Flashcards in Physiology - Mouth to Stomach Deck (35):
What enzymes/secretions are present in the oral cavity? What roles do they play?
- saliva is the only secretion of the oral cavity; it begins carbohydrate digestion
- it is 99.5% H2O and 0.5% electrolytes + proteins
- the proteins: amylase (begins breakdown of carbohydrates into maltose), mucus (lubrication), and lysozyme (antibacterial)
- a condition characterized by decreased salivary secretion
- symptoms: difficulty chewing, swallowing, speaking, increased incidence of cavities (caries)
What is the basal rate of salivary secretion? How can this be increased?
- basal rate: 0.5 mL/min
- increased via the simple or conditional salivary reflexes
- simple reflex: presence of food in mouth (chemoreceptors and pressure receptors)
- conditioned reflex: thinking about food, smelling it, seeing it
What are the parasympathetic and sympathetic effects on salivary secretion?
- BOTH increase it! but parasympathetic input increases its secretion much more so than sympathetic
- parasympathetic is for digestion, sympathetic is to facilitate respiration
What are the 2 stages of swallowing a bolus? What types of peristalsis are involved in swallowing?
- the oropharyngeal stage and the esophageal stage
- oropharyngeal: about 1 second; bolus is moved from the mouth to the pharynx to the esophagus
- esophageal: about 5-9 seconds; peristaltic contractions move the bolus down the esophagus and into the stomach
- primary wave peristalsis is for normal swallowing
- secondary wave peristalsis is for when a bolus gets stuck and needs the extra push to make it into the stomach
During the oropharyngeal stage of swallowing, what measures ensure that the bolus moves in the proper direction?
- the tongue's position during swallowing prevents the bolus from re-entering the mouth
- the uvula seals off the nasal passages
- the apposition of the vocal folds + the closed epiglottis prevent the bolus from entering the respiratory tract
What secretions/enzymes are found in the esophagus? What roles do they play?
- the sole secretion is mucus, and it serves a protective/lubricating purpose
What are the two sphincters of the esophagus? When is each closed? What function do they provide?
- the upper pharyngoesophageal sphincter: opens only when swallowing food to prevent air from entering the digestive system (prevents eructation/"burping")
- the lower gastroesophageal sphincter: opens only when a bolus is to enter the stomach to prevent reflux of gastric contents (prevents GERD/"heartburn")
What are the roles of the stomach? Which is its main role?
- main role: storing food and beginning digestion
- other roles: continuing carbohydrate digestion, beginning protein digestion, converting food boli into chyme
- (no absorption occurs in the stomach; although alcohol and aspirin absorption DOES begin here)
What are the 4 aspects of gastric motility?
- filling, storage, mixing, and emptying
Where are the pacemaker cells (interstitial cells of Cajal) of the stomach found?
- in the upper fundus
Gastric filling occurs via what mechanism? Given that the relaxed, non-distended stomach is approximately 50 mL, to what volume can the stomach expand to to accommodate food?
- gastric filling involves receptive relaxation (as food enters the stomach, it relaxes and expands)
- the stomach usually expands from 50 mL to 1 L! it can expand even further, but at this point, you will feel discomfort
Where does gastric mixing take place?
- in the antrum
- (this is what creates chyme)
What factors control gastric emptying into the duodenum?
- gastric and duodenal factors
- gastric: distension (amount of food) and the fluidity of the chyme; both increase emptying
- duodenal: distension, hypertonicity, and the presence of fat and acid; these DECREASE/SLOW DOWN emptying
T or F: emesis is the reverse peristalsis of the stomach.
- emesis involves the contraction of the respiratory muscles (the diaphragm and the abdominals)
What are the 2 distinct areas of gastric mucosa? Where is each found?
- the oxyntic mucosa (in the fundus and body)
- the pyloric gland area/PGA (in the antrum)
Which cell types are found in the oxyntic gastric mucosa?
- 3 exocrine cells types: mucous, chief, and parietal cells
- mucous cells: line the gastric pits, secrete watery mucus
- chief cells: deeper part of the glands, secrete pepsinogen
- parietal cells: deeper part of the glands, secrete HCl and intrinsic factor
- 1 paracrine cell type: ECL (enterochromaffin-like) cells which secrete histamine
What type of cell is found between the gastric pits? What does it secrete?
- the mucosa between the pits is lined with surface epithelial cells
- they secrete a thick, alkaline mucus
How does HCl assist in digestion?
- HCl activates pepsinogen into pepsin which can then go on to activate other pepsinogen molecules and begin protein digestion
What does intrinsic factor do? What performs this role before intrinsic factor takes over?
