Vomiting: emetics and anti-emetics Flashcards

1
Q

define haematemesis

A

V blood

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2
Q

emetic vs anti-emetic

A

stimulates/ inhibits V

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3
Q

what are the 3 causes of V? give examples of each

A

primary gastric conditions - gastritis, ulcer, foreign body, obstruction, neoplasia
intestinal conditions - enteritis, colitis, obstruction, constipation
secondary to systemic (non-GI) causes - toxaemia, motion sickness, CNS disease, otitis media, hepatitis, peritonitis, drugs e.g. digoxin

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4
Q

what is dysphagia?

A

failure to prehend/ swallow food

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5
Q

what is expectoration?

A

coughing up phlegm

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6
Q

what is regurgitation?

A

passive reflux of oesophageal contents

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7
Q

where is the V centre

A

the medulla

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8
Q

where does the medulla receive inputs from?

A

vagus and glossopharyngeal nerves mediate control of closure of airway and motor changes of GI tract

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9
Q

name 5 afferent inputs to the V centre

A

higher brain centres, vestibular, CRTZ, V centre, peripheral receptors

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10
Q

how do higher brain centres influence V?

A

Psychogenic - fear, stress, excitement

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11
Q

How do vestibular inputs influence the V centre?

A

motion sickness/ labyrinthitis

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12
Q

how does the CRTZ influence V?

A

outside BBB so exposed to blood.
drugs e.g. digoxin, morphine
metabolic - acidoses, toxins etc

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13
Q

How might the V centre influence V?

A

CNS inflammation, raised intracranial pressure; hydrocephalus/ brain tumour

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14
Q

What about peripheral receptors?

A

CNX/ CNIX - inflammation, irritation, distension

anatomy of where nerves are?? think

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15
Q

what are the stages of the V reflex?

A

prodromal, retching, expulsion, relaxation

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16
Q

describe the prodromal stage

A

nausea. restlessness, depression, salivation, relaxation of LES

17
Q

describe the retching stage

A

uncoordinated contractions of resp muscles. inhibition salivation, duodenal retroperistalsis, mixing of gastric contents

18
Q

describe the expulsion phase

A

coordinated abdominal contractions, stomach squeezed, inhibition of breathing, closure of glottis and nasopharynx to protect airway. reduced LES and UES tone.

19
Q

describe the relaxation phase

A

abdominal muscles, resp and diaphragm relax, nasopharynx and glottis relax and breathing resumes

20
Q

give 2 consequences of V

A

dehydration due loss of Na and water

acid-base disturbances

21
Q

describe a metabolic acidosis

A

more common. loss of duodenal juice therefore HCO3.

GI loss of K so hypokalaemia

22
Q

describe a metabolic alkalosis

A

loss of HCl (hypochloraemia) due to pyloric blockage therefore retention of HCO3.
renal excreation of NaHCO3 to compensate and Na/K exchange to compensate for Na loss. Also leads to hypokalaemia

23
Q

what are emetics used for? give examples of contra-indications

A

to induce vomiting of substances that are safe to be vomited back.
sharps, detergents, batteries, some medicines

24
Q

what is the main problem with emetic/ anti-emetic drugs?

A

species differences in receptor location so some drugs may only work in certain situations in some species

25
define V
forceful, reflex ejection of gastric (and upper intestinal) content from the stomach. ACTIVE PROCESS with forceful contraction of abdominal muscles
26
give 3 examples of emetic drugs
ipecacuanha, apomorphine, xylazine (alpha-2 agonist)
27
how does Ipecacuanha work?
contains emetine, stimulates gastric chemoreceptors
28
how does apomorphine work?
stimulates dopaminergic receptors in CRTZ - powerful in dogs (not cats)
29
how does xylazine work?
stimulated adrenergic receptors in V centre. rapid induction in cats but sedation (inhalation)
30
name other chemicals known to induce V
salt, hydrogen peroxide, washing soda (sodium carbonate) no longer recommended as most also contain caustic sodium hydroxide
31
how might chemotherapy drugs stimulate V?
fear/ anticipation (higher brain), direct action CRTZ, serotonin receptors GI/ damage to ep
32
describe the properties of maropitant
effective drug, broad spectrum drug. blocks substance P receptors (NK). licensed in D and C, will inhibit V due to chemo agents, motion sickness and gastroenteritis. Highly protein-bound so once daily dose. given IV, SC (pain) and PO (poor bio so double dose) metabolised by liver (disease) store in fridge
33
describe the properties of metoclopramide
licensed oral and injectable forms, CRI puppies and kittens. lower doses D2, higher 5HT3 antagonists. also a prokinetic, urinary excretion (dose). SE = hyper CNS
34
how do anti-histamines work?
H1 receptor antagonists in vestibular and CRTZ. less effective in animals than people. some efficacy in motion sickness and vestibular disease in dogs, no vet licensed products and mostly used in allergic skin disease. SE = drowsiness H2 antagonists block gastric acid production e.g. promethazine (human)
35
how do anti-muscarinics work?
inhibit parasymp. antagonise M1 Ach receptors. unlicensed and SE = dry mouth, tachycardia, mydriasis and constipation e.g. scopolamine
36
how do serotonin antagonists work?
antagonise 5HT3 receptors, unlicensed. often used for chemo induced vom as expensive e.g. Ondansetron
37
how do phenothiazines work?
dopamine receptor antagonists. unlicensed + antagonise other receptors. SE = sedation, vasodilation (sedatives)
38
what other drugs can be used to inhibit V?
glucocorticoids, cannabinoids
39
name 6 drug groups used as anti-emetics
maropitant, metoclopramide, anti-histamines, anti-muscarinics, serotonin antagonists, phenothiazides