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Flashcards in Tranfusion medicine Deck (69)
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1

What kind of antibodies are the antibodies aagainst the ABO blood groups?

IgM

2

How does IgM bound to ABO to cause hemolysis within seconds?

triggers the complement cascade - phagocytic cells - coagulation from free hgb - systemic inflammation and scavenger NO

(intravascular hemolysis)
can kill you

3

How is the IgM activity different from IgG bound to blood cells?

doesn't trigger complement cascade, but will stay on the RBC until it gets to the spleen hwich will then take it out. NO systemmic reaction and it won't kill them.

(extravascular hemolysis)

4

Where else in the body are the ABO antigens?

on RBCs
on vascular endothelium
platelets
epithelial surfaces

soluble forms just floating in our blood, saliva, milk, urine, meconium, feces, etc.

5

What are some diseases we see from ABO incompatibility?

hemolytic transfusion reactions

solid organ transplantation (hyperactue rejection)

mild hemolytic disease of fetus and newborn (this is Igm antibodies and very few will get through the placenta, so it's not as severe)

6

What is the most common presenting symptom of an ABO incompatible RBC transfusion?

fever

7

What are some other symptoms?

feeling of dread
flushing
pain at infusion site
low back and flank pain
chest abd pain
n/v
shock
SOB, hyperventilation, cyanosis

8

THere are multiple antigens in the Rh group, what is the most important one?

D antigen

9

Why do we care about the Rh group?

it's the most immunogenic blood group outside of ABO

10

What kind of antibodies do we have against D?

IgG

note - can only happen after a previous exposure

11

WHy do Rh antibodies cause a more severe hemolytic disease of the newmorn than the ABO antibodies?

This is IgG instead of IgM, so it's all going through the placenta.

12

How do you track hemolysis in a fetus?

dopplers of the middle cerebral artery (higher flow suggests anemia)

used to need to use a Liley curve to track bilirubin in the amniotic fluid by gestational age

13

What do you do for treatment of these babies?

intrauterine transfusions

14

What does "weak D" mean?

there are lower levels of D antigen on the surface of RBC (normal antigen, but not highly expressed)

low enough levels that when we test the patient, we can't tell in all cases. So we might call them D negative, which can be dangerous

15

What does "partial D" mean?

there are mutations in the antigen structure, so some will be missed because our lab test may use a monoclonal antibody against part of the normal antigen they don't have

so these people will also be called D negative

16

Why is this an issue particularly for the partial D patients?

They are called D negative, which they sort of are because their D might be different enough from normal D that if they did receive D+ blood they could develop an antibody against it

17

Do we actually know that rhogam won't work after 72 hours?

nope - prison story

so just give it even if it's late

18

How many antigens in the Kell system?

24

19

Why is Kell important?

1. it will cause immediate or delayed hemolysis
2. Kell alloantibodies are very hard to detect, so you wouldn't be concerned about it unless you did a special test or you saw a Kell- person received a Kell+transusion in the past

20

Most people are Kell ____

negative

21

Why is a pregnant mom getting Kell antibodies during pregnancy an even bigger deal than ABO and Rh?

Kell antigen is expressed on the placenta very early and causes suppression of erythropoiesis

22

The Mcleod phenotype (missing the XK protein that goes with the Kell on RBC membrane) is associated with what two diseases?

chronic granulomatous disease
Duchenne's

23

WHy is this important to think about for these patients?

they can't get regular blood - so they need their own stored for them

24

Why is the Kidd blood group system clinically significant?

it's famous for disappearing and reappearing and can cause a roaring delayed hemolytic transfusion with amnestic response leading to intravascular hemolysis

25

Duffy is a six antigen system that causes a problem in what patient population?

Sickle cell patients; because duffy antigen is the receptor for plasmodium vivax. So basically all caucasians are duffy positive and african americans (especially sicklers) are mostly negative

and caucasians tend to give blood more often

26

WHat is the P-antigen group?

it's the receptor for parvovirus B19

27

After a viral illness, kids in general can develop an autoantibody against he P-antigen and develop what?

paroxysmal cold hemoglobinuria

(antibody binds in the extremities and then activate complement and hemolysis when they reach the warm body core)

28

How do you test for paroxysmal cold hemoglobinuria?

the Donath-Landsteiner test

basically intubate three tubes at different temperatures and positive test has lysis at 37 C

29

How does paroxysmal cold hemoglobinuria present?

rarely paroxysmal, precipitated by cold and it's not necessarily hemoglobinuric

kids usually presenting with an acute anemia following viral infection

30

How does the I and i work on RBCs - how do we all have both?

i is the long carbohydrate on young RBCs

as the RBC matures, the carbohydrate folds and it becomes I