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MOD > Fetal Hydrops (10) > Flashcards

Fetal Hydrops (10) Flashcards

1
Q

What is Fetal Hydrops?

A

Accumulation of edema fluid in fetus during intrauterine growth

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2
Q

Accumulation of edema fluid in fetus during intrauterine growth

A

Fetal Hydrops

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3
Q

What are the 2 types of fetal hydrops?

A
  1. Immune

2. Nonimmune

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4
Q

What is the current most common form of hydrops and why?

A

Nonimmune due to successful prophylaxis

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5
Q

What is Immune Hydrops?

A

Hemolytic disease cause by blood group antigen incompatibility between the mother and fetus!

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6
Q

What pregnancy does immune hydrops affect?

A

2nd!

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7
Q

Describe the setup for immune fetal hydrops to occur

A

Rh - mother and Rh + father

= Rh + 1st child

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8
Q

When will the mother become sensitized to the Rh + antigen?

A

During her first pregnancy with an Rh + child, at the last trimester

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9
Q

How does Rh + fetal blood reach maternal circulation at the last trimester?

A

Due to loss of cytotrophoblast barrier or during birth iteself

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10
Q

What is the most common Rh + antigen that causes incompatibility?

A

D

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11
Q

During the first pregnancy, when fetal Rh D+ blood reaches maternal circulation of Rh - , what antibodies will be made?

A

IgM - cannot cross placenta

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12
Q

When the mother becomes sensitized, what antibodies does she produce and why is the first child not affected?

A

IgM antibodies cannot cross the placenta

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13
Q

When the second child is Rh D+, what antibodies will become active?

A

IgG! - can cross placenta

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14
Q

With the second child, how does hemolytic disease begin?

A

If the fetal blood crosses into maternal circulation, the IgG antibodies will cross the placenta and degrade the fetal RBCs

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15
Q

Greater than ___ ml of fetal Rh + blood into maternal circulation will cause an antibody response

A

1 mL

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16
Q

The mother’s antibody response depends on the dose of the antigen that reaches her blood stream. How much will need to cross?

A

1 mL

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17
Q

Once IgG antibodies attach and begin to degrade the fetal RBCs, describe what happens as anemia progresses.

A
  • Anemia
  • Causes liver injury and cardiac decompensation
  • Liver injury results in decreased albumin synthesis
  • Decreased albumin synthesis causes decreased oncotic pressure = edema
  • Cardiac decompensation = edema
    == Fetal hydrops
18
Q

Once IgG antibodies attach and begin to degrade the fetal RBCs, describe what happens are hemoglobin is degraded.

A
  • Hb is degraded and releases heme
  • Heme is converted to bilirubin
  • Increased levels of bilirubin
  • Bilirubin deposits in the basal ganglia of the brain
    = Jaundice and Kernicterus
19
Q

A level of bilirubin in the blood greater than ___ will usually cause kernicterus

A

20

20
Q

Where does bilirubin get deposited in the brain for kernicterus to occur?

A

Basal ganglia

21
Q

What treatment is given to the Rh - mother now?

A

Rhesus Immune Globin with Anti - D antibodies (RhIg)

22
Q

When is Rhesus Immune Globin with anti - D antibodies given to the Rh - mother?

A

28 weeks gestation and within 72 hours of birth of the child

23
Q

Is RhIg also given after abortions?

A

Yes

24
Q

3 causes of nonimmune hydrops?

A
  1. Cardiovascular
  2. Chromosomal anomalies
  3. Fetal anemia
25
Q

What cardiovascular defects can cause nonimmune hydrops?

A

Malformations and arrhythmias

26
Q

What chromosomal anomalies can cause nonimmune hydrops?

A

Turner’s syndrome (45X), Trisomy 18 and 21

27
Q

How do chromosomal anomalies like Trisomy 18 and 21 cause nonimmune hydrops?

A

They have associated cardiac abnormalities

28
Q

What is the most common cause of fetal anemia that can cause nonimmune hydrops?

A

Homozygous alpha-thalessemia

29
Q

What does Homozygous alpha-thalessemia do?

A

Deletes all 4 alpha globin chains = fetal anemia

30
Q

What virus can cause fetal anemia that results in nonimmune fetal hydrops?

A

Transplacental infection by Parvovirus B19

31
Q

Describe how Parvovirus B19 causes fetal anemia and thus nonimmune hydrops

A
  • Parvovirus B19 gains entry into normoblasts
  • The virus replicates
    = RBC apoptosis and aplasia
32
Q

In nonimmune hydrops associated with fetal anemia, what color are the fetus and placenta?

A

PALE

33
Q

In nonimmune hydrops associated with fetal anemia, describe the bone marrow.

A

Bone marrow exhibits compensatory hyperplasia of erythroid precursors

34
Q

In nonimmune hydrops associated with fetal anemia, describe what is seen in other places?

A

Extramedullary hematopoiesis is present in other tissues!

35
Q

How do RBCs look in nonimmune hydrops due to fetal anemia?

A

LARGE number of IMMATURE RBCs

– reticulocytes and erythroblasts

36
Q

A large number of reticulocytes and erythroblasts is known as?

A

Erythroblastosis Fetalis

37
Q

Erythroblastosis Fetalis

A

Large number of immature RBCs due to Fetal anemia c

38
Q

Turner’s syndrome (45X) is susceptible to what type of fluid accumulation?

A

Postnuchal fluid = cystic hygroma

39
Q

Cystic Hygroma

A

Postnuchal fluid accumulation seen with turner’s syndrome of hydrops

40
Q

Once the IgG antibodies reach fetal blood and begin degrading, describe what results after anemia.

A
  • Anemia
  • Liver injury (hypoxia) and cardiac decompensation
  • Liver injury causes decreased synthesis of albumin
  • Decreased albumin causes decreased oncotic pressure
    = Edema = Hydrops
41
Q

Once the IgG antibodies reach fetal blood and begin degrading, describe what results with hemoglobin degradation.

A
  • Hemoglobin is degraded to heme
  • Heme is degraded to bilirubin
  • Bilirubin levels greater than 20 accumulate in the brain (basal ganglia) and tissues
    = Jaundice and Kernicterus

MOD (68 decks)

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