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66 Cards in this Set

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  • Back
segment contractions
peristaltic contraction
segment: most common form of movement, main function is to mix chyme back and forth

peristaltic: vectoral movement, slow waves of smooth muscle cotrol these contractions, is slow to allow chyme several hours digestion
Slow waves of the small intestine

slow waves may have AP's superimposed on the peak of the wave, AP cause larger smooth muscle contractions

control of electrical rhythym is INTRINSIC via enteric NS, indirect control is symp/parasym on intrinsic plexuses
intestinointestinal reflex
overdistension of one segment relaxes smooth muscle in the rest of the intestin to protect it from potential rupture
gastroileal reflex
high stomach acidity increases chyme movement from the terminal ileum into the colon
MMC and small intestine
same as in stomach, one every 75-90 min
critical concept of intestinal secetions
although small intestine abs nearly all nutrients it also secretes a large amount of isotonic salt soln
Epithelial cell secretion of small intestine
(epithelial cells in crypts of lieberkuhn)
high volume 1.8L/day of isotonic mostly nacl soln to dilute chyme to simplify abs
how do epithelial cells of small intestine secrete this isotonic solution
Na/K/Cl is taken up into the cell from the body. Cl is spit into lumen using a Cl channel CFTR (regulated by Ca and cAMP),
Lumen is now negative cause it has so much Cl, so Na follows paracellularly
cholera toxin binds basolateral R and causes increased adenylate cyclase, cAMP which upregulates CFTR channel and increases heavily nacl secretion
name the two incretins
GIP and GLP-1, released in response to small intestina glucose, cause insulin secretion
exocrine pancreas secretes?
secretes enz water and bicarb
what two H signal exocrine pancrease secretions?
CCK - stim enz's
Secretin - stim bicarb
innervation of the pancreas
celiac and mesenteric plexuses are sympathetic to pancreatic blood vessels

vagus parasymp release Ach
Aqueous component of pancreatic juice
ducts secrete water and salt(no enz's) isotonic with plasma

initially aqueous portion is hypertonic, then as it moves through the ducts water comes in to make it isotonic

between meals only intralobular ducts secrete, during meal secretin causes extralobular ducts whose secretion is high in bicarb to turn on
Bicarb secretion by pancreas
two ways
Carbonic Anhydrase: H is removed by Na/H countertransporter and an H ATPase

Na/HCO3 cotransporter brings in na and bicarb, uses the Na/K atpase gradient

Bicarb for both is secreted using a Cl/HCO3 exchanger driven by CFTR channels that secrete Cl into lumen (this is called cl recycling)
how does secretin increase bicarb secretion
it activates adenyk cyclase cAMP and PKA to phos the CFTR and open it. This increases Cl recycling and therefore bicarb secretion
how does Ach increase bicarb of pancreas?>
increases cellular Ca
where are pancreatic enz's secreted?
acinar cells
what causes pancreatic enz secretion
Ach CCK gastrin and substance P through increased Cellular Ca and IP3
discuss the enzymes produced by acinar cells
zymogen granules trypsinogen chymotrypsinogen, procarboxypeptidase, lipase and colipase
once in duod enterokinase breaks down trypsinogen which can then activate the others.
Acinar cells secrete trypsin inhibitor to inhibit premature trypsin formation

amylase is secreted in active form
three phases on pancreatic secretion
cephalic: thinking causes vagus to stim high enz low volume pancreatic juice

Gastric: vagovagal reflex induces small vol high enz

Intestinal: Acid in chyme stim large vol low enz pancreatic juice with lots of bicarb, high bicarb is released via secretin, aa stim CCK which causes enz release
what bonds does alpha amylase break?
alpha1-4 linkages, alpha1-6 linkages cannot be broken

leaving glucose polymers 2-9 long, and limit dextrins
what breaks down:
1) dextrins
2) glucose polymers
3) disaccharides lactose and sucrose
dextrin: alpha dextrinase
Glucose polymers: glucoamylase
Lactose(gluc-galac) :lactase
Sucrose(gluc-fruc): sucrase
describe intestinal uptake of sugars
SGLT1 Na/gluc or galac cotransporter, uses [na]grad

Glut5 transports fructose

GLut2 takes gluc galac and fruc into blood from cell
congenital lactose intolerance
babies have no lactase and will die if limited to milk, different from lactose malabsorption synd
what percentage of protein is abs? what percentage of starch
100% protein abs
80-90% starch abs
explain protein digestion and abs
protein broken down by pancreatic enz to oligopeptides, these are broken down by membrane amino-oligopeptidase enz. Amino acids are then transported into epithelial cells by 5 Na/aa cotransporters and two non sodium dependent

di and tripeptides are transported in via a H+/di-tri-peptide transport protein
once inside cell peptides are broken down to aa and two na-dep and 3 na-indep basolateral transporters shove them into blood
water absorption
no water absorbed in duod, a great deal is secreted

ileum and jej abs a lot
colon abs the rest and leaves .1L/day in feces
Absorption of sodium
duod secretes mostly
so ileum and jej abs mostly
Na/aa and Na/sug and Na/H cause sodium abs
Na/K pumps na out of cell
Abs of cl and bicarb
Cl is paracellular, driven by mass influx of na

duodenum and Jejunum: bicarb from pancreas is injected in and reacts with acidic chmye to make Co2 and H2O, Co2 then diffuses across epithelial cell layer

ileum: bicarb is SECRETED in exchanged for chloride across apical membrane, it is sucked into the cell from blood via a Na/HCO3 cotransporter (note this is different from the alkaline tide seen in the stomach)
Absorption of potassium in small intestine
nacal sugar and aa are transported into blood, water follows, K concentration increases untill its enough to drag it between cells
Absorption of Ca
Moves down chemical gradient

