Symptoms of GI Disease: Nausea & Vomiting Flashcards
What is nausea?
Nausea is a sensation personal, self reported associated with physiological changes unpleasant triggers aversion
What is vomiting?
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
Describe the relationship between Nausea and vomiting
Nausea is produced by the same stimuli as vomiting
Nausea is generally a prodrome (ie premonitory symptom) of vomiting
BUT nausea may clear up without triggering vomiting
AND vomiting can occur without prior nausea
What are the causes of nausea and vomiting (emetic stimulus)?
GI infection (eg norovirus) Pregnancy Travel sickness Other people being sick Metabolic disturbance Drugs (e.g. morphine chemotherapy) Raised intracranial pressure GI disease (e.g. gastritis, kidney stones) Emotional upset
Describe when vomiting and nausea is advantageous
Poisoning (eg contaminated food, poisonous plants, chemical agents)
Obstruction
Excessive alcohol
Excessive eating
How are we protected against ingested toxins?
Taste and smell can potentially prevent ingestion
we have a built-in dislike of bitter flavours
children are wary of novel flavours; we learn from our elders what is safe
Explain how gastric and GI afferents help expel ingested toxins
can potentially expel harmful agents before they have (much) chance to be absorbed
associated with chemoreceptive cells that respond to:
irritants
inflammatory mediators
bacterial (and some other) toxins
What effect do non-ingetsed toxins have?
non-ingested toxins will have the same effect as ingested toxins – eg chemotherapy, systemic infection, metabolic disturbance, iv
What is the chemoreceptor trigger zone
The chemoreceptor trigger zone is the area postrema in the brainstem responds to circulating poisons
blood-brain barrier has to be “leaky”
What is the blood brain barrier?
Within the brain, capillaries have endothelial walls with tight junctions, so substances have to be carried into / out of brain tissue - protection
In area postrema blood brain barrier is leaky so substances from plasma can cross into the tissue to trigger nausea
What is the vestibular system?
This is 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 Nausea & Vomiting in response to un-natural motion
How do we prevent ingesting toxins in the future?
If we survive a mistake we avoid repeating it (unpleasantness reinforces learning)
aversion may hard-wire avoidance
But can create incorrect associations
What are our anti-poison defences co ordinated by?
Our anti-poison defences are coordinated by the nucleus tractus solitarius (NTS), found in the medulla of the brainstem
What are the other functions of the NTS?
It also integrates cardiac, respiratory and gastrointestinal functions
What are the 4 different types of ‘warning’ inputs received by the NTS?
- Visceral Afferents
- Area Postrema
- Viestibular system
- Higher Centres
Describe how the visceral afferents cause a response to toxins
axons run through parasympathetic nerves, Vagus → directly into brainstem associated with receptors that respond to toxins, irritants, distension etc.
Where is the area postrema located?
Chemoreceptive zone (no blood-brain barrier) in medulla, below cerebellum and very close to foramen magnum
What is the foramen magnum?
the hole in the base of the skull through which the spinal cord passes
Explain how raised intercranial pressure causes nausea and vomiting
Raised intracranial pressure causes nausea and vomiting, as the increased pressure can only be relieved by pressing brainstem down, through foramen magnum - area postrema compressed
Describe the vestibular system
Organ of balance, inner ear
Toxins in blood (disrupting vestibular receptors)
Triggers motion sickness
How does the NTS cause Nausea?
NTS signals hypothalamus to release ADH to conserve fluid, increases sympathetic activity and decreased Parasympathetic activity to upper GI tract to stop gastric emptying - paleness & sweating
How does the NTS cause vomiting?
NTS coordinates muscles involved to increase pressure on abdomen and release of anti-reflux barriers to prevent reflux of gastric contents up oesophagus
Explain the mechanism of the vagus nerve to produce vomiting and nausea
- Reduced mixing & peristalsis due to decreased Parasympathetic activity
- Relaxation of the Proximal stomach
- Giant retrograde contraction
Explain how reduced peristalsis due to decreased p/s activity causes nausea and vomiting
Reduced mixing & peristalsis due to decreased Parasympathetic activity
Prevents toxins from being carried further through the system
Stop processing food and stop pushing it down
Explain how relaxation of the stomach causes nausea and vomiting
Proximal stomach relaxes
Prepares stomach to receive additional contents
Relaxed muscle = very distensible
How does giant retrograde contraction cause vomiting and nausea?
