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Craniofacial > Midterm > Flashcards

Midterm Flashcards

1
Q

Prevalence of clefts by type

A

Cleft lip AND palate (50%); cleft lip only (25%); cleft palate only (25%)

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2
Q

Sex bias

A

cleft lip & palate: m>f; cleft palate only: f>m (african populations b> girls both, chinese g>b both)

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3
Q

Racial bias

A

NA Indians (1 in 267)> asian (1 in 500) > caucasian (1 in 1,000) > african american (1 in 2,500); maybe asian/caucasian same

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4
Q

Cleft occurence rates

A

1 in 500 to 750 (2,000) live births; most frequent facial birth defect

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5
Q

Clefts of primary palate

A

structures anterior to incisive foramen (lip, alveolar ridge)

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6
Q

Clefts of secondary palate

A

Structures posterior to incisive foramen (hard palate, soft palate, uvula)

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7
Q

Types of cleft (frequency occurrence)

A

unilateral 2x than bilateral

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8
Q

What point are arches formed

A

4 weeks

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9
Q

form to nasal maxillary

A

6 weeks

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10
Q

when does hard palate begin to form

A

8 weeks

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11
Q

non syndrome (isolated CL/CLP)

A

70% CL(P); 50% CPO

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12
Q

Recurrence risk for CL(P)

A

increases w/ severity, # affected relatives, sex of person, how closely related

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13
Q

by 10th week development, _______ developed

A

maxillary incisors

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14
Q

by ______ weeks, they can reliably diagnose if fetus will have CL(P)

A

20

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15
Q

Types of cleft lip

A

bilateral/unilateral, medial/left/right, complete/incomplete

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16
Q

Types of cleft palates

A

cleft of hard palate only; sub mucous cleft; cleft of hard and soft palate

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17
Q

Posterior boundary of the primary palate

A

Incisive foramen

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18
Q

Surgical interventions (age)

A

lip repair- 3 months; palate repair- 9-12 months; teeth repair- 8 years; Maxillary advancement- 18 years

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19
Q

Roughly what % of kids w/ repaired cleft will have articulation disorder?

A

60-70%

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20
Q

5 dental anomalies of children w/ CL(P)

A

placement (cross bite); number (missing teeth); collapsed maxilla; protruding pre-maxilla (bilateral primary palate cleft); malocclusions (open bite); oral nasal fistula

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21
Q

Most frequent kind of cleft

A

left unilateral

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22
Q

Lip repair usually (timing)

A

3 months

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23
Q

Palate (soft/hard) repair (timing)

A

9-12 months (often 18+ months, pierre robin); 20-30% need secondary, 4-5 years

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24
Q

Alveolar cleft repair (timing)

A

7-9 years

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25
Q

How many children w/ CL/P have ST in Kindergarten/1st grade

A

60-70% for arctic (reduced hearing, marginal VP function, abnormal dental/alveolar structures)

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26
Q

Dental/Alveolar anomalies of children w/ CL(P)

A

Missing teeth (misshapen/rotated when present)’ Supernumerary (ectopic) teeth (normal tooth in wrong position); Cross bites (lower teeth overlap upper); protruding prefixal; oro-nasal fistula

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27
Q

How many consonants involve alveolar/palatal structures?

A

16/24 (67%)

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28
Q

Hearing issues in children w/ CL(P)

A

high prevalence of ET dysfunction (due to abnormal muscle insertion into posterior hard palate order, horizontal position of tube in infancy)

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29
Q

Langauge delays in children w/ CL(P)

A

limited babbling, delayed first words (until AFTER palate repair)

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30
Q

Speech Characteristics do VPI in children w/ CL(P)

A

obligatory: hypernasality, ANE (audible nasal emissions) turbuluent/nasal flutter, weak pressure consonants; Compensatory: misartiuclations

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31
Q

Speech in CL(P)

A

respiration; laryngeal; arctic (m/b, glottal stop for p), resonance

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32
Q

Compensatory Misarticulations

A

manner maintained, place altered (posteriorly) to compensatory for structural defects

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33
Q

PSNE (Phoneme specific nasal emission)

A

Turbulent NE: production of sibilants/africatives (s, z, sh, j, ch, zzzsh)

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34
Q

Palatal shelves move together and fuse from ______ to ______. Interruption can lead to a ______

