GI Deck 1 Flashcards
2 functions of the GI system
1- absorb nutrients/electrolytes/H20
2- excrete waste
4 basic properties that underly 2 functions
1- motility
2- secretion
3- digestion
4- absorption
what is the cephalic phase?
activation of the GI tract in readiness for a meal (idea of food, smell, sight, sound)
which cranial nerves carry the impulse to activate salivary secretion?
CN 7 & 9 (facial and glossopharyngeal)
what is the pathway from sensory input to readiness of GI tract?
sensory input -> cortex/hypothalamus -> lower pons/upper medulla -> DMN of vagus activates parasympathetics -> increase salivary secretion (7&9), gastric secretion, pancreatic secretion, etc.
what is the oral phase?
same as the cephalic, but food is present in the mouth
what do you add with the oral response?
- chemoreceptors in tastebuds & mechanoreceptors in mouth & pharynx
what is xerostomia?
- dry mouth which reduces the pH in oral cavity, causing tooth decay, difficulty swallowing, esophageal errosion
what is the purpose of chewing?
- break down food into tiny particles
- mix with enzymes (amylases, lipases)
- mixing with mucin to lubricate
what are the main muscles of chewing and what are they innervated by?
temporalis, masseter, pterygoids
innervated by mandibular branch of trigeminal
where do GI secretions come from (3 locations)?
1) glands associated (salivary, pancreas, liver)
2) gut wall (Brunner’s) - mostly mucus/bicarb
3) intestinal mucosa
what are secretions elicited by? which systems can they come from?
secreatogogues; can be endocrine, paracrine, neurocrine
3 pairs of major salivary glands
1) parotid
2) submandibular
3) sublingual
3 types of secretion cells and how they stain
serous (dark), mucous (light), mixed
which gland is primarily serous?
parotid
which gland is primarily mucous?
sublingual
which gland is mixed?
submandibular
what are the units of secretion?
acini cells
what are demilunes?
in a mixed group of secretion cells, mucous cells swell and push serous cells into caps
What are myoepithelial cells?
present around acini cells and intercalated ducts; contain actin & myosin to contract and expel saliva forward
what are the 3 functions of saliva?
lubrication
protection
initial digestion
what does the composition of saliva depend on?
the rate of secretion & flow
how is saliva compared to the composition of blood? due to which ions?
- hypotonic
- because Na/Cl are low in saliva
3 transporters of the luminal side of acinus cell
Na/H antiporter, Cl/Bicarb antiporter, H/K antiporter (also have Na/K pump on blood side)
what is the net result of acinus cells?
- net absorption of Na/Cl; (net secretion of bicarb & K+)
at highest flow rate, (4 mL/min) what does saliva look like?
- less time for modification, looks similar to plasma but is still hypotonic
how is bicarb altered with flow rate? how does it compare to other secretions?
secrete more bicarb with flow, (normal pattern is less- secrete less K+)
what are the ways in which acinar cell secretion is regulated?
neural (symp and PARASYMP)
which CN does PS use to regulate acini cells? which neurotransmiters?
CN 7 & 9
Ach acting on muscarinic receptors, increasing IP3/Ca, increasing saliva
where does sympathetic regulation for the acini cells come from?
T1-T3/superior cervical ganglion
Ne acting on Beta adrenergics, increasing cAMP and increasing salavia
3 increases stimulation of salivary cells causes
1) saliva production
2) bicarb & enzyme secretion
3) contraction of myoepithelial cells
what does atropine block?
PS muscarinic receptors, decreasing saliva production
during which phase is swallowing voluntary?
short segment in oral phase
where is the regulatory swallowing center?
medulla & lower pons
what are the steps of the swallowing reflex?
stretch receptors near opening of pharynx - medulla/ower pons - respiratory center/ motor CNs to pharynx&upper esophagus / vagus to esophagus
what are the 3 phase of swallowing?
oral, pharyngeal, esophageal
what are the 2 functions of the UES and LES?
- propel food from pharynx to stomach
- protect airway & esophagus from acid reflux
how many waves of peristalsis do you have?
1* peristalsis - doesn’t clear entire bolus to stomach
2* peristalsis- under control of enteric NS, caused by distention of esophagus
what is receptive relaxation? which NTs cause it?
when orad stomach & LES relax at the same time; VIP and NO
which molecule causes the LES to relax?
