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ca 1 Flashcards

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1
Q

Haemolytic reactions is due to?
and describe haemolysis

A

incompatible blood transfusions
rupture of RBC leakage of their contents to extravascular or intravascular surface

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2
Q

haemolytic reactions can be x or y mediated

A

immune or non-immune mediated

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3
Q

immune haemolytic reactions is due to?

A

incompatibility between donor and patient products

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4
Q

non-immune haemolytic reactions are due to ?

A

thermal, osmotic or mechanical activity to RBC.

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5
Q

non-haemolytic reactions are due to?

A

accumulation of cytosines or patient leukocyte antibody reacting with donor leukocyte antigens on lymphocytes, granulite’s or platelets

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6
Q

what is dosage

A

when stronger expression of a gene

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7
Q

what BGS does dosage effect - Doesn’t affect?

A

MNS, Kidd and Duffy - don’t effect ABO

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8
Q

Example of dosage - effect

A

when anti-M is added to MN- 2+ but MM-3+
#Greater antigen-antibody response

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9
Q

A antigen - causes,? , is it naturally occurring
A gene encodes for? function? - products
extra serum activity occurs

A

immune response
Yes [naturally/expected]
N-acetylgalactosaminyl transferase- transfers N-acetylgalactomine to H precursor - H antigens and A antigens
A1 cells = used for reverse group as Group A2 & A2B can make anti-A1 - extra serum reactivity

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10
Q

B gene encodes for ?

A

D-galactosyltransferase
transfers D-galactose to H PS

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11
Q

LISS- principle
limitation

A

reduces ions as they cause cloudy effect allows antibody to detect antigen more easily
if ion strength is too low - complement will bind and coat - false positive

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12
Q

Enzyme technique enhances.?
enzymes used.?
mechanism of this technique
benefit of enzyme technique
Limitation

A

detection of IgG antibodies especially Rh ab
papain, bromelin, ficin, trypsin
strips negatively charged ions from surface of RBC- reduces zeta potential- reduces steric hinderances- proteins adjacent - antigens -antibodies have greater access
allows IgG to spam distance + agglutination occurs
B- Rapid method - identifies antibodies when mixture - denatures some anti-c and anti-fya [MNS & Duffy]
damages some antibody’s - can’t use by itself

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13
Q

List controls used for ABO grouping

A
  1. Reverse grouping - O, A, B, known cells = mixed with serum should match forward grouping result. If group A FG - positive for anti-A RG positive with B cells as has antigen against them
  2. Known cells should be tested against known anti-sera i.e., Anti-A reacting with A cells.
  3. Rh control- should always be negative has everything anti-D reagent does except D antibodies
  4. IgM monoclonal anti-D carried out in duplicate as if true D positive must react with both - directed against different epitopes
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14
Q

ABO is the most - BGS. Naturally occurring antigens are present on -. Antigens in this blood group are - - -.
The presence of the gene determines x
For every missing antigen there will be.
O gene is known as x because?

A

significant
RBC surface
A, B, O antigens
the Antigen
the corresponding antibody
amorph as its product does not produce a trait

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15
Q

what are 2 types of antiglobulin test
Principle of antiglobulin reagent

A

DAT & IAT
antibodies are gamma globulins, so an antibody directed against gamma globulins is added and helps form bridges between IgG antibodies and other antigens

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16
Q

DAT principle - what does it detect

A

RBCS + Coombs reagent = added- detects antibodies on cell surface - autoimmune antibodies and alloimmune haemolysis
can detect compliment

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17
Q

List Risk assessment 4 major categories
List 5 interior categories

A
  1. Biological Hazards
  2. Chemical Hazards
  3. Physical Hazards
  4. Electrical Hazards
    Interior categories
  5. Hazard identification - blood, reagents, chemicals, centrifuge
  6. Control measure - PPE + correct handling and disposing, maintaining centrifuge correctly, safety locks - clean up spills
  7. Risk assessment- blood is screened for disease - not 100% sure no disease in it like HIV- anti-D may have components from cell line - not 100% sure = removed
    Chemicals like Na alzide .1% - explosive if comes in contact with lead + plumbing
    - electrical fault
    spillage, aerosols, uncapped tubes -contaminated residues in centrifuge
  8. Category - low
  9. Person InCharge- lecturer/ lab technician
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18
Q

frequency is expressed as.?

