Skip to main content
UploadLanguage (EN)Support
BusinessMobileSocial MediaMarketingTechnologyArt & PhotosCareerDesignEducationPresentations & Public SpeakingGovernment & NonprofitHealthcareInternetLawLeadership & ManagementAutomotiveEngineeringSoftwareRecruiting & HRRetailSalesServicesScienceSmall Business & EntrepreneurshipFoodEnvironmentEconomy & FinanceData & AnalyticsInvestor RelationsSportsSpiritualNews & PoliticsTravelSelf ImprovementReal EstateEntertainment & HumorHealth & MedicineDevices & HardwareLifestyle
MedicoseAcademics, profile picture
Uploaded byMedicoseAcademics
75 views

Blood grouping and typing, Transfusion Reaction

🧠 Explore Blood Groups, Blood Transfusion, and Tissue & Organ Transplantation with Dr Faiza 🧠 Build a clear understanding of the physiological and immunological principles behind blood grouping, transfusion reactions, Rh incompatibility, and transplantation. This lecture connects basic physiology with clinically important concepts such as ABO and Rh matching, hemolytic transfusion reactions, erythroblastosis fetalis, blood storage changes, tissue typing, graft rejection, and immunosuppressive therapy. It is designed to strengthen concept building for undergraduate and postgraduate medical studies and support preparation for professional and licensing examinations including USMLE, PLAB, FCPS, NEET PG, and similar exams worldwide. 🎓 Speaker 🎓 Dr Faiza is a physiology educator with qualifications including MBBS as Best Graduate from Allama Iqbal Medical College, FCPS Physiology, MHPE from Riphah International University Islamabad, ICMT, CHPE, DHPE from STMU, MPH from Government College University Faisalabad, and MBA from Virtual University of Pakistan. Her academic expertise includes medical physiology, health professions education, and medical teaching. 🎯 Learning Objectives 🎯 Describe the physiological basis of major blood grouping systems. Explain the genetic and immunological basis of the ABO and Rh blood groups. Discuss the pathophysiology, features, treatment, and prevention of ABO and Rh incompatibility. Interpret the principles of blood typing and compatibility testing. Enlist the major changes that occur in stored blood. Discuss the features and complications of mismatched blood transfusion. Describe the major hazards and reactions associated with blood transfusion. Explain the principles of tissue and organ transplantation. Describe tissue typing and the role of HLA matching. Explain the prevention of graft rejection through immunosuppressive therapy. 🔬 Topics Covered 🔬 ABO blood group system A and B antigens and plasma agglutinins Genetic basis of ABO blood groups H antigen and formation of A and B antigens ABO genotypes and phenotypes Development and origin of naturally occurring antibodies Agglutination and hemolysis Blood typing and interpretation Rh blood group system D antigen and Rh-positive versus Rh-negative blood Formation of anti-Rh antibodies Rh transfusion reactions Erythroblastosis fetalis and hemolytic disease of the newborn Kernicterus and complications of fetal hemolysis Treatment and prevention of Rh incompatibility Anti-D immunoglobulin and prevention of maternal sensitization Indications for blood transfusion Acute and delayed hemolytic transfusion reactions Jaundice and acute kidney injury after incompatible transfusion Febrile non-hemolytic transfusion reactions Allergic and anaphylactic reactions TRALI Graft-versus-host disease Post-transfusion purpura Changes in stored blood Alternatives to conventional blood transfusion Autografts, isografts, allografts, and xenograft

Health & Medicine◦
medicoseacademics@gmail.com 0310-7990649 Blood Types, Transfusion, and Tissue and Organ Transplantation Dr Faiza MBBS (Best Graduate, AIMC Lahore) FCPS Physiology, MHPE (Riphah Int University, Islamabad) ICMT, CHPE, DHPE (STMU) MPH (GC University, Faisalabad) MBA (Virtual University of Pakistan)
medicoseacademics@gmail.com 0310-7990649 Physiological Basis of Blood Grouping Dr Faiza MBBS (Best Graduate, AIMC Lahore) FCPS Physiology, MHPE (Riphah Int University, Islamabad) ICMT, CHPE, DHPE (STMU) MPH (GC University, Faisalabad) MBA (Virtual University of Pakistan)
medicoseacademics@gmail.com 0310-7990649 Learning Objectives • Describe the physiological basis of major blood grouping systems. • Discuss pathophysiology, features, and treatment of ABO and Rh incompatibility.
