Gastric Physiology 2 Flashcards
Protease secretion
Chief cells produce proteases by producing an inactive enzyme called pepsinogen
Proteases are synthesised in inactive form called zymogen
Pepsinogen mediated by input from enteric nervous system (ACh)
Secretion parallels HCl secretion- as we need pepsin and HCl at the same time as they have the same purpose- help us break down proteins
Requires luminal activation
Protease activation- positive feedback loop
Seeing, smelling, chewing food leads to the production of both HCl acid from a variety of cells and pepsinogen from the chief cells in the gastric wall
In the gastric lumen there is a mixture of pepsinogen and HCl acid. HCl acid cleaves pepsinogen to make pepsin
Pepsin can then also digest pepsinogen into pepsin- positive feedback loop
Why do we secrete pepsinogen rather than pepsin?
As we don’t want the pepsin to digest our own cells as cells are made of proteins so its dangerous to have pepsin inside of cells
Protease activation
Conversion of pepsinogen to pepsin is pH dependant
Most efficient when theres a low pH of pH<2
Pepsin is only active at a low pH. Irreversible inactivation in small intestine by HCO3- which neutralises pH of the material coming from the stomach
Role of pepsin in protein digestion
Not essential (protein digestion can occur if the stomach is removed)
Accelerates protein digestion
Normally accounts for 20% of total protein digestion
Breaks down collagen in meat- helps shred meat into smaller pieces with greater surface area for digestion
Gastric motility
Empty stomach has a volume of approx 50mL
When eating the stomach can accommodate approx 1.5L with little increase in luminal pressure
Smooth muscle in body and fundus undergoes receptive relaxation to allow accommodation of greater volume with little increase in luminal pressure
This receptive relaxation of smooth muscle and so allowing of increasing in volume without pressure increasing, is mediated via the vagus nerve (parasympathetic nervous system acting on enteric nerve plexuses and so the coordination is afferent input via the vagus nerve ) and is triggered by the sight, smell and chewing of food.
This occurs due to the release of nitric oxide and serotonin from the nerve endings in the stomach- released by enteric nerves mediate relaxation
Peristalsis
Peristaltic waves begin in gastric body
Weak contraction in the body (little mixing)
When stomach is empty theres weak contractions but a lot of food increases the strength of contractions, which leads to gastric mixing.
The coordinated contractions of the stomach start in the fundus of the stomach so at the top of the stomach where they are quite weak. They then become stronger as they head into the pylorus so they serve to churn material
As the peristaltic wave is coordinated the wave of chi faction heads towards the pylorus, so its driving its gastric contents towards the duodenum and then hits the ‘closed door’, effectively the pylorus where it then slushes back into the stomach so it churns and mixes gastric contents
Little chyme enters the duodenum
Only when the stomach starts to empty is there significant movement
Basic electrical rhythm
Frequency of peristaltic waves determined by pacemaker cells in muscularis propria and is constant (3/minute). The pacemaker cells of the GI are called interstitial cells of cahal
Pacemaker cells undergo slow depolarisation-repolaristaion cycles
Depolarisation waves transmitted through gap junctions to adjacent smooth muscle cells
Do not cause significant contraction in empty stomach- it would be a waste of energy
Strength of peristaltic contractions- increase
Can increase with excitatory neurotransmitters and hormones (Gastrin)- this increases the amplitude of the wave which causes further depolarisation, sufficient (when threshold is reached) to trigger an action potential and muscle contraction
Gastrin increases strength
Gastric distension (medicated by mechanoreceptors)
Strength of peristaltic contractions- decrease
Duodenal distension
Increase in duodenal luminal fat
Increase in duodenal osmolality
Decrease in duodenal luminal pH
Increase in sympathetic NS action
Decrease in parasympathetic NS action
Gastric emptying
Capacity of stomach is much larger than the capacity of the duodenum
The volume of the duodenum between them cannot undergo receptive relaxation and doesn’t like to have a large volume of hypertonic acidic material
Overfilling of duodenum by a hypertonic solution causes dumping syndrome:
Vomiting, bloating, cramps, diarrhoea, dizziness, fatigue, weakness, sweating
This occurs because duodenal overfilling will lead to an outpouring of fluid through the Lumina of the duodenum into the wall of the duodenum into the lumen. This shift in fluid in electrolytes leads to diarrhoea
Change in blood pressure and ion concentrations leads to the other symptoms
Gastroparesis
Delayed gastric emptying caused by
Idiopathic
Autonomic neuropathies (e.g. in Diabetes mellitus)
Drugs – next slide
Abdominal surgery
Parkinson’s disease
Multiple sclerosis
Scleroderma
Amyloidosis
Female gender
Gastroparesis drugs
On slide
Gastroparesis- delayed gastric emptying
Nausea
Early satiety
Vomiting undigested food
GORD
Abdo pain/bloating
Anorexia
