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Pathology Finals > Disease Of Infancy And Childhood > Flashcards

Disease Of Infancy And Childhood Flashcards

1
Q

Congenital anomalies

Multifactorial in origin

A

Malformations

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2
Q

Congenital anomalies

Result from secondary destruction of an organ or body region that was previously normal in development.

A

Disruptions

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3
Q

Congenital anomalies

Localized or generalized compression of the growing fetus by abnormal biochemical forces, leading to structural abnormalities.

A

Deformations

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4
Q

Congenital anomalies

Cascade anomalies triggered by one initiating aberration

A

Sequence

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5
Q

Congenital anomalies

Usually occur singly: sometimes multiple

A

Sequence

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6
Q

Congenital anomalies

Extrinsic disturbance in morphogenesis

A

Disruptions

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7
Q

Congenital anomalies

Example of malformations

A

Congenital heart defects

Anencephaly (absence of brain)

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8
Q

Congenital anomalies

Example of disruptions

A

Amniotic bands

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9
Q

Congenital anomalies

Example of deformations

A

Club feet

Uterine constraint

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10
Q

Congenital anomalies

35-38th week gestations, rapid increase in the size of the fetus outspaces growth of uterus and decrease amniotic fluid.

A

Deformations

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11
Q

Congenital anomalies

Example of sequence

A

Oligohydramnios

Potter sequence

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12
Q

Cannot be explained on single initiating defect

Most often caused a single etiologic agent.

A

Malformation syndrome

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13
Q

Malformation syndrome

Causes of anomalies

A

Genetic
Environmental
Multifactorial

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14
Q

Malformation syndrome

80-90% of fetuses with aneuploidy and other abnormalities of chromosome number die in utero, the majority in the earliest stages of gestation.

A

Genetic causes

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15
Q

Malformation syndrome

Genetics follow _____________ pattern of inheritance

A

Mendelian

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16
Q

Malformation syndrome

Genetics

How many percent are autosomal dominant or recessive and xlinked

A

90% autosomal and recessive

10% x linked

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17
Q

Malformation syndrome
Genetics

Most common developmental defect of the forebrain and midface.

A

Holoprosencephaly

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18
Q

Malformation syndrome
Genetics

A critical role in morphogenesis and loss of function mutations

A

Hedgehog signaling

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19
Q

Malformation syndrome

Environmental causes

At risk period shortly before conception to the 16th week of gestation, greater hazard in the first 8weeks.

A

Rubella

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20
Q

Malformation syndrome

Environmental causes

Congenital rubella

A

Cataracts
Heart defects
Deafness
Mental retardation

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21
Q

Malformation syndrome

Environmental causes

Mostly asymptomatic
Most common fetal viral infection

A

Intrauterine CMV infection

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22
Q

Malformation syndrome

Environmental cause

CMV highest risk during

A

Second semester

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23
Q

Malformation syndrome

Environmental causes

CMV is CNS involvement is a major feature are

A

Mental retardation
Microcephaly
Deafness
Hepatosplenomegaly

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24
Q

Malformation syndrome

Less than 1% congenital malformations

A

Teratogens

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25
Q

Malformation syndrome
Drugs and other Chemicals

Most widely used teratogen

A

Alcohol

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26
Q

Malformation syndrome
Drugs and other Chemicals

Alcohol disrupts 2 signaling pathways

A

Hedgehog

Retinoic acid

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27
Q

Malformation syndrome
Drugs and other Chemicals

Spontaneous abortion, premature labor placental abnormalities; low birth weight babies, and prone to sudden infant syndrome

A

Nicotine

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28
Q

Malformation syndrome
Drugs and other Chemicals

Radiation

A

Microcephaly
Blindness
Skill defects
Spina bifida

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29
Q

Malformation syndrome
Drugs and other Chemicals

Maternal diabetes

A

Cardiac anomalies
Neural tube defects
CNS malformations

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30
Q

Malformation syndrome
Drugs and other Chemicals

Organomegaly and increase body fat and mass

A

Maternal diabetes

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31
Q

Malformation syndrome
Drugs and other Chemicals

Most common genetic causes of congenital malformation
Cleft lip and palate
Neural tube defect (folic acid)