VIP
what is greater- intraesophageal pressure or abdominal pressure?
abdominal pressure- hard to keep air & acid out of esophagus
what is LES resting tone like?
pressure is higher than esophagus or orad stomach
what thick layer of cells protects esophagus and anal canal from friction?
stratified squamous epithelium
what is GERD, and during chronic GERD what disappears?
gastroesophageal reflux disaease; LES tone is not enough, stratified squamous epithelium disappears
what factor is known to cause GERD?
increase in intrabdominal pressure- pregnancy and obesity
what is a hiatal hernial and in what population do you find them?
muscular problem, stomach sneaks through esophageal hiatus into diaphragm; found in older patients
what is achalasia?
SM does not have normal peristalsis & LES does not relax; myenteric plexus is lost
what can you use to treat achalasia temporarily?
- use atropine
What are the two types motility in the small intestine and which neural systems do they use?
Segmental (enteric NS)
Peristaltic (Ach/Substance P/VIP/NO)
What is the MMC and what is it stimulated by?
Migrating motor complex
Every 90 minutes get periodic contraction
Stimulated by motilin
major functions of gastric phase
- storage
- motor activity
- secrete IF
- secrete H+ (kills stuff & activates pepsin)
- secrete mucus & bicarb (simple columnar)
- secrete water
what is the essential factor of gastric secretion?
intrinsic factor (required to absorb B12)
how is the gastric phase regulated?
- neural (extrinsic and ENS)
- paracrine (histamine)
- endocrine (gastrin, somatostatin)
Which region prevents reflux, causes burping, accepts food? what is it closest to?
- cardia region
- closest to LES
In which region are most of the secretory cells?
fundus
In which region are the g-cells?
antrum
What are the 3 regions based on glandular tissue of gastric mucosa?
- small cardiac
- oxynitic/parietal (fundus)
- pyloric (antrum)
6 types of secretory cells in fundus/antrum
1- parietal/oxynitic cells (HCl/IF) 2- Mucous neck cells 3- peptic/chief cells (pepsinogens) 4- ECL cells (histamine) 5- D cells (somatostatin) 6- G cells
what makes up gastric juice?
HCl, pepsinogen, bicarb, mucus, IF
net secretion in stomach? net absorption?
secretion- HCl
absorption- bicarb
pathway for gastric secretion of acid
extrinsic efferents of vagus- intrinsic nerves that innervate parietal cells, ECL cells, g-cells
neurocrine, endocrine & paracrine regulators of gastric acid secretion
neurocrine- Ach,
endocrine- gastrin
paracrine- histamine
What percent of HCl is secreted during the cephalic/oral phases vs. gastric phase
30% vs 60%
5 pathways for HCl secretion during gastric phase?
1- direct- vagal on parietal cells 2- indirect- vagus - GRP- etc. 3- indirect- Ach/gastrin(?) on ECLs 4- vagovagal (distention of stomach) 5- small peptides & AAs
what is negative feedback on HCl pathway stimulated by and where?
low pH (<3) in antrum
direct and indirect effects of somatostatin
direct- SS antagonizes cAMP
indirect- SS inhibits ECL & g-cells
motility division of stomach
orad- thin walled
caudad- thick walled
GD junction functions
1) filter
2) controls rate of emptying
3) prevents reflux
gastric vs duodenal ulcer
gastric- NOT HIGH ACID; have something wrong with mucosal barrier (e.g. H. pylori)
duodenal- have high H+ (damaged pancreas, high stomach secretions)
what is Zollinger-Ellison syndrome? what 2 things does it cause?
- gastrin secreting tumor in pancreas
- increased H+ secretion, increased parietal cell mass
which electrolytes are high and which are low in saliva?
high K+, bicarb
low Na, Cl
6 changes that represent the intestinal phase of the response to the meal
(1) increased pancreatic secretion
(2) increased gallbladder contraction
(3) relaxation of the sphincter of Oddi
(4) regulation of gastric emptying
(5) inhibition of gastric acid secretion
(6) interruption of the migrating motor complex (MMC).
4 things that must happen for gastric emptying
1) increase in tone in proximal stomach
2) increased antral contraction strength
3) forced opening of the pylorus
4) inhibition of duodenum
what is the vagal pathway that inhibits gastric emptying?
