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Alimentary > Vomiting + Regurgitation > Flashcards

Vomiting + Regurgitation Flashcards

0
Q

Give 3 forms of obstructional oesophageal disease

A

Mural (stricture)
Luminal (foreign bodies)
Extralumenal (mass)

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1
Q

Give 4 anatomical oesophageal diseases

A

Vascular ring anomaly
Cricopharyngeal disease
Hiatal hernia
Diverticulum

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2
Q

Give 3 causes of oesophagitis

A

Trauma, reflux (anaesthesia), irritation

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3
Q

Give 3 motility disorders of the oesophagus

A

Megaeosophagus
Neuropathy
Myopathy

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4
Q

What are the 3 most common causes of oesophageal disease?

A

Oesophagitis
Oesophageal foreign body
Mega-oesophagus

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5
Q

Outline the clinical signs associated with regurgitation

A

Hypersalivation
Odynophagia
Dysphagia (pharyngeal problem more likely)
Nasal discharge
Coughing (due to 2ry aspiration pneumonia)

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7
Q

Outline the differences between vomiting and regurgitation

A

Vomiting: abdominal effort, nausea, digested food, no swallowing pain (May be alkaline or acidic substance) MOST COMMON
Regurgitation: passive, no nausea, undigested food, possibly painful (usually alkaline)

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8
Q

Which questions may distinguish vomiting from regurgitation?

A
  • abdominal effort/wretching?
  • digested food being brought up?
  • when in relation to eating?
  • swallowing difficulties?
  • pain on eating?
  • do they look nauseous?
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9
Q

What does physical exam usually reveal for oesophageal disease?

A

Nothing - usually normal
Lung auscultation may reveal aspiration pnumonia
Underlying/concurent disease
Body condition may indicate how chronic the disease is

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10
Q

What are the most common investigations to carry out? What else may be carried out?

A

Diagnostic imaging -plain/contrast radiographs
Heamotology and biochemistry
Endoscopy

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11
Q

What are the most common differential diagnoses for megaoesophagus?

A

Idiopathic (dogs)
Myasthenia gravis (generalised or focal)
Thymoma
Hypoadrenocorticism

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12
Q

What is the prognosis of megaoesophagus? What is the treatment?

A

Poor
Death usually results from repeated aspiration pnumonia
Treatment aimed at minimising occourence of pnumonia eg. elevate food and water
Hold vertical after feeding
Experiment with food consistency - liquid go down better but may be aspriated, solids harder to swallow but less likely to be aspirated
Manage pnumonia

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13
Q

Why is aspiration pnumonia associated with megaoesophagus?

A

Regurgitation not associated with reflex closure of the larynx (vomiting IS)

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14
Q

What are the causes of oesophagitis?

A
  • chemical injury: corrosive agents, medications (doxycycline esp in cats if gets stuck)
  • gastro-oesophageal reflux: GA, hiatal hernia, persistent vomiting, feeding tubes if positioned incorrectly
  • Oesophageal foreign bodies
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15
Q

How can oesophagitis be treated?

A

Dietary - small meals high protein low fat food to minimise reflux ± gastric feeding tube
Sucralfate liquid - “chemical bandage”
Inhibitors of gastric acid secretion - H2 blockers, proton pump inhibitors

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16
Q

What is a possible serious complication of oesophagitis?

A

Strictures due to serious irritation if FB remains for >24hours

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17
Q

Where do oesophageal FBs usually lodge?

A

Lodge at thoracic inlet, heart base, hiatus

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18
Q

What is required to assess and treat oesophageal FBs? What is a potential complication?

A

Endoscopy - retrieval/push to stomach

Potential for mucosal damage/perforation

19
Q

What is vomiting?

A

Foreful expulsion of GI contents
Symptom NOT disease
Primitive toxin elimination mechanism

20
Q

What may stimulate vomiting?

A

Brainstem vomiting centre responsible, inputs from:
Cortex
Vagal and sympathetic afferents from gastirits
Brainstem chemoreceptor trigger zone (CRTZ)

21
Q

Once vomiting has been diagnosed, what is the next step?