A

Multifactorial inheritance

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32
Q

Two phases of intrauterine fetal developmant

A

Embryonic period - 1st 9weeks of pregnancy

Early embryonic period - 1st 3weeks after fertilization - abortion and death

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33
Q

Extremely susceptibility to teratogenesis, peaks at 4th-5th week

A

3rd-9thweek

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34
Q

Growth retardation, injury to already formed organs

A

Fetal period until birth

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35
Q

Craniofacial abnormalities including holoproncephaly and cyclopia (single fused eye)

A

Cyclophosphamide

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36
Q

HOX proteins

HOX mutations

A

Valproic acid

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37
Q

2nd most common cause of neonatal mortality

AOG

A

Prematurity

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38
Q

Major risk factors of prematurity

A

PPROM
Intra uterine infection
Uterine, cervical and placental abnormalities
Multiple gestation

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39
Q

Responsible for as many as third of all preterm deliveries

A

PPROM

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40
Q

PPROM refers to spontaneous ROM occuring before

A

37 week

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41
Q

In contrast to PPROM. PROM rupture of membranes after

A

37weeks

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42
Q

Pathophysiology of PPROM

A

Inflammation of placental membranes,

Enhanced collagen degradation by MMP

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43
Q

PPROm risk factors

A

Smoking
HS of vaginal bleeding
Low socioeconomic status

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44
Q

Major cause of premature labor with or without intact membranes
Present at 25% preterm births

A

Intrauterine infection

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45
Q

Example of intrauterine infection

A

Chorioamnionitis (inflammation of placental membranes)

Funisitis ( inflammation of fetal umbilical cord )

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46
Q

Most common microorganism of intra uterine infection

A 
U. Urealyticum
Mycoplasma hominis
G. Vaginalis
Trichomonas 
Gonorrhea
Chlamydia
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47
Q

Hyaline membrane disease
NecrotiIng enterocolitis
Sepsis
Intra ventricular and germinal matrix hemorrhage

A

Hazards of prematurity

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48
Q

Neonatal respiratory distress syndrome

A

Hyaline membrane disease

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49
Q

Infants who weights less than 2500gm are born at term (small for gestational age) suffers from

A

FGR fetal growth restriction

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50
Q

Factors known to result to FGR

A

Fetal abnormalities
Placental abnormality
Maternal abnormality
Confined placental mosaicism

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51
Q

Fetal abnormalities

A

Chromosomal disorders
Congenital anomalies
Congenital/fetal infections

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52
Q

Congenital /fetal infections considered in all infants with FGR

A

TORCH

Toxoplasmosis
Other viruses and bacteria
Rubella
CMV
Herpes
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53
Q

Proportionate FGR, meaning all organ systems are similarly affected

A

SGA

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54
Q

Asymmetric, disproportionate GR with relative sparing of the brains

A

Placental abnormality

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55
Q

Placental abnormality usually during

A

3rd trimester

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56
Q

Placental abnormality

A

Placenta previa
Thrombosis
Multiple gestation

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57
Q

Most common factors associated with SGA

A

Maternal abnormality

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58
Q

Maternal abnormality conditions that result in decreased placental blood flow.

A

Pre eclapmsia
Narcotic abuse
Malnutrition
Etc

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59
Q

Recently discovered causes of FGR

Mutations occur later and within the dividing trophoblast or extra embryonic progenitor cells

A

Confined placental mosaicism

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60
Q

Most common cause is respiratory distress syndrome also known as hyaline membrane disease

A

Neonatal respiratory distress syndrome

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61
Q

Major cause of NRDS

A

Sedation of mother
Fetal head injury
Aspiration of Blood
Hypoxia

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62
Q

Clinical findings of NRDS

A

Preterm
Male
DM
CS

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63
Q

Dx of NDRS

A

Fine rhales

Ground glass picture

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64
Q

Pathogenesis of NRDS

A

Immaturity of the lungs

RDS inversely proportional with gestational age

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65
Q

Etiology of NDRS

A

Deficiency of lung surfactant-fundamental defects in RD
Di palmitoyl phosphatidyl choline
Phosphatidyl glycerol
Surfactant associated proteins

