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SGU Physiology Final - GI


layer of GIT that contains luminal epith, lamina propria, immune cells, glands,and M.mucosa


CT layer of GIT, contains bl + lymph vessles, Meissner's nerve plexus

Muscularis externa

GIT layer: contains inner circular + outer longitudinal muscle layers with Aurbach's myenteric nerve plexus in between


GIT layer: thin CT where vessels + nerves enter, gen cont w/ peritoneal mes


where enterokinase, maltase, sucrase, lactase, trehalase, isomaltase, aminooligopeptidase, and dipeptidase are secreted


where amylase, trypsin, elastase, chymotrypsin, carboxypeptidase, colipase, phosphoplipase A2, and CholE nonspec lipase are secreted

dense bodies

what actin filaments in smooth mm are connected to instead of tropomyosin


the smooth mm equivalent of T-tubules, where Ca2_ flows in to


movement of subst from lumen -> bl


movement of subst from bl -> lumen


side of membrane that contains ENa+, Na+/nutri, Na+/Cl- cotransporter, Na+/H+ antiporter, Cl-/HCO3- antiport


side of memb that cont Na+/K+ ATPase, Cl- chans, K+chans

leaky epithelia

epith w/ lowe electrical resistance => have low ionic gradients, ex: prox tubule, SI, gallbladder, choroid plexus


type of transport char by passive Na+ entering from Lumen and active Na exiting to blood => negative potential -> passive Cl- paracellular from lumen to blood


type of transport char by passive Cl- exiting to lumen and Na+/Cl-/X entering from bl, active Na+ exiting to bl -> passive Na+ from bl to lumen paracellular

Liddle's Syndrome

clinicaL: AD mut -> inc ENaC -> in Na reabs -> hypertension

Cystic Fibrosis

clinical: loss of apical Cl- chan, thick mucus in airways, very comm, dec Cl- excr -> dec HCO3- excr -> dec Na+/H2O -> dec pancreatic duodenal secr -> dec enzme Fx in gut

Meissner's (submucosal) plexus

ENS: controls absorption and secretions, innerv gland epith, intestine, endocrine, bl vessels

Myenteric Plexus

betw long + circ layers of M. extera, controls motility

Hirschprung Disease

clnical: lack of ENS in large intestine => inc tone, colon distension, const constipation, Tx = surgery

VIP (Vasoactive Intestinal Peptide)

NT: inhib smooth mm, but excites secretory enterocytes

FGIDs (Functional GI Disorders)

clinical: have no obvious path but lots of symptoms, change sense + motor GI physio, ex: IBS


enzyme: AAs in stomach -> Vagus -> ACh -> GRP -> G cells -> inc secretory activity w/ gastric acid in ECL + parietal cells, inhib by low pH or SS

CCK (CholeCystoKinin)

enzyme: found in SI enocrine, ENS, stim by SI FAs-> I cells -> increase pancreatic enzynes, inc satiety, inhib by SS


enzyme: low pH in SI -> S cells in pancreas + stomach -> inc HCO3- + dec gastric acid, inhib by S


enzyme: hypoglycemia, low eight -> X cells in stomach -> inc hunger, GH rel


enzyme: fasting -> M cells -> in SI endocrine (Antrum + duod smooth mm) -> inc MMC


enzymes that increase insulin: GIP, GLP-1

GIP (Glc-dep Insulinotrpic Polypeptide/Gastric Inhib Peptide)

enzyme: carbs, FAs, AAs -> K cells in pancreatic beta cells -> inc insulin

GLP-1 (Glucagon-Like Peptide-1)

enzyme: Carbs -> L cells in pancreas -> inc insulin, dec glucagon

Serotonin (5-HT)

paracrine mediator: ECL in mucosa -> inc gut motil + secr

SS (Somatostatin)

paracrine mediator: in stomach D cells + pancreatic delta cells -> dec GI, vasoconstriction


paracrine mediator: in mast + ECL -> inc gastric acid


GI phase: see/smell food -> medulla -> X/ENS -> inc saliv, GI, motil


GI phase: distend stomach/AAs in stomach -> ENS -> hormones, paracrines, NTs -> inc secr + motil -> pepsin digest prots, make chyme -> chyme enters SI


GI phase: chyme enters SI -> var reflexes


fancy word for toothless


made of ions (Na+, Cl-, K+, HCO3-, Ca2+, PO4), enzymes (amylase, lipase, lysozyme), and prots (mucus, kallikrien), 1.5L/day, Fx = lube, protect, digest, alkaline

submandibular glands

salivary gland responsible for most saliva


clinical: virus that attacks salivary glands (esp parotid), children, involves testis -> sterility, poss attack pancreas -> diabetes


clinical: congenital lack of salivary glands, difficulty swallowing, bacterial overgrowth


mediates esoph relax


mediates esoph contract

Acid reflux

clinical: bad LES -> GERD (Gastro-Esoph Reflux Disease) -> pyrosis (heartburn), mucosal dmg


clinical: "absense of relax", LES does NOT relax -> hard to swallow -> dysphagia

body (corpus)

part of stomach where most HCL is secreted


part of the stomach where most hormones are secreted


grinding of food in the stomach


food forced back into stomach by pyloric sphincter

Dumping syndrome

clinical: etio = gastrectomy -> inc undigested chyme in LI => diarrhea, Tx = octreotide, diet, surgery

pyloric stenosis (CHPS)

