Download Free Medical Blood Group by Subhendu Sahu PowerPoint Presentation

Blood Group by Subhendu Sahu PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : blood grouping

Tags : blood group,blood,blood types,blood transfusion

Published on : May 23, 2023 | Views : 587 | Downloads : 1

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Subhendu Sahu 1st Semester Group-18 GUIDED BY- BLOOD GROUPING Dr.Bakyt Bekzhan Kulambaev Associate professor of AZMI
Slide 2-

Blood Typing RBC surfaces are marked by genetically determined antigens - Agglutinogens or isoantigens Blood is typed (grouped) based on surface antigens At least 30 common antigens and 100s of rare antigens have been found on the surfaces of human blood cells The ABO and Rhesus (Rh) systems of antigens are of major clinical importance as they are associated with transfusion reactions when mismatched Other antigens are less likely to cause reactions; however, they are of forensic importance (establish parentage).
Slide 3-

Karl Landsteiner 1901: was the first to discover the ABO blood agglutinins & classified blood groups accordingly. 1930: awarded the Nobel Prize in Physiology & Medicine for his discovery 1937: With Alexander S. Wiener, he identified the Rh factor.
Slide 4-

Blood Typing ABO blood group: A and B antigens are found in: Most cells: RBCs, WBCs and platelets In secretions: saliva, sweat, semen They are glycoproteins, complex oligosaccharides that differ in their terminal sugar RBCs with A antigen = Type A blood RBCs with B antigen = Type B blood RBCs with neither antigens = Type O blood RBCs with both antigens = Type AB blood Detection of A and B antigens in dried blood stains is of forensic importance
Slide 5-

ABO Blood Group Frequency Frequency of ABO has ethnic variation
Slide 6-

Two genes (one maternal and one paternal in origin), one on each of the two paired chromosomes number 9, determine the O-A-B blood type. These genes can be any one of three types but only one type on each of the two chromosomes number 9: type O, type A, or type B. The type O gene is either functionless or almost functionless, so that it causes no significant type O agglutinogen on the cells. Conversely, the type A and type B genes do cause strong agglutinogens on the cells. The type A and type B genes are co-dominant. This meant that if a person inherited one type A gene and one type B gene, their red cells would possess both the A and B antigens Genetic Determination of ABO Antigens
Slide 7-

ppt slide no 7 content not found
Slide 8-

Rh factor (D): There are eight different Rh agglutinogens, three of which (C, D, and E) are common Rh factor (antigen) are a complex system of antigens with Mendelian inheritance Cc, Dd, Ee Rh factor (antigen) was first discovered in blood of Rhesus monkey. Rh factors only detectable on RBCs C, D & E antigens (D is the most immunogenic) RBCs with D protein = Rh+ RBCs without D protein = Rh– 85% of caucasians, 95% of black Americans, 99% of chinese and nearly 100% of black Africans are Rh+ Locus of alleles responsible of ABO system is on long arm of chromosome 9 while Rh locus is on chromosome 1
Slide 9-

Agglutinins Plasma contains isoantibodies or agglutinins (IgM) to the A or B antigens not found in the blood: Anti-Rh antibodies (IgG) develop only in Rh- blood type and only with exposure to the antigen: transfusion of positive blood. during a pregnancy with a positive blood type fetus. anti-A antibody reacts with antigen A. anti-B antibody reacts with antigen B. Anti-A and Anti-B antibodies are not present at birth. Two to 8 months after birth, an infant begins to produce agglutinins. A maximum titer is usually reached at 8 to 10 years of age, and this gradually declines throughout the remaining years of life. Normal plasma contains no anti-Rh (anti-D) antibodies. LANDSTEINER's LAW: If an agglutinogen is present on red blood cell membrane ,the corresponding agglutinin must be absent in the plasma. If an agglutinogen is absent on red blood cell membrane, then corresponding agglutinin must be present in the plasma. This law is only applicable to ABO blood grouping system.
Slide 10-

Agglutinins Anti-Rh antibodies (IgG) develop only in Rh- blood type and only with exposure to the antigen: transfusion of positive blood. during a pregnancy with a positive blood type fetus. Anti-Rh antibodies are not spontaneously formed in Rh– individuals. However, if an Rh– individual receives Rh+ blood, anti-Rh antibodies form. Anti-Rh agglutinins develop slowly (2-4 months). Once produced they persist for years and can produce serious transfusion reaction during 2nd transfusion. This immune response occurs to a much greater extent in some people than in others. With multiple exposures to the Rh factor, an Rh-negative person eventually becomes strongly "sensitized" to Rh factor.
Slide 11-

Agglutinins
Slide 12-

ABO Blood Typing With ABO, person makes antibodies (agglutinens; IgM) against factors (agglutinogens) he/she does NOT have on his/her cells
Slide 13-

