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Clin Med Fall 2015 > Developmental Disorders 2 Test 1 > Flashcards

Developmental Disorders 2 Test 1 Flashcards

1
Q

Flexion elongates extensors to prepare them for function

A

premature -often more extended/ flaccid- problem for motor development

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2
Q

Respiratory function

-surfacant ( respiratory enzyme) not produced until___

A

29th week of gestation

-surfactant keeps alveoli from collapsing and allows gas exchange

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3
Q

peak production of surfactant at __

A

34 weeks

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4
Q

alveolar development and lung maturation are not complete until__

A

35th week of gestation
- creates issues related to survial; hpoxia, anoxia, inadequate oxygen delivery, alterations in BP, unable to regulate homeostatsis

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5
Q

BPD- Bronchopulmonary Dysplasia

A
  • adult RDS
  • continuous positive airway pressure to keep airways open
  • can cause scaring to lungs/bronchioles leading to fibrosis or development of asthma later in life
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6
Q

RDS- Respiratory distress syndrome

A

peds disorder

  • require ventilation beyond corrected gestational age ( 40 weeks)
  • high level of O2 to survive may casue damage to lung tissue
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7
Q

Retinopathy of prematurity

A
  • retina/ vasculature in eye is not fully developed
  • changes in BP cause damage to BV -> retina
  • limitations in vision/ cortical blindness is possible
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8
Q

Necrotizing Enterocolitis

A

intestinal death due to blood compromise in GI tract

  • intestines not fully ready to handle breast milk or formula-> inflammation or death of tissue
  • may have to remove part of GI tract
  • sustain w/ IV
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9
Q

seizures

A

brain not fully developed

-imbalances in polarity causing impaired connections by NT

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10
Q

Hyperbilirubinemia

A
  • child is born yellow/jaundice
  • liver working incorrectly
  • full term
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11
Q

Germinal Matrix

A

thin fragile mesh work of blood vessels forms in floor of lateral ventricle at 24-25 weeks of gestation

  • remains in place until 35 weeks gestation(then reabsorbed into floor of ventricle)
  • area susceptible to bleeds due to spikes in BP~linked to intraventricular hemorrhages
  • premature infant has trouble with homeostasis; regulating body temp, BP and respiration
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12
Q

Intraventicular hemorrhage (IVH)

A
  • difficulty regulating respiration
  • abrupt changes in BP
  • collapse or rupture of vessels in germinal matrix
  • leakage of blood and CSF into periventricular region (internal capsule)
  • fluid may be reabsorbed or encapsulated forming cysts
  • presence of cysts is termed (Periventricular leukomalcia- cysts appear white around ventricles)
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13
Q

Periventricular leukomalcia

A

presence of cysts around ventricles (appear white)

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14
Q

Incidence of IVH

A

increases with increased prematurity and a birth weight less than 1000 grams

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15
Q

grade I IVH

A

bleeding confined to a small are where it begins

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16
Q

grade II IVH

A

blood is also within the ventricles

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17
Q

grade III IVH

A

more blood in ventricles, results in ventricles increasing in size

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18
Q

Grade IV IVH

A

collection of blood within the brain tissue

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19
Q

management of IVH

A

no cure; preventive in maintaining homeostasis

  • hydyrocephalus is a common complication that can be managed surgically ( untreated causes brain damage due to increased pressure on brain)
  • infants w/ gr III and IV are at increased risk of brain damage
  • motor and sensory systems can be affected
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20
Q

Failure to Thrive (FTT)

A
  • weight consistently below 3rd percentile
  • 1% of all children admitted to hospital
  • FFT before 1 yr of age may affect brain development
  • Organice /non organic / combination
  • txt- increase calorie intake
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21
Q

Organic causes of FTT

A

growth inhibiting disorder, cancer (high metabolic rate)

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22
Q

non- organic cause of FTT

A

environmental neglect

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23
Q

mixed cause of FTT

A

combination ie child with respiratory problems may not or has difficulty eating

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24
Q

FTT

A

should measure head circumference- should be growing in proportion to body- too large= hydrocephalus?