A

Define/refine the problem

  • chronic/acute
  • primary GI/ secondary GI
22
Q

List 4 causes of ACUTE primary GI vomiting

A

Dietary - indiscretion/intolerance/hypersensitivity
Infection - Parasites/parvovirus
Obstruction - Neoplasia/FB/gastric hypertrophy
Motility disorders/gastic volvulus

23
Q

List 2 causes of CHRONIC primary GI vomiting

A

Inflammatory disease - Gastritis/IBD/ulceration

Neoplasia

24
Q

List 6 causes of secondary (metabolic) causes of vomiting. How would you distinguish the cause as secondary?

A

Ureamia (vUSG, PUPD associated with chronic renal failure)
Addison’s disease (adrenocoritcal insufficiency)
Hepatic disease
Pancreatitits
Toxin ingestion
Drugs (iatrogenic)
> often NOT the only clinical sign

25
Q

How can you rule out secondary (metabolic) causes of vomiting?

A

Heamaology/biochemistry

Urinalysis

26
Q

How can diagnositc imaging be used when working up a vomiting animal?

A

Radiographs for obstruction

Ultrasound for other organ involvement

27
Q

Give 6 causes of stomach ulcers. Which is most common?

A

Neoplasia - lymphoma, carcinoma, leiomyoma/sarcoma
Inflammation - Gastritis
Iatrogenic - NSAIDS Most common
Systemic - Hypoadrenocorticism, liver dysfunction, uraemia, mast cell tumour->hyperhistamineamia, gastrinoma->hypergastrinaemia.
Hypotension - shock, DIC, sepsis
Other/idiopathic - stress, spinal surgery

28
Q

What is the treatment of acute and chronic vomiting?

A

Acute: fasting and treat symptoms
Chronic: find underlying cause!

29
Q

Give 3 classes of drug used to treat vomiting

A

Anti-histamines
Anti-cholinergics
Proton-pump inhibitors eg. Omeprazole

30
Q

What is the mechanism of action of sucralfate? What is it good for?

A
  • Aluminium hydroxide and sucrose octasulfate, dissociates in acid and becomes sticky polymer which adheres to proteinaceous exudate found at ulcer sites.
  • Provides a protective barrier and stimulates HCO3-, mucus and PG secretion.
  • Good for oesophageal as well as gastirc ulceration
31
Q

What is another name for Sucralfate?

A

Antepsin, sulcrate, pepsigard

32
Q

What is the dosing of Sucralfate?

A

20kg: 1mg/dog q6-8hrs

33
Q

What are some names of H2 receptor antagonists?

A

Cimetidine
Rinitidine (zantac)
Famotidine

34
Q

What is the mechanism of action of cimetidine/ranitidine/famotidine? What are the disadvantages of them?

A

H2 receptor antagonist - inhibition of gastric acid and some gastric PROKINETIC activity
Disadvantages:
No evidence of its efficacy in cats/dogs
Expensive
BID/TID

35
Q

What is the mechanism of action of omeprazole?

A

Proton pump inhibitor
- binds H+/K+
> long T1/2 -> SID

36
Q

What is omeprazole indicated for?

A

Gastric hyperacidity
GI ulcers
Zollinger-Wllison syndrome (gastrinoma)
> good evidence for this in vet use

37
Q

When is anti-emetic therapy indicated?

A

Vomiting is debilitating
- pain
- marked fluid/electrolyte loss
Remember vomiting can be debilitating

38
Q

Which MODERATE antiemetic is licensed for vet use?

A

Metoclopramide
- PABA derivative with central and GI effects - antagonises CRTZ and peripheral cholinergic effect
- Upper GI prokinetic
> moderate activity (not strongest)

39
Q

How can metoclopramide be given?

A

Tablets, suspension, injection

- 0.2-0.5mg/kg im, sc, po q6-12hrs or as CRI

40
Q

Which is the most potent anti-emetic? Why is it rarely used? When would it be indicated?

A 
Ondansetron (zofran)
- 5HT antagonist 
- CRTZ action only
>expensive
- indicated for chemotherapy patients and pancreatitis
41
Q

Which antiemetic works on the final step before the vomiting centre?

A

Maropitant

  • NK1 R ant
  • Laos has peripheral effects
42
Q

Why should care be taken when using maropitant?

A

Very potent. May mask underlying disease.

43
Q

Which species is maropitant licensed in? What are the dose rates for these species?

A

Dogs (1mg/kg sc q24hrs or 2mg/kg po q 24hrs)

Cats (0.5-1mg/kg po, sc q 24hrs)

Alimentary (30 decks)

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