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66
Q

Severe respiratory failure in neonates with congenital deficiency of surfactant caused by

A

Mutation of SFTPB and SFTBC

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67
Q

Surfactant is accelerated after

A

35th week of gestation

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68
Q

Compounded by soft thoracic wall that I spelled in as diaphragm descend q

A

Stiff atelectatic lung

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69
Q

Barriers to gas exchange leading to carbon dioxide retention and Hypoxemia

A

Fibrin hyaline membranes

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70
Q

Surfactant synthesis is modulated by

A 
Cortisol
Insulin 
Prolactin 
Thyroxine
TGF-B
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71
Q

Intrauterine stress and FGR increase

A

Corticosteroid and lower risk for RDS

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72
Q

Labor increase what

A

Surfactant of synthesis

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73
Q

Before onset of labor may increase risk of RDS

A

CS section.

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74
Q

Gross of RDS

A

Normal size
Solid
Airless
Reddish purple liver

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75
Q

RDS microscopic

A

Poorly developed alveoli with atelectasis

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76
Q

Major thrust in control of RDS is focuses or prevention either

A

Delaying labor until fetal lung reaches maturity

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77
Q

Prophylactic administration of exogenous surfactant at birth to extremely premature infants has been shown very beneficial

A

Less than 28 weeks of gestation

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78
Q

RDS

2 known complication

A

Retrolental fibroplasia

Bronchoplumonary Dysplasia

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79
Q

RDS

Anternal corticosteroids to mothers with threatened preterm delivery at

A

24-34 weeks

80
Q

Retrolental fibroplasia has 2 phase pathogensis

A

Phase 1- hyperoxic phase RDS

Phase 2 - hypoxic room air ventilation

81
Q

VEGF decreased

A

Phase 1

82
Q

VEGF increased

A

Phase 2

83
Q

RDS

Caused by impairment in the development of alveolar septation

A

BPD

Bronchoplumonary Dysplasia

84
Q

Infant who recover from RDS, have increase risk of

A

PDA
Intraventricular hemorrhage
Necrotizing enterocolitis

85
Q

Most common premature infants; inversely proportional to gestational age

A

Necrotizing enterocolitis

86
Q

NEC Multifactorial in etiology

A

Premature
Enteral feeding
Infections

87
Q

NEC manifestations

A

Bloody stools
Abdominal distention
Circulatory collapse
Gas within the intestinal wall

88
Q

NEC gross

A

Distented part
Gangrenous
Intestinal perforation
Peritonitis

89
Q

NEC microscopic

A

Transmural coagulation necrosis
Ulceration
Bacterial colonization and
Submucosal gas bubbles

90
Q

NEC treatment

A

Conservatively 20-60% resection of the bowel

91
Q

Usually acquired by cervicovaginal route

Most bacteria and virus (herpes simplexII )

A

Transcervical (ascending) infection

92
Q

Transcervical

In general fetus acquires infection either by

A

Inhaling of infected amniotic fluid shortly before birth

By passing thru the infected birth canal

93
Q

Transcervical

Preterm birth is common and unfortunate consequence of infection due to

A

Damage and rupture of amniotic sac as consequence of inflammation
Prostaglandins released from neutrophils

94
Q

Transcervical

Inhalation of amniotic fluid

A

Pneumonia

Sepsis and meningitis

95
Q

Hematogenous gain access thru chorionic villi

A

Transplacental (hematologic) infections

96
Q

Transplacental

Chorionic villi

A

Parasitic (toxoplasma, malaria)

Bacterial (listeria, treponema)

97
Q

Transplacental

May occur at any time during gestation

A

Hep B and HIV

98
Q

Transplacental

Delivery via maternal-fetal transfusion

A

Parvovirus B 19

TORCH

99
Q

Erythema infectious 5th disease of childhood

Can infect seronegative (non immune) pregnant women

A

Parvovirus B19

100
Q

Early onset within 1st 7days of life

A

Perinatal sepsis

101
Q

Most common cause of early onset sepsis

A

Group B strep

102
Q

Perinatal sepsis from 7days to 3 months

A

Late onset

Listeria
Candida

103
Q

Accumulation of edema fluid in fetus during intrauterine growth
Progressive and generalized edema of the fetus

