Symptoms of GI disease Flashcards

1
Q

What is the difference between nausea and vomiting?

A
Personal, self reported 
Associated with physiological changes
Unpleasant
Triggers aversion 
Aversion- a strong dislike or disinclination
Vomiting (emesis) is a physical act:
Expels contents of upper GI tract via mouth
Forceful (cf regurgitation, reflux)
Complex, co-ordinated reflexive events 
Associated with sensation of relief
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the difference between nausea and vomiting?

A
Personal, self reported 
Associated with physiological changes
Unpleasant
Triggers aversion 
Aversion- a strong dislike or disinclination
Vomiting (emesis) is a physical act:
Expels contents of upper GI tract via mouth
Forceful (cf regurgitation, reflux)
Complex, co-ordinated reflexive events 
Associated with sensation of relief
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes nausea and vomiting?

A
GI infection (e.g. norovirus)
Excessive alcohol
Pregnancy
Excessive eating 
Travel sickness
Metabolic disturbance
Other people being sick
i.v. drugs (e.g. morphine, chemotherapy)
Raised intracranial pressure
GI disease (e.g. gastritis)
Obstruction
Emotional upset
Poisoning (e.g. contaminated food, poisonous plants, chemical agents)
Kirusikan in a nurse's outfit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do gastric and upper GI afferents influence nausea and vomiting?

A

Can potentially expel harmful agents before they have (much) chance to be absorbed
Associated with chemoreceptive cells that respond to:
Naturally occurring toxins
Damaging chemicals
Inflammatory mediators
BUT non-ingested toxins will have the same effect- e.g. chemotherapy, systemic infection, metabolic disturbance
Chemoreceptor trigger zone:
The area postrema in the brainstem
Blood-brain barrier is “leaky”
Chemoreceptors that can detect toxins in the blood
BUT non-ingested toxins will have the same effect- e.g. chemotherapy, systemic infection, metabolic disturbance
Vestibular system:
The organ of balance, but also a potent trigger for emesis
Poisoning is thought to produce aberrant activity in vestibular neural pathways
BUT also triggers N & V in response to un-natural motion
Protection against ingested toxins
Prevention of ingestion- learning and aversion:
If we survive a mistake we avoid repeating it (unpleasantness reinforces learning)
Aversion may hard-wire avoidance
BUT can create incorrect association

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the mechanisms of nausea and vomiting?

A

Our anti-poison defences are co-ordinated by the nucleus tractus solitarius (NTS)
Found in the medulla of the brainstem
It also integrates cardiac, respiratory and gastrointestinal functions
It receives four different types of “warning” inputs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the visceral afferents?

A

The afferents are the sensory nerves that run up into the brainstem
They get their input from chemoreceptor cells that are found in the wall of the stomach and the duodenum
These chemoreceptor cells are responsive to toxins, irritants, inflammation and (some abnormal distension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the area postrema?

A

Aka chemoreceptive tigger zone (CTZ)
It is found in the brain stem very close to the NTS
There is no blood brain barrier, so brain cells here can respond to toxins in the blood
If you have raised intercranial pressure the brain swells and the extra volume tends to gets squeezed out of the foramen magnum with the area postrema and NTS getting pushed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the vestibular system?

A

Organ of balance, inner ear

Its sends its axons through the with cranial nerve to the NTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do higher centres influence vomiting and/or nausea?

A

Things that your social groups find disgusting
Other people in your group being sick
Things that made you sick in the past

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does the NTS trigger nausea and vomiting?

A

Inputs from the higher centres produces nausea
NTS projecting to the hypothalamus increases ADH hormone to save water (if you’re going to vomit you will lose a lot of fluid)
NTS to autonomic efferent which increases salivation, to give a good fluid lining to the mucosa, and vasoconstriction of the GIT to reduce the absorbance of substances into the bloodstream
The autonomic efferents also changes the gut motility so peristalsis won’t carry that food further down to be absorbed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the steps that are taken for the NTS to trigger nausea and vomiting?

