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Cleft Palate Wendy Elliot > Midterm > Flashcards

Midterm Flashcards

1
Q

What does foramen mean?

A

hole or opening in bone

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2
Q

What is the uvula made up of?

A

mucosa, glandilar tissue, adipose, vascular

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3
Q

Does the uvula have a function?

A

No

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4
Q

What is the pharynx made up of?

A

oropharynx, nasopharynx, hypopharynx

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5
Q

What does the eustachian tube connect?

A

connects middle ear w/ pharynx

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6
Q

What are the muscles of the VP?

A
  • Levator Veli Palatini
  • Superior Pharyngeal -Constrictor
  • Palatopharyngeus
  • Palatoglossus
  • Musculus Uvulae
  • Tensor Veli Palatini
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7
Q

WHat does the levator veli palatini do?

A

Velar elevation

“sling”

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8
Q

What does the superior pharyngeal constrictor do?

A

Constricts pharyngeal walls to narrow vp against

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9
Q

What does the palatopharyngeus do?

A

Narrows the pharynx

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10
Q

What does the palatoglossus do?

A

Depresses the velum or elevates the tongue

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11
Q

What does the musculus uvulae do?

A

“bulges” for seal on nasal surface

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12
Q

What does the tensor veli palatini do?

A

Opens the E-tubes

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13
Q

Which VP nerves are motor?

A
  • Trigeminal V
  • Facial VII
  • Glossopharyngeal IX
  • Vagus X
  • Accessory XI
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14
Q

Which VP nerves are sensory?

A
  • Glossopharyngeal IX

- Vagus X

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15
Q

Which VP nerves are both sensory & motor?

A
  • Glossopharyngeal IX

- Vagus X

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16
Q

What are the physiological subsystems for speech?

A
  • Respiration
  • Phonation
  • Resonation
  • Articulation
  • Prosody
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17
Q

What types of movement is needed for VP physiology/closure?

A
  • Velar movement
  • Lateral pharyngeal wall movement
  • Posterior pharyngeal wall movement
  • Passavant’s Ridge
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18
Q

What is a Passavant’s Ridge?

A

A shelf-like ridge of muscles projecting from posterior pharyngeal wall into pharynx.

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19
Q

What are the VP closure variations?

A
  • Coronal
  • Sagittal
  • Circular
  • Circular with Passavant’s Ridge
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20
Q

What is a coronal VP closure?

A

VP meeting posterior pharyngeal wall

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21
Q

What is a sagittal VP closure?

A

Lateral walls

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22
Q

What is a circular VP closure?

A

Sinched sac

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23
Q

What types of activity is needed for VP closure?

A
  • Speech
  • Swallow
  • Gag
  • Vomit
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24
Q

What is the timing for VP closure?

A

VP must be completely closed before phonation begins

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25
Q

What types of phonemes does the VP create the greatest force?

A

Fricatives and consonants

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26
Q

What is the ratio between Rate/Fatigue and closure force?

A

Increased rate and fatigue equals decreased closure force

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27
Q

What are factors that affect VP function?

A
  • Lack of muscle bulk (esp. levator)
  • Abnormal muscles insertion
  • Malposition of repaired muscle
  • Velum scar tissue
  • Short velum
  • Deep pharynx
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28
Q

Until when do facial bones continue growing?

A

Early adulthood

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29
Q

How long is a newborn pharynx compared to an adult?

A

Newborn is 4 cm long

Adult is 20 cm long

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30
Q

What the changes in the nasopharynx through adulthood?

A

infancy>adult = +80% volume

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31
Q

T/F VP function deteriorates as a factor of aging

A

False it does not deteriorate

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32
Q

What is a cleft?

A

-an abnormal opening (fissure) in an anatomical structure that is typically closed

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33
Q

T/F There are missing structures/flesh in a cleft.

A

False: All structures are present, but not fused or developed normally

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34
Q

What is the prevalence of clefts in live births in the USA?

A

1:600

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35
Q

When is the lip and alveolus developed in embryological development?

A

6-7 weeks

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36
Q

When does the tongue begin to drop down in embryological development?

A

7-8 weeks

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37
Q

When is the palate developed in embryological development?

A

8-9 weeks

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38
Q

When is the fusion of the hard palate and velum complete in embryological development?

A

by 12 weeks

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39
Q

What are causes of cleft?

A
  • Embryologic under-development
  • Chromosomal disorders
  • Genetic disorders_Maternal factors
  • Environmental teratogens
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40
Q

What are two types of embryologic under-development?

