Oesophageal diseases and vomiting lecture Flashcards

1
Q

3 most common causes of oesophageal disease

A

Oesophagitis
Oesophageal FB
Mega-oesophagus

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2
Q

How can oesophageal diseases be categorised?

A

Anatomic - vascular ring anomaly, cricopharyngeal disease, hiatal hernia, diverticulum
Obstruction - mural (stricture), luminal (FB), extraluminal (mass)
Oesophagitis - trauma, reflux (anaesthesia), irritation
Motility disorders - megaoesophagus, neuropathy, myopathy

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3
Q

What is an oesophageal disorder?

A

Failure of transport and/or reflux

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4
Q

Clinical signs of regurgitation (6)

A
  • hypersalivation
  • odynophagia
  • anorexia (uncommon)
  • dysphagia
  • nasal discharge
  • coughing
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5
Q

How is vomiting different to regurgitation (4)?

A

Vomiting = abdominal effort, prodromal nausea, usually digested food, no swallowing pain, (alkaline or acidic)

Regurgitation = passive, no prodromal nausea, undigested food, possibly painful, no prodromal nausea

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6
Q

How do you diagnose oesophageal disease? (5)

A

PE normal usually, upper oesophageal palpation, lung auscultation, underlying concurrent disease, BCS

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7
Q

Which investigations are normally focused on with oesophageal disease? (3)

A
  • Diagnostic imaging (plain then contrast radiography)
  • Haematology and biochemistry - others too
  • Endoscopy
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8
Q

Will plain radiography be able to rule out the 3 main causes of oesophagitis?

A

No - will show radio-opaque FB and mega-oesophagus but not oesophagitis. It WIll allow you to determine if problem is functional or structural.

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9
Q

What are the common causes of mega-oesophagus?

A
  • Idiopathic (dogs)
  • MG (generalised or focal)
  • Thymoma
  • Hypoadrenocorticism
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10
Q

Other, rarer causes of megaoesophagus?

A
  • Polyneuritis
  • polymyositis
  • dysautonomia (cats)
  • CNS disease
  • botulism/tetanus
  • SLE
  • lead/thallium toxicity
  • Hypothyroidism
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11
Q

How does aspiration pneumonia show up on a radiograph?

A

Alveolar lung pattern = the lungs fill with fluid (aspirated and inflammatory) which appears white.

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12
Q

What are the 3 main causes of oesophagitis?

A
  • Chemical injury
  • Gastro-oesphageal reflux
  • Oesophageal FBs
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13
Q

Name one medication that can cause chemical injury-induced oesophagitis?

A

Doxycycline

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14
Q

What are the treatment options for oesophagitis? (3)

A
  • Dietary (small meals, high protein, low fat, +/- fastric feeding tube)
  • Sucralfate liquid (provides chemical bandage)
  • Gastric acid secretion inhibitors (H2 blocker or proton pump inhibitor)
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15
Q

Serious treatment complication of oesophagitis?

A

Stricture

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16
Q

Where do oesophageal FB lodge? (3)

A

Thoracic inlet, heart base, hiatus

17
Q

How is it best to remove an oesophageal FB?

A
  • Endoscopic retrieval or push to stomach (usually this)

- Consider emergency referral

18
Q

What diseases is the symptom of vomiting associated with? (5)

A
  • GIT/abdominal,
  • systemic
  • neuro
  • metabolic/endocrine
  • toxicity
19
Q

Where do most vomiting pathways converge? (2)

A
  • Vomiting centre (brainstem)

- CRTZ (chemoR trigger zone) for blood borne substances

20
Q

Primary (GIT causes of vomiting =? (4 most common; Others)

A

MOST COMMON =

  • Dietary (acute: indiscretion, intolerance or hypersens.)
  • Infection (acute: parasites)
  • Inflammatory disease (chronic: gastritis, IBD, ulceration)
  • Obstruction (acute: FB)

OTHERS=

  • Infection (acute: parvo)
  • Neoplasia (chronic)
  • Obstruction (acute: neoplasia, gastric hypertrophy)
  • Motility disorders/gastric volvulus (acute)
21
Q

List some secondary metabolic causes of vomiting (6)

A
  • Uraemia (i.e. CRF thus PU/PD)
  • Addison’s
  • Hepatic disease
  • pancreatitis
  • toxin ingestion (acute)
  • drugs
22
Q

How do you go about a workup of dogs and cats with A.) acute vomitting? B.) chronic vomiting?

A

A.) Radiograph for blocking FB. Otherwise treat symptomatically and fasting

B.) Bloodwork (hame/biochem to ID organ disease); Urinalysis (concentrating ability of kidney); Imaging (radiography for obstruction, ultrasound for other organ involvement); endoscopy (if no answers).

23
Q

What is the commonest cause of gastric ulceration?

A

Iatrogenic - NSAIDs

24
Q

Other causes of gastric ulceration? (5)

A
  • Neoplasia
  • Inflammation
  • Systemic
  • Hypotension
  • Other/idiopathic
25
Q

What causes gastric acid secretion?

A
  • Parietal cells - H+
  • Vagus –> Ach –> M2 receptor on parietal cell
  • Mast cell –> histamine –>H2 receptor on parietal cell
  • Food (esp. aa) and antral distension –> G-cell (antrum) –> gastrin –> gastrin R on parietal cell
26
Q

Name 3 pharmacological ways acid secretion can be regulated

A
  • Antihistamines
  • Proton pump inhibitors (Omeprazole)
  • Anti-cholinergics
27
Q

SUCRALFATE:
what is it made of?
What happens in acid?
What does it do?

A
  • Aluminium hydroxide and sucrose octasulfate
  • Dissociates in acid: sucrose octasulgate reacts with HCl and is polymerised to viscous sticky susbtance that binds to porteinacious exudate usually found at ulcer sites.
  • Forms protective barrier (stimulates HCO3-, mucuos and PG secretion)
28
Q

What are cimetidine/ranitidine and famotidine examples of ?

A

H2 R antagonist –> inhibits gastric acid and has some gastric prokinetic activity.

-Frequently usedd for any kind of V/R, no EBVM for cats/dogs, relatively expensive, 2-3/day

29
Q

How does Omeprazole work? When do you use it (3)?

A

Proton pump inhibitor: binds parietal cells irreversibly blcks H+/K+ ATPase.
Use for gastric hyperacidity, GI ulcers and erosions, Zollinger-Ellison syndrome (gastrinoma).
Long duration of activity

30
Q

Name 3 anti-emetic drugs.

A

Metoclopramide, Ondansetron, Maropitant

31
Q

When do you use anti-emetics?

A

If V is debilitating, pain, marked fluid/electrolyte loss

32
Q

How does metoclopramide work?

A

PABA derivative –> central and GI effects
CENTRAL: Antagonises D2 and 5HT3 receptors in CRTZ
GI: Peripheral cholinergic effects

33
Q

How does Ondansetron work?

A
  • 5-HT3-serotonergic antagonist
  • expensive, best for chemo-induced nausea/V
  • also good for pancreatitis
34
Q

Where and how does maropitant work?

A
  • NK- R antagonist (centrally and peripherally) which is involved in eliciting the last step in the pathway before V
  • Stops binding of SP
  • V potent - can mask underlying diseases
  • useful for any sort of V