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25
Q

Cerebral Palsy History

A

first named by surgeon William Little in 1860s “ little’s
disease”
1897 cp observations made by sigmund frued

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26
Q

Cerebral Palsy defined

A

NOT a disease, it is a category of developmental disabilities with an early onset

  • Non-progressive CNS ( brain) deficit*
  • single site of damage or multifocal
  • results in motor impairments and possible sensory abnormalites
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27
Q

Prevalence of CP

A

CDC estimates that 500,000 americans have CP

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28
Q

Incidence of CP

A
  • Controversial:
  • 2 :1,000 live births to 7: 1,000 live births or
    2. 6 : 1,000 live births
  • not always present at birth could be post delivery
  • over the past 30 years incidence rates of CP have remained the same due to ; environmental toxins, advances in technology leading to better survival of premature babies with increased risk of disability or damage to CNS
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29
Q

Causes of CP

A

no one cause , depends on individual case

  • Congenital: born with, occurs during development
  • Acquired: occurs post natal
  • Genetic
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30
Q

Congential Causes of CP

A

intrauterine or at the time of labor and delivery
prenatal;
-heredity -Rh compatibility
-infection -metabolic disorders
-jaundice -errors in brain development
-anoxia (premature separation of placenta)
-aspiration of meconium

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31
Q

Prenatal Congential causes

A
  • Problems of pre-maturity
    • gestational age rather than size is the greatest predictor of future outcomes
  • Compression of brain or ruptured blood vessels in prolonged or difficult deliveries
  • Asphyxia drug induced, premature separation of placenta, mechanical obstruction(cord around neck)
  • problems associated with post maturity;large child beyond 42 weeks
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32
Q

Acquired CP

A

10-20% of cases

-results in brain damage in the first few months to years of life (2-5 y/o)

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33
Q

Causes of acquired CP

A
  • Brain infection ( bacteria, meningitis, viral encephalitis, HIV,-> inflammation and damage to CNS)
  • head injury (MVA, fall, child abuse[shaken baby syndrome)
  • seizures, tumors, near drowning ( anoxia)
  • intracranial hemorrhage, vascular accidents
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34
Q

Genetic Causes of CP

A

3 types:

  • familial spastic paraplegia
  • generalized choreoathetoid tremor
  • familial ataxia
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35
Q

Classification of CP by body region

A
  • Monoplegia
  • Diplegia
  • Hemiplegia
  • Quadriplegia
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36
Q

Monoplegia

A

1 extremity is involved ( motor)

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37
Q

Diplegia

A

2 extremities involved ( LE > trunk> UE)

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38
Q

Hemiplegia

A

one sided involvement ( damage on opposite side of brain)

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39
Q

Quadreplegia

A

involvement of UE, LE & trunk

- difference from Diplegia bc of the level of involvement for UE

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40
Q

Primary impairments of CP

A
  • increased mm tone
  • decreased cordination
  • decreased strength
  • inability to stand or transfer
  • decreased balance
  • decreased ROM
  • decreased sensation
  • reflexes: hyper or hypo present or never develop.
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41
Q

Secondary impairment of CP

A

mm atrophy

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42
Q

Classification of CP by motor related impairment:

A
  • Spastic
  • Hypotonic
  • Athetoid or Dyskinetic ( basal ganglia)
  • Ataxic
43
Q

Spastic

A

motor cortex or projections to and from sensorimotor cortex

- increased tone / stiffness

44
Q

Hypotonic

A

no link to specific structures

  • decreased tone and ability to generate mm force
    • typically quadreplegia
45
Q

Athetoid or Dyskinetic ( basal ganglia)

A
  • intermittent tone in extremities and trunk (changes w/ mvmt)
  • involuntary movement patterns
  • lack of smooth mvmt: choreic (chorea) continuous jerky mvmt
  • dysmetria- trouble reaching towards objects
46
Q

