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SBL exam 2 - MY > DSA- Transfusion Medicine (martin) > Flashcards

DSA- Transfusion Medicine (martin) Flashcards

1
Q

RBC membrane contains:

A

proteins - Rhesus (Rh) system
carbs- ABO system

**note: there are >400 RBC blood group antigens

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2
Q

what are the mechanisms of immunization to RBC antigens?

A

primary and secondary (amnestic) response

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3
Q

primary response vs secondary response

A

primary- seen after first immune exposure to foreign protein Ag (days or weeks after exposure)

secondary- seen upon REPEAT exposure to foreign protein Ag (noticed much quicker)

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4
Q

typical primary response for most blood group antigens:

A

sustained HIGH [IgM]

some formation of IgG

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5
Q

typical secondary response for most blood group antigens:

A

sustained HIGH [IgG]

transient rise in IgM

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6
Q

ABO system components

A

3 antigens expressed: H, A, B

terminal sugar units

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7
Q

“O” blood type

A

H Ag only

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8
Q

A blood type

A

H+ A

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9
Q

B blood type

A

H+B

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10
Q

AB blood type

A

H+ (A+B)

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11
Q

describe a secretor

A

someone who is capable of making ABO antigens in their secretions and plasma

  • about 80% population carries at least one allele called “Se” –> encodes enzyme that allows that individual to make the H antigen on long carbohydrate-rich chains (type 1 chains) which are found in secretions and plasma
  • once H antigen is made: then person can make either A or b antigens (or both) on type 1 chains
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12
Q

naturally occurring antibodies seen in serum of each group

A

O –> anti-A, anti-B, anti-A,B
A–> anti-B
B–> anti-A
AB–> none

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13
Q

What can cause compatibility issues when transfusing a patient?

A

subtypes (ex. A is subdivide into A1 and A2)

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14
Q

leukemia can alter expression of ABO Ag, how?

A

decrease Ag on individual RBCs

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15
Q

how can you get “Acquired B” ag

A

intestinal obstruction–> increases bowel permeability, leading to bacterial polysaccharides into circulation being absorbed by grp A cells

bacterial enzymes will remove some of the acetyl groups from the A Ag–> produces B specific sugar

Mariya’s interpretation: so basically you have a person that has blood group A get infected by bacteria that will then get into their blood which will cause the person to react to B weakly also (since that person is acquiring the group B enzymes of galactose)

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16
Q

What is the Bombay phenotype

A

absence of H Ag (Oh; h/h) which is typically found on virtually all RBCs and is the building block for pdtion of antigens within the ABO blood group

Bombay: RBC has NO antigen
(anti-A, Anti-B, AntiA,B, and AntiH)

*anti-H IgM binds complement and lyses cells

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17
Q

what blood does a person with a bombay phenotype need to receive in a transfusion?

A

can ONLY receive Bombay blood

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18
Q

Which Ig is more common in someone w/ a Bombay phenotype

A

IgM > IgG

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19
Q

why is it impt to know if someone has the bombay phenotype?

A

bc of anti-H reactivity–> capable of hemolysis (can activate complement cascade which lyses RBCs while theyre still in circulation)–> intravascular hemolysis

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20
Q

Are there transfusion reactions in someone with bombay phenotype

A

YES- can cause an acute hemolytic transfusion rxn

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21
Q

What could arise in mothers with the Bombay phenotype?

A

Hemolytic Dz of the newborn(HDN) is possible

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22
Q

universal donor vs recipient

A 
donor = blood group O-
recipient = blood group AB+
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23
Q

Rh (rhesus) system most important antigens:

A

multiple antigens (2 genes- one for D and one for CcEe)

D- Rhesus factor/Ag
d= absence of D ): (he smol so he gone)
C= codominant w/ c (vice versa)
E= codominant w/ e (vice verse)

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24
Q

are antibodies naturally occurring in the rhesus system

A

NO (unlike ABO)

you need exposure to Ags in order to produce ABs (pregnancy or transfusion)

25
Q

indication for RhoGAM

A

used in preventing Rh immunization for pregnancy and other obstetric conditions in Rh- women unless baby father is conclusively Rh-

other usage:
transfusion of Rh+ blood to Rh neg individual
treatment of ITP

26
Q

when is RhoGAM contraindicated

A

in Rh+ individuals and in pts w/ known history of anaphylactic or severe systemic rxns to the administration of human immune globulin pdts

27
Q

why is RhoGAM risky?

A

products from human blood may carry risk of transmitting infectious agents (viruses, vCJD awhen usingnd CJD agent)

28
Q

What will yield positive serologic testing results after administration of Rho(D) immune globulin (rhogam)?

A

transitory increase of various passively transferred antibodies in pts blood

29
Q

what system ranks second in immunogenicity after D (Rh)

A

Kell system

30
Q

what are the most impt antigens and phenotypes in the kell system

A

Ags: K= Kell, k= Cellano

phenotypes observed: kk>Kk>KK

31
Q

are alloantibodies to K common

A

YES

IgG and rxn at 37C
–> HDN + hemolytic transfusion rxn

32
Q

what is more common in the Kell system: anti-K or anti-k

A

anti-K (since kk is the more common phenotype in caucasians and african americans)

33
Q

antigens involved in the Kidd system

A

Jk^a or Kidd (a)

Jk^b or Kidd (b)

both seen commonly, but low titer and weak avidity–> disappear rapidly

34
Q

what reactions are common with the Kidd system?

A

3/4 delayed hemolytic transfusion rxns (IgG)

activates complement–> rapid hemolysis due to synergistic activation of complement and cell-bound Ab

35
Q

during initial Ab screen and Xmatch what is seen with the Kidd antibodies?

