Developmental Disorders Flashcards

1
Q

Define incidence.

A

Incidence is the number of new cases in a given time frame.

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2
Q

Define prevalence.

A

The number of individuals who currently have the disease in a particular area.

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3
Q

How many weeks are considered full term?

A

37-42 weeks

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4
Q

For gestational age, what is considered pre-term? what is considered post-term?

A

Pre-term: < 37 weeks
Post-term: > 42 weeks

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5
Q

How long can an infant survive in-utero?

A

22-weeks gestation

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6
Q

How long do we “correct” for prematurity? How do we “correct” it?

A

We correct premature infants’ age for up to one year. Depending on how many weeks or months early the infant was born, you subtract the number of weeks or months from their true age.

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7
Q

Why do we use APGAR?

A

To determine whether a neonate needs recussitation.

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8
Q

What does APGAR stand for?

A

Appearance, pulse, grimace, activity, and respiration.

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9
Q

If you are 7-10 on the APGAR, what does that indicate? 4-6? 0-3?

A

7-10 means the baby is normal; 4-6 means the baby is moderately depressed; and 0-3 means the baby needs immediate recussitation.

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10
Q

What is full-term birth weight?

A

2500 grams - 4100 grams (5.5 lbs - 9.0 lbs)

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11
Q

What is considered low birth weight (LBW)?

A

Below 2500 grams (5.5 lbs)

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12
Q

What is considered very low birth weight (VLBW)?

A

Below 1500 grams (3.3 lbs)

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13
Q

What is considered extremely low birth weight (ELBW)?

A

Below 1000 grams (2.2 lbs)

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14
Q

What does SGA stand for? According to length and weight percentiles, where will these infants fall?

A

Small for gestational age; they will fall below the 10th percentile.

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15
Q

What does LGA stand for? According to length and weight percentiles, where will these infants fall?

A

Large for gestational age; they will fall above the 90th percentile.

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16
Q

If an infant is consistently below the 3rd percentile for length and weight, what are they considered?

A

Failure to thrive (FTT)

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17
Q

If an infant has fetal alcohol syndrome and cannot put on weight, even with a steady caloric intake, would that be considered organic or non-organic, in regard to FTT? If an infant is not receiving enough caloric intake, would that be considered organic or non-organic?

A

The first would be organic because these are growth-inhibiting disorders; it doesn’t matter that the child is being fed, they will not gain weight or grow. The second would be non-organic because this is environmental neglect that is limiting weight gain and growth.

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18
Q

What is the treatment for children suffering FTT?

A

Increase their caloric intake

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19
Q

What is Meconium staining and how can it be life-threatening to the neonate? If this occurs, is there anything done to help during the birthing process?

A

Meconium comes from the large intestine of the fetus/newborn at the time of birth. During vaginal birth, infants can aspirate on meconium, especially if they are LGA. Aspirating on the meconium can cause damage to the neonate’s respiratory system and could lead to hypoxia/anoxia. If this occurs, the infant will receive suctioning and clearing of their airway right away.

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20
Q

How can we prevent a fetus/newborn from aspirating on meconium?

A

If a mother has a C-section, it is not likely that the baby will aspirate because you are decreasing the birthing process and difficulty of delivery, especially if the infant is LGA.

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21
Q

What is Erb Palsy?

A

Paralysis of the UE due to a traction injury to the brachial plexus during the birthing process.

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22
Q

What are the 3 types of Erb Palsy? Briefly describe them and the positioning of the infant during birth.

A

Erb Duchenne palsy: involve C5-C6 nerve roots; typically occurs due to shoulder dystocia, which involves the shoulder being stuck under the mother’s pubic symphysis.
Whole-arm palsy: C5-T1 nerve roots
Klumpke palsy: C8-T1 nerve roots; typically occurs due to shoulder hyperabduction, most likely occurring from an occiput-posterior positioning of the infant during birth.

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23
Q

With a child that has Erb Duchenne palsy, what position of the UE will be displayed after birth? Klumpke palsy?

A

Erb Duchenne palsy: the elbow is extended, shoulder IR and adducted, wrist pronated, and fingers flexed.
Klumpke palsy: wrist and long fingers flexed, with the hand intrinsics involved as well.

