disorder, significance, blood clotting and its mechanism and more.
Blood
• Blood (connectivetissue)
• pH alkaline (7.3-7.4).
• Blood volume:
– Males: 5-6 L
– Females: 4-5L
Blood plasma
Formed elements
• Cells
• Cell fragments
Liquid extracellular
matrix
(1)
Rashmi M G
3.
Functions of blood:
•Transportation
• Regulation
• Protection
Gases (oxygen and carbon dioxide)
Nutrients
Hormones
Heat
Wastes
pH
Body temperature
Water content of
cells
Blood loss- clotting
Disease – phagocytic activity
Rashmi M G
4.
Components of blood
Bloodplasma Formed elements
55% volume 45% volume
Straw colored RBC- red color
WBC – no color
Platelets no color
Blood- formed elements= blood plasma Blood- blood plasma= formed elements
Components:
90-92% water
8-10% solutes (approx 7% proteins-
albumin, globulin, fibrinogen)
Minerals- sodium, calcium, magnesium,
bicarbonates, chlorine
3 components:
RBC
WBC
platelets
HEPATOCYTES
PLASMA PROTEINS
ALBUMINS
GLOBULIN
FIBRINOGEN IMPORTANT CLOTTING FACTOR
Rashmi M G
5.
FORMED ELEMENTS
ERYTHROCYTES LEUKOCYTESPLATELETS
Red blood cells (RBC)
complete cell
White blood cells (WBC)
Complete cell
Thrombocytes
Cell fragments
Normal range:
Male- 5.4 millions/micro litre
of blood
Female
Female- 4.8 million/ micro
litre of blood
Normal range:
5000-10000 cells/ micro litre
of blood
Normal range:
150000-400000/ micro litre
of blood
Features:
No nucleus and membrane
bound organelles
Biconcave
Red colour - hemoglobin
Features:
Nucleus present
Colorless- No hemoglobin
Features:
No nucleus
Cytoplasm small enclosed by
piece of plasma membrane
Origin:
hemopoietic stem cells
erythrocytes
Origin:
Hemopoietic stem cells
leukocytes
Origin:
Hemopoietic stem cells
megakaryocytes
thrombocytes
Rashmi M G
6.
Types of Leukocytes(White blood cells)
GRANULOCYTES
Conspicuous chemical filled cytoplasmic granules (vesicles) present and visible after
staining
EOSINOPHILS BASOPHILS NEUTROPHILS
Features:
Nucleus- bilobed
Cytoplasmic granules- red
Features:
Nucleus- bilobed
Cytoplasmic granules-
blue
Features:
Nucleus- multilobed ,
(polymorphonuclear
leukocytes)
Cytoplasmic granules- pink
Function:
Detoxification
Function:
Synthesis of Histamine
and heparin
Function:
Phagocytic activity
Rashmi M G
7.
Types of Leukocytes(White blood cells)
•AGRANULOCYTES
AGRANULOCYTES
Conspicuous chemical filled cytoplasmic granules are may be present or absent but
invisible after staining
LYMPHOCYTES MONOCYTES
Features:
Small cells with round nucleus and little
cytoplasm
Features:
Cells with single nucleus (Kidney shaped/
horse shoe shaped)
Azurophilic granules present
B-LYMPHOCYTES T- LYMPHOCYTES NO SUCH TYPES
Produce antibodies
which binds to
antigen of foreign
particle and causes
destruction
Directly destroy
cells that have
antigens of
pathogen
Functions:
Immune response
Functions:
Phagocytic activity
Rashmi M G
8.
FUNCTIONS OF FORMEDELEMENTS
ERYTHROCYTES LEUKOCYTES THROMBOCYTES
Oxygen and carbon dioxide
transport
Defense
Detoxification
Anticoagulant synthesis
Phagocytic activity
Immune response
Clotting
Serotonin synthesis
(2)
Rashmi M G
9.
BLOOD CLOTTING
Coagulation.
Transformation of liquid blood into solid gel
“clot”
Clot consists of insoluble proteins “fibrin”;
formed elements are trapped.
Formation of fibrin threads.
Substance required for clotting are: clotting
factors
Calcium ions.
Inactive enzymes by hepatocytes.
Molecules associated with platelets/ released by
damaged tissues.
Main reaction:
SOLUBLE FIBRINOGEN INSOLUBLE FIBRIN
(3)
Rashmi M G
10.
12 Clotting factors
FACTORSOURCE DESCRIPTION
FACTOR I LIVER FIBRINOGEN
FACTOR II LIVER PROTHROMBIN
FACTOR III DAMAGED TISSUE, PLATELETS THROMBOPLASTIN
FACTOR IV DIET, BONES, PLATELETS CALCIUM IONS
FACTOR V LIVER, PLATELETS PROACCELEREIN
FACTOR VII LIVER PROCONVERTIN
FACTOR VIII LIVER ANTIHEMOPHILIC FACTOR- A
FACTOR IX LIVER ANTIHEMOPHILIC FACTOR- B
FACTOR X LIVER THROMBOKINASE
FACTOR XI LIVER ANTIHEMOPHILIC FACTOR-C
FACTOR XII LIVER ANTIHEMOPHILIC FACTOR-D
FACTOR XIII LIVER, PLATELETS FIBRINASE
Rashmi M G
11.
