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Acute Abdomen > The Vomiting Patient > Flashcards

The Vomiting Patient Flashcards

1
Q

What is vomiting?

A

The forceful expulsion of contents of the stomach and proximal small intestine

Vomiting involves a complex series of events initiated by the vomiting centre in the medulla oblongata.

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2
Q

Where is the vomiting centre located?

A

In the medulla oblongata, comprising the reticular formation and the nucleus of the tractus solitarius

The vomiting centre contains receptors that respond to various stimuli.

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3
Q

What receptors are found in the vomiting centre?

A
  • α-adrenergic
  • 5-hydroxytryptamine 3 (5-HT3, serotonin)

These receptors can be stimulated directly by irritants or indirectly by inputs from other brain areas.

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4
Q

What is the role of the chemoreceptor trigger zone (CRTZ)?

A

It detects circulating toxins/drugs that can stimulate vomiting

The CRTZ is located in the area postrema at the floor of the 4th ventricle and is not protected by the blood-brain barrier.

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5
Q

What receptors does the CRTZ stimulate?

A
  • Dopamine (D2)
  • 5-HT3
  • α-adrenergic
  • Neurokinin (NK1)
  • Histamine (H1)
  • Acetylcholine/muscarinic (M1)
  • Enkephalinergic opioid

These receptors contribute to the vomiting reflex.

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6
Q

What triggers vomiting from the vestibular nuclei?

A

Nausea and vomiting due to motion sickness

Stimuli travel from the inner ear via the vestibulocochlear nerve.

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7
Q

What higher brain centres are involved in vomiting?

A

Cerebral cortex and thalamus

These centres are implicated in emotionally charged stimuli that can cause nausea and vomiting.

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8
Q

What is the initial phase of vomiting in humans?

A

Hypersalivation and the subjective feeling of nausea

This phase may be observed in veterinary patients as well.

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9
Q

What is the process of retching?

A

Spasmodic contraction and relaxation of the abdominal muscles and diaphragm

Retching occurs before the final phase of vomiting.

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10
Q

Differentiate between vomiting and regurgitation.

A
  • Vomiting: Active expulsion of food from the stomach +/- small intestine
  • Regurgitation: Passive expulsion of ingesta from the oesophagus

The two conditions have distinct causes and implications.

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11
Q

What are common signs associated with vomiting?

A
  • Prodromal signs of nausea
  • Hypersalivation (lip-smacking, discomfort)
  • Active abdominal contractions

These signs help in identifying vomiting as opposed to regurgitation.

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12
Q

What are potential causes of vomiting?

A
  • GI causes: obstruction, inflammatory, infectious, others
  • Extra-GI causes: endocrine, liver disease, drug/toxin induced

A complete history and physical examination are essential for diagnosis.

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13
Q

What does haematemesis indicate?

A

Gastric or duodenal ulceration or coagulopathy

Fresh blood or coffee grounds appearance in vomit suggests underlying pathology.

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14
Q

What is the significance of physical examination in vomiting patients?

A

It helps narrow down differential diagnoses and localize the lesion

Examination includes assessing GI and extra-GI systems.

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15
Q

What is the role of basic bloodwork in diagnosing vomiting?

A

To evaluate for extra-GI causes and sequelae of vomiting

Basic bloodwork includes PCV, TS, blood glucose, and electrolytes.

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16
Q

What diagnostics should be performed in acute abdomen cases?

A
  • Extended minimum database
  • Point of care ultrasound (POCUS)
  • Abdominocentesis

These diagnostics are critical in managing severe cases.

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17
Q

What does urinalysis help to rule out?

A

Renal versus pre-renal causes of azotaemia

Urinalysis is important before initiating intravenous fluid therapy.

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18
Q

What are second-line diagnostic tests for vomiting?

A
  • Upper GI contrast radiography
  • Upper GI endoscopy

These tests are used when initial diagnostics are inconclusive.

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19
Q

What should be included in the general approach to treating vomiting?

A

Address major body system abnormalities, provide pain relief

Basic emergency principles apply to vomiting patients.

