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General Pathology > Exam #3: Diseases of Childhood & Infancy II > Flashcards

Exam #3: Diseases of Childhood & Infancy II Flashcards

1
Q

What is an ascending infection?

A

Infection of the neonate via the uterus

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2
Q

What bacteria cause asecnding infection?

A

E. coli

GBS

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3
Q

What virus causes ascending infection?

A

HSV II

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4
Q

What are the diseases/ inflammations caused by ascending infection?

A

1) Chorioamnionitis= inflammation of the fetal membranes (amnion and chorion)
2) Funisitis= inflammation of the connective tissue of the umbilical cord
3) Placentitis
4) Villitis= inflammation of the chorionic villi

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5
Q

What are the consequences of ascending infection?

A
  • Preterm birth
  • Recurrent miscarriage
  • Fetal Growth Restriction
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6
Q

Describe the microscopic appearance of villitis in perinatal ascending infection.

A

Remember that this is an inflammation of the chorionic villi & shows LYMPHOCYTIC infiltration of the chorionic villi

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7
Q

What is the difference between early onset & late onset neonatal sepsis?

A 
Early= < 1 week
Late= 8 days- 3 months
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8
Q

What pathogens typically cause early onset neonatal spesis? What diseases are these pathogens associated with?

A

GBS: (meningitis)

Gram negatives:

  • E. Coli
  • Klebsiella

Note that the gram negative organisms cause pneumonia & meningitis

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9
Q

What pathogens are associated with late-onset neonatal sepsis?

A
  • Staphylococci
  • H. influenzae
  • Listeria
  • Chlamydia
  • Mycoplasma
  • Candidia
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10
Q

What are the major risk factors for early-onset neonatal sepsis (5)?

A

1) Previous infant with GBS
2) GBS bacteriuria during pregnancy
3) Delivery before 37 weeks (preterm)= diminished immune system
4) Ruptured membranes (amniotic sac) >18 hours
5) Intrapartum temp >38 C/ 100.4 F

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11
Q

Describe the microscopic appearance of neonatal congenital pneumonia.

A

Many neutrophils infiltrating immature bronchioles

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12
Q

What are the causes of NRDS (Neonatal Respiratory Distress Syndrome)?

A

1) Prematurity
2) Lack of surfactant
3) Fetal head injury
4) Sedation
5) Aorta abnormalities
6) Umbilical cord coiling
7) Amniotic fluid aspiration

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13
Q

What is the period for surfactant production in the neonate?

A

26-32 weeks

Type II pneumocytes

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14
Q

What is hyaline membrane disease?

A
  • This is the most common cause of NRDS i.e. most common specific disease process that causes NRDS, which is due to a lack of surfactant production
  • Leading cause of mortality & morbidity in infants

**Hyaline Membrane Disease is characterized by a surfactant deficiency, which leads to alveolar collapse and noncompliant lungs

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15
Q

What are the risk factors for Hyaline Membrane Disease?

A

1) Preterm
2) Maternal DM
3) C-section
4) Male gender

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16
Q

Outline the pathophysiology of Hyaline Membrane Disease.

A

N/A

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17
Q

Describe the microscopic appearance of Hyaline Membrane Disease.

A

Alternating atelectic alveoli & dilated aleolar ducts lined with pink fibrin rich hyaline & necrotic cells

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18
Q

What is the clinical presentation of Hyaline Membrane Disease?

A
  • Respiratory Distress
  • Cyanosis
  • Hypoxemia
  • Hypercarbia
  • Metabolic acidosis (mixed)
19
Q

What are the complications of Hyaline Membrane Disease?

A

1) Intraventricular hemorrhage
2) PDA
3) Necrotizing enterocolitis
4) Bronchopulmonary dysplasia
5) Retinopathy of prematurity

*****All are associated with hypoxemia & metabolic acidosis

20
Q

What is Bronchopulmonary Dysplasia?

A
  • Reduced total numbers of alveoli
  • Alveolar wall thickening
  • Epithelial hyperplasia
  • Squamous metaplasia
  • Interstitial fibrosis
  • Sponge-like radiology
  • Predisposition to respiratory infection

All associated with preterm neonates treated with oxygen therapy > 4weeks & positive pressure ventilation

21
Q

What is post-mortem exterior cobblestone surface of the lung associated with?

A

This is pathognemonic for Bronchopulmonary Dysplasia

22
Q

Describe the microscopic appearance of Bronchopulmonary Dysplasia.

A
  • Interstitial fibrosis
  • Epithelial hyperplasia
  • Squamous metaplasia
  • Alveolar wall thickening
23
Q

What is the clinical presentation of Necrotizing Enterocolitis?

