Symptoms of GI Disease Flashcards
Define nausea
- personal, self-reported
- associated with physiological changes (pale, sweaty)
- Nausea is a SENSATION
Define vomiting (emesis)
- Expels contents of the upper GI tract via the mouth
- Forceful (regurgitation, reflux)
- Emesis is a PHYSICAL ACT
List some things that could cause nausea and vomiting. PART 1
- poisoning
- GI infection
- pregnancy
- excessive alcohol
- travel sickness
- metabolic disturbance
List some things that could cause nausea and vomiting. PART 2
- drugs
- emotional upset
- travel sickness
- metabolic disturbance
Outline the importance of taste and smell against ingested toxins.
- can potentially prevent indigestion
- we have a built-in dislike for bitter flavours
- children are naturally wary of novel flavours
Outline the importance of gastric and upper GI afferents against ingested toxins.
- can potentially expel harmful agents before they have much chance to be absorbed
- associated with chemoreceptors that respond to: irritants, inflammatory mediators and bacterial toxins
Outline the importance of the chemoreceptor trigger zone against ingested toxins
- the postrema in the brainstem
- Can detect toxins because the blood-brain barrier is leaky, chemoreceptors can detect toxins in the blood
Outline the importance of the vestibular system against ingested toxins
- part of the ear that detects movements of the head and direction of gravity
- trigger for emesis
- poisoning is thought to produce aberrant activity in vestibular neural pathways
Outline the importance of learning against ingested toxins
- if we survive a mistake we avoid repeating it
- aversion may hardwire avoidance
List 4 things that will feed into and trigger nausea and vomiting.
- visceral afferents (respond to toxins, irritants and distentions)
- area postrema (responds to toxins in the blood)
- vestibular system (responds to toxins in the blood, disrupting vestibular receptors)
- higher centres of the brain (responds to aversive and emotional stimuli)
Where are signals sent by the factors that trigger nausea and vomiting?
- To the brainstem i.e the NTS
- Integrating centre for the heat, respiratory and GI systems
List the mechanisms of nausea. PART 1
Reduced mixing and peristalsis - prevents toxins from being carried further through the system
Proximal stomach relaxes - prepares stomach to receive additional contents
List the mechanisms of nausea. PART 2
Giant retrograde motion - sweeps up from the mid-intestine and returns upper intestinal contents to stomach
List the mechanisms of vomiting. PART 1
Retching
- 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
List the mechanisms of vomiting. PART 2
Vomiting (emesis)
- oesophageal sphincters and the crural diaphragm relax
- further waves of contraction expel the stomach contents
What do pain receptors respond to?
Noxious stimuli
What are pain receptors commonly known as?
Nociceptors
What do nociceptors respond to?
- distention
- inflammation
- muscle spasms
What do nociceptors do upon distension?
- Nociceptors respond to the stretching of the wall, with the further stretching being potentially damaging.
- The higher the distention, the higher the frequency firing.
What factors can cause inflammation?
Injury, irritants, toxins, infection
How does a nociceptor respond upon occurrence of inflammation?
- Triggers additional nociceptor activity. RESULT - Pain
- Positive feedback because the nociceptor releases inflammatory mediators when depolarised
Describe nociceptor pathways.
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.
What can cause chronic pain?
- Pain pathways can become potentiated, so normal signals from nociceptors are magnified, leading to chronic pain.
How is visceral pain different from somatic pain?
Somatic pain is very precisely located. This is not the case for visceral pain.
Why is somatic pain precisely located?
Ordered pathways, allowing for the pinpointing of the location of the pain
What is the basis of viscero-somatic convergence?
REFERRED PAIN
- If there is pain in the internal organs, it will be felt in a precise location on the surface of the body.
What are some characteristics of visceral pain? PART 1
Often diffuses and poorly localised.
- has a relatively small number of afferents
- imprecise wiring
Generally ‘referred’ to regions of the body wall due to viscero-somatic convergence
What are some characteristics of visceral pain? PART 2
Each organ has a characteristic pattern of referral.
- a dermatome is an area of skin supplied by a single spinal nerve sending somatic afferents to each spinal cord segment
- initially, the pain is sent to dermatomes matching the embryonic origin of the organ
- however, this may evolve as other tissues are affected
What is the difference between nausea and vomiting?
→Nausea is produced by the same stimuli as vomiting
→Nausea may clear up without triggering vomiting
→Vomiting can occur without prior nausea
Why do receptors in the gut wall respond to non ingested toxins?
→Receptors in the gut wall that detect poison have a blood supply
→are in contact with the circulation so they respond to toxins in circulations
Describe the setup of the blood-brain barrier.
→Within the brain the capillaries have endothelial walls that have tight junction
→ in other places there are big gaps between the endothelial cells so plasma can enter.
→Substances have to be carried across into and out of the brain tissue
What are visceral afferent receptors associated with?
→ Afferents that run through the parasympathetic nerves through the vagus and into the brainstem.
Where is the area postrema?
→sits below the cerebellum and the foramen magnum
What happens if pressure goes up in the skull?
→If pressure goes up in the skull then it presses the brainstem down through the foramen magnum
Why does vomiting occur if pressure goes up in the skull?
→The area postrema is sensitive to the change in pressure so vomiting occurs
How does the NTS cause antireflux barriers to relax? PART 1
→The NTS integrates the information and produces the outputs
→NTS triggers the hypothalamus to increase ADH
→Fluid starts to be conserved
→Sympathetic activity increases
How does the NTS cause antireflux barriers to relax? PART 1
→Reduced parasympathetic activity to upper GI tract
→Pallor and sweating (result of sympathetic activation)
→NTS coordinates muscular activity
→The antireflux barriers are relaxed
Where are the endings of nociceptors found?
→ Under the skin
What does activation of nociceptors trigger?
→The nociceptor triggers activity in a pathway that goes to the primary somatosensory cortex
What are the oesophageal nociceptors?
→The oesophageal nociceptors have broad spreading axons that make connections.
- The stimulation of receptors can activate a large part of the somato cortex
- Pain appears to be coming from a wide surface
What do each of the visceral organs send?
→Each of the visceral organs send inputs to the spinal cord segment
