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MOD > Chapter 10 Part 2 > Flashcards

Chapter 10 Part 2 Flashcards

1
Q

Definition of vertical transmission

A

infectious agent passed from mother to fetus via three routes: placental-fetal, during birth, postnatal

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2
Q

Definition of placental-fetal transmission

A

Occurs when mother is infected during pregnancy, interferes with fetal development; effects vary depending on gestational age of fetus

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3
Q

Infection transmission during birth

A

contact with infectious agent during passage through birth canal

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4
Q

Postnatal transmission of infectious agents

A

agents transmitted through maternal milk like CMV, HIV, HBV

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5
Q

What are the two major routes of perinatal infections

A

Transcervical, transplacental

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6
Q

How does a transcervical infection pass to a newborn?

A

Inhalation of amniotic fluid before delivery or passage through infected birth canal

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7
Q

What is one mechanism responsible for preterm delivery as a result of transcervical infections?

A

Inflammation causing rupture of amniotic sac and release of prostaglandins from neutrophils

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8
Q

What are the most common conditions associated with bacterial transcervical infections?

A

Meningitis, sepsis, pneumonia

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9
Q

What type of infections pass transplacentally via the chorionic villi?

A

Parasites and viruses

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10
Q

Parvovirus B19 mode of infection and clinical outcome

A

Transplacentally; spontaneous abortion, hydrops fetalis, still birth, congenital anemia; commonly seen in erythroid cells

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11
Q

Clinical manifestations of TORCH infections

A

fever, encephalitis, chorioretinitis, hepatosplenomegaly, pneumonitis, myocarditis, hemolytic anemia, skin lesions

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12
Q

Long term clinical manifestations of TORCH infections

A

intellectual disability, growth retardation, cataracts, congenital cardiac anomalies, bone defects

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13
Q

Bacteria of TORCH infection group

A

Toxoplasmosis, other (syphilis, parvovirus B19), rubella, cytomegalovirus, herpesvirus

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14
Q

Definition of fetal hydrops

A

accumulation of edema fluid in two or more fetal compartments during intrauterine growth, most commonly pleural, pericardial, peritoneal, skin; can be generalized or local

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15
Q

Cause of immune hyrdrops

A

blood group antigen compatibility between mother and fetus

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16
Q

Antigens that cause immune hydrops

A

D Rh and ABO blood groups (Rh- mother and Rh+ father)

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17
Q

Etiology of immune hydrops

A

Immunization of mother by exposure to other blood type via placenta or birth causes formation of IgM abs, exposure during a second pregnancy leads to an IgG response

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18
Q

What would protect the mom from Rh immunization?

A

ABO incompatibility, no transplacental bleed during birth

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19
Q

Common treatment for Rh Immunization

A

RhIg containing anti-D antibodies

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20
Q

Major consequences of hemolysis in immune hydrops

A

Anemia (cardiac decomp and extramedullary hematopoiesis) and Hgb degradation (kernicterus and jaundice)

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21
Q

Three major etiologies of non-immune hydrops

A

chromosomal defects, csomal anomalies, fetal anemia (alpha thalassemia, twin-twin transfusion, parvovirus B19)

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22
Q

Gross morphological changes in hydrops

A

pale fetus and placenta, enlarged liver and spleen, compensatory erythrocyte hyperplasia in bone, extramedullary hematopoiesis,

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23
Q

Where is kernicterus most prominent?

A

basal ganglia

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24
Q

Mechanism for generalized hydrops

A

severe hemolysis leads to hypoxic injury to heart and liver, decreasing albumin and leading to heart failure; increased hydrostatic pressure and decreased oncotic pressure

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25
Q

Erythroblastosis fetalis

A

Alloimmune hemolytic anemia, Rh incompatibility

Microscopically: polychromatophilic macrocytes (CHARACTERISTIC), nucleated RBCs, ejected nuclei

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26
Q

Clinical manifestations of fetal hydrops

A

pallor, hepatosplenomegaly, jaundice, generalized edema, neuro injury

27
Q

Definition of inborn errors of metabolism

A

group of rare genetic diseases resulting from defect in enzyme or transport protein that results in a block of metabolic pathway

28
Q

Common abnormalities suggesting IEM

A

deafness, abnormal hair, hydrops, seizures, hypotonia, poor feeding, cataract, cherry red macula, myopathy

29
Q

Two categories of IEM

A

disorders that result in toxic accumulation, disorders of energy production and utilization

30
Q

Goals of IEM treatment

A

prevent substance accumulation, eliminate toxic metabolite, correct metabolite abnormality

31
Q

PKU etiology

A

deficiency of phenylalanine hydroxylase and resultant hyperphenylalanemia

32
Q

When do PKU signs start to appear?

