3. History of Blood Groups and Blood Transfusions
•Experiments with blood transfusions
have been carried out for hundreds
of years. Many patients have died
and it was not until 1901, when the
Austrian Karl Landsteiner
discovered human blood groups, that
blood transfusions became safer.
• He found that mixing blood from
two individuals can lead to blood
clumping. The clumped RBCs can
crack and cause toxic reactions. This
can be fatal.
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4. • Karl Landsteiner discovered that blood
clumping was an immunological reaction
which occurs when the receiver of a blood
transfusion has antibodies against the donor
blood cells.
•Karl Landsteiner's work made it possible to
determine blood types and thus paved the
way for blood transfusions to be carried out
safely. For this discovery he was awarded the
Nobel Prize in Physiology or Medicine in
1930.
History of Blood Groups and Blood
Transfusions (Cont.)
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5. • There are more than 20 genetically determined
blood group systems known today
• The AB0 and Rhesus (Rh) systems are the
most important ones used for blood
transfusions.
• Not all blood groups are compatible with each
other. Mixing incompatible blood groups leads to
blood clumping or agglutination, which is
dangerous for individuals.
What are the different blood groups?
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6. According to the ABO
blood typing system there
are four different kinds of
blood types:
A, B, AB or O (null).
ABO blood grouping system
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9. Blood group A
the blood group A, means
A antigens on the surface of
your RBCs and B antibodies
in blood plasma.
Blood group B
the blood group B, means
B antigens on the surface of
RBCs and A antibodies in
blood plasma.
AB0 blood grouping system
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10. Blood group AB
the blood group AB, means
both A and B antigens on the
surface of RBCs and no A or B
antibodies at all in blood plasma.
Blood group O
the blood group O (null), means
neither A or B antigens on the surface of
your RBCs but have both A and B
antibodies in blood plasma.
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11. • The ABO gene is autosomal (the gene is not on either sex
chromosomes)
• The ABO gene locus is located on the chromosome 9.
• Each person has two copies of genes coding for their ABO
blood group (one maternal and one paternal in origin)
• A and B blood groups are dominant over the O blood group
• A and B group genes are co-dominant
ABO inheritance and genetics
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12. This meant that if a person inherited one A group gene
and one B group gene their red cells would possess both
the A and B blood group antigens.
These alleles were termed A ( which produced the A
antigen ),
B (which produced the B antigen) and O (which was non
functional and produced no A or B antigen)
What do co-dominant genes mean?
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14. Parent
Allele
A B O
A AA AB AO
B AB BB BO
O AO BO OO
Possible Blood group Genotypes
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15. The ABO blood groups
• The most important in assuring a safe blood transfusion.
•The table shows the four ABO phenotypes ("blood groups")
present in the human population and the genotypes that give
rise to them.
Blood
Group
Antigens
on RBCs
Antibodies in Serum Genotypes
A A Anti-B AA or AO
B B Anti-A BB or BO
AB A and B Neither AB
O Neither Anti-A and anti-B OO4/15/2014 16BLOOD AND ITS COMPONENTS
16. Why group A blood must never be
given to a group B person?
Giving someone blood from the wrong ABO
group could be fatal.
The anti-A antibodies in group B attack group
A cells and vice versa.
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17. more complicated, because there's another antigen to be
considered - the Rh antigen.
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
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18. • 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.)
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19. Blood
Type
Genotype
Alleles
Produced
Rh positive
RR R
Rr R or r
Rh negative rr r
Rh Blood Group and Rh Incompatibility
A person with Rh- blood does not have Rh antibodies
naturally in the blood plasma
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20. Why is an Rh incompatibility so dangerous
when ABO incompatibility is not during
pregnancy?
• Most anti-A or anti-B antibodies are of the IgM
class (large molecules) and these do not cross the
placenta.
•In fact, an Rh−/type O mother carrying an
Rh+/type A, B, or AB foetus is resistant to
sensitisation to the Rh antigen.
•Her anti-A and anti-B antibodies destroy any foetal
cells that enter her blood before they can elicit anti-
Rh antibodies in her.
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21. •This phenomenon has led to an effective
preventive measure to avoid Rh sensitisation.
•Shortly after each birth of an Rh+ baby, the
mother is given an injection of anti-Rh
antibodies (or Rhogam).
