O1ii / 22A14 / 14A03: Vomiting

22A14: Exam Report

Describe the neural integration of vomiting, highlighting the site and mechanism of action of antiemetics

60% of candidates passed this question

The examiners commented that a well-drawn and labelled diagram was a very useful adjunct to answering this question.

Consideration of stimulus, sensors, integrators/processors, and effectors was also useful to ensure that all components of the question were covered by a candidate’s answer.

Incorrect facts or a lack of detail about the various receptors and their locations was a common theme in answers that scored poorly.

Classes of antiemetics, with specific drugs given as examples, were expected to gain marks.

14A03: Exam Report

Describe the neural integration of vomiting. (60% of marks) Describe the pharmacology of ondansetron. (40% of marks)

58% of candidates passed this question

Candidates who failed the question did not answer the actual question. They did not discuss the  neural  integration  but  instead  listed  various  inputs  into  the  CTZ  and  vomiting  centre.

It was expected candidates could detail the pathways involved (afferent and efferent limbs) and describe  the  relationship  with  the  coordinating  centres.

For  example, afferent  pathways  to the vomiting centre include stretch and chemoreceptors located throughout the GIT via vagal and  sympathetic nerves,  pharyngeal  touch  receptors  via glossopharyngeal  nerves etc.

Again structuring pharmacology answers was often poor.

O1ii / 22A14 / 14A03: Describe the neural integration of vomiting (60 marks). Describe the pharmacology of ondansetron (40 marks)

Definition

Vomiting = involuntary, forceful + rapid expulsion of gastric contents through mouth

  • Neutral integration involves:
    1. Afferent input
    2. Central integration
    3. Efferent outputs

1) Sensory Inputs

  • Stomach/intestinal irritants → vagal afferents  → stimulate CTZ & vomiting centre (5HT3)
  • Systemic toxins (drugs) → activate chemoreceptor cells of CTZ (5HT3, D2)
  • Motion sickness → vestibulocochlear n.  → activates vestibular centre  → CTZ (ACh, H1)
  • Emotion/pain/foul sights & smells → CNS afferent pathway  → directly stimulates VC
  • Head injury → direct central effect on VC

2) Central Integration

  • CTZ
    • Located on 4th floor ventricle, medulla, outside BBB
    • Relays stimuli to vomiting centre
    • Receptors for all emetic stimuli (M1, D2, 5HT3, NK1, H1)
  • Vomiting Centre
    • Located in Medulla
    • Mainly muscarinic receptors
    • Activated by:
      1. CTZ impulses
      2. Higher brain centres
      3. Visceral afferents (directly)

3) Efferent Outputs

  • Brainstem causes abdominal contraction & expulsion of gastric contents via:
    1. Vagus, glossopharyngeal n. → upper gut
    2. Spinal nerves → diaphragm + abdominal m’s

Mechanism:

deep inspiration + closure of glottis

↓

LOS relaxation, reverse peristalsis

↓

Strong abdominal m. contraction

↓

Diaphragm descends  → ↑↑↑abdominal P

↓

↑pressure on stomach forces contents into oesophagus

↓

UES relaxation & contents expelled through mouth

Efferent Outputs

Classes of anti-emetics

Class

Example

Class

D2 Antagonist

Example

  • Phenothiazine
    • Chlorpromazine
    • Prochloperazine
  • Butyrophenones
    • Droperidol
    • Domperidone
  • Benzamides
    • Metoclopramide

Class

Anticholinergic

Example

  • Hyoscine
  • Atropine

Class

5HT Antagonis

Example

  • Tropisetron
  • Ondansetron

Class

H1 Antagonist

Example

  • Phenothiazine
  • Promethazine

Class

Other

Example

  • Steroids
  • Cannabis
  • Propofol
  • Benzodiazepines