A

% For particular trait

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19
Q

Clinical significance Kell BGS💕
Kell antigens are very x
list 5 antigens and describe likely hood of antibody production against them
What immunoglobulin group do they have
Reactive in x and therefore can?
Disease’s it can cause
it most common phenotype is
3rd most x

A

very immunogenic
Anti-Kp^a Js^a - rare because these antigens are uncommon
Anti (antibodies)-k, Kp^b Js^b - rare because antigens are so common
IgG
antiglobulin test
can bind complement
K-k+
HTR HDN
polymorphic diff forms - genetic variation

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20
Q

Example of enzyme technique

A

Patient plasma mixed with 1, 2, 3 screen cells - 2+, 3+, 1+ antibody detected
Pos control - 2+, 2+ , N/A
Neg control - N/A, N/A, 2+

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21
Q

Rh BGS
how much antigens -how much do the work
they are x proteins
Rh complex is made of x and y & z
compare Rh D and CE x4

A

50 antigens
5 do work - C, c, E, e, D.
transmembrane proteins
RhD, RhCE & glycoproteins
share 97% identity
hydrophobic
not glycosylated
function unknown - shares homology with ammonia transporter

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22
Q

Define weak D antigen
weak-D testing required

A

has D antigen - just fewer + weaker phenotype
Donor ensures truly negative - Rh negative patients can’t get blood Rh pos
Anetal testing - pregnant women don’t get anti D unnecessarily (prevents mother from making antibody D when Rh negative against child RBC)
Recipient - ensure truly negative prevent Rh neg blood # waste

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23
Q

Define Partial D
most significant?
testing done

A

Missing some epitopes of D ag
D^VI missing most epitopes
Donor - if has partial D typed as positive recp. won’t make ab
Recipient - negative will make ab - missing its epitopes on donor RBC

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24
Q

Discrepancy - Leukaemia used to be RhD - don’t produce N-acetylgalactosaminyl transferase

A

weak forward reaction - A antigen is not produced- 1+, 2+
reverse group B cells fewer reaction- less antibodies - fighting cancer cells/necrosis

