Diseases of Infancy and Childhood: Perinatal infections, fetal hydrops Flashcards

1
Q

Microbes can enter the host by doing what?

A

breaching epithelial surfaces, inhalation, ingestion, or sexual transmission

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2
Q

in general, fetal and perinatal infections are acquired through one of two primary routes. What are these routes?

A

transcervically (aka ascending) or transplacentally (hematologic)

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3
Q

Occasionally, infection occur by a combination of the two routes- how so?

A

ascending microorganism infects the endometrium and then invades the fetal bloodstream via the chorionic villi

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4
Q

perinatal sepsis can be grouped clinically based on what?

A

early onset (within the first 7 days of life) versus late onset (from 7 days to 3 months)

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5
Q

most cases of early-onset sepsis are acquired at or shortly before birth and tend to result in clinical signs and symptoms of what?

A

PNA, sepsis, and occasionally meningitis within 4-5 days of life

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6
Q

what is the most common cause of early onset sepsis as well as early-onset bacterial meningitis?

A

group B streptococcus

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7
Q

what could be the source of perinatal infections?

A

bacteria, fungus, parasites, viruses, TORCH

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8
Q

What are the different routes in which vertical transmission can occur?

A

placental-fetal transmission, transmission during birth, and postnatal transmission in maternal milk

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9
Q

What are 2 examples of infections caused via transmission during birth?

A

gonococcal and chlamydial conjunctivitis

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10
Q

what are 3 examples of infections transmitted via postnatal transmission in maternal milk?

A

cytomegalovirus (CMV), HIV, and hepatitis B virus

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11
Q

what does fetal hydrops refer to?

A

the accumulation of edema fluid in the fetus during intrauterine growth

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12
Q

there are 2 general patterns of fluid accumulation in fetal hydrops, what are they?

A

hydrops fetalis (generalized) and cystic hygroma (localized)

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13
Q

What are the two different etiologies of fetal hydrops?

A

immune hydrops and non-immune hydrops

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14
Q

what is immune hydrops caused by?

A

a hemolytic disease caused by blood group antigen incompatibility between mother and fetus

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15
Q

what are the three major causes of non-immune hydrops?

A

cardiovascular defects, chromosomal anomalies, and fetal anemia

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16
Q

Immune hydrops is what type of reaction?

A

a type II hypersensitivity reaction (antibodies react with antigens present on cell surfaces or in the extracellular matrix)

17
Q

What happens if there is IgG antibody attachment to Rh+ erythrocytes? and what does this cause/lead to?

A

removal and destruction of the erythrocyte-antibody complex; causes anemia and hemoglobin degradation

18
Q

what does anemia in the fetus lead to?

A

extramedullary hematopoiesis and cardiac decompensation

19
Q

what does hemoglobin degradation lead to in the fetus?

A

an excess of bilirubin; which leads to jaundice and kernicterus

20
Q

What does the cardiac decompensation that results from anemia in the fetus lead to?

21
Q

the incidence of maternal Rh isoimmunization has decreased significantly since the use of what?

A

Rhesis immune globulin (RhIg) containing anti-D antibodies

22
Q

when should administration of RhIg take place?

A

at 28 weeks of gestation and within 72 hours of delivery to Rh-negative mothers; also administered following abortions because these too can lead to immunization

23
Q

what are some of the cardiovascular defects that could cause non-immune hydrops?

A

structural and functional anomalies (congenital malformations and arrhythmias)

24
Q

what are some of the chromosomal anomalies that could cause non-immune hydrops?

A

45, XO (turner syndrome) and trisomes 21 and 18

25
what is an example of fetal anemia that could cause non-immune hydrops?
alpha thalassemia (most common cause), transplacental parovovirus B19 and twin-twin transfusion
26
What are the two consequences of excessive destruction of red cells in the neonate?
anemia and jaundice
27
What is the mechanism for the development of generalized hydrops?
with more severe hemolysis, progressive anemia develops and may result in hypoxic injury to the heart and liver; because of the liver injury, plasma protein synthesis (albumin) decreases. Cardiac hypoxia may lead to cardiac decompensation and failure; the combination of reduced plasma oncotic pressure and increased hydrostatic pressure in the circulation (secondary to cardiac failure) results in generalized edema and anasarca
28
What accounts for the presence in the peripheral circulation of large numbers of immature red blood cells,, including reticulocytes and erythroblasts?
the increased hematopoietic activity