Digestive System, Lecture 2 Flashcards
GI Tract - pharynx - deglutition - 1st stage
deglutition - swallowing
- highly complex, coordinated activity involving 22 muscle groups
- ~8 sec for solid food / ~1-2 sec for liquids
1 stage: voluntary or buccal stage
- in mouth; voluntary (control over what it happens)
- once bolus formed it is pushed into oral pharynx by action of tongue against palate (soft and hard palate)
my notes:
- 1 stage still in mouth, 2nd: pharynx, 3rd: esophagus
- still in oral cavity within mouth
- bolus: create something that is fairly well structured and lubricated so it moves down more easily
1st stage, where tongue pushes up or against the palate and that is going to push bolus from oral cavity to oral pharynx
GI Tract - pharynx - deglutition - 2nd stage
2nd stage: pharyngeal stage
- in pharynx; involuntary (receptors in oral pharynx that sense bolus is in there, which sends signal to medulla, which will send responses to number of directions)
- oral pharynx receptors signal swallowing centre in medulla oblongata, bolus present
- medulla has a cluster of neurons that make up the swallowing centre (my note)
swallowing centre sends signal to:
- move structures to blocking positions uvula; nasal pharynx (blocks it from going back up) / epiglottis; laryngeal pharynx (block passageway to lungs) / tongue; oral pharynx (preventing bolus going into oral cavity)
- inhibitory respiratory muscles; stop breathing briefly
- relax upper esophageal sphincter (controlling the opening into esophagus) - a bit like vasodilation (a lot larger opening / diameter gets bigger); bolus enters esophagus
once in esophagus; signal to swallowing centre stops (as soon as you remove it from the location; receptors are no longer detecting it as it is no longer in that position)
- structures moving back to non blocking positions (the blocking structures return to normal position - initial position)
- respiratory muscles re-engage; breathing resumes
- upper esophageal sphincter contracts; blocking backflow
GI Tract - pharynx - deglutition - 3rd stage
3rd stage: esophageal stage (moving through esophagus)
- in esophagus; involuntary
- peristalsis:
◦ circular muscles – contract to constrict above
bolus (can constrict further down as well, not just
in one set place)
◦ longitudinal muscles – contract along esophagus
length to push bolus down (along the length)
- circular and longitudinal: creating a barrier and then pushing it along
- lower esophageal sphincter relaxes (lower esophagus to stomach); bolus enters stomach (relax when wanting to enter)
once bolus in stomach:
- lower esophageal sphincter contracts to prevent regurgitation (backward movement)
- alcohol, smoking: can relax lower esophageal sphincter (can cause things to move back up; heart burn)
GI Tract - stomach (filling and storage)
- can expand during meals
- needed to slow down movement through GI tract (ingestion faster than digestion/reabsorption)
my notes: - storage is one of the first important parts of the GI system
- we have to slow everything down cause digestion and reabsorption takes times; or else digestion can be incomplete (in stomach for period of time)
GI Tract - stomach (gastric motility)
mixing waves composed of propulsion and retropulsion (waves ~15-25 sec) (waves that go up are retropulsion, while waves that go down that stomach are propulsion)
- pacemaker cells in smooth muscles that set a basic wave rhythm (altered by neural and hormonal)
- strong motility in body and antrum (more stomach actions here); minimal in fundus
- bolus broken down to chyme (soupy liquid) -> semisolid to fully liquid
my notes:
- could make waves faster or slower altered by neural and hormonal factors
- combination of longitudinal and circular muscle in just two directions (propulsion and retropulsion)
- mixing waves are waves that go down and back up the stomach (mix everything up together with the bolus and secretions we add)
- fundus is a key storage area rather than mixing, becoming a continuation of digestion in that way
GI Tract - stomach (gastric emptying)
- small amount of chyme per mixing waves moves into duodenum (mainly liquid cause sold cannot really get through the passage)
- takes ~2-4 hours depending on chyme composition
- if it is more fat dominant takes more time (more like 4 hours); whereas more carb dominant would be around the 2 hour mark (my note)
GI Tract - stomach - gastric gland
key stomach cell types in gastric gland:
mucous cells:
- secrete mucus, bicarbonate (can protect some of the wall from highly acidic lumen)
◦ into stomach along inner surface
exocrine cells:
- parietal cell: secrete hydrochloric acid (HCl)
