transfusion Flashcards

1
Q
ABO blood group
antigens - what class of molecules?
A
carbs. 
antibodies naturally occuring
predominantly IgM. 
clinically significant - bind complement (membrane attack complex formes) 
cause intravascular hemolysis
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2
Q

intravascular hemolysis

A

agglutination & complement fixation = membrane attack to destroy rbc.

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3
Q

rh blood group

A

Antigen = protein
d-type most immunogenic.
Ab = not naturally occuring. primary and secondary response needed.
IgG
clinically significant. extravascular hemolysis

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4
Q

extravascular hemolysis

A

destroy rbc by macrophage englufing.

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5
Q

other clinically significant blood groups

A
kell
kidd
MNS
duffy
- IgG, react at body temp, cause extravascular hemolyssis
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6
Q

clinically insignificant blood groups

A

lewis
P
MNS
react at low temp, IgM. no hemolysis

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7
Q

type and screen

A

ABO RH screen - type the blood. then check antibodies for RH, Kell, Kidd, MNS, Duffy
* screen only valid for 3 days because Ab may have formed.

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8
Q
acute hemolytic transfusion reaction
- what blood groups?
effects?
cause?
symptoms?
A

immediate
anti-A/B Ab present in pateint plasma bind donor cells - fix complement = IVH
cause: mis-ID when collecting, infusing.
symptoms = fever, chills, hemoglobinuriea, decrease bp, renal failure.

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9
Q

indicators of IVH

A
  • increase plasma Hb
  • decrease haptoglobin (binds free Hb)
    increase lactate dehydrogenase (comes from inside of lysed rbc)
    hemoglobinuriea
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10
Q

delayed hemolytic transfusion reaction
-what blood groups
symptoms

A

delayed.
Ab formed removed in spleen (EVH)
rh, kell, kidd, duffy
symptoms: fever, chill, jaundice (due to bilirubin increase from rbc breakdown)

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11
Q

indicators of EVH

A
increase bilirubin
decrease Hb
increase lactate dehydrogenase
positivity antibody screen
positive direct antiglobulin test = detect antibody coating rbc
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12
Q

immune response in IgG vs IgM

A

IgG = larger secondary response than IgG primary and IgM secondary.

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13
Q

hemolytic disease of fetus and newborn

A

maternal rbc cross placenta and attach to fetal cells causing hemolysis.
- anemia & erythropoiesis
mild to severe.
first pregnancy unaffected. Rh (-) mom delivering Rh (+) baby.

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14
Q

HDFN - in utero
severe case
treatment

A

severe case - profound anemia, hepatosplenomegaly (increase size of liver & spleen because removing coated red cells
hypoproteinemia - less proein because liver focusing on making new rbc’s
cardiovascular failure - enlarged heart
hydrops fetalis - severe edema

treat: intrauterine transfusion (IUT) - transfuse blood that has antigens negative to moms blood into umbilical cord.

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15
Q

HDFN - post partum

A

severe cases: anemia, hyperbilirubinemia, hemolysis
treatment: exchange transfucion (swap 5 mL with “good blood” slowly exchange all the blood.
prevention - screen pregnant women for RBC antibodies. Rh (-) greatest risk. Rh Ig (anti-d) if mother delivers positive baby. high dose will quickly bind to any D+ cells from baby, remove before immune system can react.

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16
Q

RhIg

A

human source anti-D. given to mother intravenously to attach to fetal cells in her blood. cleared before immune system recognizes and reacts - no memory cells made.