A
  1. Cell migration delay

2. Cell disruption

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41
Q

What are maternal factors of cleft occurrences?

A
  • older age
  • utero factors
  • maternal malnutrition
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42
Q

What are environmental teratogens of cleft occurrences?

A
  • Cigarette smoke
  • Dilantin
  • Thalidomide
  • Valium
  • Lead
  • Corticosteroids
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43
Q

What are clefts of the primary palate?

A

lip and alveolus (structures anterior to the incisive foramen)

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44
Q

What are the cleft types of the primary palate?

A
  • Complete (through to incisive foramen)
  • Incomplete (e.g. lip only
  • Unilateral and Bilateral
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45
Q

What is a cleft of the secondary palate?

A

Hard palate and velum

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46
Q

What are the cleft types of the secondary palate?

A

-Complete (uvula to incisive
foramen)
-Incomplete (bifid uvula into velum)
-Can be with or without cleft lip

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47
Q

What are the types of submucous cleft palate?

A
  • Overt (bifid uvula, zona pellucida, posterior hard palate notch)
  • Occult (hidden on nasal surface)
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48
Q

How is an overt submucous cleft palate and an occult submucous cleft palate identified?

A

Overt-intraoral exam

Occult-nasoendoscopy

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49
Q

What types of facial clefts are there?

A
  • Oblique

- Midline (median)

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50
Q

What are oblique facial clefts?

A
  • Unilateral or bilateral
  • Affects skeletal and soft tissue
  • Begins at mouth>lateral, horizontal, upward (extreme disfigurement)
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51
Q

What are midline facial clefts?

A

-Mild

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52
Q

What do midline facial clefts cause?

A

Cranial base anomalies

  • Encephalocele
  • Absent corpus callosum
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53
Q

Where is genetic material found?

A

In the nucleus of the cell

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54
Q

What does the nucleus of the cell communicate with?

A

With endoplasmic reticulum (a complex system of membranes that control transport of proteins and lipids)

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55
Q

What does DNA stand for?

A

Deoxyribonucleic acid (substance that carries hereditary information)

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56
Q

What is DNA made of?

A

A nucleic acid made of building blocks called nucleotieds

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57
Q

How is DNA arranged?

A 
Double Helix
In antiparallel (opposite directions)
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58
Q

What is the process of DNA replication?

A

Process of creating two identical DNA molecules from one

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59
Q

How does DNA replication happen?

A

The two double strands separate and a newly synthesized strand is added, each original

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60
Q

How many nucleotieds must be precisely matched for each cell division in humans?

A

3.5 x 10^4 nucleotides

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61
Q

What is a mutation?

A

A change in the DNA sequence

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62
Q

What does RNA stand for?

A

Ribonucleic acid

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63
Q

What does RNA do?

A

Transports genetic information from the nucleus to the cytoplasm

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64
Q

How is RNA arranged differently than DNA?

A

RNA is a single stranded molecule rather than a double helix

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65
Q

How is RNA created?

A

Through Transcription

-Creates a single complementary strand of a DNA template

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66
Q

What is the flow of genetic information?

A

Proceeds from DNA through transcription to RNA

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67
Q

What are chromosomes?

A

Linear double strands of DNA

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68
Q

How many human chromosomes are in most human cells?

A

46 chromosomes

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69
Q

How can we “see” chromosomes?

A

In karyotypes seen in visual profiles

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70
Q

What are the copies of 22 chromosomes called?

71
Q

What is the 23rd pair of chromosomes?

A

The sex chromosomes (X and Y) because of their role in gender determination

72
Q

What are types of chromosomal mutations of the changes in the copies of individual chromosomes?

A
  • Monosomy
  • Trisomy
  • Mosaicism
  • Deletions
  • Duplications
  • Inversions
  • Translocations
73
Q

What is monosomy?

A

Loss of one copy of an individual chromosome

74
Q

What is Trisomy?

A

Gain of 1 extra copy of an individual chromosome for a total of three

75
Q

What is mosaicism?

A

The presence of cells with 2 or more different genetic contents in a single individual

76
Q

What do most monosmy and trisomy mutations result in?

A

Miscarriage

77
Q

What does autosomal recessive inheritance mean?

A

All people carry genes with mutations capable of causing disease

Inheriting two copies of each gene with one copy that functions is sufficient

78
Q

What does it mean to be a “carrier”?

