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MODULE 16 - Alimentary Tract Disease > PATHOLOGY - Vomiting > Flashcards

PATHOLOGY - Vomiting Flashcards

1
Q

Which four regions input information into the vomiting centre of the brain to trigger the vomiting reflex?

A

Chemoreceptor trigger zone
Gastrointestinal tract
Cerebral cortex
Vestibular system

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2
Q

What is the chemoreceptor trigger zone?

A

The chemoreceptor trigger zone detects emetic agents within the blood and relays this information to the vomiting centre to trigger emesis

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3
Q

Give three examples of emetic agents that are detected by the chemoreceptor trigger zone

A

Uraemic toxins
Ketoacidosis
Drugs (e.g. apomorphine, chemotherapy)

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4
Q

How does the gastrointestinal system relay information to the vomiting centre of the brain?

A

The gastrointestinal system relays information to the vomiting centre via the vagus nerve (CN X)

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5
Q

Give three examples of gastrointestinal changes that are relayed to the vomiting centre of the brain

A

Chemicals/irritants
Inflammation
Excessive stretch of the gastrointestinal tract

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6
Q

How does the vestibular system relay information to the vomiting centre of the brain?

A

The vestibular system relays information to the vomiting centre via the vestinbulocochlear nerve (CN VIII)

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7
Q

What is the difference between vomiting and regurgitation?

A

Regurgitation is the passive evacuation of food and/or fluid from the oesophagus due to oesophageal disease, whereas vomiting is the forceful evacuation of the stomach and/or duodenal contents

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8
Q

How do you differentiate between regurgitation and vomiting?

A
  1. Vomiting will usually be preceded by signs of nausea such as lip smacking and drooling
  2. Vomiting presents with retching/abdominal effort whereas regurgitation does not
  3. Vomiting may occur minutes to hours after eating whereas regurgitation is more likely to occur not long after eating
  4. Vomit is partially digested food or liquid and often contains bile, whereas regurgitation is typically undigested food
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9
Q

What are the gastrointestinal causes of acute vomiting?

A

Acute gastritis
Acute enteritis
Dietary indiscretion
Gastrointestinal foreign body
Mesenteric torsion
Intussusception
Gastric dilatation volvulus (GDV)

Remember GDV is unproductive vomiting

Image of mesenteric torsion
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10
Q

What are the systemic causes of acute vomiting?

A

Acute pancreatitis
Acute hepatobiliary disease
Acute kidney disease
Endocrine disease
Peritonitis
Pyrometra
Acute neurological insult
Toxin ingestion

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11
Q

Which endocrine disease can cause acute vomiting?

A

Hypoadrenocorticism (Addison’s disease)

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12
Q

How do you approach investigation of acute vomiting?

A
  1. Assess history, signalement and clinical signs
  2. Clinical examination
  3. Symptomatic management if mild clinical signs
  4. Symptomatic management and further investigation if severe vomiting and/or signs of systemic disease
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13
Q

Which history questions are useful to ask when investigating acute vomiting?

A
  1. Has there been any recent dietary changes?
  2. Is the patient a scavenger?
  3. How frequently is the patient vomiting?
  4. Is the vomiting productive or unproductive?
  5. Is the vomit undigested food? partially digested food?
  6. Does the vomit have a faecal odour?
  7. Is there blood (haematemesis) or coffee grounds in the vomit?
  8. Are there any other concurrent gastrointestinal signs?
  9. Is the patient on any medications?
  10. Is the patient systemically unwell? (such as PUPD, jaundice, signs of endocrine disease, lethargic, etc.)
  11. How is the patient’s appetite?
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14
Q

What are the two main aims of the clinical examination when investigating acute vomiting?

A

Determine if there are any clinical signs that can help discriminate the cause of the acute vomiting and determine the clinical status of the patient

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15
Q

What should you assess in detail during the clinical examination when investigating acute vomiting?

A

Signs of systemic disease
Pyrexia
Signs of hepatobiliary disease (jaundice)
Signs of kidney disease
Assess if the abdomen is painful
Palpate for any abdominal masses
Ascites
Assess for dehydration
Assess for hypovolaemia

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16
Q

Which diagnostic tests can be used when investigating acute vomiting?