medicoseacademics@gmail.com 0310-7990649 Blood Types ABO Blood Grouping Rh Blood Grouping
medicoseacademics@gmail.com 0310-7990649 Antigenicity and Immune Reactions in Blood • Plasma antibodies of one person can react with antigens on RBCs of another person • This interaction forms the basis of blood transfusion reactions
medicoseacademics@gmail.com 0310-7990649 Antigenicity and Immune Reactions in Blood • RBC membranes contain many antigens • At least 30 common antigens exist • Hundreds of rare antigens are also present • Any of these antigens may occasionally cause immune reactions • Most RBC antigens are weak • They are mainly useful for studying genetic inheritance • These antigen patterns may help in parentage testing
medicoseacademics@gmail.com 0310-7990649 Major Antigen Systems in Transfusion • Two antigen systems are most important in blood transfusion: • ABO (O-A-B) blood group system • Rh blood group system • These systems cause most clinically significant transfusion reactions
medicoseacademics@gmail.com 0310-7990649 Antigens/Agglutinogens • Two major antigens are present on the surface of red blood cells • A antigen • B antigen • Responsible for most blood transfusion reactions • Agglutinogens can cause clumping of RBCs when they react with antibodies
medicoseacademics@gmail.com 0310-7990649 Genetic Basis of ABO Blood Groups • A and B antigens are complex oligosaccharides • They differ in their terminal sugar structure • Role of H Antigen • The H gene codes for an enzyme (fucosyltransferase) • This enzyme adds terminal fucose • This forms the H antigen • Present in almost all individuals • Acts as a precursor for A and B antigens
medicoseacademics@gmail.com 0310-7990649 Genetic Basis of ABO Blood Groups Formation of A and B Antigens • Type A individuals: • Have an additional enzyme (A transferase) • Modify H antigen → A antigen • Adds terminal N-acetylgalactosamine • Type B individuals: • Have B transferase • Modify H antigen → B antigen • terminal galactose
medicoseacademics@gmail.com 0310-7990649 Distribution of A and B Agglutinogens • Because of genetic inheritance, RBCs may contain: • No agglutinogen • Only A agglutinogen • Only B agglutinogen • Both A and B agglutinogens • This variation forms the basis of the ABO blood group system
medicoseacademics@gmail.com 0310-7990649 Genetic Basis of ABO Blood Groups • ABO blood group is determined by three alleles • IA • IB • IO • These alleles represent different forms of the same gene
medicoseacademics@gmail.com 0310-7990649 Genetic Basis of ABO Blood Groups • IA and IB produce A and B agglutinogens on RBC surface • IO allele does not produce agglutinogens • IA and IB show codominance • IO allele is recessive to both IA and IB
medicoseacademics@gmail.com 0310-7990649 Genotypes of ABO Blood Groups • Each person inherits two alleles (one from each parent) • Possible genotype combinations: • OO • OA • OB • AA • BB • AB • These combinations are called genotypes • Genotype determines the blood group phenotype
medicoseacademics@gmail.com 0310-7990649
medicoseacademics@gmail.com 0310-7990649 Major ABO Blood Types • Blood groups are classified based on presence or absence of agglutinogens • Type O: No A or B agglutinogens • Type A: A agglutinogen present • Type B: B agglutinogen present • Type AB: Both A and B agglutinogens present
medicoseacademics@gmail.com 0310-7990649 Frequency of ABO Blood Groups • Approximate prevalence in a studied population: • Blood group O: 47% • Blood group A: 41% • Blood group B: 9% • Blood group AB: 3% • O and A genes occur more frequently than B gene
medicoseacademics@gmail.com 0310-7990649 Antigenicity of Blood • Blood types differ in antigenic properties • Plasma antibodies of one blood type may react with RBC antigens of another type • If incompatible blood is transfused: • Agglutination (clumping) occurs • Hemolysis of RBCs may follow • Proper blood matching helps prevent transfusion reactions
medicoseacademics@gmail.com 0310-7990649 Plasma Antibodies (Agglutinins) • Antibodies develop against absent antigens • Type O blood • Anti-A antibodies • Anti-B antibodies • Type A blood • Anti-B antibodies • Type B blood • Anti-A antibodies • Type AB blood • No antibodies
