Nausea, Vomiting, Pain Flashcards

1
Q

What’s nausea?

A

Sensation:

personal, self reported, associated w physiological changes, triggers aversion

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2
Q

What’s vomiting (emesis)?

A

Physical act:

expels contents of upper GI via cf regurgitation+ reflux, coordinated reflexive events,associated w sensation of relief

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3
Q

What’s the relationship between nausea + emesis?

A

Nausea is produced by the same stimuli as vomiting, generally a prodrome (ie premonitory symptom) of vomiting, can clear up w/o vomiting
Vomiting can occur w/o nausea

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4
Q

How taste + smell protects against ingested toxins?

A

built-in dislike of bitter, children wary of novel flavours,

learn from elders what’s safe

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5
Q

How gastric+upper GI afferents protects against ingested toxins?

A

Expel harmful agents before absorbed associated w chemoreceptive cells that respond to: irritants,🐛toxins, inflammatory mediators

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6
Q

How Chemoreceptor Trigger Zone protects against ingested toxins?

A

the area postrema in the brainstem, BBB ‘s “leaky”, chemoreceptors detects toxins in the blood

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7
Q

How vestibular system protects against ingested toxins?

A

organ of balance, potent trigger for emesis poisoning produces aberrant activity in vestibular neural pathways

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8
Q

☹ of vestibular system?

A

vestibular malfunction triggers N+V

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9
Q

☹ of gastric+upper GI afferents, Chemoreceptor Trigger Zone?

A

no effect on non-ingested toxins eg chemotherapy, systemic infection, metabolic disturbance

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10
Q

How learning + aversion protects against ingested toxins?

A

after mistake we avoid repeating it ∵unpleasantness reinforces learning
aversion hard-wires avoidance

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11
Q

☹ learning + aversion

A

create incorrect associations

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12
Q

What’s anti-poison defense coordinated by?

A

Nucleus Tractus Solitarius NTS -in the medulla, integrates ❤, respiratory and GI functions

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13
Q

What inputs does NTS receive?

A

addominal afferents
area posterma
vestibular system
higher centres

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14
Q

What are abdominal afferents?

A

involve upper GI tract signals from vagus: toxins, irritants, distention

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15
Q

What are the signals from area posterma?

A

located on 4th base ventricle of the brain-toxins detected here sends signals

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16
Q

What are the signals from vestibular system?

A

vestibular receptors disrupted by toxins∴imbalance in the body sends signals

17
Q

What are the signals from higher centres?

A

processes world +👁emesis stimuli-visual, emotional,aversive–>anticipatory N+V (eg anticipating chemotherapy)sends signals

18
Q

What 💊 ↓N+V?

A

5HT3 antagonists ∵ area postrema + abdomen have 5HT3 receptors

19
Q

How’s N caused?

A

NTS sends signals to:
frontal cortex + some limbic area
hypothalamus
organs via autonomic efferents

20
Q

How’s N sensation caused

A

NTS sends signals to frontal cortex + some limbic area

21
Q

What happens when NTS sends signals to hypothalamus?

A

⇶ADH- retain H2O as fluid will be lost while vomiting

22
Q

What happens when NTS sends signals to organs via autonomic efferents?

A
  • ↓gut motility -↓substance passes
  • vasoconstriction of gut-↓ toxin absorption
  • sweating+salivation
23
Q

Mechanism of N via vagus?

A
  • ↓Mix+peristalsis prevents toxins carried further
  • Proximal stomach relaxes-prepares stomach to receive extra contents
  • Giant retrograde contraction-sweeps up from mid-small intestine returning upper intestinal contents to stomach
24
Q

Mechanism of V via phrenic + somatic nerves?

A
  • Retching/dry heaves-coordinated contractions of abdominal muscles+diaphragm –>🌊of high p in abdomen –> compresses stomach but anti-reflux barriers intact ∴ no expulsion
  • Emesis-oesophageal sphincters + crural diaphragm relax, ↑🌊of contraction expels contents
25
Q

Situations where vomiting occurs?

A
  • Poison- remove harmful substances detected by chemoreceptors
  • Gastroenteritis (noravirus)- remove viral toxins detected by chemoreceptors
  • ⇑🥤- poisonous,detected by chemoreceptors
  • 🤰- chemicals + hormones produced stimulates chemoreceptors
  • Emotional upset-via higher centers
  • ⇑eating-evolutionary so man could re-eat undigested matter
  • GI diseases-so food doesn’t go to obstructed area
  • ↑ intracranial p-presses on NTS
  • 💊-poisonous detected by chemoreceptors
  • Metabolic disturbance-others 🤮,precautionary measure preventing poisoning from food being eaten by the group
  • ✈🤮-stimulates vestibular system
26
Q

Where are visceral afferents?

A
Greater splanchnic (sympathetic) nerves  ~T1-9
Lesser splanchnic (sympathetic) nerves  ~T10-12
27
Q

Where’s visceral input?

A

Nociceptors= respond to ‘noxious’ stimuli eg distension, inflammation,muscle spasm

28
Q

How do nociceptors respond to inflammatory?

A

responds to inflammatory mediators + stretching of the gut wall

29
Q

What do nociceptors do when depolarised?

A

⇶ pro-inflammatory chemicals–>+ve feedback loop - contributes to inflammatory bowel disease

30
Q

Why chronic pain w/o main cause?

A

Abnormal activity potentiates synapses –>↑ nociceptor signals –>self-sustaining

31
Q

Diff between somatic vs visceral pain?

A
  • precisely localised

- referred to body surface, location of pain reported following activation of oesophageal nociceptors imprecise

32
Q

What’s viscero-somatic convergence?

A

visceral pathways ‘piggy back’ on somatic pathways + 🧠interprets the origin of pain like somatic

33
Q

Dermatomes?

A

Afferents synapse in segments matches embryonic origin of each organ∴ nociceptor inputs can cause pain at places that are nowhere near the organ

34
Q

Features of visceral pain?

A

-“referred” to regions of the body wall ∵ viscero-somatic convergence
-Diffuse+poorly localised ∵ few afferents+imprecise wiring
-Each organ has a characteristic pattern of referral∵
dermatomes matches embryonic origin of the organ but may evolve as other tissues affected