Ca that enters the cell binds calbindin or enters vesicles

Ca channel in apical mem, and Ca-Atpase and Na/Ca exchanger shoves it out into blood.
Vit D and Ca abs
Vit D stim the synthesis of calbindin Ca channels and Ca Atpases
Absorption of iron in the small intestine
most iron not abs'd
Iron reductase on brush border reduces Fe3 to Fe2, transported into cell via DCTH1 H/Fe2 cotransporter
In cell Fe2 is oxidized to Fe3 by ferroxidase. Fe3 binds mobilferrin or ferritin

Iron is also absorbed at heme, transported in via HCP-1, Iron is removed from heme by heme oxidase
Abs of iron, secretion into blood
IREG1 transports fe out of cell, in blood binds transferrin
what do GLP-1 and oxyntomodulin do for hunger?
decrease food intake, cross BBB, unsautrable
In the arcuate nucleus what two centers control hunger and what signal do they send
NPY/AgRP = increases hunger
POMC/CART = decreases hunger
what chemical signals inhibit npy/agrp? what signals stim?
inhib: leptin, insulin and PYY
stim: Growth H and Ghrelin
what chemical signals inhibit pomc/cart? what signals stim
stim = leptin insulin oxyntomodulin and GLP
inhib = ?
what three hormones work on thirst?
Ang II = increases thirst
ANP = cardiac myocytes stretch, decrease thirst
Relaxin - corpus luteum, increase thirst

all three work through Subfornical organ in brain
how does neural thirst work
arterial baroR(aorta/carotid bodies) cardiopulmonary baroR and visceral osmoR fall silent as BP decreases, this facilitates thirst
how does neural thirst work in respect to SFO OVLT and visceral osmoR
sense OSM, as it increases thirst increases
bile synthesis
bile acids cholesterol and phospholipids are the primary secretions, cells in the ducts secrete fluid with bicarb
what stimulates primary secretion? what stimulates bicarb fluid?
CCK does primary
secretin does bicarb
gall bladder and the standing osmotic gradietn hypothesis
gall bladder concentrates liver bile 5-20 fold by:
actively transporting Na across cells into the space BETWEEN cells. Cl and bicarb follow to maintain electroneutrality and water follows.
during what phase of digestion does the gall bladder contract and sphincter of oddi relax
what H is responsible?
cephalic and gastric phase, this is mainly due to CCK!
Bile secretion and recycling
the body doesnt produce enough bile acid as it needs to must recycle, abs by Na-dep/indep transport proteins in ileum, returned to liver in portal blood via Na-dep transport
bile composition
65% bile acids, 20% phospholipids, chlesterol, bile pigments and protein,
most important bile acid is cholic acid which is conj to glycine or taurine, amphipathic
critical micellar concentration

mixed micelle
bile acid concentration required for micelle formation

mixed: contain phospholipids cholesterol in addition to bile acids
review liver secretion of bile
bile acids, choles, etc are primary secretions stim by CCK, aqueous ductal part is stim by secretin which increases cAMP to open CFTR channels and allow cl recycling to push HCO3 into lumen, much like in the exocrine pancrease (not like small intestine which uses paracell and bicarb/cl)
discuss lipase and co lipase
co lipase moves the bile acid out of the way in a micelle to expose the fat and allow lipase to degrade it to 2FA's and 2-monoacyl glycerol
what degrades cholesterol?
cholesterol esterase breaks cholesterol esters to cholesterol and a FA

PLA2 degrades phospholipids to FA and lysolipid
how do digested fats enter blood?
diffusion, (note bile acids aren't abs with them in the duoud and jej, they instead travel to ileum where they are abs)

MG(monoacylglycerol) FA ets diffuse through the unstirred layer, this is mediated by intestinal motility, once in cells FABP transports FA's and MG's to ER where they are remade to TG's and phospholipids, and CE's . They all combine in the golgi to make a chylomicron and then are secrete4d into lecteals. Glycerol is diffused straight through the cell
out of the fat soluble vitamins which one requires E carrier-mediated transport
what controls the ileocecal sphincter
itnramural plexuses and intrinsic nervous system
describe the parasymp and symp innervation of the colon
parasymp: cecum, asc, and transverse colon come from vagus(initiates segment contraction). desc, sigmoid colon and rectum come from pelvic nn(expulsion of feces)

symp (stops motility): early colon = superior mesenteric plexus, late colon = inferior mesenteric and superior hypogastric plexus
describe control of anal sphincters
internal anal sphincter = circular smooth mm involuntary

external anal sphincter = skeletal innerv by pudendal nn
Motility of colon
cecum and early colon = segmental contractions seen as haustra

central and distal colon = mass movement 1-3 X a day, remain contracted for several minutes
describe myenteric potential oscillations vs slow wavesn in the colon
slow waves are 6/min are low in frequency but have high amplitudes

myenteric potential oscillations are much more frequent but have a lower amplitude
Ach VIP Substance P and NO on colonic waves
Stimulatory motor nn release acH and substance P
inhibitory mottor neurons release VIP and NO

when ach is released by enteric nn's it stimulates circular muscle to increase the length of the slow wave to produce contraction(as colon rarely produces AP's by itself)
does sympathetic or parasympathetic control the coloncolonic reflex
sympathetic - one part of the colon is distended the others relax
gastrocolic reflex
autonomic innervation: food enters stomach colonic smooth muscle contracts producing mass movement and need to defecate
NACL absorption in the colon (late and early)
early colon: have Na/H and HCO3/Cl apical exchangers that shunt NACL in

late: have an sodium channel and CFTR (also cl is abs paracellular but not as important)
how does aldosterone affect the kidney and colon
promotes na reabsorption by increasing na channels and potassium secretion
get net bicarb and K secretion or reabs in colon