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blood trans semester 1 > ca 1 > Flashcards

ca 1 Flashcards

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
Q

identify discrepancy Elderly patient - low antibody titre

A

low reverse group age increases antibodies present decreases with age

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26
Q

RhD controls

A

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

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27
Q

True weak D result should be?
If less than this?

A

2+ or more
mixed field agglutination - if Rh- patient got Rh+ blood - patient history

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28
Q

Application of antiglobulin testing

A
  • routine pretransfusion testing
  • in-vivo sensitisation
29
Q

2 examples of antiglobulin

A

Poly specific- directed against complement + human globulins - anti-C
Monospecific - direct against human globulin- anti-IgG

30
Q

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

A

glycoproteins called glycophorins
cleavage by protease
S s = fewer copies + smaller
MN - extracellular segment of transmembrane molecules
M-N+
NN

31
Q

Anti-M Anti-N facts-5 can it be clinically significant

A

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
Q

Anti-N is x reactive how common, compliment, enzyme treated cells, immunoglobulin class, is it clinically significant + why

A

cold reactive, rare, doesn’t activate complement, doesn’t react with enzyme treated cells, IgG, only if it reacts at 37 degrees

33
Q

Anti-S + Anti-s common? temp? occur after? clinically significant?

A

uncommon, react at 37 degrees, red cell stimulation, yes -HDN, HTR- IgG

34
Q

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

A

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
Q

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

A

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
Q

Test done on donor blood before issued to hospital

A

ABO grouping Rh testing - negative - weak D + Partial D, screened for disease

37
Q

Prevention of HDFN

A
  • 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
Q

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

A

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
Q

Compare IgG -IgM

A

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
Q

Applications of DAT x4
detects ?

A
  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
Q

what reason for positive cross match when negative antibody screen

A

unexpected antibody

42
Q

monoclonal antibodies

A

directed against specific epitopes on antibody - made from homogenous B cell - large amounts from cell culture detect antigens on cancer cells

43
Q

polyclonal antibodies

A

mixture of antibodies directed against different epitopes humans usually have these D - Da Db Dc Dd

44
Q

purpose of antibody screen

A

detects presence or absence unexpected RBC antibodies
result - antibody detected or no-antibody detected

45
Q

when is antibody detected usually
reagents / procedures

A

after blood transfusions or 1st pregnancy
known screen cells with patient cells (incubated with O cells)

46
Q

Reasons for false negative x5

A
  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
Q

False Positive x4

A
  1. RBC agglutinated before test
  2. dirty glassware
  3. contaminated saline
  4. over centrifugation
48
Q

IAT detects? application x3

A

in vitro-sensitization - coating not complement
1. antibody screen
2. antigen typing
3. antibody identification

49
Q

Gel agglutination
what is spun for reverse and forward group explain the positive and negative result

A

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
Q

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?

A

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
Q

Role of complement - can cause

A

in-vivo RBC destruction if antibody can bind complement after incompatible blood transfusions

52
Q

which blood groups can activate initial steps of complement

A

All except MNS and Rh

53
Q

The complement system is a system of x which are involved found on x and y

A

greater or equal to 30 proteins on membrane and serum (proteins)
involved in cell lysis + opsonisation - coating of foreign substance facilitate phagocytosis

54
Q

complete antibodies -
incomplete antibodies -

A

c- capable of agglutinating cells suspended in saline -IgM
inc- attach cells but don’t cause agglutination

55
Q

which BGS can cause entire cascade

A

ABO, Lewis, Kidd

56
Q

similarities between Duffy and ABO x3

A
  1. can bind complement
  2. clinically significance
  3. react at 37 degrees
57
Q

Differences between ABO and Duffy x5

A
  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
Q

how to prepare 5% suspension
2% suspension
1% suspension

A

add 19 drops of saline and 1 drop packed RBC
4 drops saline 1 drop 5%
2 drops saline 1 drop 5%

59
Q

Method for IAT

A

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
Q

how to antibody’s come about

A

B lymphocytes differentiate to plasma cells and secrete antibody

61
Q

what’s cellular immunity

A

immune response mediated by cells

62
Q

Different classes of immunoglobulins differ by? x3

A

molecular weight - heavy chains - carbohydrate concentration

63
Q

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

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
Q

What antigens are found in the P1PK system, how are they formed- most common antigen

A

P1 & Pk
addition of sugar residues to glycosphingolipids P1

65
Q

Give name and class of the antibody in P1Pk BGS what temperature does it react, is it associated with HDN

A

Anti-P1 IgM- 4 degrees Celsius - not associated with HDN

66
Q

Xga is the only antigen found where?

A

on X chromosome

67
Q

is Fy (a+b-) heterozygous or homozygous

A

homozygous as does not contain b—-negative but does contain a [+]

68
Q

what are the BGS that display dosage therefore must show?

A

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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