medicoseacademics@gmail.com 0310-7990649 Development of Agglutinins with Age • At birth: Agglutinins almost absent • Between 2–8 months of age • Infant begins producing antibodies • Maximum antibody levels reached around 8–10 years • Antibody levels decline gradually with age
medicoseacademics@gmail.com 0310-7990649 Origin of Agglutinins • Agglutinins are gamma globulin antibodies • Produced by bone marrow and lymphoid cells • Mainly IgM and IgG immunoglobulins • Exposure to A or B antigens in food and bacteria stimulates antibody formation • Neonates have few antibodies, showing production occurs after birth
medicoseacademics@gmail.com 0310-7990649 Agglutination in Transfusion Reactions Occurs when antibodies meet corresponding antigens • Anti-A reacts with A antigen • Anti-B reacts with B antigen Antibodies bind to multiple RBCs (2-10) RBCs become linked together This produces clumping (agglutination)
medicoseacademics@gmail.com 0310-7990649 Agglutination Followed by Hemolysis Clumped RBCs block small blood vessels RBC membranes are destroyed by: • Physical distortion • Phagocytic white blood cells Hemoglobin released into plasma This process is called hemolysis
medicoseacademics@gmail.com 0310-7990649 Sometimes hemolysis occurs immediately Antibodies activate the complement system Complement forms membrane attack complex Pores form in RBC membrane Leads to osmotic lysis of RBCs Mainly caused by IgM antibodies (hemolysins) Far less common than agglutination followed by hemolysis Acute Hemolysis in Transfusion
medicoseacademics@gmail.com 0310-7990649 Blood Typing Before Transfusion • Steps in blood typing: • Separate RBCs from plasma • Dilute RBCs with saline • Mix samples with: • Anti-A serum • Anti-B serum • Observe under microscope for agglutination
medicoseacademics@gmail.com 0310-7990649 Interpretation of Blood Typing
medicoseacademics@gmail.com 0310-7990649 Rh Blood Group System Dr Faiza MBBS (Best Graduate, AIMC Lahore) FCPS Physiology, MHPE (Riphah Int University, Islamabad) ICMT, CHPE, DHPE (STMU) MPH (GC University, Faisalabad) MBA (Virtual University of Pakistan)
medicoseacademics@gmail.com 0310-7990649 Rh Blood Group System • Rh system is the second major blood group system after ABO • Important in blood transfusion compatibility • Unlike ABO system, Rh antibodies do not form naturally • Antibodies develop only after exposure to Rh antigen • Exposure occurs through • Blood transfusion • Pregnancy
medicoseacademics@gmail.com 0310-7990649 Rh Antigens • Six common Rh antigens exist • These are called Rh factors • Types include: • C, D, E, c, d, e • Each person inherits one antigen from each pair • Examples of antigen pairs • C or c • D or d • E or e
medicoseacademics@gmail.com 0310-7990649 Rh Positive and Rh Negative • D antigen is the most important Rh antigen • It is highly antigenic • If D antigen is present → Rh positive • If D antigen is absent → Rh negative • Other Rh antigens may still cause reactions, but these are usually mild
medicoseacademics@gmail.com 0310-7990649 Distribution of Rh Blood Types • Approximate prevalence in populations: • Whites • Rh positive: 85% • Rh negative: 15% • Black Americans • Rh positive: 95% • Black Africans • Nearly 100% Rh positive • Native Americans and East Asians • Over 95% Rh positive • Worldwide frequency • Rh positive: ~95% • Rh negative: ~5–6%
medicoseacademics@gmail.com 0310-7990649 Formation of Anti-Rh Antibodies • Occurs when Rh-positive RBCs enter Rh-negative person • Immune system recognizes Rh antigen as foreign • Anti-Rh antibodies develop slowly • Maximum antibody levels appear after 2–4 months • Repeated exposure causes strong sensitization
medicoseacademics@gmail.com 0310-7990649 Rh Transfusion Reactions First exposure to Rh-positive blood in an Rh-negative person Usually no immediate reaction Antibodies develop over 2–4 weeks Transfused cells later undergo hemolysis Reaction is usually delayed and mild If the same person receives Rh- positive blood again Immune system is already sensitized Reaction becomes rapid and severe Similar to reactions seen in ABO incompatibility