•These passively acquired antibodies destroy
any foetal cells that got into her circulation
before they can elicit an active immune
response in her.
Rh incompatibility during pregnancy (cont.)
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22. People with blood group O
are called "universal
donors" and people with
blood group AB are called
"universal receivers."
Blood transfusions – who can
receive blood from
whom?
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24. Blood
Group
Antigens Antibodies Can give
blood to
Can receive
blood from
AB A and B None AB AB, A, B, O
A A B A and AB A and O
B B A B and AB B and O
O None A and B AB, A, B, O O
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26. Non immunological transfusion reaction
1. Bacterial contamination reactions.
2. Circulatory overload.
3. Transfusion haemosiderosis.
4. Complications of massive transfusion.
5. Non immune hemolytic reaction
6. Disease transmission.
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27. 1. Bacterial contamination reaction.
• Although uncommon,but this type of specific
reaction can have a rapid onset and high mortality in
recipients.
• The presence of bacteria in transfused blood may
lead either to febrile reactions in the recipient ( due
to pyrogens ) or serious manifestations of septic or
endotoxic shock.
• Commonly caused by endotoxin produced by
bacteria capable of growing in cold temperatures
such as Pseudomonas species, E. coli, Yersinia
enterocolitica.
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28. Source of infection.
• Infection of stored blood is extremely rare.
• Skin contaminants are not infrequently present in
freshly donated blood but these organisms (
predominantly staphylococci ) do not survive storage at
4 º C although they will grow profusely in platelet
concentrates stored at 22 º C.
• Healthy donor who are bacteremic at the time of
donation. The majority are due to Yersinia
enterocolitica, which grows well in red cell components
due to its dependence on citrate and Iron.
• Gram negative, endotoxin – producing contaminants
found in dirt, soil and faeces may rarely grow in the
storage condition of blood.
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29. •According to CDC , most are caused by blood
components contaminated by Yersinia enterocolitica.
•Since 1987, from 20 cases reported to CDC, 12 are
caused by this organism.
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30. Clinical manifestation
• Usually appear rapidly during transfusion or
within about 30 minutes after transfusion
with dryness, flushing of skin.
• Fever, Hypotension, Chills, Muscle pain,
vomiting, Abdominal cramps, Bloody
diarrhoea, Hemoglobinuria, Shock, Renal
failure, DIC.
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31. Management.
• Rapid recognition is essential
• Immediately stop the transfusion.
• Therapy of shock, steroids, vassopressors, fluid
support, respiratory ventilation and maintenance of
renal function.
• Broad spectrum IV antibiotics
• The blood component unit and any associated fluids
and transfusion equipment should be sent
immediately to blood bank for investigation ie: gram
stain and culture.
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32. Prevention
• Strict adherence to policies & procedures
regarding blood component collection, storage,
handling,and preparation is essential to reduce
the risk.
• Visual Inspection of components before release
from the transfusion service include any
discolouration, visible clots, or hemolysis.
• Ensure the blood components are infused within
standard time limits ( 4 hours ).
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33. Prevention
• Blood packs should never be opened for
sampling, if any open method of preparation
has been used, the unit should be transfused
within 24 hours.
• Blood should always be kept in accurately
controlled refrigerators (with alarms),
maintained strictly at 2 – 6 º C, the blood
should never be removed and taken to the
ward or OT until it is recquired.
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34. 2. Circulatory overload
• All patient will experience a temporary rise in blood
volume and venous pressure following the
transfusion of blood or plasma except for those who
are actively bleeding. However, young people with
normal cardiovascular function will tolerate this
changes provided it is not excessive.
• Pregnant women, patient with severe anaemia,
elderly with compromised cardiovascular function
will not tolerate the increase in plasma volume and
acute pulmonary oedema may develop.
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35. Clinical manifestation
• Frequently due to transfusion of a unit at too
fast rate.
• Signs of cardiac failure – raised JVP, basal
crepitations in both lungs, dry cough,
breathlessness.
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36. Management
• Stop the transfusion immediately.
• Prop up the patient
• Oxygen therapy
• Intravenous diuretics should be used
appropriately.
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37. Prevention
• Packed cell should be used instead of whole blood.
• Packed cells should be given slowly over 4 hours.The
usual rate of transfusion is about 200 ml per hour. In
patient at risk rate of 100 ml per hour or less are
appropriate.
