Brief descriptions of the said topics for concept clearing

1. BLOOD COAGULATION; ABO BLOOD
GROUP & Rh FACTOR
Microteaching(2020)
Date-31.07.2020
NAME- Susmita Shaw
C.U Roll No.-183411-11-0208
College Roll No-18ZOOA032
Semester IV
Department of Zoology
BKGC

3. HAEMOSTASIS
[Haem - blood, Stasis-making something motionless]
● Haemostasis is the process of forming clots in the walls of damaged
blood vessels and preventing blood loss while maintaining blood in
the fluid state within the vascular system.
● MECHANISM - 1) Vascular Spasm
2) Platelet Plug Formation
3) Blood Clotting
4) Growth of fibrous tissue in blood clot area

4. VASOCONSTRICTION
●Vasocontriction is the narrowing of blood vessels.
●Reduces flow of blood from injured vessels.
●It lasts for 20-30 minutes
● Causes :-
1) Local myogenic spasms
2) Nervous reflexes
3) Release of vasoconstrictors
(Thromboxane A2, Serotonin,ADP)
from platelet that adhere to the walls
Of damaged vessels.
Mechanism Of Vasoconstriction

5. PLATELET PLUG FORMATION
●This is the second phase of haemostasis.
●It occurs in three major steps-1)Platelet adhesion
2) Platelet activation
3) Platelet aggregation
MECHANISM
●Platelet adhesion occurs when von Willibrand factor connects
collagen & platelets.
●The platelet release reaction is the release of ADP,Thromboxane A2
and other chemicals that activate other platelets.
●Platelet aggregation occurs when activated sticky platelets
Stick to each others and platelet plug is formed by the accumulating
mass of platelets.

6. Platelet Plug Formation
Contact of Platelets to
damaged vascular wall

7. BLOOD COAGULATION IN RUPTURED
VESSELS
●Coagulation is a complex sequence of chemical reaction which
results in the deposition of insoluble proteins to form a clot.
●Clot is composed of a meshwork of fibrin threads which adhere to
damaged surfaces of blood vessels.
●The process of formation of clot is called as clotting.
●Clot begins to develop –
▪severe trauma – 15 to 20 seconds
▪minor trauma – 1 to 2 minutes

8. INITIATION OF COAGULATION
FORMATION ─ OF FIBRIN
●There are two pathways involved in fibrin clot formation-
1) Intrinsic Pathway
2) Extrinsic Pathway
●After initial activities both pathways converge in a final common
pathway.
●In intrinsic, extrinsic & final common pathways, a series of
different plasma proteins called as Blood-clotting Factors
play a major role.

10. INTRINSIC PATHWAY FOR INITIATING
CLOTTING
●The intrinsic pathway involves factor VIII,IX,X,XI,XII as well as high
molecular weight kininogen (HK),Prekallikrein , Ca2 ,platelet
phospholipids. This results in the formation of factor Xa.
●The initial factors originate from within the blood.
●The formation of prothrombinase activator is initiated by factor XII.

11. Sequences of events in Intrinsic Pathway
1)The factor XII is activated to factor XIIa upon proteolysis by kallikrein and HMW
kininogen.
2)The activated factor XII then converts factor XI into XIa in the presence of HMW
kininogen.
3) XIa activates factor IX in the presence of factor IV(Ca2 ).
4) A little amount of thrombin (probably produced by extrinsic pathway
activation)activates factors VIII to factor VIIIa.
5)Factor IX a along with factor VIIIa , platelet phospholipid and Ca2 (formation of
tenase complex) convert factor X to factor Xa.

12. INTRINSIC
PATHWAY

13. EXTRINSIC PATHWAY FOR INITIATING
CLOTTING
●In this pathway the initial factors are found from injured tissue.
●The formation of prothrombin activator is initiated by the tissue thromboplastin ,
which is formed from the injured tissue.
Sequences of events in Extrinsic Pathway
1) Tissues that are damaged during injury release factor III(thromboplastin)
2) Factor III complexes with factor factor VII & converts it to factor VIIa.
3) Factor VIIa, tissue factor , Ca2 cleaves factor X to form factor Xa.

