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125 Cards in this Set
- Front
- Back
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PNS afferents lead to... |
nausea distention satiety |
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PNS efferents |
Vagus nerve vaGo-vagal reflexes S2-4 outflow |
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SNS afferents lead to... |
conscious pain |
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SNS efferents |
preganglionic fibers (arise in spinal cord) |
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enteric NS controls... |
GI secretions motor activity sphincter contraction blood vessels |
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SNS projects to the GI tract from the .... |
spinal cord: thoracic and lumbar regions |
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PNS projects to the GI tract from the.... |
medulla & spinal cord S2-S4 |
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where is enteric nervous system located? |
within GI wall: submucosal and myenteric plexuses between the longitudinal and circular muscle layers and within the submucosal layer of GI tract |
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somatotomotor pudendal nerve responsible for |
sensory and motor control of external anal sphincter |
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where do parasympathetic post-ganglionic neurons synapse? |
directly on myenteric plexus (muscarinic acetylcholine receptors) |
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layers of the gut |
inner --> outer mucosa: epithelial cells submucosal plexus circular muscle myenteric plexus interstitial cells of cajal longitudinal muscle serosa |
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myenteric plexus |
continuous throughout entire length of GI tract primarily involved in coordination of smooth muscle activity regulates circular and longitudinal smooth muscle electrical & contractile activities |
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submucosal plexus |
primarily in small and large intestines controls fluid & electrolyte secretion/absorption regulates local tissue blood flow regulates luminal surface properties |
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interstitial cells of cajal |
regulate motor activities of enteric nervous system mesenchymal non-neuronal tissue of origin pacemaker cells which regulate membrane potential of BER (basal electrical rhythm) |
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enteric motor neuron inhibitory junction potentials mediated by... |
nitric oxide vasoactive intestinal peptide inhibitory |
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enteric motor neuron excitatory junction potential mediated by |
substance P acetylcholine |
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basal electrical rhythm (BER) |
slow waves below threshold ... give no smooth muscle contractions (if below Ca++ threshold) |
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force and duration of smooth muscle contraction in gut are directly related to... |
amplitude and frequency of electrical action potentials (increased probability from parasympathetic stimulation and other inputs) smooth muscle contractions = mechanical evens |
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where do long sweeps of peristalsis occur? |
esophagus (swallowing) descending colon Migrating motor complex (MMC during fasting) |
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peristalsis |
generally movements of SHORT distance upstream: activators (muscarinic receptors) downstream: inhibitors/ relax muscle |
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segmentation |
stationary contraction dominated by circular smooth muscle |
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MMC |
migrating motor complex/ "intestinal housekeeper" during interdigestive (postprandial) state w/ food in intestine, neural programming defaults to continuous motor activity of small intestine w/out food in upper small intestine for a period of roughly 2 hrs, release burst of motilin --> segmentation activity is arrested/ replaced w/ MMC |
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where is MMC initiated? |
stomach antrum |
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effect of opiods and Mu receptors in gut |
inhibit enteric nerve activity --> inhibit forward motility and water/electrolyte secretion -->constipation suppress: -excitability -ACh release (decreases longitudinal muscle contraction) -VIP/NO release (increased circular smooth muscle segmental tone) -VIP/PGE1 (decreased secretions) |
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muscles of esophagus |
upper 1/3: striated distal 2/3: smooth muscle lower esophageal sphincter remains contracted except when swallowing, vomiting, or eructation (belching) |
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dysphagia |
difficulty swallowing failure of propulsive force incoordination of contraction & relaxation obstruction to flow UES can be involved |
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achalasia |
cannot swallow idiopathic degeneration of ganglion cells of myenteric plexus and/or dorsal motor nucleus, and/or vagal fibers failure of LES to relax normally |
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common factors lowering LES pressure leading to GERD |
high fat diet chocolate peppermint ETOH smoking hyperchlorohydria (SX stomach acid) progesterone gastric distension (aerophagia, gastroparesis) |
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defecation: gastroileal reflex |
vago-vagal reflex: stomach distended/chemoreceptors and stretch send afferent signal to medulla, efferent vagus to ileum "move things along because another cargo load is coming" |
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defecation: colic reflex |
eat something --> stomach --> dorsalmodal reflex (less vagus) synapse to S2-S4 pelvic splanchnic nerves --> myenteric plexus efferent vagus innervates distal colon (??) |
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defecation: orthocolic reflex
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awake/sit upward sends info to ileum and distal colon to undergo motor activity |