Giant retrograde contraction
(reverse of peristalsis) squeezing mechanism to bring food back up
Sweeps up mid-small intestine
Returns upper intestinal contents to stomach
How do the phrenic nerves cause vomiting and nausea?
- retching (dry heaves)
5. Vomiting (emesis)
Explain how retching causes nausea and vomiting
Retching (dry heaves)
coordinated contractions of abdominal muscles and diaphragm
waves of high pressure in abdomen
compresses stomach but anti-reflux barriers intact so no expulsion
Explain how the phrenic nerves cause vomiting
Vomiting (emesis)
oesophageal sphincters and crural diaphragm relax
further waves of contraction expel stomach contents
How is visceral pain detected?
“Pain” receptors respond to “noxious” stimuli, and are called nociceptors They respond to: distension inflammation muscle spasm resulting in pain
Describe the innervation resulting in pain
Nociceptor receptors associated with axons running through sympathetic nerves into thoracic segments
Describe the normal gut distension
these are the normal levels of distension seen during peristalsis / mixing movements. We are unaware of this occurring
Explain pathological distension
← Pathological distention will stretch the gut wall to a potentially damaging degree, producing pain.
How is pain produced during pathological gut distension?
Nociceptive fibres are present in the gut wall that respond to the stretching of the gut wall. The more stretched the gut wall = the more action potentials produced by the nociceptive fibres per second
The brain only produces visceral pain sensation in response to high frequency of action potentials firing
What induces inflammation in the gut?
Nociceptors respond to inflammatory mediators, as well as stretching of the gut wall: Injury Toxins Irritants Infection Autoimmunity
How do inflammatory mediators affect nociceptive fibres?
Inflammatory mediators will depolarise nociceptors, make them fire action potentials, sensitising them to being stretched to produce a higher level of firing
When does chronic sensitisation of visceral pain pathways occur?
In GI disease
Explain how inflammatory bowel disease is contributed towards by nociceptor fibres
Nociceptors respond to inflammatory mediators but also release pro-inflammatory chemicals when depolarised (e.g substance P)
Causes Positive feedback loop between inflammation and the release of pro-inflammatory chemicals from nociceptors which may contribute to inflammatory bowel disease
How is chronic pain caused by nociceptive fibres?
The pain pathways can become potentiated so that normal signals from nociceptors are magnified, and can become self sustaining leading to chronic pain with no obvious cause.
What is somatic pain?
precisely localised (somatosensory cortex → T3 somatic nociceptor activated to specific area) e.g. if stabbed with pin in chest: Nociceptive fibre fires axon to T3 T3 somatic pathway leads to somatosensory cortex, where pain is specified on map
What is visceral pain?
is diffuse & variable, (viscerosomatic convergence, C2 - T4 somatosensory → oesophagul & somatic nociceptive receptors)
Describe how visceral pain is felt
location of pain reported following activation of oesophagul nociceptors to T3 which also follows somatic pathway to produce pain in chest wall despite initiating in oesophagus as oesophagus not represented on somatosensory cortex
Explain why visceral pain is poorly localised?
Often diffuse and poorly localised
relatively small number of afferents
imprecise wiring
Why is visceral pain referred to regions rather than precisely located?
Generally “referred” to regions of the body wall due to viscerosomatic convergence (C2 - T4)
Explain how visceral pain is referred to different areas of the body
Each organ has a characteristic pattern of referral
Afferents synapse in segments matching the embryonic origin of each organ
May evolve as other tissues are affected
Pain is felt in the dermatome belonging to the segment of origin of the organ
What are dermatomes?
Regions of the body sending somatic afferents to each spinal cord segments
Each visceral organ sends input to spinal cord segment correlating with the somite the organ developed from in the embryonic state