medicoseacademics@gmail.com 0310-7990649 Erythroblastosis Fetalis
medicoseacademics@gmail.com 0310-7990649 Erythroblastosis Fetalis • Also called Hemolytic Disease of the Newborn • Occurs when: • Mother is Rh negative • Fetus is Rh positive • Fetal RBCs enter maternal circulation • Mother forms anti-Rh antibodies • These antibodies cross the placenta and attack fetal RBCs
medicoseacademics@gmail.com 0310-7990649 Erythroblastosis Fetalis Hemolytic Disease of the Newborn Pathogenesis Mother: Rh negative Fetus: Rh positive Fetal RBCs enter maternal circulation Mother forms anti-Rh antibodies Antibodies cross placenta, attack fetal RBCs Severe response in second or subsequent pregnancies Mechanism Findings in newborn
medicoseacademics@gmail.com 0310-7990649 Erythroblastosis Fetalis Hemolytic Disease of the Newborn Pathogenesis Mechanism Maternal anti-Rh antibodies cross placenta Cause agglutination of fetal RBCs RBCs undergo hemolysis Hemoglobin is converted to bilirubin Leads to jaundice in the newborn Antibodies may also damage other fetal cells Findings in newborn
medicoseacademics@gmail.com 0310-7990649 Erythroblastosis Fetalis Hemolytic Disease of the Newborn Pathogenesis Mechanism Findings in newborn Severe anemia Jaundice Excess bilirubin may deposit in brain tissue Causes neuronal damage Leads to condition called kernicterus Mental impairment Motor dysfunction Permanent neurological damage Enlarged liver and spleen Rapid RBC production in hematopoietic tissues Release of immature nucleated RBCs Hence erythroblastosis fetalis
medicoseacademics@gmail.com 0310-7990649 Erythroblastosis Fetalis Hemolytic Disease of the Newborn Pathogenesis Mother: Rh negative Fetus: Rh positive Fetal RBCs enter maternal circulation Mother forms anti-Rh antibodies Antibodies cross placenta, attack fetal RBCs Severe response in second or subsequent pregnancies Mechanism Maternal anti-Rh antibodies cross placenta Cause agglutination of fetal RBCs RBCs undergo hemolysis Hemoglobin is converted to bilirubin Leads to jaundice in the newborn Antibodies may also damage other fetal cells Findings in newborn Severe anemia Jaundice Excess bilirubin may deposit in brain tissue Causes neuronal damage Leads to condition called kernicterus Mental impairment Motor dysfunction Permanent neurological damage Enlarged liver and spleen Rapid RBC production in hematopoietic tissues Release of immature nucleated RBCs Hence erythroblastosis fetalis
medicoseacademics@gmail.com 0310-7990649 Incidence in Pregnancies • First Rh-positive baby usually not affected • Because sensitization occurs during first pregnancy • Incidence increases in later pregnancies: • Second Rh-positive baby about 3% affected → • Third baby about 10% affected → • Risk rises with each subsequent pregnancy
medicoseacademics@gmail.com 0310-7990649 Treatment of Erythroblastosis Fetalis • Main treatment: Exchange transfusion • Procedure: • Neonate’s Rh-positive blood removed • Replaced with Rh-negative blood • Process takes about 1.5 hours • May be repeated during first weeks of life • Goals: • Reduce bilirubin levels • Prevent kernicterus
medicoseacademics@gmail.com 0310-7990649 Outcome After Treatment • Transfused Rh-negative cells circulate temporarily • Infant gradually produces own Rh-positive RBCs • Maternal antibodies disappear within 6 weeks • Disease resolves as antibodies are cleared from circulation
medicoseacademics@gmail.com 0310-7990649 Prevention of Erythroblastosis Fetalis • Prevention uses Rh immunoglobulin (Anti-D antibody) • Given to Rh-negative pregnant women • Administered at 28–30 weeks of gestation • Also given after delivery of Rh-positive baby • Prevents maternal sensitization to D antigen
medicoseacademics@gmail.com 0310-7990649 Mechanism of Rh Immunoglobulin • Anti-D antibodies work by: • Binding to Rh-positive fetal RBCs • Removing them before maternal immune system reacts • Suppressing B-cell antibody production • Preventing formation of anti-Rh antibodies • This greatly reduces the risk of hemolytic disease in future pregnancies.
