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Swallowing > Midterm I > Flashcards

Midterm I Flashcards

1
Q

Oral preparatory stage (part of oral phase)

A
  • voluntary but overly routinized
  • Important for the sensory recognition of food: visual, olfactory, auditory, kinesthetic
  • Different prep of food materials; liquid = tongue cups around bolus; puree = tongue manipulates and holds bolus; solid = prepare to chew
  • Mastication = relatively complex act; upper and lower teeth crush bolus with rotary/lateral movement of jaw to manipulate bolus, not just up and down; saliva mixed with bolus by tongue and by chewing
  • Posterior aspect of oral cavity is closed (soft palate and back of tongue), anterior aspect of oral cavity is closed by lips, larynx is at rest
  • Time to complete = as long as necessary
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2
Q

Oral transit stage

A

• Oral transit starts when tongue begins to propel the bolus posteriorly
• Tongue tip and sides to the alveolar ridge
o So not to lose food laterally
• Soft palate elevates - tongue base drops
o Closure of oral cavity from nasal cavity
o Opening becomes even bigger when tounge base drops
• Pressure exerted by the tongue increases as viscosity increases
• Oral phase ends when bolus reaches ramus of mandible
• Time to complete oral phase is 1 - 1.5 seconds depending upon viscosity and age
• .3 seconds longer for people over 60

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3
Q

• Bolus containment
• Action: Provide anterior seal of lips, especially for larger boluses, highly active during straw suck
Innervation?

A 
Orbicularis oris (superior and inferior)
Invisivus labii (superior & inferior)
• Innervation: VII
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4
Q

• Bolus control
• Action: - Provide check tension to keep bolus between occlusal surfaces of the teeth; reduce area of lateral sucli
Innervation?

A

Buccinator
Risorius
• Innervation: VII

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5
Q

• Bolus control
• Action: Anterior depression of tongue tip; creation of midline depression or channe
Innervation?l

A

Genioglossus
Intrinsic tongue muscles
• Innervation: XII

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6
Q

Muscles of bolus containment

Innervation?

A
  • Orbicularis oris (superior/inferior) - VII

* Invisivus labii (superior/inferior) - VII

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7
Q

Muscles of bolus control

Innervation?

A
  • Buccinator - VII
  • Risorius - VII
  • Genioglossus - XII
  • Intrinsic tongue muscles - XII
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8
Q
  • Mastication
  • Action: Raise mandible

Innervation?

A

Masseter
Medial pterygoid
Temporalis

• Innervation: V

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9
Q
  • Mastication
  • Action: Lower mandible

Innervation?

A

Lateral pterygoid - V
Anterior belly of digastric - V
Mylohyoid - V
Geniohyoid - XII

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10
Q
  • Mastication
  • Action: Collectively moves in coordination with jaw and tongue during chewing

Innervation?

A 
Levator anguli oris
Depressor anguli oris
Levator labii superioris
Depressor labii inferioris
Zygomaticus
Mentalis

• Innervation: VII

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11
Q

Muscles of mastication

Innervation?

A 
Masseter - V
Medial Pterygoid - V
Temporalis - V
Lateral Pterygoid - V
Anterior Belly of Digastric - V
Geniohyoid  - XII
Mylohyoid - V
Levator anguli oris - VII
Depressor anguli oris- VII
Levator labii superioris- VII
Depressor labii inferioris- VII
Zygomaticus- VII
Mentalis- VII
• Action: raise mandible, lower mandible, move with jaw during chewing
• Innervation: V, VII, XII
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12
Q
  • Oral bolus propulsion
  • Action: Press lips together and obliterate anterior labial sulcus during onset of bolus transfer

Innervation?

A

Orbicularis oris (superior & inferior)

• Innervation: VII

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13
Q
  • Oral bolus propulsion
  • Action: Tense cheeks and obliterate lateral sulci during onset of bolus transport

Innervation?

A

Buccinator

• Innervation: VII

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14
Q
  • Oral bolus propulsion
  • Action: Create channel in midline of tongue, progressive and sequential pressing of the tongue against palate

Innervation?

A

Intrinsic lingual muscles
Genioglossus

• Innervation: XII

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15
Q

Muscles of oral bolus propulsion

Innervation?

A

Orbicularis Oris (S/I) - V
Buccinator - V
Intrinsic lingual muscles - V
Genioglossus - XII

• Innervation: V, XII

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16
Q
  • Velopharyngeal Closure
  • Action: Elevate velum

Innervation?

A

Levator veli palatine
Musculus uvulae

• Innervation: X

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17
Q
  • Velopharyngeal Closure
  • Action: tenso anterior velum and open auditory tube

Innervation?