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24
Q

What is the prognosis for Erb Duchenne Palsy? Klumpke Palsy?

A

If the child has not achieved elbow flexion in an anti-gravity position by 3 months of age, the recovery process will be poor. Most gains are made prior to 18 months. For Klumpke palsy, the prognosis has a poorer outcome in the long-term.

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25
Q

What are Teratogens?

A

Chemicals in the environment that affect fetal development.

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26
Q

What can occur if a mother has deficient amounts of Folic Acid during pregnancy?

A

There may be issues during the folding of the fetus’s neural tube.

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27
Q

What is anencephaly? What is the prognosis?

A

It is a neural tube defect because the cephalic end of the tube fails to close. This will result in the absence of the forebrain and cerebrum, scalp, and skull. Prognosis typically involves the infant being stillborn or they will usually die within hours or days after birth.

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28
Q

What is microcephaly? What is the prognosis?

A

Circumference of the head is significantly smaller than average for age and gender. The face continues to develop at a normal rate while the head fails to grow. Typically involves a poor prognosis for normal brain function; motor abilities range from clumsiness to quadriplegia and we suspect a decreased life expectancy.

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29
Q

What is porencephaly? What is the prognosis?

A

Cyst-like cavities forms in the cerebral hemisphere. This could be due to a bleed or stroke inutero or of an infection. Prognosis depends on the location of the lesion, but we often see a hemiplegic type presentation, delayed development, seizures, hydrocephalus, and ID.

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30
Q

What is Lissencephaly? What is the prognosis?

A

Lack of normal convolutions in the brain because of defective neuronal migration during development. Many die before the age of 2, range of near normal development and cognition to no significant development past a 3-5-month-old level.

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31
Q

What does STORCH stand for? What does it represent?

A

Syphilis, toxoplasmosis, other (HIV, enterovirus, influenza, chicken pox, Epstein-Barr), rubella, cytomegalic inclusion disease, and herpes.
Infections

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32
Q

What is syphilis, how is it given to the infant, and what is the clinical picture?

A

It is an STD and is transferred to the fetus through the placenta of the mother. 25% fetal death occurs by the second trimester and 25% die soon after birth. Of those that survive, 25% show signs of jaundice, anemia, pneumonia, skin rash, and bone inflammation; 75% show no signs at birth, but later manifest abnormalities of teeth, blindness, skeletal anomalies, ID, and sensorineural deafness.

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33
Q

What is toxoplasmosis, how is it given to the infant, and what is the clinical picture?

A

Toxoplasmosis involves a protozoan found in cat feces. If a mother handles cat feces while pregnant, she can contract the protozoan that will be passed through the placenta. Affected infants typically have LBW, an enlarged liver/spleen, jaundice, and anemia.

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34
Q

How do infants acquire HIV, and what is the clinical picture?

A

Infants acquire virus inutero, through transplacental transfer or through mothers’ breast milk. Infants will have opportunistic infections, pneumonitis, microcephaly, and neurologic abnormalities.

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35
Q

What is rubella, how is it given to an infant, and what is the clinical picture?

A

Togavirus can multiply in the upper respiratory tract and pass into the bloodstream. The transmission occurs while inutero. It may cause spontaneous abortions, blindness, deafness, ID, LBW, rash, heart defects, enlarged liver/spleen, microcephaly, and cataracts.

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36
Q

What is cytomegalic inclusion disease, how is it given to the infant, and what is the clinical picture?

A

It is a virus that is transmitted through intimate contact. It may cause intrauterine death or premature death. The transmission occurs while inutero. An infant can present with LBW, jaundice, rash, deafness, diseases of the retina, and developmental delays.

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37
Q

What is herpes, how is it given to the infant, and what is the clinical picture?

A

It is a virus that is transmitted to the fetus during the birthing process, rather than through the placenta. If mild, the infant can have a disease of the skin and mucous membranes of the eyes and mouth. If severe, it will involve all the body organs, retinal disease, and developmental delay.

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38
Q

What are examples of Teratogens?