A

anterior to posterior; soft palate cleft (NOT isolated hard palate cleft)

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35
Q

Genetic causes of CL/P present it how many cases

A

20 to 50%

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36
Q

Family factors in CL/P etiology

A

younger and older fathers; subclinical abnormalities of orbicular oris muscle; prenatal health/teratogens (smoking x@ increase, actuate, anticonvulsants) need folic acid and not too much vitamin A

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37
Q

Embryos have two layers:

A

epiblast, hypoblast

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38
Q

Embryos have 3 germ layers

A

ectoderms (from epiblast), mesoderm and endoderm

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39
Q

Ectoderm

A

neural ectoderm- CNS and surface ectoderm- will cover outside of body

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40
Q

endoderms

A

gut

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41
Q

Embryo: developing brain shifts the cariogenic region more_______ and forms the _______

A

caudal, ventral; foregut

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42
Q

First pharyngeal arch (in embryo)

A

22 days (branchial, visceral arch)

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43
Q

1st and 2nd pharyngeal arch

A

27 days

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44
Q

Developing inner ear is called ____ and emerges day ____

A

the otic pit; 27

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45
Q

First pharyngeal arch has ____ & _____ prominences that form the _________

A

maxillary, mandibular; upper and loer jaw

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46
Q

Tongue comes from what pharyngeal arches?

A

anterior two thirds of tongue: first arch; posterior one third: 3rd arch

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47
Q

Following anterior neuropore closure, the ectoderm that will line the nasal cavities (olfactory places) is located _________

A

lateral aspects of frontonasal prominence

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48
Q

During the _____ week human gestation, the olfactory places line the nasal pits and medial and lateral nasal prominences form around nasal pits

A

fifth

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49
Q

Normal development of of the upper lip requires union of __________ which occurs during the _________ week of gestation

A

medial nasal prominence, lateral nasal prominence and maxillary prominence; sixth

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50
Q

The secondary palatal shelves are part of the _________

A

maxillary prominence

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51
Q

The ________ contribute tissue that forms the anterior part of the primary palate

A

medical nasal prominences

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52
Q

the tongue is initially interposed between the _______

A

secondary palatal shelves; they later become positioned above the tongue to allow for midline fusion

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53
Q

Secondary palatal shelves fuse____

A

anteriorly and posteriorly from midpoint

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54
Q

the 4 maxillary incisors develop within the _______

A

primary palate

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55
Q

spontaneous mutation

A

change in genes at formation of egg/sperm

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56
Q

deformation

A

abnormal structure/position due to mechanical force (more common in multiple births)

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57
Q

Disruption

A

defect caused by extrinsic breakdown/interference normal development

58
Q

malformation

A

defect caused by intrincix abnormality; genetic (e.g. cleft lip, craniosynostosis)

59
Q

sequence

A

one anomaly causing cascade of secondary anomalies

60
Q

syndrome

A

multiple anomalies occurring together from single cause

61
Q

van der Woude syndrome

A

lower lip pits w/ w/out cleft; autosomal dominant (50% recurrence)

62
Q

Apert syndrome

A

synostosis of coronal suture –> long, vertical skull short from front to back; mid face hypoplasia; protruding eyes; prognathism; v-shape maxilla (palatal arch); Class III (severe) malocclusion; pseudo cleft palate, 30% true or SMCP; small pharynx w/ large soft palate (airway problems); channel atresia, tracheal anomalies, fusion on hands and feet (syndactyly); CNS problems (ICP, hyrocephalus, cognitive impairment); early surgery (

63
Q

Pierre Robin sequence

A

Micrognathia (precipitating factor) –> glossoptosis (retracted tongue), respiratory distress, u-shaped cleft palate; common feeding problems, delayed cleft repair (50% part of other syndromes); distraction osteogenesis

64
Q

Stickler syndrome

A

most common cause of pierre robin; micrognathia; flat facial profile & epicentral folds, myopia, risk of retinal detachment/cataracts; hearing loss; small nose/flat nasal bridge; mid face hyoplasia; cleft palate; progressive joint/orthopedic problems

