Digestion And Absorption Flashcards

1
Q

Gross anatomy of small intestine

A

. Kekring’s mucosal folds
. Villi on folds
. Microvilli on apical surface of enterocytes forming brush border

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2
Q

Salivary and pancreatic amylase

A

. Digest complex carbs at internal alpha 1,4 links to either maltotriose, alpha-limit dextrins, and maltose

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3
Q

Brush border enzymes

A
. Glycosidases is the general category 
. Lactase: digests lactose to glucose and galactose 
. Maltase 
. Sucrase 
. Alpha-dextrinase
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4
Q

Final monosaccharides formed by action of brush border enzyme

A

. Glucose
. Fructose
. Galactose

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5
Q

Main transporters for absorption of glucose, galactose, and fructose in the small intestine

A

. GLUT-5: apical side, transport fructose into enterocyte from lumen, Na-independent
. SGLT-1: apical side, ransport of glucose/galactose into enterocyte from lumen, Na-dependent (Na-K ATPase drives gradient)
. GLUT-2: basolat. Membrane, transports glucose, galactose, and fructose out of enterocyte to interstitial space, Na-independent

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6
Q

Pepsin

A

. In lumen of stomach

. Digests some dietary protein (10-20% total) to oligopeptides

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7
Q

Function of brush border enzymes and aminopeptidases

A

. Apical membrane of enterocyte

. Hydrolyzes most, but not all, of remaining oligopeptides, Tori-peptides, and di-peptides to AAs

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8
Q

Cytoplasmic peptidases

A

. Inside enterocyte
. Digests tripeptides and dipeptides that have been absorbed intact
. Complete hydrolysis to AAs

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9
Q

Absorption of tri and di-peptides into enterocyte

A

. Pept-1: H-dependent, linked to apical Na/H exchanger
. Specific hydrolysis transport proteins for di-peptides on brush border that hydrolyze them and transport AA formed
. Intact absorption (pinocytosis) by M cells (can also be entry route for bacteria)

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10
Q

Absorption of AAs into enterocyte

A

. Na-dependent transporters (need Na-K ATPase to make gradient)
. Na-independent transporters
. Transporters specific for AA structure: neutral/acidic/basic

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11
Q

Classifications of dietary fat

A
. Triglycerides 
. Phospholipids
. LCFFA
. Cholesterol
. Medium chain FFA
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12
Q

Triglycerides

A
. Dietary fat mostly this 
. 3C glycerol sterilized w/ 3 FAs
. Not H2O-soluble 
. Do not form micelles w/ bile salts 
. Must be hydrolyzed to 2-monoglyceride (2-MG) and long-chain FFAs then 2-MG forms micelles
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13
Q

Phospholipids

A

. Digested by phospholipase A2 to release

. Lysophospholipids and LCFFA form micelles w/ bile salts

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14
Q

Long chain free fatty acids (LCFFA)

A

. Over 12C in chain

. Form micelles w/ bile salts

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15
Q

Cholesterol

A

. Sterol w/ same physical and chemical characteristics as fat
. Form micelles w/ bile salts

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16
Q

Medium chain FFA

A

. 8-12 FFA attached

. Do NOT form micelles

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17
Q

2 main problems in fat digestion

A

. Dietary fats are not water soluble but form large droplets in the aqueous lumen
. Enzymes for fat digestion are not lipid-soluble

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18
Q

Enzymatic cleave of fats must occur at ____

A

. Oil-water interface
. Fat digestion and absorption requires coordination of gastric emptying, all sections, and physiochemical events of emulsification and micelle formation

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19
Q

Steps in triglyceride digestion

A

. Emulsification
. Gastric lipase
. Binding of colipase
. Lipase

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20
Q

Emulsification

A

. Reduces large globules of fat into small spheres inc. SA for enzyme activity
. Physical (mastication, peristaltic contractions in stomach, phasic contractions in upper SI)
. Chemical: bile salts and phospholipids in lumen of SI

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21
Q

Gastric lipase

A

. In lumen of stomach
. Digests about 15% of dietary TG to DAG and FFAs
. Important in digestion for infants bc pancreatic lipase in low in them
. In adults it cannot fully compensate for insufficient pancreatic lipase

