MBBS

1. BLOOD GROUPS

2. INTRODUCTION
 Agglutinogens–
Antigens present on cell
membrane of RBC
 Agglutinins–antibodies
against Agglutinogens
present in plasma.
 Agglutination –of RBCis
reaction between these 2

3. BLOODGROUPINGSYSTEM.
 Majorbloodgroupsystem–based on Agglutinogens on cell
membrane, present widely & causes severe transfusion
reaction


ABO
Rhsystem
 Minorbloodgroupsystem–based on Agglutinogens but
present in few populations & causes mild transfusion
reaction.


MNS
P
 Familialbloodgroupsystem–found in few families
 KELL.DUFFY,LUTHERAN,BOMBAYLEWIS, DEIGO,KIDD

4. LANDSTEINER’SLAWKARL
LANDSTEINER1900
 Ifan Agglutinogens is
present on surface of RBC
corresponding
agglutinins must be
absent in plasma.
 & if an Agglutinogens is
absent on surface of RBC
corresponding
Agglutinins must be
present in plasma.

5. CLASSICALABOBLOOD
GROUPINGSYSTEM
 A& B Agglutinogens- these are complex
oligosaccharides differing in terminal sugar
 InAntigenA–N-acetylgalactosamine & in
AntigenB–galactose.
 OtherthanRBCalso present in salivary
glands, pancreas, kidney, liver, lung, testes also
in body fluids like saliva, semen & amniotic
fluid

6.  Anti-A (α)and anti-B (β) Agglutinins –IgM
type & cannot cross placenta.
 Absence of these are determined by
Landsteiner’s law
 Act best at low temperature so calledCold
Antibodies.

7. TYPESOFABOBLOOD
GROUPS.
BLOODGROUP ANTIGEN ANTIBODIES
A A ANTI--B OR β
B B ANTI–A OR α
AB AB ---------------------
O ----------- ANTI-A(α) & ANTI--B (β)

8. POPULATIONDISTRIBUTION OF
ABOBLOODGROUPS
BLOODGROUPS PERCENTAGE(%)
A 20
B 40
AB 08
O 32

10. H Antigen(not antegenic)
The H gene codes for an enzyme that
adds the sugar fucose to the terminal
sugar of a precursor substance (PS)
The precursor substance (proteins
and lipids) is formed on an
oligosaccharide chain (the basic
structure)

11. RBC Precursor Structure
Glucose
Galactose
N-acetylglucosamine
Galactose
Precursor
Substance
(stays the
same)
RBC

12. Formation of the H antigen
Glucose
Galactose
N-acetylglucosamine
Galactose
H antigen
RBC
Fucose

13. Formation of the A antigen
Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose
N-acetylgalactosamine

14. Formation of the B antigen
Glucose
Galactose
N-acetylglucosamine
Galactose
RBC
Fucose
Galactose

15. APPERANCEOFANTIGENS&
ANTIBODIES
 Antigens A& B appears
in 6thweek of fetal life, at
birth 1/5th of adult level
& rises during puberty
& adolescence.
 Antibodies are absent at
birth, appear 10-15
days after birth, reach
maximum at 10 yrs.

16. MECHANISM
 Antigens similar to A& B are present in
intestinal bacteria & foods, when newborn
exposed to these absorbed in blood,
stimulate formation of antibodies against
antigens recognized as non-self by immune
system.

17. DETERMINA
TIONOFABO BLOOD
GROUPS
 Covered in
Practicals “
Determinationof
BloodGroups”

18. Well, it gets more complicated here, because there's
another antigen to be considered - the Rh antigen.
Some of us have it, some of us don't.
If it is present, the blood is RhD positive, if not it's RhD
negative.
So, for example, some people in group A will have it, and
will therefore be classed as A+ (or A positive).
While the ones that don't, are A- (or A negative).
And so it goes for groups B, AB and O.
The Rhesus (Rh) System

19. •Rh antigens are transmembrane proteins with loops
exposed at the surface of red blood cells.
•They appear to be used for the transport of carbon
dioxide and/or ammonia across the plasma membrane.
•They are named for the rhesus monkey in which they
were first discovered.
•RBCs that are "Rh positive" express the antigen
designated D.
•85% of the population is RhD positive, the other 15% of
the population is running around with RhD negative
blood.
The Rhesus (Rh) System (Cont.)

20. Rhesus (Rh) Group
Group Agglutinogen Agglutinin
Rh +ve D No Agglutinin
Rh –ve No Agglutinogen No Agglutinin

21. RhAntibodies.
 Nonatural antibodies like
ABOblood groups system
 Rhantibodies are produced
when Rh-ve individual is
transfused with Rh+ve
blood.
 These are IgGtype & crosses
placenta.
 WarmAntibodies.

