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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
If there is bile in the vomitus* is it more likely to have occurred via vomiting or regurgitation?
Vomiting | Bile from duodenum enters stomach due to reverse peristalsis
26
How would you expect the ‘food’ to appear in vomitus if vomiting has occurred?
Digested
27
Could both vomiting and regurgitation occur?
YES If patient has been vomiting for an extended period they can develop oesophagitis which can cause regurgitation
28
When can vomiting be treated symptomatically? When do you have to be careful ?
- first instance of vomiting - acute onset - patient clinically stable - no other clinical concerns - high likelihood of dietary indiscretion or gastroenteritis ——COULD BE GI OBSTRUCTION ——
29
When shouldn’t vomiting be treated symptomatically?
- no response to symptomatic therapy - vomiting is persistent and severe - other clinical signs presenting
30
What might be the causes of other clinical signs presenting alongside vomiting? What could be an example of these clinical signs?
Secondary GI disease Severe primary GI disease ``` PU/PD Jaundice Anaemia Weight loss Chronicity ```
31
Give an example of when symptomatic therapy is not appropriate
When patient presents with primary regurgitation | - they rarely respond to symptomatic treatment
32
What is meant by primary GI disease? Where is the problem most likely to be in the vomiting patient?
Stomach to anus Most likely upper GI tract - gastric, duodenal (jejunal/ileal) or multi-loc
33
When can vomiting be caused by pathology of the colon?
Vomiting associated with obstipation/severe constipation
34
Define the term: obstipation
Intestinal obstruction by faeces - can’t pass.
35
What secondary GI diseases could cause vomiting?
Pancreas - pancreatitis Electrolyte imbalance - Na, K, Calcium Hypoadrenocorticism Endogenous toxins Exogenous toxins Primary CNS disease
36
What could be the source of endogenous toxins which result in vomiting?
Kidney Liver Ketoacidosis (diabetic) Infection
37
How can the timing of vomiting differ in primary GI disease?
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
What might you expect to be the problem if vomiting was delayed for some hours after eating?
Primary GI | Non-inflammatory gastric disorder
39
What might you expect to be the problem if a patient is vomiting despite not eating?
Foreign body or secretory disorder
40
What might you expect to be the problem if vomiting occurs at variable times after eating?
Lower bowel disorder
41
What clinical presentations could you expect from animals with primary GI disease?
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
When should Primary GI disease be strongly suspected?
- abnormality palpated in gut - vomiting with diarrhoea - vomiting PRECEDED signs of malaise - vomiting consistently related in time to eating
43
What abnormalities might you be able to palpate in dogs with primary GI disease?
Foreign body Intussuception
44
When should secondary GI disease be strongly suspected?
— vomiting started AFTER the onset of malaise (inappetance and/or depression) — other clinical signs present (e.g. jaundice, PU/PD — history indicates otherwise
45
How might a patients history indicate that it has secondary GI disease?
Dietary indiscretion Toxin access
46
When would you expect a patient presenting with vomiting to be metabolically ill?
Secondary GI
47
When might a patient with secondary GI disease NOT be metabolically ill? What clinical signs could you look for ?
Early pancreatitis — mild abdominal discomfort Hyperthyroid cats (early) — losing some weight, increased activity
48
What can be gained from carrying out a CBC, biochemistry and urinalysis on a patient with primary GI disease?
Gives information about the clinical status of the patient, not the underlying cause
49
What would a hypoalbuminaemia or hypoglobuminaemia tell you about a patient?
The gut is not absorbing proteins as it should be
50
What is cobalamin? Where is it largely absorbed?
Vitamin B12 Ileum
51
What would low cobalamin tell us?
Gut/Ileum is not absorbing as it should be
52
What MIGHT cause hypoalbuminaemia and hypoglobuminaemia?
Vomiting associated with protein losing enteropathy (PLE) Changes associated with diffuse inflammatory bowel disease
53
Why would it be useful to know the electrolyte balance of a vomiting animal?
Helps manage patients fluid balance if you know about electrolyte derangements.