1/150 males, pyloric sphincter hypertrophy -> projectile vomiting, Tx = surery

post-prandial alkaline tide

oxyntic cells neutralize CO2 to produce a huge amount of HCO30 that causes gastric venous plasma to have a high pH


hormones from SI endocrine cells that inhibit gastric function, includes Secretin, GIP, CCK

Type I

enzyme: pepsinogens from peptic + mucus cells in oxyntic area

Type II

enzyme: pepsinogens from mucus cells in pyloric area

duodenal ulcers

clinical: high H+ + pepsinogen secr

H. (Helicobacter) pylori

clinicaL: gram (-) bact that counts for 80% of peptic, 90% of duod, and 70% of gastric ulcers, RF for gastritis, gastric carcinoma, survives in stomach due to urease (converts urea into ammonia => buffer H+)

PUD (peptic ulcer disease)

clinical: can be either Duod (acidic chyme enters duod -> hypergastrinemia or Gastric (dmg mucosal barrier)

Zollinger-Ellison Syndrome

clinical: etio = pancreatic adenoma = gastrinoma -> inc gastric acid -> inc gastrin/HCl

Pernicious Anemia

clinical: dec IF -> dec P cells -> inc Gastrin, BUT NO HCl secr


enzyme located outsed the pancreas that cleaves trypsinogen to trypsin -> activate major panreatic zymogens

classic lobule

liver model: hepatocytes around portal v, hepatic a drains bl to hepatic/central v

portal lobule

liver model: around triad, drain bl from hepatocytes -> bile duct

portal acinus

liver model: around sinusoids, supply O2 bl to hepatocytes, main midel

portal vein

provides 75% of hepatic bl (hepatic a = oth 25%)

Zone I

portal acinus: zone with highest O2 and nutri delivery, closer to hepatic arteriole, for ox metab, ureagenesis, bile acid production

Zone II

portal acinus: transitional zone

Zone III

portal acinus: zone with loest O2 + nutri delivery => most affected by drug tox, farthest from hepatic arteriole, for glycolysis, ketogenesis, detox


epith cells lining biliary tree that are sim to pancreatic duct cells (stim by secretin to secrete HCO3-rich fl)

canalicular lumen

formed by adj apical memb domains of hepatocytes around bile canaliculi


composition = 70% cholic + chenoxydecholic acid, 20% Plipids, 4% chol, pigments

critical micellar concentration

[bile acid] when micelle aggregates form

primary bile acids

include cholic acid + chenodeoxycholic acid, found in duod, synth from chol in the liver

secondary bile acids

dehydrox primary bile acids by int. bact -> deoxycholic + lithocholic acid, MUCH less solub

conjugated bile acid

synth from bile acids, include glycocholate + taurocholate, easily ionize to bile salts


formed from bile salts, dissolve hydrophobic molecs

ileal resection

clinical: dec BA abs -> inc excr -> dec bile salt pool -> dec lipid abs => steattorhea

glucouronyl transferase

in hepatocyte ER, converts bili -> conj bili -> excr

free bilirubin

form of bili bound to albumin, formed from biliverdin, which is formed from heme oxygensase


metab conj bili, colorless, 20% reabs and returned to liver via portal v


gives poo brown color, formed from metab urobili in colon


filtered stercobilin in the kidneys that is ox, gives pee it's color

contracting segment

peristalsis: seg where circ m contracts -> push bolus forward, long m relax + downstream (receptive relax)

receiving segment

peristalsis: seg where long. m contracts -> pull bowel wall over bolus like a sleeve

valvulae conniventes

fancy term for transverse folds in SI that inc SA by 3x


functional unit of intestine w/ goblets,ECL, endocrine, cont tip, matur, crypt regions, where absorption occurs


part of villi where secretion occurs, cont stem cells


clinical: bact that produces enterotoxin that inc cAMP in intestinal cell (norm due to inc VIP/Histm) -> inc CFTR -> inc [Cl-]lumen => Secretory Diarrhea

Clostridium difficile

clinical: bact that produces enterotoxin that inc Ca2+ in intestinal cell (norm due to ENS -> ACh or ECL -> 5-HT) -> inc CACC -> inc [Cl-]lumen -> Secretory Diarrhea


major cation secreted by LI but not by SI


binding prot that carries Ca2+ to avoid inc [Ca2+]i since it acts as a second messenger


bound to Fe in tissue for storage


bound to Fe in plasma for transport

DCT-1 (Divalent Cation Transporter-1)

mediates free Fe2+ uptake


stim by full Fe stores in the liver -> dec ferroportin in basolat memb


basolat transport prot that transports Fe out of cell


clinical: Fe less than body's needs or inc loss => Tx = FeSO4 (ferrous salts)