65
Q

hemifacial microsomia

A

spectrum; ear defomities, max/mandib hypoplasia; tongue ankylosis; 15% CL/P; VPI due to asymmetry/unilaeral paresis; tempromandibular joint disorders; colombomas (retina, upper eyelid); absent corpus callosum, hydrocephalus; cervical anomalies 15%; aka Goldenhar syndrom if eye cysts; 1 in 3-5,00; right > left but 30% bilateral; boys > girls; speech- dental malocclusion, limited mouth opening, CP or velar paresis

66
Q

Velocardiofacial (VCF) syndrome

A

most common syndrome involving clefts; autosomal dominant; 75% micro deletion 22q11.2; FISH detects deletion; DiGeorge if thyroid involved; SMCP/VPI; ventricular septal defect; long face w/ ear anomalies; 40% cog impairment; pharyngeal hypnotic, slender hands, risk adult schizophrenia

67
Q

Treacher Collins Syndrome (mandibulofacial dysostosis)

A

autosomal dominant; 1 in 50,000; eyes: coloboma of iris, missing lower eyelashes, downward slant, malaria hypoplasia; hypVPI/SMCP in 30-40%; small pharynx (*airway problems) cup-de-sac speech; ear ossicular malformations, deformities, hypo plastic TM/middle ear

68
Q

Ectrodactyly-Ectodermal Dysplasia

A

“claw like” hands & feet; poorly developed skin, hair, teeth, nails; bilateral C>/P common; nasolacrimal duct obstruction; autosomal dominant; rare (260 cases)

69
Q

Turner Syndrome

A

x chromosome disorder; short; hearing loss (conductive to sensorineural; high arched palate & retrognathia; learning disabilities

70
Q

Fragile X Syndrome

A

most common cause of inherited cognitive impairment and known cause ASD; FMR1 gene mutation; mod to severe speech & lang delays; peculiar rate/prosody

71
Q

Beckwith-Wiedemann Syndrome

A

pre & post natal overgrowth; risk of neonatal seizures/hypoglycemia; childhood hemi-hypertrophy;macroglossia (respiratory distress); kidney tumor risk

72
Q

CHARGE Syndrome

A

retinal *Coloboma; Heart defects; choanal *Atresia(back of nasal passage); Retarded growth; Genitourinary anomalies (micropenis, undescended testicles); Ear anomalies; often cognitive impairment

73
Q

Down (Trisomy 21)

A

1 in 700, most common chromosome disorder; cognitive impairment, hypotonia, short, nasopharyngeal resonance (low CL/P risk)

74
Q

Fetal Alcohol Syndrome (now a spectrum disorder)

A

low birth weight, microcephaly, narrow palepbral fissures (eyes), thin upper lip, short nose, flat philtrum; VSD; cognitive/developmental delays: occasional CL/P

75
Q

Neurofibromatosis Type 1

A

1 in 3,000; autosomal; neurofibromas; cafe au last spots; often VPI but no cleft

76
Q

Craniosynostosis Syndromes

A

premature fusion of bony sutras restricting growth at right angles to fused sutures

77
Q

Crouzon Syndrome

A

like Apert but no limb deformities; 1 in 25,000 births; mutation of chromosome 10 gene; synostosis of coronal and often sagittal and lambdoidal sutures

78
Q

Maxillary advancement surgery (timing)

A

15-17 years

79
Q

Double opposing Z plasty (furrow repair)

A

to reposition musculature of palate in more posterior position; oral and mucous w/ muscle, muscle moves posterior & flaps w/out muscle moves anterior; lengthens palate, puts muscle in normal anatomic positions; residual alveolar cleft remains

80
Q

Rationale for 3-month Lip Repair surgery

A

10 weeks age, weigh 10 lbs, 10g hemoglobin for surgical safety; time to dx other conditions prior to surgery

81
Q

rationale for 9-12 month timing palate repair

A

after 20 months, restricts maxilla & mid face growth; repair before 11 months less effects SO compromise 2-12 months; But 60s/70s excessive scarring which restricted growth of gum ridge/midface

82
Q

Rational for 7-9 year Alveolar bone graft repair

A

based on emergence of permanent teeth in cleft area

83
Q

American Cleft Palate Craniofacial Association (ACPA)

A

started by dentists; 35% dentists, 35% plastic surgeons, 16% SLPs to emphasis of surgical repairs on facial growth, aesthetics and teeth

