BLOOD GROUPING
AND
BLOOD
COAGULATION
Prepared by :
Miss. Asha Golasangimath
lecturer
Sanjeevini School of Pharmacy
Vijayapur
BLOOD GROUPS
THE 2 MAIN BLOOD GROUP SYSTEMS ARE :
1. ABO SYSTEM
2. Rh SYSTEM
ABO SYSTEM OF BLOOD GROUPING :
 Antigen –foreign bodies (agglutinogen)
 Antibody –fight against antigen (aglutinin)
 This is classified into A, B, AB,O groups .
 The classification is based on presence of
Agglutinogen A, B, AB, or none of them is O
respectively.
 Membrane of erythrocytes contain antigens called
agglutinogen and human have natural antibodies
i.e. aglutinins.
 Agglutinogen are genetically determined & are 2
types : “A”(group A) and “B(group B)” or both
“A&B”(group AB).
 No antigen in red cells – group “O”
 Aglutinins(antibody) in the plasma are
globulin and are opposite type.
BLOOD GROUPS SHOWING THEIR COMPATIBILITY
RH SYSTEM OF BLOOD GROUP
 There is another antigen called Rh antigen or Rh
factor found in the RBC’s .
 As A,B,&O these Rh factor also inherited from one’s
parents.
 Rh factor is a blood protien that plays a critical role in
some pregnancies.
 People without Rh factor are known as Rh negative,
while people with Rh factor are known as positive.
 If Rh factor present in blood is +ve .
 If Rh factor absent in blood is –ve.
 Rh = Rhesus factor
 Rh factor is discovered in 1937 by Karl Landsteiner and
Alexander wiener .
Incompatibilities of Rh factor :
When a woman and her unborn baby carry different Rhesus
(Rh) protien factors, their condition is called as Rh-
incompatibility.
If a women who is Rh negative is pregnant with a fetus who is
Rh positive , her body will make antibodeis against the fetus
‘s blood .
This can cause Rh disease also known as hemolytic disease of
new born baby & in severe cases Rh desease leads to brain
damage and even death.
Since 1968,a vaccine has existed to prevent the mother’s body
from making anti-bodies against the fetus blood .
 AB is universal accepter.
 O is universal doner.
COAGULATION OF BLOOD OR BLOOD CLOTTING
 When blood is collected in a container due to
expose into environment it looses its purity and
converted onto jelly like mass is called as
coagulation as a result form
fibrinogen(glycoprotien).
FACTORS INVOLVE IN COAGULATION :
1. Factor I – Fibrinogen
2. Factor II-Prothrombin
3. Factor III- Thromboplastin
4. Factor IV- Calcium
5. Factor V- Labile factor
6. Factor VI – not yet been proved
7. Factor VII – stable factor
8. Factor VIII – anti hemophilic factor
9. Factor IX – christmas factor
10. Factor X – stuvert pover factor
11. Factor XI – plasma thromboplastin
12. Factor XII –kegmen factor
13. Factor XIII – fibrin stabelising factor
SEQUENCE OF BLOOD CLOTTING MECHANISM
 Blood will not clot because the factors which are present in
coagulation are in inactive form during injury they become
activated as a result fibrin will form i.e. blood is clotted.
 Clotting or coagulation occur in 3 stages :
1. formation of prothrombin activator
2. conversion of prothrombin to thrombin
3. conversion of fibrinogen to fibrin
1. Formation of prothrombin activator : is formed by 2 ways
I Extrinsic pathway- production of prothrombin activator
inside the cell.
II Intransic pathway – production of prothrombin activator
outside the cell.
(Kegmen factor)
(Plasma
thromboplastin)
(Christmas factor)
(anti hemophilic factor )
Stuvert pover factor
Labile factor
(Stable
factor)
Tissue factor
CONVERSION OF PROTHROMBIN TO THROMBIN
CONVERSION OF FIBRINOGEN INTO FIBRIN
ANTICOAGULANTS
 Anticoagulants are commonly known as
blood thinners, are chemical substances that
prevent or reduce coagulation or clotting of
blood , prolonging the clotting time .
