Pharyngeal and oesophageal disease Flashcards

1
Q

What are the 3 phases of swallowing?

A

Oral
Pharyngeal
Oesophageal

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2
Q

Outline the oral phase of swallowing

A

Stimulated by oral tactile receptors
Afferent signals transmitted to the medulla
Integration in swallowing centre
Motor impulses propogated to pharynx/ oesophagus by Cranial nerves
Food is moved in a dorso-caudal direction by tongue pressing on the soft palate
Bolus arrives in the pharynx
This initiates tactile receptors that start in the pharyngeal phase

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3
Q

Outline the pharyngeal phase

A

Soft palate is pulled dorsally
The palatial folds move medially preventing food from going into the nasal pharynx
Vocal cords move medially
Epiglottis covers the larynx
Upper Oesophageal sphincter relaxes to receive bolus

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4
Q

Outline the oesophaeal phase

A

The cricopharyngeal muscle constricts after the bolus has passed
Waves of peristalsis occur in the oesophagus

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5
Q

What are some of the more specific Hx/ PE/ MDB tests you should consider for pharyngeal/ oesophageal disease Ix?

A

Observe patient eating

Include CK on MDB

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6
Q

Compare pharyngeal and oesophageal disorder eating

A
Pharyngeal - Immediate ejection of undigested food
Repeated swallow attempts
Poor ability to drink
Possible pain on swallowing
Oesophageal - Variable time after eating to eject undigested food (normally within couple of hours)
Single swallow attempt
Variable ability to drink
Possible pain on swallowing
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7
Q

What are the Ddx for pharyngeal disease?

A

Physical disorders - FB, neoplasia, inflammation, trauma, TMJ issues
Functional disorders - CNS dz, CN dz, NM dz
Other - cricopharyngeal achalasia

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8
Q

How can you investigate physical pharyngeal disease?

A

GA and direct exam
Endoscopy
Radiography/ CT

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9
Q

How can you investigate functional pharyngeal disease?

A

Fluoroscopy
ACh receptor antibody titre for MG
Muscle/ nerve biopsy
EMG

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10
Q

What is cricopharyngeal achalasia?

A

Failure of the cricopharyngeal muscle to relax in swallowing
Cockers predisposed to the congenital form, which can be treated with cricopharyngeal myotomy
Acquired may be associated with hypothyroidism or part of a polymyopathy

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11
Q

Outline nasopharyngeal polyps

A

More cats than dogs
Nasal signs/ phonation changes
Can be removed by Sx or traction, but traction has a 1/3 recurrence rate
Ideally CT to assess
If the middle ear is affected, the bulla osteotomy will help

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12
Q

Compare canine and feline oesophaguses

A

Feline - bottom third is made up of smooth muscle, whereas in dogs it is all skeletal.
Can see the blood vessels in cats when you can’t in dogs

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13
Q

How is investigation of oesophageal disease different to pharygneal

A

With physical, can do contrast radiography
Can’t really do just a direct exam
Functional is the same

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14
Q

What are the differentials for physical oesophageal disease?

A

Extramural obstruction - PRAA, mediastinal disease, thymoma
Mural - neoplasia/ abscess/ stricture, oesophagitis
Intramural - FB
Other - hiatal hernia

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15
Q

What are the DDx for Functional oesophageal diseases

A

Muscle - polymyopathy, dermatomyositis, Addisons
Nerve - Polyneuropathy, dysautonomia
NMJ - MG
Other - mega oesophagus

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16
Q

Outline the causes of oesophagitis

A

Causes - increased acid secretion/ regurge/ caustic substances/ v+
Can lead to strictures (65% strictures associated with GA)
Inflammation leads to decreased motility

17
Q

How do you treat oesophagitis?

A

Anti acid - the best is omeprazole
Prokinetics not great for direct treatment but may reduce reflux and allow healing (cisapride better than metoclop)
Unclear benefit of sucralfate
Low fat liquid food to enhance clearance

18
Q

How can a hiatal hernia be diagnosed?

