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GI > Physiology and Pharmacology of Nausea and Vomiting > Flashcards

Physiology and Pharmacology of Nausea and Vomiting Flashcards

1
Q

what is emesis

A

vomiting

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2
Q

what is nausea

A

highly unpleasant subjective urge to vomit. Felt in stomach and throat as a sinking feeling, doesn’t necessarily lead to vomiting

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3
Q

what is vomiting

A

the forceful expulsion of stomach contents through the mouth/nose by contraction of the abdominal muscles and diaphragm

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4
Q

what autonomic influences are seen in nausea

A

paleness, sweating, excessive salivation, elevation of heart rate, relaxation of smooth muscle of stomach and oesophagus, upper intestinal contractions with reverse peristalsis

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5
Q

what is retching

A

repetitive reverse peristalsis of the stomach and oesophagus without vomiting

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6
Q

what is regurgitation

A

effortless movement of swallowed food contents/ stomach acid back into the mouth (not associated with nausea or vomiting)

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7
Q

why is there excessive salivation in nausea

A

reduces acidic content entering the oesophagus helps reduce damage

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8
Q

why do you stop breathing when you vomit

A

to close the glottis and elevate the soft palate which helps seal off the nasal passage

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9
Q

does vomiting involve the active contraction of the stomach- why

A

no- smooth muscle of stomach relaxed so it can receive contents from the small intestine

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10
Q

what muscle contract to allow vomiting

A

skeletal muscles and diaphragm- increases intra-abdominal pressure

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11
Q

what state are the sphincters of the oesophagus in during vomiting

A

relaxed

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12
Q

what are the different pathways that stimulate vomiting

A

vestibular (motion sickness, labyrinth), central (brainstem), CNS, mechanical

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13
Q

what do all pathways stimulate

A

the vomiting centre in the medulla

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14
Q

how do absorbed toxins stimulate the vomiting centre

A

via CTZ within the AP of the brainstem

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15
Q

how do mechanical stimuli or pathologies within the GI tract stimulate the vomiting centre

A

via vagal afferents to brain stem

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16
Q

how does the vestibular system stimulate the vomiting centre

A

vestibular nuclei, CTZ

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17
Q

how do stimuli within the CNS stimulate the vomiting centre (pain, repulsive sights, odours, fear, anticipation, psychological factors

A

cerebral cortex, limbic system,

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18
Q

what do enterochromaffin cells in the mucosa release which causes the stimulation of vagal nerve fibres to the brainstem

A

5-HT and substance P

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19
Q

what are CTZ IMPORTANT

A

chemoreceptor trigger zone

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20
Q

where do vagal fibres from the gut terminate IMPORTANT

A

in CTZand NTS, both in the brain stem

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21
Q

what are NTS IMPORTANT

A

nucleus tractus solitarius

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22
Q

what prevents harmful toxins entering the CNS

A

blood brain barrier- CTZ lack this

23
Q

what is the medullas proper name

A

the medulla oblongata

24
Q

where can you eject GI contents from

A

ileocecal valve

25
Q

what effect do the vagal afferents have to the GI organs during vomiting

A

oesophagus shortens,

proximal relaxation of the stomach, retrograde contraction of the small intestine

26
Q

what effect do the somatic motor neurones have during vomiting

A

contraction of abdo muscles and diaphragm

27
Q

what are the prodromal signs that precede vomiting

A

increase HR and force, increased salivation, pallor of skin and cold sweating

28
Q

what nerves cause the constriction of the sphincters of the bladder and anus

A

autonomic/ somatic afferents

29
Q

what are the consequences of severe vomiting

A

dehydration,
loss of gastric proton and chloride= hypochloraemic metabolic alkalosis,
proton loss is accompanied by potassium excretion= hypokalaemia,
mallory-weiss tear,
aspiration

30
Q

when can severe vomiting cause metabolic acidosis (rare)

A

loss of duodenal bicarbonate

31
Q

why does chemotherapy and radiotherapy cause nausea and vomiting

A

releases 5-HT and substance P

32
Q

what is PONV

A

post operative N&V occurs with administration of general anaesthetic

33
Q

why do dopamine agonists cause N&V

A

as dopamine receptors prevalent in CTZ

34
Q

name a cardiac drug that causes N&V

A

cardiac glycosides e.g. digoxin

35
Q

what are setron drugs and how do they work

A

5-HT3 receptor antagonists- competitive block the receptors at peripheral and central terminal

36
Q

when are setrons used

A

to suppress chemo and radio therapy N&V and PONV

37
Q

what are setrons not effective against

A

motion sickness, agents increasing dopaminergic transmission

38
Q

what are the SE of setrons

A

constipation and headaches

39
Q

what is the main use of muscarinic acetylcholine receptor antagonists

A

prophylaxis and treatment of motion sickness

40
Q

how do muscarinic acetylcholine receptor antagonists relieve N&V

A

inhibit GI movements and relax GI tract

41
Q

what are the SEs of muscarinic acetylcholine receptor antagonists

A

blockade of para system causes blurred vision, urinary retention, dry mouth

and centrally mediated sedation

42
Q

how do histamine H1 receptor antagonists work to prevent N&V and what are they used for

A

motion sickness and acute labyrinthisitis N&V caused by irritants of the stomach

block receptors

43
Q

what are the SEs of histamine H1 receptor antagonists

A

depression and sedation

44
Q

what are dopamine receptor antagonists sued for

A

drug induced vomiting and GI disorders- not effective against motion sickness

45
Q

what dopamine receptor antagonist is safer and why

A

domperidone as does not cross the blood brain barrier so produces less side effects

46
Q

when are NK1 receptor agonists used

A

in combo with 5-HT3 receptor antagonists in chemotherapy

47
Q

when is cannabinoid (CB1) receptor agonists used and what are the SEs

A

in cytotoxin chemo thats unresponsive to other anti emetic drugs

drowsiness, dizziness, dry mouth, mood swings

48
Q

what is metaclopramide used to treate

A

antiemetic, GORD, migraine

49
Q

what does an NK1 receptor block

A

substance P

50
Q

what causes pregnancy N&V

A

placenta produces HCG

51
Q

when does morning sickness happen

A

begins weeks 4-8, peaks 7-12, subsides 16

52
Q

what are the non pharmcological treatments for morning sickness

A

changes in diet, ginger/ pyridoxine, wrist acupressure

53
Q

what is hyperemesis gravidarum

A

Fluid and electrolyte disturbances or nutritional deficiency develops from intractable vomiting in pregnancy

54
Q

what is the treatment for hyperemesis gravidarum

A

First line recommended treatment is an antihistamine such as promethazine or cyclizine.
Second line treatments are prochlorperazine and metoclopramide.

GI (64 decks)

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