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Pediatrics > Congenital disorders > Flashcards

Congenital disorders Flashcards

1
Q

How may congenital infections occur?

A
  • during pregnancy, labor and delivery
  • transmission: through placenta, amniotic fluid, vaginal canal
  • prevention with prenatal care of mom is key!!
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2
Q

How do first trimester infections affect the fetus?

A
  • affect virtually any of the developing organ systems

- find symmetrically growth restricted infants

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3
Q

Presentations of congenital infections?

A
  • growth retardation
  • premature delivery
  • CNS abnormalities: microcephaly, intracranial calcifications, chorioretinitis, hydrocephaly
  • hepatosplenomegaly: can have accompanying jaundice
  • bruising or petechiae: thrombocytopenia, hemolytic anemia
  • skin lesions
  • pneumonitis
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4
Q

What does TORCH stand for?

A
  • T: toxoplasmosis
  • O: other - syphilis, HIV, parvovirus B-19, varicella, hepatitis, enterovirus
  • R: rubella
  • C: cytomegalovirus
  • H: herpes simplex
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5
Q

Source of Toxo? Maternal sxs, and neonate sxs?

A
  • Toxoplasma gondii, found in cat feces, raw or undercooked meat, contaminated soil or water
  • maternal sxs: nonspecific, such as fatigue, fever, HA, malaise, and myalgia
  • sxs in neonates: fever, maculopapular rash, hepatosplenomegaly, microcephaly, seizures, jaundice, thrombocytopenia (petechiae), and rarely, generalized lymphadenopathy
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6
Q

Classic triad signs of congenital toxo?

A
  • chorioretinitis
  • hydrocephalus
  • intracranial calcifications
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7
Q

Primary focus of toxo infection in neonate?

long term complications?

A
  • CNS:
    necrotic, calcified cystic lesions dispersed within the brain (can find similar lesions in liver, lungs, heart, skeletal muscle, and spleen)
  • long term complications: seizures, mental retardation, spasticity, relapsing chorioretinitis
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8
Q

Dx Toxo? Tx?

A
  • 85% are asx
  • IgM anti-toxoplasma ab at 20-26 weeks (mother)
  • isolation of parasite in fetal blood or amniotic fluid
  • postnatal: IgM abs in serum
  • prenatal US: symmetric ventricular dilation, intracranial calcifications, increased placental thickness, hepatosplenomegaly, ascites
  • labs: may show anemia, thrombocytopenia, eosinophilia, abnormal CSF
  • tx: pyrimethamine and sulfadiazine or Spiramycin
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9
Q

HIV transfer?

A
  • educate and address mother’s infection, lower viral load = lower chance of transfer
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10
Q

Enterovirus?

A
  • usually acquired around time of birth, good prognosis
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11
Q

Parvovirus B-19?

A
  • possible fetal hemolytic crisis assoc
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12
Q

Varicella?

A
  • perinatal exposure can be very severe, immune globulin given if suspected
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13
Q

Hepatitis?

A
  • type B, HBIG and vaccine if mom + - give to baby at time of birth
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14
Q

Syphilis transmission?

A

organism: Treponema pallidum

- if mom in primary or secondary stage transmission is nearly 100%

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15
Q

Syphilis infection can result in what?

A
  • stillbirth
  • Hydrops fetalis (fluid overload)
  • prematurity and assoc long term morbidity
  • hepatomegaly
  • edema
  • thrombocytopenia
  • anemia
  • skeletal abnormalities, saddle nose deformity
  • rash: maculopapular, vesicular
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16
Q

When does transmission of syphilis occur?

- early sxs?

A
  • transplacental infection generally occurs in 2nd half of pregnancy
  • if mother has primary or secondray infection there is high risk of transmision to fetus
  • half of infected infants are sx
  • early sxs:
    hepatosplenomegaly, skin rash, anemia, jaundice, metaphyseal dystrophy, periostitis, CSF with increased protein and PMNs
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17
Q

Congenital syphilis manifestations in infancy and childhood?

