Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
34 Cards in this Set
- Front
- Back
What are short reflexes in git?
|
reflexes controlled by ganglia outside the GI tract eg, celiac ganglion
|
|
When does swallowing occur?
|
when a food bolus comes in contact with pressure receptors in the pharynx
|
|
Where is swallowing center?
It's efferents? |
-Medulla
- Efferents are vagus and glossopharyngeal nerves |
|
Stages of esophageal phase of swallowing?
|
-Respiration is inhibited
- Bolus is moved into oral pharynx - larynx is raised and glottis closes - esophageal sphincter is relaxed and bolus enters the upper esophagus -peristalsis initiates and leads to downward movements -larynx descends, glottis opens, respiration restarts |
|
Function and importance of upper esophageal sphincter?
|
- contracted at rest, by the action of continuously firing motoneurons
- prevents the entry of air which would otherwise follow the -ve intrathoracal pressure - relaxes prior to swallowing due to inhibition of discharge of somatic nerves (cns mediated) |
|
What is receptive relaxation in stomach?
|
Stomach relaxes after receival of food, increasing its volume
- involves a long reflex (vagovagal) and a local reflex in myenteric plexus. - mediated by atp or vip. -continues until swallowing ceases |
|
What controls the basic electrical rythm of stomach?
Where is this pacemaker located? |
A pacemaker located in the proximal region of greater curvature, in longitudinal muscle
-frequency of basic electrical rythm is about 3 per minute |
|
what does basic electrical rythm initiate?
|
low amplitude contraction waves
|
|
how are high amplitude contraction waves created?
|
acetylcholine(or gastrin, substance P) further depolarize smooth muscle cells creating high amplitude contractions, bursts of action potentials.
|
|
Which factors influence gastric emtpying?
|
-fat
-protein -acid - hyper/hypo-osmotic solutions -----> slow gastric emptying |
|
What is gastrin? How is it produced?
what are the effects of gastrin? |
-A hormone produced by G cells in the stomach antrum
- is produced after stomach distension - causes secretion of highly acidic gastric juice - stimulates stomach wall contraction -enhances activity of pyloric pump |
|
How do fats/protein delay stomach emptying?
|
upon entering the duodenum proteins/fats stimulate release of cholecystokinin. cck blocks the actions of gastrin on antral muscle
|
|
How do acids influence gastric emptying?
|
acid in duodenum releases secretin,which acts directly on smooth muscle and relaxes it
|
|
how does sympathetic system affect gastric emptying?
|
it blocks the response of myenteric neurons to acetylcholine
|
|
What is the migrating myoelectric complex? (stomach& small intestine)
|
-A series action potentials triggering powerful contractions that clears any undigested food or chyme in stomach/intestine.
|
|
What is segmentation in small intestine?
|
Standing waves produced by the pacemakers, creating randomly standing waves of contractions along the small intestine.
- these ensure chyme contact against the epithelium |
|
Describe stages in peristalsis
|
1. Distention of ileum activates met-enkephalin neurons with ascending axons, that mediate contraction above the distended portion.
2. Distention also stimulates VIP neurons that trigger relaxation in the area ahead of distention 3. other sets of neurons, serotonin, substance p, stimulate later contraction in the relaxed area. 4.chyme is pushed forward,distends the region there and the whole process repeats |
|
What reflexes control peristalsis? (long,short, local?)
|
Local reflexes in myenteric plexus.
|
|
When does the ileocecal valve open allowing its contents into cecum?
|
When pressure in ileum rises 15-20mmHg above colon.
|
|
Which hormone is linked to generation of migrating myoelectric complex?
|
motilin produced by the epithelium of the upper intestine
|
|
3 motility 'stages' of small intestine
|
- migrating myoelectric complex during interdigestive phase
-segmentation -peristalsis |
|
term for motility in colon?
|
haustral shuttling
|
|
gastrocolic reflex
|
the incease of colon motility during or shortly after a meal.
|
|
which cells secrete which compounds in the stomach?
|
-mucus cells
-parietal cells : HCL and intrinsic factor - chief cells: pepsinogen -g-cells : gastrin and somatostatin |
|
how is HCL secreted by parietal cells?
|
co2 + h2o -> h2co3 (under enzymatic activity of carbonic anhydraze)
-h2co3 -> hydrogen ions and hydrogen carbonate -hydrogen ions are exchanged with K from lumen -bicarbonate ions are exchanged with Cl and enter venous blood. -Cl follows the hydrogen pumped into lumen |
|
stages of stimulation of gastric secretion
|
-cephalic phase (imagining, smelling etc)
- gastric phase : *long reflexes *local reflexes *humoral factors (gastrin) -intestinal phase : secretion of chyme into intestine affects gastric secretion |
|
stages of inhibition of gastric secretion.
|
cephalic phase : symp. stimulation increases somatostatin release (inhibits parietal and G cells)
gastric phase: -ve feedback of acidic milieu in antrum, inhibits release of gastrin -intestinal phase: acids in duodenum stimulate release of secretin (inhibits parietal cells and gastric motility) |
|
What are the secretions of pancreas ? (acinar and epothelial cells)
|
Acinar cells secrete:
-nucleases,peptidases,amylases,lipases Ductal cells secrete: -water, bicarcarbonate and Na ions. |
|
what are the saliva components?
|
-sodium,potassium,calcium,bicarbonate
- IgA, lysozyme, lactoferrin - alpha-amylase(ptyalin) -mucoproteins for lubrication |
|
how is sodium bicarbonate formed in pancreas? (NaHCO3)
|
1. co2+ h2o -> h2co3 (carbonic anhydrase)
2. h2co3 -> H + HCO3 3. hco3 transported (with Na) out of cell into lumen 4. hydrogen ion is exchanged for sodium ions at the basal site of cell. |
|
what factors stimulate panreatic secretion?
|
-smell, taste of food, hypoglycemia (cephalic phase)
- distention of stomach : gastropancreatic reflex -factors stimulating the release of gastrin eg.proteins,amino acids, calcium cause a low-volume high-enzyme secretion from pancreas Intestinal phase: -entry of chyme(proteins/fats) in duodenum stimulates CCK-> secretion of high protein low volume juice -secretin ->rich in bicarbonate secretion |
|
What are the stimulants and effects of CCK? (cholecystokinin)
|
chyme with fats/proteins entering duodenum stimulates cck formation.
- inhibits gastric emptying - Pancreas: it binds to specific receptors on the acinar cells, mobilizes Ca and cGMP causing a secretion high in protein and low-volume -contracts the bladder |
|
Stimulants and effects of secretin
|
stimulated by acid entering duodenum
- inhibits gastrin activity in stomach -inhibits gastric motility - in pancreas: via cAMP stimulates secretion of juice rich in bicarbonate |
|
activation and protection from pancreatic proteases
|
- trypsinogen, chymotrypsinogen, procarboxypolypeptidase
-trypsinogen is secreted along with trypsin inhibitor in pancreas - in duodenum it is converted to trypsin by enterokinase or by already activated trypsin (aytocatalysis) -trypsin activates the other 2 enzymes |