- enterochromaffin-like (ECL) cells: secrete histamine
- chief cells: secrete pepsinogen
◦ into stomach lumen
enteroendorine cells:
- G cells: secrete gastrin
- D cells: secrete somatostatin
◦ into bloodstream
-circulate till it finds target cells and binds onto them
GI Tract - stomach - gastric gland (2)
pepsinogen - inactive:
- so does not digest cells forming it
- activated to pepsin by HCl (key thing)
- pepsin breaks proteins into peptide fragments; most active in highly acidic environment
- mucus, bicarbonate secretions form protective barrier for epithelium against HCl
HCl also:
- increases activity of lingual lipase and inactivates salivary amylase
- partially denatures proteins
- kills some pathogen
GI Tract - stomach - acid regulation
parietal cell
- forms hydrogen and bicarbonate
- hydrogen crosses the stomach lumen
- bicarbonate into bloodstream
- chloride from bloodstream into stomach lumen
- hydrogen and chloride combine in stomach lumen to HCl
my notes on diagram information:
- counter transport (secondary) bicarbonate and chloride (basolateral membrane)
- hydrogen crosses apical apical membrane to lumen (primary active transport (ATP) hydrogen-potassium pump)
◦ potassium into parietal cell
◦ K and Cl come out through facilitated diffusion
across apical membrane
◦ want hydrogen and chloride in lumen
GI Tract - stomach - acid regulation (HCl)
HCl levels in stomach - variable
- secondary messengers regulate how many hydrogen-potassium pumps inserted on apical membrane:
- gastrin, histamine, acetycholine - increase secondary messengers - more pumps - so more acid in stomach lumen (more pumps on apical membrane - more hydrochloric acid in lumen - more secretion) - excitatory
- somatostatin - decrease secondary messengers - less pumps - so less acid in stomach lumen (inhibitory)
* what is causing what - gastrin in not effecting number of pumps, instead it effects number of secondary messengers - does not directly go to that (2 steps)
Gastrointestinal Regulation - cephalic phase
cephalic phase in mouth: salivation
cephalic phase in stomach:
- food not present in stomach
- preparation for food coming
- increases in HCl triggered by gastrin, histamine, acetylcholine (Ach) secretions
- as food in not yet present, there are relatively small changes in acid secretion compared to to when food arrives in stomach
-> as far as we get before food in actually in stomach
Gastrointestinal Regulation - gastric phase
gastric phase - food arrives in stomach (stronger effects than cephalic phase)
- stomach receptors detect change in distension, acidity, amino acids, peptides
neural - parasympathetic and enteric
- increase in HCl secretion (sympathetic can inhibit HCl secretion)
- increase in gastric motility (more mixing waves) so greater gastric emptying (motility increasing goes to greater emptying)
hormonal - gastrin secretion
- increase in HCL secretion
- increase in gastric motility (more mixing waves) and relax pyloric sphincter so greater gastric emptying
◦ if opening gets larger, more will go out (under the
influence of gastrin) - every mixing waves that
comes in can splash more into duodenum
- increase in lower esophageal sphincter contraction - regurgitation prevention (constrict that valve; the enterence to prevent backflow into esophagus)
regulation - negative feedback
- too much HCl secretion inhibits gastrin secretion and stimulates somatostatin secretion (inhibit acid secretion)
◦ both decrease HCl secretion
Gastrointestinal Regulation - intestinal phase
intestinal phase - food arrives in duodenum (small intestine)
duodenum stimuli detected by receptors and can alter gastric emptying
* neural (enterogastric reflex) - short and long reflexes (just difference of water level you go to but result is the same of decreasing gastric emptying)
◦ effect directly on stomach or higher up then
coming down to level stomach
◦ long - change balance of parasympathetic and
sympathetic (increase sympathetic and decrease
parasympathetic)
* hormonal- enterogastrones (secretin, CCK)
◦ can just keep it to the 2 hormones
◦ if we increase secretion of those hormones, we
get higher levels in blood that will decrease
gastric emptying
Gastrointestinal Regulation - intestinal phase (response)
response - decreased gastric emptying
- decreased gastric motility (less mixing waves) - to get optimal level of gastric emptying, since majority of it before was increasing it
- increased contraction of pyloric sphincter
- trying to match gastric emptying to small intestine digestion/absorption
- overload duodenum - dumping syndrome - nausea, sweating, dizziness, diarrhea, vomiting