A

congenital syphilis can result in:

  • late abortion or stillbirth
  • infantile: rash, osteochondritis, periostitis, liver and lung fibrosis

-childhood: interstitial keratitis, hutchinson teeth, 8th nerve deafness

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18
Q

Sxs of syphilis? Dx, and Tx?

A
  • may be asx, may develop sxs weeks or months later
  • snuffles: nasal obstruction, initially clear d/c then purulent or sanguineous d/c
  • Dx: IgM FTA-ABS (fluorescent treponemal ab absorption) in newborn blood: not always + at first, recheck in 3-4 weeks
  • Tx: PCN G
  • monitor for vision changes, hearing, developmental abnormalities
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19
Q

How common is Rubella in US? When is it the most transmissable?

A
  • rare in US due to immunizations, 0.5/1000 live births
  • in adults causes mild self limited illness
  • high maternal to fetal transmission rate if infected in first trimester
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20
Q

Clinical manifestations of congenital rubella?

A
  • deafness, cataracts, glaucoma, strabismus, nystagmus, cardiac malformations (PDA, pulmonary artery hypoplasia), and neuro and endocrinologic sequelae
  • growth retardation (SGA), radiolucent bone disease, hepatosplenomegaly, thrombocytopenia, purpuric skin lesions (Blueberry muffin lesions that represent extramedullary hematopoiesis), hyperbilirubinemia
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21
Q

Dx Rubella? Long term complications?

A
  • increased anti-rubella IgM titer in perinatal period
  • increased anti-rubella IgG titer in the 1st few years of life
  • isolate virus from throat swab, CSF or urine
  • long term complications:
    communication disorders, hearing defects, mental or motor retardation, microcephaly, learning deficits, balance and gait disturbances, behavioral problems
  • tx: prevention with vaccination, if immunocompromised baby - may try ganciclovir
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22
Q

How common is CMV? How is it transmitted? Are sxs usually present?

A
  • most common congenital viral infection
  • virus is ubiquitous
  • transmitted by saliva, urine or bodily fluids
  • can be transmitted to fetus even if maternal infection occurred prior to conception secondary to virus reactivation
  • if transmitted from a newly acquired maternal infection then increased severity of infection and worse prognosis
  • 40,000 infants born with CMV in US yearly
  • 5-20% are sx:
    30% mortality rate, 80% neurologic
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23
Q

Sxs of CMV?

A
  • leading cause of SNHL, mental retardation, retinal disease, and cerebral palsy
  • SGA, microcephaly, thrombocytopenia (petechiae, purpura), hepatosplenomegaly, hepatitis, intracranial calcifications
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24
Q

Herpes Simplex - transmission? Tx and prevention?

A
  • most commonly acquired at time of birth during transit through infected birth canal
  • transmission more likely if primary outbreak
  • C-section often performed to prevent transmission
  • tx acyclovir
  • mortality rate high (encephalitis)
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25
Q

HSV transmission rates?

A

Primary genital herpes in mother with vaginal delivery transmission rate about 33-50%

  • mother with reactivated infection transmission rate is 5%
  • more than 75% of infants who acquire HSV infection are born to mothers with no previous hx or clinical findings consistent with HSV infection
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26
Q

Sxs of neonatal HSV? Tx

A
  • disseminated disease: sepsis, liver (elevated liver enzymes), lungs
  • localized: CNS (seizures, encephalopathy), skin, eyes, mouth
  • tx: acyclovir
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27
Q

Clincal manifestations of congenital varicella?

A
  • cutaneous scars
  • cataracts
  • chorioretinitis
  • micropthalmos
  • nystagmus
  • hypoplastic limbs
  • cortical atrophy
  • seizures
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28
Q

Workup for perinatal infections?

A
  • review maternal hx
  • assessment of physical stigmata consistent with various intrauterine infections
  • CBC, LFTs,
  • long bone X-rays
  • ophthalmologic eval
  • audiologic eval
  • neuroimaging - U/S
  • LP
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29
Q

What infections are asx at birth?

A
  • toxo
  • syphilis
  • CMV
  • HSV
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30
Q

Which infections cause deafness at birth and later on?