Clotting cascade
EXTRINSIC PATHWAYINTRINSIC PATHWAY
Shorter pathway Longer pathway
Rapid process Slow process
Activator is from cells outside the blood
vessels
Activators is in direct contact with blood/
within blood
First reaction:
Proconvertin active Proconvertin
First reaction:
Hageman factor active Hageman
factor
Rashmi M G
12.
INTRINSIC PATHWAY
Damaged surfaceof blood vessel
XII Hageman factor XII Active Hageman factor
XI AHF-C XII Active AHF-C
IX AHF-B IX Active AHF-B
VIII Active AHF-A
X Thrombokinase X Active thrombokinase
V Active Proaccelerin
II Prothrombin II Active thrombin
I Fibrinogen I Fibrin
XIII Fibrinase
Cross linked fibrin clot
Rashmi M G
13.
EXTRINIC PATHWAY
Injury
VII ProconvertinVII active Proconvertin
X Thrombokinase X Active thrombokinase
V Active Proaccelerin
II Prothrombin II Active thrombin
I Fibrinogen I Fibrin
XIII Fibrinase
Cross linked fibrin clot
Thromboplastin
Rashmi M G
14.
Anemia- Reduced Oxygencarrying capacity
of blood
Iron deficiency anemia
Inadequate absorption of iron or loss
of iron in body
Megaloblastic anemia
Inadequate intake of Vit B12, red bone
marrow produces abnormal RBCS
Pernicious anemia
Inability to produce intrinsic factor
needed for absorption of Vit B12 in
small intestine
Hemorrhagic anemia
Excessive loss of RBC through
bleeding, stomach ulcers and over
menstruation
Hemolytic anemia
Premature rupture of plasma
membrane of RBCs due to invasion of
RBC by malarial parasite or sickle cell
(defective cells)
Thalassemia
Deficient synthesis of globins,
hereditary hemolytic disease
Aplastic anemia
Destruction of red bone marrow,
failure of bone marrow to produce RBC
Rashmi M G
15.
Blood group
Type- ABLOOD GROUP RBC
ANTIGEN- A
ANTIBODY- B
Type- B BLOOD GROUP RBC
ANTIGEN- B
ANTIBODY- A
Type- AB BLOOD GROUP RBC
ANTIGEN- A and B
ANTIBODY- NO
Type- O BLOOD GROUP RBC
ANTIGEN- NO
ANTIBODY- A and B
Rashmi M G
16.
Predicting blood groups
Bloodgroup- A Genotype: IA
IA
/ IA
i
IA
i
Blood group- O Genotype: ii i
Blood group- B Genotype: IB
IB
/ IB
i
IB
i
Blood group- AB Genotype: IA
IB
IA
IB
4 MATERNAL
BLOOD GROUP
✕
4
PATERNAL
BLOOD GROUP
=
16
DIFFERENT
COMBINATIONS
Rashmi M G
17.
Parents
genes
AA BB ABOO AO BO
AA AA AB AA,AB AO AA,AO AB,AO
BB AB BB AB,BB BO AB,BO BB,BO
AB AA,AB AB,BB AA,AB,B
B
AO,BO AA,AB,A
O,BO
BB,BO,A
B,AO
OO AO BO AO,BO OO AO,OO BO,OO
AO AA,AO AB,BO AA,AB,A
O,BO
AO,OO AA,AO,O
O
AO,BO,A
B,OO
BO AO,AB BB,BO AB,BO,A
O,BB
BO,OO AB,AO,B
O,OO
BB,BO,O
O
AA, AO- BLOOD GROUP-A
BB,BO- BLOOD GROUP-B
OO- BLOOD GROUP-O
AB- BLOOD GROUP-AB
Rashmi M G
18.
Rh- blood group
•Rh blood group-1940- Landsteiner and Wiener
• System based on presence/ absence of Rh-
antigen/ Rh-factor on plasma membrane of RBC
• Rh factor- Rhesus monkey- Macacus rhesus
• Rh- Negative- RBC lack Rh-D antigen
• Rh- Positive- RBC has Rh-D antigen
Parent Genotype Passes genes
Rh-Negative Rh-
/Rh-
Rh–
Allele
Rh- Positive Rh+
/Rh+
Rh+
/Rh-
Rh+
/Rh-
Rashmi M G
Mother
Child Rh-Positive Blood
Rh-NegativeBlood
Fetal and mother blood
Separate -Placenta
During Pregnancy =
Usually mother’s Rh-
Negative blood is not
exposed to Rh-Positive
blood of Fetus
There is possibility of Exposure of
Maternal Blood to small Amount of
Rh-Positive Blood From Fetus during
Delivery of 1st
Child
Mother produces Antibodies Against Rh- Antigen
These antibodies cross Placenta in Subsequent Pregnancy
Causes Hemolysis of Rh- Positive RBC of Fetus
Anemia-
Erythroblastosis Fetalis
Prevention: Injecting Rh-Negative mother with Antibody prepared against Rh-Antigen
(Anti-Rh Antibodies) within 72hours after birth of each Rh- Positive baby
(Passive Immunization)
Rashmi M G