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22
Q

Binding of colipase

A

. LCFFAs stimulate pancreatic acinar secretion through CCK
. Trypsin activates pro-colipase to form active cofactor colipase
. Anchors lipase to oil/water interface so lipase can efficiently digest dietary triglyceride
. Dietary triglyceride digestion is severely impaired in absence of colipase

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23
Q

Lipase

A

. Found in salivary, gastric, and pancreatic secretions
. Most important is pancreatic lipase
. Secreted in active form from pancreatic acinar cells
. Bile salts inhibit activity (don’t allow access to oil/water interface)
. Colipase displaces bile salts to lipase can access it
. When it adheres to interface, it generates LCFFAs and 2-MG from dietary TG which can when be incorporated into micelles

24
Q

Absorption of lipid contents of micelle

A

. Micelles diffuse to apical membrane of enterocyte
. Micelles break down, they are not absorbed intact
. Contents diffuse through lipid membrane of enterocyte and enter the cytoplasm

25
Absorption of medium-chain FFA
. Do not require micellar solubilization for absorption . Absorbed by simple diffusion . Go directly into capillaries by going in between enterocytes
26
Process of chylomicron formation
. LCFFA and 2-MG or DAGare converted back into TG and phospholipids are synthesized in smooth ER . Cholesterol enters cholesterol pool in the cell and can be esterified to cholesterol esters . In smooth ER lipids are packaged for export . TG, cholesterol, cholesterol esters, and phospholipids form droplets w/ protein coat apo-B (chylomicrons) making it water-soluble . In Golgi chylomicrons are packaged then exocytosed across basolateral membrane of enterocyte . Chylomicrons diffuse onto lacteal of villus and pass into larger lymph channels and ultimately enter venous system
27
Fat soluble vitamin absorption
. Incorporated into micelles for absorption
28
Vitamin B12 absorption
. In gastric lumen, pepsin digests protein and B12 is attached to proteins . Free vit. B12 binds to salivary R protein in gastric lumen . When chyme enters duodenal lumen, pancreatic proteases degrade salivary R protein . Vi. B12 binds to intrinsic factor secreted by parietal cells because it is resistant to H and pancreatic proteases . IF forms dimers and binds to receptors in brush border of ileum allowing for absorption of vit. B12 . Absorbed into plasma where it attached to binding protein
29
Most ingested Ca is in ____form
. Nonionic form as salts . insoluble at neutral pH . Gastric acid solubilizes some salts and permits absorption in the SI
30
Dissolved Ca
. Absorbed through tight junctions by solvent drag . Absorbed through Ca channels . Absorbed primarily in the duodenum
31
Calcium absorption
. Enters enterocytes down its electrochemical gradient through an epithelial Ca channel (TRPV5/6) . Inside enterocytes, Ca binds to binding protein calbindin . At basolateral membrane Ca-ATPase and Na/Ca exchangers extrude Ca against an electrochemical gradient
32
Vitamin D in relation to Ca absorption
. Inc. number of apical m membrane Ca channels Inc. number of cystolic CaBP (calbindin protein) . Inc, activity of basolateral Ca-ATPase
33
Main mechanisms of Na absorption in small intestine
. Co-transport w/ glucose/galactose or AA | . In exchange w/ H
34
Na absorption in colon
. ENaC channels . Inc. by aldosterone . Inc. number of channels and insertioni of ENaC into apical Membrane of enterocyte
35
Mechanisms for iron absorption by duodenal enterocytes
. Divalent metal transporter 1 (DMT 1): ferric iron (Fe3+) is reduced to ferrous iron by ferrireductase DCYTB in apical membrane . Heme gets transported into enterocyte and inside cell released Fe2+ via heme oxygenase
36
Inside cell, ferrous Fe2+ is ___
. Stored as ferritin | . Exported across basolateral membrane by ferroportin 1
37
Iron in circulation
. Hephaestin is a ferroxidase in basal membrane that oxidizes Fe 2+ to 3+ . Ferric iron binds to apotransferrin in plasma . Hepcidin synthesized by liver can bind to ferroportin and block iron export under conditions of Fe overload
38
Digestion and absorption of carbs in colon
. Digested by colonic bacteria . Produce short chain FFA (under 8C) and gases . Short chain FFA are absorbed by simple diffusion and. Promote Na and H2O absorption . Gases eliminated as farts
