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Labs Medicine > Tranfusion medicine > Flashcards

Tranfusion medicine Flashcards

1
Q

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

A

IgM

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2
Q

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

A

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

(intravascular hemolysis)
can kill you

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3
Q

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

A

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)

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4
Q

Where else in the body are the ABO antigens?

A

on RBCs
on vascular endothelium
platelets
epithelial surfaces

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

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5
Q

What are some diseases we see from ABO incompatibility?

A

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)

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6
Q

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

A

fever

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7
Q

What are some other symptoms?

A 
feeling of dread
flushing
pain at infusion site
low back and flank pain
chest abd pain
n/v
shock
SOB, hyperventilation, cyanosis
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8
Q

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

A

D antigen

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9
Q

Why do we care about the Rh group?

A

it’s the most immunogenic blood group outside of ABO

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10
Q

What kind of antibodies do we have against D?

A

IgG

note - can only happen after a previous exposure

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11
Q

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

A

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

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12
Q

How do you track hemolysis in a fetus?

A

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

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13
Q

What do you do for treatment of these babies?

A

intrauterine transfusions

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14
Q

What does “weak D” mean?

A

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

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15
Q

What does “partial D” mean?

A

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

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16
Q

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

A

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

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17
Q

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

A

nope - prison story

so just give it even if it’s late

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18
Q

How many antigens in the Kell system?

A

24

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19
Q

Why is Kell important?

A
  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
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20
Q

Most people are Kell ____

A

negative

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21
Q

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

A

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

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22
Q

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

A

chronic granulomatous disease

Duchenne’s

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23
Q

WHy is this important to think about for these patients?

A

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

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24
Q

Why is the Kidd blood group system clinically significant?

A

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

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25
Q

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

A

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

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26
Q

WHat is the P-antigen group?

A

it’s the receptor for parvovirus B19

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27
Q

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

A

paroxysmal cold hemoglobinuria

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

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28
Q

How do you test for paroxysmal cold hemoglobinuria?

A

the Donath-Landsteiner test

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

29
Q

How does paroxysmal cold hemoglobinuria present?

A

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

kids usually presenting with an acute anemia following viral infection

30
Q

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

A

i is the long carbohydrate on young RBCs

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

31
Q

Anti-I antibodies are associtaed with what infection

A

mycoplasma in adults

32
Q

Anti-i is associated with what infection?

A

mono in kids

33
Q

“Type” determines what?

A

the ABO

34
Q

the “screen” determines what?

A

presence of antibodies against commonly clinically important RBC antigens (Kidd, Kell, Rh, etc.)

35
Q

What is “front type”?

A

you mix patient’s RBCs with anti-A and anti-B monoclonal antibodies and see if ti reacts

36
Q

What is the “back type”?

A

mix the patient’s PLASMA with known RBCs to see if it reacts

37
Q

Since anti-A and anti-B are IgM, how long will it take for agglutination to occur on these tests?

A

happens immediately

38
Q

What type of test is used for the screen?

A

indirect antiglobulin test

take plasma, add RBCs with known antibodies, add anti-human globulin (anti-Fc) or Coomb’s reagent

this will lead to agglutination if the plasma had antibodies against the RBCs that were added

39
Q

How long does a negative type and screen take?

A

30-60 min

40
Q

How long does a positive type and screen take?

A

1-4 hours or maybe more

41
Q

How long will a type and screen last (when would you need to repeat it)?

A

72 hrs

42
Q

What is the cross match?

A

Patient’s plasma with donor RBCs

just to check one more time that there aren’t antibodies that were missed

43
Q

What is the electronic cross match?

A

scan the blood batch and patient’s MRN and the computer will tell you if it’s compatible if they have no hx of unexpected antibodies and currently negative antibody screen

this means blood is ready immediately, but there still continues to be a small risk that patient may have an antibody against a rare antigen, which is why nurse needs to be in the room to watch for a reaction

44
Q

The direct antibody test looks for antibody directly bound to the surface of the RBC in vivo. So in this setting, what do we use the DAT for?