A
  • CMV (SNHL), rubella
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31
Q

What infections can be assoc with thrombocytopenia and purpura or petechiae?

A
  • Rubella, CMV, syphilis, toxoplasmosis
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32
Q

Which infection has elevated LFTs?

A
  • HSV
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33
Q

Which infections cause chorioretinitis and possible blindness?

A
  • congenital varicella
  • HSV
  • CMV
  • Rubella
  • toxoplasmosis (chorioretinitis)
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34
Q

Maternal conditions that may cause birth defects?

A
  • med use
  • metabolic disorders
  • substance abuse
  • mechanical forces
  • toxins
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35
Q

Teratogens - medications?

A
  • ACEI
  • anticonvulsants
  • antineoplastic agents
  • thalidomide, retinoic acid, methylene blue
  • misoprostol, penicillamine, fluconazole
  • lithium, isotrentinoin, acitrentin
  • tetracycline, sulfa meds
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36
Q

Maternal medical disorders that can cause birth defects?

A
  • diabetes: LGA, hypoglycemia
  • PKU: delayed growth, developmental delay
  • Androgen producing tumors of adrenal glands or ovaries
  • SLE: ANAs, miscarriages
  • obesity: gestational diabetes, HTN, pre-term labor, babies - overweight
  • fever: over 103 - cause baby to be stillborn
  • HTN: SGA
  • hypothyroidism: if not tx - developmental delays, premature birth, respiratory distress
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37
Q

Maternal substance use/abuse?

A
  • alcohol
  • ilicit drugs
  • inhaling paints, solvents
  • tobacco
  • caffeine (a little is ok)
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38
Q

features assoc with FAS?

A
  • skin folds at corner of eye
  • low nasal bridge
  • short nose
  • indistinct philtrum
  • small head circumference
  • small eye opening
  • small midface
  • thin upper lip
  • dislocated joints, aberrant palmar creases
  • low IQ
  • SGA
  • learning and behavioral difficulties
  • facial dysmorphism
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39
Q

Mechanical forces that may cause congenital defects?

A
  • amniotic bands
  • too much or too little amniotic fluid - restrict growth
  • position of fetus
  • uterine fibroids
  • placental issues: infarction, detachment
40
Q

Maternal toxins?

A
  • mercury
  • Lead
  • ionizing radiation
  • CO
  • poor nutrition
41
Q

What is VSD?

A
  • 25% of all congenital heart defects
  • opening b/t R and L ventricles
  • some close spontaneously, others need patching
  • degree of sxs correlates with size of the shunt
42
Q

Sxs of VSD?

A
  • fatigue
  • diaphoresis with feedings
  • poor growth
  • pansystolic murmur***
  • may not be sx at birth due to normally elevated pulmonary vascular resistance but as PAP decreases, the amt of L to R shunt increases
43
Q

What is ASD?

A
  • hole b/t the 2 atria
  • blood flows from L to R
  • can be caused by PFO
  • R heart becomes dilated
44
Q

Sxs of ASDs?

A
  • infants and children are rarely sx with ASDs
  • soft systolic ejection murmur
  • fixed split S2
  • larger shunts need to be closed if still present around 3 yrs of age
45
Q

What is a PDA?

A
  • ductus arteriosus allows blood to flow from PA to AO during fetal life
  • this vessel normally closes within first 24 hrs after birth
  • failure to close results in a PDA
  • going to have a widened pulse pressure
  • continuous machine like murmur that can be heard over left side of back as well
  • closure with prostaglandin inhibitors such as indomethacin or with catheter based methods by coiling or using a closure device
46
Q

RFs for PDA?

A
  • prematurity
  • other heart defects
  • high altitudes over 10,000 ft
  • relative hypoxia (causing increased pulmonary vascular resistance)
  • maternal rubella infection
47
Q

COA is often assoc with what other congenital heart abnormalities?

A
  • hypoplastic aortic arch, abnormal aortic valve and VSD

- occurs where ductus arteriosis inserts into the aorta

48
Q

Sxs and tx of COA?