A

Tensor veli palatine

• Innervation: V

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18
Q
  • Velopharyngeal Closure
  • Action: Move lateral pharyngeal walls medially; create Passavant’s pad on posterior pharyngeal wall

Innervation?

A

Superior constrictor muscle
Horiztonal fibers of palatopharyngeus

• Innervation: IX, X

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19
Q
  • Velopharyngeal Closure
  • Action: Perhaps provide initial anterior depression of velum as set up response; helps form faucial pillars

Innervation?

A

Palatoglossus

• Innervation: IX, X

 Palatoglossus one of the muscles that helps to form the faucial pillars; also helps to modify the shape of the velum as velopharyngeal closure is taking place

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20
Q

Muscles of velopharyngeal closure

Innervation?

A 
Levator veli palatine - X
Musculus uvulae - X
Tensor veli palatine - V
Superior Constrictor - IX, X
Horizontal fibers of palatopharyngeus - IX, X
Palatoglossus - IX, X

 Swallowing has an effect on pressure in the ear
 Closure occurs at the end of the oral phase and at the beginning of the pharyngeal phase

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21
Q

Muscles of Pharyngeal Elevation & Constriction

Innervation?

A

Superior, middle, and inferior constrictor - pharyngeal plexus: IX, X
Salpingopharyngeus - pharyngeal plexus: IX, X
Stylopharyngus - IX

  • Action: Progressive contraction and elevation of the pharynx
  • Innervation: IX, X
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22
Q

Muscles of Hyolaryngeal Elevation

Innervation?

A

Anterior belly of digastric - V
Mylohyoid - VII
Geniohyoid - XII

  • Action: Elevate and anteriorly displace hyoid - suprahyoid muscles
  • Innervation: V, VII, XII
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23
Q
  • Laryngeal Protection
  • Action: Elevate and anteriorly displace hyoid

Innervation?

A

Interarytenoids (TV + Oblique IA)
Lateral cricoarytenoid - adduction of VF
Thyroarytenoid

• Innervation: X

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24
Q
  • Laryngeal Protection
  • Action: Invert epiglottis

Innervation?

A

Thyrohyoid - contraction helps pull forward epiglottis in posterior aspect
Aryepiglottic (?)

• Innervation: X

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25
Q

Muscles of Laryngeal Protection

Innervation?

A 
Interarytenoids (TV + Oblique IA)
Lateral cricoarytenoid - adduction of VF
Thyroarytenoid
Thyrohyoid - contraction helps pull forward epiglottis in posterior aspect
Aryepiglottic (?)

Innervation: X

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26
Q

Labial sulcus
Buccal sulcus
Faucial arches/pillars
Ramus of the mandible

A
  • labial sulcus = indentations in oral cavity that can pocket food; between lips and osseous structures
  • buccal sulcus = between line of dentition and buccal cavity shaping muscles
  • faucial arches/pillars = two bands of tissue around tonsils; can trigger a gag reflex
  • ramus of the mandible = important landmark in determining end of oral phase and beginning of pharyngeal phase
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27
Q

Cranial nerves of intraoral sensation

A
  • CN V = lips, cheeks, anterior 2/3 of tongue, palate, gums, and front of mouth; sensory information is very important swallowing process; importance of sensation in preparing oral cavity for food
  • CN IX = posterior 1/3 of tongue; very important for triggering the pharyngeal phase when it loses its seal from the velum as it elevates while bolus material is passing by;
28
Q

Cranial nerves for taste sensation

A

o Anterior 2/3 of tongue - CN VII

o Posterior 1/3 of tongue - CN IX

29
Q

Swallowing center of the brain

A

nucleus tractus solitarius
• Bolus stimulates superficial and deep sensory receptors, many of which project via IX, X, and XI to a medullary reticular formation called the nucleus tractus solitarius (NTS)
• Likely incorporates sensory information from V, VII, and XII as well
• Center integrates sensory information and begins reflexive movements that characterize the pharyngeal phase of the swallow

30
Q

Pharyngeal Stage

A
  • Anterior and superior displacement of the hyolaryngeal complex
  • Closure of the false and true vocal folds
  • Progressive pharyngeal contraction
  • Opening of the upper esophageal sphincter (UES)/PES - pharyngo-esophageal segment

Pharyngeal Transit
 Base of tongue retraction and contract with the posterior pharyngeal wall
 Sequential contraction of the upper, middle, and inferior constrictors
 The bolus moves inferiorly via a combination of base of gravity, base of tongue retraction, pharyngeal wall contraction, and pressure differentials

Time = 1 second (?)