22. INHERIT
ANCEOFRhBLOOD
GROUPS

23. Other Examples
Mom Dad Offspring Blood
Group
AA BB 100% AB
BO OO 50% each of B
or O
OO OO 100% O
OO AO 50% each of A
or O

24. HEMOLYTIC
DISEASE OF
NEWBORN.


25. Incompatibility of Rh blood
groups between fetus & mother.

26.  Is a disease of fetus and newborn
 Mother is Rh –ve ,Father Rh +ve
 Danger is only when fetus acquires Rh +ve from father
 The first pregnancy usually proceeds without problems
 At birth, mother may receive some of baby’s RBCs
 Mom’s immune system is sensitized
 Makes antibodies against Rh
 In a subsequent pregnancy:
 Mother’s blood carries antibodies
 Anti-Rh antibodies cross placenta
 Attack the Rh+ blood in the fetus Antigen – Antibody
reaction
 Agglutination of RBCs of fetus

27.  Anemic or jaundiced
 Hepatomegaly and splenomegaly
 Nucleated blastic forms appear in blood
 Permanent brain impairment or damage to
motor areas of brain due to deposition of
bilirubin in the neuronal cells--- Kernicterus

28. MECHANISMOF HEMOLYTICDISEASE OF
NEWBORNIN RHINCOMPATIBILITY
.
 Entrance of Rh+ve fetal
RBCinto Rh–vemother’s
circulation duringfirst
pregnancy.
 Production of Rh
antibodies.
 Rhincompatibility
reaction during second
pregnancy.

29. MANIFESTATIONSOFHEMOLYTIC
DISEASEOFNEWBORN.
 Erythroblastosisfetalis.


Erythroblastosis
Anaemia.
 Icterus gravis Neonatorum.


Jaundice
Enlarged liver & spleen.


Kernicterus–excess (<18mg%) bilirubin
deposition in brain mainly basal ganglia
Hydropsfetalis–Grossly edematous
fetus.

30. PREVENTIONOFHEMOL
YTIC
DISEASEOFNEWBORN.
 Injecting single dose of
Rhantibodies (anti-D)
to mother soon after
child birth.
 So active antibodies
will not be formedby
mother.

31. TREATMENTOFHEMOL
YTICDISEASE
OFNEWBORN.
 Replacement of baby’s
Rh+ve blood by Rh –ve
blood.
 This is called Exchange
Transfusion.

32. Treatment :
Exchange Transfusion
- Removes Rh +ve cells
- Removes Bilirubin
- Removes Anti-D
Rhesus (Rh) Group

33. Determination of ABO blood
groups
Slide method

34. Bombay( o bld grp)
 The hh causes NO H antigen to be produced
 Results in RBCs with no H, A, or B antigen (patient
types as O)
 Bombay RBCs are NOT agglutinated with anti-A,
anti-B, or anti-H (no antigens present)
 Bombay serum has strong anti-A, anti-B and anti-H,
agglutinating ALL ABO blood groups
 What blood ABO blood group would you use to
transfuse this patient??

35. Gal
NAGA Gal
Bombay phenotype
Gal
NAGA Gal
Fuc NAGA
A antigen
Gal
NAGA Gal
Fuc Gal
B antigen
Gal
NAGA Gal
Fuc
H substrate ( 0 group)
H antigen
Gal  Galactose
NAGA  N Acetyl Galactosamine
FUC  Fucose

36. CLINICALAPPLICATIONSOF BLOOD
GROUPS.
 Inbloodtransfusion.
 InPreventing HemolyticDisease.
 InPaternityDisputes.
 InMedicolegalCases.
 InknowingSusceptibility toDiseases.

37. BLOODTRANSFUSION.
 Lifesaving measure
 Should be carried out
when absolutely
necessary.

38. INDICATIONS
 Bloodloss –Accidents, major operations, rupture
peptic ulcer, rupture aortic aneurysm & rupture
ectopic pregnancy.
 ForQuickrestorationof haemoglobin.
 Exchange transfusion.
 Blooddiseases- Aplastic anaemia, agranulocytosis,
leukemias, purpurae & clotting defects
 Acutepoisoning–carbon Monoxide poisoning.

39. DONORS&RECIPIENT
.
 Donor–person who
donate the blood
 Recipient –person who
receives the blood.
 Universaldonor–O
Rh Negative.
 Universalrecipient–
ABRh positive

40. PRECAUTIONSTOBET
AKEN WHILE
SELECTINGDONOR.
 Should be Healthy
 Age–18- 60 yrs
 Contraindicated in
pregnant & lactating
mothers
 Screeningfor –AIDS,viral
hepatitis, malaria, syphilis.
 Hb& PCVshouldbe
normal

41. PRECAUTIONSDURINGBLOOD
TRANSFUSION.


Absoluteindication.
Crossmatching


Major –Donor’s RBC +
Recipient plasma
Minor -Donor’s plasma+
Recipient RBC



42. Cross matching
 Major cross matching
 Mixing of donor’s cells with recipient’s plasma
 Minor cross matching
 Mixing of recipient’s cells with donor’s plasma

43. PRECAUTIONSDURINGBLOOD
TRANSFUSION.
 Blood bag/bottle should be checked.
 Blood transfusion should be given at slowrate.
 Proper Aseptic measures.
 Careful watchon recipient condition –for first 10-
15min.
 Should stopif any reaction

44. HAZARDSOFBLOOD
TRANSFUSION.
 Mismatchedtransfusion reaction.
 Agglutination of donor’s RBC
 Tissue ischemia –chest pain or back pain
 Haemolysis of agglutinated RBC- Haemoglobinemia
 Haemolytic Jaundice
 Renal vasoconstriction
 Circulatory shock
 Haemoglobinuria.
 Renal tubular damage, acute renal shutdown &Uraemia.