- secreted by parietal cells in the stomach
- necessary for the absorption of vitamin B12 (crucial for RBC production)
- *it is the most important substance secreted by the stomach!* (pepsin is important too, but it is NOT essential because we have pancreatic proteases)
- haptocorrin binds vit B12 in the stomach before transferring it over to intrinsic factor
Where is pepsinogen stored in the chief cells?
- in the cytoplasm in zymogen granules
Which cell types are found in the pyloric gland area (PGA) of the gastric mucosa?
- 2 endocrine cell types: G cells and D cells
- G cells: secrete gastrin
- D cells: secrete somatostatin
- 2 exocrine cell types: mucus and chief cells (pepsinogen)
Which compounds stimulate HCl secretion? Pepsinogen secretion? Which compounds inhibit HCl secretion?
- HCl stimulation: gastrin, ACh, and histamine
- pepsinogen stimulation: gastrin and ACh
- HCl inhibition: somatostatin, prostaglandin, secretin, and GIP (slightly)
What are the 3 phases of gastric secretion?
- cephalic, gastric, and intestinal
- cephalic: an increase in HCl and pepsinogen secretion before food is swallowed (thinking about food, smelling food, chewing food, etc.); due to vagal stimulation of enteric NS (increased ACh = increased HCl and pepsinogen) and of G cells (increased gastrin = increased HCl, pepsinogen, and histamine)
- gastric: presence of protein in the stomach triggers vagal stimulation as above
- intestinal: decreased HCl and pepsinogen secretion as food empties into the duodenum; distention, hypertonicity, fat, and acid result in decreased gastric secretion
Which gastrointestinal hormones regulate gastric function?
- secretin (S cells), CCK (I cells), and somatostatin (D cells); decrease gastric function (slow down motility and decrease secretion)
- gastrin (G cells); increases gastric function
When is somatostatin released?
- in the presence of acid (low pH), to inhibit further acid production
- (ex: when food is no longer in the stomach, it can't buffer the gastric acid and pH decreases, triggering somatostatin release)
Which nutrients are absorbed in the stomach?
- however, alcohol and aspirin absorption begin here
Why do we say to eat a fatty/greasy meal before or during a big night out?
- because alcohol is absorbed more slowly in the stomach than in the small intestine
- by eating a high fat meal, we slow down gastric motility and secretion (because fat in the duodenum will trigger these responses), allowing the alcohol more time to be absorbed slowly in the stomach vs. rapidly in the small intestine
Why does the presence of fat in the duodenum slow down gastric function? Why not carbohydrates and proteins?
- because the only fat digesting enzyme is secreted by the pancreas (lipase). by slowing down gastric function, less chyme is pushed into the duodenum, allowing the chyme already in the duodenum more time to be digested by the lipase
What role do ECL cells play in gastric digestion?
- enterochromaffin-like cells release histamine in response to gastrin
- *histamine is the MAIN trigger for increasing acid secretion via the parietal cells (even though gastrin, itself, stimulates acid secretion; as does ACh)
Pathway for Vagal Stimulation of HCl Release
- vagal stimulation causes ACh release --> ACh binds to M3 receptors on the parietal cell --> Gq (a GPCR) triggers the PIP2 pathway (IP3/Ca2+ and DAG/PKC) --> activation of K+-H+-ATPase pump
- (atropine blocks this pathway)
- vagal stimulation also stimulates G cells and ECL cells via GRP receptors and M1 receptors, respectively (these also lead to increased HCl secretion)
- (GRP: gastrin releasing peptide; this is NOT ACh)
Pathway for Gastrin Stimulation of HCl Release
- G cells (stimulated by distension, amino acids, aklalinization, vagus) secrete gastrin --> gastrin binds to CCK-B receptors on the parietal cell --> Gq (a GPCR) triggers PIP2 pathway (IP3/Ca2+ and DAG/PKC) --> activation of K+-H+-ATPase pump
- (proglumide blocks this pathway)
- gastrin also stimulates ECL cells, which also increases HCl release
Pathway for Histamine Stimulation of HCl Release
- gastrin stimulates ECL cells to release histamine --> histamine binds to H2-receptors on the parietal cell --> Gs (a GPCR) activates cAMP/PKA pathway --> activation of K+-H+-ATPase pump
- *this is the main mechanism for gastric acid secretion*
- (H2 blockers block this pathway)
How do prostaglandins and somatostatin inhibits HCl release?
- both bind to respective receptors on the parietal cell and trigger Gi (a GPCR), which inhibits cAMP/PKA pathway, thus inhibiting the K+-H+-ATPase pump
- prostaglanin analogs (misoprostol) use the same pathway