11.6: Transfusion II Flashcards

(40 cards)

1
Q

WHat is HDN?

A

“Hemolytic disease of the newborn”

- Hemolytic process in perinatal period resulting in abnormal RBC production

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2
Q

What is the perinatal period?

A

The time during pregnancy

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3
Q

Main cause of HDN?

A
  • Unexpected alloantibodies
  • These are not ABO antibodies
  • Most are IgG and do not bind complement
  • Associated with delayed, extravascular hemolysis
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4
Q

What detects alloantibodies?

A

Antibody screen

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5
Q

Why does HDN occur?

A
  • Fetus inherits half of paternal RBC antigens
  • Fetal RBC passes transplacentally into mother
  • Mother produces IgG against fetal antigens that she does not share
  • IgG can freely cross placenta
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6
Q

Which antibodies freely cross into fetal circulation?

A
  • IgG
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7
Q

Normal progress in HDN?

A
  • 1st pregnancy mother RH-, fetus RH+
  • Pregnancy goes fine but mother now sensitized
  • 2nd pregnancy, maternal antibodies cross placenta to attack RH + newborn
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8
Q

What is an FMH?

A

“Fetal maternal hemorrhage”

  • Incidence allowing fetal RBCs to cross placenta to mother
  • Risk increases w/ gestational age: highest risk at pregnancy
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9
Q

What is erythroblastosis fetalis?

A
  • What happens to baby in HDN
  • Peripheral smear of baby showed nucleated RBCs and erythroblasts
  • Not normally found in marrow
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10
Q

What are erythroblasts?

A
  • RBC precursors
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11
Q

What is another name for RH factor?

A
  • Anti D
  • D positive fetus’ mother makes anti D
  • Fetus RBCs are thus sensitized and will agglutinate in antiglobulin test
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12
Q

Where do fetus’s make RBCs>

A
  • Liver and spleen
  • Not in marrow until born
  • Thus HDN babies demonstrate hepatosplenomegaly with liver failure
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13
Q

Where are coag factors made?

A
  • Liiver

- Baby with HDN cant form clots

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14
Q

Symptoms of fetus with HDN?

A
  • Hepatosplenomegaly
  • Decreased coagulation and platelets
  • Lowe liver function
  • Shortened RBC life
  • Hypoalbuminemia, leading to edema / hypotension and CHF
  • Jaundice / hyperbilirubinemia
  • High risk of kernicterus and neurologic damage
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15
Q

What is anasarca?

A
  • Whole body edema
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16
Q

HDN IV or EV?

A

Extravascular

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17
Q

What is kernicterus?

A
  • Staining of basal ganglia due to severe hyperbilirubinemia
  • Causes neuronal damage
18
Q

When does HDN occur with isoagglutinins?

THIS WILL BE ON EXAM*

A
  • Normally when mother is “O” so has anti A/B/AB
  • DAT will be positive
  • Disease is usually milder
19
Q

What usually causes HDN?

A
  • D antigen of RH blood group

- This is only type we have prophylaxis for

20
Q

How do we prophylaxis for HDN?

A
  • Give mother protein concentrate of anti D: “RH immune globulin”
  • This prevents mothers from making own alloantibodies
  • Given at delivery and at 28 and 30 weeks
  • We do not know how it works but it does
21
Q

What happens when mother is already sensitized and makes anti D?

A
  • Pregnancy is high risk and taken care of specialists
22
Q

What is amniotic fluid made of?

23
Q

Old way of monitoring high risk sensitized mother?

A
  • “Ultrasound guided amniocentesis”

- Sample amniotic fluid with needle and US

24
Q

New way of monitoring fetus for HDN?

A
  • Ultra sound monitoring of cerebral blood flow for kinetics
  • Anemic blood flows faster so we can test for anemia
  • If anemia, intrauterine transfusion needed into umbilical vein while in placenta
  • Monitor bilirubin once born
25
How to treat baby with high bilirubin?
"Bili lights" - Phototherapy with UV lights - Solubilize unconjugated bilirubin - Urobilinogen then excreted in kidneys * **If lights don't work exchange transfusion performed
26
What is bilirubin?
- Yellow breakdown product of normal heme catabolism, caused by clearance of aged RBCs which contain hemoglobin - Bilirubin is excreted in bile and urine - Elevated levels may indicate certain disease
27
What are cold and warm antibodies?
Cold: dont work at body temp so inconsequential Warm: React at body temp ***Both are non specific and directed against RBC membrane antigens
28
How do you dectect autoantibodies?
AIT: antibody screen
29
Which autoantibodies cause most trouble?
- Warm, IgG in nature cant coat RBC or be in plasma | - Will cause positive DAT or IAT
30
Characteristic of cold autoantibodies?
- Usually silent and don't cause problems - IgM - Activate complement pathway
31
Danger or warm autoantibodies?
- Cause cross matching compatibility with all RBCs
32
Disease associated with unexpected autoantibodies?
1. Systemic Lupus Erythematosus 2. Chronic lymphocytic leukemia 3, Normally idiopathic
33
Markers of immune hemolysis?
1. Falling hemoglobin and hematocrit 2. Hyperbilirubinemia 3. Elevated LDL 4. Positive DAT /IAT 5. Low haptoglobin 6. Spherocytes
34
Clinical findings in anemia?
- Fatigue - Exercise intolerance - Weakness - Pallor
35
Treatment of warm hemolytic anemia?
1. Corticosteroids 2. IV gammaglobulin 3. RBC transfusion: safe as long as on steroids - Even if cross math is incompatible
36
Unique symptoms for cold agglutinin disease?1
1. Acrocyanosis when cold
37
What is acrocyanosis?
- Bluish or purple coloring of the hands, lips and feet caused by slow circulation
38
How to treat ptn. with cold agglutinin disease?
- Keep warm | - Prednisone
39
Which hemolytic anemias associated with positive DAT?
- All
40
Is Igm see on RBC in cold autoimmunity?
No only complement