A

Haematology
Biochemistry
Urinalysis
Diagnostic imaging

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17
Q

What are the aims of haematology and biochemistry when investigating acute vomiting?

A

Haematology and biochemistry can be used to identify primary disease as well as gather more information on the patient’s clinical status

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18
Q

Which systemic disease processes can be identified using haematology and biochemistry?

A

Acute pancreatitis
Acute hepatobiliary disease
Acute kidney disease
Endocrine dysfunction

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19
Q

What is a distinctive feature of hypoadrenocorticism (Addison’s disease) on biochemistry?

A

High potassium levels and low sodium levels

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20
Q

Which additional test can be done to diagnose acute vomiting secondary to hypoadrenocorticism (Addison’s disease)?

A

ACTH stimulation test

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21
Q

Which factors should you assess to determine patient status based on haemoatology and biochemistry results?

A

Is the patient dehydrated?
Are there any electrolyte disturbances
Is there metabolic acidosis
Are there changes that are compatible with sepsis?

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22
Q

Which imaging techniques can be used to investigate acute vomiting?

A

Radiography
Ultrasounds

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23
Q

Which questions should you consider when assessing a radiograph when investigating acute vomiting?

A

Is there evidence of a gastric dilatation volvulus (GDV)?
Is there evidence of a gastrointestinal foreign body?
Is there evidence of gastrointestinal obstruction?
Is there evidence of a gastrointestinal perforation?
Is there evidence of peritonitis?

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24
Q

What are the key signs of a gastrointestinal perforation on radiography?

A

Loss of serosal detail due to free fluid
Gas bubbles in the abdomen
Bunching of the intestines

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25
Q

What are the benefits of using abdominal ultrasound when investigating acute vomiting?

A

Abdominal ultrasound allows for the assessment of the gastrointestinal tract, liver, pancreas and reproductive tract, as well as allows for ultrasound guided aspiration of free abdominal fluid

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26
Q

What are the aims of symptomatic management of acute vomiting?

A
  1. Address fluid and electrolyte imbalances caused by vomiting
  2. Decrease the frequency/stop the vomiting
  3. Reduce gastric acid production if there are suspicions of ulceration
  4. Improve gastric emptying
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27
Q

How do you carry out symptomatic management of acute vomiting?

A
  1. Intravenous fluids with appropriate electrolyte supplementation
  2. Antiemetics
  3. Gastroprotectants to reduce gastric acid production
  4. Prokinetic drugs to improve gastric emptying
  5. Starve for 24 hours and reintroduce a bland, low fat food with small frequent meals if appropriate
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28
Q

List three examples of antiemetic drugs

A

Maropitant
Metoclopramide
Ondansetron

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29
Q

What is the mechanism of action of maropitant?

A

Maropitant is a neurokinin 1 receptor antagonist which acts on the chemoreceptor trigger zone and the vomiting centre of the brain to inhibit emesis

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30
Q

(T/F) Maropitant is both an efficacious antiemetic and antinausea drug

A

FALSE. Maropitant is an efficatious antiemetic however it is not a very effective antinausea drug

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31
Q

What is the mechanism of action of metoclopramide?

A

Metoclopramide is an dopamine (D2) receptor antagonist which acts on the chemoreceptor trigger zone and the gastrointestinal tract to inhibit emesis and have a prokinetic effect

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32
Q

Which method of administration is the most effective for metoclopramide?

A

Metaclopramide is most effective when administered as a continuous rate infusion (CRI)

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33
Q

What is the mechanism of action of ondansetron?

A

Ondansotron is a 5HT3 serotonin receptor which acts of the chemoreceptor trigger zone and the gastrointestinal tract to inhibit emesis

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34
Q

(T/F) Ondansetron is both an efficacious antiemetic and antinausea drug

A

TRUE.

Can be very useful but has to be used under the cascade

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35
Q

Which antiemetic drugs are liscenced in the UK?