84
Q

Speech development and repaired status of CL/P

A

0-3 months cooing before lip repaired; 1-12 months babbling/first words before palate repaired; 1-2 years first words and combos before alveolar cleft repaired; 2-3 years rapid vocab/sentence growth, `80% speech should be intelligible before alveolar cleft repaired then mastery phonetic inventory

85
Q

Artic problems due to dentition

A

lisping (dentalized- Class III malocclusion (underbite) or lateralized- posterior cross bit/lateral open bite); backed/retracted artic 9palatalized t, d, s due to narrow/collapsed maxillary arch/ONF)

86
Q

Prevention of dental/artic problems in kids w/ CL/P

A

pre surgical orthopedics; early alveolar bone graft, early lip and palate repair (normal feeding/interactions more ONF)

87
Q

Who’s on the team?? (cleft palate)

A

Core: SLP, Dentist (orthodontist), plastic surgeon; desired- ENT, surgeon, nursing, audiologist, geneticist, pediatric dentist, prosthodontist, OMF surgeon, psychologist, social worker

88
Q

Focus of specialists over time

A

birth/infancy: feeding specialist, social worker, plastic surgeon; preschool/school: SLP & Psych; Middle/late childhood: dentistry/orthodontist; late adolescence/early adulthood: OMFS and plastic surgeon

89
Q

Who’s on the team?? (craniofacial)

A

for ACPA recognition: neurosurgeon, ophthalmologist, @ least 10 cranial surgeries/year

90
Q

Learning disabilities in children w/ CL/P

A

15-20% general population; 30-40% children w/ CL/P

91
Q

Infant/toddler psychosocial issues

A

CPO below developmental norms at one year for motor, language, and play (CL only NOT); VP and Hearing Status account for cognitive/linguistic delays

92
Q

Reading study- Zajac replication

A

Good readers use sight reading more than phonemic decoding to greater extent than poor readers for children w/ AND w/out CL/P

93
Q

Maternal attachment predicted by

A

infant facial attractiveness (ugly=higher attachment); 84% CL/P and 54% CP)

94
Q

Structural anomalies that disrupt “suck, swallow, breathe” cycle

A

CL/P; micrognathia; macroglossia; pharyngeal stenosis; laryngeal cleft; choanal atresia

95
Q

Feeding problems of cleft palate

A

poor oral suction/ formula volume intake; prolonged time; nasal regard; choking & gagging; excessive air intake

96
Q

What kind of cleft shows poorest weight gain (68% delayed surgery) ?

A

isolated cleft palate

97
Q

Feeding concerns and interventions for cleft lip only

A

decreased lip seal and intra oral pressure; breastfeeding possible; bottle feeding using wide base nipple

98
Q

feeding concerns and intervention for cleft alveolar ridge

A

may have decreased compression, lip seal, intraoral pressure and have poor bolus control; breast feeding possible (mother may manually seal lips to nipple); bottle feeding w/ easy flow nipple

99
Q

feeding concerns and intervention for complete cleft palate

A

special bottle for feeding w/ clefts; soft nipple w/ large cross cut (increases flow and fluid control); supplemental breast feeding system; baby in cross cradle/football position & mother manually squeezes breast

100
Q

For poor intraoral pressure/compression

A

Mother may manually squeeze bottle (soft plastic or plastic liners)

101
Q

Orthodontic nipple

A

low flow; facilitates infant’s suck to develop proper tongue position

102
Q

obturator (feeding plate)

A

orthodontic device to provide stable area for tongue compression, reduce nasal regurgitation, help infant generate negative intraoral pressure

103
Q

Psychosocial adjustment of children with CL/P determined by degree of _______

A

parental support; higher with visible clefts

104
Q

CL/P & Self-concept

A

CL/P less self-concept than CPO and CL; girls > affected than boys

105
Q

Trigonocephaly

A

traingle-shaped forehead (metopic)

106
Q

Brachycephaly

A

short head; coronal bilaterally

107
Q

Dolichocephaly

A

long head; sagittal

108
Q

Plagiocephaly

A

flat back of head; coronal & lambdoid unilaterally

109
Q

Turricephaly

A

pointed top of head; coronal & lambdoid

110
Q

Triad of SMCP

A

split (bifid) uvula; midlis divison/diastasis of muscles (aka zona pellucida); v-shaped notch of hard palate (palpate)