A
  • poor feeding
  • respiratory distress
  • shock
  • femoral pulses weak compared to radial or brachial pulses
  • older kids may have lower extremity claudication
  • systolic murmur best heard on L upper back
  • tx: try to keep ductus arteriosus open until surgery
49
Q

What is tetralogy of fallot?

A
  • combo of VSD, pulm stenosis, overriding aorta, right ventricular hypertrophy
  • R to L shunt
  • cyanosis varies depending on size of shunt
  • surgical repair at about 6 months
50
Q

TOF sxs?

A
  • loud, harsh systolic ejection murmur
  • hypoxia
  • cyanosis
  • sxs worsen after PDA closes
  • tachypnea
  • tet spells: cyanosis worsens with crying, toddlers will squat to relieve sxs, may have syncope, hemiparesis, seizures or death may occur
51
Q

Cornerstone test for workup of congenital heart disease?

A
  • Echo or pre-natal US
52
Q

What is cyantoic congenital heart disease?

A
  • R to L shunt
  • 5 Ts of cyanotic congenital heart disease:
    TOF
    transposition of great arteries
    tricuspid atresia
    truncus arteriosus
    total anomalous pulm venous return
53
Q
  • Acyanotic congenital heart disease types?
A
  • PDA
  • VSD
  • ASD
  • obstructive lesions: aortic stenosis, pulmonary stenosis, COA
54
Q

Eval of cyanotic newborn?

A
  • central cyanosis is indicative of a significant underlying condition
  • cardiopulmonary disease is the most common:
    Respiratory distress syndrome
    sepsis
    cyanotic heart disease
55
Q

Workup of cyanotic newborn?

A
  • CXR
  • CBC, CMP: blood glucose
  • ABGs
  • blood cultures
  • echo
  • involve your supervising physician early and refer
56
Q

Numerical autosomal abnormalities?

A
  • down syndrome (Trisomy 21)

- Trisomy 13

57
Q

x’somal deletion disorders?

A
  • deletion 22q11 syndrome
58
Q

Numeric sex x’somal disorders?

A
  • turner syndrome XO

- Klinefelter syndrome XXY

59
Q

How common is Down syndrome? What is it assoc with?

A
  • most common abnormality of x’somal number 1:800
  • assoc with developmental and medical comorbidities
  • increased risk when maternal age is greater than 35
60
Q

Characteristics of Down syndrome?

A
  • normal size baby
  • hypotonic
  • brachycephaly
  • flattened occiput
  • hypoplastic midface
  • flattened nasal bridge
  • upslanting palpebral fissures
  • epicanthal folds
  • large protruding tongue
  • short broad hands
  • transverse palmar crease
  • wide gap b/t 1st and 2nd toes
61
Q

Medical problems assoc with Down syndrome?

A
  • 40% congenital heart defects
  • 10% GI tract abnormalities
  • 1% hypothyroidism
  • increased risk of leukemia (20x)
  • increased risk of infection
  • increased risk of cataracts
  • 10% have alantoaxial instability = predispose to spinal cord injury
  • over 35 - may develop alzheimers like features
62
Q

Most constant characteristic of Down syndrome?

A
  • mental retardation with IQs mostly b/t 40-50
  • goal is to help these children develop to their full potential (PT, OT, ST)
  • differing degrees of disability
63
Q

Down syndrome screening and management?

A
  • growth (have specific growth chart) - will be slower at reaching developmental milestones
  • sleep - sleep apnea
  • thyroid screening in newborns
  • hearing screening
  • vision screening
  • echo
  • CBC
  • support with OT, ST, PT
64
Q

What is Trisomy 13?

A
  • multipe dysmorphic features and complications

- most die of heart failure or infection in infancy or by 2nd year of life, marked developmental retardation

65
Q

What is Deletion 22q11 syndrome?

A
  • assoc with variety of syndromes:
    velocardiofacial syndrome, conotruncal anomaly facial syndrome, Shprintzen syndrome, DiGeorge syndrome, CATCH 22
  • most of them have congenital heart disease and cleft palate
  • can affect virtually all body systems
66
Q

Manifestations of Deletion 22q11 syndrome?

