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FM 4 > Developmental Pathology > Flashcards

Developmental Pathology Flashcards

1
Q

Symmetric IUGR
Causes
Timing of diagnosis
How common?

A

Caused by fetal factors: chromosomal defects, infection.
Diagnosed earlier
Less common than asymmetric.

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2
Q

Asymmetric IUGR
Causes
Timing of diagnosis
How common?

A

Due to placental / maternal factors: uteroplacental insufficiency, abnormal cord, placenta previa (covers cervical os) / abruption (clot), pre-eclampsia (HTN, proteinuria, edema), eclampsia (add CNS sxs), chronic HTN, drugs, alcohol, smoking, diabetes.
Diagnosed later
More common than symmetric IUGR

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3
Q

Potter sequence
Causes
Characteristics

A

Oligohydramnios from renal agenesis, urethral obstruction, or amniotic fluid leakage → pulmonary hypoplasia, flat face, varus (deformation), amnion nodosum (squamous metaplasia of amnion)

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4
Q

Deformation
Causes
Examples

A

Caused by mechanical forces / pressure during phenogenesis, such as oligohydramnios, malformed uterus, leiomyomata, or impaired CNS w/ fetal mobility problems.
Ex: varus, valgus, clubfoot (talipes equinovarus / equinovalgus)

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5
Q

Disruption

A

Teratogens. Occur during organogenesis

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6
Q

TORCHS

When is risk highest?

A

Toxoplasma, Others (HIV, Influenza, Varicella) Rubella, Cytomegalovirus, Herpes, Syphilis
1st trimester during organogenesis is highest risk.

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7
Q

Congenital Toxoplasma
Problems
Timing of transmission

A
  • Periventricular calcifications and chorioretinitis.

* More transmissible later in gestation, but most severe early

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8
Q

Congenital Rubella
Triad / Tetrad
Timing of transmission

A
  • Rubella triad (tetrad): cataracts, PDA, deafness via CN VIII damage, (MR / microcephaly)
  • Easier transmission early (opposite toxo). Highest risk during organogenesis.
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9
Q

Congenital Herpes

Limited vs Disseminated

A
  • Limited / External → SEM disease: skin, eyes, mucous membranes
  • Disseminated → liver failure / hepatic necrosis, brain. Often fatal.
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10
Q

Congenital Cytomegalovirus
Timing of infection
Problems (4)
Characteristics (2)

A
  • Primary maternal infection in 2nd trimester causes MR, microcephaly, deafness, hepatospenomegaly
  • Characterized by chronic villitis (lymphocytes in placenta) and viral intranuclear inclusions (Owl Eyes)
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11
Q

Congenital Syphilis
Early (infantile) vs Late (tardive)
Timing

A
  • Early (Infantile)
  • Manifests in first 2 years of life.
  • “Snuffles” = nasal congestion w/ ulcers
  • Bullous skin rash
  • Hepatomegaly (fibrosis)
  • Skeletal abnormalities – saddle nose, saber shins (outward boning of proximal tibia)
  • Late (Tardive)
  • Manifests after 2 years
  • Hutchinson Triad: notched central incisors, interstitial keratitis (blindness), deafness
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12
Q

What is the Hutchinson triad?

A

Occurs in late / tardive syphilis

Notched central incisors, interstitial keratitis (blindness), deafness

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13
Q

What does hyperthermia cause (hot tub)?

A

Anencepaly

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14
Q

Thalidomide

A

Thalidomide – limb defects (meromelia / amelia) via down-regulation of Wingless (WNT) signaling. Lenalidomide is derivative used for CLL w/ similar effects.

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15
Q

Warfarin (3)

A

Warfarin – clitoral hypertrophy, labial fusion, MR

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16
Q

Valproic acid (3)

A

Valproic acid – affects limb, vertebral, and craniofacial development via disruption of homeobox (HOX) TF proteins.

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17
Q

1,3-cis retinoid acid (3)

A

1,3-cis retinoic acid (acutane for acne) – cleft lip / palate, CNS, and cardiac defects via TGFb signaling.

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18
Q

Alcohol (3)

A
  • Alcohol – growth retardation, facial anomalies, CNS dysfunction
  • Fetal Alcohol Syndrome is a more severe form of Fetal Alcohol Spectrum Disorder.
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19
Q

Maternal diabetes (6)

A

LGA (due to high insulin) and hypoglycemia. Large size increases risk for birth injury. Also associated w/ heart defects, spina bifida, and other CNS malformations.

20
Q

Radiation (5)

A

Microcephaly, blindness, skull defects, spin bifida, cleft palate

21
Q

Kleinfelter Syndrome

A

47, XXY, male

22
Q

Turner Syndrome

A

45, X, female

23
Q

Down Syndrome (6)

A

AV septal defect, epicanthic folds, simian crease, macroglossia, leukemias, dementia (amyloid precursor is upregulated → neurofibrillary tangles / plaques)

24
Q

Patau Syndrome (3)

A

Trisomy 13 – 3 p’s: polydactyly, palate (facial clefts), puny eyes (microphthalmia)

25
Q

Edwards Syndrome (2)

A

Trisomy 18 – micrognathia (small jaw) and overlapping fingers

26
Q

Causes of hydrostatic and oncotic edema in hydrops

A

Cardiac ischemia / heart failure (anasarca) causes hydrostatic. Ischemic dysfunction of liver → poor protein production (oncotic).

27
Q

3 causes of non-immune hydrops

A
  • CV defects (heart failure)
  • Turner Syndrome (45X)
  • Non-immune fetal anemia (parvovirus B19 / hemoglobinopathy)
28
Q

3 names for Parvovirus B19 in kids

A

Slapped cheek / 5th disease / erythema infectiosum. Tropism for RBC precursors in marrow.

