BLOOD PHYSIOLOGY

Guyton chapter = 35
Blood Types; Transfusion; Tissue and Organ Transplantation

By Dr. Mudassar Ali Roomi (MBBS, M. Phil.) Assistant Professor Physiology

Blood group antigens are present on the surface of RBCs

O-A-B Blood Types
• A and B Antigens—Agglutinogens:
– Two antigens—type A and type B. – occur on the surfaces of the red blood cells

• When neither A nor B agglutinogen is present, the blood is type O. • When only type A agglutinogen is present, the blood is type A. • When only type B agglutinogen is present, the blood is type B. • When both A and B agglutinogens are present, the blood is type AB.

Agglutinins/antibodies
 When type A agglutinogen is not present in a person’s red blood cells, antibodies known as anti-A agglutinins develop in the plasma.  Also, when type B agglutinogen is not present in the red blood cells, antibodies known as anti-B agglutinins develop in the plasma.

Average titers of anti-A and anti-B agglutinins in the plasma of people with different blood types.
• The agglutinins are gamma globulins (antibodies) and they are produced by plasma cells • Most of them are IgM and IgG immunoglobulin molecules. • agglutinin formation occurs almost entirely after birth when type A and/or B antigens enter the body in food, in bacteria, and in other ways.

Landsteiner’s law
• The reciprocal relationship between antigens on the red blood cells and antibodies in the serum is known as Landsteiner’s law • It states that:
– If an agglutinogen is present in the red cells of a blood, the corresponding agglutinin must be absent from the plasma. – If an agglutinogen is absent in the red cells of a blood, the corresponding agglutinin must be present in the plasma

Relative Frequencies of the Different Blood Types in western population

Rh Antigens-“Rh-Positive” and “Rh-Negative”
People.

 There are six common types of Rh antigens, each of which is called an Rh factor. These types are designated C,D, E, c, d, and e

Rh Antigens-“Rh-Positive” and “RhNegative” People.

 A person who has a 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 antigens. D Ag: Anyone who has this type of antigen is said to be Rh positive, whereas a person who does not have type D antigen is said to be Rh negative. 85 % people are Rh +ve

– –

it is on the basis of presence or absence of antigens on red cells blood is grouped for purpose of transfusion
- Blood spot on weapon, clothing or some other site - To solve the issue of Disputed paternity and maternity

- Peptic ulcer is common in blood group O - Carcinoma stomach is more common in blood group A

Antisera for blood grouping
• These are prepared in the body of a horse. • Stored in fridge at 4 degree C.

For blood transfusion we consider
• Donor’s antigen on RBCs • Recipient’s antibody in serum • Donor’s antibodies are diluted in the plasma of recipient, that’s why are not considered.

Who can donate and who can receive blood?

Pre-requisites of blood transfusion
• Blood grouping/typing of donor and recipient • Cross matching • Screening for infections e.g. hepatitis B, hepatitis C, HIV/AIDS

Cross matching of blood
• cross matching is done after Blood typing • Cross matching is Performed prior to blood transfusion and it serves as the last guard to ensure a safe transfusion • We mix recipients serum and donor’s RBCs to check the full compatibility of donor’s blood with that of recipient. • Significance: It is to rule out the incompatibility of other minor antigens b/w donor and recipients.

Erythroblastosis Fetalis (“Hemolytic Disease of the
Newborn/HDN)

• Why called so?
– Because blasts are seen in blood circulation.

• Erythroblastosis fetalis is a disease of the fetus and newborn child characterized by of the fetus’s red blood cells
• The mother is Rh-negative, the father is Rh- positive and the baby is Rh-positive

Erythroblastosis Fetalis (“Hemolytic Disease of the Newborn/HDN)

Effect of the Mother’s Antibodies on the Fetus

 After Ig-G anti- Rh antibodies have
formed in the mother, they diffuse slowly through the placental membrane into the fetus’s blood. There they cause agglutination of the fetus’s RBCs followed by their lysis.