31
Q

Four mechanisms of airway protection

A

1) Hyoid/laryngeal elevation away from path of bolus
2) Epiglottic retroflection
• Suprahyoid, geniohyoid, and mylohyoid are responsible for anterior movement of the hyoid and subsequent tipping of the epiglottis to a horizontal position
• Elevation of the larynx to approximate the hyoid (via thyrohyoid contraction) results in flipping the epiglottis over to a more vertical position
3) Adduction of the true vocal cords
• Apneic event usually interrupting expiration; most people exhale-swallow-exhale
• Recurrent laryngeal nerve - responsible for innervating muscles that have to do with adduction of the true vocal folds
4) Closure of the laryngeal vestibule (bounded by the epiglottis, aryepiglottic folds, and arytenoid cartilage, and ends at the false vocal folds)
• Anterior tilting of the arytenoids creates tighter closure as hyolaryngeal complex moves anteriorly
• False vocal fold adduction
• Lateral septal nucleus, CN V, CN VII, cervical nerves 1-4
• Expelling penetrated material - if something has accidentally “penetrated” into the larynx, the closure of laryngeal vestibule will help to expel the material

32
Q

Pharyngeal stage (from website)

A
  • Complete closure of the velopharyngeal port to prevent material from entering the nasal cavity
  • Elevation and anterior movement of the hyoid and larynx. Elevation contributes to airway protection Forward movement contributes to opening of the Upper Esophageal Sphincter which soon allows the bolus to move into the Esophagus.
  • Closure of the Larynx (vocal folds) begins in a bottom - up sequence in order to clear any penetration. -Bottom-up sequence for VF to laryngeal vestibule to clear penetration = -True vocal folds contract and respiration ceases -Laryngeal vestibule closes -False folds contract -Arytenoids move in a downward, forward, and inward direction which narrows the laryngeal opening -At same time, larynx is elevated and pulled forward which thickens the epiglottic base -Laryngeal framework is pulled up, the epiglottis inverts
  • Epiglottis inverts and comes into contact to further protect the airway
  • Top to bottom contractions of pharyngeal constrictor muscles
  • Opening of the cricopharyngeal sphincter to allow material to pass from pharynx to epiglottis -Tension released -Yanked open due to laryngeal elevation
  • Tongue base to posterior pharyngeal wall contact delivering bolus to pharynx -Food is directed around the epiglottis
  • Relaxation of cricopharygeus muscle & opening of upper esophageal sphincter region
  • Pharyngeal phase ends when the esophageal phase begins as the bolus passes through the Upper Esophageal Sphincter (UES) entirely
  • Breathing is reinitiated
33
Q

Oral Transit Stage (from website)

A

1) Oral Transit Phase begins when the tongue begins posterior movement of the bolus
2) Food on anterior tongue
3) Bolus is moved posteriorly due to the midline of the tongue sequentially squeezing against the hard palate
4) Anterior to posterior rolling action of the midline of the tongue
5) Tongue elevation progresses sequentially more posteriorly to push the bolus backward
6) Sides and tip of the tongue are anchored to the alveolar ridge
7) As food viscosity thickens, greater muscle activity is required to squeeze the bolus back
8) Oral transit phase typically lasts approximately less than 1 to 1.5 second, .3 seconds longer for people over 60 & this increases slightly with increased viscosity
9) As tongue propels bolus back, sensory receptors in the oropharynx and tongue itself are stimulated and pharyngeal swallow is triggered

34
Q

Important landmarks of the larynx/pharynx: Valleculae, lateral channels, aryepiglottic folds, false vocal folds, pyriform sinuses

A
  • Valleculae = Higher - located in depression anterior to epiglottis
  • Lateral Channels = Form the passage alongside and outside the main laryngeal structures bypassing laterally the opening into the trachea
  • Aryepiglottic folds = Large folds on either side of the larynx, coursing from the lateral aspect of the epiglottis towards the laryngeal cartilages
  • False vocal folds = Not really vocal folds innervated to open and close; Superior to the true vocal folds; They don’t entirely close they do constrict and can form a barrier in that region
  • Pyriform Sinuses = Inferior and posterior to the valleculae; Formed in lateral aspect of the laryngeal vestibule
35
Q

Muscles of the pharyngo-esophageal segment

A
  • Cricopharyngeus (major contributor, thought to be part of the inferior pharyngeal constrictor)
  • Inferior pharyngeal constrictor
  • Proximal end of the esophagus

Called the pharyngo-esophageal segment because it’s not only one muscle

36
Q

Opening of the Upper Esophageal Sphincter

A
  • Opening of the UES allows the bolus to enter the esophagus
  • Opening occurs before the bolus arrives and contributes to the pressure differential within the pharynx
  • UES relaxes during the swallow
  • Elevation of the larynx pulls UES open: fibers of the cricopharyngeus are attached anteriorly to the laminae of the cricoid cartilage
  • Duration of opening increases as bolus volume increases; With small bolus, UES opening is shorter
  • Contraction of pharynx also contributes to the opening;
  • It is “contracted” - relaxes for bolus, then contracts back to stop reflux;
37
Q

Reflexive Cough & Gag reflex

Innervation?