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20
Q

What imaging technique may be indicated if the history and physical examination suggest upper GI disease?

A

Survey radiographs

Survey radiographs may be unremarkable

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21
Q

What are the risks associated with the administration of barium in vomiting dogs?

A

Aspiration

Barium is contraindicated if gastrointestinal perforation is suspected

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22
Q

What is the purpose of upper GI endoscopy?

A

Diagnostic and therapeutic removal of oesophageal or gastric foreign bodies

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23
Q

What should be prioritized in the treatment of vomiting patients?

A

Major body systems abnormalities and pain management

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24
Q

What treatment is often required for dehydrated patients with vomiting?

A

Intravenous fluids

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25
What were traditional guidelines regarding nutrition for vomiting patients?
Nutrition was withheld for the first 24 hours
26
What is the modern approach to feeding critical vomiting patients?
Early enteral feeding
27
What are antiemetics used for?
Reduce frequency of vomiting, fluid loss, nausea, and prevent electrolyte imbalances
28
True or False: Antiemetics treat the underlying cause of vomiting.
False
29
What is Maropitant?
An NK1 receptor antagonist used as an antiemetic
30
What is the recommended dosage for Maropitant?
1 mg/kg once daily for up to 5 consecutive days
31
What is a significant adverse effect associated with Maropitant?
Pain on subcutaneous injection
32
What is Metoclopramide used for?
Antiemetic via dopamine (D2) antagonism and prokinetic action
33
What are the main adverse effects of Metoclopramide?
Neurological extra-pyramidal signs
34
What is Ondansetron?
A serotonin 3 (5HT3) receptor antagonist with central and peripheral action
35
What is the typical dosage for Ondansetron?
0.5-1.0 mg/kg q 8-12 h
36
What class of drugs do chlorpromazine and prochlorperazine belong to?
Phenothiazides
37
What is the main action of Phenothiazides?
Dopamine (D2) and histamine (H1) receptor antagonism
38
What are potential adverse effects of Phenothiazides?
Sedation, vasodilation, hypotension
39
What should be considered before administering Metoclopramide?
Rule out gastrointestinal obstruction
40
Fill in the blank: Maropitant provides some _______ unrelated to its antiemetic activity.
Visceral analgesia
41
What is a contraindication for using NSAIDs in vomiting patients?
Risk of gastrointestinal issues
42
What is the effect of Metoclopramide on gastric emptying?
Accelerates gastric emptying
43
What is the mechanism of action for Maropitant?
NK1 receptor antagonist ## Footnote Used for its antiemetic properties and visceral analgesia
44
What is the recommended dose of Maropitant?
1 mg/kg SC, IV q 24 hours (max 5 days) ## Footnote May cause pain on subcutaneous injection and is recommended to be kept in the fridge
45
What are the potential side effects of Maropitant?
Bone marrow hypoplasia in puppies ## Footnote Other properties include visceral analgesia
46
What receptors does Metoclopramide act on?
Dopamine and 5HT3 receptor antagonist, 5HT4 receptor agonist ## Footnote Acts as a prokinetic agent
47
What is the recommended dose of Metoclopramide?
1-2 mg/kg/day IV CRI ## Footnote Protect from light and rule out gastrointestinal obstruction before use
48
What are the side effects associated with Metoclopramide?
Extrapyramidal CNS adverse effects ## Footnote These effects can impact the nervous system
49
What is the mechanism of action for Ondansetron?
5HT3 receptor antagonist ## Footnote Commonly used as an antiemetic
50
What is the recommended dose of Ondansetron?
0.5-1 mg/kg IV, PO q 8-12 hours ## Footnote It is considered expensive
51
What receptors does Chlorpromazine target?
D2 and H1 receptor antagonist, M1/M2 receptor antagonist, α-adrenergic receptor antagonist ## Footnote Used for its antiemetic properties
52
What is the recommended dose of Chlorpromazine?
0.1-0.5 mg/kg IV q 8-12 hours ## Footnote Should not be used in hypotensive patients
53
What are the potential side effects of Chlorpromazine?
