S1: Nausea, Vomiting and Pain Flashcards

1
Q

What is nausea?

A

Nausea is a sensation

  • it is personal and self reported.
  • associated with physiological changes
  • unpleasant
  • triggers aversion which is a feeling of repugnance towards something with a desire to avoid
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2
Q

What is vomiting?

A

Vomiting is a physical act

  • it expels content of the upper GI tract via the mouth
  • it is forceful
  • it is a complex, coordinated reflective event
  • associated with a sensation of relief
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3
Q

What is the medical name for vomiting?

A

Emesis

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4
Q

Is nausea produced by the same stimuli as vomiting?

A

Yes

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5
Q

Nausea is recognised as a prodrome. What does this mean?

A

Prodrome is a warning symptom

Nausea is therefore a warning symptom of vomiting

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6
Q

List some causes of nausea and vomiting

A
Poisoning 
Gastroenteritis
Excessive alcohol
Pregnancy
Excessive eating
Travel sickness
Metabolic disturbances
Drugs
GI disease
Emotional upset
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7
Q

What is the benefit to vomiting?

A

It acts as protection against ingested toxins

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8
Q

What is the first defence against ingested toxins?

A

Taste and smell

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9
Q

How does our body protect us from toxins - especially in children?

A

Children are wary of new flavours and we have a built in dislike of bitter flavours.
Children also learn from elders and aversion hardwired this knowledge

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10
Q

What happens when our body creates incorrect associations to stimulus?

A

People can feel nausea and vomit at normal stimuli e.g. seafood

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11
Q

Explain how our gastric and upper GI afferent fibres help prevent ingested toxins

A

They expel potentially harmful agents before they have much chance to be absorbed in the body

Afferents are associated with chemoreceptive cells embedded in the gut wall

They respond to contaminants in blood

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12
Q

Where is the chemoreceptors trigger zone?

A

The area postrema in the brain stem (medulla)

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13
Q

Explain the chemoreceptor trigger zone

A

The chemoreceptor trigger zone is found in the brain stem (medulla)

The blood brain barrier is leaky and chemoreceptors can detect toxins in the blood

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14
Q

What is the vestibular system?

A

It is the organ of balance and potential trigger of emesis.
It may be activated by toxins in the blood or disequilibrium resulting in poisoning

Poisoning is thought to produce aberrant activity in vestibular neural pathways

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15
Q

What is the disadvantage with the vestibular system?

A

It triggers nausea and vomiting in response to unnatural motion e.g. on boat as it assumes that poison may have been ingested

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16
Q

Where is the nucleus tractus solitaries found and what’s its role?

A

It is located in the medulla of the brain stem and integrates cardiac, respiratory and gastrointestinal functions.

The NTS is the coordinator/regulator

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17
Q

Where do the abdominal afferents travel to?

A

The nucleus tractus solitaries by vagus nerve

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18
Q

Where are visceral afferent receptors found?

A

They are found in the fundus and duodenum

19
Q

Examples of visceral afferents that can trigger nausea and vomiting

A

Toxins
Irritants
Distension

20
Q

Briefly explain the pathway the visceral afferents take

A

The afferents take information via the vagus nerve (parasympathetic system)

21
Q

Where do fibres from the vestibular system travel?

A

They travel to the NTS (nucleus tractus solitarius) after detecting toxins or disequilibrium

22
Q

What do the fibres from the area postrema do?

A

They detect toxins in the blood

23
Q

What reduces area postrema and abdominal afferent signalling to NTS?

A

5-HT3 antagonist

It reduces nausea and vomiting

24
Q

Name 3 mechanisms of nausea

A
  1. Reduced gut motility (mixing and peristalsis) prevents toxins from being carried further through the system
  2. Proximal stomach relaxes to receive additional contents
  3. Giant retrograde contraction occurs, that sweeps up from the midsmall intestine and returns upper intestinal contents to stomach
25
Q

Name the structure that the NTS signals to for nausea

A

Frontal cortex

26
Q

What happens when NTS signals the hypothalamus?

A

The hypothalamus will release ADH which helps conserve water so less is lost during vomiting

27
Q

What happens when NTS signals the the frontal cortex?

A

Nausea

28
Q

What happens when NTS signals the autonomic efferents?

A
  1. Changes in gut motility

2. Salivation, vasoconstriction in GIT and skin, sweating

29
Q

Name the 2 structures that the NTS signals to for vomiting

A

Autonomic efferents

Hypothalamus

30
Q

Mechanism of vomiting

A
  1. Vomiting is going to occur, typically there will be RETCHING (dry heaves). These are coordinated contractions of the abdominal muscles by phrenic nerve. Waves of Hugh pressure in the abdomen compress the stomach but the anti reflux barriers (oesophageal sphincters and crural diaphragm) are intact, so there is no expulsion
  2. Then is emesis. The oesophageal sphincters and crural diaphragm relax and further waves of contractions of the stomach expel stomach contents
31
Q

How is the mechanism of vomiting different to nausea

A

In vomiting, NTS will use somatic and autonomic efferents to cause changes in gut motility and expulsion as well as salivation , vasoconstriction and sweating

32
Q

What nerve innervates the abdominal muscle?

A

Somatic nerve

33
Q

What nerve innervates the diaphragm?

A

Phrenic nerve

34
Q

Name the 2 anti-reflux barriers

A

Oesophageal sphincters and crural diaphragm

35
Q

What are sensory receptors for pain called?

A

Nociceptors

36
Q

Name the 2 nociceptors in the GI

A

Arc stretch receptors

Chemoreceptors

37
Q

Name some noxious stimuli

A
Distension 
Inflammation 
Ischaemia
Traumatic injury 
Muscle spasm
38
Q

Are most GI nociceptors afferent axons sympathetic or parasympathetic?

A

They mostly run in the sympathetic nerves (the greater and lesser splanchnic nerves)

39
Q

Explain distension of the stomach

A

Wide dynamic range cell fires infrequent AP when gut is not very distended.
The AP frequency increases as distension increases.

Nociceptors specific cells only start to fire when the amount of distension becomes grossly abnormal so signal to the brain. The brain produces signals felt as pain.

40
Q

Nociceptors respond to inflammatory mediators and produce some of their own.

What happens to the GI if cell receptors become hypersensitive due to inflammation?

A

Normal levels of inflammation and normal gut distension will feel painful

The wide dynamic range cell will fire more frequently at low levels of distension as will the nociceptors specific cell

41
Q

Characteristics of visceral pain

A
  1. Diffuse and poorly localised
  2. Pain is generally referred to regions of the body wall
  3. Each organ has a characteristic pattern of referral
42
Q

Explain how visceral pain is diffuse and poorly localised

A

There are relatively small number of afferents and there is diffuse innervation of organs.

The pathways are divergent

43
Q

Explain how visceral pain is often referred to regions of the body wall

A

This is due to viscera-somatic convergence. This means that visceral afferents travel with somatic nerves which innervate a similar body wall

44
Q

Explain how each organ has a characteristic pattern of referral for visceral pain

A

Pain is referred to the dermatomes marching the embryonic origin of the organ.

The site and nature may change as well as other tissues that are affected