A
  • Reflexive cough = CN X: both motor and sensory
  • Reflexive cough occurs in response to material entering deep into the laryngeal vestibule
  • Damage to CN X motor/sensory means no reflexive cough that doesn’t stop food penetrating to laryngeal vestibule - no longer normal swallow
  • Gag reflex = sensory CN IX, motor CN X
  • The absence of a gag reflex is not predictive of pharyngeal stage dysphagia severity or aspiration risk
  • Many individuals with normal swallowing have an absent gag reflex
38
Q

Esophageal Stage

A
  • PES/UES already opened
  • After entrance of bolus into the esophagus, the food is carried to the stomach via gravity and esophageal peristalsis
  • Lower esophageal sphincter (LES) must open and close after bolus
  • Passage of food through the hypopharynx is not considered to be due to “peristalsis”
  • Malfunction of the LES can lead to disorders like reflux
  • Esophagus joins the stomach through the opening in the diaphragm called the “diaphragmatic” or “esophageal” hiatus
  • Problems can include lack of peristalsis, difficulties opening/closing sphincters, travel of food material in the wrong direction
  • Esophageal phase usually takes around 8-12 seconds; Most lengthy of the three phases discussed
39
Q

What do we know about the aging process in general?

A

Decreased motor skills and decreased acuity for sensory information

  • Tissue elasticity decreases; especially in cartilaginous structures - e.g., the epiglottis becomes less flexible as we age
  • Sensory receptors decrease in number. Includes kinesthetic structures; Fewer receptors to take info to the brain; Ones that are there are less slower, less effective in processing sensory stimuli
  • Muscle wasting (sarcopenia)
  • Fatigue. Many aspects of eating are associated with effort; Less social demands; Eating requires sustained attention to a task
  • Geriatric failure to thrive (decreased appetite, less intake at meals). Failure to thrive = failure to take in enough nutrients for healthy living; Decrease in sensory receptors - can’t smell, food doesn’t taste as good
  • Physicians say that skills (swallowing) become decompensated; e.g., skills become less effective, integrated, coordinated, don’t accomplish the purpose we have for those skills
40
Q

What do we know about the aging process as it relates to swallowing structures?

A

Eating is less rewarding, meals may take longer

  • Decreased saliva production
  • Decreased sense of taste (decreased sensation)
  • Loss of dentition. TMJ may have reduced ROM; Dentition is included in loss of bone mass; TMJ is affected by ossification & sarcopenia
  • Larynx becomes more calcified. Cartilage becomes more like bone (ossified); Affects readiness in which structures in the larynx can change position and move
  • Sensory receptors decrease in number
  • Muscle wasting (sarcopenia) = Masseter, muscles in the tongue, muscles responsible for elevating velum, sarcopenia can affect pharyngeal constrictors
41
Q

Changes in deglutition in normal elderly = Oral stage

A

Oral stage(s):
 Slowing of movement, reduced efficiency of structures, increased oral transit time
 Bolus position more posterior or more anterior in the oral cavity than in younger adults
 “Tipper” and “dipper” types of oral swallows
• Tipper: swallowing initiated with tip of tongue; bolus is supralingual - often found in young adults
• Dipper: bolus initially positioned beneath the anterior portion of the tongue; tongue dips under bolus first. Occurs in all ages, but more prevalent in older individuals
 Premature spillage into valleculae: when normal?
• There is some premature spillage into the valleculae
• Considered normal as long as the pharyngeal phase of the swallow is triggered as the tail of the bolus is leaving the ramus of the mandible

it may be the case there is a range of normal that we expect from a competent swallower, either very young or elderly

42
Q

Changes in deglutition in normal elderly = Pharyngeal/Esophageal

A

o Pharyngeal stage(s)
 Timing slowed: increased transit time, slowed pharyngeal contraction, longer apnea duration
 Swallow triggered lower in pharynx and needs larger bolus to elicit trigger
 Decreased excursion of the hyolaryngeal complex
 More coughing after swallowing, but decreased pharyngeal sensitivity
 Delayed onset PES opening
• Slower timing, bolus is lower before swallow is triggered

o Esophageal stage:
 Reduced esophageal peristalsis
 Slower transit to stomach

43
Q

Esophageal stage (from website)