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parasympathetic innervation of defecation |
pelvic splanchnic nerves |
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somatomotor innervation of defecation |
pudendal and levator ani nerves |
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vomiting |
chemoreceptor trigger zone (area of postrema), higher centers of brain, GI vagal or sympathetic Afferents --> vomiting center (medulla) stimulated --> LES relaxed, glottis closed, contract diaphragm--> antiperistalsis |
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serotonin |
aka 5HT receptors in gut initiate afferents that go to medulla, trigger emesis |
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enterochromaffin cells |
endocrine cell that releases serotonin from stomach to trigger emesis triggered by various stimuli (staph enterotoxin, syrup of ipecac) |
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phases of integration of GI responses to food |
cephalic gastric intestinal (food is in intestine, tells other organs what to do) inter-digestive (nothing in GI sys; MMC) |
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acinus |
salivary gland |
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types of saliva |
serous (watery w/ enzymes) mixed mucus (glycoprotein mucins lubricate food) |
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composition of saliva |
hypotonic K+, HCO3- solution containing elctrolytes of plasma and organic compounds |
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what disease inhibits salivon? |
sjorgren's disease autoimmune dz that attacks salivon, antibodies against NK1 receptors |
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pancreatic acinar cell responsible for... |
(inactivated) enzyme secretion (zymogen granules) |
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pancreatic duct epithelial cell responsible for... |
HCO3- secretion |
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what activates trypsinogen |
entero-kinase formed in duodenal enterocytes |
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fxn of trypsin |
activate pancreatic enzymes that flow into jejunum lumen |
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what components are responsible for lubrication, protection of the stomach |
mucus, HCO3-, trefoil peptides |
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what components are responsible for protein digestion, B12 binding in the stomach? |
H+, intrinsic factor |
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what components are responsible for protein and fat digestion in the stomach |
pepsinogen, gastric lipase |
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what components are responsible for regulating acid secretion in the stomach |
gastrin somatostatin histamine |
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layers of onxyntic gland in corpus (stomach) |
superficial epithelial cell mucus neck cell stem/regenerative cell parietal (onxyntic) cell chief cell endocrine cells (G, D, ECL (histaminal) cells) |
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chief cells make... |
pepsinogen |
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where did onxyntic cells get their name? |
full of mitochondria- which are responsible for oxidative phosphorylation
very high oxygen consumption! |
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GRP |
gastrin-producing peptide post-synaptic neurotransmitter controlling gastrin release |
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fxn of parietal cell
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HCl and intrinsic factor production to release into lumen |
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fxn of ECL cell |
produce histamine to release into lamina propria |
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acid in antrum (of stomach) stimulates ___ to inhibit ____ |
stimulates somatostatin release to inhibit meal-stimulated gastric secretion by binding G cell |
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what chemicals stimulate parietal cells? |
acetylcholine, gastrin, histamine |
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Tx for peptic ulcers |
stop NSAID use abx (H. pylori) PPI stomach lining protector |
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gastric emptying factors |
meal factors: volume, acidity, osmolarity, caloric density, fat in ileum, particle size, certain amino acids other factors: ileal fat, rectal/colonic distention, pregnancy, blood glucose, posture, circular mostion and vection |
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dumping syndrome |
uncontrolled gastric emptying due to lack of feedback inhibition by duodenum (post-surgical, neuro deficit) undigested food makes it to colon pt barely makes it to toilet |
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pyloric stenosis |
projectile vomiting pediatric disease (failure to thrive, projectile vomiting after breast feeding, caused by improper formation of duodenum) |
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duodenum regulation of gastric emptying and secretion |
chyme entering duodenum activates intestinal receptors ENS short reflexes --> increased motility of duodenum, decreased contraction of stomach --> delays gastric emptying enterogastrones |
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enterogastrones |
hormones released by duodenum and feedback on stomach to decrease gastric emptying and secretions -secretin in response to acid -CCK in response to free fatty acids, certain amino acids |
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leptin |
suppresses appetite |
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ghrelin |
stimulates appetite |
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___ and ___ oppositely regulate appetite via the ___ |
gastric ghrelin; adipose leptin; hypothalamus |
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acid feedback control occurs via: |
somatostatin inhibition of gastrin release |
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acid production in the stomach can be reduced by... |
blocking parietal cell H2 receptors or inhibiting the H+/K+ ATPase |
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intestinal phase of gastric acid secretion involves what kind(s) of feedback? |