Ataxic

A

general instability of movemnt

47
Q

Degree of severity of CP

A

relates top amount of motor involvement

  • mild
  • moderate
  • severe (ie Lejohnny, cant hold up head, wheelchair bound, or cant do ADLs etc)
48
Q

Percentage of Presentation of CP

A 
Spastic:85%
   - Hemiplegia:36.4%
     -Diplegia:41.5%
     -Quadriplegia:7.3%
Athetoid/Dyskinetic 10%
Ataxic:5%
49
Q

Early Clinical Picture of CP

A

-slow to reach developmental milestones
(rolling, sitting, crawling, creeping)
-abnormal mm tone (hyper, hypo, ataxia, athetoid)
-unusual posture or favor one side of body or unusual mvmt strategies

50
Q

Diagnosis of CP

A
  • assessment of motor skills
  • examination of hx
  • rule out other disorder which can cause motor problems
  • establish non-progressive nature of problem
51
Q

Diagnostic test for CP

A

CT, MRI, Ultrasound

52
Q

Prognosis for CP

A

CP is a non progressive disorder. Lesions within the brain are not increasing in size or severity of damage to surrounding tissue structures, however the child may appear to be getting worse as the grow and develop

53
Q

Pathophysiology of Reye’s Syndrome

A
  • true cause unknown
  • post natal
  • tends to follow some acute viral infection (influenza, Epstein -Barr (mono), Varicella(chicken pox))
  • may be associated with aspirin use (increased salicilates in blood-> increased ammonia levels-> damage to meinges/brain/viscera coverings)
  • related causes may include exogenous toxins or intrinsic metabolic defects
  • acute encephalopathy and fatty degeneration of the viscera surrounding brain (acute toxic encephalopathy)
54
Q

Reye’s syndrome incidence

A
  • related to viral infection rates

- 2-18 y.o population most common

55
Q

Clinical picture of Reye’s syndrome

A

Fever, rhinorrhea(runny nose), sore throat, cough, abdominal pain, diarrhea, rash

  • onset of encephalitis-mild amnesia- lethargy, disoriented/agitated, coma and unresponsiveness, decerebrate posture (Extension throughout) or decorticate posture (flexion or increased tone of UE, extension or decreased tone of LE-result of damage to cerebral hemisphere or higher level)
  • seizures, flaccidity, fixed dilated pupils, respiratory arrest
  • can be life threatening
  • red flag is change in mental status
56
Q

Diagnosis of Reye’s syndrome

A
  • significant increases in sera ammonia levels

- presentation usually follows acute viral infection

57
Q

Medical Management of Reye’s syndrome

A
  • periotoneal dialysis (flush perineatium w/ saline solutionto remove ammonia from tissue-hemodialysis if severe), blood transfusion, restoration of blood levels, IV electrolytes, endotrachial tube and controlled ventilation, meds to overcome urea cycle deficiency and intracranial pressure
  • may see permanent neurological damage if treatment is delayed ( due to damage to brain from inflammation, Increased pressure due to increased fluid buildup due to increased proteins in CSF)
58
Q

Pathophysiology of Rett Syndrome

A

unknown, possible x-linked dominant condition, lethal to males

59
Q

Rett Syndrome incidence

A

1: 12,000-15,000 live female births

- often missed due to small incidence

60
Q

Clinical picture of Rett Syndrome

A

Period of normal development to 6 months with deterioration between 6-18 months

  • normal head size at birth with decreased rate of growth
  • loss of acquired behavioral/social/psychomotor skills
  • severe/profound MR, loss of language skills
  • loss of purposeful hand skills, replaced by stereotypic hand writing(wring hands at midline), clapping, waving, or mouthing
  • scoliosis( severe to point where can’t walk, vasomotor disturbances, seizures, breathing dysfunction(apnea-stop breathing for 45 s to 1 min), teeth grinding, growth retardation
61
Q

Rett Syndrome diagnosis

A
  • via clinical presentation- often misdiagnosed

- decreased life expectancy( become immobile -> increased risk of infection/ respiratory illness)

