Haematology Flashcards
red cell structure and function:
haemaglobin breakdown
broken into haem and globin
haem becomes bilinogen and excreted in faeces/urine
globin becomes aa
the iron from haem gets transported via transferrin and stored in bone marrow/recycled
haemophillia A
deficiency of F8
haemophillia B
deficiency of F9
universal recipient
AB+ (cos it has the antigen of everything)
universal donor
O- (cos it does not have the antigen of anything)
O type RBCS
universal donor for giving cells
AB type plasma
universal donor for giving serum- in an emergency if need to give plasma, give AB plasma
AB type blood
universal recipient
What happens when antibodies meet the antigen?
IgM antibodies fix complement -> permeabilises RBC membrane -> intravascular haemolysis.
ABO blood system
Body naturally makes antibodies against antigens it doesn’t have
Antibodies are type IgM
A, B, O antigen is an oligosaccharide (sugar)
Anti A, B, O antibodies cant cross the placenta
Rhesus blood system
Body doesn’t naturally make antibodies against antigen it doesn’t have- must need exposure eg a wrong transfusion-befor body makes antibodies
Antibodies are type IgG
D antigen is a PROTEIN
Anti-D antibody can cross the placenta and cause HDN
blood grouping:
forward group
- pt’s red cells are tested with antibodies.
* If pt has either A, B or D antigen, the antibodies will bind to the antigens –causing agglutination
blood grouping:
In the Backward group:
- Mix pts serum with A, B and AB cells
* If pt has either A antibody, B antibody or both, it will bind to the A, B or AB cells and cause agglutination.
Indications for Red cell transfusion
If pts haemoglobin level was less than 70 g
But if no symptoms then u might not need transfuion
70-100 appropriate with ongoing blood loss
100- unlikely to be appropriate
FFP
contains all coagulation factors
when to give platelet transfusion
u normally want platelet count mroe than 50
so if less than that, give platelet transufison
wat bac contamination common for blood transfusion
gram neg organism- yersinia enterocolita
wat do we screen for in blood?
Syphilis antibodies Hepatitis B Surface Antigen Hepatitis C antibody HIV antibody HTLVI and II antibody HIV Nucleic acid testing HCV Nucleic acid testing
indications for blood transfusion
acute major blood loss: surgery, post part
marrow problems: ALL, AML
haemoglobinopathies: thalassaemia major
chronic disae; malignancy
direct coombs test
to detect antibodies already on cell
get pts cells (with antibodies on them) and add anti-human antibodies. everything sticks together
agglutination=positive result
indirect coombs test
to detect antibodies in recipeints serum
take pt’s serum (with antibodies in it) , add donor rbcs, add anti-human antibodies. if donors rbcs had the antigen, everything will agglutinate= positive result
conditions that cause a right shift:
increase in temperature, 2,3-DPG, or PCO2, H+
a decrease in pH
these conditions REDUCES haemoglobin’s affinity for oxy
hence need high PO2 for same O2 saturation
foetal hb and hb dissociation curve
Foetal haemoglobin (HbF) is left shifted compared to adult Hb. It is not sensitive to 2,3DPG (so can’t move the curve to the right).
haemophillia
X-linked recessive, women asymptomatic
haemathrosis, haemartoma,
prolonged aPTT
forming a platelet plug
platelets bind to collagen via glycoprotein IIa/Ia
vWF helps platelets bind to collagen (forms extra links bw platelet’s glycoprotein Ib and collagen)
activated platelets release granules like ADP and thromboxane A2 to call more platelets to come
PT tests for factors
7, 10, 5, 2, 1
PTT or aPTT test for factors
12, 11, 9, 8, 10, 5, 2, 1
thrombin time TT test for factor
1
Target INR in anticoagulation therapy
2-3
prolonged Prothrombin time (PT)
vitamin K deficiency
DIC
warfarin use
liver disease
prolonged aPTT
anticoagulation therapy, DIC, hemophilia, severe liver disease, lupus coagulant, factor inhibitors
inhbitors of coagulation cascade
Protein C
protein S
Antithrombin III
DIC
S&S – haemorrhage symptoms (stroke, bruising, haematuria, epistaxis), clotting symptoms (stroke, focal ischaemia
Coagulation times prolonged (PT, aPTT and thrombin)
Von Willebrand Factor (vWF)
Synthesised by endothelial cells
carrier for FVIII; without vWF, FVIII has a very short survival period in the blood
Von Willebrand’s Disease
Abnormal platelet adhesion, prolonged bleeding time.
Heavy periods
Hence detected more in females
Mildly prolonged aPTT.
factors dependent on vit K
2,7, 9, 10