54
What would you look for in diagnostic imaging of a patient with primary GI disease? What techniques would you use?
— thickening and loss of layering —mass lesions — foreign bodies X ray and ultrasound Endoscopy/colonoscopy Barium study
55
How could you collect a tissue sample non-invasively?
Endoscopy/colonoscopy
56
Describe the pros and cons of non invasive tissue sampling.
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
Describe the pros and cons of an Exploratory Laporoscopy
Allows full thickness biopsies Pathology in muscularis can be identified —More invasive
58
How could you assess whether the cause of the secondary GI disease was: The pancreas
Pancreatic lipase test
59
How could you assess whether the cause of the secondary GI disease was: Electrolyte imbalance
Biochemical profile
60
How could you assess whether the cause of the secondary GI disease was: Endogenous toxins - Kidney
Biochemical profile and urinalysis CBC
61
How could you assess whether the cause of the secondary GI disease was: Endogenous toxins - Liver
Biochemical profile CBC BA stim Ammonia
62
How could you assess whether the cause of the secondary GI disease was: Ketoacidosis
Biochemical profile and urinalysis Acid-base Ketones CBC
63
How could you assess whether the cause of the secondary GI disease was: Infection
CBC Biochemistry Urinalysis
64
How could you assess whether the cause of the secondary GI disease was: Exogenous toxins
History - access to a drug/toxin CBC Biochemistry
65
How could you assess whether the cause of the secondary GI disease was: Primary CNS
Historical information - neuro exam Rule out other conditions
66
When would you do an exploratory laparotomy to investigate secondary GI disease?
ONLY: If blood work normal If you need a definitive diagnosis (e.g. to obtain biopsies of liver etc)
67
What lesions in the stomach could cause GI disease?
Gastritis Gastric foreign body Gastric ulcer Disorders of the pelorus Abnormal gastric motility
68
What lesions in the interestine could cause GI disease?
Enteritis e.g. viral (parvo, corona) or dietary indiscretion Intestinal obstruction by foreign body IBD/chronic enteropathies Neoplasia
69
What are the common primary GI causes of vomiting?
Gastritis - spoiled food/dietary indiscretion/ food intolerance Viral infection - Parvo/Corona/Rotavirus Foreign body GI neoplasm
70
What are the common secondary GI causes of vomiting?
Pancreatitis Liver disease Renal disease Endocrine disease - diabetic ketoacidosis - Hypoadrenocorticism - Hypercalcaemia
71
Would you perform an exploratory laparotomy to investigate regurgitation?
NO - DANGEROUS GA increases risk of regurgitation Increased risk of aspiration pneumonia Will not give diagnosis and wasting money!
72
What categories of conditions can result in regurgitation?
``` Anatomic Megaoesophagus External compression Internal obstruction- physical or functional Oesophagitis Intramural lesions in oesophageal wall ```
73
What are some anatomic causes of regurgitation ?
Cricopharyngeal disease Hiatal hernia (esp. BRACHYCEPHALICS) Oesophageal diverticulum
74
What external compression can result in regurgitation?
Persistent right aortic arch Mediastinal lymphoma Thyroid tumours
75
What internal obstruction can cause regurgitation?
Foreign bodies Strictures
76
How can oesophagitis cause regurgitation?
Trauma Reflux of gastric acid Irritation
77
What kinds of intramural lesions can result in regurgitation?
Neoplasms Abscesses Granulomas
78
How should you investigate regurgitation?
Imaging of the oesophagus Secondary investigations: CBC/chemistry
79
What imaging should you do to look investigate regurgitation?
1. PLAIN RADIOGRAPHS — ideally when animal conscious to rule out MO Thoracic CT, Dynamic studies and Endoscopy also possible
80
How could dynamic imaging studies help to investigate regurgitation?
Fluoroscopy assesses motility and contraction
81
Why might you carry out CBC and biochem in a patient that is regurgitating?
Evaluate the metabolic EFFECTS of regurgitation | - WONT TELL YOU WHY

BVetMed3 Alimentary (16 decks)

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