A
  1. Reduced mixing and peristalsis- prevents toxins from being carried further through the system (vagus nerve)
    1. Proximal stomach relaxes- prepares stomach to receive additional contents (vagus nerve)
    2. Giant retrograde- sweeps up from mid-small intestine, returns upper intestinal contents to stomach (vagus nerve)
    3. Retching (dry heaves):
      Co-ordinated contractions of abdominal muscles and diaphragm
      Waves of high pressure in abdomen (phrenic nerve)
      Compresses stomach but anti-reflux barriers intact so no expulsion
    4. Vomiting (emesis)
      Oesophageal sphincter and crural diaphragm relax
      Further waves of contraction expel stomach contents (Somatic nerves)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What causes nausea and vomiting?

A
GI infection (e.g. norovirus)
Excessive alcohol
Pregnancy
Excessive eating 
Travel sickness
Metabolic disturbance
Other people being sick
i.v. drugs (e.g. morphine, chemotherapy)
Raised intracranial pressure
GI disease (e.g. gastritis)
Obstruction
Emotional upset
Poisoning (e.g. contaminated food, poisonous plants, chemical agents)
Kirusikan in a nurse's outfit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do gastric and upper GI afferents influence nausea and vomiting?

A

Can potentially expel harmful agents before they have (much) chance to be absorbed
Associated with chemoreceptive cells that respond to:
Naturally occurring toxins
Damaging chemicals
Inflammatory mediators
BUT non-ingested toxins will have the same effect- e.g. chemotherapy, systemic infection, metabolic disturbance
Chemoreceptor trigger zone:
The area postrema in the brainstem
Blood-brain barrier is “leaky”
Chemoreceptors that can detect toxins in the blood
BUT non-ingested toxins will have the same effect- e.g. chemotherapy, systemic infection, metabolic disturbance
Vestibular system:
The organ of balance, but also a potent trigger for emesis
Poisoning is thought to produce aberrant activity in vestibular neural pathways
BUT also triggers N & V in response to un-natural motion
Protection against ingested toxins
Prevention of ingestion- learning and aversion:
If we survive a mistake we avoid repeating it (unpleasantness reinforces learning)
Aversion may hard-wire avoidance
BUT can create incorrect association

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the mechanisms of nausea and vomiting?

A

Our anti-poison defences are co-ordinated by the nucleus tractus solitarius (NTS)
Found in the medulla of the brainstem
It also integrates cardiac, respiratory and gastrointestinal functions
It receives four different types of “warning” inputs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the visceral afferents?

A

The afferents are the sensory nerves that run up into the brainstem
They get their input from chemoreceptor cells that are found in the wall of the stomach and the duodenum
These chemoreceptor cells are responsive to toxins, irritants, inflammation and (some abnormal distension)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the area postrema?

A

Aka chemoreceptive tigger zone (CTZ)
It is found in the brain stem very close to the NTS
There is no blood brain barrier, so brain cells here can respond to toxins in the blood
If you have raised intercranial pressure the brain swells and the extra volume tends to gets squeezed out of the foramen magnum with the area postrema and NTS getting pushed

17
Q

What is the vestibular system?

A

Organ of balance, inner ear

Its sends its axons through the with cranial nerve to the NTS

18
Q

How do higher centres influence vomiting and/or nausea?

A

Things that your social groups find disgusting
Other people in your group being sick
Things that made you sick in the past

19
Q

What are the characteristics of visceral pain?

A

Generally “referred” to regions of the body wall
Due to viscerosomatic convergence
Often diffuse and poorly localised
Relatively small number of afferent
Imprecise wiring
Each organ has a characteristic pattern of referral
Initially to dermatomes matching the embryonic origin of the organ
But may evolve as other tissues are affected

20
Q

What are the steps that are taken for the NTS to trigger nausea and vomiting?