 Ex : heparin (inactivate IX,X,XI,XII)
coumarin derivative (inactivete factors
II,VII,IX,X & inhibit vit.K)
EDTA(remove calcium from blood )
MAJOR DISORDERS OF BLOOD
I )Anemia : it is the condition in which the oxygen
carrying capacity of blood is reduced or is less than
the normal quantity of heamoglobin in the blood .
Symptoms of Anemia :
• Weakness
• Tiredness
• Pale skin
• Fast heartbeat
• Shortness of breath
• Fatigue
• Chest pain
TYPES OF ANEMIA
Causes of Anaemia :
 Anemia can be caused by blood loss, decreased red blood cell
production, and increased red blood cell breakdown.
 Causes of blood loss include trauma and gastrointestinal bleeding.
 Causes of decreased production include iron deficiency, vitamin B12
deficiency, thalassemia, and a number of neoplasms of the bone
marrow.
 Causes of increased breakdown include genetic conditions such
as sickle cell anemia, infections such as malaria, and certain
autoimmune diseases.
Anemia can also be classified based on the size of the red blood
cells and amount of hemoglobin in each cell.
i. If the cells are small, it is called microcytic anemia
ii. if they are large, it is called macrocytic anemia and
iii. if they are normal sized, it is called normocytic anemia.
The diagnosis of anemia
in men is based on a hemoglobin of less than 130 to 140 g/L (13
to 14 g/dL);
TYPES OF ANEMIA
Impaired RBCs production could be impaired
due to the following reasons :
a) Iron deficiency anaemia
b) Megaloblastic anaemia
c) Pernicious anaemia
d) Hypoplastic anaemia
Increased RBCs loss :
a) heamolytic anaemia
b) Haemorrhagic anaemia
a) Iron deficiency Anaemia :
• It is a common type of anaemia results due to inadequate absorption
of iron, excessive loss of iron increased iron requirement or
insufficient intake of iron.
• Women are at greater risk for anaemia due to menstrual blood loss
and increased iron demands of the growing foetus during pregnancy.
• Causes if body does not make enough RBC. Bleeding causes
loss of RBC more quickly. Common cause of this is infestation
due to parasitic worms, round worms etc. Malaria and
vit A deficiency can also cause IDA.
b) Megaloblastic Anaemia :
It is also called as folic acid anaemia or vitamin B12 deficiency anaemia.
 It is a condition in which the bone marrow produces unusually large,
structurally abnormal, immature RBC or megaloblasts.
 Deficiency of vitamin B12(cobalamine) and vitamin B9(folate ) are 2
most common causes for megaloblastic anaemia.
 These 2 are serve as building blocks and essential for production of
healthy cells.
SYMPTOMS :
 Fatigue
 Paleness of skin
 Shortness of breath
 Dizziness
 Irregular heartbeat
 Muscle weakness
Treatment
• Deficiency can be treated with apprpriate changes to the diet
and the administration of suppliments.
C) Pernicious Anaemia :
 It is the condition in which decrease in RBC that occures
when the intestine cannot properly absorb vitamin B12.
D) Aplastic Anaemia :
• It is the condition that occures when yoour body stops
producing enough new blood cells.
HEAMOLYTIC ANAEMIA :
 It is a disorder in which RBCs are destroyed
faster than they can be made.
Heamorrhagic Anaemia :
 excessive loss of RBCs resulting from large
wound, stomach ulcer, and heavy
menstruation leads to heamorrhagic
anaemia.
SICKLE CELL ANAEMIA :
 It is a serious disorder in which body makes sickle
shaped(crescent shaped) RBCs.
 Sickle cells contain abnormal heamoglobin called as sickled
heamoglobin or heamoglobin S.
 This heamoglobin causes the cells to develop sickle or crescent
shape.
 Sickle cells are stiff and sticky .
 They tend to block blood flow in the bood vessels of the limbs
and organ, it is due to genetic mutation that causes substitution of
wrong amino acid in particular portion of globin.
 At low oxygen concentration in many cappillaries, heamoglobin
molecules combine with each other to formfibre like structures to
form sickle shape.
 Sickle cell Anaemia can leads to stroke, organ damage,
blindness, leg ulcer, etc.
TREATMENT
 Rehydration with intravenous fluid helps RBC
to return its normal shape .