A

Alcohol, smoking, drugs (Acutain, Thalidomide, Marijuana, Tranquilizers).

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39
Q

What is phocomelia?

A

It is the developmental anomaly of the absence of the upper portion of one or more limbs.

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40
Q

What Teratogen causes phocomelia, and the attachment of the feet or hands to the trunk?

A

Thalidomide

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41
Q

What does neonate mean?

A

Newborn

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42
Q

When is surfactant produced? When is peak production?

A

Not until the 29th week of gestation; peak production occurs at 34 weeks.

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43
Q

When are alveolar development and lung maturation complete?

A

Not until the 35th week of gestation.

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44
Q

If an infant is born premature, what will happen to their respiratory function?

A

Since the infant may not reach peak production of a surfactant or achieve alveolar development and lung maturation, it can lead to issues related to survival. The infant can experience hypoxia, anoxia, inadequate oxygen delivery, and alterations in BP.

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45
Q

What is the germinal matrix? When does it form, and how long does it stay in place?

A

The germinal matrix is a thin and fragile meshwork of blood vessels that form on the floor of the lateral ventricle at 24-25 weeks of gestation. The matrix remains in place until the 35th week of gestation.

46
Q

Why are we concerned about pre-mature infant and their germinal matrix?

A

Since a premature infant will be born before 37 weeks of gestation, they have a greater likelihood of still maintaining their germinal matrix since it has not been absorbed yet. In a premature infant, they will struggle to maintain homeostasis, consisting of abrupt changes in BP. These abrupt changes can cause a rupture or collapse of the blood vessels within the matrix, with the potential for blood and CSF to leak out of the ventricles or an intraventricular hemorrhage.

47
Q

If an infant suffers an intraventricular hemorrhage, what will happen to the fluid?

A

The fluid may be reabsorbed or encapsulated, forming cysts.

48
Q

What is the acronym, IVH?

A

Intraventricular hemorrhage

49
Q

What are the grades of IVH?

A
  1. Bleeding is confined to a small area where it first begins.
  2. Blood is also within the ventricles.
  3. More blood in the ventricles, usually with ventricles increasing in size.
  4. A collection of blood within the brain tissue.
50
Q

How do you diagnose an IVH?

A

Ultrasound of the head, in between the fontanelles of the infant.

51
Q

What is a common complication with an IVH?

A

Hydrocephalus

52
Q

What is the acronym, PVL?

A

Periventricular Leukomalacia

53
Q

What is periventricular leukomalacia? What do these children end up being categorized as having?

A

Following a hemorrhage in the periventricular, the infant will develop PVL. After the bleed resolves, we will see white cysts appear, along with scarring and fibrosis. These children end up being categorized as having CP.

54
Q

What is the acronym, BPD?

A

Bronchopulmonary dysplasia

55
Q

What is the acronym, RDS? Will this be an acute or chronic issue?

A

Respiratory distress syndrome; is an acute issue.

56
Q

What is the acronym, RDS? Will this be an acute or chronic issue?

A

Respiratory distress syndrome; is an acute issue.

57
Q

What is retinopathy of prematurity?

A

The infant’s eyes are not as developed at the time a child is born, and it impacts the vasculature of the retina, leading to visual impairments for that child.

58
Q

What is necrotizing enterocolitis?

A

The GI system is not as developed, and infants may have difficulty with digestion because the production of enzymes and motility may not be working properly. This can lead to inflammation, damage to the walls of the intestine, and rupture of the walls.

59
Q

What is hyperbilirubinemia? What is the treatment for it?

A

There is too much bilirubin in the infant’s blood. Bilirubin is made by the breakdown of red blood cells, a function of the liver. If the infant cannot rid of the bilirubin, we will see jaundice. Treatment for hyperbilirubinemia is direct exposure to UV light or the sun to help break down the excess bilirubin into iron.

60
Q

Define Cerebral Palsy.

A

It is NOT a disease, it is a category of developmental disabilities with an early onset. It is non-progressive and can come from a single site of damage or be multifocal. It will result in motor impairments and possible sensory abnormalities.

61
Q

Over the past 30 years, incidence rates of CP have remained steady or increased. Why?