14. EXTRINSIC PATHWAY

15. FINAL COMMON PATHWAY
●The common pathway of coagulation starts with the conversion of factor X to Xa; in
the intrinsic pathway this is caused by factor IXa, in the extrinsic pathway this is
caused by tissue factor.
●In both intrinsic and extrinsic pathway ,the initially formed thrombin activates factor
V.
●Factor Va in turn accelerates formation of both intrinsic and extrinsic Prothrombin
activator.
●The prothrombin complex consists of platelet phospholipid , Ca2 , factor Va ,factor
Xa .
●The prothrombin activator converts prothrombin into thrombin.

16. Coagulation Pathway

17. FORMATION OF STABLE CLOT
Fibrinogen
Thrombin, Ca2
Fibrin monomer
Fibrin Polymer
Factor XIIIa , Ca2
Cross-linked Fibrin threads

18. CLOT RETRACTION
●Once the clot forms, it undergoes contraction & usually expresses most of the
fluid from the clot within 20-60 minutes.
●The straw- coloured fluid squeezed out during clot retraction is called Serum.
●Serum lacks fibrinogen & clotting factors I,II,V,VIII & XIII which up used during
clot formation.
● Platelets stimulate the process of clot retraction in the
following steps-
1)Platelets themselves interconnect different fibrin fibres.
2)Factor XIII released by platelets forms multiple covalent bonds between
neighboring fibrin threads.
3) Active contraction of contractile proteins in platelets such as actin, myosin
causes shrinkage of the attached fibrin fibres & this causes clot retraction.

19. ANTICLOTTING MECHANISM IN THE BODY
1) Physical Factors-
i) continuous circulation of blood prevents blood clotting.
ii) smoothness of endothelial lining prevents platelets adhesion & extension of
clot in the blood vessel.
iii)negatively charged particles (such as glycocalyx, a mucopolysaccharide)
present over the endothelium lining, repels clotting factors.
2) Chemical Factors – Natural Anticoagulants –
i) Presence of heparin prevents blood clotting in vessel.
ii) Production of thermodulin by endothelium of the blood vessels (except brain
capillaries).Thermodulin binds with thrombin ,this complex activates protein C
that acts as an anticoagulant.
iii) Prostacyclin inhibits platelet aggregation & prevents of progress of clotting.

20. IMPORTANCE OF BLOOD CLOTTING
1) Prevent excessive blood loss.
2) Prevent infection by microorganisms & foreign particles.
3) Maintain the blood pressure.
4) Maintain circulation of blood in a close circulatory system.

21. ABO BLOOD GROUP SYSTEM
& Rh Factor

22. ABO BLOOD GROUP SYSTEM
●The most well-known and medically
important blood types are in the
ABO group.
●All humans and many other
primates can be typed for the ABO
blood group.
●Based on the presence or absence
of antigen A and antigen B , Blood
is divided into i) A group
ii) B group
iii) AB group
iv) O group
HISTORY
● The ABO blood group system was
discovered in 1900 by Karl
Landsteiner in the process of
trying to learn why blood
transfusions sometimes cause
death and at other time saves a
patient.
● He belatedly received the Nobel
Prize for his discovery of blood
types.

23. A and B Antigens
●Two antigens – type A and type B ,occur on the surfaces of the red blood cells in
a large proportion of human beings.
●These antigens are called as agglutinogens that cause most blood transfusion
reactions.
●Agglutinogens are present not only in RBCs but also present in many organs like
salivary glands,pancreas,kidney ,liver, lungs etc.
●Agglutinogens appear during the 6th month of fetal life.
●A or B antigen expression fully developed at
2-4 years of age and remain constant throughout
life.

24. AGGLUTININS
●Antibodies against agglutinogens present in plasma are known as Agglutinins.
●When type A agglutinogen is not present in a persons red blood cells ,
antibodies known as anti-A agglutinins develop in the plasma.
●Also when type B agglutinogen is not present in the RBCs, antibody known as
anti-B agglutinins.
●Type O individual develops both agglutinins and type AB individuals develops
neither.