There is an increased incidence in BOAS dogs
Normally needs surgical correction

A

Radiographs - v hard
Fluoroscopy - still may be missed as is intermittent. Increase the chance by increasing intra abdominal pressure by raising the hind legs
Sometimes endoscopy may work

19
Q

Outline oesophageal FBs

A

Terriers predisposed
Normally occur at the heart base, thoracic inlet or cardia
Leads to spasm, oedema, abrasion, ulceration, perforation

20
Q

How do you treat an oesophageal FB

A

Remove with endoscopy - use long rigid forcepts and assess after removal
Should x ray after to check for pneumomediastinum (which would need surgery)/ aspiration pneumonia

21
Q

Outline post op management of oesophageal FBs

A

Nil per os - PEG tube
Omeprazole to prevent reflux
Little evidence for sucralfate but makes sense to use

22
Q

What can cause a stricture?

A

Post FB (1-3 weeks after)
Oesophagitis (can be quick)
Doxycycline (can be quick)

23
Q

How can you treat an oesophageal stricture?

A

Conservative - liquid diet

Interventional - balloon dilation with intralesional steroid injection or bougienage (similar success rates)

24
Q

Outline investigation/ treatment of a vascular ring anomaly

A

Should occur post weaning in young animals
contrast radiographs or endoscopy
Treatment is sx
Oesophageal diverticulae will continue post op ad require ongoing management

25
Q

Outline congenital megaoesophagus

with all MO, there is decreased to absent motility leading to dilation

A

Predisposed breeds are mini schnauzers, Irish setters, great danes
Guarded prognosis but some gain function with age
N.B some young terriers have signs consistent with MO without dilation, these gain function with age.

26
Q

Which breeds are predisposed to acquired MO?

A

GSDs
Great danes
Irish setters

27
Q

What are some of the Ddx for MO?

A

CNS - neoplasia/ trauma/ brainstem lesions/ distemper
Peripheral neuropathies - lead, acrylamide, thallium/ polyneuritis/ polyradiculoneuritis/ gangioradiculitis/ dysautonomia/ bilateral vagal damage/
NMJ dz - MG/ botulism/ tetanus/ acetylcholinesterase toxicity
Myopathy - oesophagitis/ SLE/ glycogen storage disease/ polymyositis/ dermatomysositis/ cachexia/ Addisons/ hypothyroidism
Misc - pyloric stenosis/ GDV/ pituitary dwarfism/ thymoma/ idiopathic/ mediastinitis

28
Q

What is myasthenia gravis?

A

Immune mediated disease of the neuromuscular junction
ABs produced against the acetyl choline receptors
This reduces NMJ transmission
Can be focal or generalised
Predisposed breeds = Akita, GSD, retrievers, Scotties, Pointers
GSD/ Retriever predisposed to focal disease
Test with AB titre test although not 100% sensitive

29
Q

How can you treat MG?

N.B remission common in 1month to 1 year - a decreasing AB titre can suggest impending remission

A

Acetyl choline esterase inhibitors
Don’t use immunosuppressives - aspiration pneumonia common and steroids reduced muscle strength
Even in MO cases where the titre test is -ve, consider trial tx

30
Q

How can you treat MG?

N.B remission common in 1month to 1 year - a decreasing AB titre can suggest impending remission

A

Acetyl choline esterase inhibitors
Don’t use immunosuppressives - aspiration pneumonia common and steroids reduced muscle strength
Even in MO cases where the titre test is -ve, consider trial tx

31
Q

How can you treat MO?

A

High calorie food
Feed in specific posture (consider bailey chair)
Tailor make diet to the patient - trial meat balls first but may need to do liquid
If drinking is a struggle trial ice
Consider gastrotomy tube, however this does not address saliva issue and also possible poor welfare never getting to eat
Prokinetics do not help