H+/hyperosmolarity act on vagal afferents - activates vagal efferents to decrease the strength of antral contractions, contract pylorus, and decrease proximal gastric motility
two major factors that contribute to the inhibition/slowing of gastric emptying?
- presence of fat in duodenum
- presence of H+ in duodenum
what mediates the effect of fat on slowing gastric emptying?
- CCK secreted in the presence of FAs
- causes pylorus contraction, regulates gallbladder contraction, relaxation of sphincter of Oddi, pancreatic secretion
what mediates the effect of H+ on slowing gastric emptying?
- reflexes in enteric NS
- H+ receptors in duodenal mucosa - relay info to myenteric plexus & smooth muscle
- results in ample neutralization by pancreatic bicarb
what part of the pancreas has significant contributions towards the digestion process?
EXOcrine pancreas
- 90% of pancreas volume
- secretes enzymatic and aqueous components
what are the two components of pancreatic secretion, and what are the two cells they are secreted by?
aqueous (high bicarb) - centroacinar & ductal cells
enzymatic- acinar cells
3 things that secrete bicarb to maintain neutral pH in duodenum so pancreatic enzymes can be active
1) pancreas ductal cells *** largest contributor
2) duodenal surface epithelial cells
3) biliary ductules
what are the main effector arms of the pH regulatory system? which hormone are they acted upon by?
ducts
secretin - stimulates secretion of bicarb (& negative feedback)
which cycle does low pH in duodenum signal?
low pH in duodenum- stimulates S cells in intestinal epithelium- secretin is released- secretin stimulates secretion of bicarb- negative feedback on low pH
what does secretin increase in ductal cells? what does this product do?
- increases cAMP which opens CFTR Cl- channels so Cl- is spilled into lumen
what does an elevation of Cl in the lumen stimulate?
Cl reabsorption and bicarb secretion (antiporter)
what are the two sources for bicarbonate?
- absorbed across basolateral membrane via NBC-1 symporter (Na dependent!!)
- carbonic anhydrase breaking down H20 & CO2 intracellularly (extrudes proton into pancreas venous blood)
net result of pancreatic ductal secretion
secrete bicarb into lumen
absorb H+, acidify pancreatic venous blood
what is mutated in cystic fibrosis? what problem does this cause in the pancreas?
CFTR, decreases ductal secretion, precipitates enzymes in duct & destroys gland
if you administer secretin, what should happen? which disorder is this altered in?
- ductal cells should produce bicarb
- Zollinger-Ellison, gastric-like cells in pancreas that respond to secretin by releasing gastrin
what stimulates CCK release from I cells in small intestinal epithelium?
1) FAs & AAs binding to I cells
2) FAs & AAs binding to paracrine cells that release CCK-RP
3) Neural stimulation of pancreas releasing monitor peptide
2 ways CCK stimulates pancreatic acinar secretion
1) binding to CCK1 receptors on acinar cells (endocrine)
2) paracrine effect stimulates neural reflex, causing vagovagal reflex in pancreas, releasing Ach, GRP, & VIP
How do CCK, Ach, and GRP act?
mobilize intracellular Ca2+, causes fusion of zymogen granules & exocytosis
how does trypsin inhibit pancreatic secretion in absence of protein
- trypsin can bind to protein, CCK-RP & messenger peptide and degrades what it binds
- with low protein, it degrades CCK-RP and messenger peptides, don’t get release of CCK to stimulate exocytosis of vesicles
what are pancreatic proteases activated by?
trypsin
what is pancreatitis (inflammation of pancreas) caused by?
premature activation of proteases by trypsin
what activates trypsinogen to trypsin and where?
- enterokinase as a brush border enzyme in the small intestine
pathways for stimulation of pancreatic secretion (cephalic, gastric, intestinal)
- cephalic- thought of food- vagal/enteric nerves
- gastric- stomach distension- vagovagal
- intestinal
- low pH- secretin
- peptides- CCK
- distension- enteropancreatic reflexes
- CCK sensory enteric neurons- vagovagal
what is the ASBT and where is it found?
apical sodium bile transporter, found in terminal ileum, recycles 90-95% of bile when lipid absorption is complete
what is the majority of our diet?