medicoseacademics@gmail.com 0310-7990649 Hazards of Blood Transfusion Dr Faiza MBBS (Best Graduate, AIMC Lahore) FCPS Physiology, MHPE (Riphah Int University, Islamabad) ICMT, CHPE, DHPE (STMU) MPH (GC University, Faisalabad) MBA (Virtual University of Pakistan)
medicoseacademics@gmail.com 0310-7990649 Learning Objectives • Enlist changes occurring in stored blood • Discuss features and complications of mismatched blood transfusion • Describe hazards of blood transfusion • Elaborate transplantation of tissues and organs • Explain the process of tissue typing • Explain prevention of graft rejection by immune suppression
medicoseacademics@gmail.com 0310-7990649 Requirement for Blood Transfusion • A typical blood bag contains 1 pint of blood (approximately 450 ml) • Most of the times, 1 pint of blood is transfused at one instant • Blood transfusions are commonly required for the following conditions: 1. Anemia (iron deficiency, thalassemia) 2. Hemorrhage (accidental, during surgery) 3. Kidney and liver disorders 4. Cancers
medicoseacademics@gmail.com 0310-7990649 Blood Transfusion Reactions • Hemolysis • Acute • Delayed • Jaundice • Acute Kidney Failure
medicoseacademics@gmail.com 0310-7990649 Transfusion Reactions from Mismatched Blood When donor and recipient blood types are incompatible Recipient antibodies react with donor RBC antigens This causes agglutination (clumping) of donor red cells Agglutinated cells are later destroyed in circulation
medicoseacademics@gmail.com 0310-7990649 Why Donor Cells Are Usually Affected • Donor plasma becomes diluted in recipient plasma • This dilution reduces donor antibodies • Therefore, donor antibodies rarely affect recipient RBCs • Recipient plasma antibodies remain concentrated • These antibodies attack donor RBCs
medicoseacademics@gmail.com 0310-7990649 Hemolysis in Transfusion Reactions Hemolysis following transfusion Immediate hemolysis Caused by hemolysins Delayed hemolysis Occurs after phagocytosis of agglutinated RBCs RBC destruction releases haemoglobin into plasma Bilurubin Jaundice
medicoseacademics@gmail.com 0310-7990649 Agglutination in Transfusion Reactions Occurs when antibodies meet corresponding antigens • Anti-A reacts with A antigen • Anti-B reacts with B antigen Antibodies bind to multiple RBCs (2-10) RBCs become linked together This produces clumping (agglutination)
medicoseacademics@gmail.com 0310-7990649 Agglutination Followed by Hemolysis Clumped RBCs block small blood vessels RBC membranes are destroyed by: • Physical distortion • Phagocytic white blood cells Hemoglobin released into plasma This process is called hemolysis
medicoseacademics@gmail.com 0310-7990649 Sometimes hemolysis occurs immediately Antibodies activate the complement system Complement forms membrane attack complex Pores form in RBC membrane Leads to osmotic lysis of RBCs Mainly caused by IgM antibodies (hemolysins) Far less common than agglutination followed by hemolysis Acute Hemolysis in Transfusion
medicoseacademics@gmail.com 0310-7990649 Formation of Bilirubin
medicoseacademics@gmail.com 0310-7990649
medicoseacademics@gmail.com 0310-7990649 Jaundice After Hemolysis • Large amounts of hemolysis increase bilirubin levels • High bilirubin causes jaundice • Skin and tissues become yellow • Jaundice usually appears only if more than 400 mL of blood is hemolyzed in one day
medicoseacademics@gmail.com 0310-7990649 Acute Kidney Failure in Transfusion Reaction • One of the most dangerous complications is acute kidney injury • Can begin within minutes to hours • May progress to acute renal failure • Can lead to death if untreated
medicoseacademics@gmail.com 0310-7990649 Acute Renal Failure Renal Vasoconstriction Antigen–antibody reaction releases toxic substances These substances cause severe constriction of renal blood vessels Renal blood flow decreases Kidney function becomes impaired Circulatory Shock Massive RBC destruction reduces oxygen transport Toxic substances enter circulation Blood pressure falls sharply This leads to circulatory shock Renal blood flow and urine output decrease Tubular Blockage by Hemoglobin Excess hemoglobin is released into blood plasma Normally it binds to haptoglobin When haptoglobin becomes saturated Free hemoglobin enters kidney tubules High concentration causes hemoglobin precipitation Tubules become blocked