hormonal and neural |
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driving force of osmotic flow in canaliculus |
bile acid active transport |
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what is excreted in canaliculus |
non-filterable lipohpilic compounds (as opposed to water-soluble waste products that are processed in the kidney) |
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process of bile formation |
1. excreted lipophilic compounds in hepatocyte 2. bile acid secretion active co-transport w/ Na+ 3. Facilitated transporter secretion of primary solutes 4. H2O osmotically follows secreted solutes 5. Reabsorption of Cl- and other solutes FROM the forming bile 6. active secretion of HCO3- and other solutes INTO ductile lumen (stimulated by secretin) 7. H20 moves osmotically with lumen solutes |
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major components of bile |
bile electrolytes bile acids bile lipids |
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bile electrolytes |
active secretion of HCO3- in exchange for Cl- by ductile cells stimulated by secretin water and cations follow passively in the ductules plasma electrolytes are concentrated w/in gallbladder |
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precursor for bile acids
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cholesterol |
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bile acids |
detergent (surfactant properties) concentrated in gallbladder bile acid + Na+ = bile salt |
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method of secretion from hepatocytes for bile acids |
Na+-dependent active transport secretion into canaliculi against concentration and pressure gradients |
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bile lipids |
cholesterol's major excretory path via the bile excretion is coupled w/ that of bile acids concentrated in gallbladder |
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steps of release of bile from gallbladder (and lipases from pancreas
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1. bile synthesized in liver, stored in gallbladder 2. CCK liberated from duodenum "I" cells in response to fatty acids (hormone circulates in blood, stimulates vagus afferent receptors w/in intestinal wall) 3. CCK stimulates pancreas acinar cells to make/ d/c lipases and pro-colipase 4. contraction of gallbladder smooth muscles 5. relaxation of sphincter of oddi 6. discharge of bile into duodenum lumen |
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contraction of gallbladder smooth muscle triggered by... |
-CCK direct effects -vagus efferents via plexus of ENS interneurons |
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what stimulates relaxation of spincter of oddi? |
vagus efferents via plexus of ENS interneurons |
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process of recycling bile |
1. secreted bile salts 95% recycled 2. bile storage/concentration in gallbladder 3. bile mvmnt throughout sm intestine 4. Na+ dependent active transport system for conjugated bile 5. 95% of bile salts absorbed in terminal ileum 6. reabsorbed bile salts recycled by enterohepatic circulation 7. 5% of bile salts lost in feces |
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functions of bile |
excretion of solutes poorly filtered by kidney (lipid-soluble, protein-bound trace minerals, antigen-antibody complexes, IgA) enhancement of intestinal absorption (lipids, Ca++ and Fe++) |
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process of bilirubin excretion
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1. heme converted --> free bilirubin 2. bound to albumin in plasma 3. stripped off albumin & absorbed by hepatocytes 4. conjugated (in hepatocytes) 5. secreted as part of bile 6. bacteria metabolize it in in sm intestine 7. elminiated in feces (stercobilin) or urine (urobilin) |
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jaundice |
excessive amnts of either free or conjugated bilirubin in blood circulation (accumulate in tissue extracellular fluid) --> yellow discoloration of skin, sclera, mucous membranes |
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gallstone formation |
-form as crystals based on physical interactions of cholesterol, phospholipids, and bile salts w/in "micelles" |
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consequences of cholestasis |
jaundice inflammation fat/vitamin malabsorption sm intestine |
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what controls release of bile into small intestine? |
cholecystokinin (CCK) |
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sm intestinal villi are lined with... |
epithelial cells called enterocytes |
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enterocytes connected by... |
tight junctions |
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enterocyte function |
responsible for digestion and absorption of organic compounds, water, electrolytes |
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crypt enterocyte function |
secretion of fluids and electrolytes *supplied by blood capillaries |
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steps of carbohydrate digestion and absorption |
1. partial hydrolysis of starch by salivary amylase 2. hydrolysis of starch and complex carbohydrates by pancreatic amylase 3. hydrolysis of disaccharides and alpha-dextrins by brush border enzymes 4. transport of monosaccarides across apical membrane of absorptive enterocyte 5. transport of monosaccarides across basolateral membrane into portal blood |
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carbohydrate digestion |
1. starch & glycogen (long polymers)
2. hydrolyzed by pancreatic alpha-amylase to give smaller glucose polymers 3. hydrolyzed by apical membrane dextranase and glucoamylase to generate free glucose 4. monosaccharide products of enzyme hydrolysis are transported into enterocyte via apical membrane transporters |
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SGLT1 |
transports D-glucose via Na+ dependent secondary active transport |
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GLUT5 |
transports fructose via facilitated diffusion |
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enterocyte apical membrane transporter(s) |