 Blood transfusion can improve transport of
oxygen and nutrients as needed.
 Supplemental oxygen is given through the
mask .

Blood group & blood coagulation

  • 1.
    BLOOD GROUPING AND BLOOD COAGULATION Prepared by: Miss. Asha Golasangimath lecturer Sanjeevini School of Pharmacy Vijayapur
  • 2.
  • 3.
    THE 2 MAINBLOOD GROUP SYSTEMS ARE : 1. ABO SYSTEM 2. Rh SYSTEM
  • 4.
    ABO SYSTEM OFBLOOD GROUPING :  Antigen –foreign bodies (agglutinogen)  Antibody –fight against antigen (aglutinin)  This is classified into A, B, AB,O groups .  The classification is based on presence of Agglutinogen A, B, AB, or none of them is O respectively.  Membrane of erythrocytes contain antigens called agglutinogen and human have natural antibodies i.e. aglutinins.  Agglutinogen are genetically determined & are 2 types : “A”(group A) and “B(group B)” or both “A&B”(group AB).  No antigen in red cells – group “O”
  • 5.
     Aglutinins(antibody) inthe plasma are globulin and are opposite type.
  • 6.
    BLOOD GROUPS SHOWINGTHEIR COMPATIBILITY
  • 7.
    RH SYSTEM OFBLOOD GROUP  There is another antigen called Rh antigen or Rh factor found in the RBC’s .  As A,B,&O these Rh factor also inherited from one’s parents.  Rh factor is a blood protien that plays a critical role in some pregnancies.  People without Rh factor are known as Rh negative, while people with Rh factor are known as positive.  If Rh factor present in blood is +ve .  If Rh factor absent in blood is –ve.  Rh = Rhesus factor
  • 8.
     Rh factoris discovered in 1937 by Karl Landsteiner and Alexander wiener . Incompatibilities of Rh factor : When a woman and her unborn baby carry different Rhesus (Rh) protien factors, their condition is called as Rh- incompatibility. If a women who is Rh negative is pregnant with a fetus who is Rh positive , her body will make antibodeis against the fetus ‘s blood . This can cause Rh disease also known as hemolytic disease of new born baby & in severe cases Rh desease leads to brain damage and even death. Since 1968,a vaccine has existed to prevent the mother’s body from making anti-bodies against the fetus blood .  AB is universal accepter.  O is universal doner.
  • 11.
    COAGULATION OF BLOODOR BLOOD CLOTTING  When blood is collected in a container due to expose into environment it looses its purity and converted onto jelly like mass is called as coagulation as a result form fibrinogen(glycoprotien).
  • 12.
    FACTORS INVOLVE INCOAGULATION : 1. Factor I – Fibrinogen 2. Factor II-Prothrombin 3. Factor III- Thromboplastin 4. Factor IV- Calcium 5. Factor V- Labile factor 6. Factor VI – not yet been proved 7. Factor VII – stable factor 8. Factor VIII – anti hemophilic factor 9. Factor IX – christmas factor 10. Factor X – stuvert pover factor 11. Factor XI – plasma thromboplastin 12. Factor XII –kegmen factor 13. Factor XIII – fibrin stabelising factor
  • 13.
    SEQUENCE OF BLOODCLOTTING MECHANISM  Blood will not clot because the factors which are present in coagulation are in inactive form during injury they become activated as a result fibrin will form i.e. blood is clotted.  Clotting or coagulation occur in 3 stages : 1. formation of prothrombin activator 2. conversion of prothrombin to thrombin 3. conversion of fibrinogen to fibrin 1. Formation of prothrombin activator : is formed by 2 ways I Extrinsic pathway- production of prothrombin activator inside the cell. II Intransic pathway – production of prothrombin activator outside the cell.
  • 14.
    (Kegmen factor) (Plasma thromboplastin) (Christmas factor) (antihemophilic factor ) Stuvert pover factor Labile factor (Stable factor) Tissue factor
  • 15.
  • 16.
  • 19.
    ANTICOAGULANTS  Anticoagulants arecommonly known as blood thinners, are chemical substances that prevent or reduce coagulation or clotting of blood , prolonging the clotting time .  Ex : heparin (inactivate IX,X,XI,XII) coumarin derivative (inactivete factors II,VII,IX,X & inhibit vit.K) EDTA(remove calcium from blood )
  • 20.