large ferritin agg due to Fe tox


clinical: high amount of heosiderin

hemochromatosis (bronze diabetes)

clinical: inc Fe abs -> hemosiderosis -> tissue dmg, dark skin + diabetes, due to failure of neg feedback via hepcidin


part of SI that absorbs bile acids + Vit B12


part of SI that absorbs most carbs, Fe, Ca

small intestine

part of GI where most nutri abs occurs


minor form of starch w/ long, unbranched alpha1,4 Glc


major form of starch w/ a-1,4 links + a-1,6 branches


rand oligos produced by amylase


enzyme: breaks down most a-1,6 branches in a-amylopectin


a-1,1 Glc dimer


exch 2Na+ for Glc or Gal transport


facil diff of Glc, Gal, or Frc out of cells into bl


transports Frc into cell via facil diff (not Na+ coupled)

lactase deficiency

clinical: can't digest lactose to Glc + Gal => ferment lac in colon -> bloating

Amino acids

form of prots that are cotransported with Na+, 40% of products


form of prots that are cotransported with H+, acted upon by cytosolic enzymes, 60% of products


enzyme: secreted by pancreas -> elastase, chymotrypsin, trypsin

carboxypeptidase A

enzyme: ectopeptidase for products of chymotrypsin and elastase

carboxypeptidase B

enzyme: ectopeptidase for products of trypsin


enzyme: major proteolytic brush border enzyme

kinetic advantage

phenomenon where AAs reabs more slowly then peptides due to var carriers that are not as saturated as easily as AA carriers


clinical: basic AA defect => kidney stones

Hartnup's Disease

neutral AA defect => cerebellar ataxia, pellagra, psychosis

acid lipases

enzyme: accounts for 20% of lipid hydrolysis in adults, 50% in babies and people with pancreatic probs, includes lingual + gastric lipases, removes 1 FA from TAG

pancreatic lipase

enzyme: alkaline lipase, only 10% that is secreted is actually necc, co-lipase needed ELSE displaced by bile salts, produces MAG + 2 FAs

Phospholipase A2

enzyme: degrades lecithins + oth Plipids

Carboxyl Ester Lipase (nonspecific lipase)

hydrolyzes CholEs

fat malabsorption

clinical: indicated by > 7g fat in stools/day


clinical: defective TAG + Apo assembly


glycoprot secreted into saliva + gastric that complexes w/ VitB12, digested by pnacreatic proteases in SI, while IF remains

IF (intrinsic factor)

enzyme: deficient in Pernicious Anemia, couples w/ VitB12/haptocorrin in SI, req for abs in distal ileum


ferries VitB12 from bl to liver for storage, post-ileal abs

right colon

colon: from cecum -> prox/TC, has mixing contractions for mucosal contact to inc abs

left colon

colon: from distal TC to end of SC, has segmenting contractions (more rapid than right colon)

teniae coli

three discrete strips of longitudinal mm in LI, discont around wall => haustra


outpouching of teniae coli due to discont, pos dep on contraction of circ mm

haustral shuttling

cont form + reform haustra to dig over fecal content, bidir, not as strong propulsion as mass movements

mass movements

major propulsive contractile events, move fecal content at least 20cm, 3-4x/day

ENaC (Epithelial Na+ Channel)

maj target for mineralocorticoids, for Na+ uptake from lumen, mainly found in distal colon


bact fermentation making H2, CH4, CO2, H2S -> gas


made by bact fermentation -> include acetate, proprionate, butyrate, weak acids that prevent bact overgrowth


increase in stool fl volume of more than 200 mL in 24 hours => diarrhea, freq results in hypokalemia due to inc rate of fl flow in distal colon, metabolic acidosis (due to loss of HCO3-)

BER (basic electrical rhythm)

slow waves of electricity that det rate of contraction (freq), generator potentials

spike potentials

cause contractions by open Ca2+ chans at the peak of a slow wave, last 10-40x longer than nerve Ap's

ICCs (Interstitial Cells of Cajal)

origin of slow waves, loc betw long + circ mm, act as pacemaker for smooth mm surrounding GI, close assoc w/ myenteric plexus -> electrical syncytium

ileogastric reflex

reflex: ileum distends -> slow gastric emptying, mediated by ext + intrinsic nn

ileal break

nutrients (esp lipids) abs by ileum -> reduce gastric emptying + SI motil, mediated by GLP-1 and Peptide YY

gastroileal reflex

reflex: stomach distends -> inc ileal motil, releax ileocolic valve, mediated by extrinsic nn, gastrin, cck

MMC (Migrating Motor Cortex)

powerful peristaltic wave present every 90 minutes in the fasted distal stomach + SI, prevents bact overgrowth in SI, propels undigested material

CTZ (Chemoreceptor Trigger Zone)

area postrema region on wall of 4th ventricle that is stim by emetics like morphine, digitalis, CuSO4 -> 5-HT + dopa -> NTS -> Vomit

splanchnic circulation

largest reservoir of bl that can be redirected to oth vasc beds, affected by ANS, ENS (post-prandial hyperemia), metabolic hyperemia

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