25. ● Agglutinins are the gamma-globulins which are mainly of IgM immunoglobulin.
●Therefore these agglutinins cannot cross placental barrier.
●Agglutinins is produced in response to A or B agglutininogens which enter the
body through respiratory system or digestive system along with bacteria.
●Agglutinin is not produced during fetal life. It starts appearing only 2 or 3 months
after birth , reach adult level at 5-10 years of age and decreases in elderly.
● They are produced by the same bone marrow and lymph gland cells that produce
antibodies to any other antigens.
●Specific agglutinins act best at low temperature and called cold antibodies.

26. I) If a particular agglutinogen (antigen) is
present on red blood cells , the corresponding
agglutinin ( antibody) must be absent in the
plasma.
II) If a particular agglutinogen is absent on red
blood cells, the corresponding agglutinin
must be present in the plasma.
Landsteiner’s Law

27. Blood types with their corresponding agglutinogens & agglutinins

28. GENETIC INHERITANCE PATTERN
●The locus of ABO gene is on chromosome 9 occupied by one of the three major
allelic genes i.e. A,B or O.
●There is gene responsible for the specificity of our ABO blood group.
●Other gene which plays an important role in the determination of ABO blood
groups is H gene with locus on chromosome 19.
●Each individual inherits two ABO genes, one from each parent and these genes
determine the ABO antigen present on their red cells.

29. ●The A and B genes are dominant while O is recessive thus is not directly detected.
●The serological typing reveals the Phenotype and the family studies reveal the
genotype.
●The six possible combinations of genes are OO,OA,OB,AA,BB and AB. These
combinations of genes are known as the genotype.
●Each person is one of the six genotype.
Blood types with their different Genotypes

30. Agglutination Process In Transfusion Reaction
●When bloods are mismatched so that anti-A or anti-B plasma agglutinins are
mixed with red blood cells that contain A or B agglutinogens respectively.
● A single agglutinin can attach to two or more RBCs at the same time thereby
causing the cells to be bound together.
●This binding causes the cells to clump, which is the process of agglutination.

31. Blood Typing
• Blood typing is done on the basic of agglutination.
• It is the process by which blood group is determined.
• This is performed in the following way :-
i) The RBCs are first separated from the plasma
and diluted with saline.
ii) one portion is then mixed with anti-A agglutinin
and another portion with anti-B agglutinin.
iii) After several minutes, the mixtures are
observed .
If the RBCs become clumped- that is agglutinated.

32. Transfusion reactions due to ABO
incompatibility
●Transfusion reactions are the adverse reactions in the body ,which occur
Due to transfusion error that involves transfusion of incompatible blood.
●Severity of the transfusion reactions varies from mild (fever and chills) to severe
(acute kidney failure ,shock and death).
● Transfusion of incompatible blood produces hemolytic reactions.
Hemolytic transfusion reaction - It may be acute or delayed.
□ The acute hemolytic reaction occurs within few minutes of transfusion.
□ It develops because of rapid hemolysis of donor’s RBCs.
□ Symptoms include fever, chills, nausea, chest pain, low blood pressure etc.

33. □ The delayed hemolytic reaction occurs from 1 to 5 days after transfusion.
□ The hemolysis of RBCs results in release of large amount of hemoglobin into the
plasma. This leads to several complications.
Complications of mismatched blood transfusion

34. Rh-factor
●Rh-factor is an antigen present in RBC.
● The Rh blood group system is one of most immunogenic systems known in
human.
● It is the most complex system, with over 45 antigens.
●It is the most important blood group system after ABO blood group system.

35. DISCOVERY OF Rh-factor
● The antigen was discovered by Karl Landsteiner & Alexander Wiener in 1940.
●They injected RBCs of Rhesus Monkey (monkeys with red ischial callosity) into
rabbit. The rabbit respond to the presence of an antigen in these cells by
forming an antibody with agglutinates Rhesus RBCs.
●If the immunized rabbit’s serum is tested against human RBCs, agglutination
occurs in 85% of people.
●The red cell surface substance of man which is similar to monkey’s is called the
Rh-factor.

36. Rh-antigens
●Blood group antigens are the result of the action of the genes which are present
in the chromosome.
●There are six common types of Rh-antigens.
●They are protein in nature with an active phospholipid component.
●These types are designated C,D,E,c,d and e.
●A person who has C antigen does not have the c antigen , but the person missing
the C antigen always has the c antigen. The same is true for the D-d and E-e
antigen.
●The type of D antigen is widely prevalent in the population and considerably
more antigenic than the other Rh-antigens.
●Production of antibody to D requires exposures to the antigen.