111
Q

levator veli palatini

A

most important; pulls soft palate superior and posterior

112
Q

tensor veli palatini

A

anchors to hummus bone; assists elevator to pull up palate

113
Q

palatoglossus

A

anterior faucial pillar; elevates posterior part of tongue, maybe pulls palate down

114
Q

palatopharyngeus

A

posterior faucial pillar; closes off entrance to nose

115
Q

musculus uvulae

A

incrases bulk (surface area) of velum to contact, close off

116
Q

muscles of the velum

A

curtain; levator veli palatini, tensor veli palatini, palatoglossus (AFP), palatopharyngeus (PFP), musculus uvulae

117
Q

Superor pharyngeal constrictor

A

velo-pharyngeal closure

118
Q

Occult SMCP

A

No visible features; facet in muscles uvulae (lack muscle bulk, seen as nasal trough on endoscopy, LVP insertion into hard palate)

119
Q

Passavant’s ridge

A

short palate; treat surgically w/ z pasty

120
Q

Pre surgical orthodontics

A

for severe (wide) clefts; to reduce width, align maxillary segments, reposition protruding premaxilla

121
Q

Presurgical intraoral places

A

prevents medial mxaillary segment collpase; guides growth of maxillary segments; passive or active (w/ jack screws or springs)

122
Q

Presurgical taping

A

traction

123
Q

Surgery goals

A

avoid fistulas; competence velum for adequate speech (delayed goal)

124
Q

Indications for fulow z-plasty

A

submucous cleft short; cleft posterior soft palate; v shaped cleft of entire soft palate; previous straight-line repair w/ inadequate length (5-10 mm)

125
Q

indications for 2-flap palatoplasty

A

wider cleft of soft palate; u shaped clefts; cleft entire secondary palate

126
Q

indications for vomer flaps

A

wide anterior cleft; bilateral cleft; redo palatoplasty for large fistula

127
Q

intravelar veloplasty

A

separation of muscle from poster edge hard palate; free underlying nasal w/ overlying oral layer; suture muscle as separate layer to recreate velar sling

128
Q

Velopharyngeal Insufficiency

A

inadequate function of soft palate; hyper nasal speech (telex, nasoendoscopy)

129
Q

Nadoendoscopy closure patterns

A

coronal- soft palate posterior movement (min lateral pharyngeal wall contribution); circular- posterior displacement of soft palate AND medial displacement of lateral pharyngeal walls

130
Q

Muscles of ET

A

tensor veli palatini (dilator rubae inferior bundle); levator veli palatini

131
Q

Causes of ET dysfunction in CP (high prevalence)

A

abnormal insertion of muscles into posterior border hard palate; pliant; wider nasopharynges; horizontal (during infancy)

132
Q

Result of ET dysfunction

A

bilateral conductive hearing loss, mild-moderate; negative middle ear air pressure (retraction TM, bacteria from ET drawn up, fluid to effuse from middle ear mucosa)

133
Q

Otitis Media types & sequence

A

OME (w/ effusion)- fluid in middle ear w/o symptoms; AOM acute- symptoms of infection

134
Q

Otitis media in children w/ CP

A

> 95%; early myringotomies and PE tubes (usually at time of palate repair or lip repair if needed; increase risk for cholesteatoma) BUT 70% still had after palate repair ; in CL only: 22% (19% control)

135
Q

If bilateral ear atresia

A

bone-conduction aids; BAHA implanted

136
Q

Non-cleft causes of VPI

A

occult SMCP; short velum/deep nasopharynx; post adeniodectomy; adenoid atrophy; mechanical obstruction (posterior pillar web or tonsils) ; neuromotor involvement (CN infection)

137
Q

Effects of large adenoids

A

sleep apnea; hyponasality; adenoid0assisted VP closure

138
Q

Articulation difficulty in children with CL/P and VPI

A

nasalized plosives; hypernasality; reduced volume; nasal air emission; wak oral pressure; omissions, sub, friacative & affricate>plosive>glide; l and r; more voiceless than voiced; tongue tends to be high and retracted

139
Q

Compensatory misarticulations in children with CL/P

A

Place change posterior to preserve manner (pharyngeal fricative, glottal stop); 25-30% of children w/ CL/P

140
Q

cul-de-sac resonance

A

pharyngeal cavity resonance; due to obstruction (from tonsils, small jaw & glossoptosis; VPI anterior nasal blockage)

Craniofacial (2 decks)

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