50% carbs, mostly polysaccharides
what can be absorbed through the intestinal epithelium?
carbs- 3 monosaccharides (GFG)
proteins- AAs, di & tripeptides
fats- cholesterol, monoglycerides, lysolecithin, fatty acids
what is trehalose broken down into and by what?
2 glucose molecules by trehalase
what is sucrose broken down into and by what?
glucose & fructose by sucrase
what is lactose broken down into and by what?
glucose & galactose by lactase
what is the most significant enzyme to break down starch and what does it break down? what can it not digest?
- pancreatic alpha amylase
- only hydrolyzes alpha 1,4 linkages (straight chains)
- can not digest beta 1,4 linkage (cellulose)
what are the products of alpha amylase and their enzymes?
maltose (maltase), maltotriose (sucrase), alpha-dextrins (alpha-dextrinose)
how are carbohydrates transported across the apical membrane?
- SGLT1- symporter w/ Na for gulcose & galactose, is 2* active
- GLUT5- fructose
how are carbohydrates transported across the basolateral membrane?
Glut2- passive, does glucose/galactose/fructose
where does protein digestion start and with which peptide? what does it give?
stomach, pepsin; gives intact proteins and large peptides
what are 5 major pancreatic proteases secreted as inactive precursors/what are their active forms?
trypsinogen/trypsin chymotrypsinogen/chymotrypsin proelastase/elastase procarboxypeptidase A/carboxypeptidase A procarboxypeptidase B/carboxypeptidase B
what are the two classes the 5 major pancreatic proteases secreted as inactive precursors are divided into?
endopeptidases - hydrolyze interior peptide bonds (pepsin, trypsin, chymotrypsin, elastase)
&
exopeptidase- hydrolyze one amino acid at a time from C-terminal end (carboxypeptidase A&B)
how are AAs, dipeptides & tripeptides absorbed?
AAs- w/ Na symporter (and Na/K ATPase on bl side)
Di/tripeptides- with H+ symporter (broken down with peptidase inside cell)
AAs leave via facilitated diffusion
what is the major supply of lipids in the diet? what is it broken down into and by which enzymes?
triglycerides
- monoglycerides & 2 FAs
- lingual, gastric & pancreatic lipases
what is used for emulsification in the stomach & small intestine? what are the emulsifications called in the SI?
stomach- dietary proteins
SI- bile acids & lysolecthin (caused micelles)
what are the 3 major pancreatic lipolytic enzymes that work at a neutral pH?
pancreatic lipase
phospholipase A2
cholesterol ester hydrolase
which cofactor is important to prevent bile acids from inhibiting phospholipase activity?
colipase
what are the 5 steps of lipid absorption?
1) lipids are released from micelles at the apical membrane
2) lipid digestion products are re-esterified with free fatty acids
3) products packaged with apoproteins to form chylomicrons
4) chylomicrons are secreted by exocytosis
5) chylomicrons are transported by lymphatic capillaries
what is a phospholipid broken down into and by which enzyme?
lysolecithin & FA
by phospholipase A2
what is the main way in which water is reabsorbed in the small intestine?
paracellularly via leaky tight junctions
what is the major site for Na reabsorption in SI? using which transporters? what is it absorbed with in this region?
jejenum
SGLT, AAs, Na/H+ exchanger
absorbed with bicarb
in addition to the 3 Na transporters, what does the ileum also have?
bicarb/Cl exchanger with basolateral Cl transporter
in the small intestine, which cells are responsible for absorption? secretion?
absorption- brush border epithelial cells
secretion- crypts
what does cholera do?
causes the overproduction of cAMP, stimulating the CFTR Cl- channel and causing the secretion of water > water absorption
what are the two types of diarrhea and examples of things that cause them?
osmotic- lactose intolerance
secretory- cholera, e. coli
what do you have on the basolateral side of intestinal crypt cell?
- Na/K+ ATPase
- Na/K/2Cl- cotransporter
- receptor for hormones/neurotransmitters that activates cAMP to open CFTRs
what is required for Ca2+ absorption? what does it induce?
active form of vitamin D (1,25 dihydroxycholecaliferol)
induces synthesis of calbindin D-28K to bind Ca2+ in cell
what is required for B12 absorption? where does it occur, and by which mechanism?
intrinsic factor, ileum, cotransport with IF