A

Maropitant
Metaclopramide

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36
Q

Describe the physiology of gastric acid production

A

Distension of the stomach stimulates the neuroendocrine cells - G-cells and enterochromaffin-like cells - to release gastrin and histamine which act on receptors on the parietal cells to produce and release gastric acid (HCl)

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37
Q

List four classifications of gastroprotectants

A

Proton pump inhibitors
Histamine (H2) blockers
Sucralfate
Synthetic prostaglandins

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38
Q

Give an example of a proton pump inhibitor

A

Omeprazole

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39
Q

What is the mechanism of action of omeprazole?

A

Omeprazole inhibits the proton pumps within the parietal cells which are involved in gastric acid (HCl) production, resulting in decreased gastric acif (HCl) production

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40
Q

(T/F) Omeprazole is very efficacious at reducing gastric acid production

A

TRUE. Omeprazole is very efficacious at reducing gastric acid production as it directly targets the proton pumps in the parietal cells

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41
Q

What is the mechanism of action of histamine (H2) blockers?

A

Histamine (H2) inhibitors antagonise the H2 receptors on the parietal cells, inhibiting histamine binding which would usually trigger gastric acid secretion

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42
Q

Why are histamine (H2) blockers not as efficacious as omeprazole at reducing gastric acid?

A

Gastrin also stimulated the release of gastric acid from the parietal cells, making histamine (H2) blockers less efficacious than omeprazole which directly targets the proton pumps within the parietal cells

43
Q

Give three examples of histamine (H2) blockers

A

Cimetidine
Ranitidine
Famotidine

44
Q

What are the main limitations of cimetidine as a gastroprotectant?

A

Only available in an oral form in the UK
Not very potent

45
Q

What is the most potent histamine (H2) blocker?

A

Famotidine

However not liscenced in the UK so has to be used under the cascade

46
Q

What is the mechanism of action of sucralfate?

A

Sucralfate triggers a polymerisation reaction at a low pH, forming a viscous gel which binds to exposed proteins - such as ulcerated tissue

47
Q

What is the mechanism of action of synthetic prostaglandins?

A

Synthetic prostaglandins trigger prostaglandins production within the gastrointestinal mucosa. Within the gastrointestinal tract, prostaglandins inhibit gastric secretion and cause vasodilation to increase blood flow to the stomach and increase mucus production to protect the gastric mucosa

48
Q

When are synthetic prostaglandins particularly useful gastroprotectants?

A

Synthetic prostaglandins are particularly useful gastroprotectants when managing NSAID overdoses

49
Q

Give an example of a synthetic prostaglandin

A

Misoprostol

50
Q

Which gastroprotectants are licenced in the UK?

A

Cimetidine

51
Q

Give two examples of prokinetic drugs

A

Metoclopramide
Ranitidine

52
Q

Which prokinetic drug is liscenced in the UK?

A

Metoclopramide

53
Q

What are the gastric causes of chronic vomiting?

A

Bilious vomiting syndrome
Chronic gastritis
Chronic gastric foreign body
Gastric ulceration
Gastric neoplasia
Pyloric outflow obstruction/pyloric stenosis
Motility disorder

54
Q

What is bilious vomiting syndrome?

A

Bilious vomiting syndrome is the vomiting of bile early in the morning

55
Q

What are the intestinal causes of chronic vomiting?

A

Inflammatory bowel disease (IBD)
Intestinal foreign body
Extra-intestinal obstruction
Intestinal ulceration
Intestinal neoplasia
Intussusception
Parasitism

56
Q

What are the systemic causes of chronic vomiting?

A

Chronic pancreatitis
Chronic hepatobiliary disease
Chronic kidney disease
Endocrine disease
Neurological disease
Chronic drug/toxin exposure

57
Q

Which two endocrine diseases can cause chronic vomiting?

A

Hypoadrenocorticism (Addison’s disease)
Hyperthryroidism (more common in cats)

58
Q

How do you approach investigation of chronic vomiting?

