nausea and vomiting

Question 1

what can cause nausea and vomiting?

Answer 1

• ingestion of irritants, toxins, bacteria or virus, toxins have a rapid onset while bacteria and viruses are usually slower.
• motion sickness - this is due to a disconnect between visual stimuli and proprioception
• distension of the stomach after large meals
• pharyngeal reflex
• psychological stress
• opiod therapy
• early pregnancy
• cytotoxic drug therapy

Question 2

what is nausea?

Answer 2

the sensation of imminent vomiting possibly with discomfort in the stomach, it doesnt always lead to vomiting.

Question 3

why are there less treatments for nausea?

Answer 3

it is difficult to test nausea as we cant tell how animals feel and not many humans would volunteer, its therefore difficult to find treatments.

Question 4

what is vomiting?

Answer 4

the forceful expulsion of stomach contents

Question 5

whats the mechanism behind vomiting?

Answer 5

somatic motor nerves to the skeletal muscle causes contraction of the diaphragm abdominal muscles and external intercostal muscles causing expulsion of stomach contents, the motor nerves also cause closure of the glottis and pharynx so that vomit doesnt enter the windpipe.

Question 6

vomiting involves parasympathetic activation - what does this cause?

Answer 6

increased salivation, retroperistalsis in the duodenum (food at the beginning og the small intestine gets pushed up), opening of the pyloric sphincter, opening of the oesophageal sphincter.

Question 7

what does sympathetic activation cause during vomiting?

Answer 7

sweatig, palpitations and a racing heart

Question 8

what were emetics originally used for?

Answer 8

historically emetics were used to treat ingestion of poisons.

Question 9

why are emetics no longer used in humans?

Answer 9

• it can cause increased damage if corrosives are ingested
• has a limited effect on the absorption of poisons
• risk of acid aspiration and oesophagitis - this is where repeated exposure of the oesophagus to acid can cause tissue damage which may lead to barrets oesophagus - this increases your risk of oesophageal cancer.
• poisons may cause drowsiness so vomiting in this case would be dangerous

Question 10

emetics are still sometimes used in veterinary medicine for non corrosive poisons. what are some examples of emetics used?

Answer 10

h2o2 solution for non drowsy dogs after consumption of chocolate or sugar coated tablets
apomorphine given parenteral
xylazine - an a2 agonist

Question 11

how does peripheral stimuli cause vomiting?

Answer 11

after digestion of harmful substances or overingestion (causing mechanical distension) the enterochromaffin cells of the stomach and duodenum wall will release 5HT that stimulates 5HT3 receptors on vagal afferent sensory nerve endings, activating the nerve so it sends signals to higher centres.

Question 12

how can chemotherapies cause peripheral vomiting?

Answer 12

cytotoxic chemotherapies can damage the GI tract and activate abdominal vagal afferents of the emetic pathway

Question 13

what plays a pivotal role in the neurotransmission that occurs in nemesis?

Answer 13

serotonin, sp and dopamine acting on 5ht3, NK and d2 receptors respectively are thought to play a pivotal role in the neurotransmission that occurs in emesis.

Question 14

what is the dorsal vagal complex?

Answer 14

the dorsal vagal complex consists of the emetic centre, the area postrema and the vagal afferent terminals. sensory inputs are integrated at the dorsal vagal complex resulting in activation of abdominal muscles, diaphragm, stomach and osophagus triggering the emetic response.

Question 15

the emetic centre is located in the medulla oblangata - where does it recieve signals from?

Answer 15

• vagal afferent fibres from the GI tract
• cerebral cortex from smells emotion and pain
• vestibular system (inner ear) due to motion and balance
• chemoreceptor trigger zone
  inputs into the emetic centre cause vomiting

Question 16

whats the CTZ?

Answer 16

the chemoreceptor trigger zone is within the medulla oblongata but outside the BBB hence toxins in the blood can trigger the ctz, from here it will send signals to the emetic centre.