A

• Upon entry of the bolus through the cricopharyngeal muscle, the esophageal phase is initiated
• Esophageal propulsion begins via muscle contractions occurring initially in response to the arrival of a bolus that stretches the esophageal lumen and then continue as each segment of the esophagus is stretched by the bolus in a feed-forward fashion Here there is no spinal/brainstem mediation.
Once the bolus has entered the esophagus, it is carried to the stomach by a mixture of esophageal peristalsis and gravity
• Esophagus produces a proximal to distal (top to bottom or “anterograde”) sequence of contractions that propel material distally toward the digestive system.
• At the bottom of the esophagus, the lower esophageal sphincter relaxes so that the bolus can enter the stomach.
• Esophageal transit takes approximately 8 to 20 seconds
• It normally takes two peristaltic waves to clear the esophagus
• The bolus enters the stomach, the swallowing process has finished, and digestion begins.

44
Q

Purpose of the clinical swallow assessment

A
  • Much more detailed type of dysphagia assessment - not just determining the presence or absence of dysphagia, as nurses might, but also the physiologic factors that are contributing to the dysphagia, and the stage of the swallow that seems to be impaired
  • Figure out what assessments/tests are needed to complete the picture and understand the nature of the disorder
  • Make recommendations for safest means of intake, including diet (PO substances), or perhaps on basis of clinical swallow that the patient is safe for oral diet and may need non-oral hydration and nutrition needs.
  • Is the swallowing pattern you observe consistent with the medical history? Is the pattern you are seeing consistent with their medical disorder? Does what you’re seeing suggest there is an additional medical problem not mentioned in the chart or by the family? If so, you may want to let the physician know you are seeing problems not consistent with the impairments expected from their medical condition.
  • Take your findings to their logical conclusion - what should the treatment be needed for this patient? Is there follow up needed? What kind of follow up?
45
Q

Penetration vs Aspiration

A
  • Penetration - you want to determine the extent to which p.o. material enters the airway and exits as the swallow continues
  • Aspiration - P.O. material is below the level of the vocal folds and is no longer retrievable - it won’t exit on its own.
  • Biggest threat to airway safety, and thus healthy p.o.
46
Q

Who is at risk for dysphagia?

A

Neurogenic dysphagia: disorders of the cerebral hemispheres and brainstem = CVA, Brainstem lesions, TBI

Neurogenic Dysphagia: Progressive Disease = Parkinson’s disease, Multiple sclerosis, Huntington’s disease, ALS, Dementia, Motor unit abnormalities (Guillaine-Barre Syndrome, Myasthenia Gravis)

Surgical trauma
Respiratory difficulties
Medication
Obstructive diseases (COPD)
Restrictive diseases
Tracheotomy

Esophageal Disorders of Swallowing = Zenker’s diverticulum; constrictions from GERD; Tracheoesophageal fistula (hole); Diffuse esophageal spasms; Achalasia (incomplete relaxation)

47
Q

Characteristics of dysphagia typical for CVA

A
  • Up to 40% of stroke survivors can have dysphagia at some point
  • Dysphagia can occur due to a unilateral CVA or bilateral
  • May be slightly higher incidence with R CVA, but many individuals of both R and L have dysphagia.
  • Swallowing problems often only show up for a few days after the stroke - there will be a rebound effect. Others can have swallowing problems for a long time.
  • The muscles involved with swallowing are bilaterally innervated; unilateral UMN damage in the right or left hemisphere won’t cause noticeable and significant dysphagia.
  • Some individuals with RHD may have a prolonged delay in swallowing.
  • With bilateral strokes and bilateral UMN damage, there are noticeable effects on the muscles of swallowing. That patient probably needs feeding tubes.
  • Can cause damage to reticular formation in medulla
48
Q

Characteristics of dysphagia typical for brainstem lesions

A
  • Oral and/or pharyngeal stage dysphagia depending on where the damage is. You can expect a range in the stage and the severity - seems to correlate with the size of the area damaged in the stroke
  • Typically affect the swallowing centers in the brainstem (CVA, neoplasm, congenital defects, and TBI)
  • Results in mild to profound dysphagia
  • Brainstem strokes are much more difficult on swallowing - takes out multiple crainial nerve nuclei. These are not as common.
49
Q

