Embryonic Development Issues
Overview of Congenital Anomalies in Embryonic Development
Key Conditions: Anencephaly, Spina Bifida, Cleft Lip and Palate, Tetralogy of Fallot, Renal Agenesis, Omphalocele, Gastroschisis, Hydrops Fetalis.
Anencephaly
Etiology: Congenital neural tube defect; incomplete brain/skull development.
Genetic and Environmental Factors: Chromosomal abnormalities, teratogens, folic acid deficiency.
Pathogenesis: Failure of anterior neuropore closure leads to developmental failures of cerebral tissue.
Clinical Significance: Poor prognosis; prevention includes folic acid supplementation.
Spina Bifida
Etiology: Congenital neural tube defect; incomplete spinal column closure.
Genetic and Environmental Factors: Similar to anencephaly.
Pathogenesis: Failure of posterior neuropore closure leads to spinal exposure and damage.
Clinical Importance: Varies based on defect severity; prevention via folic acid supplementation.
Cleft Lip and Palate
Etiology: Failure of facial structure fusion during embryonic weeks 4-12.
Genetic and Environmental Factors: Family history, teratogens (e.g., medications, alcohol).
Pathogenesis: Disruptions in maxillary and nasal processes lead to gaps in lip/palate.
Clinical Impact: Feeding difficulties, speech challenges; surgical interventions usually in infancy.
Tetralogy of Fallot
Etiology: Genetic mutations (e.g., NKX2-5, GATA4) and environmental risks.
Pathogenesis: Comprises four defects (pulmonary stenosis, VSD, overriding aorta, RVH) affecting circulation.
Clinical Significance: Cyanotic condition with potential for complications like heart failure.
Renal Agenesis (Potter Syndrome)
Etiology: Genetic mutations, chromosomal anomalies, environmental influences.
Pathogenesis: Normal kidney development disrupted; leads to oligohydramnios and resultant deformities.
Clinical Impact: Bilateral agenesis incompatible with life; unilateral affects future kidney function.
Omphalocele
Etiology: Genetic factors, infections during pregnancy.
Pathogenesis: Failure of intestines to return to the abdominal cavity leads to a membrane-covered sac of organs.
Clinical Significance: Risk of infection; surgical intervention needed after birth.
Gastroschisis
Etiology: Thought to be multifactorial; involves vascular disruptions.
Pathogenesis: Ischemia leads to a defect in abdominal wall, with intestines exposed.
Clinical Implications: Requires urgent surgical intervention; risk of bowel dysfunction.
Hydrops Fetalis
Etiology: Primarily due to Rh incompatibility leading to hemolysis.
Pathogenesis: Results in increased fluid accumulation and fetal anemia.
Clinical Findings: Generalized edema, detected via ultrasound; treatment may include RhIg administration and possible early delivery.