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25
identify discrepancy Elderly patient - low antibody titre
low reverse group age increases antibodies present decreases with age
26
RhD controls
3 tubes = control 1= patient sample tube 1 - patient cells and anti-D 2= Rh control + patient cells - ensures patient is not reacting with anything but D components NEG=VLR 3. Neg control - known weak-D cells + saline - NEG=VLR 4. Pos control- known weak D cells and anti-D ensures anti-D can detect even weak D antigen
27
True weak D result should be? If less than this?
2+ or more mixed field agglutination - if Rh- patient got Rh+ blood - patient history
28
Application of antiglobulin testing
- routine pretransfusion testing - in-vivo sensitisation
29
2 examples of antiglobulin
Poly specific- directed against complement + human globulins - anti-C Monospecific - direct against human globulin- anti-IgG
30
MNS antigen are x and called sensitive to? similarity/ diff. M N & S s M N are ? molecules ? phenotype + genotype if cell don't react with anti-M but react with anti-N
glycoproteins called glycophorins cleavage by protease S s = fewer copies + smaller MN - extracellular segment of transmembrane molecules M-N+ NN
31
Anti-M Anti-N facts-5 can it be clinically significant
M - frequently occurs 1. saline agglutinin RT/below 2. don't bind complement 3. don't react with enzyme treated cells 4.ususally IgM yes - has implicated HDN - rarely implicated HTR
32
Anti-N is x reactive how common, compliment, enzyme treated cells, immunoglobulin class, is it clinically significant + why
cold reactive, rare, doesn't activate complement, doesn't react with enzyme treated cells, IgG, only if it reacts at 37 degrees
33
Anti-S + Anti-s common? temp? occur after? clinically significant?
uncommon, react at 37 degrees, red cell stimulation, yes -HDN, HTR- IgG
34
where are I antigens found, what biomolecule are they + associated with? x encodes i antigen x = PS of y when is I developed I =common? immunoglobulin class + temp. how to overcome autoantibody x2
cell membrane carbohydrates associated with glycoproteins and glycosphingolipids glycosyltransferase encodes i antigen i = PS of I common autoantibody - attack own antigens cold reactive IgG overcome by heating cell + serum - 37C Cord blood - don't display I antigen - result indicates I present
35
Serological Characteristics of Duffy BGS what biomolecule = they, found where immunogenicity? role? antigens? how common are antibodies against above, clinically significant? react at + in? complement? immunoglobin class, enzyme detected
glycoproteins - transmembrane proteins, not immunogenic, chemokine receptors, Fya Fyb, - antibodies = infrequent, clinically sign (associated with HTR HDN), optimally - IgG bind complement - dosage 0 not detected by enzyme technique
36
Test done on donor blood before issued to hospital
ABO grouping Rh testing - negative - weak D + Partial D, screened for disease
37
Prevention of HDFN
- Rh D testing - early in pregnancy - if neg - test for weak D - if neg anti-D injections prevent mother's antibodies attack foetus RBC
38
what are antigens in Kidd BGS ab found when? which results with? after x which can result in? immunogenicity? why? ? biomolecule = they r they found? function? antibodies = x mediated class, enzyme, disease? complement
Jk a + b usually with other antibodies- strong anamnestic response (after several pregnancies or transfusion) - very severe delayed HTR not v. immunogenic effected by dosage glycoproteins - cell membrane urea transporters - on red cell membrane + endothelial cells of vasa recta in kidney immune mediated IgG, enzyme detected (enhanced), HTR, HDN, bind complement Jk (a-b-) = rare
39
Compare IgG -IgM
IgM- pentamer-10 binding sites- formed first in immune response-cannot cross placenta - blood lymph IgG- monomer - smaller-2 binding sites- formed later in immune response - can cross placenta -all body fluids
40
Applications of DAT x4 detects ?
1. HDN- detects sensitising infant cell with maternal antibody 2. HTR - sensitizing of IgG or complement on donor cells in patient 3. Autoimmune haemolytic anaemia - autoantibody or complement coating patient cells 4. Drug related haemolytic anaemia in-vivo sensitisation - coating by IgG or C3
41
what reason for positive cross match when negative antibody screen
unexpected antibody
42
monoclonal antibodies
directed against specific epitopes on antibody - made from homogenous B cell - large amounts from cell culture detect antigens on cancer cells
43
polyclonal antibodies
mixture of antibodies directed against different epitopes humans usually have these D - Da Db Dc Dd
44
purpose of antibody screen
detects presence or absence unexpected RBC antibodies result - antibody detected or no-antibody detected
