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BVetMed3 Alimentary > Vomiting in Small Animals > Flashcards

Vomiting in Small Animals Flashcards

1
Q

What is the generic ‘diagnostic approach’ which we can apply to vomiting cases?

A

Problem
System
Location
Lesion

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2
Q

What might owners confuse with vomiting?

A

Regurgitation
Gagging
Coughing

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3
Q

What are the phases of vomiting?

A

Nausea phase
Retching
Vomiting

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4
Q

What happens during the nausea phase of vomiting?

A
  1. Salivation and sensation of nausea
  2. Reduced gastric tone
  3. Reverse peristalsis

This results in depression, hypersalivation and repeated swallowing

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5
Q

What is meant by the term anti-peristalsis?

A

Proximal duodenum emptying back into the stomach - moving in the wrong direction.

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6
Q

What happens during the vomiting phase?

A
  1. Glottis closes
  2. Breath is held mid inspiration
  3. Abdominal wall muscle contraction
  4. Chest held on fixed position
  5. Lower oesophageal sphincter and oesophagus relax
  6. Gastric contents ejected
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7
Q

Why does the glottis close during vomiting?

A

Prevents aspiration of vomitus

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8
Q

How is the intra abdominal pressure increased during vomiting?

A

Holding breath,
Chest held in fixed position,
Contraction of abdominal muscle.

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9
Q

How can the CVRS be affected by vomiting?

A

Cardiac rhythm disturbances - arrhythmias

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10
Q

What is a potential GI effect of vomiting?

A

Changes in colonic motility - diarrhoea

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11
Q

Physiology of vomiting:

Pharyngeal stimulation

A

Pharyngeal stimulation — CNIX —> Nucleus tractus solitarius —> Programmed vomiting response vomiting centre Medulla Oblongta.

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12
Q

Physiology of vomiting:

Gastric irritation

A

Gastric mucosa — CNX —> Nucleus tracts solitarus —>Medulla oblongata

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13
Q

What is the area postrema ?

A

A medullary structure not protected by BBB (privileged) therefore can act as a sensor for circulating chemicals in blood.

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14
Q

Physiology of vomiting:

Drugs (opiates and chemo), Uraemia (renal failure), radiation

A

Circulating chemicals sensed by chemoreceptors in AREA POSTREMA —> Nucleus tractus solitaries —> MO vomiting centre

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15
Q

Physiology of vomiting:

Pain, anticipation

A

Higher centres : diencephalon and limbic system —> MO vomiting centre

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16
Q

Physiology of vomiting:

Motion/ vertigo, middle ear disease

A

Labyrinth —> cerebellum —> MO vomiting centre

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17
Q

How can antihistamines help with vomiting?

A

Act on chemoreceptor trigger zone (area postrema)

Act on vestibular system

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18
Q

How can phenothiazine help with vomiting?

A

Act on vestibular system,
Act on vestibular system
Act on vomiting centre of MO

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19
Q

How can NK1 receptor antagonists help vomiting?

A

Act on CRTZ, MO and vestibular system

Act on peripheral receptors

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20
Q

How can anticholinergic drugs help with vomiting?

A

Act on vestibular system and peripheral receptors

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21
Q

What is regurgitation ?

A

Passive process - no coordinated movements

Facilitated by gravity when head and neck are held down

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22
Q

What can induce/exacerbate regurgitation ?

A

Alterations in food consistency

Exercise

Excitation

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23
Q

How could you use behaviour to distinguish between nausea and regurgitation?

A

Nausea and salivation

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24
Q

How could you use the pH of the vomitus to determine whether vomiting or regurgitation had taken place?

A

Acidic pH is more likely to be vomiting

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25
Q

If there is bile in the vomitus* is it more likely to have occurred via vomiting or regurgitation?

A

Vomiting

Bile from duodenum enters stomach due to reverse peristalsis

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26
Q

How would you expect the ‘food’ to appear in vomitus if vomiting has occurred?

A

Digested

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27
Q

Could both vomiting and regurgitation occur?

A

YES

If patient has been vomiting for an extended period they can develop oesophagitis which can cause regurgitation

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28
Q

When can vomiting be treated symptomatically?

When do you have to be careful ?

A
  • first instance of vomiting
  • acute onset
  • patient clinically stable
  • no other clinical concerns
  • high likelihood of dietary indiscretion or gastroenteritis

——COULD BE GI OBSTRUCTION ——

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29
Q

When shouldn’t vomiting be treated symptomatically?

