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Dawn Harpham

on 20 September 2012

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Transcript of Antiemetics

photo (cc) Malte Sörensen @ flickr Dawn Harpham Antiemetics Understand problems caused by emesis.
Appreciate those patients likely to be at high risk of PONV.
Understand the pathways involved in emesis.
Be able to classify antiemetics.
Understand the mechanisms by which antiemetics work.
Be able to discuss commonly used antiemetics. Objectives Unpleasant and uncomfortable (patient distress)
Delayed discharge
Late mobilisation
Dehydration and reduced oral input (drugs, nutrition)
Loss of hydrogen, chloride, potassium and sodium ions.
Metabolic alkalosis
Increased pain
Poor surgical outcome (dressing/wound disturbance, bleeding) Problems with emesis Cause of emesis are multifactorial. Risk Factors Classified according to receptor types at which they act.
1. Dopamine antagonists
2. 5HT3 antagonists
3. Anticholinergics
4. Antihistamines
5. Miscellaneous (cannabinoids etc) Classification of Antiemetics Abdominal muscles contract and relax (retching) followed by sustained contraction of abdominal muscles, co-ordination of intercostal, pharynx and larynx muscles during expulsion of gastric contents.

Large autonomic involvement causes pallor, salivation, hypotension, sweating. Emesis Controlled by efferent neurones in the medula oblongata in an undefined area known as the vomiting centre.
Many neural pathways and receptors involved.
Vomiting centre in stimulated by various afferent inputs:
1. CTZ
2. Vestibular system
3. Higher centres
4. Vagal stimuli (GIT) Control of Vomiting Opiod - CTZ
Dopamine (D2) - CTZ
mACh - PNS (GIT distension), vestibular
Histamine (H1) - vestibular apparatus Receptors Patient Factors Young
Female (especially menstruation age)
Previous PONV or motion sickness
Non smokers
Hypotension Surgical Factors Pain
Laparoscopy Anaesthetic Factors Opiod analgesics
Anasthetic agents (etomidate, nitrous)
Prolonged anaesthesia Antiemetics eg. Ondansetron
Carbazole structure
Presentation:4mg tablets, 16mg suppository or 2mg/ml clear sol.
Mechanism: Blocks 5HT3 centrally and peripherally
Effects: well tolerated (headache, flushing, bradycardia, constipation).
Kinetics: Rapidly absorbed, 60% oral bioavailability, 75% protein bound, hepatic metabolism by hydroxylation and glucoronide conjugation to inactive metabolites. Reduce dose in hepatic impairment. Half life 3h.
Uses: CTX/RTX, periop including rescue. 5HT3 antagonists Identify high risk patients and procedures.
Minimise triggers.
Review notes (previous antiemetics used etc)
Consider additional periop antiemetics (dex+8mg ondansetron)

Consider cause (eg hypotension)
Understand actions of antiemetic classes (onset, duration etc)
Minimise side effects.
Use different group from prophylaxis with different mode of action and rapid acting. PONV Considerations eg Cyclizine
Piperazine derivative
Mechanism: H1 antagonist, some anticholinergic action.
Effects: Painful injection, reduced oesophageal sphincter tone, anticholinergic, tachyarrythmias.
Kinetics: Well absorbed orally, 80% bioavailable. Metabolised in liver to norcyclizine. Elimination half life 10 hours..
Uses: Motion sickness, RTX/opiod/PONV, menieres disease H2 antagonists D2 Antagonists Hyoscine

Effects: CNS (sedation, central anticholinergic syndrome) CVS (bradycardia), resp (bronchodilation, reduced secretions), anti-sialagogue
Kinetics: Rapid but unpredictable oral absorption, 50% plasma protein bound, liver esterase metabolism.
Uses: premedication with im opiod to reduce PONV, sedative Anticholinergics Dexamethasone (effective, long half life/slow onset - prophylaxis rather than rescue, unclear mechanism).

Cannabinoids (nabilone, actss on VC, useful post chemotherapy)

Neurokinin 1 antagonists (aprepitant, NK1 R in GIT activated by substance P which is released from gastric mucosa when damaged, may act in association with 5HT3 to trigger vagal afferents, potential target for antiemetics) Other
Complex area in reticular formation.
Efferent fibres leading to vasomotor, respiratory and salivary nuclei.
Vagal, phrenic and spinal nerves go to GIT to initiate vomiting. Vomiting Centre NTS 1 of 3 nuclei which form origin of the vagus nerve.
Visceral afferent nucleus of the brainstem.
Receives afferents from vagus, glossopharyngeal, facial nerve by way of the solitary tract.
Hence receives sensory fibres from larynx, pharynx, GIT, heart, lungs. Vagus Nerve Visceral afferent effects are transmitted mainly by the vagus nerve. Vestibular Nucleus Stimulation from the labyrinth in the inner ears is projected via vestibular and cerebellar nuclei to the VC. CTZ In caudal end of 4th ventricle
and functionally lies outside BBB (suited for detecting circulating toxins in blood and CSF). Pathways Benzamides Phenothiazines Divided into 3 groups based on structure.

1. Propylamine (chlorperazine)
2. Piperadine (thioridazine)
3. Piperazine (prochlorperazine)

Mechanism: antagonises D2, muscarinic, noradrenergic, H1, 5HT3 receptors.
Effects: CNS (extrapyrimidal, neuroleptic malignant syndrome, increased prolactin, hypothermia), CVS (hypotension), anticholinergic, jaundice, leucopenia, haemolytic anaemia.
Kinetics: good absorption but large hepatic first pass metabolism (oral availability 30%)
Uses: schizophrenia, terminal care, PONV, hiccoughs.

Effects: Same as chlorpromazine (especially acute dystonia, akathisia)
Kinetics: Erratic oral absorption, low bioavailability,
Uses: PONV, vertigo, psychosis Metoclopramide

Procainamide derivative
Presentation: tablets, syrup, solution (PO/IV/IM)
Mechanism: D2 antagonism at CTZ, some 5HT3 antagonism.
Effects: CNS (extrapyrimidal especially young females, neuroleptic malignant syndrome) CVS (hypotension, tachy/bradycardia)
Kinetics: well absorbed, varied frist pass metabolism (oral bioavailability 30-90%), conjugated in liver.
Uses: prokinetic, antiemetic, reflux (prokinetic), migraine
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