Pediatric Pathology Flashcards by Stacey Hansen

Inability to aerate lungs easily due to lack of pulmonary surfactant
Aka Hyaline Membrane Disease
Mostly a disease of premature infants and infants of diabetes mothers

Neonatal respiratory distress syndrome

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Neonatal respiratory distress syndrome is caused by this

Lack of pulmonary surfactant

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Pulmonary surfactant is produced by this

Type II pneumocytes

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Pulmonary surfactant contains glycoproteins and lipids, and this which can be measured to determined how mature a fetus is

Phosphatidylcholine (lecithin)

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Birth before 37 weeks GA

Preterm

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In Neonatal respiratory distress syndrome, alveolar walls produce this

Exudative effusion
Fluid fills alveoli –> increased lung stiffness, labored breathing

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Alveoli lined by eosinophilic material

Hyaline membrane

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Hyaline membrane is seen in this condition

Neonatal respiratory distress syndrome

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4 risk factors of Neonatal respiratory distress syndrome

Prematurity
C section
Maternal diabetes
High O2 ventilation

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Prematurity, C section, Maternal diabetes and High O2 ventilation are risk factor for this

Neonatal respiratory distress syndrome

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Antenatal corticosteroid and postnatal surfactant are prevention/treatment for this

Neonatal respiratory distress syndrome

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2 preventatives/treatments for Neonatal respiratory distress syndrome

Antenatal corticosteroid
Postnatal surfactant

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Production of pulmonary surfactant is increased by this

Cortisol

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Production of pulmonary surfactant is decreased by this

Insulin

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Cortisol has this effect on production of pulmonary surfactant

Increased

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Insulin has this effect on production of pulmonary surfactant

Decreased

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Bronchopulmonary dysplasia and Retinopathy of prematurity are complications of this

Neonatal respiratory distress syndrome

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Complication of Neonatal respiratory distress syndrome that may result in fibroproliferative pulmonary distress (if late prematurity) or lack of branching and septation (at extreme prematurity)

Bronchopulmonary dysplasia

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Result of bronchopulmonary dysplasia in baby born with late prematurity (33 weeks) in Neonatal respiratory distress syndrome

Fibroproliferative pulmonary distress

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Result of bronchopulmonary dysplasia in baby born at extreme prematurity (24 weeks) in Neonatal respiratory distress syndrome

Lack of branching and septation

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Complication of Neonatal respiratory distress syndrome that involves vascular proliferation due to repair process (VEGF)

Retinopathy of prematurity

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Intestinal necrosis due to abnormal microbial flora

Necrotizing Enterocolitis

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What causes necrotizing enterocolitis in premature infants?

Abnormal microbial flora
Much more common with formula feeding

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Bloody stools, abdominal distension, and Pneumatosis intestinalis are seen in this condition of premature infants

Necrotizing enterocolitis

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Pneumoperitoneum if perforated is seen in this condition in premature infants

Necrotizing Enterocolitis

Long-term consequence of intracranial hemorrhage

Periventricular leukomalacia (lack of myelination, upper motor neuron lesion)

Intracranial hemorrhage begins with hemorrhage into this

Subependymal germinal matrix (lining of ventricles)

Intracranial hemorrhage in premature infants may produce this

Infarction

Periventricular leukomalacia is a long-term consequence of this

Intracranial hemorrhage

Early onset (first 7 days) perinatal sepsis is most commonly due to this infection

Group B Strep Pneumonia, sepsis, and meningitis also common

Group B strep is most common in perinatal sepsis of this onset

Early onset (first 7 days)

Later onset perinatal sepsis is due to this type of organisms acquired at delivery/prenatal

Long latency organisms like Listeria or Candida

Long latency organisms like Listeria or Candida are more commonly seen in perinatal sepsis of this onset

Later onset (7 days - 3 months)

Intrauterine accumulation of fetal edema

Fetal Hydrops

Fetal hydrops are intrauterine accumulation of this

Fetal edema

Immune hydrops are due to this

Blood group incompatibility (ABO, Rho)