A

Fetal hydrops

104
Q

Most serious threat in fetal hydrops is CNS damage

A

Kernicterus

105
Q

Kernicterus affected brain is enlarged and edematous

A 
Basal ganglia
Thalamus
Cerebellum
Cerebral gray matter
Spinal cord
106
Q

Fetal hydrops

Clinical features

Infants

A

Pallor

Hepatosplenomegaly

107
Q

Fetal hydrops

Clinical features

Neonates

A

Jaundice
Generalized edema
Neurologic injury

108
Q

Fetal hydrops

These infants may be supported by

A

Phototherapy

Total exchange transfusion

109
Q

Hemolytic diseases in the newborn caused by blood group incompatibility between mother and child.

A

Immune hydrops

110
Q

Immune hydrops

During

A

3rd trimester

111
Q

Immune hydrops

Initial exposure to _________ evokes the formation of ____

A

Rh antigen

IgM

112
Q

Immune hydrops

Exposure during a subsequent pregnancy generally leads to a brisk ___

A

IgG

113
Q

Immune hydrops

Concurrent ABO incompatibility protects the mother against Rh immunization because fetal RBC

A

Coated with ant A/B IgM

114
Q

Immune hydrops

Dose of immunizing antigen; hemolytic disease develops only when the mother has experienced a significant

A

Transplacental bleed

115
Q

Immune hydrops

Treatment and prevention

A

Administration of the Rhesus immune globulin (RhIg) containing anti D antibodies at 28 weeks and within 72 hours of delivery to the Rh negative mothers

116
Q

Immune hydrops

Antenatal identification and management of the at risk fetus have been greatly facilitated by

A

Amniocentesis

Fetal blood sampling

117
Q

Immune hydrops

ABO incompatibility

A

Mother O

Infant AB

118
Q

Immune hydrops
ABO incompatibility

Do not cross placenta

A

Most anti A and B antibodies are of IGM type

119
Q

Immune hydrops
ABO incompatibility

Certain group O women possess IgG antibodies directed against group A or B antigens even without

A

Prior sensitization

120
Q

2 consequences of excessive RBC destruction in neonates

A

Anemia

Jaundice

121
Q

Immune hydrops

May result in hypoxic injury to the heart and liver
Result in edema and anasarca, culminating in hydrops fetails

A

Anemia

122
Q

Immune hydrops

Jaundice

A

Unconjugated bilirubin
Poorly developed BBB
Damage CNS causing Kernicterus

123
Q

Non immune hydrops

A

Cardiovascular
Chromosome anomalies
Fetal anemia

124
Q

Non immune hydrops

Most common cause of no immune hydrops

A

Fetal anemia due to homozygous alpha thalasemmia

125
Q

Inborn errors of metabolism

Most common form, common in persons of Scandinavian descent

A

PKU

126
Q

PKU

Enzyme def

A

Phenylalanine hydroxylase

127
Q

PKU

6 months of life

A

Severe mental retardation

128
Q

PKU

Inability to convert

A

Phenylalanine to tyrosine

129
Q

PKU

Excreted in urine cause

A

Mousy odor

130
Q

PKU

Without tyrosine no

A

Melanin

131
Q

Galactosemia

Accumulation of

A

Galactose 1 phosphate in tissue

132
Q

Galactosemia

Two variants

A

Total lack of galactose 1 phosphate uridyl transferase (GALT) involved reaction 2
Deficiency of galactose, reaction 1