A

Babies are surviving earlier in the pregnancy progress. The likelihood that the child will have an impairment, the earlier they are born, will increase their risk of having CP.

62
Q

True or False: There is one cause of CP.

A

False, there is NO one cause.

63
Q

What are some pre-natal congenital causes of CP?

A

Heredity, infection, anoxia, or jaundice.

64
Q

What are some of the peri-natal causes of CP?

A

Problems of prematurity, compression of brain or rupture of blood vessels during prolonged or difficult deliveries, problems associated with post-maturity, premature separation of the placenta, or mechanical obstruction.

65
Q

What is it called when there is premature separation of the placenta?

A

Placenta previa

66
Q

If a child is categorized as having CP due to an acquired cause, what is it a result of?

A

Brain damage in the first few months to years of life

67
Q

If CP is acquired, what are some things it can be caused by?

A

Brain infection, head injury, seizures, tumors, near drowning, intracranial hemorrhage, or vascular accidents.

68
Q

What are the 3 types of CP caused by genetics?

A

Familial spastic paraplegia, generalized choeroathetoid tremor, and familial ataxia.

69
Q

What are the classifications of CP, by motor impairment, and briefly describe them?

A

Hypotonic (no link to specific structure): decreased tone and ability to generate muscle force.
Dyskinetic (due to damage to the basal ganglia): intermittent tone in extremities and trunk; involuntary movement patterns.
Ataxic (due to damage to cerebellum): general instability of movement.

70
Q

What is dystonia?

A

Cyclical pattern of being very stiff in certain muscles.

71
Q

What is athetosis?

A

The patient will have high peaks and valleys of changes in tone; they may be more in motion and cannot hold things in midline.

72
Q

What is chorea?

A

Twisting movement presenation.

73
Q

What is the general clinical picture of children who are classified as having CP?

A

Slow to reach development milestones; abnormal muscle tone; atypical reflex development/integration; unusual posture or favor one side of the body; sensory impairments - proprioception, vision, hearing, others; with or without cognitive impairments.

74
Q

What does ADDM stand for?

A

Autism and Developmental Disabilities Monitoring

75
Q

How do you classify CP? (NOT DIAGNOSE)

A

Assessment of motor skills, examination of history, rule out other disorders which can cause motor problems, and establish non-progressive nature of problem.

76
Q

CP is a non-progressive disorder, however, the child may appear as though the condition is worsening as they grow and develop, why?

A

Children with CP are not able to meet motor milestones in a timely manner; therefore, they will have challenges in their MSK system, relating to strength, ROM, and misalignment. These factors will make the child look like they are getting worse.

77
Q

What does FAS stand for?

A

Fetal Alcohol Syndrome

78
Q

When does alcohol damage a fetus during pregnancy?

A

Anytime during pregnancy

79
Q

How much alcohol are women safe to consume while pregnant?

A

NO ESTABLISHED AMOUNT OF ALCOHOL IS SAFE

80
Q

What is the clinical picture for a child with FAS?

A

Pre and post-natal growth deficiency; microcephaly, small wide-set eyes, thin upper lip, shortened upturned nose, receding chin, drooping eyelids, cleft palate, small mouth, wide space between the nose and upper lip. They will also have muscle changes, visual disturbances, congenital heart disease, and behavior problems.

81
Q

What are the 3 criteria that must be present to diagnose a child with FAS?

A

Characteristic facial features: a flattened midface, thin upper lip, indistinct/absent philtrum, and short eye slits.
Growth retardation: lower birth weight, disproportional weight not due to nutrition, height, and/or weight below the 5th percentile.
CNS neurodevelopmental abnormalities: impaired fine motor skills, learning disabilities, behavior disorders, or a mental handicap.

82
Q

Pathophysiology of Reye’s Syndrome.

A

The true cause is unknown, but it tends to follow some acute viral infection; it may also be associated with aspirin use.

83
Q

Clinical picture of Reye’s syndrome.

A

Fever, rhinorrhea, sore throat, cough, abdominal pain, diarrhea, and rash; seizures, flaccidity, fixed dilated pupils, and respiratory arrest.

