Nausea, Vomiting and Pain Flashcards
What is vomiting?
Vomiting (emesis) is a physical act:
- expels contents of upper GI tract via mouth
- forceful
- complex, co-ordinated reflexive events
- associated with sensation of relief
What is the relationship between nausea and vomiting?
Nausea is produced by the same stimuli as vomiting
Nausea is generally a prodrome (premonitory symptom) of vomiting
Nausea may clear up w/o triggering vomitingAND vomiting can occur w/o prior nausea- eg sticking finger down throat
List some causes of nausea and vomiting
Why can obstruction cause vomiting?
Si hay obstruction in your intestines, hay que remove as much of the contents of your GI tract bc peristalsis will keep pushing that stuff down there.
Your intestine wont be able to pass contents down so it will expand
It will stretch its walls and be v painful- could do a lot of damage.
How does our taste and smell protect us from toxins?
How do our gastric and upper GI afferents protect us from toxins?
Gastric & upper GI afferents can expel harmful agents before they’re absorbed
They’re associated w chemoreceptive cells that respond to:
naturally occurring toxins
damaging chemicals
inflammatory mediators
why do some non ingested toxins, eg chemotherapy produce the vomiting reflex?
Chemoreceptor cells sit in the gut wall in tissue w good blood supply.
Substances mix from capillaries into the ECF that surrounds those key receptive cells.
So substances circulating in the blood can trigger responses from these cells which trigger responses from the efference. This produces the vomiting reflex.
How does the chemoreceptor trigger zone protect us from toxins?
Chemoreceptor Trigger Zone
Found in the area postrema in the brainstem. Here the blood-brain barrier is “leaky”, so toxins can enter
Hay chemoreceptors that can detect toxins in the blood
BUT again non-ingested toxins will have the same effect – eg chemotherapy, systemic infection, metabolic disturbance
How does the chemoreceptor trigger zone protect us from toxins?
Chemoreceptor Trigger Zone
Found in the area postrema in the brainstem. Here the blood-brain barrier is “leaky”, so toxins can enter
Hay chemoreceptors that can detect toxins in the blood
BUT again non-ingested toxins will have the same effect – eg chemotherapy, systemic infection, metabolic disturbance
How does the vestibular system protect against toxins?
Vestibular system is the organ of balance, but also a potent trigger for emesis
Poisoning produces aberrant activity in vestibular neural pathways:
Axons from the receptors are sent out through the 8th cranial nerve (vestibulocochlear nerve) and straight into the NTS
BUT also triggers nausea and vomiting in response to un-natural motion
How does learning and aversion protect us from toxins?
If we survive a mistake we avoid repeating it (unpleasantness reinforces learning)
Aversion may hard-wire avoidance
BUT can create incorrect associations
Describe visceral afferents
Visceral afferents are the sensory nerves that run up into the brainstem.
They get their input from chemoreceptor cells found in the walls of the stomach and the top of the small intestine.
Chemoreceptors respond to toxins, irritants, inflammatory mediators.
Also hay some afferent nerves that have endings that respond to abnormal distension of the GI tract.
How does increased intracranial Pa cause nausea and vomiting?
If intracranial Pa goes up, the brain swells. Extra volume gets squeezed out through the foramen magnum. The brain gets pressed down into area prostrema and the nucleus tractus solitarius.
Those areas cause aberrant signals that will trigger nausea and vomiting.
What is the mechanism of nausea and vomiting?
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
Describe the higher centre input for n+v
What is important about the area postrema and afferent pathways?
The two pathways that are involved in detecting actual poisons, area postrema and abdominal afferents, use 5-HT3 receptors as a key location.
Therefore 5-HT3 antagonists can be used to treat ONLY these two types of nausea and vomiting
How does the NTS prepare for and trigger nausea and vomiting?
Why does the NTS stimulate autonomic efferents to trigger nausea?
Increase in salivation gives protective fluid lining to your mucosa if you throw up v acidic stomach contents.
Constriction in the GIT will reduce absorption from inside the GI tract into the bloodstream. This reduces the amount of toxin that gets into your bloodstream.
The autonomic efferents also change the pattern of gut motility.
Describe various processes controlled by efference in the vagus nerve to trigger nausea.
Describe various processes controlled by efference in the vagus nerve to trigger vomiting
What do these green pathways represent?
these green pathways come from throughout the GI tract. They’re associated w afferents which can detect damaging stimuli and which project to the spinal cord to the thoracic regions.
They converge onto the greater and the lesser splanchnic nerves.
What are receptors for visceral pain?
“Pain” receptors respond to “noxious” stimuli, and are called “nociceptors”
They respond to:
Distension- abnormal levels of stretching cause pain
Inflammation- inflammatory chemicals sensitise nociceptors
muscle spasm
What does this show?
Sensory afferents innervate the wall of the gut and produce action potentials.
This shows a.potential firing for each level of distension.
As distension increases, a.potential firing Hz increases.
In normal distension, a.potentials give feedback to the neural network that controls gut movement, but it’s not producing sensation- you don’t feel anything
Once afferent activity reaches higher levels due to abnormal distension, signals are interpreted by the brain as damage to the system. Pain sensation is produced and will increase as a.potential firing rate increases.
What else do nocireceptors respond to apart from distension?
Nociceptors respond to inflammatory mediators, as well as stretching of the gut wall:
Inflammatory mediators are detected by sensitive afferent endings which depolarise.
These endings release pro inflammatory mediators which increase inflammation again, which increase depolarization etc- positive feedback
What does this demonstrate?
Extra a.potentials from normal distension AND inflammation mean that pain threshold decreases
How can the positive feedback loop of inflammation and depolarisation cause Chronic sensitisation of visceral pain?
The positive feedback loop increases responses This can produce long term potentiation of synapses, strengthening and increasing power of the synapses.
Both + feedback in the gut & strengthening of the synapses in the pathway produce bigger responses.
It may produce a situation where people who have had a trigger which has been cured can STILL continue to feel GI pain.
Describe somatic pain
Pain in a precise area activates somatic nociceptors which project to the spinal cord and enter T3.
Somatic nociceptors synapse w a pathway that carries the info to the somatosensory cortex.
In the somatosensory cortex, hay a map of the body (somatosensory homunculus). This helps afferents from various parts of the body terminate in a very organised way.
This pathway will carry the information to a v precise spot within the chest region of that map. Therefore sera a very highly localized pain sensation at that point.
Describe viscero somatic convergence
Viscero-somatic convergence piggy backs onto the somatic pathway
Hay v few nociceptors which make messy connections. This produces activity over an extended part of the somatosensory map.
Therefore pain sensation is poorly localized, and is referred to the body wall even though it’s coming from a visceral organ.
This is viscero-somatic convergence and results in referred pain
Each organ has a…
Each organ has a specific pattern of referral
initially the site of the pain is on the dermatome it was linked to in the embryo
How does inflammation of the gallbladder lead to shoulder pain?
Referred pain from the gall bladder is in the T9 dermatome bc the gall bladder gets its innervation from T9
Inflammation of the gall bladder can spread to surrounding structures, eg the diaphragm and parietal peritoneum- these get their innervation from C3 to C5 bc they get their innervation from the phrenic nerve.
Therefore if gallbladder inflammation worsens/spreads it leads to shoulder pain
describe characteristics of visceral pain.
