Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
24 Cards in this Set
- Front
- Back
Basic Anatomy of the Small Intestine
|
pyloric sphincter->duodenum->jejunum->ilium->ilocecal sphincter
1. duodenum: 1st 10-12in -arcs around head of pancreas -passes to the left & ends at sharp bend called duodenojejunal flexure 2. Jejunum: ~8ft long 3. Ileum: ~12ft & joins large intestine @ ileocecal valve |
|
Villi & Microvilli of Small Intestine
|
3 components of brush border:
1. level 1 mucuosal lining -referred to as "rugae" of SI 2. Villi: larger bumps, can see w/ naked eye or low powered microscope 3. Microvilli: bumps contained on larger bumps (increase SA) |
|
Simple Columnar Epithelium
|
-enterocytes = simple columnar
-lots of mitochondria (high ATP) for absorption -> active transport -highly energetic -also have goblet cells: mucus producers, dumped into lumen -protect from acid & help neutralize |
|
GI Secretions:
1. Saliva 2. Gastric Secretion 3. Pancreatic Secretion |
1. high HCO3, high K, hypotonic, a-amylase, lingual lipase
-stim by para/sympNS -inhib by sleep, dehydration, atropine 2. HCl (Gastrin, paraNS, histamine), Pepsinogen (paraNS), Intrinsic Factor -inhib by: low pH, chyme in duod (secretin/GIP), atropine, cimetidine, omeprazole 3. high HCO3 (secretin), isotonic (CCK, paraNS), pancreatic lipase/amylase/protease (CCK, paraNS) |
|
Type of digestion in...
1. mouth 2. stomach 3. duodenum 4. liver 5. pancreas 6. jejunum & ileum 7. colon |
1. mxl, biochem = no absorp
2. mxl, biochem = minimal absorp 3. coordination mxl, biochem = important absorp 4. biochem = no absorp 5. biochem = no absorp 6. mcl, biochem = absorp very imp 7. minimal digest = imp. absorp. |
|
Digestion of Carbohydrates
|
-Polysaccharides: starch, glycogen, cellulose, fiber
-Disaccharide: sucrose, maltose, lactose -Monosaccharide: glucose, fructose, galactose -pancreatic amylase: degrades polysaccharides into disaccharides -disaccharidases: disaccharides are degraded by group of brush border enzymes -brush border enzymes: series/fam. of enzymes embedded in cell mem. -imp that SI has good peristalsis so all chyme gets contact w/ brush border |
|
Absoprtion of Carbohydrates
|
INTO ENTEROCYTES:
1. SGLT1: secondary active transport -Na-dependent co-transport of Na w/ galactose or glucose -ATP indirectly affects 2. GLUT5: fructose enters by facilitated diffusion OUT OF ENTEROCYTES: 3. GLUT2: all monosaccharides to bloodstream -core of villus = highly vascularized -2 types of capillaries: 1. blood 2. lymph (lacteals) 3. |
|
Lactose Intolerance
|
-lactose enzymes slow down = mxn unknown
-normal lactose digest = lactase enzyme -intolerance= SI incapable of digest/absorp, creat osmotic gradient -osm. gradient increases H2O retention in SI (SI stretch = increase motility) -lactose not broken down->goes to LI, where bacteria ferment -lots of particles w/ nowhere to go cause: gas, cramps, bloat, diarrhea |
|
Overview of Digestion & Absorption of Proteins
|
-stomach denatures protein, but not as effective of cleave off aa (pepsin)
-cleave aa occurs mainly in SI -pancreas release 4 inactive enzymes: 1. trypsinogen 2. chymotrypsinogen 3. procarboxypeptidase 4. proelastase -when deposit in SI: trypsinogen converted into trypsin by brush border enzyme enterokinase (enteropeptidase) -trypsin cleaves aa & convert/activate enzymes -aa/small peptides after digest absorb via cotransport (same as glucose, Na-dependent) or facilitated diffusion |
|
What are the Brush Border Ezymes?
