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150 terms

SGU Physiology - GI

SGU Physiology Final - GI
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Mucosa
layer of GIT that contains luminal epith, lamina propria, immune cells, glands,and M.mucosa
Submucosa
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
Serosa
GIT layer: thin CT where vessels + nerves enter, gen cont w/ peritoneal mes
Duodenum
where enterokinase, maltase, sucrase, lactase, trehalase, isomaltase, aminooligopeptidase, and dipeptidase are secreted
Pancreas
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
caveoli
the smooth mm equivalent of T-tubules, where Ca2_ flows in to
absorption
movement of subst from lumen -> bl
secretion
movement of subst from bl -> lumen
apical
side of membrane that contains ENa+, Na+/nutri, Na+/Cl- cotransporter, Na+/H+ antiporter, Cl-/HCO3- antiport
basolateral
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
absorption
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
secretion
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
Gastrin
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
secretin
enzyme: low pH in SI -> S cells in pancreas + stomach -> inc HCO3- + dec gastric acid, inhib by S
ghrelin
enzyme: hypoglycemia, low eight -> X cells in stomach -> inc hunger, GH rel
motilin
enzyme: fasting -> M cells -> in SI endocrine (Antrum + duod smooth mm) -> inc MMC
incretins
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
Histamine
paracrine mediator: in mast + ECL -> inc gastric acid
cephalic
GI phase: see/smell food -> medulla -> X/ENS -> inc saliv, GI, motil
gastric
GI phase: distend stomach/AAs in stomach -> ENS -> hormones, paracrines, NTs -> inc secr + motil -> pepsin digest prots, make chyme -> chyme enters SI
intestinal
GI phase: chyme enters SI -> var reflexes
edentulous
fancy word for toothless
saliva
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
MUMPS
clinical: virus that attacks salivary glands (esp parotid), children, involves testis -> sterility, poss attack pancreas -> diabetes
xerostomia
clinical: congenital lack of salivary glands, difficulty swallowing, bacterial overgrowth
NO
mediates esoph relax
ACh
mediates esoph contract
Acid reflux
clinical: bad LES -> GERD (Gastro-Esoph Reflux Disease) -> pyrosis (heartburn), mucosal dmg
Achalasia
clinical: "absense of relax", LES does NOT relax -> hard to swallow -> dysphagia
body (corpus)
part of stomach where most HCL is secreted
antrum
part of the stomach where most hormones are secreted
trituration
grinding of food in the stomach
retropulsion
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
enterogastrones
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
enterokinase
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
cholangiocytes
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
bile
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
micelles
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
urobilinogen
metab conj bili, colorless, 20% reabs and returned to liver via portal v
stercobilin
gives poo brown color, formed from metab urobili in colon
urobilinogen
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
villi
functional unit of intestine w/ goblets,ECL, endocrine, cont tip, matur, crypt regions, where absorption occurs
crypts
part of villi where secretion occurs, cont stem cells
cholera
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
pottasium
major cation secreted by LI but not by SI
calbindin
binding prot that carries Ca2+ to avoid inc [Ca2+]i since it acts as a second messenger
ferritin
bound to Fe in tissue for storage
transferrin
bound to Fe in plasma for transport
DCT-1 (Divalent Cation Transporter-1)
mediates free Fe2+ uptake
hepcidin
stim by full Fe stores in the liver -> dec ferroportin in basolat memb
ferroportin
basolat transport prot that transports Fe out of cell
anemia
clinical: Fe less than body's needs or inc loss => Tx = FeSO4 (ferrous salts)
hemosiderin
large ferritin agg due to Fe tox
hemosiderosis
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
ileum
part of SI that absorbs bile acids + Vit B12
duodenum
part of SI that absorbs most carbs, Fe, Ca
small intestine
part of GI where most nutri abs occurs
alpha-amylose
minor form of starch w/ long, unbranched alpha1,4 Glc
alpha-amylopectin
major form of starch w/ a-1,4 links + a-1,6 branches
dextrins
rand oligos produced by amylase
isomaltase
enzyme: breaks down most a-1,6 branches in a-amylopectin
trehalose
a-1,1 Glc dimer
SGLT-1
exch 2Na+ for Glc or Gal transport
GLUT-2
facil diff of Glc, Gal, or Frc out of cells into bl
GLUT-5
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
peptides
form of prots that are cotransported with H+, acted upon by cytosolic enzymes, 60% of products
endopeptidases
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
aminooligopeptidase
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
Cystinuria
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
abetalipoproteinemia
clinical: defective TAG + Apo assembly
haptocorrin
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
transcobalamin
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
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
flatulence
bact fermentation making H2, CH4, CO2, H2S -> gas
SCFAs
made by bact fermentation -> include acetate, proprionate, butyrate, weak acids that prevent bact overgrowth
diarrhea
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
post-prandial hyperemia
where splanchnic flow inc up to 8x after ingestion, mediated by VIP + CCK + adenosine -> vasodil