45. HAZARDSOFBLOOD
TRANSFUSION.
 Transmissionofbloodborneinfections–AIDS,viral hepatitis
 Pyrogenicreactions –fever with chills Allergic
reactions –skin rashes ,asthma Hyperkalemia–
after excessive transfusion
 Hypocalcaemia–Tetany due to chelation of Caby citrate Reduced
tissueoxygenation–stored RBChas low 2,3-DPG Haemosiderosis–Iron
overload & deposition in liver, heart Thrombophlebitis –at
Venepuncture site
 Airembolism–entry of air into blood.
 Circulatory overload- Hypervolemia










46. Hazards :
- Effect of Incompatible Blood
Inapparent Hemolysis
Post-transfusion Jaundice
Haemoglobinuria
- Mechanical Overloading of Circulation
- Chemical Risks
- Pyrogenic Reactions
- Allergic Reactions
- Transmission of Diseases
Blood Transfusion :

47. ABO in compatibility / Mismatched
transfusion reaction
Agglutination of donor’s RBC in the recipient circulation
Tissue ischaemia
Violent pain in back & tightness of chest
Haemolysis – release of Hb
Haemolytic jaundice

48. Renal vaso constriction
Circulatory shock
Haemoglobinuria
Renal tubular damage
Acute renal shutdown
Uraemia
Coma and death

49. AUTOLOGOUSBT.
 Transfusion of
individual ownblood
withdrawl & stored
 Forelective surgery
 Duringsurgery
 Sportspersons

50. STORAGEOFBLOODFOR
TRANSFUSION.
 One unit 420 ml mixed with 120 ml ACD( Acid
citrate dextrose)
 Contents –
 Acid citrate 0.48gm
 Trisodium citrate –1.32 gm
 Dextrose –1.47gm
 Distilled water -100ml
 Dextrose–provide energy for Na-Kpump

51. IMPORTANTFACTSABOUT
BLOODTRANFUSION.
 One can safely donate 1 unit of blood every 6
month.
 Blood can be stored for 21 dayswithabove
conditions
 WBC&platelet virtually absent after 24 hrs of
storage.
 After transfusion 80% RBCsurvive for 24 hrs &
destroyed at a rate of 1% per day.

53. LYMPHOID
TISSUES AND
LYMPH

54. Reticulo endotheial system
• Mononuclear phagocyte system/ monocyte macrophage system
• Lymphoid tissues are fundamental importance in all types of
immune response.
• SITES:
• BM, spleen, lymph nodes, tonsils, peyer’s patch, appendix thymus
• It contains 3 types of cells
1. Tissue macrophages
2. Lymphocytes
3. Plasma cells

55. Tissue macrophages
• These are special group of phagocytic cells-body having common
characterstics features to ingest large foreign colloidal particles –
macrophages
1. Littoral cells- cells that form part of the lining of blood sinuses in
the BM
2. Kuffersr’s cells :cells that lie at frequent intervals along vascular
capillaries in the liver
3. Reticulum cells :found in both red &white pulp of the spleen.
4. Lymph nodes :that line the lympatic paths.
5. Pulmonary alveolar macrophages.
6. Osteoclats in the bones.
7. Microglia in the brain
8. In subcutaneous tissues.

56. Functions
• Ingest & destroy RBC; form and release bilirubin .also destroy
WBC and platelets.
• Defence of the body against infections
• They ingest and processs antigen which then stimulate antibody
formation in plasma cells.

57. LYMPH
• Lymph is a aqueous fluid derived from the interstitial fluid present
in the small channels called lymphatic capillaries.
 Chemistry :
• Lymph is a modified tissue fluid ,transparent, yellowish fainty
alkaline in raction and clot slowly.
• Its colloidal osmotic pressure is less than that of plasma
 Formation and flow :
• Formation based on the trans capillary exchange
• 2-4 lit of lymph seeps back in to the blood stream in 24 h and flow
is very slow (0.5-1ml/ min )

58. Functions of the spleen
1- Cleanses the blood by removing
old RBCs and platelets, as well as
debris from the blood.
2- Stores the breakdown products of
RBCs site of erythrocyte production
in the fetus
The spleen
spleen
The largest lymphoid organ , it sites of lymphocyte proliferation
and immune surveillance and response

59. • Lymphatics are absent in cartilage, bones , epithelial tissues and
brain.
• Serves very imp role of returnining the materials lost from blood
into interstitial fluid.
• Obstruction of the lymphatics as in filariasis leads to development
of oedema in affected part –called elephantiasis.
• Lymphatics form a route of spread of cancer cells.