29
Q

Complications of non-immune fetal anemia

A

Jaundice / kernicterus due to Hb breakdown

30
Q

Cystic Hygroma / Posterior Cervical Hygroma

A

Fluid accumulation in lymphatics of posterior neck caused by structural defects. Basically a localized form of hydrops.

31
Q

Prune bell
Cause
Population
Characteristics (5)

A

Caused by urethral obstruction
More common in males
Thin / absent abdominal muscles due to distention
Dilated bladder / ureters and hydronephrosis
Renal dysplasia due to back-pressure
Cryptoorchidism
Hypoplastic prostate

32
Q

What causes conjectures / pterygium?

A

Oligohydamnios

33
Q

Causes of polyhydramnios

A

Esophageal atresia / obstruction or CNS dysfunction preventing swallowing

34
Q

2 manifestations of single umbilical artery (SUA)

A

Growth retardation and CV defects

35
Q

Ascending (bacterial) infections
Pathophysiology
Bacteria
Hallmark of ascending infection

A
  • Ascending (bacterial) infections → chorioamnionitis → PPROM (not IUGR).
  • Bacteria that cause PROM / PPROM are usually STD bugs (Chalmydia, mycoplasma, Trichomonas), rather than those that cause meningitis (Listeria, E coli, Group B strep)
  • Hallmark is Chorioamnionitis = acute inflammation of fetal membranes due to MATERNAL PMNs. PPROM occurs due to inflammation, cytokines, and endogenous binding of TLRs to bacterial components → disruption of prostaglandins.
36
Q

Characteristics of infected amniotic fluid
Which bugs?
Complications (3)

A
  • Infected amniotic fluid = acute inflammation of umbilical cord w/ FETAL PMNs.
  • Vasculitis / funisitis = fetal PMNs marginating in cord
  • Organisms include gram negs and group B strep
  • Fetal / neonatal infections may include pneumonia, meningitis, and sepsis
37
Q

Transplacental / hematologic infections
Causes
General effect on fetus
Hallmark of transplacental infection

A

TORCHS. Usually viral (parvovirus, CMV). May be parasitic (toxo) or bacterial (Listeria / syphilis).
Causes IUGR and stillbirth
Hallmark is chronic villitis or villitis of unknown etiology (VUE; most likely autoimmune)

38
Q

Congenital Parvovirus B19
Site of replication
Problems
Histology

A
  • Replicates in erythroid precursor cells.
  • Reduced RBCs → anemia → hydrops / extramedullary hematopoiesis (EMH). No hemolytic disease of newborn b/c it prevents RBC production from the start
  • Histology - Large cells in bone marrow. Homogenation of chromatin (ground glass) w/ margination of chromatin and nuclear enlargement.
39
Q

Early vs late perinatal sepsis. Which bugs?

3 most common causes of neonatal sepsis and morphology

A
  • Early onset (1st week of life) – E coli, group B strep
  • Late onset (>1 week after birth) – Listeria, Candida
  • LEG = 3 most common causes of neonatal sepsis
  • Listeria = gram positive rod
  • E coli = gram neg rod
  • Group B strep = gram positive coccus
40
Q

What is considered premature delivery?

What is limit of viability?

A

Less than 37 weeks

Limit: 22-23 weeks

41
Q

What causes PROM / PPROM?

A

Ascending infections

42
Q 
Problems that occur w/ PPROM
Brain (3)
GI (1)
Heart (1)
Liver (1)
Lungs
A
  • Brain –germinal matrix (near ventricles, make new neurons) / intraventricular hemorrhage may cause increased intracranial pressure and herniation of medulla → death. Also associated w/ cerebral palsy. May have problems w/ homeostasis, including temperature, blood glucose, and vasomotor tone.
  • GI = necrotizing enterocolitis – dead small bowel due to infection. Poor immune response to infection. Surgical resection is necessary.
  • Heart – PDA
  • Liver – physiologic jaundice may lead to kernicterus
  • Lungs - Hyaline membrane disease / Respiratory distress syndrome. Also pneumonia. Complication includes bronchopulmonary dysplasia.
43
Q 
Hyaline membrane disease / neonatal Respiratory Distress Syndrome (RDS)
Pathophysiology
Histology
Difference from DAD
Timing of onset
Treatment
A

•Alveolar atelectasis → hypoxemia → CO2 retention / acidosis → poor pulmonary perfusion → endothelial damage → leakage of plasma / fibrin → hyaline membranes (made of fibrin, fibrinogen, and cell debris)
•Necrotic cellular debris early and eosinophilic hyaline membranes later.
•DAD does not cause atelectasis
•Occurs hours after birth (NOT in utero).
TREATMENT
•Glucocorticoid steroids are given to mom prior to impending premature delivery to induce surfactant synthesis
•Baby requires assisted ventilation w/ high O2 levels. Give prophylactic exogenous surfactant.

44
Q

Complication of hyaline membrane disease
Cause
Characteristics

A
  • Chronic bronchopulmonary dysplasia
  • Caused by long-term O2 / ventilator dependence (>28 days). May involve oxygen toxicity and barotrauma from ventilator.
  • Characterized by epithelial hyperplasia, interstitial fibrosis, alveolar wall thickening, and reduced number of airspaces (alveolar hypoplasia)
45
Q

Retinopathy of prematurity (aka retrolental fibroplasia)
Association
Cause

A

Associated w/ PPROM

Caused by VEGF-mediated retinal neovascularization

FM 4 (5 decks)

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