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MNI (bones and joints path) > L45- Pediatric Pathology II > Flashcards

L45- Pediatric Pathology II Flashcards

1
Q

define:

  • (1) premature birth
  • (2) SGA and LGA
  • (3) LBW
A

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

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2
Q

______ are the common causes of LBW

A

(low birth weight)

  • prematurity
  • fetal growth restriction for their gestational age (SGA)
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3
Q

list the risk factors for Premature birth

A
  • structural abnormalities of uterus, cervix, placenta
  • multiple gestation (twins, ect)
  • preterm placental rupture of membranes (vaginal discharge)
  • intrauterine infections
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4
Q

list the general causes of Fetal Growth restriction

A
  • fetal –> symmetric fetal growth restriction
  • placental –> asymmetric (typically small body and normal head size)
  • maternal –> asymmetric
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5
Q

list the fetal causes of fetal growth restriction

A
  • chromosomal disorders (17%)
  • congenital malformations
  • congenital infections
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6
Q

list the placental causes of fetal growth restriction

A
  • placenta previa
  • placenta abruption
  • placental infarction
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7
Q

list the maternal causes of fetal growth restriction

A
  • toxemia of pregnancy – pre-eclampsia
  • chronic hypertension
  • alcoholism, narcotic abuse, smoking
  • drugs (phenytoin)
  • malnutrition (eg. prolonged hypoglycemia)
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8
Q

Apgar score:

  • (1) times it is completed, include reason
  • (2) normal score range
  • an abnormal score indicates (3)
A

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

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9
Q

list the common complications of prematurity

A
  • 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

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10
Q

______ is the hallmark radiographic feature of RDS

A

diffuse symmetrical ground glass infiltrates: grainy appearance of lungs

-also bell-shaped thorax

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11
Q

RDS:

  • (1) all alternate names
  • (2) risk factors
A

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)

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12
Q

in RDS, the alveolar damage consisting of endothelial and epithelial damage leads to formation of…..

A

hyaline membranes: fibrin and necrotic cells

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13
Q

describe the progression of RDS

A
  • normal appearance at birth (usually)
  • w/in mins to hrs –> labored, grunting respirations –> progressively worsens

CXR- shows ground glass alterations

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14
Q

RDS gross appearance

A
  • normal size
  • solid, airless, reddish-purple in color (like a sac of blood)

resembles liver appearance

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15
Q

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
A

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)

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16
Q

RDS prevention (pre-birth and after-birth)

A

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
17
Q

list the long-term sequelae for RDS and what the causes are

A
  • Retrolental fibroplasia
  • Bronchopilmonary dysplasia

results from O2 toxicity (high concentration of ventilator administered oxygen for prolonged periods)

18
Q

Retrolental fibroplasia, aka (1):

  • results from (2) causing decreased levels of (3)
  • (4) is the end result
A

1- retinopathy of prematurity

2- O2 toxicity
3- low VEGF

4- permanent blindness

19
Q

Bronchopulmonary dysplasia:

  • (1) risk factors
  • (2) preventative measures
A

1- hyperventilation, vascular maldevelopment

2- gentler ventilation, glucocorticoids, prophylactic surfactant

20
Q

Bronchopulmonary dysplasia results from (1) and (2), causing (3) changes in lungs

A

1- arrested development of alveolar septum (at saccular stage)
2- RDS –> ventilator / hyperventilation

3- (dec alveolar septation) –> large simplified alveolar structures + dysmorphic capillary configuration

21
Q

NEC = (1):

  • disease affecting (2) at (3) timeline
  • (4)% mortality
A

1- neonetal necrotizing enterocolitis
2- premature and or LBW infants
3- 3rd wk of life
4- 25-50%

22
Q

list the predisposing factors for NEC

A
  • intestinal ischemia
  • bacterial colonization of gut
  • administration of formula feeds (not breast milk)
23
Q

NEC clinical features:

  • (1) status of infant before Sxs
  • (2) Sxs
  • (3) involved GIT segments
A

(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

24
Q

NEC gross appearance

A

(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)
25
Q

NEC radiograph appearance (diagnostic)

A

(neonatal necrotizing enterocolitis)

  • dilated loops of bowel
  • pneumatosis intestinalis –> gas bubbles win intestinal wall
26
Q

NEC microscopic appearance

A

(neonatal necrotizing enterocolitis)
-mucosal coagulative necrosis –> extends into and often thru submucosa and muscular layers

  • small air-filled spaces beneath mucosa = pneumatosis intestinalis
  • thinning of GIT walls
27
Q

NEC:

  • (1) early complications
  • (2) delayed complications
A

(neonatal necrotizing enterocolitis)
1- sepsis, shock, acute tubular necrosis, DIC, intestinal perforation

2- (usually after intestinal resection) short gut syndrome, malabsorption, strictures

28
Q

Neonatal Intraventricular Hemorrhage involves a bleed into (1) area with extension into (2) and beyond, define (1). (3) is the eventual progression, include occurrences that causing it. (4) are the resulting features of survivors.

A

1- germinal matrix: source of nerve cells in embryo/fetuses up to 33 wks gestation

2- ventricles

3- death is massive hemorrhage w/ tears in falx cerebri or tentorium

4:

  • cavitations / pseudocysts surrounded by hemosiderin laden macrophages, gliosis
  • hydrocephalus in 10-15% survivors

MNI (bones and joints path) (10 decks)

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