Question 17

what receptors does the ctz have?

Answer 17

the chemoreceptor trigger zone expresses numerous transmitter receptors like 5ht3 (serotonin), dopamine, neuropeptide and opiod .
substances that cant cross the bbb wont directly trigger the emetic centre as it will go via the ctz.

Question 18

what receptors are involved with vomiting?

Answer 18

muscarinic receptors - a g protein coupled receptor in the vomiting centre recieving data from vestibular nucleus

dopamine receptors d2, a g protein coupled receptor in the chemoreceptor trigger zone.
5ht3 - serotonin - a ligand gated ion channel - chemoreceptor and baroreceptor in the emetic centre

H1 - a g protein coupled receptor recieving signal from vestibular nucleu, chemoreceptors, baroreceptors and pain receptors in the emetic centre.

Question 19

whats a muscarinic receptor antagonist?

Answer 19

hyoscine is a muscarinic receptor antagionist that crosses the bbb acting on m1 receptors from the vestibular system, blocking parasympathetic nerve transmission. it is useful in motion sickness but can have antimuscarinic side effects like dry mouth and blurred vision.

Question 20

what are some h1 antagonists?

Answer 20

cinnarazine, promethazine and cyclizine are all h1 antagonists that will block many pathways to the emetic centre however it has limited efficacy in ctz mediated vomiting. they can cause a sedative effect and some antimuscarinic activity. antihistamines are useful in motion sickness and promethazine can be used for severe morning sickness in pregnancy.

Question 21

what are 5ht3 antagonists?

Answer 21

ondansitron and granisetron are 5ht3 antagonists that have action in both the ctz and the gi tract - they are useful in post operative vomiting.

Question 22

what are d2 receptor antagonists ?

Answer 22

metoclopramide and phenothiazines like prochlorperazine are d2 receptor antagonists that have action in the cts and the gi tract - they are useful in post operative vomiting

Question 23

what are cannabinoid receptor agonists?

Answer 23

CB1 receptors regulate antisickness therefore cannabinoid receptor agonists like nabilone are used to target cb1 in the gi tract as an anti emetic. they are used for treatment of chemotherapy induced nausea and vomiting and vomiting that is resistant to other treatments. they frequently cause drowsiness, dizziness and make patients ‘high’

Question 24

what are neurokinin antagonists?

Answer 24

aprepitant is a neurokinin antagonist that targets the ctz emetic centre and the gi tract. they are usually used as part of cotherapy and typically for treatment of chemotherapy induced nausea and vomiting.

Question 25

how are corticosteroids used for vomiting?

Answer 25

dexamethasone is an analogue of corticosteroidss that acts on steroid receptors in the emetic centre having a direct action. it interacts with transmitters release and receptors whilst reducing inflammation and stress. it is used for chemotherapy induced nausea and vomiting

Question 26

whats p6 accupoint stimulation?

Answer 26

a non pharmacological approach to treating nausea and vomiting - pressure is applied to the p6 accupoint either via massage bands or electrical stimulation.

Question 27

what are some herbal remedies for nausea and vomiting?

Answer 27

ginger mint chamomile and lemon oil are all possible remedies. ginger may act as a 5ht3 antagonist.

Question 28

how can nausea and vomiting affect pregnancy?

Answer 28

historically it was a cause of maternal death due to dehydration - this is now managed with iv infusions. some abortions are due to severe nausea and vomiting. we want to avoid drugs in pregnancy due to unkown side effects to foetus. nice suggests ginger p6 accupoint and antihistamines.

Question 29

whats menieres disease?

Answer 29

a disorder of the inner ear causing vertigo tinnitus nausea and hearing loss. treatment includes h1 antagonists, betahistidine - this is a weak h1 receptor agonist and a h3 antagonist - it increases the release of neurotransmitters by removing presynaptic inhibition it also increases inner ear blood flow to reduce pressure