3-17 Small Intestinal phase Flashcards
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A: Intense motility / Intense Secretions and [Large surface area of mucosa cells] are the basis for significant digestion/absorption of nutrients in small intestine
B: Control of the Pylorus plays a BIG ROLE in the small intestinal phase since it regulates gastric emptying
B2: Emptying of gastric contents to duodenum is slow & takes 3 hours. Liquids empty faster and Isotonic contents empty faster.
B3: Gastric emptying allows TIME for [1 mm3 food bolus] to be digested & absorbed b4 next bolus comes WHILE ALSO allowing time for acid neutralization from pancreatic HCO3. It involves 4 actions:
1) INC tone and [intraluminal pressure] of proximal stomach
2) INC [gastric antral] contraction strength
3) Opening of Pylorus
4) Simultaneous INHIBITION of [duodenal SEGMENTAL contractions]
C: Chyme entering duodenum initiaties [feedback INHIBITION] and SLOWS [gastric emptying]. This can be [vagal neural] or hormonal.
º[Vagal neural Afferents] responds to [H+ and HYPERosmotic] nutrients in chyme via [enteric nervous system]
º[Vagal neural EFFERENTS] outflow will DEC proximal stomach motility / DEC [gastric antral] contraction strength / closes pylorus
D: Once Chyme moves further down small intestine, [feedback INHIBITION] is “lifted” and gastric emptying resumes
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A: 3 Factors contribute to provoking the INHIBITION of gastric emptying
1. [Fatty Acids] in the Duodenum —> CCK secretion—> Inhibits gastric emptying
- low pH in Duodenum (H+ receptors in duodenal mucosa detect Chymes low pH and relay to gastric smooth m. via [myenteric plexus interneurons]
- HYPERosmotic content of Chyme in Duodenum
\: In addition to SLOWING gastric emptying, CCK also.. •Closes Pylorus •Contracts Gallbladder •Relaxes [Sphincter of Oddi] •induces pancreatic Secretion
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A: Pancreatic secretions are the LARGEST contributors to enzymatic digestion. Exocrine pancreas is MOST important in digestion and secretes 1L/day into duodenal lumen (10x its weight). The secretions have 2 components:
1) MAJORITY= Aqueous component - HIGH IN HCO3 [FROM DUCTAL CELLS]
2) minority= enzymatic component [from Acinar cells]
B: 3 Locations of HCO3 Secretions (used to maintain pH 7)
1. PANCREAS = LARGEST CONTRIBUTOR
2. Biliary Ductal Cells
3. [Duodenal epithelial]
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B2: HCO3 is SOURCED from..
1) [Pancreatic Duct Cell] Intracell Carbonic anhydrase rxns (remaining H+ is transported into blood via [Na/H NHE1 exchanger]–>acidifies Pancreatic Venous blood
B3: H+ is transported
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C: HCO3 neutralization is IMPORTANT since pancreatic enzymes DO NOT work in acidic environments AND since the intestinal mucosa can be damaged by [free H+ & pepsin]
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A: Saliva’s Route of Passage from [Initial Isoosmotic] to [Final hypOosmotic]
B: [ENdocrine Pancreas] is 2% of Pancreatic volume and is composed of [islet Langerhan Cells] which produce
-insulin
-glucagon
-Somatostatin (inhibits G stomach cells)
-pancreatic polypeptide
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A1: [EXOcrine Pancreas] is 90% of Pancreatic volume and is organized similar to salivary glands with Ducts and Acinar cells. {Note: Pancreatic Juice is ISOTONIC ALL THROUGHOUT ROUTE OF PASSAGE unlike Saliva}
- {[Acinar] secrete enzymatic component of Pancreatic Juice= small volume–>uses [Aqueous HCO3 solution] to get out into duodenum} and
- {[Pancreatic Ductal epithelial] which extends upward to [Centroacinar cells] Secrete [Aqueous HCO3 solution] = MAJORITY OF PANCREATIC JUICE. These do this when stimulated by Secretin!
A2: [Pancreatic Ductal epithelial] are pH responsive so when [small intestine pH is LESS THAN 4.5] —> S cells in [small intestine epithelium] release Secretin which travels up to Pancreas–>
ºINC cAMP in [pancreatic ductal epithelial]–>
ºOpens [CFTR Cl- channels] and allows Cl to passively diffuse into [pancreatic duct Lumen]–>
B: [Na / K / HCO3 / Cl] are all transferred INTO ACINAR FLUID from Plasma but Cl is taken out in the duct to import MORE HCO3
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A: Liver sends Freshly made Bile–(hepatic duct)
–>GallBladder –(Bile Duct)–>[Sphincter of Oddi]—-> DUODENUM
Note: Bile Has NO ENZYMES but does have [Bile Acids] which emulsify Fat and forms micelles
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C: Cystic Fibrosis occurs when the [CFTR channel] became inactively mutated—>NO Cl TO DRIVE HCO3 into Pancreatic Juice.