A
  • hypoplasia of thymus and/or parathyroid gland
  • conotruncal cardiac defects
  • facial dysmorphism
  • clinical manifestations may include neonatal hypocalcemia, increased infections, as well as predisposition to autoimmune diseases later in life
  • mild to moderate learning difficulties are common
67
Q

Incidence of Turner Syndrome? Comorbidity risks?

A
  • XO
  • 1:10000 females
  • maternal age at birth is often advanced
    comorbidity risks:
    -renal anomalies (40%)
    -congenital heart defect (coarctation - 20%)
    -autoimmune thyroiditis is common
68
Q

Dysmorphic features of Turner syndrome

A
  • lymphedema (hands and feet)
  • webbing of neck
  • short stature
  • mult pigmented nevi
  • gonadal dysgenesis: ovaries fail to respond to gonadotroponin stim ( amenorrhea at puberty and failure of development of secondary sexual characteristics
69
Q

Turner syndrome tx? What can occur as these women get older?

A
  • estrogen replacement therapy
  • growth hormone therapy can be used to increase ht
  • hearing loss, hypothyroidism, and liver fxn abnormalities can occur as these women get older
70
Q

What is Klinefelter syndrome?

When is it detected usually?

A
  • XXY
  • most common congenital abnormality causing hypogonadism
  • other than thin build and long arms, prepubertal boys have normal phenotype
  • incidence approx 1:500 live male births
  • often not detected until about 15 or 16 when the testes remain small and they lack secondary sexual characteristics
71
Q

Dymorphic features of Klinefelter syndrome?

A
  • taller stature/wider arm span
  • small testes/decreased testosterone/decreased spermatogenesis
  • incomplete masculinization/ decreasd body hair
  • female habitus/gynecomastia
72
Q

Clinical features of Klinefelter’s?

Tx?

A
  • immaturity
  • normal to borderline low IQ, some variations manifest severe mental retardation
  • behavioral problems
  • tx:
    testosterone, replacement therapy
73
Q

What is fragile X syndrome?

A
  • 1:4000 males, 1:8000 females
  • mutation of DNA that codes for protein helps plays a role in development of synapses
  • mental retardation, oblong face with large testicles, autistic like behavior
74
Q

What is cause of Marfan’s syndrome?

A
  • caused by mutation in FBN1 gene that determine the structure of fibrillin
  • fibrillin is a protein that is impt part of connective tissue and elastic fibers which affect multiple parts of body such as bones, joints, eyes, blood vessels, and heart
75
Q

Who is likely to have marfan’s?

A
  • inherited disease and can affect men and women of any race or origin
  • there are some very serious cases but most are mild
  • 1 in 10 affected cases are serious
  • Abe was suspected of having this disease
76
Q

Frequency of Marfans?

A
  • about 200,000 people in US have marfan syndrome
  • each child of a person who has marfans has 50% chance of inheriting the disease
  • 2 unaffected parents have only 1 in 10000 chance of having child with Marfans
  • about 25% of all marfan cases are due to spontaneous mutation at time of conception
77
Q

Marfan sxs?

A
  • muscle weakness of legs
  • increased risk of hernia
  • increased risk of spontaneous pneumothorax
  • lens dislocation
  • AAA
  • vascular dissection
  • flat feet
  • scoliosis
  • long and skinny fingers and toes
  • pectus excavatum
  • arachnodactyly
  • stretch marks
  • loose/hyperflexible jts
  • tall, thin stature
78
Q

Leading cause of death of Marfans?

A
  • AAA
79
Q

Dx Marfans?

A
  • AAA and ectopia lentis (dislocated lenses) are cardinal features
  • clinical signs typical of dx
  • genetic testing
80
Q

Tx of Marfans?

A
  • BBs: decrease stres along vascular walls
  • losartan - ARB
  • control of sxs from valvular disease
  • there is no cure for Marfans but there are some txs to help improve quality of life
81
Q

Life expectancy of marfans?

A
  • now about that of average person, this has grown b/c there is currently better tx and dx
82
Q

What is PKU? Clinical presentation?