A
  1. Assess history, signalement and clinical signs
  2. Clinical examination
  3. Symptomatic management if mild clinical signs
  4. Symptomatic management and further investigation if increased frequency of vomiting, severe vomiting and/or signs of systemic disease
59
Q

Which history questions are useful to ask when investigating chronic vomiting?

A
  1. How long after eating does the vomiting begin?
  2. Is there blood (haematemesis) in the vomit and/or meleana
  3. Is there concurrent diarrhoea? (indicates intestinal disease)
  4. Is the vomiting in the morning and is it always bile?
  5. Are there any concurrent signs of systemic disease (such as PUPD, jaundice, signs of endocrine disease, lethargic, etc.)
60
Q

Which diagnostic tests can be used when investigating chronic vomiting?

A

Haematology
Biochemistry
Urinalysis
Diagnostic imaging

61
Q

Which imaging techniques can be used to investigate chronic vomiting?

A

Radiography
Ultrasound
Endoscopy

62
Q

Which questions should you consider when assessing a radiograph and ultrasound when investigating chronic vomiting?

A

Is there evidence of a gastrointestinal foreign body?
Is there evidence of a gastrointestinal neoplasia?
Is there evidence of pyloric ouflow obstruction/stenosis?
Is there evidence of chronic pancreatopathy? (has to be done on ultrasound)

63
Q

What are the benefits of ultrasound when investigating chronic vomiting?

A

The main benefits of ultrasound when investigating chronic vomiting is the ability to assess the gastrointestinal lumen and wall for signs of neoplasia, obstruction, to assess the pancreas for pancreatopathy, and to determine if endoscopy is required for further diagnosis

64
Q

Which components of the gastrointestinal tract can be evaluated using endoscopy?

A

Oesophagus
Stomach
duodenum

65
Q

When is endoscopy indicated when investigating chronic vomiting?

A

If primary gastrointestinal disease is suspected (usually done after systemic disease is ruled out with haematology and biochemistry)
Investigate haematemesis
Endoscopic foreign body removal
Endoscopic mucosal biopsy

66
Q

Why is it so important to investigate haematemesis with endoscopy?

A

Haematemesis can be indicative of neoplasia

67
Q

What is chronic gastritis?

A

Chronic gastritis is chronic inflammation of the gastric mucosa

68
Q

What are the potential causes of chronic gastritis?

A

Dietary hypersensitivities
Gastrointestinal parasites
Fungal infection
Bacterial infection

Often the cause of chronic gastritis is not identified

69
Q

Which gastrointestinal parasite can cause chronic gastritis in cats?

A

Ollunalanus tricuspis

70
Q

Which fungal infection can cause chronic gastritis?

A

Pythiosis

Very rare

71
Q

Which bacterial infection can cause chronic gastritis?

A

Helicobacter

72
Q

How do you treat chronic gastritis?

A

Dietary modifications (e.g. hypoallergenic diets).
Immunosuppressive therapy in severe cases
Antiemetics
Treat the underlying cause

73
Q

(T/F) Gastric neoplasia is very common

A

FALSE. Gastric neoplasia is very rare

74
Q

What are the different forms of gastric neoplasia?

A

Adenocarcinoma
Adenoma
Lymphoma
Leiomyosarcoma
Leiomyoma
Gastrointestinal stromal tumour (GIST)
Carcinoid

75
Q

What is the most common form of gastric neoplasia?

A

Gastric adenocarcinoma

76
Q

Which dog breeds are predisposed to gastric adenocarcinoma?

A

Belgian Shepherds
Collies
Staffordshire Bull Terriers

77
Q

What are the clinical signs of gastric adenocarcinoma?

A

Chronic vomiting
Haematemesis
Meleana
Hypersalivation
Weight loss
Anorexia
Lethargy

78
Q

How do you diagnose gastric neoplasia?

A

Gastric neoplasia is usually diagnosed based on ultrasound scanning which can show thickening and a loss of layering of the stomach wall, and evidence of gastric ulceration on endoscopy. Endoscopic mucosal biopsies are very important for definitive diagnosis

79
Q

What is the prognosis for gastric neoplasia?

A

Very poor prognosis

80
Q

What are the potential causes of gastrointestinal ulceration?

