L45- Pediatric Pathology II Flashcards
define:
- (1) premature birth
- (2) SGA and LGA
- (3) LBW
1- before 37wks gestation
2:
- small for gestational age, <10th percentile
- large for GA, >90th percentile
3: Low Birth Weight, <2.5 kgs (5.5 lbs) at birth
______ are the common causes of LBW
(low birth weight)
- prematurity
- fetal growth restriction for their gestational age (SGA)
list the risk factors for Premature birth
- structural abnormalities of uterus, cervix, placenta
- multiple gestation (twins, ect)
- preterm placental rupture of membranes (vaginal discharge)
- intrauterine infections
list the general causes of Fetal Growth restriction
- fetal –> symmetric fetal growth restriction
- placental –> asymmetric (typically small body and normal head size)
- maternal –> asymmetric
list the fetal causes of fetal growth restriction
- chromosomal disorders (17%)
- congenital malformations
- congenital infections
list the placental causes of fetal growth restriction
- placenta previa
- placenta abruption
- placental infarction
list the maternal causes of fetal growth restriction
- toxemia of pregnancy – pre-eclampsia
- chronic hypertension
- alcoholism, narcotic abuse, smoking
- drugs (phenytoin)
- malnutrition (eg. prolonged hypoglycemia)
Apgar score:
- (1) times it is completed, include reason
- (2) normal score range
- an abnormal score indicates (3)
1:
- 1 minute, how well was birthing process tolerated
- 5 minutes, how well is infant tolerating new environment
2- 7-9/10
3- <7/10 –> neonate to the ICU
list the common complications of prematurity
- RDS (respiratory distress syndrome) / hyaline membrane disease
- necrotizing enterocolitis
- intraventricular and germinal matrix hemorrhage
Long-term sequelae: inc risk for developmental delay and other chronic diseases
______ is the hallmark radiographic feature of RDS
diffuse symmetrical ground glass infiltrates: grainy appearance of lungs
-also bell-shaped thorax
RDS:
- (1) all alternate names
- (2) risk factors
1- respiratory distress syndrome, hyaline membrane disease, neonatal bronchiectasis
2: **prematurity (90% of cases)
- perinatal asphyxia
- maternal DM
- C-section before onset of labor (no cortisol)
- twins
- males (2:1)
in RDS, the alveolar damage consisting of endothelial and epithelial damage leads to formation of…..
hyaline membranes: fibrin and necrotic cells
describe the progression of RDS
- normal appearance at birth (usually)
- w/in mins to hrs –> labored, grunting respirations –> progressively worsens
CXR- shows ground glass alterations
RDS gross appearance
- normal size
- solid, airless, reddish-purple in color (like a sac of blood)
resembles liver appearance
RDS microscopic appearance:
- (1) if infant dies w/in first several hrs of life
- (2) if infant survives for 12-24hrs
- (3) if infant dies several days later
1- necrotic cellular debris in terminal bronchioles, alveolar ducts
2:
- smooth homogenous pink membranes lining terminal / respiratory bronchioles and alveolar ducts
- membranes: necrotic alveolar type II pneumocytes, fibrin
- minimal neutrophilic inflammatory reaction
3: (evidence of reparative changes)
- proliferation of type I pneumocytes
- interstitial fibrosis
- residual hyaline membranes (fibrin, necrotic cells)
RDS prevention (pre-birth and after-birth)
Prebirth:
- delay labor until lungs mature
- induce maturation via steroids (acts as cortisol replacement)
- evaluate amniotic fluid: lecithin:sphinogomyelin >2.4 is normal — <1.5 is high risk for RDS
Postbirth:
- ventilatory support –> O2 supplementation
- surfactant replacement therapy
list the long-term sequelae for RDS and what the causes are
- Retrolental fibroplasia
- Bronchopilmonary dysplasia
results from O2 toxicity (high concentration of ventilator administered oxygen for prolonged periods)
Retrolental fibroplasia, aka (1):
- results from (2) causing decreased levels of (3)
- (4) is the end result
1- retinopathy of prematurity
2- O2 toxicity
3- low VEGF
4- permanent blindness
Bronchopulmonary dysplasia:
- (1) risk factors
- (2) preventative measures
1- hyperventilation, vascular maldevelopment
2- gentler ventilation, glucocorticoids, prophylactic surfactant
Bronchopulmonary dysplasia results from (1) and (2), causing (3) changes in lungs
1- arrested development of alveolar septum (at saccular stage)
2- RDS –> ventilator / hyperventilation
3- (dec alveolar septation) –> large simplified alveolar structures + dysmorphic capillary configuration
NEC = (1):
- disease affecting (2) at (3) timeline
- (4)% mortality
1- neonetal necrotizing enterocolitis
2- premature and or LBW infants
3- 3rd wk of life
4- 25-50%
list the predisposing factors for NEC
- intestinal ischemia
- bacterial colonization of gut
- administration of formula feeds (not breast milk)
NEC clinical features:
- (1) status of infant before Sxs
- (2) Sxs
- (3) involved GIT segments
(neonatal necrotizing enterocolitis)
1- premature infant OR at term LBW infant with h/o asphyxia (RDS) requiring ventilation
2- (development of intestinal obstructions after oral feedings begin)
- abdominal distension, bloody stools
- shock, DIC —> progression to death
3- terminal ileum, cecum, R colon
NEC gross appearance
(neonatal necrotizing enterocolitis)
-involved bowel distended
- thin, delicate walls w/ spotty areas of necrosis and possible perforation
- pneumatosis intestinalis –> gas cysts in affected / necrotized areas (w/in intestinal wall)