A
  • most common AA metabolism disorder, 1:12000 births
  • decreased activity of phenylalanine hydroxylase, the enzyme that converts phenylalanine to tyrosine
  • clincal presentation:
  • asx in early infancy
  • hypopigmentation
  • neuro manifestations: tremors, hypertonicity, behavioral disorders, seizures
  • severe mental retardation
83
Q

Management of PKU?

A
  • when tx early will be normal physically and developmentally
  • dietary restrictions: diet for life
  • especially impt during pregnancy if woman has PKU
  • restriction of foods high in Phenylalanine: red meat, chicken, fish, eggs, nuts, cheese, legumes, milk and other dairy products
  • infants may be breastfed
  • avoid aspartame
  • supplementation of tyrosine and other nutrients that may be deficient
84
Q

What is Galactosemia? Clinical presentation?

A
  • autosomal recessive disorder
  • deficiency of galactose 1 phosphate uridyltransferase leading to buildup of unmetabolized galactose
  • clinical presentation:
    appears within days to weeks of birth
  • hepatomegaly
  • vomiting, anorexia
  • growth failure (FTT)
  • aminoaciduria
85
Q

Tx of Galactosemia?

A
  • eliminate galactose from diet (if tx early - excellent prognosis) - soy based formula
  • prognosis: untx - death, mental and or growth retardation, cataracts
86
Q

Neural tube defects incidence? 2 diff types? Dx? Prevention?

A
  • this is why you do spine exam in newborns - manifest in diff ways
  • failure of neural groove to fuse completely
  • 1-2 in 1000 births
  • Risk factors: maternal age (teenage and older women), maternal health (meds, diabetes, nutrition)
  • 2 major types:
    anencephaly (no cranium), meningomyelocele (spina bifida) - distal to brain
  • dx: prenatally - elevated alpha-fetoprotein
  • prevention: prenatal (antenatal) folic acid supplementation
87
Q

Orofacial clefts incidence?

A
  • cleft lip with/without cleft palate
  • incidence: 1-2/1000 births
  • 2:1 male-female ratio
  • highest incidence in Asian and Native American pops
  • isolated cleft palate: increased incidence of other congenital abnormalities - congenital heart disease
88
Q

What is cerebral palsy?

A
  • static encephalopathy (won’t improve)
  • encephalopathy: brain injury that is non-progressive disorder of posture and movement
  • variable etiologies
  • often assoc with epilepsy, speech problems, vision compromise, and cognitive dysfxn
89
Q

Prevalence of cerebral palsy?

A
  • 2.5/1000 births

- during past 3 decades considerable advances made in obstetric and neonatal care, but no change in incident of CP

90
Q

Etiology of CP?

A
  • prenatal: infection, anoxia, toxic, vascular, Rh disease, genetic, congenital malformation of brain
  • natal: anoxia, traumatic delivery, metabolic
  • postnatal: trauma, infection, stroke
91
Q

Clinical features of CP?

A
  • muscle spasticity
  • dyskinesia: defect in ability to perform voluntary movement
  • ataxia: defective muscle coordination, especially manifested when voluntary movements attempted
  • epilepsy
  • mental retardation
  • learning disabilities
  • behavior problems
  • strabismus
92
Q

When is CP usually dx?

A
  • in first 18 months of life when they fail to meet developmental motor milestones
93
Q

Complications of CP?

A
  • spasticity
  • weakness
  • increased reflexes
  • clonus
  • seizures
  • articulation and swallowing difficulty
  • visual compromise
  • deformation
  • hip dislocation
  • kyphoscoliosis
  • constipation
  • UTI
94
Q

Management of CP?

A
  • refer to neuro and possible physical medicine and rehab physician
  • OT and PT
  • speech
  • adaptive equipment
95
Q

Screening for neonatal congenital disorders?

A
  • complete medical, surgical, social, family hx
  • amniocentesis
  • quad screen (maternal blood sample) and fetal U/S
  • newborn disease screening
  • TORCH screening

Pediatrics (20 decks)

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