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MHD > Humoral Immune Mediated Hemolysis, Blood Banking, Transfusions > Flashcards

Humoral Immune Mediated Hemolysis, Blood Banking, Transfusions Flashcards

1
Q

What are isoagglutinins?

A

Expected immunoglobulins that circulate in our blood

Do not cause disease normally

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2
Q

What are alloantibodies?

A

Antibodies made against one’s own species with different genetics

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3
Q

What are autoantibodies?

A

Antibodies made against your own tissues

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4
Q

What is the A antigen on RBC cell membranes?

A

N-acetylgalactosamine

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5
Q

What is the B antigen on RBC cell membranes?

A

D-galactose

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6
Q

What blood type is the universal donor? Why?

A

O Type.

Has no A or B antigen on RBC cell surface

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7
Q

What blood type is the universal recipient? Why?

A

AB Type.

Has no isoagglutinin against either A or B antigen.

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8
Q

What is the most common procedure performed on hospitalized patients?

A

Blood transfusion

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9
Q

What are two most common places for mistakes in blood transfusion?

A

Specimen ID

Patient ID

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10
Q

What is “forward” blood typing? What reagents would you use for it?

A

Used to determine ABO and D blood type of individual.

Take the patient’s RBCs and coat with anti-A, anti-B, and anti-D

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11
Q

What is “reverse” blood typing? What reagents would you use for it?

A

Used to determine what isoagglutinins are present in a patient’s serum

Use stock Type A and stock Type B RBCs to test for isoagglutinins in patient serum

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12
Q

What is the Antibody Screen test?

A

Screening for antibodies in patient serum that are against other common antigens (Not ABO type).

Mix patient serum with these RBCs and perform an IAT to see if they have antibodies

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13
Q

Once the patient serum and stock RBCs have been mixed, what do you add to induce agglutination if antibodies have bound antigen?

A

Anti-human globulin

Antibody made by a non-human animal against human Ig and/or complement proteins

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14
Q

What is sensitization?

A

When the first antibody has bound an antigen on the cell surface of the RBC

Does not cause agglutination

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15
Q

Describe the indirect agglutination test (IAT)

A

In vitro test = Antibody Screen

Given a stock of RBCs, add the patient’s serum and let any antibodies bind to RBC membrane. Then add anti-human globulin and see if agglutination occurs. This will tell you whether the patient has any alloantibodies against your sample of RBCs

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16
Q

What are the required pretransfusion compatibility testings?

A

Typing (ABO and Rh)

Screening (testing for clinically significant antibodies)

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17
Q

What is a Type and Crossmatch?

A

Type/Screen (ABO, Rh, and antibody screening)

Crossmatch (mix patient serum with donor RBCs to see if agglutination occurs)

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18
Q

When would you order a Type and Screen?

A

When the need for transfusion is remote (5% or lower)

Asymptomatic with chronic anemia
Surgical pts with low risk of bleeding
Prior positive antibody screens

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19
Q

When would you order a Type and Crossmatch?

A

High likelihood that RBC transfusion will be required

Actively bleeding patients
Surgical pts with high risk of bleeding

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20
Q

How do you perform a Direct Agglutination test (DAT)?

A

In vivo test
Add anti-human globulin to the patient’s RBCs (that you suspect may be sensitized already)

Positive DATs are always abnormal

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21
Q

What are methods of avoiding Acute Hemolysis from pre-formed IgM?

A

ID (Specimen and Patient)
Blood typing
Antibody Screen
Crossmatching

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22
Q

Describe the pathogenesis of Acute Immune Mediated Hemolysis.

A

IgMs in serum activate complement and cause intravascular hemolysis.
Free hemoglobin will be released into circulation and bind to haptoglobin.

Occurs rapidly

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23
Q

List symptoms of Acute Immune Mediated Hemolysis.

A 
Fever
Constriction of chest
Lumbar pain
Hemoglobinuria
Hemolysis
Hypoalbuminemia
Hypotension
Bleeding
Renal failure
24
Q

Why is a secondary immune response of greater magnitude and speed than the primary response?

A

Plasma cells and memory B cells already exist and will be able to respond more quickly

25
Q

How are patients commonly exposed to RBC antigens they lack?

A

Pregnancy
Transfusions
Transplants

26
Q

List some common Lab Results you will see when you suspect Hemolysis

A 
Falling hemoglobin and hematocrit
Low haptoglobin
DAT Positive
Elevated LDH
Peripheral blood smear findings (spherocytes, polychromasia)
27
Q

What are unexpected alloantibodies?

A

IgG antibodies that are made by patients who lack the corresponding antigen.
They are stimulated upon exposure to RBCs from other humans

28
Q

Describe the kinetics and pathogenesis of Unexpected Alloantibodies (Delayed immune mediated hemolysis)

A

Slow kinetics (10-14 days)

Most do NOT bind complement

Associated with extravascular hemolysis

29
Q

How would you test for Unexpected Alloantibodies

A

Detected using the antibody screen

Could cause crossmatching incompatibility

DAT will be positive as long as the sensitized cells are in circulation

30
Q

When you have a patient with an Unexpected Alloantibody reaction in their history, how will you need to address in future transfusions?