medicoseacademics@gmail.com 0310-7990649 Acute Renal Failure Renal Vasoconstriction Antigen–antibody reaction releases toxic substances These substances cause severe constriction of renal blood vessels Renal blood flow decreases Kidney function becomes impaired Circulatory Shock Massive RBC destruction reduces oxygen transport Toxic substances enter circulation Blood pressure falls sharply This leads to circulatory shock Renal blood flow and urine output decrease Tubular Blockage by Hemoglobin Excess hemoglobin is released into blood plasma Normally it binds to haptoglobin When haptoglobin becomes saturated Free hemoglobin enters kidney tubules High concentration causes hemoglobin precipitation Tubules become blocked
medicoseacademics@gmail.com 0310-7990649 Acute Renal Failure Renal Vasoconstriction Antigen–antibody reaction releases toxic substances These substances cause severe constriction of renal blood vessels Renal blood flow decreases Kidney function becomes impaired Circulatory Shock Massive RBC destruction reduces oxygen transport Toxic substances enter circulation Blood pressure falls sharply This leads to circulatory shock Renal blood flow and urine output decrease Tubular Blockage by Hemoglobin Excess hemoglobin is released into blood plasma Normally it binds to haptoglobin When haptoglobin becomes saturated Free hemoglobin enters kidney tubules High concentration causes hemoglobin precipitation Tubules become blocked
medicoseacademics@gmail.com 0310-7990649 Acute Renal Failure Renal Vasoconstriction Antigen–antibody reaction releases toxic substances These substances cause severe constriction of renal blood vessels Renal blood flow decreases Kidney function becomes impaired Circulatory Shock Massive RBC destruction reduces oxygen transport Toxic substances enter circulation Blood pressure falls sharply This leads to circulatory shock Renal blood flow and urine output decrease Tubular Blockage by Hemoglobin Excess hemoglobin is released into blood plasma Normally it binds to haptoglobin When haptoglobin becomes saturated Free hemoglobin enters kidney tubules High concentration causes hemoglobin precipitation Tubules become blocked
medicoseacademics@gmail.com 0310-7990649 Mechanism of Renal Shutdown • Three processes together cause kidney failure: • Renal vasoconstriction • Circulatory shock • Tubular obstruction by hemoglobin • These lead to complete renal shutdown • Outcome of Severe Transfusion Reaction • Persistent renal failure can occur • If untreated, death may occur within 7–12 days • Survival requires artificial kidney (dialysis) or rapid medical treatment
medicoseacademics@gmail.com 0310-7990649 Complications of Blood Transfusion 1. Incompatible blood transfusion 2. Non-hemolytic febrile reactions 3. Allergic reaction 4. Hyperkalemia 5. Hypocalcemia 6. Transmission of infections 7. Hemosiderosis 8. Circulatory failure 9. Air embolism 10. Hypothermia 11. Thrombophlebitis
medicoseacademics@gmail.com 0310-7990649 • To avoid complications of blood transfusion: 1. Crossmatching should be done to rule out ABO and Rh incompatibility 2. Donor should be screened for transmissible infections 3. Blood should be stored in sterile conditions and at adequate temperature 4. Whenever possible, fresh blood should be transfused
medicoseacademics@gmail.com 0310-7990649 Blood Transfusion Reactions Compatible Acute Immunologic Acute hemolytic (ABO mismatch) Febrile non- hemolytic Allergic / anaphylaxis TRALI Non-immunologic Circulatory overload Mechanical hemolysis Hypocalcemia Hypothermia Air embolism Dilutional thrombocytopeni a Delayed Immunologic Delayed hemolytic (Rh, Kell) GVHD Post- transfusion purpura Non-immunologic Iron overload Infections HIV, Hepatitis B/C Mismatched Immunologic Acute hemolytic → IgM + complement Delayed hemolytic → IgG, spleen/liver destruction
medicoseacademics@gmail.com 0310-7990649 Blood Transfusion Reactions Compatible Acute Immunologic Acute hemolytic (ABO mismatch) Febrile non- hemolytic Allergic / anaphylaxis TRALI Non-immunologic Circulatory overload Mechanical hemolysis Hypocalcemia Hypothermia Air embolism Dilutional thrombocytopeni a Delayed Immunologic Delayed hemolytic (Rh, Kell) GVHD Post- transfusion purpura Non-immunologic Iron overload Infections HIV, Hepatitis B/C Mismatched Immunologic Acute hemolytic → IgM + complement Delayed hemolytic IgG, spleen/liver → destruction
medicoseacademics@gmail.com 0310-7990649 Blood Transfusion Reactions Compatible Acute Immunologic Acute hemolytic (ABO mismatch) Febrile non- hemolytic Allergic / anaphylaxis TRALI Non-immunologic Circulatory overload Mechanical hemolysis Hypocalcemia Hypothermia Air embolism Dilutional thrombocytopeni a Delayed Immunologic Delayed hemolytic (Rh, Kell) GVHD Post- transfusion purpura Non-immunologic Iron overload Infections HIV, Hepatitis B/C Mismatched Immunologic Acute hemolytic → IgM + complement Delayed hemolytic IgG, spleen/liver → destruction