Incidence of the Disease

Clinical Features of Erythroblastosis Fetalis (“Hemolytic
Disease of the Newborn/HDN)

• Jaundice • Kernicterus (deposition of unconjugated bilirubin in the brain) can occur. It can lead to mental retardation and cerebral palsy • Hemolytic Anemia • Nucleated Erythroblast are present in the peripheral blood • Hydrops fetalis (fetus is swollen) • Abortion may occur • Enlarged spleen and liver

1. Exchange blood transfusion
• 400 ml Rh+ blood of the baby is removed and same quantity of Rhblood is transfused. • This procedure is repeated several times till the mother’s antibodies are cleared from the plasma of baby.

2. phototherapy
• UV-rays convert unconjugated bilirubin (lipid soluble) into water soluble form which is excreted in urine.

Prevention of Erythroblastosis Fetalis

 an that is administered to the expectant Rh –ve mother starting at 28 to 30 weeks of gestation.

Prevention of Erythroblastosis Fetalis

within 24 – 48 hours of delivery & these neutralize RBCs of baby in mother’s circulation. This prevents the mother’s sensitization by baby’s RBCs.

Rh+ Blood transfusion to an Rh- person?
(e.g. A+ transfusion to A- person)

• In contrast to ABO system, in Rh system Anti Rh antibodies are not present naturally. These are produced when an Rh- person is transfused with Rh+ blood • Such transfusion can be done one time. Not more than once! • Such first Rh+ transfusion sensitizes the RhPerson. Second Rh+ transfusion will cause hemolysis

ABO incompatibility b/w mother and fetus
(e.g. mother is B+ and Fetus is A+)

• It is very less common than Rh incompatibility • Reason: The antibodies in ABO system are of Ig M type, which being five times larger than Ig G antibodies, cannot cross the placenta.

Acute complications of blood transfusion
1. Acute haemolytic transfusion reaction due to mismatch of donor’s and recipient’s blood groups 2. Septic/infective shock due to bacteria 3. Transfusion related acute lung injury (TRALI) 4. Fluid overload and lung edema in case of multiple transfusion over a short period of time 5. Non-haemolytic febrile reactions (fever, chills) 6. Severe generalized allergic reaction or anaphylaxis 7. Hyperkalemia (inc. K+) due to lysis of RBCs 8. Hypocalcemia (dec. Ca++): as Ca++ binds with citrate in the transfusion bags 9. Air embolism (air can enter in the blood vessels)

Delayed complications of blood transfusion
1. Delayed haemolysis of transfused RBCs 2. Development of antibodies that react with antigens of WBCs or platelets 3. Post-transfusion purpura (pin point hemorrhage) due to decrease in number of platelets. 4. Iron overload due to frequent transfusions e.g. in thalassemia 5. Transmission of Infection e.g. Hepatitis B, Hep. C and HIV.

Acute Transfusion Reactions Resulting from Mismatched Blood Types

• Red blood cells of the donor blood are agglutinated. • The plasma portion of the donor blood immediately becomes diluted by all the plasma of the recipient • Hb bilirubin jaundice

• These are the result of antibodies in the recipient's plasma directed against antigens on the donor's RBCs. • This results in rapid intravascular hemolysis of the donor RBCs. • ABO incompatibility due to clerical error is the most frequent cause. • immunoglobulin M (IgM) typically result in severe, potentially fatal complement-mediated intravascular hemolysis

1. 2. 3. 4. 5. 6. 7. 8. 9.

Fever Chills Flushing Nausea Burning at the intravenous (IV) line site Chest tightness Restlessness and Apprehension Back pain Difficulty in breathing, increase in heart rate, fall in B.P., circulatory Shock 10. No urine production (oliguria) due to acute renal shut down

Acute Kidney Shutdown After mis-matched Transfusion  One of the most lethal effects of transfusion reactions is kidney failure.  The kidney shutdown seems to result from three causes:
1. 2. 3. Renal vasoconstriction Circulatory shock Obstruction of renal tubules

2.Circulatory Shock
1. Renal Vaso constriction

3.Renal Tubular Blockage

Acute Renal Shutdo wn

1. Renal vasoconstriction

2. Circulatory shock

• ↓ BP • ↓ Renal blood flow • ↓ urine formation (oliguria)

3. Obstruction of renal tubules
• Haptoglobin can bind up to 10 % free Hb. • Excess Hb precipitates and blocks many of the kidney tubules.

Other blood group systems
• Thirty-three major blood group systems (including the AB and Rh systems) have been recognised • a few other systems are :MNS system, Kell system, Lewis system.

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