• Diuretics should be given at the start of the transfusion
and only one or two units of concentrated red cells
should be transfused in any 24 hour period.
• Blood transfusion should be given during the daytime,
Overnight transfusion should be avoided wherever
possible.
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38. 3. Transfusion haemosiderosis
• A complication of repeated long term blood
transfusion.
• Most commonly seen in thalassaemic patient.
• Each unit of blood has about 200 mg of iron, while
the daily excretion rate is about 1 mg. The body has
no way of excreting the excess unless the patient is
bleeding.
• Assessment of storage iron levels such as ferritin
levels should be done.
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39. The use of Iron chelating agent, Desferrioxamine
does not completely overcome the Iron load, but
has delayed the onset of problems due to
haemosiderosis.
Transfusion of neocytes or young red cells is the
other alternative. However, it is expensive, time
consuming, and the result are not as favourable as
expected.
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40. 4. Complication of massive transfusion
• Massive transfusion is defined as the replacement of total
blood volume within a 24 hour period.
• This will inevitably lead to :
1. Dilution of platelets.
Blood effectively has no functional platelets after 48 hours
storage, after 8 to 10 units of blood transfusion,
thrombocytopenia will usually seen.
Bleeding due to a slightly low platelet is uncommon,
therefore routine administration of platelet after certain
amount of blood transfusion is unnecessary.
Regular monitoring of platelet count is more important.
Platelet transfusion may be recquired if platelet count <100
x 10 9 /L with continous bleeding or surgical intervention.
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41. 2. Dilution of coagulation factors.
Stored Whole blood < 14 days has adequate levels of
most coagulation factors for haemostasis.
If stored blood of more than 14 days, or plasma reduced
blood or red cells in optimal additive solution is used,
replacement of coagulation factors with FFP is necessary.
3. Hypothermia ( defined as core body temperature
less than 35 c ) is associated with large volumes of cold
fluid transfusion. This may results in cardiac irregularities in
particular VF. Therefore the use of blood warmer is
important.
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42. 4. Excess citrate can act on the patient’s plasma free
ionized calsium and results in hypocalcaemia (transient
).Citrate toxicity occur with extremely rapid transfusion (
one unit every 5 minute ), in premature infant having ET
with blood stored in citrate for longer than 5 days.
5. Hyperkalemia
Can be caused by intracellular loss of potassium from RBC
during storage or infusion of intracellular potassium
depleted RBC blood components such as washed RBC or
frozen washed RBC .
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43. The most important consideration in massive
blood transfusion is to replace blood loss quickly
and adequately. Too little blood , too late has
more serious consequences than massive blood
transfusion itself.
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44. 5.Non immune hemolytic reaction
• Mechanical – heat damage from blood
warmer, cold, small gauge needle.
• Environment – hypotonic or hypertonic
solution.
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45. 6. Disease transmission.
• Hepatitis
• Syphilis
• Malaria
• Cytomegalovirus
• Human immunodeficiency virus
• Human T cell leukaemia viruses.
Donor selection criteria and subsequent screening of all
donations are designed to prevent disease transmission, but
these do not completely eliminate the hazards.
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46. White blood cells
• Different from RBC
– Larger in size
– Irregular in shape
– Nucleated
– Many types
– Granules are present in some type of WBC
– Life span is shorter
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52. Eosinophils
• Coarse granules in the cytoplasm, which stain
pink or red with eosin
• Bilobed nucleus
• Diameter - 10 to 14 µM
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53. Basophils
• Coarse cytoplasm in the cytoplasm
• Stain purple blue with methylene blue
• Bilobed nucleus
• Diameter - 8 to 10 µM
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55. Monocytes
• Largest leukocytes with diameter of 14 to 18
µM
• Cytoplasm is clear without any granules
• Nucleus is round, oval horse shoe shaped,
bean shaped or kidney shaped
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58. lymphocytes
• No granules
• Two groups based on size:
– Large – diameter – 10 to 12mm
– Small – diameter – 7 to 10mm
• Two groups based on function
– T – lymphocytes
– B - lymphocytes
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59. • B – LYMPHOCYTES
– B cells make antibodies that bind to pathogens to enable
their destruction. (B cells not only make antibodies that
bind to pathogens, but after an attack, some B cells will
retain the ability to produce an antibody to serve as a
'memory' system.)
