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PBL SEM 4 > oral, pharyngeal and oesophageal physiolgoy and dysphagia > Flashcards

oral, pharyngeal and oesophageal physiolgoy and dysphagia Flashcards

1
Q

what 3 phases are there in a normal swallow?

A

oral, pharyngeal, oesophageal

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2
Q

oral phase of swallowing : muscle, neural control and voluntary control

A
  • striated muscle
  • neural control = cortex/medulla
  • full voluntary control
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3
Q

pharyngeal phase of swallowing : muscle, neural control and voluntary control

A
  • striated muscle
  • neural control = medulla
  • some voluntary control
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4
Q

oesophageal phase of swallowing : muscle, neural control and voluntary control

A
  • striated/smooth muscle
  • neural control = medulla/ENS (mainly vagal nerve and ENS)
  • no voluntary control
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5
Q

what are the 3 components of preparation of bolus and initiation of swallowing in the oral phase?

A

chewing, salivation, movement of bolus

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6
Q

what is the function of chewing? effectors?

A
  • prepare solid food for transfer through pharynx
  • effectors = teeth, jaws masseter muscles
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7
Q

what is the function of salivation? effectors?

A
  • lubricate bolus and begin digestion
  • mucus, amylase, lipase, water, HCO3-
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8
Q

what is the function of bolus movement? effectors?

A

deliver prepared bolus to oropharynx — tongue

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9
Q
A
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10
Q

describe the upper oesophageal sphincter (UOS)

A
  • pressure = 100mmHg (atm = 0)
  • relatively high pressure zone
  • protects are ability to avoid laryngopharyngeal reflux (reflux from oesophagus into airway)
  • opens as pharyngeal phase starts
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11
Q

describe intraoesophageal pressure

A

-5mmHg
- -ve pressure — as longs and pleura pull against oesophagus
- bolus pulled into oesophagus

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12
Q

describe the lower oesophageal sphincter (LES)

A
  • pressure = 20mmHg
  • pressure higher than intragastric pressure
  • opens to allow food to enter stomach
  • barrier to avoid intragastric contents entering into oesophagus = reflux
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13
Q

what do sphincters do?

A

prevent influx of air and reflux of gastric contents into the oesophagus

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14
Q

what has the role of organising in the neuroanatomy of swallowing?

A

brain stem central programme generator (CPG)

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15
Q

what cranial nerves are involved in swallowing?

A

V, VII, IX, X, XII — have input from sensory receptors in oropharynx, larynx and oesophagus

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16
Q

what is a main afferent relay centre?

A

nucleus solitarius (X)

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17
Q

what efferent nucleus is very critical in swallowing, and damage to it can cause severe dysphagia?

A

nucleus ambiguous (IX, X)

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18
Q

mid to low oesophagus is mainly under what neural input?

A

enteric nervous system — vagal and spinal pathways

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19
Q

what 2 nuclei in the brain are important efferent centres for the oesophagus?

A

dorsal motor nucleus and nucleus ambiguous

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20
Q

peristalsis is the result of what?

A

excitation and inhibition in parallel

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21
Q

how are swallowing regions in the brain organised?

A

topographically

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22
Q

what does function MRI (FMRI) look at?

A

areas associated with increased changes in BOLD (blood oxygen level dependency)

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23
Q

there is integration between what systems?

A

taste, flavour and swallowing

increased flavour = increased activity in FMRI

24
Q

describe oropharyngeal dysphagia

A
  • abnormal bolus transfer to the oesophagus
  • difficulty initiating a swallow
  • only one manifestation of the primary disease (eg. a stroke)
25
Q

describe oesophageal dysphagia

A
  • abnormal bolus transport through the oesophagus
  • food stops after initiation of swallow
  • oesophagus is location of the primary disease (eg. achalasia)
26
Q

how common is dysphagia after stroke?

A

common — around 50% of all stroke victims

27
Q

what type of dysphagia is most common after stroke?

A

oropharyngeal

28
Q

dysphagia after stroke increases mortality risk by what %?

A

30%

29
Q

what is the most important complication of dysphagia after stroke?

A

aspiration

30
Q

why do dysphagic stroke patients recover swallowing function?

A

stroke on opposite side to activation of swallowing system in recovery — compensation in non-dominant side — plasticity

31
Q

describe conventional manometry

A

> senses the pressure and constriction of muscles in the esophagus as you swallow

  • pressure recordings in the oesophagus using channles following catheterisation
  • has simple pressure transducers
32
Q

how do the majority of dysphagia after stroke sufferers recover?

A

natural swallowing recovery

33
Q

describe high resolution manometry

A
  • more precise measurement of upper GI motility
  • catheters with multiple sensory <2cm apart (24+ arrays)
  • spatiotemporal or topographic plot of pressure data (Clouse Plots)
  • evolutionary technology

high resolution manometry uses more pressure sensors therefore more accurate

34
Q

describe Spatiotemporal (Clouse) Plot

A
  • for high resolution manometry
  • gives locational, temporal and pressure info — gives us a visual plot

red = higher pressure

35
Q

what is the definition of achalasia?

A

the failure of a ring of muscle fibres, such as a sphincter of the oesophagus, to relax

36
Q

what is achalasia associated with (genetic component)?

A

HLA-DQw1

37
Q

what suggest that achalasia may be an autoimmune disorder?

A

circulating antibodies to enteric neurones

38
Q

unconfirmed, but what may achalasia result from?

