GI mod 2 Flashcards
what is digestion
secretion of gastric juices
digests food into chyme
what is chyme
partially digested food
absorption in stomach?
none, except aspirin, NSAIDS, alcohol
how much alcohol absorbed in stomach vs SI
20% stomach
80% SI
carbonated drink and empty stomach - absorption rate
absorbs faster
stomach and motility
after initial digestive processes the stomach propels food into duodenum
what stimulates relaxation of stomach to prepare for bolus
swallowing
relaxation of the stomach musculature allows what?
allows the stomach to serve as a reservoir for the incoming food
stomach has ability to accommodate large volume changes?
true
what is the vago-vagal reflex
food enters stomach - stomach distension stimulates vagal mechanoreceptors which reflexively stimulate vagal VIP (vasointestinal peptide) release to relax smooth muscle of stomach wall
what is the stimulus of gastric emptying
parasympathetic activity
sequence of gastric emptying
- retropulsion: contractions push food back towards the body of the stomach - 4-5 sequential peristaltic waves push chyme back and forth (churn)
- the last wave forces pyloric sphincter to open and allow small amount of chyme is pushed into duodenum
how open does the pylorus get?
just a small amount 1-2cm
-not enough to have duodenum regurg back into pylorus
another name for pylorus
antrum
what passes faster liquids or solids
liquids
why type of solids pass faster than others?
carbs and proteins empty faster than fats
how long does it take to empty 50% of stomach
2-3hrs
total emptying time of stomach?
4-5hrs
rate of gastric emptying is dependent on what
volume . osmotic pressure and type of food ingesteed
factors that increase rate of gastric emptying
larger food volume increases rate of gastric emptying
factors that decrease rate of gastric emptying
- hyper/hypotonic fluid
- fatty foods
- increased rate of acids entering duodenum
* *these act as a negative feedback loop from the duodenum
how does hyper/hypotonic fluid decrease rate of gastric emptying
receptor in stomach/duodenum detect osmotic pressure
–this allows time to create/facilitate an isoosmotic environment for duodenum
how does fatty foods decrease rate of gastric emptying
- -CCK (cholecsystokinin) synthesized and released by duodenum/SI will inhibit gastric motility and decrease acid production
- -fats are digested in the duodenum - if too much fat enters SI then feedback loop slows down rate to allow time to properly digest fats
how does increased rate of acids entering the duodenum decrease the rate of gastric emptying
acid is neutralized in duodenum so if too much entereing then feedback is to inhibit gasyric emptying to decrease acid entering duodenum
regions of the stomach
- cardiac
- funcus
- body
- pyloric
- lesser/greater curvature
affect of decreased blood glucose - affect on gastric motility and gastric emptying
increases gastric motility but does not increase emptying (hunger pains)
what is pyloric stenosis
how is it treated
AKA infantile hypertrophic pyloric stenosis (IHPS)
- hypertrophy of the pyloric sphincter - impairs gastric emptying
- treated as soon as possible with surgery (Pyloromyotmy performed by laproscopically)
what is gastric juice made of
combo of acid, mucus, and pepsinogen
major secretions of the stomach
mucus acid (HCl) Pepsinogen hormones intrinsic factor
what is the active form of pepsinogen
pepsin
what hormones are secreted from stomach
gastrin histamine somatostatin serotonin ghrelin
function of mucus
- protects the mucosal layer from acid and pepsin (protease)
- provides transitional layer to protect the epithelium of the stomach
- this layer has a neutral pH (7.0) at the epithelial surface
- the mucus contains high levels of bicarb (HCO3-) to neutralize the H+
pH of stomach
1.5
what is the stimulus of mucus secretion
- prostaglandins
2. nitric oxide
what can disrupt the mucus barrier
- aspirin, NSAIDS, and alcohol
- bile salts - regurgitated from SI
- helicobacter pylori
what happens if mucus barrier is disrupted
inflammation/ulceration
function of acid secretion
- dissolve food
- inactivation of digested bacteria/microbes
- convert pepsinogen to pepsin
what secretes acid in the stomach
parietal cells
process of acid secretion from parietal cells
- acid formation/secretion occurs in exchange for bicarb
- increased gastric acid secretion will increase bicarb entering plasma
- proton pump (H+/K+ + ATPase) of parietal cells secrete H+ into stomach while HCO3- is secreted in GI interstitial/plasma fluid
what are the stimuli of acid secretion in the stomach
- synergystic with:
- ACh - via vagus nerve (parasympathetic)
- gastrin
- histamine
* *syngergy of all three stimulate large amount of acid production - if just one present then smaller amount of acid production
inhibition of acid secretion
- somatostatin
- prostaglandin E2 (PGE2)
- secretin
- gastric inhibitory peptide (GIP)
- glucagon
3 gastric phases of acid secretion
- cephalic phase
- gastric phase