A

To diagnose a hemolytic reaction

order it especially in the ED when someone’s been dropping hemoglobin and they’re a little symptomatic with relatively recent hx of a transfusion

45
Q

What’s the volume of blood in a RBC unit?

A

250-350 ml with 200-250 ml or RBCs

46
Q

How much will hematocrit increase and hemoglobin increase after an RBC?

A

Hematocrit should increase 3%

Hemoglobin should increase 1%

47
Q

If that 3:1 ratio is off after a transfusion, what does that tell you?

A

volume status

48
Q

Wha is the transfusion indication for RBCs?

A

to correct anemia and increased O2 delivery

49
Q

Without co-morbidities, what hemoglobin is the cutoff for transfusion?

A

7

50
Q

If they do have co-morbidities, what hemoglobin is the cutoff?

A

you can still use the 7 or 8-10; depending on the study you look at

51
Q

What are some co-morbidities that you would want to use 8 as the cutoff?

A 
cardiac disease
tachycardia
respiratory failure
bone marrow failure
hematologic disease
cerebrovascular disease
52
Q

Neonates should get a transfusion with a hgb less than?

A

13 (although there’s really no data for this - we’re conservative with babies)

53
Q

People with cyanotic heart disease should get a transfusion with a hgb less than?

A

13

54
Q

WHat’s in FFP?

A

200-250 ml

400 mg of fibrinogen
1 unit/ml of all the coagulation factors

55
Q

Which factor in FFP has the shortest half life?

A

Factor 7; so if they have a coagulopathy, that FFP transfusion will start to not be enough within about 4 hrs because the 7 will degrade in vivo

56
Q

WHat’s the difference between FFP an FP24?

A

FFP must be frozen within 8 hrs

FP24 (plasma) is frozen within 24 hrs, containing less factor 5, factor 8, protein S and C

57
Q

What are the indications for FFP?

A

INR>1.8

PTT>45’’

58
Q

What shoudl the dosage of FFP be?

A

10-20 ml/kg

s 2 units should increase factor levels by 20-30% in a 70 kg person

59
Q

FFP can be used for emergent reversal of warfarin, but what should you use instead if time permits?

A

vitamin K

60
Q

What’s the universal plasma donor?

A

AB (no antibodies)

61
Q

A platelet unit from a single donor = __whole blood derived platelet unit.

A

6 (so consider this when you’re ordering)

62
Q

One single donor platelet unit should increase platelet count by how much?

A

25-40,000

63
Q

What platelet count is sufficient to maintain vascular integrity?

A

5,000/ul, but about 7000/ul are consumed each day to repair the microvasculature

you should be completely safe at 10,000 as long as they’re still making their own platelets

64
Q

So when do you transfuse platelets?

A 
<10K for normal patients
<20K with mucosal bleed
<50 for active bleeding, surgery 
<50K for infant under 1 mo
<100,000 for neuro or ophthalmologic surgery bc bleed would be devastating
65
Q

WHat does Cryoprecipitate contain?

A 
250 mg fibrinogen
vWF
Factor VIII
Factor XIII
Fibronectin
66
Q

WHat’s the indication for cryo?

A

mainly a fibrinogen deficiency

67
Q

What does leukoreduction do?

A

reduces the # of leuklocytes present in RBC and platelet units in an effort to reduce febrile non-hemolytic transfusion reactions from WBC cytokines

68
Q

WHo needs to have irradiated blood? Why?

A

patients with compromised T-cell function

the transfusion of donor lymphocytes can cause transfusion-associated graft vs host disease and start to attack the bone marrow, killing them within 21 days with 100% mortality

69
Q

What is the risk with using irradiated blood?

A

it increases the potassium level, so in an infant or a patient with a cardiac arrythmia or hyperkalemic already, this can cause cardiac arrest

Labs Medicine (27 decks)

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