    MAJOR DISORDERS OFBLOOD I )Anemia : it is the condition in which the oxygen carrying capacity of blood is reduced or is less than the normal quantity of heamoglobin in the blood . Symptoms of Anemia : • Weakness • Tiredness • Pale skin • Fast heartbeat • Shortness of breath • Fatigue • Chest pain
  • 22.
  • 23.
    Causes of Anaemia:  Anemia can be caused by blood loss, decreased red blood cell production, and increased red blood cell breakdown.  Causes of blood loss include trauma and gastrointestinal bleeding.  Causes of decreased production include iron deficiency, vitamin B12 deficiency, thalassemia, and a number of neoplasms of the bone marrow.  Causes of increased breakdown include genetic conditions such as sickle cell anemia, infections such as malaria, and certain autoimmune diseases. Anemia can also be classified based on the size of the red blood cells and amount of hemoglobin in each cell. i. If the cells are small, it is called microcytic anemia ii. if they are large, it is called macrocytic anemia and iii. if they are normal sized, it is called normocytic anemia. The diagnosis of anemia in men is based on a hemoglobin of less than 130 to 140 g/L (13 to 14 g/dL);
  • 24.
    TYPES OF ANEMIA ImpairedRBCs production could be impaired due to the following reasons : a) Iron deficiency anaemia b) Megaloblastic anaemia c) Pernicious anaemia d) Hypoplastic anaemia Increased RBCs loss : a) heamolytic anaemia b) Haemorrhagic anaemia
  • 25.
    a) Iron deficiencyAnaemia : • It is a common type of anaemia results due to inadequate absorption of iron, excessive loss of iron increased iron requirement or insufficient intake of iron. • Women are at greater risk for anaemia due to menstrual blood loss and increased iron demands of the growing foetus during pregnancy. • Causes if body does not make enough RBC. Bleeding causes loss of RBC more quickly. Common cause of this is infestation due to parasitic worms, round worms etc. Malaria and vit A deficiency can also cause IDA. b) Megaloblastic Anaemia : It is also called as folic acid anaemia or vitamin B12 deficiency anaemia.  It is a condition in which the bone marrow produces unusually large, structurally abnormal, immature RBC or megaloblasts.  Deficiency of vitamin B12(cobalamine) and vitamin B9(folate ) are 2 most common causes for megaloblastic anaemia.  These 2 are serve as building blocks and essential for production of healthy cells.
  • 26.
    SYMPTOMS :  Fatigue Paleness of skin  Shortness of breath  Dizziness  Irregular heartbeat  Muscle weakness Treatment • Deficiency can be treated with apprpriate changes to the diet and the administration of suppliments. C) Pernicious Anaemia :  It is the condition in which decrease in RBC that occures when the intestine cannot properly absorb vitamin B12. D) Aplastic Anaemia : • It is the condition that occures when yoour body stops producing enough new blood cells.
  • 27.
    HEAMOLYTIC ANAEMIA : It is a disorder in which RBCs are destroyed faster than they can be made. Heamorrhagic Anaemia :  excessive loss of RBCs resulting from large wound, stomach ulcer, and heavy menstruation leads to heamorrhagic anaemia.
  • 28.
    SICKLE CELL ANAEMIA:  It is a serious disorder in which body makes sickle shaped(crescent shaped) RBCs.  Sickle cells contain abnormal heamoglobin called as sickled heamoglobin or heamoglobin S.  This heamoglobin causes the cells to develop sickle or crescent shape.  Sickle cells are stiff and sticky .  They tend to block blood flow in the bood vessels of the limbs and organ, it is due to genetic mutation that causes substitution of wrong amino acid in particular portion of globin.  At low oxygen concentration in many cappillaries, heamoglobin molecules combine with each other to formfibre like structures to form sickle shape.  Sickle cell Anaemia can leads to stroke, organ damage, blindness, leg ulcer, etc.
  • 31.
    TREATMENT  Rehydration withintravenous fluid helps RBC to return its normal shape .  Blood transfusion can improve transport of oxygen and nutrients as needed.  Supplemental oxygen is given through the mask .