HRR: secretions and motility III Flashcards
What are secretions of the LES and cardia?
Mucus and bicarb
What is unique about the cardia of the stomach?
It has the oblique layer of muscle in the ME. It helps the valve function of the LES
What are secretions of the fundus and body?
Protons, IF, mucus, bicarb, lipase, pepsinogens
What motility functions occur in the fundus and body?
Reservoir, tonic force during emptying
What are secretions of the antrum and pylorus?
Mucus and bicarb
What motility functions occur in the antrum and pylorus?
Mixing, grindings, regulation of emptying
What do surface epithelial cells do?
Secrete bicarb and mucous to protect the epithelium
What do mucus neck cells do?
Secrete mucus; higher in cardia and antral regions
What do parietal cells do?
Secrete HCL and IF. Higher amount in body and fundus
What do chief cells do?
Secrete pepsinogens
What do enterochromaffin cells do?
Secrete histamine
What do D cells do?
Secrete somatostatin
When are stomach acids produced?
Prior to the gastric phase; their production is initiated in the cephalic and oral phases from vagal stimulation
What are the stimuli for increased gastric acid secretion during the gastric phase?
Distension of the stomach and partially digested proteins or amino acids sensed by G cells
Describe what happens when food enters the stomach and causes distension.
The vagovagal reflex is activated, resulting in ach and GRP release that will lead to activation of parietal cells. Local ENS reflex pathways are also activated, leading to Ach release and further activation of parietal cells
Describe how partially digested proteins increase gastric acid secretion.
G cells sense the proteins and secrete gastrin that will act on parietal cells to increase HCL secretion. Enterochromaffin cells will secrete histamine and activate parietal cells
Which cells does vagal efferent outflow impact?
Parietal cells, ECL cells, G cells, and chief cells
How does the vagus nerve impact the stomach?
Through the enteric nervous system
What stimulates parietal cells to make acid?
Gastrin, ach, histamine
What receptor in the parietal cell responds to gastrin?
CCK2
What receptor in the parietal cell responds to histamine?
H2
What molecules are inhibitory for parietal cells?
Somatostatin and prostaglandin
Describe what happens to parietal cells upon stimulation to become activated.
They undergo cytoskeletal rearrangement, resulting in fusing of tubulovesicular and canalicular membranes. This increases their surface area. They also add a bunch of HK pumps, K channels, and Cl channels to the canalicular membrane
How do parietal cells produce acid?
Water and CO2 enter the cell, where carbonic anhydrase forms carbonic acid. Carbonic acid dissociates into H and bicarb. The proton will be secreted into the lumen by the HK pump, and the bicarb gets exchanged into the blood
What is the major pump for protons to move into the gastric lumen?
HK pump
What do D cells do?
Sense when the pH falls below 3. When this happens, they secrete somatostatin to inhibit gastrin secretion to decrease parietal cell function and HCL secretion
What are some effects of somatostatin?
Splanchnic vasoconstriction, decreases pepsinogen secretion, reduces pancreatic enzyme and bile secretion, and overall reduces GI motility and gastric emptying
What happens to gastric pH when we eat a meal?
It actually will initially drop! The food we eat is more neutral than stomach pH.
What is a gastrinoma?
A neuroendocrine tumor that produces gastrin autonomously; it does not respond to negative feedback. This overwhelms the stomach and may lead to ulcers, heartburn, and diarrhea
What is autoimmune atrophic gastritis?
Antibody and T cell mediated destruction of parietal cells that causes a lack of IF secretion leading to pernicious anemia as well as low HCl secretion that causes iron deficiency and high gastrin
What can cause chronic atrophic gastritis?
H pylori
What is the main stimulator of chief cells?
Ach
What is pepsinogen?
Inactive proenzyme of pepsin secreted by chief cells
What is required for pepsinogen activation?
Low pH
When does pepsin become inactivated?
In the neutral environment of the duodenum
Describe how NSAIDs impact the GI system.
They inhibit prostaglandin production. Normally, prostaglandins reduce gastric acid secretion and stimulate gastric mucus and bicarb secretion. Inhibiting prostaglandins leads to more stomach acid and potential damage to gastric epithelium
How does the stomach achieve emptying?
Contraction of proximal and distal stomach and relaxation of pyloric sphincter
What is adaptive relaxation?
Relaxation of the stomach in response to food entering
Describe the process of adaptive relaxation.
Mechanoreceptors sense distension, leading vagal afferent nerves to signal the vagal ganglion, then vagal efferent nerves stimulating ENS to relax smooth muscle. The ENS itself will also stimulate interneurons followed by motor neurons to stimulate relaxation of smooth muscle
Which portion of the stomach has thicker muscle: proximal or distal? Why?
Distal to aid in churning and mixing to create chyme
What impacts the rate of gastric emptying?
Food composition, volume, medications, nerve/muscle conditions, and hormones
Which macronutrient empties the fastest?
Carbs
Describe the process of gastric emptying.
As gastric contents become chyme, antral contraction and transient relaxation of the pyloric sphincter results in some entering the duodenum. The proximal stomach will increase tone and distal stomach contractions become more forceful to propel chyme into the transient openings of pyloric sphincter and into the duodenum. When pylorus is open, distal portion relaxes and chyme just flows
What is the enterogastric reflex?
The process by which signals travel to the CNS resulting from duodenum sensing distention/fats, followed by signals back to the GI tract to stop gastric emptying, decrease gastric motility, and decrease gastric acid production
What is gastroparesis?
Delayed emptying of the stomach due to damage to the stomach’s neural network and interstitial cells of cajal
What is the most common cause of gastroparesis?
Diabetes