May cause sedation ## Footnote Avoid use with Metoclopramide
54
What is the purpose of gastrointestinal protectants?
To prevent gastric mucosal damage and treat gastric ulceration ## Footnote These drugs are widely used in veterinary medicine
55
What is a significant concern regarding the use of gastrointestinal protectants in veterinary medicine?
Lack of clinical trials in veterinary species ## Footnote Many studies focus on pharmacological efficacy rather than clinical outcomes
56
What triggers the production of gastric acid?
Gastrin, acetylcholine, and histamine ## Footnote These substances bind to receptors on gastric parietal cells
57
What is the common endpoint of the pathways activated by gastrin, acetylcholine, and histamine?
Proton pump activation (H+/K+ ATPase) ## Footnote This process involves the fusion of pumps with the luminal membrane
58
What mechanisms protect the stomach from gastric acid?
* Mucous layer * Rapid epithelial cell turnover * High rate of mucosal blood flow * Prostaglandin production ## Footnote These mechanisms help in maintaining gastric integrity
59
How do gastrointestinal protectants function?
Prevent activation or inactivate the proton pump and/or enhance stomach's protective mechanisms ## Footnote They aim to reduce gastric lesions and improve outcomes
60
61
What type of receptor does ranitidine act on?
H2 receptor antagonist ## Footnote Ranitidine's efficacy in reducing gastric pH is questionable and it has prokinetic activity.
62
What is the recommended dose of famotidine for dogs?
0.5-1 mg/kg IV, PO q 12-24 hours ## Footnote Famotidine is the most potent of the H2 blockers.
63
What are proton pump inhibitors (PPIs) known to inhibit?
Hepatic P-450 enzymes ## Footnote This inhibition can lead to decreased metabolism of some drugs.
64
What adverse effect is associated with misoprostol?
Abortion ## Footnote Owners should be warned and must wear gloves when handling misoprostol.
65
What is the primary action of sucralfate?
Forms a viscous paste that binds to eroded mucosa ## Footnote Sucralfate stimulates mucosal repair and needs to be administered separately from other medications.
66
True or False: Proton pump inhibitors are more effective than H2 blockers.
True ## Footnote Studies indicate that PPIs are more effective at reducing gastric acid than H2 receptor blockers.
67
Fill in the blank: The dose for omeprazole is _______.
0.5-1 mg/kg IV, PO q 12 ## Footnote It takes 2-3 days for omeprazole to reach full effect.
68
What should be done before starting antibiotics in a vomiting patient?
Sample the source of infection ## Footnote This can include cystocentesis, airway wash, or faecal culture.
69
What is a common reason for antibiotic use in vomiting patients?
Underlying bacterial infection ## Footnote Indications include septic peritonitis, pyometra, pyelonephritis, and suspected sepsis.
70
What is the recommended administration method for antibiotics in critical patients?
Broad spectrum intravenous coverage ## Footnote Oral administration is inappropriate for vomiting patients.
71
What is the effect of tachyphylaxis associated with H2 blockers?
Need to increase dose for the same clinical effect ## Footnote This phenomenon can limit the efficacy of H2 receptor antagonists over time.
72
What is the role of cytology in diagnosing infections?
Provides rapid results to identify gram-positive or gram-negative infections ## Footnote The presence of cocci suggests gram-positive, while bacilli indicate gram-negative infections.
73
What is the effect of misoprostol on gastric mucosa?
Stimulates secretion of mucous and bicarbonate ## Footnote It increases gastric mucosal blood flow and has protective mechanisms.
74
What adverse effect can PPIs cause in people?
Diarrhoea and dysbiosis ## Footnote Dysbiosis in humans has been associated with increased risk of bacterial pneumonia following aspiration events.
75
What is the recommended timing for administering oral omeprazole?
One hour pre-feeding ## Footnote This maximizes drug uptake into the cell.
76
What should be done with antibiotic therapy based on culture results?
Deescalate the antibiotic therapy ## Footnote This means reducing to a narrow spectrum if the organisms are susceptible or stopping altogether.

Acute Abdomen (1 decks)

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