39
Digestion and absorption of protein in colon
. Digested by colonic bacteria into ammonia and cadavarine | . Gases leave as farts
40
Digestion and absorption of triglycerides by colon
. Not digested by colonic bacteria or absorbed in colon | . Excreted intact in feces (steatorrhea)
41
Digestion and absorption of bile salts in colon
. Salts Not absorbed in terminal ileum are converted into secondary bile salts by colonic bacteria . Secondary bile salts are lipid-soluble and are absorbed by simple diffusion
42
How much fluid is absorbed by intestine every day
. 2L of ingested fluid . 7L of secreted fluid . Less than 2% lost in poo
43
Functions of water in small intestine
. Maintains osmolarity of luminal contents equal to plasma . Maintains fluidity of luminal contents . Fluid luminal contents distend visceral smooth m. To activate mechanoreceptive IPANS and inc. frequency of phasic contractions . Brings digestive enzymes into contact w/ food particles . Allows diffusion of digested nutrients to apical surface of enterocytes so absorption can occur
44
Water flux occurs in response to ____
. Osmotic gradients produced by luminal accumulation of nutrients and electrolytes (Na) and absorption of nutrients and electrolytes into extracellular space . Hydrostatic pressures generated by presence of water in extracellular space or intestinal lumen
45
If net water flux is from blood to lumen it is called ____
. Secretion
46
If net water flux is from lumen to blood it is called ___
Absorption
47
Water absorption from intestinal lumen to blood
. H2O from lumen enters extracellular space by following osmotic gradient established by absorbed solutes and-or electrolytes . Entrance of water into extracellular space inc. hydrostatic pressure w/in space . Inc. hydrostatic pressure causes bulk flow of H2O and solutes into fenestrated capillaries
48
Passive diffusion of water is much greater in SI than colon because of ___
. Leakier barriers btw adjacent enterocytes allowing for easier paracellular transport of water . Much larger SA available for H2O absorption
49
Reasons for osmotic diarrheas
. Intraluminal maldigestion (pancreatic exocrine insufficiency, reduced bile salt conc. Lactose intolerance) . Mucosal malabsorption (mucosal diseases, short bowel syndrome)
50
Pancreatic exocrine insufficiency
. Inadequate secretion of lipolytic enzymes and colipase and/or proteolytic enzymes . Over 90% pancreas must be damaged for maldigestion of fat and protein . Presence of undigested fat and protein in intestinal lumen creates osmotic driving force for water flux into lumen promoting diarrhea . Treatment: freeze-dried pancreatic extracts
51
How dec. luminal bile salt conc. Promotes osmotic diarrhea
. Impaired formation of micelles dec. digestion of dietary triglycerides and absorption of lipid digestion products . Results in water flux into lumen . Triglycerides and lipid digestion products enter colon creating osmotic driving force for retention of water in lumen and secretion of water into lumen
52
How lactose intolerance promotes osmotic diarrhea after lactose ingestion
. Lactose not digested by brush border enzyme lactase and is not absorbed . In colon it is digested by bacteria to form gas (H2 and methane) and lactic acid . Undigested lactose and lactic acid exert osmotic force promoting water flux into lumen causing diarrhea
53
Mucosal diseases
. Promote osmotic diarrhea . Disruption in integrity of mucosa and/or weakening of barrier prevents adequate absorption of nutrients by enterocytes (celiac, IBD)
54
Short bowel syndrome
. Inadequate absorptive SA prevents adequate absorption of nutrients
55
Secretory diarrhea
. Initiating event is excessive electrolyte and H2O secretion into intestinal lumen . Result from altered epithelial transport, apoptosis/necrosis of enterocytes, disruption/dysfunction of intestinal mucosal barrier . Transit time dec. . Nutrient absorption dec. . Osmotic gradients favor H2O retention and additional water secretion into lumen
56
Main causes of secretory diarrhea
. Secretory Agents assoc. w/ adenylate cyclase (entero-toxins, methylxanthines/caffeine) . Agents not assoc. w/ adenylate cyclase (bacterial endotoxins: shigella, staph, clostridium) . Mucosal injury, altered cell permeability/ tight junction issue (IBD, salmonella, E. Coli) . Tumors (gastrinoma, carcinoid syndrome, pancreatic cholera syndrome (VIP)