Gastric Secretion, Gastric Motility and Pancreatic Function Flashcards
What is the function of the Fundus, Body and Antrum
▷Fundus: Storage
▷Body: Storage, Mucus, HCl, Pepsinogen, Intrinsic Factor
▷Antrum: Mixing/Grinding, Gastrin
What cells make up the Gastric Glands?
What do each secrete?
▷Mucous Neck cells: mucus
▷Parietal/Oxyntic cells: HCl + Intrinsic Factor
▷Chief cells: Pepsinogens
What is the importance of Gastric Acid secretion?
▷Inactivates swallowed organisms -> preventing them from reaching the small intestine
▷Aids Digestion -> creates optimal pH for pepsin and gastric lipase, and also stimulates pancreatic HCO3- secretion
Which hormonal and neural mechanisms responsible for the control of Gastric Acid secretion?
▷Distension of food in the stomach -> Vagus/Local (enteric) reflexes → Ach
▷Peptides in Lumen -> G cells → Gastrin
▷Gastrin/Ach -> ECL cells → Histamine
Which cell is responsible for Gastric Acid secretion?
Parietal/Oxyntic cells!
How is Gastric Acid pumped into Stomach Lumen?
▷H+-K+-ATPase: H+ ions are pumped out of cells in exchange for K+ ions
▷Open Chloride channels: Cl- ions follow the electrical gradient of H+ ions out of the cell
▷Paracellular Pathway: Water follows the osmotic gradient created by the ions in the lumen of the stomach
NET EFFECT = HCl secretion in the stomach lumen!!
What is an Alkaline Tide?
▷Due to transient increase in HCO3- ions released into the blood after meals (post-prandially), transiently increasing blood pH
▷Occurs bc while HCl is being secreted into the lumen after meals, CO2 is being absorbed by the parietal cells from the bloodstream -> Carbonic Anhydrase inside cells combines it with H2O to form Carbonic acid, which rapidly dissociates to form HCO3- and H+ ions -> HCO3- leaves the cell in exchange for Cl- ions -> transient alkalisation of blood while Gastric acid is being secreted post-prandially!
What is the action of PPIs (ie. Omeprazole)?
▷Inhibits the H+-K+-ATPase
▷Used to treat over-secretion of gastric acid by Parietal cells
Which factors are involved in increasing proton pump activity?
Describe the intracellular effects of these factors.
▷Gastrin: (hormone) G cells -> increase intracellular Ca2+ -> Protein Kinase C -> increases Proton Pump activity!
▷Ach: (NT) Vagus nerve -> M3 Receptor -> increase intracellular Ca2+ -> Protein Kinase C -> increases Proton Pump activity!
▷Histamine: (inflammatory mediator) -> ECL cells -> H2 Receptor -> G protein (GS) -> Adenylate Cyclase converts ATP to cAMP -> protein kinase A -> increases Proton Pump activity!
Which factors are involved in decreasing proton pump activity?
Describe the intracellular effects of this factor.
▷Prostaglandins: (inflammatory mediator) -> its own receptor -> G protein (GI) -> inhibits Adenylate Cyclase conversion of ATP to cAMP -> therefore, inhibits protein kinase A -> inhibits Proton Pump activity!
What is the Cephalic phase of Gastric Acid secretion?
▷Sight, smell, taste of food
▷Stimulates the Vagus Nerve
(which stimulates G cells, and both stimulate ECL cells to release their various chemicals and trigger gastric acid secretion from the parietal cells)
What is the Gastric phase of Gastric Acid secretion?
▷Distension of stomach (Arrival of food) -> Vagus nerve -> Ach
▷Peptides in Lumen -> G cells -> Ach
▷Gastrin/ Ach -> ECL cells -> Histamine
All stimulate Parietal cells to secrete Gastric Acid!
What is the Intestinal phase of Gastric Acid secretion?
▷Acid in the Duodenum -> triggers Enterogastric (splanchnic) reflex an Secretin release -> decreases Gastrin secretion from G cells
▷Fat/CHO in the Duodenum -> triggers GIP release -> decreases Gastrin secretion from G cells
Both decrease Gastrin stimulation of Parietal cells -> reduces Gastric acid secretion!!