133
Q

Galactosemia

More common

A

Involved reaction 2

134
Q

Galactosemia

Milder form, not associated with mental retardation

A

Reaction 1

135
Q

Galactosemia

Product of excess galactose, that can accumulate to tissue

A

Galactitol

Galactonate

136
Q

Galactosemia

Clinical feature

A 
Liver
Eyes
Brain
Infants fail to thrive
Vomiting and diarrhea
137
Q

Galactosemia

Clinical features 2

A

Amino aciduria
E. coli
Hemolysis and coagulopathy

138
Q

Galactosemia

Can prevent by

A

Early removal of galactose from diet for atleast the first 2 years of life

139
Q

Galactosemia

Older patient

A

Speech disorder
Gonadal failure
Ataxia

140
Q

Autosomal recessive, Caucasian population

A

Cystic fibrosis/ mucoviscidosis

141
Q

Cystic fibrosis/ mucoviscidosis

Affect fluid secretion in

A

Exocrine glands

Epithelial lining of respi, GIT and reproductive tracts

142
Q

Cystic fibrosis/ mucoviscidosis

Abnormally viscous secretions which obstruct organ passages resulting in

A 
Lung
Pancreas
Liver 
Intestine
Steatorrhea
Malnutrition 
Male infertility
143
Q

Cystic fibrosis/ mucoviscidosis

Primary defect

A

CL-channel protein CFTR gene on chromosome 7q31.2

144
Q

Cystic fibrosis/ mucoviscidosis

Most patho physiologic relevance in

A

Interaction with ENAC

145
Q

Cystic fibrosis/ mucoviscidos

CTFR functions

A

Regulate multiple ion channels and cellular processes
Tissue specific
Regulates transport of bicarbonate ions

146
Q

Cystic fibrosis/ mucoviscidosis

CFTR is one of the most important avenues for active

A

Luminal secretion of chloride

147
Q

Cystic fibrosis/ mucoviscidosis

Class of CFTR protein

A

Class 1- defective protein synthesis
Class 2 - abnormal protein folding, processing, and trafficking
Class 3- defective regulation
Class 4- decreased conductance
Class 5- reduced abundance
Class 6- altered function in regulation of ion channels

148
Q

Cystic fibrosis/ mucoviscidosis

Produce virtual absence of membrane CFTR function are associated with the classic cystic fibrosis phenotype

A

Class 1,2&3

149
Q

Cystic fibrosis/ mucoviscidosis

Less severe

A

Class 4&5

150
Q

Cystic fibrosis/ mucoviscidosis

Remains one of the best known examples of the

A

One gene one disease

151
Q

Cystic fibrosis/ mucoviscidosis

Example of one gene one disease

A

Mannose binding lectin 2

Transforming growth factor beta1

152
Q

Cystic fibrosis/ mucoviscidosis

Morphology

A

Pancreas
Meconium ileus
Liver
Pulmonary changes (most serious)

153
Q

Cystic fibrosis/ mucoviscidosis

Clinical features

A

Meconium ileus
Pancreatic insufficiency
Cardiorespiratory complications
Recurrent sino nasal polyps

154
Q

Cystic fibrosis/ mucoviscidosis

Diagnosis

A

Le aged sweat electrolyte concentration
Abnormal newborn screening test
Family history
Clinical findings

155
Q

A disease of unknown cause

A

Sudden infant death syndrome (SIDS)

156
Q

Sudden infant death syndrome (SIDS)

Unexplained after a thorough case of investigation

A

After an autopsy
Examination of death scene
Review of clinical history

157
Q

Sudden infant death syndrome (SIDS)

What position

A

Prone or side position

Crib death or cot death

158
Q

Sudden infant death syndrome (SIDS)

Apparent life threatening event

A

Apnea
Color or muscle tone
Gagging

159
Q

Sudden infant death syndrome (SIDS)

Morphology

A

Multiple petechiaethymus

160
Q

Sudden infant death syndrome (SIDS)

Lungs

A

Congested and vascular engorgemnt with or without edema

161
Q

Sudden infant death syndrome (SIDS)

CNS

A

Astrogliosis of brain stem and cerebellum

162
Q

Sudden infant death syndrome (SIDS)

Triple risk of model of SIDS

A

Vulnerable infant
Critical development period in homeostatic control
Exogenous stressor

