Lecture 1-3, 6 Flashcards

1
Q

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

A
  • 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)

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2
Q

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

A

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
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3
Q

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

A

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

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4
Q

Naturally occuring vs Immune stimuatled antibodies

A

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
  • glycoprotein
  • igG
  • no complemetn activaiton
  • extravascular destruction
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5
Q

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

A

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

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6
Q

Protein vs glycolipid determinants of antigen

A

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

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7
Q

ABO group system

A
  • 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
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8
Q

Rh group system

A

-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)

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9
Q

Agglutination techniques

A
  • 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
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10
Q

Haemolytic disease of newborns

A

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)
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11
Q

Blood product
Blood component
Plasma derivative

A

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

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12
Q

Maintaining a safe blood supply

A
  • 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
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13
Q

Intravascular haemolytic reaction

A
  • 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

Problems

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

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

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14
Q

Extravascular haemolysis

A

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

-clinically same symtposm as intravascular

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15
Q

delayed reaction

A

transfusion successful, then haemoglobin falls and antibody starts to increase

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16
Q

febrile non haemolytic transfusion reaction

A

temp increase straight after transfusion

-when foreign white cells enter the body and cause fever

17
Q

transfusion related acute lung injury

A

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