Lecture 2 Digestion 2 Flashcards
Control of motility
Mouth: saliva/ mastication/ swallowing
Oesophagus: peristalsis (contraction/relaxation of muscles propagating forward movement along tube)
Stomach: gastric acid secretion, pepsinogen activity(active pepsin) motility and emptying
GI tract detects changes by
mechanoreceptors - distention of walls by luminal content detected by
Osmoreceptors - chyme osmolality
Chemoreceptors - chyme acidity and product conc.
(Chyme = pulpy liquid that leaves stomach mix of gastric juices and part digested food)
How GI tract responds to change:
Control systems
Neural:
autonomic (direct/enteric nervous system)
enteric - via plexuses (stomach onward)
Hormonal: endocrine secrete into blood exocrine secrete in to ducts
May have paracrine effect - local acting producing local muscle response
Long & short reflexes
Long: stimus > chemo/mechano/osmoreceptor > CNS where sight taste smell of food and emotion processed then to ANS and enteric nervous system - alt. short: stimulus > receptor > ENS.
Then endocrine cells, hormone, blood > effector > response - change in secretion or motility.
Submucous plexus
Control exo/endocrine secretion. In submucosa aka Meissner’s plexus
Myenteric plexus
Control of peristaltic activity lies between the two layers of the Muscularis externa ( circular and longitudinal). Interconnects the 2 transmits neural info up and down GI tract
Hormonal control in GI tract
Cells located in GI epithelium w/receptors on surface in contact w/luminal content.
Hormone release into interstitial fluid
- endocrine via blood
- paracrine directly to lumen
Each hormone subject to feedback control - neg or pos to regulate lumen for optimum motility for max digestion and absorption may enhance each other e.g. CCK weak stimulant of bicarb ion secretion combined with secretin creates larger response
Two families of hormone here:
Gastrins: gastrin & cholecystokinin (CCK)
Secretin: secretin, glucose dependent insulinotrophic peptide aka gastric inhibitory peptide (GIP)
Mastication
Somatic (motor) nerves linked to skeletal muscles of mouth and jaw
Mainly vol control
Reflex receptors in gums and hard palate
Saliva secretion
Swallowing ( complex reflex)
Peristalsis
Involves skeletal and autonomic neurones. Upper 1/3 leading to oesophagus is skeletal muscle, lower part is smooth muscle.Circular muscle layer contracts in a pinching movement longitudinal muscle shortens tract so that food bolus moves forward.
Gastric motility
Filing: receptive relaxation, enhances stomach ability to take extra volume of food with little rise in stomach pressure - stimulated by act of eating mediated by vagus nerve
Storage: takes place in body of stomach
Mixing: in antrum ( lowest part of stomach)
Emptying: controlled by duodenum
Gastric emptying
Factors in stomach: amount of chyme influences strength of contraction
Factors in duodenum: fat - slow to be absorbed, acid, hypertonicity, distention detected by receptors influencing future motion
Factors affecting emptying trigger
Neural: intrinsic (short) and autonomic (long) collectively enterogastric reflex
Hormonal: duodenal mucosa secretin CCK
( Emotion and intense pain also effect activity)
Exocrine cells (in oxyntic mucosa lining stomach lumen)
Digestive juices secretion
Mucous cell: Secretes alkaline mucous, stimulated by mechanical stimulation by contents. The mucous protects mucosa against mechanical, pepsin and acid injury
Chief cell: secretes pepsinogen, stimulated by ACh and gastrin. When activated begin protein digestion
Parietal cells: secrete hydrochloric acid and intrinsic factor. stimulated by ACh, histamine and gastrin. Activates pepsinogen, breaks down connective tissue, denatures proteins, kills microorganisms and facilitates B12 absorption
Endocrine cells ( in pyloric gland area)
Secretion of gastrointestinal and pancreatic hormones
Enterochromaffin-like (ECL) cells produce histamine. Stimulated by ACh and gastrin. Stimulate parietal cells
G cells: secrete gastrin. Stimulated by protein products and ACh. Stimulates parietal, chief and ECL cells.
D cells: secrete somatostatin stimulated by acid. Inhibit parietal, G and ECL cells.
Cephalic/ gastric and intestinal phases
Cephalic phase: sight smell taste chewing, link to parietal cells via parasympathetic (vagal) nerves stimulating ACh secretion at nerve endings stimulating gastrin secretion by G cells in stomach. Parietal cells release HCl and pepsin then reduction in pH inhibits gastrin secretion.
Gastric phase: vago-vagal and local reflexs stimulated by stomach distension causing ACh secretion and from that point process is the same as cephalic phase.
Intestinal phase: protein digestion products in the duodenum stimulate G cells in the intestines stimulating parietal cells and causing gastric pepsin and HCl secretion OR secretion of secretin/CCK/GIP which inhibits G cells and parietal cells reducing gastric secretions.