A

antibodies disappear–> no Abs detected (but addition of complement enhances detection)

it reappears upon transfusion w/ Kidd + unit–> hemolytic rxn):

36
Q

in vitro, what do Kidd antibodies exhibit

A

DOSAGE phenomenon - cell w/ 2 copies of same gene (homoz) has a strong rxn than a cell w/ heterozygous genes on it

37
Q

antigens involved in the Duffy system

A

Fy^a or Duffy (a)

Fy^b or Duffy (b)

38
Q

Most common antigens among african-americans; what is it resistent to ?

A

Fy (a-,b-)

resistant to Plasmodium vivax infection

39
Q

what is the Ab of Duffy system and what is it associated w/ ?

A

Ab: IgG

associated w/ HDN and hemolytic transfusion rxns

40
Q

Most impt antigens of MNS system? antibody?

A

M+ N
S+ s

Ab: IgM (occasionally IgG)

41
Q

what makes the Ab of the MNS system stand out

A

non-hemolytic usually

also has dosage effect–> react more strongly w/ homozygous cell than heterozygous cell

42
Q

what Ab does the Lewis system use? Ags?

A

IgM (Warm Abs)

Le Ag= found in secretions and plasma, then Ag adsorbed onto RBC membrane; need secretor and Hh genes also

43
Q

most common complication of transfusion

A

FEBRILE NONHEMOLYTIC rxn (fever and chills, mild dyspnea) WITHIN 6 hours of transfusion of RBCs or platelets

caused by inflammatory mediators derived from donor leukos

RESPONDS to antipyretics + are short-lived

44
Q

the frequency of febrile nonhemolytic rxns varies with what?

A

increases- w/ storage age of product

decreases - by measures that limit donor leuko contamination

45
Q

allergic rxns from transfusion

A

potentially fatal when blood pdts containing Ags are given to previously SENSITIZED recipients

increased in ppl w/ IgA deficiency (IgG antibodies recognize IgA)

46
Q

Urticarial allergic rxns from transfusion

A

rxns triggered by presence of allergen in donated blood product that is recognized by IgE antibodies in the recipient

respond to ANTIHISTAMINES, do not require discontinuation of transfusion (most instances)

47
Q

What causes an acute hemolytic rxn

A

preformed IgM Abs against donor RBCs that fix complement–> rapidly induce complement mediated lysis, intravasc hemolysis and hemoglobinuria

from: error in pt identification or tube labeling
syx: fever, shaking chills, and flank pain; may rapidly progress to DIC, shock, acute renal failure, and death

+DIRECT COOMBS

48
Q

what causes delayed hemolytic rxns

A

ABs that recognize RBC ags that recipient was sensitized to previously (prior blood transfusion)

IgG Abs

+ DIRECT COOMBS and lab fxs of hemolysis

(Abs to Ags such as Rh, Kell, and Kidd often induce sufficient complement activation to cause severe and potentially fatal rxns)

49
Q

lab features of hemolysis

A

low haptoglobin

elevated LDH

50
Q

what cells are activated in Transfusion related acute lung injury (TRALI?

A

NEUTROPHILS

51
Q

how does TRALI happen?

A

severe, frequently fatal complication - factors in transfused blood (donor leukocyte antibodies) trigger activation of neutros in lung microvasculature; occur frequently in pts with preexisting lung dz

TWO hit hypothesis; 1) priming event 2) ABs in the transfused blood product that recognize Ags expressed on neutrophils

52
Q

mc antibodies associated w/ TRALI bind what? in whom?

A

MHC 1 antigens

these antibodies are especially found in MULTIPAROUS women

more likely occur w/ pdts containing high levels of donor ABs such as FFP and platelets

53
Q

clinical px of TRALI

A

sudden onset respiratory failure, during or soon after transfusion

diffuse bilateral pulm infiltrates that DO NOT response to diuretics (on chest imaging)

other: fever, hypotension, hypoxemia

54
Q

infectious complications of transfusions

A

most bacterial are of skin flora

much more common in platelet preps than RBC preps (bc platelet preps stored in room temp- favorable to bacterial growth)

syx: fever, chills, hypotension

55
Q

viral infections seen w/ transfusions

A

-dramatically decreased w/ advances but rarely cannot detect

  • HIV, hep C, hep B
  • West Nile Virus, Trypanosomes, babesia, and Zika virus
56
Q

Blood bank donation info:

A

16+ y/o; must meet weight and Hb level requirement

NOT IF:

  • traveling to certain countries
  • medical procedures: receipt of dura mater graft, transfusion of blood/blood components w/in previous 12 mo or human derived clotting factors
  • HIV+
  • hepatiitis since 11th bday
  • Babesiosis or Chagas dz (trypanosoma cruzi antibodies are tested)
  • needle usage for drugs (not prescirbed)
  • incarceration
  • piercing or tattoo using nonsterile materials w/in last 12 mo
  • pregnancy
  • CJD or vCJD risk factors
57
Q

how do you know that a patient has a true AB or just an acquired B making it seem like they have an AB blood type?

A

get a WEAK interaction with anti-B –> producing AB blood type

but know its not truly an AB bc when test the serum, you get a strong anti-B response–> showing its an A blood type

58
Q

how does gastric or pancreatic carcinoma alter expression of ABO ag

A

serum contains excessive bld grp specific soluble substances (BGSS) which neutralize antisera used in forward grouping

get neg rxns so everyone look like group O!!!

SBL exam 2 - MY (3 decks)

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