Characteristics of dysphagia typical for TBI

A
  • Deficits at the oral stage - inability to contain bolus because of poor sensory feedback. Can have sensory & motor issues.
  • TBI can cause widespread damage - we could expect frontal lobe damage (w/ automative) plus posterior damage with widespread neuronal shearing. There is diffuse axonal damage through both hemispheres. Because damage is diffuse and bilateral, we are more likely to get bilateral UMN damage.
  • Sensory as well as motor impairments. This can cause inadequate information to be passed to the neurological swallowing center
  • The extent of the bilateral UMN damage will depend upon the severity of the head injury- anything from mild to profound dysphagias. Widespread damage will cause changes to cognition, sensory ability, motor impairments, as well as communication - language, etc.
  • The characteristic of swallowing problems for people with bilateral UMN damage, whether stroke or TBI, is slow and weak movements. In terms of muscle tone, bilateral UMN damage causes spasticity - hypertonicity. Muscles are weak and move slower.
  • Changes in cognition can affect the ability to eat safely. Changes to judgment after frontal lobe damage can cause problems with judgment when eating. This area is responsible for self-regulation. These patients who don’t chew adequately and have poor judgment about bite size = prime candidates for choking on top of aspiration.
50
Q

Characteristics of dysphagia typical for Parkinson’s Disease

A

• As Parkinson’s’ disease progresses there is more cognitive impairment and impairment of motor activity; thus, all aspects of the swallow can be impaired. Parkinson’s patients demonstrate patterns of impairment at oral stage.
• PD is a neurological impairment that results from decreased dopamine which impairs the ability to regulate and control of movement. Causes stiffness, rigidity, difficulty with movement patterns, problems with impulsivity.
• Rigidity and bradykinesia (slowness of initiating movement) underlie the disordered volitional stage of swallowing. Too much tension/rigidity. Slow rise time in muscle contraction aka bradykinesia. Disordered of volitional aspects of swallowing
• PD outpatient patients for whom medication is working show:
o Impaired lingual movement
o Characteristic frozen face = minimal jaw opening
o Stiff and abnormal head/neck posture while eating - don’t have the flexibility of structures we think of when we think about contractions of posterior pharyngeal wall, movements of hyolaryngeal complex and larynx
o Abnormal eating behavior - comes from medications that causes compulsive behaviors in general - check medications being taken, and see if those can be associated with changes that come with the swallow

Impaired lingual movement, minimal jaw opening, abnormal head and neck posture, and impulsive eating behavior lead to:
• Delayed oral transit time (tongue pumping and piecemeal deglutition).
• Delayed pharyngeal swallow and reduced contraction. Poor oral transit time will result in delay with pharyngeal swallow. Given overall stiffness, there is reduced pharyngeal contraction to help the bolus move inferiorly
• Pooling in the valleculae and pyriform sinuses. Material gets caught in pockets. Portions of the bolus are processed separately, so some material may escape prematurely into the valleculae. Might be material that pools as these different pieces are processed into the pharynx. Pooling in the pyriform sinuses result from delays at the esophageal stage (e.g., slow opening of the PES)
• Silent aspiration. Anytime you have delayed pharyngeal swallow or piecemeal deglutition, these people will be at risk for silent aspiration. Don’t have a strong cough response. The delay in pharyngeal initiation puts the opening to the airway in a positon to get pieces fo the bolus down into he airway itself.

51
Q

Characteristics of dysphagia typical for multiple sclerosis

A

• Involves an abnormal immune response directed against the CNS that leads to destruction of myelin (myelin helps project nerve impulse along the axon).
• Nerve impulses slowed or even stopped at some points. Results in spasticity and incoordination of oropharyngeal muscles and problems with the respiratory muscles. This creates functional problems with swallowing, including:
o Impairments at the oral stage - can’t have efficient oral transit if there is spasticity or incoordination of the oropharyngeal structures
o If they are having difficulty coordinating swallowing function with respiration, that makes them more likely to aspirate
• Delay and incoordination of laryngeal movements and pharyngeal constrictor dismotility. We can predict delays in laryngeal movement if there are insufficient but still present nerve impulses that head along axons of neurons in the chain.