Blood Typing and Agglutination
Slide 14-

ABO Blood Typing
Slide 15-

ppt slide no 15 content not found
Slide 16-

ppt slide no 16 content not found
Slide 17-

Rh Blood Types Only makes antibodies (agglutinens) after exposure to Rh+ blood cells (via transfusion or during birth process) Transfusion of Rh- individual with Rh+ blood results in production of anti-D agglutinens; sensitizes person to Rh factor and may result in anaphylaxis if exposed a second time. Erythroblastosis fetalis arises when Rh- mother has been exposed to Rh+ blood and is carrying Rh+ child.
Slide 18-

Universal Donor; Suitable for all? Universal donor: Blood group O, Rh negative. May be given in emergency to patients with either A, B, AB and Rh negative or positive blood groups. Antibody concentrations may be high, so may not be suitable if large volume of blood required. Universal recipient: People with type AB blood are called “universal recipients” since have no antibodies in plasma.
Slide 19-

Importance of Blood Groups In blood transfusion. In preventing hemolytic disease (Rh incompatibility). In paternity disputes. In medico-legal cases. In knowing susceptibility to disease Group O- duodenal cancer Group A- Carcinoma of stomach, pancreas & salivary glands
Slide 20-

Blood Transfusion Indications of blood transfusion: Acute hemorrhage. Sever anemia (if Hb decreased below 7 g/dL). Erythroblastosis fetalis: in this case exchange transfusion (all blood is changed) is done. To supply a necessary elements e.g. platelets, packed RBCs, and some clotting factors.
Slide 21-

Requirements Prior to Blood Transfusion Typing (grouping) of the recipient: determining red cell antigens in blood ABO typing Rh typing Cross-matching: Donor’s cells + Recipient's serum Antibody Screening: Hepatitis B and C virus Antibody to HIV HIV Antigens Syphilis Cytomegalovirus
Slide 22-

Typing and Cross-Matching Blood Typing involves testing blood with known antisera that contain antibodies anti-A, anti-B or anti-Rh. Cross-matching is mixing of donor cells with recipient’s serum. Mixing of incompatible blood causes agglutination (visible clumping): formation of antigen- antibody complex that sticks cells together (agglutination reaction).
Slide 23-

ABO Blood Grouping (Typing) in Laboratory Using Anti-sera
Slide 24-

ppt slide no 24 content not found
Slide 25-

ppt slide no 25 content not found
Slide 26-

Transfusion Reactions Incompatible blood transfusions Mixing of incompatible blood causes the formation of antigen- antibody complexes between recipient’s plasma antibodies and “foreign proteins; antigens” on donated RBC's (agglutination) Donated RBCs become leaky and burst → diminished oxygen- carrying capacity Clumped cells impede blood flow Ruptured RBCs release free hemoglobin into the bloodstream → circulating hemoglobin precipitates in the kidneys and causes kidney damage and renal failure Problems are caused by incompatibility between donor’s cells and recipient’s plasma Why do donor antibodies not attack recipient RBCs Donor plasma is too diluted to cause problems
Slide 27-

Symptoms and Signs of Transfusion Reactions Pain at site of infusion Dyspnea Nausea Flushing Hypotension Oliguria or Anuria (renal failure ) Chest Pain Back Pain Chills Shock Fever
Slide 28-

Serious Hazards of Blood Transfusion
Slide 29-

Complications of Blood Transfusion
Slide 30-

Hemolytic Disease of Newborn During birth, there is often a leakage of the baby's red blood cells into the mother's circulation. If the baby is Rh-positive (having inherited the trait from its father) and the mother Rh-negative, these red cells will cause her to develop antibodies (IgG class) against the RhD antigen unless she receives an anti-D injection soon after first delivery or abortion. Anti-D binds to fetal red blood cells and remove them from body before she reacts In 2nd child, hemolytic disease of the newborn may develop causing hemolysis of the fetal RBCs → anemia and jaundice.
Slide 31-

ppt slide no 31 content not found
Slide 32-

Hemolytic Disease of Newborn Hemolytic anemia: – If severe: treated with exchange transfusion: Replace baby blood with Rh-ve RBC (several times) Hydrops fetalis (death in utero) Prevalence of Disease Kernicterus (yellow, jaundice baby) 1st Pregnancy: 0% 2nd Pregnancy: 3 3rd Pregnancy: 10%
Slide 33-

Fetal Incompatibility Most anti-A or anti-B antibodies are of the IgM class and these do not cross the placenta. Thus, an Rh−/type O mother carrying an Rh+/type A, B, or AB foetus is resistant to sensitization to the Rh antigen. Her anti-A and anti-B antibodies destroy any fetal cells that enter her blood before they can stimulate anti-Rh antibodies in her.
Slide 34-

Prevention of Hemolytic Disease of Newborn Rh immune globulin (RhIg) or Rhogam or anti-D: Shortly after each birth of an Rh-positive baby, the mother is given an injection of anti-Rh antibodies. These antibodies destroy any Rh+ fetal cells that got into the maternal circulation before they can stimulate an active immune response in the mother. The routine administration of such treatment to Rh - ve mothers after the delivery of Rh+ve baby has reduced the incidence of disease by >90%. Fetal Rh typing from amniocenthesis, and treatment with small dose of Rh immune serum will prevent sensitization during pregnancy.
Slide 35-

ppt slide no 35 content not found