NAUSEA & VOMITING Flashcards

1
Q

Cause of N&V in gastric adenocarcinoma?

A

Tumour infiltration in gastric wall which disrupts peristalsis and thus causes a functional gastric-outlet obstruction

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2
Q

How can gastric cancer cause hiccups?

A

Stimulation of the vagus nerve as a result of gastric distension

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3
Q

Main indication for ondansetron in palliative n&v?

A

Chemotherapy-induced nausea and vomiting
(There are other indications but this is the important one to know)

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4
Q

Moa of ondansetron in CINV?

A

Selective antagonist of 5HT3
Chemotherapy is associated with release of 5HT from enterochromaffin cells of the small intensetine and induces a vomiting reflex through stimulation of 5HT3 receptors on fatal afferent
Ondansetron blocks the indication of this reflex

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5
Q

Common indications for syringe driver?

A

Persistent nausea and vomiting
Severe dysphagia
Unable to swallow e.g. due to mucositis
Reduced conscious level
Poor alimentary absorption

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6
Q

Problems associated with n&v as treatment side effects?

A

May not be able to have the full dose because of it - may impact on prognosis e.g. if chemotherapy
Can reduce compliance with drugs
Can be a concern to relatives
Impacts quality of life
Can cause physical damage
Can impair nutrition and hydration

It can impact on novel drug development

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7
Q

Where in the brain is the vomiting centre?

A

Medulla oblongata

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8
Q

Which receptors are found in the vomiting centre?

A

ACh Muscarinic receptors
H1 receptors
5HT2 receptors
NK1 receptors

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9
Q

Where is the CTZ found in the brain?

A

Dorsal surface of the medulla oblongata
Note: it’s present outside the blood brain barrier!

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10
Q

Receptors found in CTZ?

A

D2 receptors
5HT3 receptors

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11
Q

Why is the CTZ the area susceptible to cytotoxic agents?

A

As it’s situated outside the blood brain barrier!

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12
Q

Pathophysiology of motion sickness?

A

Labyrinth sends signals to the vestibular nuclei in the pons of the brainstem via the vestibulocochlear nerve
H1 receptors and Muscarinic receptors are stimulated
Signals passed on to CTZ and then on to the vomiting reflex = vomit

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13
Q

Pathophysiology of emotion, pain or stimulus-related (smell/sight) vomiting?

A

All these inputs get sent from the higher brain centre to the vomiting centre to stimulate it via muscarinic receptors and initiate the vomiting reflex

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14
Q

Pathophysiology of cytotoxic agents in stomach induced vomiting?

A

Cytotoxic agents present in the stomach = enterochromaffin cells release serotonin = stimulates 5HT3 receptors on vagal nerve fibres = signal taken to vomiting centre = vomit

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15
Q

Vomiitng reflex?

A

Relaxation of lower oesophageal sphincter
Contraction of diaphragm and abdominal muscles = increases abdominal pressure
Autonomic changes : increase peristalsis, salvation and HR
Closure of epiglottis
= expulsion of food

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16
Q

What are the 6 broad nausea and vomiting syndromes in palliative care?

A

Reduced gastric motility - may be related to opioids
Chemically mediated e.g. chemo, hypercalcaemia, drugs, toxins
Visceral/serosal - due to constipation or oral candidiasis
Raised ICP e.g. cerebral mets
Vestibular e.g. opioid related, motion related or base of skull tumours
Cortical - due to anxiety, pain, fear, anticipatory nausea

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17
Q

Features of n&v that may suggest gastric stasis as the cause?

A

Large volume of vomitus
Infrequent vomiting
Relief of Sx after vomiting
Reflux
Epigastric fullness
Early satiation
Hiccups
Succussion splash on auscultation

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18
Q

Features of n&v that may suggest gastric outflow obstruction as the cause?

A

Forceful vomiting
Rapid dehydration

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19
Q

Features of n&v that may suggest oesophageal blockage as the cause?

A

Vomiting soon after eating/drinking
Vomitus comprising what has just been swallowed
Sensation of food sticking

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20
Q

Features of n&v that may suggest bowel obstruction as the cause?

A

Intermittent nausea That is worsening
Faeculent vomiting
Abdominal pain that is colicky
Abdominal distention

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21
Q

Features of n&v that may suggest raised ICP as the cause?

A

Effortless vomiting
Worse in morning
Associated with headache and papilloedema

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22
Q

Features of n&v that may suggest chemically induced nausea as the cause?

A

Constant nausea with variable vomiting

23
Q

Investigations for vomiting in palliative care?

A

Bloods - U&Es, Ca2+, LFTs, BG - exclude hypercalcaemia and uraemia and check for hypokalaemia
Urine dip to exclude UTI
Abdominal radiography me be used to exclude constipation or US to detect ascites

24
Q

What simple measures may help nausea and vomiting in palliative care?