A
  • Abdominal distension
  • Ileus
  • Bloody stool

*****Note that this can lead to bowel perforation & stricture

24
Q

Describe the microscopic appearance of Necrotizing Enterocolitis.

A
  • Hemorrhagic necrosis
  • Few nuclei
  • Villi destruction
  • RBC infiltration of all layers of the GI mucosa

**Note that findings will begin in the mucosa & extend into the muscular wall leading to potential perforation

25
Q

What are the two forms of edema in the fetus?

A

Generalized= hydrops fetalis

Localized edema= cystic hygroma

*****Cystic hygroma= congenital multiloculated lymphatic lesion that can arise anywhere, but is classically found in the left posterior triangle of the neck and armpits

26
Q

What is the difference between immune & nonimmune fetal hydrops?

A

Immune is caused by blood group incompatibility (erythroblastosis fetalis)

Nonimmune is caused by:

  • Infection
  • Chromosomal anomalies
  • Twin pregnancy
  • Cardiovascular defects
27
Q

Describe the pathogenesis of immune fetal hydrops.

A

Immune hydrops= erythroblastosis fetalis

  • Mom= Rh D- & Dad= Rh D+
  • Maternal immune response to fetal Rh- D+ (from Dad)
  • Transplacental passage of maternal anti-D IgG & binding to fetal Rh D+ RBCs
  • Destruction of RBCs

*****Note that this has been well controlled with “Anti-D antibodies” isolated from Rhesus monkeys i.e. Rhogam

28
Q

What are the consequences of immune hydrops fetalis?

A

Hemolytic ANEMIA leading to:

  • Heart Failure (caused by ischemia)
  • Liver failure (caused by ischemia)
  • Hydrops fetalis (edema from reduced plasma oncotic pressure & increased hydrostatic pressure secondary to heart failure)

Hyperbilirubinemia

  • Jaundice
  • Kernicterus
29
Q

What is Necrotizing Enterocolitis?

A

Focal areas of bowel necrosis caused by ischemia, most often in the terminal ileum

*****Note that the etiology is mutlifactorial & contorversial

30
Q

What are the paternal risk factors for SIDS?

A
  • Young maternal age
  • Smoking
  • Drug abuse
  • Late or no prenatal care
  • Short intergestational intervals
31
Q

What are the risk factors of Necrotizing Enterocolitis?

A

1) Prematurity
2) Low birth weight

*****Complication of Hyaline Membrane Disease

32
Q

How does Necrotizing Enterocolitis appear on radiograph?

A

Gas in bowel wall

33
Q

What are the potential consequences of Necrotizing Enterocolitis?

A
  • Perforation

- Strictures

34
Q

What is the difference between capillary hemangioma & cavernous hemangioma?

A

Capillary= better prognosis & known as “strawberry type”

Cavernous= more likely to be associated with VHL disease, and form in the brain, pancreas, or liver

35
Q

What are the microscopic differences between capillary & cavernous hemangioma?

A

Capillary=

  • Thin walled capillaries
  • Scant stroma

Cavernous=
- Large cavernous blood-filled vascular spaces separated by connective tissue stroma

36
Q

What is Kernicterus?

A

Staining of brain nuclei with bilirubin in response to hyperbilirubinemia >20 mg/dL

37
Q

What is SIDS?

A

Sudden unexplained death under 1 year of age

  • 90% < 6 months
  • Most < 2-4 months
38
Q

What are the infant risk factors for SIDS?

A
  • Male

- Premature

39
Q

What are the environmental risk factors for SIDS?

A
  • PRONE sleeping position
  • Sleeping on soft surface
  • Sleeping with parents in the first 3 months
  • Hyperthermia
  • Postnatal passive smoking

**Note that the American Academy of Pediatrics ONLY accepts the SUPINE position as the acceptable sleeping position for infants & has thus generated the “Back to Sleep” Campaign.

40
Q

What are the developmental vasuclar anomalies of infancy?

A

Hemangiomas

Vascular malformations

41
Q

What is the most common tumor in infants?

A

Hemangiomas

  • Capillary hemangioma
  • Cavernous hemangioma
42
Q

What are the lymphatic tumors associated with infancy?

A
  • Lymphangioma= hamartoma or neoplasm of lymphatic origin

- Lymphangiectasis= abnormal dilations of prexisting lymphatic channels

43
Q

How does the derivation of tumors differ between children & adults?

A

Children= soft-tissue tumors of mesenchymal origin

Adults= epithelial origin

General Pathology (33 decks)

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