Lecture 1-3, 6 Flashcards Preview

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What is Haematpoetic tissue
Where does haematopoetic tissue originate from?
-what is the process from birth to getting haematopoetic tissue?

-generating non-lymphoid cells of the blood
-bone marrow, spleen

Origins - yolk sac, liver, bone marrow
Childhood - bone marrow becomes replaced with fatty cells (these can be reversed into haematopoetic tissue)


What is the Bone marrow made up of? and how does this provide support

Trabeculae bone - fat and haematopoetic tissue
-stromal cells - fibroblasts, macrophages, fat cells, endothelial cells (diagram in book)
-provide support and physical environment
-has an extracellular matrix with adhesion molecules, blood cell growth factors


Where are Haematopoetic stem cells found?
=and what antigen is expressed and how is this relevant?
-what is responsible for regulation of haematopoiesis ?

Self renewing, small population in bone marrow
have cd34 on outside - can measure htis to test how many stem cells
umbilical cord has a large amount of these
-transcription factors and cytokines are responsible for development of haematopoiesis


Naturally occuring vs Immune stimuatled antibodies

Naturally occuring
-formed in absence of exposure to specific antigen (e.g ABO)
-bacteria have similar antigens to AB system so babies will make antibodies against these antigens
-usually glycolipid
-both igm, igg
-activates complement
-intravasuclar rbc destruction

Immune stimulated
-only stimulated when individual is exposde to antigens carrying red cell e.g need expsure to the foreign red cell to produce the antibody
-no complemetn activaiton
-extravascular destruction


How is the duffy blood system and genetics related to maleria?

the duffy antigen acts as an entry poitn of material parastis into red blood cells
-Caucasians dont often have this phenotype, however is common in black ethnic background


Protein vs glycolipid determinants of antigen

Glycoproteins and glycolipids are present on the surface of red blood cells (geneitcally determind)

Protein determinants - genes code for anitgenic determinants itself - rh, kell, kidd, duffy

Glycolipid determinants - genes code for production of enzymes that add or remove carbs or lipids, ABO, lewis group


ABO group system

-antigens found not just on rbcs
-phenotype is determind by a series of glycosyltransferase enzymes - these are responsible for addition of CHO molecules to basic membrane stucture
-H antigen is the standard (O)- no molecules added
-If molecules are added either A or B type
-2 genes from parents to determine what you are
-you will make antibody against the antigen you do not have on your blood cell


Rh group system

-only on rbcs
-only following immune stimulation
-RHd + or -
-most D+ because this is dominant inheritance pattern (Dd = D+)
-if a RD- person gets a transfusion that is RD+ then will make anti D antibody against this- and this can destroy rbcs
3 minor allelic pairs (not so worreid about)


Agglutination techniques

-Red blood cells are negatively charged
-igM is big - can attract red blood cells and cause agglutination
-igG are small and not large enough to cause agglutination
-only get agglutination if igG antibody on outside of cell with igG antibody
-With ABO - if put a cells in anti a, then get agglutination becuase antibody against a antigen will cause agglutination , same for B


Haemolytic disease of newborns

occurs when a RH negative mother has an RH positive baby, when this blood gets transfered to mother, the mother will make anti D antibody which will then be transfered back to the baby and damage the rbcs (igG antibody)
-causes - stillbirth, or born with braindamage due to jaundice
-can do immunoprophylaxis - which will give mother injeciton of Anti-d immunoglobulin and this will passively protect the mother w anti-d and will lead to clearance of the red blood cells of baby and prevent the primary response form occurign
-also given after a sensitizing event e.g abortion, termination, amnioscentesis
-rarely cause by ABO becasue not often much of these antigens expressed in new borns (develops after bacterial exposure)


Blood product
Blood component
Plasma derivative

component - blood product manufactured from a signle donation into multiple donations e.g red cells, platelets
Plasma derivative - blood product manufactured from a large pool of plasma donations


Maintaining a safe blood supply

-use of voluntary donors
-exclude donors of risky behaviour (increase risk of blood borne infection)
-testing of donors for major blood borne viruses
-physical and chemical methods to destory pathoges present


Intravascular haemolytic reaction

-Due to ABO incompatibility and relate to human error
-the antibody made agaisnt anitgen is caple of activating complemetn cascade
-renal failure
-symptoms - patints feels unwell, fever, pallor, seating, loin pain, hypotenison

-microvascular bleeding due to intravascular coagulation
-vasoconstrction leading to renal failure and ishcaemic problems

-treatment- fluids to maintain blood pressure and adequate urin output


Extravascular haemolysis

presence of igG antibody against an antigen on rebc
- completment activation does not normally occur

-clinically same symtposm as intravascular


delayed reaction

transfusion successful, then haemoglobin falls and antibody starts to increase


febrile non haemolytic transfusion reaction

temp increase straight after transfusion
-when foreign white cells enter the body and cause fever


transfusion related acute lung injury

onset after about 6 hours
-donor plasma contains white cell antibodies, and this leads to agglutination and sequestration of recipient neutrophils in pulmonary vasculature
-this requires the donor antibody to recognise HLA/neutrophil "specific antigen" in recipient

-donor antibody goes into the patient, and coats the patients white cells, and then this agglutinates in the lungs