A

about 6 mo after birth - mental disability; will eventually lead to seizures, decreased pigmentation, eczema

33
Q

Maternal PKU etiology

A

hyperphenylalanemia in asymptomatic mothers leading to teratogenic effects of phenylalanine on developing fetus

34
Q

Clinical signs of PKU

A

musty odor to urine, light hair and skin, brain damage

35
Q

Diagnosis of PKU

A

not determined with screening tests because of significant number of genes involved, must use blood test to differentiate benign hyperphenylalanemia from PKU

36
Q

What form of PKU cannot be treated by dietary restriction?

A

abnormalities in recycling BH4 (cofactor for PAH)

37
Q

Etiology of galactosemia

A

Lack of galactose-1-phosphate uridyl transferase or galactokinase (rare)

38
Q

Pathogenesis of galactosemia

A

Build up of glactose-1-phosphate in liver, spleen, eye lens, kidney, heart, cerebral cortex leading to build up of galactitol and galactonate

39
Q

Clinical features of galactosemia

A

hepatomegaly, lens opacification, CNS alterations due to loss of nerve cells

40
Q

Clinical features of galactosemia in infants

A

failure to thrive, vomiting, diarrhea, jaundice, hepatomegaly, mental retardation, cataracts, hemolysis, coagulopathy

41
Q

Etiology of cystic fibrosis

A

inherited disorder of ion transport that affects fluid secretion in exocrine glands, repro, GI, and resp epithelia

42
Q

Clinical features of CF

A

chronic lung disease secondary to recurrent infections, pancreatic insufficiency, steatorrhea, malnutrition, hepatic cirrhosis, intestinal obstruction, male infertility

43
Q

Primary defect in CF

A

epithelial chloride channel coded on chromosome 7q31.2

44
Q

CFTR structure

A

two transmembrane domains, two nucleotide binding domains, regulatory domain that contains PKA and PKC phosphorylation sites

45
Q

What other channels does CFTR regulate

A

rectified chloride channels, rectified potassium channels, gap junction channels, bicarb transport, ENaC (most significant)

46
Q

Effect of loss of CFTR in sweat ducts

A

hypertonic sweat

47
Q

Pathogenesis of resp and intestinal complications in CF

A

isotonic but low volume surface fluid layer, defective mucociliary action and viscid secretions

48
Q

Class I CF

A

defective protein synthesis, complete CFTR lack

49
Q

Class II CF

A

abnormal protein folding, processing, or trafficking; MOST COMMON

50
Q

Class III CF

A

defective regulation, normal amt of CFTR but non functional

51
Q

Class IV CF

A

decreased conductance, mutation in transmembrane domain

52
Q

Class V CF

A

reduced abundance, reduced amount of normal protein

53
Q

Class VI CF

A

altered regulation of ion channels

54
Q

Clinical signs associated with atypical CF

A

idiopathic chronic pancreatitis, late-onset chronic pulmonary disease, idiopathic bronchiectasis, obstructive azoospermia

55
Q

Environmental modifiers of CF

A

virulence of organisms, therapeutic efficacy, concurrent infections, tobacco or allergen exposure

56
Q

Genetic modifiers of CF

A

gene polymorphisms in MBL2, TGFB1, IFRD1 (all modify lungs ability to resist infection

57
Q

Common gross morphological changes in CF

A

pancreatic insufficiency, defective mucociliary action; SWEAT GLANDS morphologically UNaffected

58
Q

Morphological changes of pancreas in CF

A

atrophy of exocrine portion of pancreas, impaired absorption, squamous metaplasia of pancreatic ducts, meconium ileus

59
Q

Morphological changes of liver in CF

A

bile canaliculi plugged by mucus, steatosis

60
Q

Morphological changes of salivary glands in CF

A

progressive ductual dilation, squamous metaplasia, glandular atrophy and fibrosis

61
Q

Pulmonary changes in CF

A

viscous secretions lead to obstruction and infection, distended bronchioles, hyperplasia and hypertrophy of goblet cells, abscesses

62
Q

Common organisms responsible for lung infections in CF

A

Staphylococcus aureus, Haemophilus influenzae, Pseudomonas aeruginosa, Burkholderia cepacia

63
Q

Clinical features of CF

A

meconium ileus, intussusception, persistent colonization, exocrine pancreatic insufficiency, recurrent nasal polyps, infertility, liver disease, malabsorption, fatty stools

64
Q

What is necessary for CF diagnosis?

A

Classical charcteristics, sweat chloride test, immunoreactive trypsinogen, CFTR gene sequencing

MOD (34 decks)

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