A
  • no response to symptomatic therapy
  • vomiting is persistent and severe
  • other clinical signs presenting
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30
Q

What might be the causes of other clinical signs presenting alongside vomiting?

What could be an example of these clinical signs?

A

Secondary GI disease

Severe primary GI disease

PU/PD
Jaundice
Anaemia
Weight loss 
Chronicity
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31
Q

Give an example of when symptomatic therapy is not appropriate

A

When patient presents with primary regurgitation

- they rarely respond to symptomatic treatment

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32
Q

What is meant by primary GI disease?

Where is the problem most likely to be in the vomiting patient?

A

Stomach to anus

Most likely upper GI tract
- gastric, duodenal (jejunal/ileal) or multi-loc

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33
Q

When can vomiting be caused by pathology of the colon?

A

Vomiting associated with obstipation/severe constipation

34
Q

Define the term: obstipation

A

Intestinal obstruction by faeces - can’t pass.

35
Q

What secondary GI diseases could cause vomiting?

A

Pancreas - pancreatitis

Electrolyte imbalance - Na, K, Calcium

Hypoadrenocorticism

Endogenous toxins

Exogenous toxins

Primary CNS disease

36
Q

What could be the source of endogenous toxins which result in vomiting?

A

Kidney
Liver
Ketoacidosis (diabetic)
Infection

37
Q

How can the timing of vomiting differ in primary GI disease?

A

Often will relate to time of eating

— delayed for some hours = non-inflammatory gastric disorder

— vomiting without eating = foreign body or secretory disorder

— variable times after eating = lower bowel disorder

38
Q

What might you expect to be the problem if vomiting was delayed for some hours after eating?

A

Primary GI

Non-inflammatory gastric disorder

39
Q

What might you expect to be the problem if a patient is vomiting despite not eating?

A

Foreign body or secretory disorder

40
Q

What might you expect to be the problem if vomiting occurs at variable times after eating?

A

Lower bowel disorder

41
Q

What clinical presentations could you expect from animals with primary GI disease?

A

Mix of presentations possible

—may be normal in all respects including appetite

— may be depressed and inappetsnt due to the lesion or secondary effects of prolonged vomiting

42
Q

When should Primary GI disease be strongly suspected?

A
  • abnormality palpated in gut
  • vomiting with diarrhoea
  • vomiting PRECEDED signs of malaise
  • vomiting consistently related in time to eating
43
Q

What abnormalities might you be able to palpate in dogs with primary GI disease?

A

Foreign body

Intussuception

44
Q

When should secondary GI disease be strongly suspected?

A

— vomiting started AFTER the onset of malaise (inappetance and/or depression)

— other clinical signs present (e.g. jaundice, PU/PD

— history indicates otherwise

45
Q

How might a patients history indicate that it has secondary GI disease?

A

Dietary indiscretion

Toxin access

46
Q

When would you expect a patient presenting with vomiting to be metabolically ill?

A

Secondary GI

47
Q

When might a patient with secondary GI disease NOT be metabolically ill?

What clinical signs could you look for ?

A

Early pancreatitis — mild abdominal discomfort

Hyperthyroid cats (early) — losing some weight, increased activity

48
Q

What can be gained from carrying out a CBC, biochemistry and urinalysis on a patient with primary GI disease?

A

Gives information about the clinical status of the patient, not the underlying cause

49
Q

What would a hypoalbuminaemia or hypoglobuminaemia tell you about a patient?

A

The gut is not absorbing proteins as it should be

50
Q

What is cobalamin?

Where is it largely absorbed?

A

Vitamin B12

Ileum

51
Q

What would low cobalamin tell us?

A

Gut/Ileum is not absorbing as it should be

52
Q

What MIGHT cause hypoalbuminaemia and hypoglobuminaemia?

A

Vomiting associated with protein losing enteropathy (PLE)

Changes associated with diffuse inflammatory bowel disease

53
Q

Why would it be useful to know the electrolyte balance of a vomiting animal?

A

Helps manage patients fluid balance if you know about electrolyte derangements.

54
Q

What would you look for in diagnostic imaging of a patient with primary GI disease?

What techniques would you use?

A

— thickening and loss of layering
—mass lesions
— foreign bodies

X ray and ultrasound
Endoscopy/colonoscopy
Barium study

55
Q

How could you collect a tissue sample non-invasively?