A

Individuals that have one abnormal copy of the gene but no abnormalities

79
Q

When do autosomal recessive conditions occur?

A

Only when mutations are present in both genes.

80
Q

T/F: Males and females are affected equally in autosomal recessive conditions.

81
Q

When does autosomal dominant inheritance occur?

A

When mutations are present in either of the two copies of a gene

82
Q

T/F: In autosomal dominant inheritance, it often shows that one parent is affected.

83
Q

T/F: Many autosomal dominant conditions have variable expressivity?

84
Q

What is variable expressivity?

A

Individuals can present differently (Van der Woude Syndrome-lip pits, cleft lip, cleft palate, or a combination)

85
Q

What is X-Linked Inheritance?

A

Mutations on the X chromosome

86
Q

T/F: Females are most frequently affected by recessive conditions.

A

False, Males because they receive one X chromosome.

87
Q

T/F: X-Linked dominant inheritance is rare.

88
Q

T/F: Daughters of affected X-Linked males do not inherit the disorder.

A

False, all daughters inherit the disorder

89
Q

What is multifactorial inheritance?

A

An interaction of multiple genes with environmental influences

90
Q

What are teratogens?

A

Environmental factors that increase risk of birth defects.

91
Q

What are examples of teratogens?

A

Ethanol, cigarettes, anti-epileptic meds, maternal diabetes, and congenital infections

92
Q

What is the purpose of a genetic evaluation?

A
  • Make a diagnosis
  • Determine history of the condition to assist with management
  • Determine recurrence risks for parents
  • Provide genetic psychosocial counseling
93
Q

What is involved in a genetics evaluation?

A
  • Prenatal history
  • Medical history
  • Developmental History
  • Feeding History
  • Family History
  • Physical Exam
  • Lab and Imaging studies
  • Genetic counseling
  • Psychosocial counseling
94
Q

T/F: Cleft Lip with or without Cleft Palate is a common birth defect/

95
Q

T/F: Girls are affected more that boys in a ratio of 3:2.

A

False, boys are more affected than girls

96
Q

T/F: Right sided cleft lips is more common than left sided cleft.

A

False, left sided cleft lip is more common

97
Q

T/F: Left and Right sided cleft both occur more frequently than bilateral cleft lip/cleft palate.

98
Q

Genetics of NONsyndromic Cleft Lip

A

Isolated and not generally associated with syndromes or other birth defects.

Increased risk of recurrence in siblings

99
Q

Genetics of Syndromic Cleft Lip (+- palate)

A

Some are caused by genetic syndromes or part of a multiple congenital anomaly disorder

100
Q

Genetics of Cleft Palate ONLY

A

Much more likely to be associated with underlying syndrome of other congenital anomaly

101
Q

What does the feeding and swallowing function provide for the infant?

A
  • Satisfies hunger
  • Reflexive Sucking
  • Sensory and motor stimulation
  • Mother/caregiver-infant bonding
  • Oral-motor skill development
102
Q

T/F: Normal infant structures are smaller and closer in proximity.

103
Q

What structures are ideal for sucking?

A
  • Large tongue
  • Large buccal pads
  • No teeth
104
Q

What structures are close in approximation in normal infants?

A

Close approximation of the

  • tongue
  • soft palate
  • pharyngeal wall
105
Q

In normal infants, the larynx is located where?

A

High and adjacent to C1-C3

106
Q

How is the epiglottis shaped in normal infants?

A

Tubular and narrow

107
Q

What is the physiology of infant feeding in the ORAL PHASE?

A

Sucking to stabilize nipple, create pressure gradient for fluid flow, control bolus before swallow

  • Rooting reflex
  • Nipple compression
  • Negative pressure
108
Q

What is the physiology of the PHARYNGEAL PHASE?

A

Coordination of nasal breathing, sucking, and swallowing.

109
Q

What is the physiology of the ESOPHAGEAL PHASE?

A

UES and LES

110
Q

What are s/s of pediatric dysphagia?

A

-Poor oral suction
-Inadequate volume of intake
-Lengthy feeding times
-Nasal regurgitation
-Excessive air intake (spit up or bloating)
-Coughing
-Choking
-Poor weight gain
-Excessive energy expenditure (fatigue)
Discomfort during feeding
-Stressful feeding

111
Q

What are general feeding modifications?

A
  • Relax
  • Proper feeding equipment and methods
  • Upright positioning
  • Be consistent with feeding method
  • Manage air intake
  • Limit feedings to 30 minutes or less
112
Q

What are some general feeding modifications for proper feeding equipment and methods?