|
aminopeptidase
carboxypeptidase |
|
Main players in lipid digestion:
|
1. emulsification
-critical step: w/o can't go further -lecithin & bile acid = detergents (break down into smaller bits for step 2) 2. pancreatic lipase & colipase -fat hydrolysis -emuls. makes more vulnerable for lipase to attack 3. micelles -non stable, org. of lecithin to allow absorp across brush border 4. chylomicrons -core of fast in center surround by protein coat (formed by enterocytes) -hold FFA, chol, phospholipid, TGs -lecithins recycled back to SI 5. lacteals -CM too bulky for bloodstream, capillaries so goes thru lymph |
|
Transport of Chylomicrons
Lipemia |
-don't last in circulation very long w/in hr is cleared
-once CM enter lymph-> transported up thru thoracic duct - then emptied into venous circulation at juncture of jugular & subclavian veins -occur w/in hr after eat fatty meal |
|
Fate of Chylomicrons
|
-removed from blood by liver
-CM removed from blood as pass thru capillaries of adipose tissue & liver -both contain lipoprotein lipase (tears apart CM) -enzyme esp. active in capillary endothelium: hydrolyze the TGs of CMs into FA & glycerol which diffuse into adipocytes (storage) & hepatocytes (repacked into lipoprotein & export to blood) 1) some stored in liver 2) most repack in liver-> lipoprotein new protein coat-> store in adipocytes or used as energy |
|
Types of Lipoproteins
|
5 classes:
1. CM 2. VLDL -high TGs, moderate chol & phospholipids 3. IDL: interm. dens lipoprotein -moderate TGs, chol, & phospholipids 4. LDL -low TGs, high chol & phospholipids 5. HDL -low TGs, chol & phospholipids |
|
1. LDL
2. HDL |
1. bad cholesterol:
-cells take up via receptor mediated endocytosis -LDL receptor on surface of most cells -cell digest coat & extract fat (store/use) -steroid hormone product. of cells (lydig-make male testosterone) -increase risk factor for heart attack 2. good cholesterol -low risk of heart attack -inflated beach ball -liver makes HDL shell->circulate -scavengers: looks for excess chol. that body doesn't need/want -inflated->returns to liver -liver extracts fat/chol put into bile (waste) |
|
Na, K, & Water Absorption
|
-all H2O absorp in SI is passive & secondary to solute mvmt
-solutes can be electrolytes (Na) or nonelectrolytes (glucose) -Na/glucose & Na/aa mxn stim water absorp -most K absorbed passively when luminal [K] rise bc absorp of water (solvent drag) -don't absorp all, some goes thru LI & incorp into fecal matter |
|
Ca absorption
|
-hormone regulated
-occur in duodenum & jejunum -prim. reg. by VitD (1,25 dihydroxycholecalciferol) stim synth of Ca binding protein called calbindins in enterocytes -Ca removed from lumen across brush border via passive diffucion (regulate by VitD) -inside enterocyte Ca binds to Calbinding->allow intracell level of free Ca to reamin low & maintain Ca gradient for Ca to move across brush border -at basal mem = Ca ATPase pump -in blood is bound to something (~40% albumin, 10% phosphourus) |
|
Iron absorption
|
-complex & critical for hemoglobin production
-enterocytes full of carriers sp. for iron 1) heme iron: ingeset attach to Hg (steak) -heme transporter into cell -heme oxidase: extracts & frees it to Fe2+ 2) non-heme iron: free iron -reduced and absorp by iron reductase *Ferroxidase: takes Fe2+->Fe3+ to either bind to protein or storage via Ferritin -pumped out of cell via IREG1 -transferrin: carrier molecule thru blood: either stored in liver or bone marroe to make RBC |
|
Vitamin Absorption
|
-fat sol: ADEK, absorp sim. to fat
-water sol: absorp by simple diff. -VitB12: water sol absorp w/ intrinsic factor (ileal cells across brush border) |
|
Peristalsis & Segmentation in SI
|
-peristaltic: propel & mix food along GI (esoph, stomach, & SI)
-takes chyme ~3-5hr move thru entire SI via peristalsis -seg: series of contract & relax period mxl digest -both controlled by ANS -symp inhibit -para stim |
|
Regulation of SI
1) Fat & AA |
CCK:
+ gallbladder contraction -> increase bile secretion -> increase fat digest + pancreatic enzymes -> 6 enzymes - slow motility/empty of stomach |
|
Regulation of SI
2) Acid & AA |
SECRETIN:
- inhib gastric motility +bile (allow cells to secrete electrolytes & water into bile) + pancreatic alkaline (HCO3 rich fluid) GIP: - inhib. gastric motility & empty |
|
Regulation of SI
3) Vagal Nerve |
+ intestine segmentation & peristalsis
+ secretion of pancreatic enzymes |
|
Pancreatic Enzymes
|
1. lipase
2. amylase 3. trypsinogen 4. chymotrypsinogen 5. procarboxypeptidase 6. proelastase |