Blood group incompatibility (ABO, Rho) cause this category of fetal hydrops

Immune hydrops

Anatomic or chromosomal conditions cause this category of fetal hydrops

Non-immune hydrops

Severity of fetal hydrops due to ABO blood group incompatibility

Usually mild or subclinical

Most severe cases of fetal hydrops are due to this

Rh blood group incompatibility

Only immunoglobulin that crosses the placenta

IgG

Hemolysis release this, which the liver metabolizes into bilirubin

Hemoglobin

Hemolysis releases hemoglobin, which the liver metabolizes to this

Bilirubin

Bilirubin deposits in brain

Kernicterus

Kernicterus is deposits of these in brain

Bilirubin

Bilibubin makes things this color

Yellow (jaundice)

Hemolysis has this effect on O2 carrying capacity

Decreases (anemia)

Compensatory RBC hyperplasia causes this

Hepatomegaly, Splenomegaly Hepatic hematopoiesis

Severe anemia due to hemoglobin production defect

Thalassemia

Parvovirus B19 infects these

Erythrocyte precursors

Prenatal or Postnatal infection of Parvovirus B19: Usually a self-limited infection with rash and fever

Postnatal Usually subclinical unless person has hemoglobin production disorder

Prenatal or Postnatal infection of Parvovirus B19: Infects erythrocyte precursors --> transient red cell aplasia

Postnatal

Transient Red Cell Aplasia occurs due to this

Parvovirus B19 postnatal infection

Prenatal or Postnatal infection of Parvovirus B19: Infection leads to profound anemia Also high output heart failure and fetal hydrops

Prenatal

During 2nd-3rd trimesters, there is normally very high proliferation of these cells Reason for profound anemia in prenatal infection of Parvovirus B19

RBC

Most common lethal genetic disease of Caucasians

Cystic Fibrosis

Inheritance pattern of cystic fibrosis

Autosomal recessive

CFTR gene is on this chromosome

CFTR absorbs or releases CL from/into lumen of sweat glands?

Absorbs

CFTR absorbs or releases CL from/into other glands besides sweat glands?

Releases (increase Na, increase H2O = fluid like, less thick secretions)

CFTR modifies activity of this channel

Epithelial sodium channel, ENaC

Obstructive lung disease with thick mucus and superimposed infections Caused by recurrent infections in cystic fibrosis

Chronic bronchitis

Tissue destruction of bronchial wall Caused by recurrent infections in cystic fibrosis

Bronchiectasis

Common organism for lung infections that develops alginate capsule in hypoxic environment

Pseudomonas aeruginosa

In cystic fibrosis patients, delaying this is key

Antibiotic resistance

2 most common causes of death in cystic fibrosis

Lung disease and Heart failure

Deficiencies of vitamins A, D, E, K occur in this condition

Cystic fibrosis

Foul smelling, bulky, greasy stools occur in this condition

Cystic fibrosis Due to pancreatitis; cannot absorb fats = malabsorption

Phenylketonuria is a deficiency of this

Phenylalanine hydroxylase

Accumulated metabolites cause musty "mouselike" odor in this condition

Phenylketonuria

Phenylalanine metabolites accumulate in Phenylketonuria and cause this damage

CNS damage

Galactosemia is a deficiency of this

Galactose-1-phosphate uridyl transferase

Thick secretions in the pancreas of patients with Cystic Fibrosis leads to this

Duct obstruction

Why do cystic fibrosis patients have malabsorption?

Thick secretion in pancreas lead to duct obstruction and subsequence damage/pancreatitis, pancreatic insufficiency Cannot digest fats and proteins or absorb fats

Destruction of endocrine pancreas in cystic fibrosis leads to this

Diabetes

Pancreas with morphology of cyst surrounded by scar is seen in this condition

Cystic fibrosis

5-10% of patients with this have meconium ileus at birth

cystic fibrosis

This is seen in 5-10% of cystic fibrosis patients at birth, results in no stools for days after delivery

Meconium ileus

In cystic fibrosis, bile duct obstruction leads to this

Fibrosis (50%) Cirrhosis (<10%) of liver

Bilateral vas deferens agenesis (azoospermia) and cervical mucus inpissation are reproduction results of this condition

Cystic Fibrosis

Why do female cystic fibrosis patients have decreased fertility?

Cervical mucus inspissation (thickening of fluid prevents sperm cells from traveling)

Why do male patients with cystic fibrosis have fertility issues?

Bilateral vas deferens agenesis --> azoospermia