A
  • Assistive squeezing (EBM)
  • Breaks to res or burp
  • Adaptive nipples/bottles (slower and faster flow rates, pliability, shape/size)
113
Q

What assessments are used to assess airway protection during feeds?

A
  • Videofluoroscopy (MBSS)

- Fiberoptic Endoscopic Eval of Swallow (FEES)

114
Q

What types of developmental anomalies/deficits might you see?

A
  • Dental
  • ENT
  • Language
  • Cognition
  • Psychosocial
115
Q

What are deciduous teeth?

A

Primary Teeth

1st 20 teeth (10 maxillary and 10 mandibular)

116
Q

When are deciduous teeth erupted?

A

by 29 months

117
Q

How many permanent teeth are there?

A 
Secondary Teeth
32 teeth (16 each earch)
118
Q

When are permanent teeth erupted?

A

from 7-20 years old

119
Q

What is a Class I occlusion?

A

Normal upper overlap

120
Q

What is a Class I malocclusion?

A

Incorrect line (teeth don’t match, are rotated, etc.)

121
Q

What is a Class II Malocclusion?

122
Q

What is a Class III Malocclusion?

A

Under bite

123
Q

What dental anomalies might you see with a cleft?

A
  • Missing teeth
  • Supernumerary teeth
  • Ectopic teeth
  • Rotated teeth
  • Crowding
  • Crossbite
  • Class III malocclusion
  • Open bite
  • Protruding Premaxilla
124
Q

What are supernumerary Teeth?

A

Extra teeth

125
Q

What are ectopic teeth?

A

Erupt in abnormal positions

126
Q

Why might a child with a cleft develop an open bite?

A

From missing teeth, finger/pacifier sucking, and skeletal deformities

127
Q

What speech problems might you see with cleft?

A

Misarticulation/distortion of sibilants, labiodentals, alveolars, and bilabials

128
Q

What is labioversion - Overjet?

A

Horizontal overlap of incisors (normal is 2mm)

-Lip closure problems & bilabial sound distortion

129
Q

What is linguoversion - underjet?

A

Upper incisors lingual to lowers

-Distorts sibilants and alveolars

130
Q

What is Macroglossia?

A

Narrow maxillary arch/teeth crowding

  • Lateral lisp
  • Frontal lisp
131
Q

When does a lateral lisp occur with a cleft?

A

When opening is in line with cleft (air flows around)

132
Q

When does frontal lisp occur with a cleft?

A

When maxillary central incisors are missing.

133
Q

What are ear anomalies?

A
  • Microtia
  • Aural atresia
  • Abnormal ossicle formation/fusion
  • Otitis media
  • Otic capsule abnormal development/ossification
134
Q

What is ear microtia?

A

small, deformed pinna

Leads to conductive hearing loss

135
Q

What is aural atresia?

A

Abnormal EAM and tympanic membrane

Leads to conductive hearing loss

136
Q

Abnormal ossicle formation/fusion leads to what type of hearing loss?

A

Conductive hearing loss

137
Q

What is otitis media from?

A

Malfunction of E-tube

Leads to tympanic membrane rupture and conductive hearing loss

138
Q

What type of hearing loss does otic capsule abnormal development/ossification lead to?

A

Sensorineural hearing loss

139
Q

What type of nose anomalies are there?

A
  • External deformities (facial cleft)
  • Abnormalities of nasal base (CL/CP)
  • Internal derangement
140
Q

What are examples of internal derangement?

A
  • Deviated septum
  • Pyriform aperture stenosis
  • Choanal stenosis/atresia
141
Q

What is a deviated septum?

A

Cleft palate-septum deflects into cleft side of nose

Resulting in hoponasality, cul-de-sace resonance

142
Q

What is Pyriform Aperture Senosis?

A

Narrowed nares from overgrown maxilla

143
Q

What is choanal stenosis/atresia?

A

Narrowed/blocked choanae

Leads to cholic/death

144
Q

What are facial anomalies?

A
  • Maxillary retrusion

- Facial nerve paralysis (may be partial or complete

145
Q

What are oral cavity anomalies?

A
  • Lips
  • Mouth
  • Tongue (macro or ankylo-glossia)
  • Palate-Fistula
  • Tonsils and adenoids
146
Q

What are throat/upper airway anomalies?

A

-Adenotonsillar/Adenoid/Tonsillar hypertrophy

147
Q

What developmental factors occur with IQ and brain structure?