** [Lungs / intestine / biliary system and Pancreas] ALL have [CFTR channels]***
C2: In Cystic Fibrosis, the Pancreas becomes destroyed because the HCO3 ductal secretion stops and the [acinar enzymes] become highly concentrated–>eats away Pancreas
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A: [Small intestinal epithelium - i CELLS] will secrete CCK when triggered by :
1. DIRECT interaction with [Fatty AND/OR Amino Acids]
- Binding of [Fatty AND/OR Amino Acids] to [Sensor Paracrine Cells]—> [CCK-Releasing Peptide]–> CCK Secretion
- ## Release of [Monitor Peptide] by [pancreatic Acinar cells]B: The CCK will then turn around to stimulate [pancreatic Acinar cells] secretion of enzymes by:
1) Acting as endocrine factor and binding to [pancreatic Acinar cell CCK1 receptor]
2) CCK stimulates neural reflexes that impinge on pancreas–>vagovagal reflex–> [ACh/GRP/VIP Release from pancreatic enteric neurons] —> INC phosphorylation of structural proteins–>INC Fusion of [PREMADE zymogen granules] with apical membrane and secretion of contents via EXOCYTOSIS. Enzymes are washed thru using [Ductular Aqueous HCO3]
- VIP works by INC cAMP
- ACh/GRP and [DIRECT CCK] works by mobilizing [Intracellular Ca+]
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A: [Pancreatic Protease Enzymes] from Acinar cells are secreted in INactive forms–>converted into ACTIVE by Trypsin in Duodenal Lumen. If activated too early—> PANCREATITIS!
B: premature activation of [pancreatic protease enzymes] can be Regulated by Trypsin eating itself AND [trypsin inhibitors] found within protease enzymes
C: Trypsinogen from [Pancreatic Acinar Cells] is converted into Trypsin by [Enterokinase of small intestinal epithelial cells]
D: Genetic mutations that cause Trypsin to be RESISTANT TO DEGRADATION—> PANCREATITIS
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A: Bile is made by hepatocytes and sent into [bile canaliculi] which drain into bile ducts. It’s composition is:
- 65% BILE ACID = DETERGENT
- 20% [Lecithin phospholipid]
- 6% [Isotonic Electrolytes]
- 0.3% [Bilirubin Bile Pigment]
- [4% Cholesterol AND 5% Protein]
B: Bile ACID is a detergent that [Emulsifies fat] AND [forms micelles]. Micelles protect Hydrophobic lipid monomers from aqueous small intestinal lumen.
C: [BILE ACID] is recycled from Intestine–>Liver in [Enterohepatic Circulation of Bile Acids]
º[CHARGED Conjugated] Bile Acid can ONLY be ACTIVELY ReAbsorbed using the [apical asbt symporter] found in [Terminal iLeum]–> [Portal Vein] = MAJOR RECYCLING METHOD FOR BILE ACID
º[UnCharged UnConjugated] Bile Acid can passively cross intestinal lining of duodenum and go directly to [Portal Vein] (and skip [Terminal iLeum]
ºsome Bile Acid escapes Colon and [Colonic Bacteria] converts it into [UnConjugated UnCharged]–>allows it to passively cross and travel Directly go [Portal Vein]
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Motility of Small Intestine
A: Contractile activity of Small Intestine allows fragmentation of chyme into smaller pieces–> INC chyme surface area to enzymes and detergents–>INC biochemical rxns—>even smaller micelles that can be absorbed
B: Contractile activity also propels the Bolus
C: [Segmentation vs. Peristalsis]
ºSegmentation occurs MOSTLY in [BOTH Intestine] and allows MIXING of luminal contents with secretions.
ºIt is caused by burst of localized action potentials in circular smooth m.
ºPotentially activated by CCK. SEGMENTATION PRODUCES NO FORWARD MVMNT!
vs. ——————————————————————————–
D:
ºPeristalsis which occurs mostly in pharynx/esophagus/[gastric antrum/ BOTH INTESTINE = [CONTRACTION on ORAD side using ACh & Substance P] with
[Relaxation on Caudad side using NO & VIP]
TOGETHER will produce FORWARD MVMNT
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A: [Migrating Motor Complex] (AKA Stomach Growling) occurs in the duodenum and jejunum after fasting. They are periodic contractions mediated by [motilin hormone]. They occurs at 90 min intervals.
B: [MMC] purpose is to CLEAR residual gastric & intestinal contents out and into colon. Right After Eating, [motilin hormone] DEC and MMC is suspended
- *Small Intestine special Structures**
1. Brunner Glands = Found in SubMucosa and Secrete mucus & HCO3
- [Lieberkuhn Crypt Glands]= Found on top of [Muscularis mucosae] and Secrete Peptidases & