Chapter 10 Morphology Flashcards
Appearance of lungs in children who die early
necrotic cellular debris can be seen in terminal bronchioles and alveolar ducts
Necrotic tissue in lungs of infant in distress
become incorporated within eosinophilic hyaline membranes linign the respiratory bronchioles, alveolar ducts, and alveoli
Membranes of lungs of infant in distress
- Made up of fibrin mixed with cell debris derived from necrotic type II pneumocytes
- Neutrophilic inflammatory reaction
Lungs of infants who survive more than 48 hours (3)
Alvelolar epithelium proliferates
May detach into the airspace
Undergoes partial digestion or phagocytosis by macrophages
Lung appearance of children in RDS
normal size lungs, solid, airless, reddish purple, and sink in water
Where does necrotizing enterocolitis occur?
terminal ileum, cecum, and right colon
Appearance of involved segment in necrotizing enterocolitis
distended, friable, congested, or can be gangrenous
Microscopic necrotizing enterocolitis
mucosal or transmural coagulative necrosis
ulceration
bacterial colonization
submucosal gas bubbles
Reparative changes in necrotizing enterocoitis
formation of granulation tissue and fibrosis
Hydrops associated with fetal anemia (4)
Both fetus and placenta are pale
Liver and spleen are enlarged from cardiac failure and congestion
Bone marrow has hyperplasia of erythroid precursors
Extramedullary hematopoiesis in liver, spleen, and lymph nodes
Why is there increased hematopoietic activity in hydrops?
presence in peripheral circulation of large numbers of immature red cells including retinocytes, normoblasts, and erythroblasts
*erythroblastosis fetalis
What is the most serious threat in fetal hydrops?
CNA damage known as kernicterus
Brain appearance in kernicterus (2)
Enlarged and edematous
Has yellow color - particularly in basal ganglia
Bilirubin level in blood for kernicterus
greater than 20 mg/dL in infants
Mucus secretion defect in nonclassic CF (3)
Leads to defective mucociliary action
Obstruction of bronchi and bronchioles
Crippling fatal pulmonary infections
What is not morphologically affected in nonclassic CF?
sweat glands
Pancreatic abnormalities in CF for mild cases
accumulation of mucus in small ducts
Pancreatic abnormalities in CF for severe cases
ducts are completely plugged causing atrophy of exocrine glands and fibrosis
Results from loss of pancreatic exocrine secretion in CF
impairs fat absorption and avitaminosis A can cause squamous metaplasia in pancreatic ducts
Meconium ileus
thick viscid plugs of mucus found in the small intestine that cause small bowel obstruction
Liver involvement in CF
bile canaliculi are plugged by mucus materia
Findings of a CF liver
hepatic steatosis and focal biliary cirrhosis
Histologic changes in salivary glands in CF patients
progressive dilation of ducts, squamous metaplasia of epithelium and glandular atrophy, and fibrosis
Pulmonary changes in CF patients
*most serious complication
Secondary obstruction and infection of the air passages
Bronchioles are distended with thick mucus
Marked hyperplasia and hypertrophy of cells
What are the 3 most common organisms responsible for lung infection?
haemophilus influenzae
peudomonas aeruginosa
staphylococcus aureus
What causes chronic inflammation in CF patients?
alginate-producing P. aeruginosa