medicoseacademics@gmail.com 0310-7990649 Blood Transfusion Reactions Compatible Acute Immunologic Acute hemolytic (ABO mismatch) Febrile non- hemolytic Allergic / anaphylaxis TRALI Non-immunologic Circulatory overload Mechanical hemolysis Hypocalcemia Hypothermia Air embolism Dilutional thrombocytopeni a Delayed Immunologic Delayed hemolytic (Rh, Kell) GVHD Post- transfusion purpura Non-immunologic Iron overload Infections HIV, Hepatitis B/C Mismatched Immunologic Acute hemolytic → IgM + complement Delayed hemolytic IgG, spleen/liver → destruction
medicoseacademics@gmail.com 0310-7990649 Blood Transfusion Reactions Compatible Acute Immunologic Acute hemolytic (ABO mismatch) Febrile non- hemolytic Allergic / anaphylaxis TRALI Non-immunologic Circulatory overload Mechanical hemolysis Hypocalcemia Hypothermia Air embolism Dilutional thrombocytope nia Delayed Immunologic Delayed hemolytic (Rh, Kell) GVHD Post- transfusion purpura Non-immunologic Iron overload Infections HIV, Hepatitis B/C Mismatched Immunologic Acute hemolytic → IgM + complement Delayed hemolytic IgG, spleen/liver → destruction
medicoseacademics@gmail.com 0310-7990649 Allergic Reaction • Occurs against the plasma proteins in transfused blood • Presentation includes itching, rashes, fever • Treated with antihistamine
medicoseacademics@gmail.com 0310-7990649 Anaphylactic Reaction • Severe allergic reaction • Against blood products • Presentation includes shortness of breath, hypotension, respiratory arrest, shock • Treated with epinephrine
medicoseacademics@gmail.com 0310-7990649 Febrile Nonhemolytic Reaction • Host antibodies against recipient’s HLA antigens and WBCs • Presentation includes fever, headaches, chills and flushing • Treated with corticosteroids
medicoseacademics@gmail.com 0310-7990649 Transfusion-related Acute Lung Injury (TRALI) • Acute onset of hypoxemia and pulmonary edema on CXR • Within 6 hrs of TX without evidence of cardiac failure. • Primary Suspect: • Donor antibodies to recipient WBCs • Biologically active lipids in the lungs causing edema • Symptoms • Chills, fever, cough, cyanosis, hypotension, increased difficulty breathing
medicoseacademics@gmail.com 0310-7990649 Graft vs Host Disease (GVHD) • Donor CD8+ T-Lymphocytes attack recipient (host) tissues. • Very rare in blood stored 4+ days due to WBC inactivation • Groups at risk: Immunocompromised patients (Cancer, fetus, neonatal, bone marrow transplant). • Prevention: Irradiation of blood products.
medicoseacademics@gmail.com 0310-7990649 Post-transfusion Purpura • Antibodies to platelet antigens (HP1a) • Causes abrupt onset of severe thrombocytopenia (platelet count <10,000/l) • 5-10 days following transfusion. • Signs: • Purpura, bleeding, fall in platelet count • Treatment: • IVIG, plasmapheresis or corticosteroids; platelet transfusions usually NOT recommended
medicoseacademics@gmail.com 0310-7990649 Changes Occurring in the Stored Blood: 1. RBCs become rigid, spherical and osmotically fragile 2. Platelets become non-functional and disappear within 24 hrs of collection 3. Decreased ATP 4. Decreased 2,3-DPG 5. Increased potassium 6. Decreased pH 7. Decreased levels of clotting factors V and VIII 8. Increased levels of lactate
medicoseacademics@gmail.com 0310-7990649 Alternatives to Blood Transfusion • Major Approaches under consideration • Hemoglobin-based products • Modified human/bovine/genetically engineered Hb • Liposome-encapsulated “neo RBCs” • Synthetic O₂ carriers • Perfluorocarbons (PFCs) • Artificial Hb-like molecules • Stem cell–derived RBCs • Lab-grown universal donor (O negative)
medicoseacademics@gmail.com 0310-7990649 Transplantation of Tissues and Organs Dr Faiza MBBS (Best Graduate, AIMC Lahore) FCPS Physiology, MHPE (Riphah Int University, Islamabad) ICMT, CHPE, DHPE (STMU) MPH (GC University, Faisalabad) MBA (Virtual University of Pakistan)
medicoseacademics@gmail.com 0310-7990649 Transplantation of Tissues and Organs • Cells of the body contain many antigens • These antigens are also present on RBCs and other tissues • When foreign tissue enters the body, the immune system recognizes it as non-self • This triggers an immune reaction • The body may attack transplanted tissue just like bacteria, viruses, or foreign cells
