wk 3 13 - physiology and pharmacology of nausea and vomiting Flashcards

1
Q

associated feeling of nause

A

a sinking sensation
im going to be sick
felt in throat and stomach

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2
Q

t/f nausea often relieved by vomiting

A

true

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3
Q

associated signs symptoms of nausea

A
pallor
excessive secretions - salivation 
relaxation of stomach/ lower oesophagus
upper intestinal contractions (jejunum,duodenum) 
reverse peristalsis
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4
Q

t/f vomiting can occur without nausea

A

true

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5
Q

retching

A

repetitive reverse peristalsis without vomiting

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6
Q

forceful conraction involuntary of whatt skeletal muscles is seen in retching

A

abdominal muscles
diaphragm
(cardiac part of stomach pushed into thorax)

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7
Q

medical term for vomiting

A

emesis

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8
Q

outline immediate change seen prior vomiting in mouth

A

breathing stopped(elevation of soft palate, closing of epiglotttis)

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9
Q

outline vomiting

A

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

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10
Q

t/f voomiting involved contraction of stomach

A

false

relaxed so can recieve contents from sml intestine

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11
Q

which cells are stimulated inducing vomiting

A

enterochromffin cells
release mediators -
5-HT, substance P

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12
Q

what happens when 5-ht released

A

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

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13
Q

other than toxic materials entering gut, what else can stimulate enterchromaffin cells

A

systemic toxins (cytotoxic drugs)

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14
Q

oter than mechanical stimuli or absorbed toxins, what else can induce vomiting

A

vestibular system (motion sickness)

stimuli within CNS (pain, fear, anticipation)

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15
Q

which 2 areas does the signalling pass thhrough for vomiting induced due to stimuli within th CNS

A

limbic system
cerebral cortex

then travels to medulla

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16
Q

motion sickness signals through

A

vestibular nucleus then to medulla

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17
Q

vomiting centre

A

diffuse collection of neurones

used to coordinate appropriate response

18
Q

vagal efferent effect on stomach/oesophagus/sml intestine in vomiting

A

oeso - shorterning
stomach - proximal relaxation
sml intestine - giant retrogade contraction

19
Q

effect of somatic motor neurones

A

controls skeletal muscles involved in vomiting

20
Q

autonomic/somatic ouputs effect on vomiting (immediately precede)

A

incr hr
incr secretion
skin - pallor, cold sweat (vasoconstriction of vessels)
constricyion of bladder and anus sphincters

21
Q

vomiting (prolonged/severe) causes

A

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)

22
Q

drugs and radiation induced emesis

A

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

23
Q

pattern with 5-Ht3 receptor antagonist drug names

A

all end in setron

ondansetron, palonosetron

24
Q

which type of emesis is 5-ht3 antagonists effective against

A

chemo/radiation induced

post-op nausea

25
Q

5-ht3 antagonists block peripheral and central receptors, what does this preven

A

signals travelling to AP and NTS

26
Q

t/f 5-ht3 antagonists are less effective in repeated rounds of chemo

A

true

27
Q

what may be added to 5-ht3

A

corticosteroids or neurokinin receptor antagonist (NK) (inhibits subP)

28
Q

5-ht3 is not effective in preventing vomiting due to motion sickness, what drugs are

A

histamine H1 receptor antagonists

Muscarinic ACh receptor antagonists

29
Q

2 muscarinic ach drugs

A

hyosine

scopolamine

30
Q

administration of muscarinic ach’s

A

transdermal patch

31
Q

where are muscarinic receptors that are blocked through mus.AC|h antagonists

A

vestibular nuclei
NTS
vomiting centre

32
Q
blurred vision 
urinary retention 
dry outh 
sedation
why does this occur with muscarinic Ach antagonists?
A

blockage of parasympathetic divsion of ANS

33
Q

other than prophylaxis and motion sickness, when would histamine H1 receptor antagonists be used

A

acute labrynthitis

irritant induced nausea

34
Q

t/f Histamine H1 receptors block H1 in VS and NTS

A

false

VS
NTS
Muscarinic receptor

35
Q

adverse effects of H1

A

cns depression

sedation

36
Q

domperidome and metoclopramide are

A

dopamine antagonists

37
Q

dopamine antagonists are effective in treating q

A

drug induced vomiting

vomiting from GI disorders

38
Q

phenothiazine is used in

A

severe nausea

39
Q

as well as blocking D2,D3 in CTZ, what other effect does domperidome have

A

prokinetic actioin on oesophagus/stomach/intestine

40
Q

in acute highly emetic chemotherapy, which 3 drugs would be given

A

NK1 receptor antagonist
5-HT3 receptor antagonist
Dexamethasone

41
Q

t/f for delayed emesis from chemo, same 3 drugs used in acute

A

false

only 2 - NK1 + Dexamethasone