week 1- immunohematology Flashcards
(53 cards)
• What is immunohematology?
o Specialized branch of medical science
o concepts and clinical techniques related to modern transfusion therapy
o determine blood group and type, so blood and organs are safely transfused and transplants
o prevent materno=-fetal transplacental rxns (HDN, hemolytic dz of the newborn)
• what is the sig hx of blood transfusions?
o William harvery described circulation of blood in 1616
o 1665, Lower, dog-dog transfusion -> feasibility demonstrated
o 1667, Denis, animal-human -> banned experimentation
o 1818, Blundell, human-human -> techniques, rational indications
o 1800s, Various, frequent severe reactions -> search for blood substitute (saline)
• What dis Denis do in 1667?
o Transfuse blood from docile lamb to man accused by wife of running thru streets of Paris naked w other women, in attempt to rid “wild” blood
o As soon as blood entered veins, felt heat, HR inc, sweaty face
o Upset stomach, kidney pain, felt like choking
o After sleeping all night, really black urine (Hb, bilirubin, blood)
• What are the main sxs of acute hemolytic reaction?
o Systemic: fever, chills o Heart: inc HR o Vascular: hypotension, uncontrollable bleeding o Transfused vein: heat sensation o Chest: constricting pain o Lumbar: pain o Urinary: Hb, bilirubin
• Who first described the ABO blood groups? Significance?
o Karl Landsteiner in 1901
o Until then, all blood assumed to be the same
o Often tragic consequences of blood transfusions not previously understood
• What are the Ag’s and Ab’s found in each blood type?
o A: a-B, A Ag
o B: a-A, B Ag
o AB: no Ab’s, A and B Ag’s
o O: a-A and a-B, no Ag’s
• Where are the A-B Ag’s found? What other Ag is there? What other phenotype?
o Expressed on proteins or lipid bi-layer pf RBCs
o Also H-Ag= foundation on which both A and B are created
o H-Ag: RBC-glu-gal-NAG-gal-fru (A-B attached to oligosaccharide off RBC)
o Bombay phenotype: no H-Ag, need transfusion from other H-def, 1/10000 in India, 1/million in Europe
• What is the clinical significance of blood group Ab’s?
o Abs to system destroy RBC in vivo
o Cause HDN
o Are common
• What are the AIHAs?
o Warm
o Cold: cold hemaglutinin dz, paroxysmal cold Hb-uria
• What are other types of immune hemolytic anemias?
o Alloimmune: Hemolytic dz of newborn (HDN), Hemolytic transfusion rxns
o Drug induced
• A transfusion is a tissue graft. What are the types? Blood?
o Also Abs against chemicals, drugs
o Autograft: animal has auto-Abs to its own blood
o Allograft: allo-Abs, against another individual of its own species
o Xenograft: heterologous Abs, against another species
o ABO Abs are allo-Abs; but also heterologous bc formed in response to exposure to gut and environmental bacteria, reacting w allo-Ags
• What was the first blood group system to be identified? Applications?
o ABO, most significant for transfusion practice
o Only system that reciprocal Abs are consistently and predictably present in sera of ppl who have no exposure to RBCs
o One of the first human characteristics proven to be inherited
o Used by lawyers in paternity suits, police in forensic science, anthropologists
• What are the ABO Abs?
o Occur naturally, aka natural isohemaglutinins, against A and B Ags
o Complete Abs=IgM class (u heavy chain) (st IgG, y HC)
o IgM large enough to produce visible agglutination of RBCs
o Formed w/o prior sensitization to non-self RBCs
o Form by encountering similar antigenic determinants found on micro-organisms (not present at birth)
• What are the relative amounts a-A and a-B in blood?
o Both decrease with age, highest at 10yrs
o a-A: much higher, in B and O
o a-B: about half, in A and O
• what is the difference bw sensitization and agglutination?
o S: Abs attach to a single RBC
o A: Abs attach to multiple RBCs, forming a clump of Ag-RBCs
• What is the mechaniom of immune hemolysis?
o C1,4,3 attach to sensitized RBCs
o C5,6,7,8 attach to those, signaling intravascular hemolysis
• How does complement activation occur in hemolysis (up to C1s)?
o 6 C1q subunits, 2 bind Fc of Ab to activate C’
o 1) Pentameric IgM bind Ags on cell surface, adopt “staple” form; C1q binds IgM
o OR 2) IgG bind Ags, C1q binds at least 2 IgG
o BOTH: binding of 2 C1q subunits to Ig activates C1r, cleaves and activates serine protease C1s
o IgM only requires 1 molecule, so may be better at fixing C’ and causing hemolysis
• What is the final course of C’ activation?
o C5b + C6 + C7 = complex, binds surface, basis to form membrane attack complex, binds to C8 + C9
o MAC=pore (causes lysis); C8 damages membrane, C9 polymerizes to form pore
• What is the fate of intravascular Hb after incompatible transfusion? Ssx?
o Hb Peaks in plasma at 6 hrs, after all Hpt used up
o Hpt drops to zero in first 2 hrs (bc binds all Hb, takes to liver)
o Urine Hb and serum also peak ~6 hrs, but lower levels
o All falls back to zero by 24 hrs
o Red/brown urine sign of EXTRAVASCULAR RBC destruction
o Jaundice also important sign of hemolysis
• How is ABO blood type testing done?
o Forward grouping: pt RBC added to reagent a-A and a-B antisera
o Reverse grouping: pt serum added to reagent A and B cells
o Crossmatching: last step before transfusion. Mix donor RBC w recipient plasma and test for rxn
• What are the levels of agglutination of RBCs?
o Graded on a scale of 1-4
o Negative reaction, no clumps
o +2: dispersed clumps
o +4: strongly positive, all RBCs in a single clump, can’t “de-glutinate”
• What happens if each blood type is added to a-A serum?
o A: agglutinates
o B: no rxn
o AB: agglutinates
o O: no rxn
• What happens if each blood type is added to a-B serum?
o A: no rxn
o B: agglutinates
o AB: agglutinates
o O: no rxn
• Method? Blood type? Reagent a-A binds pt RBCs, but not a-B:
o Forward grouping
o Type A