SGLT1 (glucose) GLUT5 (fructose) |
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enterocyte basolateral membrane transporter(s) |
GLUT2 (ALL monosaccarides) |
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lactase non-persistence (inheritance) |
high childhood expression of enzyme but virtually no adult expression persists autosomal recessive lactose intolerance symptoms |
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lactase persistence (inheritance) |
adults retain lactase expression autosomal dominant |
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lactose intolerance cascade |
1. ingestion of threshold amnt of lactose 2. decreased intestinal apical membrane lactase activity in sm intestine 3. increased intraluminal lactose exerts osmotic effect and draws water 4. lactose delivered unchanged to colon 5. bacteria hydrolysis 6. explosive (osmotic) diarrhea and acidic stool |
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symptoms of lactose intolerance |
abd pn/bloating gas nausea/diarrhea |
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function of incretins (names and functions) |
GLP-1 and GIP stimulate insulin secretion inhibit gastric emptying |
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intestinal "sweet taste sensors" |
L and K cells |
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cascade of protein digestion and absorption |
1. limited breakdown by stomach pepsin and HCl 2. Activated pancreatic carboxy-terminal proteases in intestinal lumen 3. hydrolysis of peptides by apical membrane aminopeptidases 4. apical membrane transport of amino acids 5. apical membrane transport of intact dipeptides 6. final hydrolysis of peptides 7. basolateral membrane transport of amino acids to portal blood 8. glutamine as enterocytes' fuel from blood |
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villus enterocyte function for protein metabolism |
absorb protein nitrogen in jejeunum and ileum |
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during interdigestive periods (fasting), enterocytes obtain their nutrition from... |
the blood via basolateral membrane transporters |
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what is the major fuel of enterocytes?
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glutamine (not glucose!) |
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what is the primary means of extracting protein nitrogen from food |
apical membran transport of dipeptides |
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3 major classes of pancreatic lipase enzymes and their dietary lipid substrates/products |
triglyceride --> pancreatic lipase --> MG, 2 FFAs lethicin phospholipid --> phospholipase A2 --> 2-lysolethicin + FFA cholesterol esters --> cholesterol esterase --> sterol + FFA |
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lipid hydrolysis and packaging within small intestinal lumen |
1. emulsified fat droplet + bile salts 2. hydrolysis on droplet surface (by lipase, colipase) 3. packaging in mixed micelle in intestinal lumen |
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chylomicron |
long-chain tryiglycerides + phospholipids + cholesterol esters + apolipoproteins formed within small intestine epithelium enterocyte absorptive cell |
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enterocyte processing of long chain FFA vs short and medium chain FFA from triglyceride |
long: packaged into mixed micelle, which spontaneously decomposes, allowing long FFA to go through transporter at apical membrane of enterocyte, packaged into chylomicron, which is exocytosed and taken into lymph capillaries in villi short/medium: go into portal circulation, passively diffuse through enterocyte membranes and pass into blood capillary in villi |
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endocrine epithelial cells |
I cells: respond to fats, produce CCK, which stimulates vagal afferent L cells: respond to sweets and fats, produce GLP-1, stimulates vagal afferent |
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central lacteal |
blind end lymphatic capillary in central core of intestinal villus |
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overall summary of lipid digestion and absorption |
1. hydrolysis of triglycerides and cholesterol esters by pancreatic esterases 2. solubilization of FA, MG, and cholesterol with bile acids 3. diffusion of mized micelle across unstirred water layer to the apical membrane 4. passive diffusion of the FA, MG and cholesterol across jejunal apical membrane. Bile salts absorbed only in ileum. 5. Re-esterification of FA and MG to triglyceride of cholesterol to cholesterol ester 6. synthesis of chylomicron 7. release of chylomicron across basolateral membrane into lymphatic system 8. short FA diffuse directly into blood |
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where are bile salts reabosrbed? |
only in the ileum! |
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what factors control pancreatic lipase release? |
CCK, vagus nerve, enteric nervous system |
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H20 transported across jejunum and ileum enterocyte apical membranes via.... |
SGLT1 mechanisms plus aquaporins |
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across basolateral membranes, what comprises the major H2O transport pathways? |
aquaporins! (more than 2x as much than the volume passing via SGLT1 route) |
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what is primary player in crypt cell secretion |
apical membrane Cl- channel (CFTR) Cl- goes into small intestine lumen, followed by Na+, which is followed by H2O |
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where is isotonic balance maintained in GI sys? |
everywhere in small intestine among lumen contents/blood/enterocytes absorption by villus cells SGLT1, secretion by crypt cells CFTR |
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mechanism behind secretory diarrhea |
crypt secretions exceed villus absorption |
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classic/prototypic cause of secretory diarrhea |
vibrio cholerae (endotoxin-mediated) |
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4 basic categories of diarrheas |
osmotic secretory exudative abnormal motility |