A

Gastritis
Gastric neoplasia
NSAID associated ulceration
Endocrine disease
Renal disease
Liver disease
Mast cell disease
Gastrinoma

81
Q

Which forms of gastric neoplasia can cause gastric ulceration?

A

Adenocarcinoma
Lymphoma
Leiomyosarcoma
Leiomyoma

82
Q

Which endocrine disease can cause gastrointestinal ulceration?

A

Hypoadrenocorticism (Addison’s disease)

83
Q

How can mast cell disease can gastrointestinal ulceration?

A

Mast cell disease causes excess histamine release which will act on H2 receptors on the parietal cells to produce excess gastric acid (HCl) which can cause gastrointestinal ulceration

84
Q

What is a gastrinoma?

A

Gastrinomas are neuroendocrine tumours which produce excessive gastrin which will act on parietal cells to produce excessive gastric acid (HCl) which can cause gastrointestinal ulceration

Gastrinomas are very rare

85
Q

What are key clinical signs of gastrointestinal ulceration?

A

Haematemesis
Meleana

86
Q

How do you treat gastrointestinal ulceration?

A

Antiemetics
Gastroprotectants
Small frequent meals
Treat the underlying cause

87
Q

Which gastroprotectants are typically used in combination for the treatment of gastrointestinal ulcers?

A

Omeprazole
Histamine (H2) blockers
Sucralfate

88
Q

How long should you administer gastroprotectants if the ulceration is caused by NSAIDs or gastritis?

A

Administer gastroprotectants for 6 - 7 weeks to allow the ulcers to heal

89
Q

What is delayed gastric emptying?

A

Delayed gastric emptying is where the food has been in the stomach for more than 8 hours post ingestion

90
Q

What are some of the potential causes of delayed gastric emptying?

A

Hypothyroidism
Post anaesthetic complication
Extramural compression of the stomach
Gastrointestinal foreign body
Pylolic stenosis

91
Q

What is pyloric stenosis?

A

Pyloric stenosis the muscular and/or mucosal thickening or the pyloric sphincter which obstructs pyloric outflow

92
Q

(T/F) Pyloric stenosis can only be congenital

A

FALSE. Pyloric stenosis can be congenital or acquired

93
Q

What is the key anatomical difference between congenital and acquired pyloric stenosis?

A

Congenital pyloric stenosis only involves muscular thickening whereas acquired pyloric stenosis involves muscular and mucosal thickening

94
Q

What are some of the key clinical signs of pyloric stenosis?

A

Projectile vomiting large volumes of fluid and food
Vomiting over 8 hours after ingestion
Intermittent regurgitation

Clinical signs are representative of delayed gastric emptying

95
Q

When do the clinical signs of congenital pyloric stenosis tend to arise?

A

The clinical signs of congenital pyloric stenosis tend to arise just after weaning where the patient is converted from liquid to solid food

96
Q

Which dog breeds are predisposed to congenital pyloric stenosis?

A

Boxers
Boston Terriers

97
Q

Which signalement is predisposed to acquired pyloric stenosis?

A

Small breed dogs

98
Q

How do you diagnose acquired pyloric stenosis?

A

Assess clinical signs
Radiography
Ultrasound

99
Q

How does pyloric stenosis appear on radiography?

A

Dilated stomach filled with fluid/soft tissue opacity (note the displacement of the gastric axis)

100
Q

How does pyloric stenosis appear on ultrasound?

A

Dilated, fluid filled stomach
‘Donut’ appearance of the pylorus due to muscular and/or mucosal thickening

101
Q

How do you treat pyloric stenosis?

A

Pyloromyotomy
Pyloroplasty

102
Q

What is a pyloromyotomy?

A

A pyloromyotomy is where a portion of the muscular pyloric sphincter is cut

103
Q

What is a pyloroplasty?

A

A pyloroplasty is a surgical procedure performed to widen the opening at the pylorus

104
Q

What is the prognosis for pyloric stenosis?

A

Good prognosis

MODULE 16 - Alimentary Tract Disease (23 decks)

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