A

Rate of acquisition of all developmental milestones

148
Q

What developmental factors occur with environmental stimulation?

A

Development of language skills in language-rich environment under age of 5

149
Q

What developmental factors occur with hearing?

A

Perception leads to acquisition of oral language skills

150
Q

What are those with a cleft palate more likely to develop (in regards to hearing)?

A

Chronic otis media

151
Q

What developmental factors occur with motivation?

A

Need and desire to learn skills “motivation to talk”

Cleft tend to revert to gestures because difficulty with speech production

152
Q

What developmental factors occur with attention?

A

Attend to environment

ADHD in 3-5% of children; most craniofcial syndromes + neuro at risk

153
Q

What developmental factors occur with A and P?

A

Vocal tract, processes (respiration, phonation, resonance, artic), neuro function

154
Q

What language and developmental learning deficits do you see?

A
  • Early deficits in cognitive development
  • Prelanguage skills
  • Lower expressive language
  • Common in syndromes
155
Q

What phonological/articulation development deficits might you see?

A
  • Disrupted tactile-kinesthetic-auditory feedback loop
  • Less vocalization
  • Predominant nasals for orals; glottals for plosives
  • Habitual compensatory productions
  • Age of palate repair
  • Apraxia co-occurrence
156
Q

What are some family psychosocial aspects of cleft?

A
  • Initial shock and adjustment

- Cleft as chronic medical condition

157
Q

What are some psychosocial school aspects of cleft?

A
  • Knowledge and expectation of teachers
  • Learning ability and performance
  • Social interaction
  • Teasing
  • Self-perception
158
Q

What are some psychosocial society aspects of cleft?

A
  • Physical attractiveness
  • Speech quality
  • Hearing impairment
  • Stigma
  • Behavioral issues
159
Q

What causes hypernasality?

A

Coupling of oral and nasal cavities during non-nasal oral sounds

-“muffled” due to damping effect (sound absorption) through turbinates

160
Q

What causes hyponasality?

A

Reduced nasal resonance of nasal sounds due to blockage “stuffed up”

161
Q

What is/causes Cul-De-Sac resonance?

A

Structural obstruction, muffled, “potato-in- mouth”

162
Q

What are mixed resonance disorders?

A

Combo on different sounds; common in apraxia

163
Q

What is nasal air emission?

A

“rustle” due to VP leak or fistula on plosives, fricatives, and affricates

164
Q

What is a nasal grimace?

A

Muscle contraction above nasal bridge in effort to achieve VP closure

165
Q

What weak or omitted consonants a result of?

A

Reduced air pressure in oral cavity.

166
Q

What causes short utterance length?

A

Frequent replacing of air pressure

167
Q

What causes altered rate and duration?

A

Longer time for utterances, longer voice onset time (VOT)

168
Q

What are some compensatory articulatory strategies?

A
  • Middorsum palatal stop
  • Backing
  • Velar fricative
  • Oral consonant nasalization
  • Vowel nasalization
  • Nasal snort
  • Nasal sniff
  • Pharyngeal
  • Posterior nasal fricative
  • Glottal stop
  • /h/ for voiceless plosives
  • Breathiness
169
Q

How might dysphonia present in an individual with a cleft?

A
  • Breathy
  • Hypernasal
  • Hoarse
  • Low intensity
  • Glottal fry
  • Hyperfunctional
  • Vocal fold nodules
170
Q

What are factors that Impact VPI and Speech?

A
  • Size of VP opening
  • Inconsistency of VP closure
  • Abnormal artic
  • Abnormal phonation
171
Q

What are causes of VPD related to the anatomy - structure of VPInsufficiency?

A
  • Cleft Palate
  • Short velum
  • Deep pharynx (cranial base anomalies)
  • Adenoid atrophy, irregularity, or adenoidectomy
  • Hypertrophic tonsils or tonsillectomy (rare)
  • Teeth malocclusion (Class III)
  • Oral cavity tumor
172
Q

What are causes of VPD related to phyiolofy - movement of VPIncompetence?

A

-Abnormal muscle insertion
-Hypotonia/poor pharyngeal wall movement
-Dysarthria, apraxia, and
neromuscular disorders
-Cranial Nerve defects (U velar paralysis/paresis)
-Velar fatigue

173
Q

What are causes of VPD related to VP mislearning?

A
  • Faulty artic
  • Bad speech habits
  • Hearing loss

Cleft Palate Wendy Elliot (1 decks)

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