A

chronic infections with herpes zoster or measles viruses

39
Q

what is pseudo achalasia?

A

an achalasia-pattern dilatation of the oesophagus due to the narrowing of the distal oesophagus from causes other than primary denervation. One of the most common causes is malignancy

40
Q

what else can cause achalasia?

A

malignancy, Chagas’ disease, Infiltration Disorders eg. Sarcoid, Amyloid

41
Q

describe the prevalence of achalasia

A
  • annual incidence of approx 1:100 000
  • men = women
  • onset before adolescence unusual
  • usually diagnosed between the ages of 25 and 60 years
42
Q

describe the frequency of symptoms in achalasia

A
43
Q

how is achalasia diagnosed?

A
  • clinical history
    > endoscopy
    > radiology
    > manometry

> = MAIN METHODS

44
Q

in one series of 87 connected patients with newly diagnosed achalasia, what was the mean duration of symptoms?

A

4.7 years

45
Q

what may endoscopy reveal in achalasia?

A
  • may reveal dilated oesophagus containing residual material
  • may appear normal
  • oesophageal stasis predisposes to candida infection that may be apparent
46
Q

describe how radiology is used in achalasia

A
  • barium swallow diagnostic accuracy = 95%
  • dilated oesophagus with beak-like narrowing — beak like - shows lower oesophageal sphincter is closed
  • dilation may be so profound that the oesophagus assumes a sigmoid shape
  • fluoroscopy reveals the absence of peristalsis
  • purposeless, spastic contractions can be observed - some radiologists call this “vigorous” achalasia
47
Q

what is usually required for confirmation of achalasia?

A

manometry = gold standard for diagnosis

48
Q

what are the 3 primary findings in manometry for achalasia?

A
  • elevated resting LES pressure — above 45 mmHg
  • incomplete LES relaxation
  • aperistalsis in the smooth muscle portion of the body of the oesophagus. for most patients, low amplitude; in some cases however, the simultaneous oesophageal contractions have higher amplitudes (eg. >60mmhg). such patients are said to have “vigorous” achalasia
49
Q

what manometry finding distinguishes achalasia from other disorders associated with aperistalsis?

A

incomplete LES relaxation

50
Q

describe the 3 subtypes of achalasia

A
  1. type I = ‘classic’ achalasia. aperistalsis — oesophagus muscles barely contract so food moves down by gravity alone
  2. type II = asynchronous contraction. the lower oesophageal sphincter is always non-relaxed and simultaneous contractions occur throughout the body of the oesophagus while a person swallows. This type is the one that responds best to endoscopic therapy.
  3. type III = vigorous achalasia. spastic contractions. can have severe chest pain (mimics heart attack)
51
Q

what are the long term risks of achalasia?

A
  • 15 year mortality of 13%
  • the time interval between the first treatment and death roughly = 9.9 +/- 1.4 years
  • 19% deaths attributable to oesophageal cancer (Risk similar for squamous and adenocarcinomas)
52
Q

describe botulinum toxin (type A) endoscopic injection into the lower oesophageal sphincter

A
  • botulinum toxin inhibits the calcium-dependent release of ACh from nerve terminals, thereby counteracting the effect of the selective loss of inhibitory neurotransmitters
    = muscle relaxant
  • it is initially effective in relieving symptoms in about 85% of patients within 6 months, possibly because of regeneration of the affected receptors

better for older attends who wouldn’t tolerate other treatment of in short term/temporary measure

53
Q

describe pneumatic dilation

A
  • the most effective non-surgical treatment option for patients with achalasia
  • involves placing a balloon across the lower oesophageal sphincter, which is then inflated to a pressure adequate to tear the muscle fibres of the sphincter
  • 50-93% of patients obtain good to excellent relief of symptoms
  • relatively safe and well tolerated
  • risk of perforation
  • sometimes need a 2nd dilation
54
Q

describe Hellers Myotomy

A
  • surgical myotomy for achalasia involves carrying out an anterior myotomy across the lower oesophageal sphincter (Heller’s myotomy)
  • however, whether myotomy should be combined with an anti reflux procedure (loose Nissen fundoplication, incomplete Toupet, or Dor fundoplication) is a cause for debate
  • myotomy ed are usualy done laparoscopically through the abdomen with a 1-2cm distal myotomy onto the stomach
  • good to excellent results are reported in 80-100% of patients
  • major complication = uncontrolled gastro-oesophageal reflux in about 10% of patients
  • wrap procedure reduces risk of reflux

LES IS CUT. BETTER IN YOUNG PATIENTS.

55
Q

what is POEMS?

A
  • Per Oral Endoscopic Myotomy

Peroral endoscopic myotomy is a procedure to treat swallowing disorders caused by muscle problems such as spasms in the esophagus. POEM uses an endoscope — a narrow flexible tube with a camera — that is inserted through the mouth (peroral) to cut muscles in the esophagus (a myotomy). Cutting the muscles loosens them and prevents them from tightening and interfering with swallowing.

POEM is not considered a surgery, since no incision is made through the skin. It is a less invasive alternative to Heller myotomy — a similar procedure that uses small incisions to reach the esophagus instead of access through the mouth. Endoscopic procedures often mean less pain and a faster recovery than open surgical procedures.

56
Q

swallowing motor cortex is _____ organised, but crucially displays inter-hemispheric ______

A
  • bilaterally
  • asymmetry

PBL SEM 4 (50 decks)

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