52
Q

Characteristics of dysphagia typical for Huntington’s Disease

A
  • Dysphagia signs stem from the oral and pharyngeal stage disorders of lingual chorea (abnormal twisting patterns) and tachyphagia (abnormally rapid eating or bolting of food)
  • Disease of movement and cognitive impairment. Early onset inherited disorder causing degeneration of neurons. Earlier onset than Parkinson’s - fairly common for symptoms to occur in the 30s
  • Characterized by lingual chorea - abnormal twisting patterns Difficulties in swallowing occur at the oral/pharyngeal stage if there is abnormal contraction or movement of the oral structures. Could be too much movement/swallowing, too early. Overall pattern of lack of control and coordination.
  • Tachyphagia = abnormally rapid eating or bolting (no chew) of food that results from cognitive impairment
  • Discoordinated out-of-sequence actions of the structures in the oral and pharyngeal stage, as well as the opening of the PES/LES
53
Q

Characteristics of dysphagia typical for Amyotrophic Lateral Sclerosis (ALS)

A

• Oral and pharyngeal stage dysphagia. Lingual movements & premature spillage (problems controlling velum) as well as difficulties with nasality in speech production
• Progressive degeneration of motor neurons themselves in the brain and spinal cord
• It eventually affects most of the motor chains in the brain and spinal cord
• Dysphagia eventually occurs in all types of ALS and in all stages
• In the initial stages of ALS, the swallowing and speech impairments are relatively mild
• Exercises not recommended because they can lead to further fatigue of the musculature.
o Actual dying of cell bodies of both upper and lower motor neurons.
o May present with spastic dysarthria, we see more LMN damage later on. May also see it with LMN first. LMN is the final pathway, it doesn’t matter how healthy everything else is.

54
Q

Characteristics of dysphagia typical for the dementias

A

• A term that is used to describe a variety of cognitive impairments. These cognitive impairments can occur in Huntington’s and Parkinson’s• Dysphagia varies by stage of disease and type of dementia
• Progressive disease whose hallmark is the cognitive impairments that affect memory, attention to task, decision making, alertness
• Affects mostly old but also young patients.
• Not just memory - also affects cognitive processes that can impact PO safety
• Sensory impairments may affect readiness to eat, awareness of bolus, etc
• Can cause inefficient/delayed processing of stimuli that affects awareness of bolus and may limit exterior stimuli that makes you ready to eat (lack of olfactory sensation)
• In the beginning stages problems are with memory, attention - these lead to lack of appropriate social interaction and decision making
• Later stage: lack of ability for self-care, goal-directed acts.
 There is a push to keep dementia patients on PO food as long as possible.

55
Q

Characteristics of dysphagia typical for Guillaine-Barre Syndrome

A
  • Affects oral and pharyngeal stage of dysphagia
  • Motor unit abnormality
  • Acute disease of the peripheral nerves that can greatly affect swallowing
  • Physicians may overlook the problems that peripheral impairments can have on patients
  • Rapid onset of weakness/paralysis of legs, arms, muscles of respiration, and face. Includes muscles that govern tongue movement, movement in the oral cavity and pharynx
  • May have abnormal sensations & tingling feelings as disease attacks the peripheral nerves
  • Typically, these patients go on to recover some/all of the control of their peripheral nerves; you may need to provide information about changes they are going through and how to adapt to the changes
56
Q

Characteristics of dysphagia typical for myasthenia graves

A
  • Motor unit abnormality
  • Disease that affects how nerve impulses are transmitted to muscle at the neuromuscular junction, the junction that allows the impulse to transfer from neuron to muscle fiber
  • Often affects muscles innervated by the bulbar nuclei
  • Progressive fatigue with use. Not good candidates for exercise programs.
  • May demonstrate weakened or delayed movements
  • MBSS before and after a meal in order to evaluate disorder when symptoms present.
57
Q

Types of surgical trauma affecting swallowing

A
  • Nerves may be stretched or cut in procedures such as cervical spinal surgeries with an anterior approach
  • Head and neck patients - nerves are being pushed/cut out of the way. Some approaches can cause more damage as nerves are moved to access particular area
  • Surgical cases where cancer has led to resection of structures thought to be crucial for swallowing: epiglottis, tongue, buccal tissue, tumors on nerves, laryngectomies
  • People that have radiation has a particular scarring affect on surface and, in some cases, deep structures
  • Almost any surgery where there is a general anesthetic the patient is intubated; putting in tube as a method to open airway can nick the larynx
58
Q

Types of medications that affect swallowing

A
  • Sedatives and anti-seizure meds may alter sensory-motor function and influence swallowing, particularly in patients with some degree of dysphagia
  • Patients with TBI may be on sedatives and anti-seizure medications. These can change sensory transmission and sensory motor function.
  • TBI Patient on anti-seizure medication may demonstrate limited sensitivity and delayed initiation of the oral phase
  • Tricyclic antidepressants and antihistamines that reduce saliva (xerostomia) can contribute to, or exacerbate, a dysphagia. Saliva is important to swallowing ability
59
Q

