Lecture - GI (Pharm Gut Motility)

Question 1

If you have slow motility or high absorption, do you get diarrhoea or constipation?

Answer 1

You get constipation with slow motility and high abs but if you have fast motility or low abs then you get diarrhoea

Question 2

In brief, what’s the anatomy of the GIT and it’s layers?

Answer 2

Mucosa - submucosa (with submucosal plexus for secretions and abs) - circular muscle layer - myenteric plexus - longitudinal muslce - peritoneum

Question 3

Alright so what’s the neurophysiology of the GIT and how does it work under

• sensory contol
• parasym
• sym

Answer 3

So it has its own set of neurons and and it’s a ‘second brain’

• If the senosry neurons sense changes (like osmotic or nutrient levels) within the gut then they send signals through interneurons to the myenteric plexus which then get translated to motor neurons and cause movement in both the muscle layers. Once we have the motor neurons activated, we can have activation of the neurons in the submucosal plexus so you have secretionsn and abs system going
• Parasym will speed things up throug the vagus nerve and the pelvic nerve - it has a positive effect on gastric motility
• Symp will do the opposite and it will essentially block the neurotransmitter relese in the gut and damepen down the secretions and motiltiy

Question 4

Ach:

1. What is it produced by?
2. Acts through what?
3. Induces what?

Answer 4

So Ach is produced by interneurons (i.e. the intermediate neurons between sensory and motor neurons)

It acts through the M receptors (muscuranic receptors) on the gastric pariteal cells and also muscle cells to induce motility and sections

Question 5

Seritonin;

1. Released by?
2. Acts through?
3. Triggers what?

Answer 5

Released by the enterochromaffin cells (in reposnse to stress and food)

It acts through the 5HT receptors on sensory neurons and then the sensory neurons work on the motor at various levels to control peristalsis

It triggers peristalsis

Question 6

Dopamine

1. Produced by what?
2. Acts on what?
3. Produces what action?

Answer 6

So dopamine is produced by the muscle and epi cells (responds to stimuli in the gut and CNS) and acts on the D receptors in the myenteric plexus and inhbits the neurotransmitter (Ach) release decreasing motility

Question 7

CNS influence on GIT function

So lots of our stimulation comes from CNS to like, vomit, I guess. and out vomitting centre causes vomittting when there is motion-induced nausea, vertigo and also histamine + Ach.

The CTZ is exposed to toxins, drugs, metabolic disturbances and infection (bc poorly developed BBB). It’s responsive also responsive to dopamine, serotonin and substance P.

So our vomitting centrea is in the medulla and is the final common pathway (aka decides at the end if you vomit or not) by accumulating responses from the GI, CTZ chemoreceptors and higher cortex + vestibulae information.

Answer 7

Okay so my understanding is that you have the CTZ and that can respond to things and send signals to vomtting centre to vomit. The vomitting centre itself can also be triggerd for that but the vomitting centre is essentially the thing that triggers vomitting

Question 8

Histamine

1. Produced by what?
2. Acts through what receptors and where?
3. Induces what?

Answer 8

Produced by mast cells, enterochromaffin cells and neurons

2. It acts through H1 in the brain (post synaptic so can cause nausea and vomiting response) and H2 (so can modulate gastruc acid sectrion) in the gut mucosa.
3. It induces nausea (bc vomtting centre is responsive to it) and gastric acid seretion

Question 9

Substance P

1. Produced by what cells in response to what?
2. Acts through what?
3. Induces what?

Answer 9

1. Produced by neurons and inflam cells in response to stress
2. Acts throughh NK-1 in brain and gut immune and mucosal cells
3. Induces vomitting bc the vommiting centre is responsive to it (so is CTZ)