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Immunology > Pediatric Pathology > Flashcards

Pediatric Pathology Flashcards

1
Q

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

A

Neonatal respiratory distress syndrome

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2
Q

Neonatal respiratory distress syndrome is caused by this

A

Lack of pulmonary surfactant

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3
Q

Pulmonary surfactant is produced by this

A

Type II pneumocytes

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4
Q

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

A

Phosphatidylcholine (lecithin)

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5
Q

Birth before 37 weeks GA

A

Preterm

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6
Q

In Neonatal respiratory distress syndrome, alveolar walls produce this

A

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

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7
Q

Alveoli lined by eosinophilic material

A

Hyaline membrane

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8
Q

Hyaline membrane is seen in this condition

A

Neonatal respiratory distress syndrome

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9
Q

4 risk factors of Neonatal respiratory distress syndrome

A

Prematurity
C section
Maternal diabetes
High O2 ventilation

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10
Q

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

A

Neonatal respiratory distress syndrome

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11
Q

Antenatal corticosteroid and postnatal surfactant are prevention/treatment for this

A

Neonatal respiratory distress syndrome

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12
Q

2 preventatives/treatments for Neonatal respiratory distress syndrome

A

Antenatal corticosteroid
Postnatal surfactant

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13
Q

Production of pulmonary surfactant is increased by this

A

Cortisol

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14
Q

Production of pulmonary surfactant is decreased by this

A

Insulin

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15
Q

Cortisol has this effect on production of pulmonary surfactant

A

Increased

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16
Q

Insulin has this effect on production of pulmonary surfactant

A

Decreased

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17
Q

Bronchopulmonary dysplasia and Retinopathy of prematurity are complications of this

A

Neonatal respiratory distress syndrome

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18
Q

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)

A

Bronchopulmonary dysplasia

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19
Q

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

A

Fibroproliferative pulmonary distress

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20
Q

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

A

Lack of branching and septation

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21
Q

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

A

Retinopathy of prematurity

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22
Q

Intestinal necrosis due to abnormal microbial flora

A

Necrotizing Enterocolitis

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23
Q

What causes necrotizing enterocolitis in premature infants?

A

Abnormal microbial flora
Much more common with formula feeding

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24
Q

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

A

Necrotizing enterocolitis

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25
Q

Pneumoperitoneum if perforated is seen in this condition in premature infants

A

Necrotizing Enterocolitis

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26
Q

Long-term consequence of intracranial hemorrhage

A

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

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27
Q

Intracranial hemorrhage begins with hemorrhage into this

A

Subependymal germinal matrix (lining of ventricles)

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28
Q

Intracranial hemorrhage in premature infants may produce this

A

Infarction

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29
Q

Periventricular leukomalacia is a long-term consequence of this

A

Intracranial hemorrhage

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30
Q

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

A

Group B Strep
Pneumonia, sepsis, and meningitis also common

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31
Q

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

A

Early onset (first 7 days)

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32
Q

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

A

Long latency organisms like Listeria or Candida

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33
Q

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

A

Later onset (7 days - 3 months)

34
Q

Intrauterine accumulation of fetal edema

A

Fetal Hydrops

35
Q

Fetal hydrops are intrauterine accumulation of this

A

Fetal edema

36
Q

Immune hydrops are due to this

A

Blood group incompatibility (ABO, Rho)

37
Q

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

A

Immune hydrops

38
Q

Anatomic or chromosomal conditions cause this category of fetal hydrops

A

Non-immune hydrops

39
Q

Severity of fetal hydrops due to ABO blood group incompatibility

A

Usually mild or subclinical

40
Q

Most severe cases of fetal hydrops are due to this

A

Rh blood group incompatibility

41
Q

Only immunoglobulin that crosses the placenta

A

IgG

42
Q

Hemolysis release this, which the liver metabolizes into bilirubin

A

Hemoglobin

43
Q

Hemolysis releases hemoglobin, which the liver metabolizes to this

A

Bilirubin

44
Q

Bilirubin deposits in brain

A

Kernicterus

45
Q

Kernicterus is deposits of these in brain

A

Bilirubin

46
Q

Bilibubin makes things this color

A

Yellow (jaundice)

47
Q

Hemolysis has this effect on O2 carrying capacity

A

Decreases
(anemia)

48
Q

Compensatory RBC hyperplasia causes this

A

Hepatomegaly, Splenomegaly
Hepatic hematopoiesis

49
Q

Severe anemia due to hemoglobin production defect

A

Thalassemia

50
Q

Parvovirus B19 infects these

A

Erythrocyte precursors

51
Q

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

A

Postnatal
Usually subclinical unless person has hemoglobin production disorder

52
Q

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

A

Postnatal

53
Q

Transient Red Cell Aplasia occurs due to this

A

Parvovirus B19 postnatal infection

54
Q

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

A

Prenatal

55
Q

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

A

RBC

56
Q

Most common lethal genetic disease of Caucasians

A

Cystic Fibrosis

57
Q

Inheritance pattern of cystic fibrosis

A

Autosomal recessive

58
Q

CFTR gene is on this chromosome

A

7

59
Q

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

A

Absorbs

60
Q

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

A

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

61
Q

CFTR modifies activity of this channel

A

Epithelial sodium channel, ENaC

62
Q

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

A

Chronic bronchitis

63
Q

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

A

Bronchiectasis

64
Q

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

A

Pseudomonas aeruginosa

65
Q

In cystic fibrosis patients, delaying this is key

A

Antibiotic resistance

66
Q

2 most common causes of death in cystic fibrosis

A

Lung disease and Heart failure

67
Q

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

A

Cystic fibrosis

68
Q

Foul smelling, bulky, greasy stools occur in this condition

A

Cystic fibrosis
Due to pancreatitis; cannot absorb fats = malabsorption

69
Q

Phenylketonuria is a deficiency of this

A

Phenylalanine hydroxylase

70
Q

Accumulated metabolites cause musty “mouselike” odor in this condition

A

Phenylketonuria

71
Q

Phenylalanine metabolites accumulate in Phenylketonuria and cause this damage

A

CNS damage

72
Q

Galactosemia is a deficiency of this

A

Galactose-1-phosphate uridyl transferase

73
Q

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

A

Duct obstruction

74
Q

Why do cystic fibrosis patients have malabsorption?

A

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

75
Q

Destruction of endocrine pancreas in cystic fibrosis leads to this

A

Diabetes

76
Q

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

A

Cystic fibrosis

77
Q

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

A

cystic fibrosis

78
Q

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

A

Meconium ileus

79
Q

In cystic fibrosis, bile duct obstruction leads to this

A

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

80
Q

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

A

Cystic Fibrosis

81
Q

Why do female cystic fibrosis patients have decreased fertility?

A

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

82
Q

Why do male patients with cystic fibrosis have fertility issues?

A

Bilateral vas deferens agenesis –> azoospermia

Immunology (21 decks)

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