62
Q

Medical management for Rett Syndrome

A
  • seizure medicatoins
  • scoliosis management
  • inability to eat (GI tube)
63
Q

Sydenhams Chorea /Rheumatic Chorea/St.Vitus’s dance pathophysiology

A
  • unclear, may be related to inflammatory complication of group A strep infections (1-3 months post)
  • short lived span of time w/ presentation, will resolve
64
Q

Incidence of Sydenhams Chorea

A

occurs in up to 10% of cases 1-3mo. After streptococcal infection and is always preceded by polyarthritis (multiple inflamed joints).
girls>boys

65
Q

Clinical Picture of Sydenham’s Chorea

A

develops as a rapid, purposeless, non-repetitive movements that may involve all the mm.s except the eye, facial grimacing, clumminess

66
Q

Prognosis of Sydenham’s Chorea

A

may last up to 1 week, several months or years without permanent impairment of CNS

  • resolves without permanent damage
  • assure family that it is temporary and will resolve without temporary damge
67
Q

Diagnosis of Sydenham’s Chorea

A

prior rheumatic fever (strep infection) episode with polyarthritis

68
Q

Medical Management of Sydenham’s Chorea

A

bed rest with mild sedation, antistreptococcal prophylaxis against recurrences of chorea and rheumatic fever
(could be dangerous for child to be up and moving without good balance)

69
Q

Tourette’s Syndrome Pathophysiology

A

unknown, may be associated with psychological problems, encephalitis, tics(habitual spasms)

70
Q

Incidence of Tourette’s Syndrome

A

rare; male to female 3:1

71
Q

Clinical picture of Tourette’s Syndrome

A

habitual spasms, vocal noises or outbursts, coprolalia ( obscene outburst -swear words), abnormal EEG
-onset 2-13 y/o may increase in serverity in childhood and resolve in adulthood, could be present throughout life

72
Q

Diagnois of Tourette’s Syndrome

A

via clinical picture

73
Q

Medical management of Tourette’s

A
  • Medication:sedatives, dopamine blockers, haloperidol to block tics
  • Psychotherapy
  • as PT see child w/ Tourette’s Syndrome bc they also have something else going on
74
Q

Definition of Mental Retardation (MR)

A

” mental retardation refers to substantial limitations in present functioning. It is characterized by significantly subaverage intellectual functioning, existing concurrently with related limitations in two or more of the following applicable adaptive skill areas: communication, self care, home living, social skills, community use, self-direction, health and safety, functional academics leisure, and work

75
Q

MR classfication by IQ

A

mild:52-68
moderate:36-51
severe:20-35
profound:

76
Q

medical classification of MR

A

based on degree of severity of intellectual impairment (IQ)

77
Q

educational classfication of MR

A

support needed for functional tasks/ educational sucess

78
Q

MR levels of support- educational classfication of MR

A
  • Intermittent
  • limited
  • extensive
  • pervasive
79
Q

Intermittent MR level of support

A

does not require constant support; live independently but someone comes &checks on them every 1-2 days, helps w/ cognitive tasks

80
Q

Limited MR level of support

A

requires ongoing support; only for certain tasks, not living independently

81
Q

Extensive MR level of support

A

requires daily and ongoing consistent levels of support- doesn’t require assistance w/ every ADL

82
Q

Pervasive MR level of support

A

requires high level of support for all activities of daily living; dressing, eating, toileting

83
Q

Incidence and Prevalence of MR

A
  • 3% population in US thought to have MR
  • only 1-1.5% diagnosed (diagnosed are likely in mild range and functioning high enough that they get by)
  • 4 times more prevalent in males than females
84
Q

MR pathophysiology

A
  • infections and toxins
  • trauma (shaken baby syndrome)
  • metabolic/nutrition deficits-
  • errors of brain formation
  • environmental deprivation
  • neonatal disorders
  • seizures
  • chromosomal abnormalities
85
Q

MR sensory impairment

A

Hypo-responsive Vs Hyper-responsive

  • visual
  • auditory
  • tactile
  • vestibular
  • self-stimulatory behavior (head banging, biting, rocking)
86
Q

MR sensory impairments cont.

