Symptoms of GI Disease: Nausea, Vomiting and Pain Flashcards
What is the difference between nausea and vomiting?
NAUSEA is a SENSATION:
- personal, self-reported
- associated with physiological changes (pale, sweaty)
- unpleasant
- triggers aversion to certain foods
VOMITING (EMESIS) is a PHYSICAL ACT:
- expels contents of the upper GI tract via the mouth
- forceful (cf regurgitation, reflux)
- complex, coordinated reflexive events
- associated with the sensation of relief
There could be exceptions:
- nausea may clear up without triggering vomiting
- vomiting may occur without prior nausea
List some things that could cause nausea and vomiting?
- poisoning (contaminated food)
- GI infection
- pregnancy
- excessive alcohol
- travel sickness
- metabolic disturbance
- drugs
- raised intracranial pressure
- obstruction
- GI disease
- emotional upset
- other people being sick
List some protections our bodies have against ingested toxins, and briefly expand on each one.
1) Taste and smell:
- can potentially prevent indigestion
- we have a built-in dislike for bitter flavours
- children are wary of novel flavours
- we learn from our elders what is safe to eat
2) Gastric and upper GI afferents:
- can potentially expel harmful agents before they have much chance to be absorbed
- associated with chemoreceptors that respond to: irritants, inflammatory mediators and bacterial (among other) toxins
[however, non-ingested toxins will have the same effect, eg. chemotherapy, systemic infection, etc.)
3) Chemoreceptor trigger zone:
- the area postrema in the brainstem
- because the blood-brain barrier is leaky, chemoreceptors can detect toxins in the blood
4) Vestibular system:
- part of the ear that detects movements of the head and direction of gravity
- the organ of balance, but also a potent trigger for emesis
- poisoning is thought to produce aberrant activity in vestibular neural pathways
5) Prevention of ingestion - learning and aversion
- if we survive a mistake we avoid repeating it (unpleasantness reinforces learning)
- aversion may hardwire avoidance
List 4 things that will feed into and trigger nausea and vomiting.
1) visceral afferents (respond to toxins, irritants and distentions)
2) area postrema (responds to toxins in the blood)
3) vestibular system (responds to toxins in the blood, disrupting vestibular receptors)
4) higher centres of the brain (responds to aversive and emotional stimuli)
All these signals are sent to the brainstem (the nucleus tractus solitarius, also the integrating centre for the heat, respiratory and GI systems)
List the mechanisms of nausea.
1) Reduced mixing and peristalsis
- prevents toxins from being carried further through the system
2) Proximal stomach relaxes
- prepares stomach to receive additional contents
3) Giant retrograde motion
- sweeps up from the mid-intestine
- returns upper intestinal contents to stomach
List the mechanisms of vomiting.
4) Retching (dry heaves)
- coordinated contractions of abdominal muscles and the diaphragm
- waves of high pressure on the abdomen
- compresses stomach but anti-reflux barriers are intact so there’s no expulsion
5) Vomiting (emesis)
- oesophageal sphincters and the crural diaphragm relax
- further waves of contraction expel the stomach contents
Describe pain receptors.
Pain receptors respond to 'noxious' stimuli and are called nociceptors. They respond to: - distention - inflammation - muscle spasms
With distention, the nociceptors respond to the stretching of the wall, with the further stretching being potentially damaging. The higher the distention, the higher the frequency firing.
Different factors can cause inflammation (eg. injury, irritants, toxins, infection, autoimmunity). The inflammation triggers activity in the nociceptor, causing pain.
But, there is some positive feedback because the nociceptor releases inflammatory mediators in response (histamine?).
Describe nociceptor pathways.
Nociceptor fibres run along with sympathetic nerves and run into the spinal cord via splanchnic nerves.
Describe how chronic sensitisation of visceral pain pathways is thought to occur in GI disease.
Positive feedback between inflammation and the release of pro-inflammatory chemicals from nociceptors may contribute to inflammatory bowel disease, and may also maintain inflammation in IBD.
The pain pathways can become potentiated, so that normal signals from nociceptors are magnified, leading to chronic pain with no obvious cause.
How is visceral pain different from somatic pain?
Somatic pain is very precisely located, as it has very ordered pathways, allowing for the pinpointing of the location of the pain.
Visceral pain isn’t precisely located.
What is the basis of viscero-somatic convergence?
The visceral pathways piggyback onto the somatic pathways, meaning that if there is pain in the internal organs, it will be felt in a precise location on the surface of the body.
This is also known as referred pain.
What are some characteristics of visceral pain?
1) It often diffuses and it poorly localised.
- has a relatively small number of afferents
- imprecise wiring
2) It is generally ‘referred’ to regions of the body wall.
- due to viscero-somatic convergence
3) Each organ has a characteristic pattern of referral.
- a dermatome is an area of skin supplied by a single spinal nerve
- initially, the pain is sent to dermatomes matching the embryonic origin of the organ
- however, this may evolve as other tissues are affected