45
when is antibody detected usually reagents / procedures
after blood transfusions or 1st pregnancy known screen cells with patient cells (incubated with O cells)
46
Reasons for false negative x5
1. weak-IgG test with known weak anti-D cells 2. improper washing - unbound antibodies mop up Coombs reagent it can't bind (C) to AHG - negative results means was positive 3. improper centrifugation - not going to agglutinate regardless 4. if AHG not working correctly - bridges will form with IgG ab for agglutination 5. number of RBC effects if too low - no agglutination
47
False Positive x4
1. RBC agglutinated before test 2. dirty glassware 3. contaminated saline 4. over centrifugation
48
IAT detects? application x3
in vitro-sensitization - coating not complement 1. antibody screen 2. antigen typing 3. antibody identification
49
Gel agglutination what is spun for reverse and forward group explain the positive and negative result
forward g- RBC and anti-sera reverse g- patient serum and reagent cells - spun into gel Pos - Cell form agglutinate at top of gel don't pass through neg - pass through gel unimpeded form button at bottom
50
How is the ABO inherited they are? dominant explain. Alleles? Chromosome? comment on dominance of each allele? Production of ABO antigens = controlled by? where are they found. A B H code for? &? are their functions? H gene codes for?
autosomal codominant - each allele can be identified A, B, O alleles on chromosome 9 A-B codominant but O-amorph product doesn't produce a trait. production = controlled by H gene on 19 chromosome. enzymes -transferases transfer sugar to carbohydrate PS H - L-fuctosyltransferase transfers fucose to H precursor makes H antigen.
51
Role of complement - can cause
in-vivo RBC destruction if antibody can bind complement after incompatible blood transfusions
52
which blood groups can activate initial steps of complement
All except MNS and Rh
53
The complement system is a system of x which are involved found on x and y
greater or equal to 30 proteins on membrane and serum (proteins) involved in cell lysis + opsonisation - coating of foreign substance facilitate phagocytosis
54
complete antibodies - incomplete antibodies -
c- capable of agglutinating cells suspended in saline -IgM inc- attach cells but don't cause agglutination
55
which BGS can cause entire cascade
ABO, Lewis, Kidd
56
similarities between Duffy and ABO x3
1. can bind complement 2. clinically significance 3. react at 37 degrees
57
Differences between ABO and Duffy x5
1. ABO - IgM Duffy -IgG 2. ABO-full cascade Duffy- can't cause full cascade 3. ABO- naturally occurring Duffy- not naturally occurring 4. ABO - not related - HTR HDN Duffy is related to these 5. ABO -don't show dosage Duffy - show effect of dosage1`65
58
how to prepare 5% suspension 2% suspension 1% suspension
add 19 drops of saline and 1 drop packed RBC 4 drops saline 1 drop 5% 2 drops saline 1 drop 5%
59
Method for IAT
patient serum + screen cells (O) is incubated 2 drops of LISS = added 37 degress 15 minutes washed 3 times AHG = added centrifuged results - observed
60
how to antibody's come about
B lymphocytes differentiate to plasma cells and secrete antibody
61
what's cellular immunity
immune response mediated by cells
62
Different classes of immunoglobulins differ by? x3
molecular weight - heavy chains - carbohydrate concentration
63
Lewis BGS list the antigens what biomolecule are they how is the phenotype acquired they are indirect gene products from action of x x influenced by x and y 2 genes are? b+ occurs when x and y occur a+ happens Le(a-b+) most common in? antibodies are only produced by? are they associated with HDN are they common can they bind complement what temp?
a and b carbohydrates - associated with glycosphingolipids and glycoproteins absorption of Lewis substance from environment Le le secretion and presence of le le Le secretor and Le Le but not secretor whites Le a- b- no very common no optimally
64
What antigens are found in the P1PK system, how are they formed- most common antigen
P1 & Pk addition of sugar residues to glycosphingolipids P1
65
Give name and class of the antibody in P1Pk BGS what temperature does it react, is it associated with HDN
Anti-P1 IgM- 4 degrees Celsius - not associated with HDN
66
Xga is the only antigen found where?
on X chromosome
67
is Fy (a+b-) heterozygous or homozygous
homozygous as does not contain b----negative but does contain a [+]
68
what are the BGS that display dosage therefore must show?
MNS, Duffy, Kidd, Rh - must show homozygous when picking cells to use for antibody identification testing- ensure don't miss low concentration antigen duffy t'he' monkey and all Kids like MNS

blood trans semester 1 (2 decks)

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