- intestinal phase
what is the cephalic phase of acid secretion
sight, smell, taste, thought of food, emotions etc stimulate acid secretion via vagus nerve (parasympathetic)
what is the gastric phase of acid secretion
- mechanical stretch from food stimulate vagus nerve to stimulate acid secretion
- peptides/amino acids in food stimulate G cells to release gastrin which stimulates acid
- food also increases pH which inhibits somatostatin release allowing an increase of acid secretion
what is the intestinal phase of acid secretion
negative feedback from food entering duodenum inhibit acid secretion in stomach
pharmaceutical strategies to reduce acid production
- H2 receptor antagonists
- inhibit histamine signaling on parietal cells
- ex. cimetidine, ranitidine, famotidine, nizatindine - PPI (proton pump inhibitors)
- inhibit H+/K+ ATPase proton pump of parietal cells
- ex. omeprazole, lansoprazole, esomeprazole, raceprazole, pantoprazole
function of pepsin secretion
proteolytic enzyme that breaks down proteins in stomach
location of pepsin secretion
secreted by chief cells of the stomach
MOA of pepsin secretion and inactivation
pepsinogen is converted to pepsin in an acidic environment (pH5.0) of duodenum
stimulus of pepsin secretion
parasympathetic stimulation, gastrin, CCK, and secretin
function/target of gastrin
- stimulates acid production from parietal cells
- indirectly by stimulating the release of histamine from enterochromaffin-like cells (ECL)
- gastrin receptors also located directly on parietal cells - stimulates gastric mucosa growth (promotes parietal cell proliferation)
location of gastrin secretion
secreted from G cells in the antrum of stomach
stimulus of gastrin secretion in the stomach
parasympathetic and presence of digested proteins
inhibition of gastrin secretion in stomach
negative feedback - increased acid in stomach inhibits gastrin release, somatostatin inhibits gastrin and histamine
what is ZES
zollinger-ellison syndrome
–caused by gastrin producing tumors results in excessive acid production
function/target of histamine
stimulates HCl secretion from parietal cells, attaches to H2 receptors on parietal cells
location of histamine secretion in stomach
secreted from enterochromaffin-like (ECL) cells in stomach
stimulus of histamine release in stomach
gastrin
inhibition of histamine release in stomach
somatostatin inhibits histamine (and gastrin)
clinical application of histamine release in the stomach
H2 receptor antagonists
what is the function of somatostatin
universal inhibitory function throughout GI tract
-inhibit parietal, chief and ECL cells
location of somatostatin release in stomach
released from D cells (delta cells) in stomach/antrum…also pancrease and intestines
stimulus of somatostatin release in stomach
acid
clinical application of somatostatin release in stomach
metabolic by products of H Pylori eventually inhibit/destroy D cells - this sets the stage for increased acid production leading to ulcer
function of serotonin (5HT)
regulate/promote gut motility, also inflammatory role
location of serotonin release in stomach
majority of serotonin is produced in GI tract by enterochromaffin cells (EC)
serotonin thought to play a role in what conditions
GI disorders (IBD, IBS, diverticulitis, CRC)
what is serotonin syndrome
diarrhea, vomiting, are GI responses (also increases cardio and CNS functions)
what is the function of ghrelin
- hunger hormone - plays a role in appetite sensation/feeding behavior
- -also stimulates growth hormone - fast acting - stimulates the sensation of hunger - levels rise just before meals
location of ghrelin release in stomach
secreted from endocrine cells mostly located in stomach
also secreted from kidneys hypothalamus pituitary placenta
stimulus of ghrelin
glucagon
inhibition of ghrelin
leptin, glucose, insulin, and other indicators of feeding
what secretes intrinsic factor
secreted by parietal cells of stomach
why is intrinsic factor necessary in stomach
- B12 - plays role in maturation of erythrocytes
2. deficiency of B12 absorption will develop pernicious anemia
what are the epithelial folds in the stomach called
ruggae
what is the cell type of the surface epithelial cells of the rugae
mucus cells
-function: produce thick mucus - production from abrasion of food and from acidic pH levels in stomach
what is located at the base of the folds of rugae
gastric glands - type of cells will vary by region of the stomach
what cells are located in the base of the rugae of stomach in the body or fundus regions
- mucus cells - located in neck of gastric glands, secrete thin watery mucus to liquefy stomach contents
- parietal cells - secrete HCl and IF
- chief cells - secrete pepsinogen to promote protein digestion
- enterochromaffin cells (EC) - secrete serotonin to increase motility/GI regulatory role
- enterochromaffin-like cells (ECL) - secrete histamine to promotes acid secretion
what type of cells are located at the base of the rugae in stomach in the cardiac region