37. ●The person having D antigen are called Rh+ and those without D antigen are called
Rh-
●Among Indian population 85% of people are Rh+ and 15% are Rh-
●The D antigen appears to be an integral membrane protein of the red blood cell.
●Rh antigens do not exist in soluble form.

38. Rh antibodies
●All Rh antibodies are immune in nature , developed after
immunizing event.
● Rh antibody is called anti-D antibody.
● Rh antibodies are of the IgG types.
● These antibodies being IgG type can cross placenta.
●Antigen – antibody reaction occurs best at the body temperature .
Therefore, the Rh antibodies are called warm antibodies.

39. Rh Inheritance
●Rh gene is inherited from both father and mother, but it is
independent of ABO blood type.
●Rh gene is inherited dominant factor.
●It may be homozygous Rh+ with DD or heterozygous Rh+
with Dd.
●Rhesus- occurs only with complete absence of D antigen(i.e
with homozygous dd).
●Just like the ABO alleles ,each biological parent donates one
of their two Rh alleles to their child.

40. Rh Transfusion Reactions
●Rh blood group does not obey the Landsteiner’s law in that a Rh- person does
not have the Rh-antigen but still does not have Rh-antibody unless exposed to
Rh+ blood.
●If a Rh- person has never before been exposed to Rh+ blood, transfusion of Rh+
blood into that person ,will likely cause no immediate reactions.
●Anti -Rh-antibodies can develop in sufficient quantities during the next 2-4
weeks to cause agglutination.
●The transfused cells are then hemolysed by the tissue macrophage system.
●On Subsequent transfusion of Rh+ blood into the same person who is now
readily immunized against Rh factor, the transfusion reaction is greatly
enhanced and can be immediate.

41. Transfusion reactions due to Rh incompatibility

42. COMPATIBILTY OF BLOOD TYPES
 During blood transfusion , only compatible blood must be used.
 While transfusing the blood, antigen of the donor and the antibody of the
recipient are considered.
 People with O - blood group are called
‘universal donors’ as O- group blood
can be given to any blood group persons.
 People With AB + group can receive
blood from any blood group persons. So,
people with this blood group are Called
‘universal recipients’.

43. Hemolytic Disease Of The Newborn
Erythroblastosis Fetalis
●Hemolytic disease is the disease in fetus & newborn characterized by abnormal
hemolysis of RBCs.
●It occurs due to the difference of Rh blood group of mother & baby.
●Hemolytic disease leads to Erythroblastosis Fetalis where the mother is Rh- &
the father is Rh+
●Small amount of fetal blood leak into the maternal circulation at the time of
delivery & some mothers develop significant titers of anti-Rh agglutinins
during the postpartum period.
●During the next pregnancy if the fetus happens to be Rh+, the mothers
agglutinins cross the placenta & enters the fetal blood.
●React with fetal red cells causing hemolysis & anemia.

44. ●RBC destruction & anemia results in compensatory hyperactivity of bone
marrow leading to liberation of erythroblasts in circulation, which is why
the condition is known as Erythroblastosis Fetalis.
HEMOLYTIC DISEASE OF THE NEWBORN

45. Various Forms Of Hemolytic Diseases In Newborns
1)Severe Anemia – Excessive hemolysis results in anemia.
Various Forms Of Hemolytic Diseases In Newborns
1)Severe Anemia – Excessive hemolysis results in anemia.
2) Hydrops Fetalis – it is a serious condition in fetus , characterized by edema.
3) Jaundice- several hemolysis in fetus leads to high billirubin level in blood
causing jaundice.
4) Kernicterus- It is a form of brain damage in infants caused by severe jaundice.
Kernicterus develops in high billirubin content.

46. IMPORTANCE OF BLOOD GROUP
1) To avoid mismatched blood transfusion .
2) For identification of a person for medicolegal purposes.
3) Association of some diseases with specific blood group.
4) The Rh blood group is specially important for prevention of
hemolytic disease of new born caused by Rh mismatching between
mother and baby.