A

Endoscopy/colonoscopy

56
Q

Describe the pros and cons of non invasive tissue sampling.

A

Can access the stomach , proximal 1/3 of the duodenum and the ileum (via colonoscopy)

  • only get superficial samples of the mucosa therefore could miss lesions
57
Q

Describe the pros and cons of an Exploratory Laporoscopy

A

Allows full thickness biopsies
Pathology in muscularis can be identified

—More invasive

58
Q

How could you assess whether the cause of the secondary GI disease was:

The pancreas

A

Pancreatic lipase test

59
Q

How could you assess whether the cause of the secondary GI disease was:

Electrolyte imbalance

A

Biochemical profile

60
Q

How could you assess whether the cause of the secondary GI disease was:

Endogenous toxins - Kidney

A

Biochemical profile and urinalysis

CBC

61
Q

How could you assess whether the cause of the secondary GI disease was:

Endogenous toxins - Liver

A

Biochemical profile
CBC
BA stim
Ammonia

62
Q

How could you assess whether the cause of the secondary GI disease was:

Ketoacidosis

A

Biochemical profile and urinalysis
Acid-base
Ketones
CBC

63
Q

How could you assess whether the cause of the secondary GI disease was:

Infection

A

CBC

Biochemistry

Urinalysis

64
Q

How could you assess whether the cause of the secondary GI disease was:

Exogenous toxins

A

History - access to a drug/toxin

CBC
Biochemistry

65
Q

How could you assess whether the cause of the secondary GI disease was:

Primary CNS

A

Historical information - neuro exam

Rule out other conditions

66
Q

When would you do an exploratory laparotomy to investigate secondary GI disease?

A

ONLY:

If blood work normal

If you need a definitive diagnosis (e.g. to obtain biopsies of liver etc)

67
Q

What lesions in the stomach could cause GI disease?

A

Gastritis

Gastric foreign body

Gastric ulcer

Disorders of the pelorus

Abnormal gastric motility

68
Q

What lesions in the interestine could cause GI disease?

A

Enteritis e.g. viral (parvo, corona) or dietary indiscretion

Intestinal obstruction by foreign body

IBD/chronic enteropathies

Neoplasia

69
Q

What are the common primary GI causes of vomiting?

A

Gastritis - spoiled food/dietary indiscretion/ food intolerance

Viral infection - Parvo/Corona/Rotavirus

Foreign body

GI neoplasm

70
Q

What are the common secondary GI causes of vomiting?

A

Pancreatitis

Liver disease

Renal disease

Endocrine disease

  • diabetic ketoacidosis
  • Hypoadrenocorticism
  • Hypercalcaemia
71
Q

Would you perform an exploratory laparotomy to investigate regurgitation?

A

NO - DANGEROUS

GA increases risk of regurgitation

Increased risk of aspiration pneumonia

Will not give diagnosis and wasting money!

72
Q

What categories of conditions can result in regurgitation?

A 
Anatomic
Megaoesophagus 
External compression
Internal obstruction- physical or functional 
Oesophagitis 
Intramural lesions in oesophageal wall
73
Q

What are some anatomic causes of regurgitation ?

A

Cricopharyngeal disease
Hiatal hernia (esp. BRACHYCEPHALICS)
Oesophageal diverticulum

74
Q

What external compression can result in regurgitation?

A

Persistent right aortic arch

Mediastinal lymphoma

Thyroid tumours

75
Q

What internal obstruction can cause regurgitation?

A

Foreign bodies

Strictures

76
Q

How can oesophagitis cause regurgitation?

A

Trauma

Reflux of gastric acid

Irritation

77
Q

What kinds of intramural lesions can result in regurgitation?

A

Neoplasms

Abscesses

Granulomas

78
Q

How should you investigate regurgitation?

A

Imaging of the oesophagus

Secondary investigations: CBC/chemistry

79
Q

What imaging should you do to look investigate regurgitation?

A
  1. PLAIN RADIOGRAPHS
    — ideally when animal conscious to rule out MO

Thoracic CT, Dynamic studies and Endoscopy also possible

80
Q

How could dynamic imaging studies help to investigate regurgitation?

A

Fluoroscopy assesses motility and contraction

81
Q

Why might you carry out CBC and biochem in a patient that is regurgitating?

A

Evaluate the metabolic EFFECTS of regurgitation

- WONT TELL YOU WHY

BVetMed3 Alimentary (16 decks)

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