A
  • noxious vs craving
  • involuntary
  • hyper-responsive:may be able to work though and desensitize or avoid stimulation
  • hypo-responsive: need extra sensation to be able to process; crave sensation, banging surfaces wth hands or head, repeated motion of feeling objects that is not functional, repeated sound ( rubbing things together), rocking or shaking head
87
Q

Learning disorders

A

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

88
Q

Learning disabilities

A
  • learning disorder which assumes normal cognitive abilities
  • specific problem in reading, arithmetic, spelling, written expression or handwriting, and understanding and/or use of verbal and nonverbal abilities
  • presumed to be due to CNS dysfunction
  • not the direct result of other disease processes or environmental infulences, but may concomitantly with other disease processes
89
Q

Attention Deficit Disorder (ADD)/Attention deficit hyperactivity disorder (ADHD)

A
  • one of the most common mental disorders among children
  • affects 3-5% of children
  • 2 million american children may have ADHD
90
Q

ADD/ADHD clinical picture

A

-inattention, hyperactivity, impulsivity, motor in-coordination, perceptual-motor dysfunctions, emotional lability, opposition, anxiety, aggressiveness, mood swings, poor social skills and peer relationships, sleep disturbances

91
Q

ADD/ADHD clinical course

A
  • onset typically before 4 years of age

- typical age of referral: 8-10 years

92
Q

ADD/ADHD diagnosis

A
  • difficult
  • need to rule out other developmental disorders/behavioral disorders
  • considered a psychiatric disorder
93
Q

ADD/ADHD prognosis and medical management

A

Prognosis: child with ADHD becomes an adult with ADHD

-Medication & counseling

94
Q

Developmental Coordination disorder (DCD)

A

also called:

  • developmental clumsiness
  • clumsy child
  • developmental apraxia
95
Q

Pathophysiology & incidence of DCD

A
  • no specific pathological process or single neuroanatomic site implicated
  • incidence: difficult to quantify, many undiagnosed
96
Q

DCD clinical picture

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
97
Q

Pervasive Developmental Disorders (PDD)

A
  • spectrum of disorders including Autism, Rett syndrome, Asperger syndrome, PDD NOS (not otherwise specified)
  • behavioral problems related to social interaction and communication are the most notable
98
Q

PDD prevalence

A
  • 10-19 cases per 10,000 individuals
  • Autism and PDD NOS: boys 5:1
  • asperger syndrome boys 10:1
  • Rett Syndrome- only girls
99
Q

Autism

A
  • effects thought, perception, and attention
  • broad spectrum of disorders ranging from mild to severe
  • NO specific or defined set of symptoms
100
Q

Autism diagnosis

A

-individual displays 6 or more of 12 symptoms in across 3 major areas: social interaction, communication, behavior

101
Q

Social Interactions- Autism diagnosis

A
  • impairments in eye gaze, facial expression, body posture, gestures
  • failure to develop peer relationships
  • lack of spontaneous seeking to share enjoyment or interests with others
  • lack of social or emotional reciprocity
102
Q

Communication- Autism diagnosis

A
  • delay in or total lack of development of spoken language
  • inadequate speech; unable to initiate/sustain a conversation with others
  • stereotyped and repetitive use of language (echolalia)
  • lack of varied, spontaneous make-believe play or imitative play
103
Q

Repetitive and stereotypic patterns of behavior- autism diagnosis

A
  • preoccupation w/ 1 or more stereotyped and restricted patterns of interest
  • apparently inflexible adherence to specific, nonfunctional routines or rituals, difficulty transitioning between activities
  • stereotyped and repetitive motor mannerisms, persistent with parts of objects
  • aversions to certain sensory modalities: olfactory, tactile defensiveness, auditory aversion

Clin Med Fall 2015 (10 decks)

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