export_gi 1 Flashcards
Motility
controlled movement of substances through the guy
secretion
release of substance and fluids
digestion
break down food into molecular compents
absorption
movement of nutrients and water into body
5 processes of GI
1) digestion
2) secretion (into GI from blood)
3) absorption (into blood from GI)
4) motility
5) barrier
Folding of intestine increases ___ which increases ___
surface area, absorption
3 types of intestinal folding
1) plicae (sub and muc)
2) villi (muc)
3) microvilli
2 types of intestinal muscle
1) circular
2) longitudinal
layers of GI (inside to out)
1) mucosa
2) submucosa
3) muscularis externa
4) serosa
paneth cells
produce antimicrobial peptides
M cells and Peyer’s patches
sample luminal antigens and activate WBCs (in PP) in response to pathogens
barrier function of GI
1) mucus production
2) acid destroys microorganisms
3) produce antimicrobial peptides
4) activate WBCs
5) IgA production
3 phases of GI regulation
1) cephalic phase (head)
2) gastric (stomach)
3) intestinal (intestine)
enteric nervous system (ENS) innervates ___ and ___ (regions)
myenteric and submucosal plexus
ENS regulates ___, ___, ___
1) motility
2) secretion
3) hormone release
signals to GI can start in __ or __
CNS or ENS
long vs. short reflexes
long- through CNS –> nerve plexus in GI –> response in lumen
short- bypass CNS, stimulus in lumen –> signals nerve plexus –> triggers response
receptor types in the GI wall
chemo, osmo, mechano
saliva functions
1) lubrication
2) buffer to dilute spice/acid
3) partial digestion (amylase)
4) clean teeth/tissues
5) antibacterial/fungal (lysozyme, histatin)
areas of saliva release
1) parotid (25%)
2) submandibular (70%)
3) sublingual (5%)
cephalic-phase control of salivary secretion
taster –> tongue mechanos –> salivary center of medulla oblongata –> ANS –> salivation
saliva secretion hormone regulation
hormone’s don’t regulate saliva secretion
sight and smell of food stimulate cephalic phase through the ___
medulla oblongata
xerostomia
dry mouth from no saliva (can lead to tooth decay)
Sjogrens Syndrome
immune damage of acinar cells, or side effects of certain drugs
pharynx
throat
food enters
esophagus function
controls swallowing, doesn’t contribute to digestion
3 phases of sawllowing
1) oral
2) pharyngeal
3) esophageal
what controls swallowing?
brain coordinates signal to pharynx, esophagus, and respiratory muscles
during pharyngeal phase: soft palate
pushed up to prevent entry into nasal cavity
epiglottis during pharyngeal phase
pushed down and glottis covers opening of trachea
phayngeal phase steps
1) soft palate up
2) epiglottis down
3) breathing inhibition
4) upper esophageal sphincter opens
esophageal phase
peristaltic contractions push food to stomach
- controlled by ENS
-contractions triggered by distension
muscles responsible for parstalsis
musularic externa (longitudinal and circular)
lower esophageal sphincter (LES)
relaxes with contraction
-normally closed
receptive relaxation
stomach relax to inc volume (50–>1500ml)
stomach functions
1) secrete intrinsic factor for vit B12 absorption
2) store meal
3) regulate output to small intestine
4) mix with secretions to form chyme
5) destroy microorganisms
3 regions of stomach
1) fundus
2) body
3) antrum
function of stomach body
secrete mucus, pepsinogen, and HCl
function of antrum
secrete mucus, pepsinogen, and gastrin
pyloric sphincter
between the antrum and duodenum
3 types of gastric glands (gland region)
1) mucous neck cells
2) chief cells
3) parietal cells
regions of stomach (inside to out)
1) gastric lumen
2) gastric pit
3) gland region
4) muscularis mucosa
conversion of pepsinogen to ___
pepsin- HCl cleaves 44aa off
active/inactive versions of pepsin(ogen)
- active- pepsin
- inactive-pepsinogen
Cells in stomach body, function, and destination
ECL cell- histamine- mucosa
Parietal- HCl IF- lumen
D cell- somatostatin- mucosa
Chief- pepsinogen- lumen
mucus- mucus- lumen
Cells in stomach antrum, function, and destination
G cell- gastrin- blood
mucus- mucus- lumen
D cell- somatostatin- mucosa
3 hormone and paracrine factors in gastic cells
histamine, gastrin, somatostatin
Inc enteric activity leads to:
+ gastrin secretion –> +his and +acid
+histamine secretion
+parietal cell acid secretion –> inc HCl
Effects of inc HCl
+somatostatin secretion –> -acid secretion
-gastrin secretion
Parietal cells effected (+/-) by:
+gastrin
+histamine
+ACh
-Somatostatin
Mechanisms of parietal cells:
secondary messengers activate H/K ATPase pumps, cells release acid
Chyme in the small intestine effects gastrin how?
decreases the secretion
inc symp/dec parasym effects stomach how?
dec gastric secretions
what turns on symp/off parasymp in long reflexes?
+acidity, +fat, +aas, distention, and hypertonicity in duodenum
short reflexes caused by what in duodenum?
+acid, +fat, +aas, hypertonicity, distention..
stim neural receptors –> dec gastric secretions
inc enterogasterones –> inc plasma enterogasterones –> dec gastic secretions
acid blockers for acid reflux
- antacids (buffers H+)
- histamines 2 receptor agonists (block hist signaling)
-proton pump inhib (inhibits H/KATPase
what is an ulcer?
break in mucosal barrier due to acid and pepsin
what is helicobacrer pylori?
bacteria that causes chronic inflammation –> ulcer –> inc stomach cancer risk
aids of gastric motility:
1) mix food w/ secretions
2) regulate output of chyme to SI
3) peristaltic contractions
4) pacemaker cells
5) force contraction regulated
6) gastric phase regulation of motility via ENS and gastrin secretion
Retropulsion
- stomach
* move it back causing turbulance (mixing)
slow wave oscillations
reach threshold briefly then long depolarization
vomiting is controlled by
vomiting center in MO
-response to extensive distension, gagging, toxins, etc
excessive vomiting leads to:
dehydration, salt imbalance, dec blood volume, metabolic alkalosis (loss of H+)
