wk 3 13 - physiology and pharmacology of nausea and vomiting Flashcards
associated feeling of nause
a sinking sensation
im going to be sick
felt in throat and stomach
t/f nausea often relieved by vomiting
true
associated signs symptoms of nausea
pallor excessive secretions - salivation relaxation of stomach/ lower oesophagus upper intestinal contractions (jejunum,duodenum) reverse peristalsis
t/f vomiting can occur without nausea
true
retching
repetitive reverse peristalsis without vomiting
forceful conraction involuntary of whatt skeletal muscles is seen in retching
abdominal muscles
diaphragm
(cardiac part of stomach pushed into thorax)
medical term for vomiting
emesis
outline immediate change seen prior vomiting in mouth
breathing stopped(elevation of soft palate, closing of epiglotttis)
outline vomiting
suspension of intestinal slow wave activity
retrogade contractions of ileum to stomach
breathing stopped (softpalate…)
relaxation of stomach -dia+abdomino contraction
ejection of gastrc contents
cycle repeated
t/f voomiting involved contraction of stomach
false
relaxed so can recieve contents from sml intestine
which cells are stimulated inducing vomiting
enterochromffin cells
release mediators -
5-HT, substance P
what happens when 5-ht released
diffises locally
stimulates vagus nerves (via 5-HT3 receptors)
causes depolarisation, from gut to brain stem (chemoreceptor trigger zone, nucleus tractus soitarious) -NEED TO KNOW
other than toxic materials entering gut, what else can stimulate enterchromaffin cells
systemic toxins (cytotoxic drugs)
oter than mechanical stimuli or absorbed toxins, what else can induce vomiting
vestibular system (motion sickness)
stimuli within CNS (pain, fear, anticipation)
which 2 areas does the signalling pass thhrough for vomiting induced due to stimuli within th CNS
limbic system
cerebral cortex
then travels to medulla
motion sickness signals through
vestibular nucleus then to medulla
vomiting centre
diffuse collection of neurones
used to coordinate appropriate response
vagal efferent effect on stomach/oesophagus/sml intestine in vomiting
oeso - shorterning
stomach - proximal relaxation
sml intestine - giant retrogade contraction
effect of somatic motor neurones
controls skeletal muscles involved in vomiting
autonomic/somatic ouputs effect on vomiting (immediately precede)
incr hr
incr secretion
skin - pallor, cold sweat (vasoconstriction of vessels)
constricyion of bladder and anus sphincters
vomiting (prolonged/severe) causes
dehydration
loss gastric contents - less protons, chloride (acid) - hypochloraemic metabolic alkalosis - incr pH of blood
hypokalaemia - proton loss = potassium loss mediated by kidney
duodenal bicarbonate may cause metabolic acidosis (v severe)
oesophageal damage (mallory-weiss tear)
drugs and radiation induced emesis
cancer chemo - cisplatin, doxorubicin
radiotherapy - 5-HT,subP release
general anaesthetic (Post Operative Nausea and Vomiting PONV)
dopamine agonists (levodopa - parkinsons) (high conc of D2 receptors in CTZ)
morphine/opiates
cardiac glycosides (digoxin)
drugs enhancing 5-HT function
pattern with 5-Ht3 receptor antagonist drug names
all end in setron
ondansetron, palonosetron
which type of emesis is 5-ht3 antagonists effective against
chemo/radiation induced
post-op nausea
5-ht3 antagonists block peripheral and central receptors, what does this preven
signals travelling to AP and NTS
t/f 5-ht3 antagonists are less effective in repeated rounds of chemo
true
what may be added to 5-ht3
corticosteroids or neurokinin receptor antagonist (NK) (inhibits subP)
5-ht3 is not effective in preventing vomiting due to motion sickness, what drugs are
histamine H1 receptor antagonists
Muscarinic ACh receptor antagonists
2 muscarinic ach drugs
hyosine
scopolamine
administration of muscarinic ach’s
transdermal patch
where are muscarinic receptors that are blocked through mus.AC|h antagonists
vestibular nuclei
NTS
vomiting centre
blurred vision urinary retention dry outh sedation why does this occur with muscarinic Ach antagonists?
blockage of parasympathetic divsion of ANS
other than prophylaxis and motion sickness, when would histamine H1 receptor antagonists be used
acute labrynthitis
irritant induced nausea
t/f Histamine H1 receptors block H1 in VS and NTS
false
VS
NTS
Muscarinic receptor
adverse effects of H1
cns depression
sedation
domperidome and metoclopramide are
dopamine antagonists
dopamine antagonists are effective in treating q
drug induced vomiting
vomiting from GI disorders
phenothiazine is used in
severe nausea
as well as blocking D2,D3 in CTZ, what other effect does domperidome have
prokinetic actioin on oesophagus/stomach/intestine
in acute highly emetic chemotherapy, which 3 drugs would be given
NK1 receptor antagonist
5-HT3 receptor antagonist
Dexamethasone
t/f for delayed emesis from chemo, same 3 drugs used in acute
false
only 2 - NK1 + Dexamethasone