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60. • T – LYMPHOCYTES
– CD4+ (helper) T cells co-ordinate the immune
response and are important in the defence against
intracellular bacteria.
– CD8+ cytotoxic T cells are able to kill virus-infected
and tumor cells.
• Natural killer cells: Natural killer cells are able to kill
cells of the body which are displaying a signal to kill
them, as they have been infected by a virus or have
become cancerous
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61. platelets
• Small colorless, non – nucleated, and
moderately refractive bodies
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63. FUNCTIONS OF PLATELETS
• Role in blood clotting
– Platelets are responsible for the formation of intrinsic prothrombin activator. This
substance is responsible for the onset of clotting.
• Role in clot retraction
– In the blood clot the blood cells including platelets are entrapped between the
fibrin threads. The cytoplasm of the platelets
contain the contractile proteins namely actin myosin and
thrombosthenin. The contractile proteins are responsible for clot retraction.
• Role in repair of ruptured blood vessel
– The platelet derived growth factor formed in cytoplasm of
platelets is useful for the repair of the endothelium and
other structures of the ruptured blood vessels.
• Role in defense mechanism
– By the property of agglutination, platelets encircle the foreign
bodies and kill them by the process of phagocytosis.
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64. • Fate of platelets
– The life span of platelets is 10 days. Platelets are
destroyed by tissue macrophage system in spleen.
– So in Splenomegaly there is decrease in platelet count
and in Splenectomy there is increased platelet count.
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65. Platelet disorders
• Thrombocytopenia
– Decrease in platelet count
Occurs in following conditions:
– Acute infections
– Acute leukemia
– Aplastic and pernicious anemia
– Chicken pox
– Smallpox
– Splenomegaly
– Scarlet fever
– Tuberculosis
– Typhoid
– Purpura
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66. • Thrombocytosis
– Increase in platelet count
Seen in
– Allergic conditions
– Asphyxia
– Hemorrhage
– Bone fractures
– Surgical operations
– Splenectomy
– Rheumatic fever
– Trauma
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67. Thrombocythemia
• Condition with persistent and abnormal
increase in the platelet count
– Carcinoma
– Chronic disease
– Hodgkin’s disease
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68. Glanzmann thrombasthenia
• Inherited hemorrhagic disorder caused by the
structural or functional abnormality of
platelets.
• Platelet count is normal
• Characterized by normal clotting time, normal
or prolonged bleeding time but defective clot
retraction
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69. Hemostasis
• Arrest or stoppage of bleeding
• Three stages
– Vasoconstriction
– Platelet plug formation
– Coagulation of blood
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75. • Bleeding time
– The time interval from oozing of blood after a cut
or injury till arrest of bleeding.
– It is determined by DUKE method using blotting
paper or filter paper method.
– Normal duration is 3 to 6 minutes.
– Prolonged in purpura
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76. • Clotting time
– The time interval from oozing of blood after a cut
injury or till the formation of clot.
– Determined by Capillary tube method
– Normal duration is 3 to 8 minutes
– Prolonged in hemophilia
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77. • Prothrombin time
– Time taken by blood to clot after adding tissue
thromboplastin to it.
– Normal duration is about 12 seconds.
– Prolonged in deficiency of prothrombin, and other
factors like 1, 5, 7 and 10
– Normal in hemophilia
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78. Blood is collected and oxalated so that, the
calcium is precipitated and prothrombin is
not converted into thrombin, thus, the
blood clotting is prevented
Large quantity of TTP with calcium is
added to the blood. calcium nullifies the
effect of oxalate. Thus TTP activates
prothrombin and blood clotting occurs.
During this procedure the time taken by
blood to clot after adding TTP is
determined
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79. • Partial prothrombin time
– The time taken for blood to clot after adding
phospholipids and calcium to it.
– This test is done to investigate the bleeding
disorders and to detect the presence of heparin in
patients treated with heparin therapy.
– Normal duration is 30 to 50 seconds.
– Prolonged in heparin therapy and deficiency of
factors like 2, 5, 7, 9, 10, 11, 12.
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80. • Thrombin time
– The time taken for the blood to clot after adding
thrombin to it.
– To investigate the presence of heparin in plasma
or to detect the fibrinogen abnormalities
– Normal duration is 12 to 20 seconds
– Prolonged in heparin therapy and during
dysfibrinogenimia ( abnormal function of
fibrinogen with normal fibrinogen level).
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