A

Make sure pt has access to large bowel, tissues and water
Calm environment away from food being prepared
Small palatable meal which are mostly carbohydrates
Cool fizzy drinks
Relaxation and acupressure bands
CBT can be considered for anticipatory n&v

25
Q

How should I treat toxicity-related nausea and vomiting from drug-induced or metabolic upset?

A

haloperidol

And Discontinue unnecessary meds

3 options: haloperidol, metoclopramide or levomepromazine

26
Q

How should I treat toxicity-related nausea and vomiting from raised ICP?

A

Cyclizine
Consider adding high-dose dexamethasone to the Cyclizine

Consider referral for radiotherapy if due to tumour

27
Q

How should I treat movement-related nausea and vomiting?

A

Cyclizine
Alternatives: Hyoscine hydrobromide, cinnarizine, levomepromazine, prochlorperazine

28
Q

How should I treat nausea and vomiting due to complete bowel obstruction with colic?

A

Cyclizine

29
Q

How should I treat anxiety-related nausea and vomiting?

A

Manage anxiety
Consider CBT
Consider a benzodiazepine or levomepromazine

30
Q

How do you manage n&v with an unknown cause?

A

Try simple measures
Levomepromazine is best option as acts on most receptors

Options for therapeutic trial: levomepromazine, metoclopramide, haloperidol, Cyclizine
If all ineffective trial of dexamethasone but seek specialist advice!

31
Q

What % of patients with advanced cancer have nausea and/or vomiting?

A

30-40%

32
Q

Examples of pro kinetic drugs that can be used to manage nausea & vomiting?

A

Metoclopramide
Domperidone

33
Q

MOA of metoclopramide for managing N&V?

A

Inhibits D2 and 5-HT3 receptrs in the CTZ
Pro kinetic effects by increasing ACh release and 5HT4 agonist = increased lower oesophageal sphincter and gastric tone which accelerated gastric emptying and transit through the gut

34
Q

Adverse efefcts of metoclopramide?

A

Extrapyramidal effects e.g. acute dystonia
Diarrhoea
Hyperprolactinaemia
Tardive dyskinesia
Parkinsonism

35
Q

Which of the prokinetics can cross the blood brain barrier?

A

Metoclopramide

36
Q

MOA of domperidone for managing N&V?

A

Blocks dopamine receptors which increases oesophageal and gastric peristalsis and lowers oesophageal sphincter pressure = fascvilitates gastric emptying
Blocks D2 and D3 in CTZ = stops n&v

37
Q

why don’t we use domperidone that often to manage N&V?

A

As it has serious cardiac adverse reactions - can cause QTc prolongation, torsades de pointes, serious ventricular arrhythmias and sudden cardiac death

38
Q

MOA of haloperidol for managing N&V?

A

D2 antagonist in CTZ = anti emetic

39
Q

MOA of Cyclizine for managing N&V?

A

Blocks H1 receptors in the vomiting centre

40
Q

MOA of levomepromazine for managing N&V?

A

Acts on 5HT2, ACh, D2 and H1 receptors

41
Q

Examples of 5-HT3 receptor antagonist?

A

Ondansetron
Granisetron
Palonosetron

42
Q

Best antiemetics for CINV?

A

Serotonin antagonists e.g. ondansetron

43
Q

Which antiemetics should you not use in parkinsons disease?

A

Metoclopramide and prochlorperazine
These can worsen parkinsons symptoms as they block dopamine receptors
Particularly bad with metoclopramide as it can cross the blood brain barrier

44
Q

Why is prednisolone used in palliative care rather than other steroids e.g. prednisolone?

A

As dexamethasone is predominantly a strong glucocorticoid and has very minimal mineralocorticoid action = prevents fluid retention

(Also 6x stronger than prednisolone)

45
Q

Moa of hyoscine hydrobromide?

A

Aka scopolamine
An anticholinergic
Competitive inhibition of Muscarinic receptors

46
Q

How should i manage n&V caused by a partial bowel obstruction i.e. without colic?

A

Metoclopramide

47
Q

Main side efefcts for levomepromazine?

A

Sedation

48
Q

SE of haloperidol?

A

Dizziness
Constipation
Dry mouth
Drowsiness
Blurred vision
Insomnia
Agitation
Movement disorders
Weight increase etc

49
Q

Moa of metoclopramide?

A

5HT4 receptor antagonist

50
Q

An absolute contraindication for metoclopramide?

A

Complete bowel obstruction - risk of perforation

51
Q

Which drugs should you never prescribe with metoclopramide and why?

A

Cyclizine or ondansetron - as they can cause constipation so further increases risk of gastric perforation

52
Q

Why can a syringe driver often reduce nausea and vomiting quite significantly compared to oral meds?

A

As when there’s a lot of vomiting there is quite often issues with absorption of the drug for multiple reasons = less drug in thr system
Syringe driver also has a psychological benefit for pt - some sort of placebo effect

53
Q

Adverse effects of 5-HT3 antagonists?

A

Prolonged QT interval
Constipation