mucus cells - secrete thin watery mucus to liquefy stomach contents
what type of cells are located at base of rugae in stomach in the pyloric (antrum) region
- mucus cells - secrete thin watery mucus to liquefy stomach contents
- G cells - secrete gastrin ( promotes acid secretion/motility and gastric mucosa growth)
- D cells - secrete somatostatin, inhibitory to parietal and chief cells
about the adjustable gastric band
LAP BAND
- placement of a band creates a small pouch at the top of the stomach
- small pouch fills with food quickly and the passage of food from the top to the bottom of the stomach is slowed
- upper part of the stomach experiences a sensation of fullness
about the vertical banded gastroplasty
stomach stapling with LAP BAND
- MC restrictive operation for weight control
- band and staples are used to create a small stomach pouch
- small opening in bottom of the pouch thru which food can pass into remainder of stomach
affect of smaller pouch with the VBG
- sense of fullness occurs with less food intake
- if continue to eat then individual will experience pain, nausea or possible vomit
- helps the person to eat smaller portions and lose weight over time
outcomes of VBG
- initial - will vary from complete wt loss( 30%) some weight loss (50%) to poor
- long term - many pts may regain wt by gradually stretching the small pouch
what is gastric bypass procedures
- reduces stomach size by creating small pouch (staples or lap ring to mimic pyloric valve)
- physically redirect anatomy of GI tract
- bypass created so chyme bypasses proximal SI to limit absorption of calories (and nutrients in SI)
outcomes of gastric bypass procedures
long and short term outcomes suggested to be better than banding/stapling procedures
complications of gastric bypass procedures
- nutritional deficiencies - long term supplementation plan necessary to compensate for by pass
- dumping syndrome - rapid gastric emptying, occurs when jejunum rapidly fills with undigested food from the stomach; results in cramping, bloating, nausea, vomiting, diarrhea, and SOB
- direct complications - bleed and infections
what is gastritis
commonly refers to inflammation of the gastric mucosa (lining of the stomach - NOT referring to peptic ulcer dz)
used to cover a variety of symptoms resulting from the inflammation and ulceration of gastric mucosa
what is acute gastritis
injury to the gastric mucosa
what causes acute gastritis
- drugs/chemicals (NSAIDS - inhibit PG which normally promote mucus secretion
- H pylori infection
- alcohol and smoking
how fast does acute gastritis heal
within a few days if offending factor removed ASAP
what is chronic gastritis
degenerative gastritis that is more common in the elderly
results in chronic inflammation, mucosal atrophy and epithelial metaplasia
two types of chronic gastritis
- Type A: chronic fundal gastritis
2. Type B: chronic antral gastritis
what is Type A gastritis
- Type A: chronic fundal gastritis
- less common
- suggested to be a result of autoimmune disorder (Abs attack parietal, chief cells, and IF)
- mucosa degerates - loss of parietal cells and chief cells lead to decreased gastric acid, pepsinogen and IF = pernicious anemia
what is type B gastritis
Type B: chronic antral gastritis
- 4x more common than type A
- NOT considered autoimmune dysfunction - no loss of acid secretion, parietal cells, or IF
- extrinsic environment cause - H pylor, alcohol, tobacco, NSAIDS
what is more common gastric ulcers or duodenal ulcers?
duodenal ulcers (gastric ulcers are 1/4 as common)
location of gastric ulcers
MC in antrum
pathophys of gastric ulcers
- chronic exposure to various substances results in break down of -protective mucosal lining of the stomach
- mucosal lining becomes permeable to H+ ions
- submucosal area exposed to digestive acids and secretions
- damaged mucosa releases histamine which increases release of acids/pepsinogen, capillary permeability
gastric ulcers possess a higher risk for what vs duodenal ulcers?
risk of cancer
two major risk factors for benign gastric ulcers
- chronic use of aspirin, NSAIDS
- H pylori infection - metabolic byproducts damage/destroy D cells which promotes increased acid production; present in 60-80% of individuals with gastric ulcer (vs duodenal ulcers 95-100%)
other risk factors for gastric ulcers
chronic gastritis chronic alcohol use smoking increasing age reflux of bile salts from duodenum
how is reflux of bile salts from duodenum a risk factor for gastric ulcers
- feedback mechanisms disrupted causing loose pyloric sphincter
- bile disrupts gastric mucosa - allows hydrogen ions to cross into mucosa
- this decreases pH of mucosa and damages sub mucosa
s/s of benign gastric ulcers
- food provoking pain pattern - immediately after eating
- -different pattern for duodenal ulcer (relief with eating and pain 2-3 hrs post eating) - gastric ulcers - more chronic in nature vs exacerbation/remission with duodenal ulcer