Swallowing and respiration

A
  • Respiration is an integral part of PO intake - in particular, you have to coordinate when you are breathing vs when you are swallowing. Swallowing and PO intake can be tricky with this population.
  • Dyspenia = difficulty breathing
  • Tachypenia = rapid breathing (applies if an adult has a breathing rate greater than 20 breaths/minute; normal adult breathing rate is 12 breaths per minute).
  • Respiratory rates above 30 per minute may be unable to safely coordinate periods of non-breathing during the swallowing cycle.
60
Q

Characteristics of dysphagia typical for obstructive diseases (COPD)

A
  • Persons with restrictive pulmonary disease are more at risk as they are more likely to inspire immediately after the swallow. They are going to be oxygen depleted - normally you breathe OUT a little bit before the swallow and after swallowing. These individuals breathe in and aspirate food
  • COPD includes a wide range of medical diagnoses such as cystic fibrosis, chronic bronchitis, asthma, bronchiectasis, and emphysema
  • As the airway is decreased/clogged/has mucus, path through the pulmonary system is full of greater resistance than in a healthy pulmonary system
  • When the air flows through the decreased space, there is more resistance and therefore more effort during respiration
  • More resistance during expiration than inspiration. Expiration is harder than normal because it is very difficult to get the air back out.
  • Fewer than normal breaths; extended expiratory phase
  • If you have COPD or perhaps bronchitis, it restricts the number of breaths you take per minute. Very fatiguing just to breathe in and out.
61
Q

Characteristics of dysphagia typical for restrictive diseases

A
  • Neuromuscular disease
  • Reduced expansion of the lungs during inspiration resulting in reduced lung capacity with low O2/oxygen saturation of the blood (hypoxic condition or hypoxemia or hypoxia) and higher than normal CO2 levels
  • Can’t get enough gas in the lungs for proper gas exchange
  • Breathing is often rapid and shallow with low 02 saturation
  • These patients are at greater risk of not beign able to tolerate PO intake
62
Q

Characteristics of dysphagia typical for tracheotomy

A
  • Surgical procedure performed when oral/nasal breathing is not adequate and produces respiratory distress:
  • breathing difficulty, shortness of breath, unusual respiratory patterns, and inadequate oxygenation of the blood
  • An emergency airway is made into the trachea, bypassing the oral cavity
  • Can have specific effects on swallowing even though PO pathway is typically clear: there can be scar tissue, affects on pressures, etc.
  • It changes natural relationship between pharynx and airway
  • Changes in pressures that affect the swallowing process
63
Q

Characteristics of dysphagia for post-radiation patients

A
  • May swallow fine after radiation treatment, but can have swallowing complaints 2-5 years later and they get progressively worse.
  • Radiation starts inflammatory process, over years the ongoing inflammatory process will cause microscarring in connective tissue around muscle fibers and bundles. Can make things extremely hard. Reduced hyolaryngeal elevation.
  • If a person does ROM exercises during radiation treatment and for the rest of their lives, they can continue to have a safe swallow.
64
Q

Characteristics of dysphagia typical for mechanical ventilation

A
  • Weight of tubing and difficulty timing the swallow with ventilator cycles add increased difficulty to that created by the cuffed trach tube
  • A machine that allows the patient to experience gas exchange, even though they are not controlling the muscles and airflow on their own
  • To maintain respiration when patient is incapable of completing gas exchange on their own
  • Pressure changes gently push air into lungs; passive forces usually govern exhalation
  • Air enters through a trach tube, a nasal mask, or through intubation
  • Some patients use these only part of the time
  • Patients with a trach tube can still (sometimes) take PO
65
Q

Esophageal disorders of swallowing

A

o Zenker’s Diverticulum is an outpouching or pocket that forms in the pharyngeal wall just superior to the UES, within the UES, or just below the UES. Content of small pockets may be refluxed later and aspirated
o Strictures/constrictions are often the result of formation of fibrotic (scar) tissue that can develop after prolonged irritation/inflammation of the esophagus (esophagitis) secondary to GERD.
o Trachoesophageal Fistula: A fistula (hole) develops between the soft tissue common wall of the trachea and esophagus. Causes PO substances to emerge through the hole and end up in the airway.
o Diffuse Esophageal Spasms (DES): simultaneous prolonged contraction of 2 parts of the esophagus rather than the normal top to bottom sequential contractions.
o Achalasia is failure of the lower esophageal sphincter (LES) to relax, or relaxation is incomplete, thus preventing passage of the bolus into the stomach. May produce backflow or pain.

Swallowing (1 decks)

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