Symptoms of GI Disease - Nausea, Vomiting & Pain

Question 1

Describe what nausea and vomiting are

Answer 1

• Nausea is a sensation -
• Personal self reported
• Associated with physiological changes
• Unpleasant
• Triggers aversion (a strong dislike)
• Vomiting is a physical act -
• Expels contents of the upper GI tract via the mouth
• Forceful - regurgitation/ reflux
• Complex, coordinated reflexive events
• Associated with sensation of relief

Question 2

Describe the relationship between nausea and vomiting

Answer 2

• Nausea is produced by the same stimuli as vomiting
• Nausea is generally a prodrome (preliminary symptom) of vomiting
• Nausea may clear up without triggering vomiting
• Vomiting can occur without prior nausea

Question 3

State some stimuli for vomiting

Answer 3

• Poisoning e.g. contaminated food, poisonous plants, chemical agents
• Emotional upset
• Obstruction
• GI disease like gastritis
• Raised intracranial pressure
• IV drugs e.g. morphine, chemotherapy
• Metabolic disturbance
• Other people being sick
• Travel sickness
• Excessive eating
• Pregnancy
• Excessive alcohol
• GI infection like norovirus

Question 4

Describe how the GI tract has mechanisms to protect against toxins

Answer 4

• Taste and smell of the toxin can prevent indigestion
• We have an intrinsic dislike of bitter flavours and children are naturally wary of new tastes
• Upper GI tract can potentially expel harmful agents before they have chance to be absorbed
• Associated with chemoreceptive cells that respond to naturally occurring toxins, damaging chemicals and inflammatory mediators
• The chemoreceptor trigger zone is an area in the postrema in the brainstem- blood brain barrier is leaky to allow chemoreceptors detect toxins in the blood
• There is a vestibular system which is an organ of balance but also is a potential trigger for emesis - poisoning is thought to produce aberrant activity in vestibular neural pathways
• Once the toxin is removed we develop an aversion to it meaning we avoid that food because we know it made us ill when we last ingested it

Question 5

State the disadvantages of these reflexes

Answer 5

• Vomiting can be produced when it isn’t necessary e.g. when there isn’t anything in the Gi tract that needs to be expelled
• This is because substances like chemotherapy drugs in the circulation can trigger chemoreceptors and cause vomiting

Question 6

Describe the mechanisms of nausea and vomiting including the 4 inputs

Answer 6

• The anti poison defences are coordinated by the nucleus tractus solitarius (NTS)
• This is in the medulla of the brainstem
• It also integrates cardiac, respiratory and gastrointestinal functions
• It receives 4 types of inputs:

1. Visceral afferents -
   - Toxins, irritants, inflammation and distension of the stomach causes signals to be sent along the vagal parasympathetic nerves to the NTS of the brain
   - The NTS then sends signals to the stomach to produce vomiting
2. Area postrema -
   - The chemoreceptive trigger zone of the brain
   - If there are toxins in the blood as there is a lack of a blood brain barrier the toxins are able to stimulate the chemoreceptors to produce the necessary response
3. Vestibular system -
   - Organ of balance present in the inner ear
   - Toxins from the blood cause disrupted vestibular signalling
4. Higher centres -
   - Things that you social group find disgusting
   - Other people in the group being sick
   - Things that have made you sick in the past

Question 7

How does the NTS trigger nausea and vomiting?

Answer 7

• It signals to the hypothalamus to increase [ADH/vasopressin]
• It signals the higher centres of the brain like the cerebral cortex and limbic system to cause nausea and future avoidance of the food
• It signals autonomic efferents to cause changes in gut motility as well as increased salivation and vasoconstriction in the GI tract

Question 8

Describe the steps of what happens during nausea and vomiting

Answer 8

• Nausea -
  1. There is reduced mixing and peristalsis to prevent toxins being carried further through the system
  2. The proximal stomach relaxes to prepare the stomach to receive additional contents
  3. There is a large retrograde contraction which sweeps up from the mid small intestine and returns the upper intestinal contents to the stomach
• Vomiting -
  4. Retching/dry heaving- coordinated contractions of abdominal muscles and the diaphragm - waves of high pressure in the abdomen - compresses the stomach but antireflux barriers are intact so there is no expulsion
  5. Vomiting (emesis) - oesophageal sphincters and crural diaphragm relax while further waves of contraction expel stomach contents

Question 9

Describe where visceral pain afferents originate and go to

Answer 9

• Originate from areas of the GI tract like the stomach, descending colon and rectum
• Send signals to the spinal cord mainly in the thoracic region
• Converge into the greater and lesser splanchnic nerves

Question 10

Describe the receptors for visceral pain

Answer 10

• Receptors that respond to noxious stimuli called nociceptors - respond to stimuli that have done damage
• They respond to - distension, inflammation and muscle spasms

Question 11

Describe how gut distension produces pain

Answer 11

• When distension becomes abnormal such as due to an obstruction
• The wall of the intestine is stretched to damaging levels which will produce pain
• As the distension of the gut increases the afferent nerve action potentials increase in frequency
• Once a certain frequency is reached the brain interprets the signals as damage or potential damage to tissues and so produces pain

Question 12

Describe how inflammation produces pain

Answer 12

• Injury, irritants, toxins, infections or autoimmune issues can all cause inflammation of the gut wall - inflammation depolarises nociceptors
• Nociceptors respond to inflammatory mediators as well as the stretching of the gut wall
• Those nerve endings are also capable of releasing pro-inflammatory mediators which makes the inflammation worse
• This is a positive feedback mechanism that aims to be helpful but it can mean inflammation is sustained even when the original cause is gone
• Inflammation increases the frequency of the afferent nerve action potentials further
• This means that normal gut distension and peristalsis can now produce pain due to the inflammation present

Question 13

Describe how pain can be localised

Answer 13

• Somatic pain is precisely localised
• Where damage occurs stimulates somatic nociceptors to send signals to the spinal cord and then through to the somatosensory cortex of the brain which processes sensations
• The signal is carried to a precise area within the somatosensory cortex which means there is a highly localised sensation of pain produced

Question 14

Describe viscero somatic convergence

Answer 14

• Some nociceptors like oesophageal nociceptors don’t have their own pathway to the somatosensory cortex
• Instead it synapses with a somatic nociceptor in the spinal cord and sends signals to the brain this way
• This is the mechanism through which referred pain is produced

Question 15

Describe how referred pain is produced with some specific examples

Answer 15

• Each organ has a characteristic pattern of referral
• Different synapses in segments match the embryonic origins of each organ
• The large intestine is innervated from T10-T12 - hence damage to the large intestine will cause synapse to somatic nociceptors that causes pain in this area of the abdomen
• Gallbladder is innervated by T9 and the stomach by T6/7 and the same can occur where referred pain is produced in these regions
• The gallbladder gets innervation from T9 but inflammation of the gallbladder can spread to the diaphragm which gets its innervation from C3-C5 hence gallbladder inflammation can cause pain where the phrenic nerve is in the right shoulder