What are Enterogastrones?
What triggers their release?
▷Hormones released from Gland cells in the Duodenal mucosa -> Secretin, CCK, GIP
▷Released in response to acid, hypertonic solutions, Monoglycerides or FAs in the Duodenum
What do Enterogastrones do?
▷They all collectively act to prevent further acid build-up in the Duodenum
▷They do this in 2 ways:
- Inhibit gastric acid secretion
- Reduce gastric emptying -> (inhibit motility/contract pyloric sphincter)
What is Pepsinogen?
How is it activated, and what is the role of its activated form?
▷Pepsinogen is a zymogen released from chief cells in the Gastric mucosa
▷It is activated to Pepsin when exposed to low pH environments
▷Pepsin is an endopeptidase -> it is needed to break down proteins into smaller peptides
What stimulates Pepsinogen secretion?
▷Ach
▷Gastrin
▷Histamine
(NB. same as Gastric Acid secretion!)
What is the role of Gastric Mucus?
Cytoprotective Role:
▷Protects mucosal surface from mechanical injury
▷Neutralises pH (HCO3-) → Protects the stomach against gastric acid corrosion and pepsin digestion (pepsin activated at low pH -> protects the stomach from that!)
Which cells produce Intrinsic Factor?
What is the function of Intrinsic Factor?
What happens if Parietal cells are damaged and you don’t get any Intrinsic Factor production?
▷Parietal cells
▷Vitamin B12 absorption in the distal/terminal ileum
▷Pernicious Anaemia (bc no B12 complex created, and hence B12 can’t get absorbed!)
Where are Brunner’s Glands found?
What is the function of its secretions?
▷Duodenal Submucosa
▷It secretes HCO3- -> important for Gastric Acid neutralisation
What triggers HCO3- secretion?
▷Long (vagal) & short (ENS) reflexes
▷Release of Secretin from S cells
What is the function of Secretin?
▷Stimulates HCO3- secretion
▷Inhibits Gastric emptying and acid secretion
What inhibits Secretin release?
▷Acid neutralisation
negative feedback control!
What mechanisms increase Gastric emptying?
▷Gastrin → increases contraction of GIT
▷Distension of stomach wall → long (vagal)/short (ENS) reflexes → increases contraction of GIT
What mechanism decreases Gastric emptying?
▷Fat/acid/amino acid/hypertonicity in duodenum → inhibition of motility
What generates Peristaltic rhythm in the GIT?
What propagates it?
▷Pacemaker cells in the Longitudinal muscle layer
▷Propagated by the BER (basal electrical rhythm) -> Slow wave rhythm (spontaneous depolarisation/repolarisation along the longitudinal muscle layer)
What is the function of the Endocrine and Exocrine Pancreas?
▷Endocrine Pancreas (Islets of Langerhans) = creates + releases hormones into the bloodstream (insulin, glucagon and somatostatin)
▷Exocrine Pancreas (duct + acinar cells) = responsible for the digestive function of the Pancreas
What is the function of the duct and acinar cells of the Pancreas?
▷Duct cells = secretes HCO3- ions
▷Acinar cells = secretes digestive enzymes (as inactive zymogen granules)
What is the action of Secretin?
What stimulates its release?
▷It stimulates HCO3- secretion from the Pancreas, Duodenum
▷It is released in response to Gastric Acid in the Duodenum
It’s release is switched off by neutralisation of the Gastric Acid -> Negative Feedback!
What is the action of CCK?
What stimulates its release?
▷It stimulates Pancreatic zymogen secretion
▷It is released in response to Fat/AAs in the Duodenum
What is the role of Enterokinase?
Where is it present?
▷Converts Trypsinogen to Trypsin
▷It is present on the brush border membrane of Duodenal enterocytes
What is the role of Trypsin?
What activates it?
▷It converts all other zymogens to their active forms
▷It is activated by Enterokinase from Trypsinogen (from the Pancreas)