medicoseacademics@gmail.com 0310-7990649 Types of Tissue Grafts • Based on the source of the transplanted tissue: • Autograft • Tissue transferred within the same person • Isograft • Transplant between identical twins • Allograft • Transplant between two individuals of the same species • Xenograft • Transplant between different species
medicoseacademics@gmail.com 0310-7990649
medicoseacademics@gmail.com 0310-7990649 Autologous Blood Transfusion • Patient’s own blood is collected before elective surgery • Blood is stored and reinfused during surgery if needed • Volume and Preparation • With iron supplementation: • 1000–1500 mL blood can be collected • Over a period of about 3 weeks • Why it is used • Reduces risk of infectious disease transmission • Seen in donor (heterologous) transfusions • Eliminates risk of transfusion reactions
medicoseacademics@gmail.com 0310-7990649 Survival of Transplanted Tissues • Autografts and isografts • Cells have same antigens as recipient • Grafts usually survive permanently • Xenografts • Strong immune response occurs • Graft cells often die within 1 day to 5 weeks unless immune reaction is suppressed
medicoseacademics@gmail.com 0310-7990649 Organs and Tissues Transplanted • Common allografts performed in medicine: • Skin • Kidney • Heart • Liver • Bone marrow • Lung • Glandular tissue • With proper matching and therapy: • Kidney grafts may survive 5–15 years • Heart and liver grafts may survive 1–15 years • Some transplanted organs now survive 20 years or more
medicoseacademics@gmail.com 0310-7990649 Preventing Immune Reactions in Transplantation • Transplant rejection occurs because of antigen–antibody reactions • Two major approaches help prevent rejection: • Tissue typing • Immunosuppressive therapy
medicoseacademics@gmail.com 0310-7990649 Tissue Typing • The most important antigens involved in graft rejection are: • Human Leukocyte Antigens (HLA) • These antigens are present on tissue cell membranes • Each person has six major HLA antigens • Around 150 different HLA types exist • Possible combinations exceed 1 trillion
medicoseacademics@gmail.com 0310-7990649 Importance of HLA Matching • Even small differences in HLA can trigger graft rejection • Exact matching is rare • Identical twins have identical HLAs • Therefore grafts between twins are rarely rejected • Good matches are often found between siblings or parents and children
medicoseacademics@gmail.com 0310-7990649 How Tissue Typing Is Done Lymphocytes are taken from blood samples These cells contain HLA antigens Lymphocytes are mixed with specific antisera and complement Cells are tested for membrane damage Dye uptake indicates antigen–antibody reaction
medicoseacademics@gmail.com 0310-7990649 Immunosuppression to Prevent Rejection • Suppressing the immune system can prevent graft rejection • T cells play the major role in destroying grafted tissue • Therefore treatment mainly targets T-cell activity
medicoseacademics@gmail.com 0310-7990649 Immunosuppressive Therapy in Tissue Transplant Ccorticosteroi d drugs Inhibit genes that produce cytokines Reduce production of interleukin-2 (IL-2) IL-2 is required for T- cell proliferation This reduces immune attack on the graft Azathioprine Toxic to lymphoid cells Inhibits formation of antibodies Reduces production of T lymphocytes Helps prevent graft rejection Calcineurin Inhibitors Cyclosporine Tacrolimus Mechanism: Inhibit calcineurin enzyme Prevent production of interleukin-2 Suppress T-cell activation Have less effect on other immune functions Immunosuppressiv e Antibody Therapy Antilymphoc yte antibodies IL-2 receptor antibodies Block activation of T lymphocytes Reduce immune attack on transplanted tissue
medicoseacademics@gmail.com 0310-7990649 Risks of Immunosuppressive Therapy • Increased bacterial infections • Increased viral infections • Higher risk of cancer • Because the immune system normally destroys early cancer cells
medicoseacademics@gmail.com 0310-7990649 Dr Faiza, FCPS Physiology Thank You References: • Guyton, A. C., & Hall, J. E. (2021). Textbook of Medical Physiology (15th ed., Chapter 36: Blood Types, Transfusion, and Tissue and Organ Transplantation). Philadelphia, PA: Elsevier. • Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong’s Review of Medical Physiology (26th ed., Chapter 31: Blood as a Circulatory Fluid & the Dynamics of Blood & Lymph Flow). New York, NY: McGraw-Hill Education. • Sherwood, L. (2015). Human Physiology: From Cells to Systems (9th ed., Chapter 11: Blood). Boston, MA: Cengage Learning.