A
  1. Reduced mixing and peristalsis- prevents toxins from being carried further through the system (vagus nerve)
    1. Proximal stomach relaxes- prepares stomach to receive additional contents (vagus nerve)
    2. Giant retrograde- sweeps up from mid-small intestine, returns upper intestinal contents to stomach (vagus nerve)
    3. Retching (dry heaves):
      Co-ordinated contractions of abdominal muscles and diaphragm
      Waves of high pressure in abdomen (phrenic nerve)
      Compresses stomach but anti-reflux barriers intact so no expulsion
    4. Vomiting (emesis)
      Oesophageal sphincter and crural diaphragm relax
      Further waves of contraction expel stomach contents (Somatic nerves)
21
Q

What are the receptors for visceral pain?

A
Pain receptors respond to "noxious" stimuli, and are called "nociceptors" and respond with pain
They respond to:
Distension
Inflammation
Muscle spasm
NB they don’t respond to "pain"
22
Q

How does gut distension trigger the receptors for visceral pain?

A

The first three are perfectly normal so you wouldn’t feel it
The last 2 would happen if you get like an obstruction of chyme and would cause pain
The sensory afferents innervate the wall of the gut and produce action potentials
The frequency of firing increases as distention increases
The normal firing is used to give feedback to the neural network that controls the movement of the gut
Once it gets to the higher levels the brain detects this as damage to the gut tissue

23
Q

What do nociceptors respond to?

A
Injury 
Irritants
Toxins
Infection
Autoimmunity
24
Q

How is the chronic sensation of visceral pain pathways thought to occur in GI disease?

A

Chronic sensation of visceral pain pathways is thought to occur in GI disease
Inflammation depolarises these nociceptors
When depolarised they release pro-inflammatory chemicals
This positive feedback increase responses which can in turn synapses
Leading to potentially self-sustaining activity that persists beyond the original cause

25
Q

How is somatic pain localised?

A

Somatic pain is very precisely localised (e.g. stabbing with a pin)
That will activate somatic nociceptors and they will project to the spinal cord entering it as T3 and synapse with the pathway that carries the information to the somatosensory cortex where there is a map of the body called the somatosensory homunculus (each region relates to a VERY specific region of the body and info gets transmitted to that specific region)

26
Q

What is viscerosomatic convergence?

A

In this case used an oesophageal nociceptor
This oesophageal nociceptor doesn’t have a private pathway up to an oesophageal part of the somatosensory cortex map
Instead it piggyback onto the somatic pathway
It sends its axon through the third thoracic spinal nerve and its synapses with the same pathway as the somatic
Therefore it will produce a pain sensation at the same point
So an oesophageal nociceptor will produce chest pain and this mechanism is called referred pain
Sometimes they make very messy connections, so might go through T2-T4, producing pain in a wider region of the chest and even in the arms
This is known as viscerosomatic convergence

27
Q

How is the pattern of referral organised? (+e)

A

Afferents synapse in segments matching the embryonic origin of organ
The large intestine gets its innervation from T10-T12 and if nociceptors activate in the large intestine they will produce referred pain in that region
Referred pain relates to the positioning and patterns of the visceral organs
But the abdomen is packed with organs
So if you have inflammation in one structure it might spread in rather random fashion to other neighbouring structures and produce, as time goes by, a change in the pattern of referred pain

28
Q

How can the pattern of referral evolve?

A

Infections in the gall bladder often spread to the parietal peritoneum and diaphragm
They get their innervation from the cervical segments (C3-5) via the phrenic nerve
So as the gallbladder inflammation gets worse they will start to feel pain in their right shoulder

29
Q

What are the characteristics of visceral pain?

A

Generally “referred” to regions of the body wall
Due to viscero-somatic convergence
Often diffuse and poorly localised
Relatively small number of afferent
Imprecise wiring
Each organ has a characteristic pattern of referral
Initially to dermatomes matching the embryonic origin of the organ
But may evolve as other tissues are affected