Nausea & Vomiting Flashcards

1
Q

What kind of response is vomiting?

A

A defensive mechanism against the external environment

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2
Q

What is vomiting?

A

A forceful expulsion of gastric contents from the mouth

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3
Q

What causes vomiting?

A
  • powerful/sustained contraction of abdominal muscles = increased abdominal pressure
  • diaphragm descent and contraction
  • gastric cardia opens
  • vomiting centre relaxes LOS
  • tachycardia
  • peristalsis
  • epiglottis closes so food doesn’t travel down the lungs

VC LOS to relax, diaphragm contracts, abdominal muscles contact, food pushed back up, increased abdominal pressure when contract muscles, tachycardia, salivation, peristalsis, epiglottis closes at top so food doesn’t travel down into lungs

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4
Q

What is retching?

A

Laboured, spasmodic, rhythmic contractions of respiratory muscles (diaphragm, chest wall, abdominal wall muscles)

  • no expulsion of gastric contents
  • generates pressure gradient which can lead to vomiting
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5
Q

What is nausea?

A

unpleasant sensation at the back of throat

urge to vomit

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6
Q

What is nausea accompanied by?

A
cold sweats
pallor
salivation
loss of gastric tone
duodenal contractions
reflex of intestinal contents into stomach
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7
Q

What happens if nausea does not stop?

A
  • life prolonged refusal of medications
  • ribs broken
    -dehydration/anorexia
    seen in cancer patient undergoing chemotherapy
    nausea can be relieved b vomiting
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8
Q

What are the 3 main types of vomiting syndrome?

A

Life prolonged nausea and vomiting (chemotherapy cancer patients)
Cyclic vomiting syndrome
Gastroparesis

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9
Q

What is cyclic vomiting syndrome?

A

nausea not relieved by vomiting
can incapacitate
rapid fire, projectile vomiting

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10
Q

What is gastroparesis?

A
delayed gastric emptying
higher with diabetes
less intense but more widespread
belching and bloating
early satiety after eating
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11
Q

What is the NTS?

A

nucleus of solitary tract

dorsal motor nucleus of vagus + reticular formation + ventrolateral medulla

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12
Q

What are some sensory inputs to the vomiting center?

A

ischaemia of heart
liver blood circulation
visual/vestibular motion sickness compression/psychogenic
pain

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13
Q

What is another word for vomiting?

A

Emesis

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14
Q

What are the 3 main anti-emetics?

A
  • muscarinic receptor antagonists
  • histamine receptor antagonists
  • dopamine D2 receptor antagonists
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15
Q

What are some examples of dopamine D2 receptor antagonists?

A
  • phenothiazines
  • metoclopramide
  • domperidone
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16
Q

What is hyoscine?

A

Muscarinic receptor antagonist
Blocks effects of acetylcholine in the brainstem/vestibular motor nuclei
For motion sickness
Cannot get through BBB to work directly on M3 in vomiting center

17
Q

What are the main histamine receptor antagonists?

A
  • diphenhydramine (crosses BBB so can act directly on muscarinic in vomiting centre, M2 receptor antagonist and H1 receptor antagonist in vestibular nuclei for motion sickness), given with Dramamine (counteracts drowsiness, motion sickness)
  • cyclizine (inhibits pre-ganglionic cholinergic activity again for motion sickness)
18
Q

What is the action of dopamine D2 receptor antagonists?

A

inhibit blood circulation from the liver to the area prostrema so it doesn’t act on nuclei

19
Q

What is metoclopramide?

A
  • dopamine D2 receptor antagonist
  • has 2 actions: anti-emetic by antagonising the dopamine receptors in the area of prostema so that cytotoxins from the blood from the liver cannot stimulate them -> not signalling to vomiting centre
  • 2nd action is that it stimulates gut motility
20
Q

When might metoclopramide be used?

A

anti-emetic: post operative care, gastritis/migraine

upper gut motility: gastro-oesophageal reflux, gastroparesis

21
Q

Where is the vomiting centre and area of prostema?

A

In the medulla oblangata

However area of prostrema is outside the BBB so more permeable to cytoxic agents (released by chemotherapy)

22
Q

What pathways feed into the vomiting centre?

A
  • CTZ (area of prostema) from chemicals in the gut travel in blood acting on dopamine receptor there(cytotoxins, poisons, damage)
  • motion sickness stimulates vestibular cochlear nerve which stimulates vestibular nuclei histamine-1 and muscarinic receptors -> CTZ -> vomiting centre
  • emotional response/smell bad/see bad detected by higher brain centre -> vomiting centre
  • enterochromaffin cells release serotonin in response to cytotoxic agents which stimulates 5HT3 receptors on bagal afferent endings -> vagus nerve brings this to the NTS -> vomiting centre
23
Q

What receptors are in the vomiting centre and the area of prostema?

A

VC - Muscarinic receptors

AOP - dopamine and serotonin

24
Q

Where are the vestibular nuclei?

A

In the pons of the brainstem

25
Q

What is a cannabinoid?

A

Can stop vomiting but not in severe cases
Work directly on CB1 receptors in brain
Treat mild
side effect limited

26
Q

What is the role of corticosteroids?

A

Dexamethasone

  • anti-inflammatory
  • increase effectiveness of other anti-emetics but also can give alone for some effect
  • can increase appetite
  • anti-nausea effects
27
Q

What should you give in severe emesis?

A

5-HT3 receptor antagonist
NK1 receptor antagonist
dexamethasone (corticosteroid)
all together

28
Q

What is the difference between partial and total bowel obstruction?

A

Partial - GI propulsion stimulated

Total - emesis, pain and retropropulsion

29
Q

How would you treat bowel obstruction?

A

Partial -> cytotoxins to the area of prostrema due to obstruction, so give metoclopramide (DT antagonist)
Total -> reduce inflammation (dexamethasone which is a corticosteroid) and reduce fluid build up in the lumen (somatostatin antagonist with NG tube)