Nausea and Emesis Flashcards

1
Q

What is nausea?

A

An unpleasant sensation vaguely referred to the epigastrium and abdomen, with a tendency towards vomiting.

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2
Q

What is regurgitation

A

Effortless return of oesophageal or gastric contents into the mouth unassociated with nausea or involuntary muscle contractions.

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3
Q

What is vomiting (emesis)?

A
Involuntary
contractions of the abdominal,
thoracic and GI (smooth) muscles
leading to forceful expulsion of
stomach contents from the mouth.
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4
Q

What is rumination?

A

food that is regurgitated
in the postprandial period, re-
chewed and then re-swallowed.

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5
Q

How does the brainstem vomiting centre (VC) coordinate vomiting?

A

Through interactions with the cranial nerves VIII and X and interactions with neural networks in the nucleus tractus solitarius (NTS) that control respiratory, salivatory and vasomotor centres.

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6
Q

Where is the vomiting centre (VC) located?

A

In the medulla oblongata in the brain.

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7
Q

What do cranial nerves VIII and X do?

A

Transfer signals from GI tract and heart to the vomiting centre stimulating vomiting.

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8
Q

What does the vestibular system do?

A

Has H1 and M1 receptors which send signals to vomiting centre in response to motion. Responsible for sea and travel sickness.

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9
Q

What does the central nervous system do to trigger vomiting?

A

The cortex, thalamus, hypothalamus and meninges send signals to the vomiting centre and to the chemoreceptor trigger zone (CTZ). Responsible for nausea due to sight of things e.g. site of blood.

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10
Q

Two types of activity the vomiting centre activates in response to stimuli?

A

1) parasympathetic

2) motor efferent

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11
Q

Which of the two centres/zones is close to the blood/brain membrane and why is this important?

A

Chemoreceptor trigger zone.
Important coz senses signals from blood to brain and detects any toxic substances in blood e.g. alcohol and stimulates vomit to try reduce level of toxic contents.

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12
Q

What stimulates post operative nausea and emesis

A

5HT3 receptor for serotonin

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13
Q

What causes nausea and emesis?

A

1) infections
2) Drugs
3) GI diseases
4) Acute abdominal disorders
5) CNS disorders
6) Metabolic disruptions
7) Pregnancy
8) others

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14
Q

Things that trigger sickness (vomiting)

A

1) pain, repulsive sight, smell, emotional factors (CNS related)
2) Motion (inner ear), signalling to vestibular nucleus (vestibular system related)
3) Pharyngeal stimulation, gastric/duodenal distension or irritation (trigger NTS and CTZ to trigger VC).
4) Endogenous toxins, drugs, vagal afferents trigger CTZ hence activating VC.

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15
Q

Consequences of vomiting?

A

1) dehydrating
2) malnutrition
3) acid-base imbalance
4) electrolyte imbalance
5) oesophageal damage
6) tooth damage

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16
Q

Things to consider when treating nausea or emesis?

A

1) treat regardless of cause
2) identify and treat underlying cause
3) provide temp relief of symptoms
4) use preventive measures in cases where vomiting can be predicted to happen e.g. in chemotherapy.

17
Q

Two types of treatment for nausea and emesis?

A

Pharmacological and non-pharmacological

18
Q

What are the non-pharmacological methods of treatment?

A

1) relaxation
2) calm environment
3) small snack, bland food
4) avoid odours
5) mouth care
6) surgery/stent
7) chemoradiation
8) acupunture/ acupressure
9 ) NG/PEG tubes

19
Q

What are the pharmacological methods of treating nausea and emesis?

A

1) D2 antagonist
2) 5HT3 Antagonist
3) Anti-histamines
4) Anti-cholinergics/ anti-muscarrinics
5) Pro-motility

20
Q

How antihistamines work?

A
  • H1 receptor antagonist
  • block muscarinic receptors as well that contribute to histamine activity
  • used for prophylaxis and treatment of motion sickness, acute labyrinthitis and PONV
  • blocks H1 receptors in vestibular nuclei
  • Cause CNS depression and sedation (causing drowsiness)
21
Q

How anticholinergics work?

A
  • muscarinic acetylcholine receptor antagonist
  • used for prophylaxis and to treat motion sickness

Mechanism:

  • block muscarinic acetylcholine receptors at multiple sites.
  • direct inhibition of GI movements and relaxation of GI tract may contribute to anti-emetic response.
  • unwanted side effects from blocking parasympathetic ANS (e.g. blurred vision, dry mouth)
  • side effects from centrally-mediated sedation
22
Q

How dopamine antagonists work?

A

*block D2 receptors, H1, Ach and alpha adenergic receptors.
*used for drug induced vomiting and vomiting in GI disorders.
Mechanism of action:
*central blocking of D2 receptors in CTZ
*peripherally exert a prokinetic action on the oesophagus, stomach and intestine.
*domperidone doesn’t cross blood/brain barrier and is less likely to result in unwanted side efffects of metoclopramide.

23
Q

why are trandsermal anticholinergics good?

A

They are’t taken orally so won’t pass through GI system so if patient was to vomit, they won’t vomit the drug back up.

24
Q

How serotonin 5HT3 receptor antagonist works?

A
  • single dose regimen same efficacy as multidose regimen
  • oral and iv routes are equivalent
  • prevents 5HT3 receptor from binding to 5HT so can’t send signal to VC so no vomitting.
25
Q

Receptors and centre for intracranial pressure, anxiety and memories?

A

R: GABA and CB
C: Cerebral cortex

26
Q

Receptors and centre for motion or vestibular disease

A

R: H1 and M1
C: vestibular apparatus

27
Q

Receptors and centre for metabolics, drugs and toxins

A

R: D2, 5HT and NK
C:chemoreceptor trigger zone(CTZ)

28
Q

Receptors and centre for GI, chemo and radiotherapy?

A

R: D2 and 5HT
Centre: Vagus afferents and splanchnic nerves