163
Q

2% of all malignant tumors

A

Tumors and tumor like lesions of the infancy and childhood

164
Q

Tumors and tumor like lesions of the infancy and childhood

Normal cells present in abnormal locations

A

Heterotopia or choristoma

165
Q

Tumors and tumor like lesions of the infancy and childhood

Overgrowth of cells

A

Hamartomq

166
Q

Tumors and tumor like lesions of the infancy and childhood

Linkage between malformations and neoplasm

A

Hamartoma

167
Q

Benign tumors and tumor like lesions

Most common tumor of infancy

A

Hemangiomas

168
Q

Benign tumors and tumor like lesions

Hemangiomas in skin

A

Port wine stain

169
Q

Benign tumors and tumor like lesions

CNS hemangioma

A

Von hippel Lindau disease

170
Q

Benign tumors and tumor like lesions

Hamartomatous or neoplastic
Occur in the skin but most often encountered in deeper regions of the neck, axilla

A

Lymphangiomas

171
Q

Benign tumors and tumor like lesions

Increases size after birth

A

Lymphangiomas

172
Q

Benign tumors and tumor like lesions

Do not extend beyond original location

A

Lymphangiectasis

173
Q

Benign tumors and tumor like lesions

Congenital infantile fibrosarcomas
ETV6- NTRK3

A

Fibrous tumors

174
Q

Benign tumors and tumor like lesions

Benign well differentiated cystic lesions

A

Mature teratomas

175
Q

Benign tumors and tumor like lesions

Lesion of intermediate potential

A

Immature teratomas

176
Q

Benign tumors and tumor like lesions

Usually admixed with another germ cell tumor such as Endodermal sinus tumor

A

Malignant teratomas

177
Q

Benign tumors and tumor like lesions

Teratomas
2 peaks of incidence

A

2 years of age (congenital neoplasm)

Late adolescent or early adulthood

178
Q

Benign tumors and tumor like lesions

Most common teratomas in childhood

A

Sacrococcygeal teratomas

Menigocele and spina bifida

179
Q

Malignant tumors

Most frequent childhood cancers arise in the

A 
Hematopoietic system
Nervous tissue
Soft tissue
Bone 
Kidney
180
Q

Malignant tumors

In adults, most common sites of tumors

A 
Skin 
Lungs
Breast
Prostate
Colon
181
Q

Malignant tumors

Most common extracranial solid tumor of childhood
Most frequently diagnosed tumor of infancy

A

Neuroblastoma

182
Q

Malignant tumors

Median age of diagnosis

A

18 months

183
Q

Malignant tumors

Major cause familial predisposition to neuroblastoma

A

ALK germline mutation

184
Q

Malignant tumors

Larger cells having more abundant cytoplasm, large vesicular nuclei and prominent nucleoli ganglion cells

A

Ganglioneuroblastoma

185
Q

Malignant tumors

Maturation of neuroblast into ganglion cells
Accompanied by Schwann cells

A

Ganglioneuroma

186
Q

Malignant tumors

Histologic prerequisite, with favorable outcome

A

Schwannian stroma

187
Q

Malignant tumors

In younger children

A

Abdominal mass
Fever
Weightloss

188
Q

Malignant tumors

In older children

A

Blueberry muffin baby

189
Q

Malignant tumors

Most pertinent prognostic factors include

A

Age and stage (mist important determinants of outcome)
Morphology
MYCN
Ploidy less than 2 yo

190
Q

Malignant tumors

Most important genetic abnormality used in risk

A

MYCN

191
Q

Most common primary renal tumor of childhood, 4th common pediatric malignancy

A

Wilms tumor

192
Q

Wilms tumor

Deletion of 11p13

A

WAGR syndrome

Aniridia
Genital anomalies
Mental retardation

193
Q

Wilms tumor

Missense, zinc finger, gonadoblastomas

A

Denys-drash syndrome

194
Q

Wilms tumor

Paternal allele (IGF-2)
Maternal allele (loss of imprinting)
A

Beckwith- wiedemann syndrome

Organomegaly

195
Q

Congenital anomalies that has a primary errors of morphogenesis

A

Malformation

Pathology Finals (7 decks)

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