84
Q

If a patient with Reye’s syndrome develops an onset of encephalitis, what can this lead to?

A

Leads to mild amnesia, then lethargy, then disoriented/agitated, to coma and unresponsiveness, then can lead to a decorticate or decerebrate posturing.

85
Q

How do you diagnose Reye’s syndrome?

A

The child will have a significant increase in sera ammonia levels; presentation usually follows an acute viral infection.

86
Q

What is the medical management for Reye’s syndrome?

A

Peritoneal dialysis to alleviate the ammonia levels, blood transfusion to dilute the amount of ammonia in the blood, restoration of blood levels, IV electrolytes, endotracheal tube and controlled ventilation, meds to overcome cycle deficiency and intracranial pressure.

87
Q

What is the clinical picture period for Rett syndrome?

A

Normal development to 6 months with deterioration between 6-18 months.

88
Q

What is the pathophysiology of Rett syndrome?

A

Unknown but possible x-linked dominant condition, lethal to males.

89
Q

Clinical picture of Rett syndrome.

A

Normal head size at birth with decrease rate of growth, loss of acquired behavioral/social/psychomotor skills, severe/profound ID, loss of language skills, loss of purposeful hand skills, replaced by stereotypical hand wringing, clapping, waving, or mouthing.

90
Q

What is the pathophysiology of Tourette’s syndrome?

A

Unknown, may be associated with psychological problems, encephalitis, tics.

91
Q

Clinical picture of Tourette’s syndrome.

A

Habitual spasms, vocal noises, coprolalia, abnormal EEG. Onset 2-13 years old, and may increase in severity in childhood and resolve in adulthood.

92
Q

What is coprolalia?

A

Yelling explicitly

93
Q

What is the definition of intellectual disability?

A

A disability characterized by significant limitations in both intellectual functioning and in adaptive behavior, which covers many everyday social and practical skills.

94
Q

When does an intellectual disability originate?

A

BEFORE the age of 18.

95
Q

What is the difference between medical vs educational regarding ID?

A

Medical: based on degree of severity of intellectual impairment.
Educational: support needed for functional tasks/educational success.

96
Q

Etiology of ID.

A

Infections/toxins, trauma, metabolic/nutrition deficits, errors of brain formation, environmental deprivation, neonatal disorders, seizures, or chromosomal abnormalities.

97
Q

Definition of a learning disorder.

A

Inability to acquire, retain, or generalize specific skills or sets of information because of deficiencies in attention, memory, perception, or reasoning.

98
Q

Does an individual with a learning disability have normal or affected cognitive abilities?

A

Normal

99
Q

What is a learning disability presumed to be caused by?

A

CNS dysfunction

100
Q

What do ADHD and ADD stand for?

A

Attention deficit hyperactivity disorder; attention deficit disorder.

101
Q

Clinical picture of ADHD.

A

Inattention, hyperactivity, impulsivity, motor incoordination, perceptual-motor dysfunctions, emotional instability, opposition, anxiety, aggressiveness, mood swings, poor social skills and peer relationships, and sleep disturbances.

102
Q

When is onset of ADHD?

A

Typically before 4 years of age.

103
Q

What are the two medications to treat ADHD?

A

Ritalin and adderall

104
Q

What does DCD stand for?

A

Developmental coordination disorder

105
Q

Clinical picture of DCD.

A

Poor strength, poor coordination, jerky movements, poor visual perception; joint laxity, poor spatial organization, poor LTM and STM, poor sequencing and feedback; low self-esteem, distractibility, delay, and poor quality of gross motor skills.

106
Q

What does ASD stand for?

A

Autism spectrum disorder.

107
Q

What is ASD?

A

Developmental disorder that affects communication and behavior. Affects thought, perception, and attention.

108
Q

True or false: there is no specific or defined set of symptoms for ASD.

A

True

109
Q

What is the diagnosis of ASD?

A

DSM-5, psychiatric diagnosis.

110
Q

Clinical picture of ASD.

A

Difficulty with communication and interaction with other people; restricted interests and repetitive behaviors; symptoms that hurt the person’s ability to function properly in school, work, and other areas of life.