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GI > Nausea and Emesis > Flashcards

Nausea and Emesis Flashcards

1
Q

What symptoms occur due to nausea?

A
  • pallor
  • sweating
  • excessive salivation
  • relaxation of stomach and lower oesophagus
  • upper intestinal contractions
    => forcing intestinal contents by reverse peristalsis into the stomach
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2
Q

Nausea and vomiting can occur independently of each other. TRUE/FALSE?

A

TRUE

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3
Q

What is retching?

A
  • forceful, involuntary contractions of abdominal muscles and diaphragm
  • the cardiac portion of stomach is pushed into the thorax
  • Retching is ‘dry’
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4
Q

How are retching and vomiting different?

A
  • Retching = ‘dry’

- Vomiting = forceful expulsion of gastric / intestinal contents out of the mouth

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5
Q

Describe what happens in the body prior to vomiting

A
  • forceful inspiration
  • reflex closure of glottis and elevation of the soft palate
    => close off the airways and nasal passages
  • stomach and oesophageal sphincters RELAX
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6
Q

What part of the body controls vomiting?

A
  • vomiting centre (VC) in medulla oblongata
  • not controlled by stomach (remember sphincters are RELAXED)
  • medulla signals to abdominal muscles to contract and compress the stomach
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7
Q

What stimuli can induce vomiting?

A

Toxic materials in gut lumen
- bacteria, salts of heavy metals, ethanol

Systemic toxins (e.g. cytotoxic drugs)

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8
Q

How do toxins cause vomiting to occur?

A
  • toxins stimulate Enterochromaffin cells in mucosa
  • these release sensory afferent signals (via 5HT) to brain
  • vagal afferents take the signal to the brainstem where the chemoreceptor trigger zone (CTZ) and nucleus tractus solitarius (NTS) are found
  • these coordinate vomiting
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9
Q

How does the vestibular system cause activation of the vomiting centre in the brain?

A
  • Signals to CTZ via vestibular nuclei in the brainstem
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10
Q

What are the potential triggers which can cause vomiting?

A
  • Pain
  • repulsive sights/ smells
  • emotional factors
  • Motion (inner ear)
  • Pharyngeal stimulation
  • gastric/duodenal distension/ irritation
  • Endogenous toxins, drugs, vagal afferents
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11
Q

What motor output nerves are involved in coordinating the action of vomiting?

A

Vagal efferents
- controls oesophagus, stomach and small bowel

Somatic motor neurones
- contracts abdominal muscles and diaphragm

Autonomic/somatic efferents
- increase HR, saliva production, sweating

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12
Q

What are the potential complications of severe vomiting?

A
  • Dehydration
  • Loss of gastric protons/chloride (=> hypochloraemic metabolic alkalosis, raised blood pH)
  • Hypokalaemia (proton loss accompanied by K+ excretion)
  • Loss of duodenal bicarbonate (HCO3) may cause metabolic acidosis
  • Oesophageal damage (Mallory-Weiss tear)
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13
Q

What types of drugs are known to cause nausea and vomiting?

A
  • Chemo + radio (release of 5-HT and substance P from enterochromaffin cells in the gut)
  • Operations under GA (post-op. N+V common)
  • Levodopa used in Parkinson’s (D2 receptors are prevalent in the CTZ)
  • Morphine and other opiate analgesics
  • Cardiac glycosides (e.g. digoxin)
  • Drugs enhancing 5-HT function (e.g. SSRIs)
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14
Q

What type of N+V are 5HT3 receptor antagonists used to treat? How do they achieve this?

A
  • chemo + radio induced N+V
  • Post-op. N+V
  • Block peripheral and central 5-HT3 receptors
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15
Q

Give examples of 5HT3 receptor antagonists

A

‘setrons’

e.g. ondansetron, palonosetron

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16
Q

What are the most common side effects of 5HT3 receptor antagonists?

A
  • constipation

- headaches

17
Q

How do Muscarinic ACh receptor antagonists work to prevent N+V?

A
  • block muscarinic ACh receptors at multiple sites (vestibular nuclei, NTS, vomiting centre)
  • Direct inhibition of G.I. movements
  • relaxation of the G.I. tract
  • can be used for prophylaxis of motion sickness
18
Q

Give an example of a Muscarinic ACh receptor antagonist

A

hyoscine

19
Q

Give examples of side effects caused by Muscarinic ACh receptor antagonists

A

block parasympathetic ANS => can cause:

  • blurred vision
  • urinary retention
  • dry mouth
  • centrally-mediated sedation
20
Q

How do H1 receptor antagonists aim to reduce N+V?

A

Histamine H1 receptor antagonists:

  • block H1 receptors in vestibular nuclei and NTS
    => used for motion sickness prophylaxis and acute labyrinthitis
  • may also potentiate blockade of muscarinic receptors which helps their effectiveness
21
Q

GIve examples of H1 receptor antagonists

A

Cyclizine

Cinnarizine

22
Q

What are the main side effects of H1 receptor antagonists?

A
  • CNS depression and sedation => drowsiness

- may affect performance of skilled tasks

23
Q

How do dopamine receptor antagonists aim to reduce N+V?

A
  • Centrally block dopamine D2 (and D3) receptors in the CTZ

- Peripherally exert a prokinetic action on the oesophagus, stomach and intestine

24
Q

When are dopamine receptor antagonsists used for N+V?

A
  • drug-induced vomiting (e.g. chemo, Parkinson’s disease agents)
  • Vomiting in GI disorders
25
Q

Give examples of dopamine receptor antagonsists used to treat N+V

A
  • domperidone

- metocloperamide

26
Q

Why does domperidone not cause as many side effects as metocloperamide?

A

Domperidone does not cross the blood brain barrier (BBB)

=> less likely to cause extrapyramidal effects (movement disorder)

27
Q

When are NK1 receptor antagonists used?

A
  • In combination with 5-HT3 receptor antagonist and dexamethasone
  • used in acute phase of highly emetogenic chemo
  • thought to antagonise substance P
28
Q

When are cannabinoid (CB1) receptor antagonists used to treat N+V?

A
  • used for in-patients

- Tx of chemo that is unresponsive to other anti-emetics

29
Q

What side effects can cannabinoid (CB1) receptor antagonists cause?

A
  • drowsiness
  • dizziness
  • dry mouth
  • mood changes

GI (33 decks)

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