A

In any future transfusions., you must provide RBCs negative for that antigen

31
Q

What is the general cause of HDN?

A

Usually due to unexpected alloantibodies (IgG) made by the mother against the fetus,

32
Q

How is the maternal immune system able to respond to the fetus?

A

Mom should become immunomodulated to the fetus. The placenta is an incomplete barrier between mother and child and there is bilateral transfer of maternal and fetal cells

33
Q

What is the D antigen? How is it important in HDN?

A

D antigen = Rh antigen
When mom is Rh- and dad is Rh+, the mother may become alloimmunized for the D antigen in the first pregnancy, which could cause HDN in the second pregnancy

34
Q

When is the highest risk for D-alloimmunization in pregnancy?

A

3rd trimester and at delivery

35
Q

Who will have a positive DAT in HDN?

A

The fetus! The positive DAT tells you that the fetal RBCs have been sensitized by IgG made by mother

36
Q

Clinical Abnormalities and Symptoms of HDN in utero

A 
Positive DAT for fetus
Shortened RBC survival in fetus
Hypoalbuminemia
Hypocoagulability
Hepatosplenomegaly
Anasarca (whole body edema)
37
Q

Clinical Abnormalities and Symptoms of HDN Postpartum

A

Jaundice
Severe hyperbilirubinemia
High risk of kernicterus
Neurological damage

38
Q

What kind of hemolysis occurs in HDN?

A

Extravascular hemolysis (of the fetal sensitized RBCs)

39
Q

What is kernicterus?

A

Severe hyperbilirubinemia can cause neuronal damage.
Can lead to visual/auditory problems, cerebral palsy-like effects.
Get yellow stain to the deep white matter of the brain

40
Q

Who is more likely to get ABO-HDN? Why?

A

Group O mothers are more likely to get ABO HDN because they have preformed anti-A, anti-B, and anti-AB in circulation

41
Q

How can we prevent HDN?

A

Prophylaxis is only available for the Rh “D” Antigen.

We can give protein concentrate of Anti-D prepared from serum pools of previously sensitized females. Given to the mothers postpartum after first delivery

Nobody knows why this works

42
Q

What will be found in amniotic fluid if the fetus is undergoing hemolysis? How can this be measured?

A

Bilirubin

Use Liley graph for optical density measurement

43
Q

How can fetal hematocrit be assessed in a non-invasive way?

A

Fetal ultrasound to assess speed of blood flow in the baby’s cerebrum

Slower speed = Higher hematocrit

44
Q

If a baby is very jaundiced and hyperbilirubinemic at birth, what is the first line therapy? Second line?

A

Phototherapy with UV light to solubilize unconjugated bilirubin. The baby will then urinate out water soluble bilirubin

If phototherapy doesn’t work, try an exchange transfusion through the umbilical vein

45
Q

What are the two categories of unexpected autoantibodies?

A

Warm autoimmune hemolytic anemia

Cold agglutinins

46
Q

What are the common etiologies of unexpected autoantibodies?

A

Idiopathic
SLE
Chronic Lymphocytic Leukemia

47
Q

Describe Warm Autoimmune Hemolytic Anemias

A

Ag-AB rxns take place near body temp
Typically IgG
Cause extravascular clearance of RBCs

48
Q

Symptoms of Warm Autoimmune Hemolytic Anemias

A

Fatigue, pallor, exercise intolerance, weakness

49
Q

Lab features of Warm Autoimmune Hemolytic Anemias

A

Positive DAT
Positive IAT

Microspherocytes seen on blood smear
Hyperbilirubinemia
Low haptoglobin

50
Q

What are the best treatments for Warm Autoimmune Hemolytic Anemias?

A

Corticosteroids
Iv gammaglobulin
Splenectomy

51
Q

Describe the clinical features of Cold Agglutinin Disease

A

Moderately severe anemia

Acrocyanosis precipitated by cold exposure

52
Q

Lab Features of Cold Agglutinin Disease

A

Ag-Ab rxns take place only at 25 celsius or lower

Positive DAT due to anti-complement only (Typically, the IgM molecule falls off)

Spherocytes and polychromasia on blood smear

Hyperbilirubinemia

53
Q

Treatments for Cold Agglutinin Disease

A 
Supportive care (RBC transfusions)
Keep the patient warm
54
Q

What is the pathogenesis of Drug Induced Hemolytic Anemias?

A

Drugs bind to RBC membrane and make it appear to be a neo-antigen

Positive DAT is seen

55
Q

How would you treat Drug Induced Hemolytic Anemias?

A

Stop taking the drug!

MHD (57 decks)

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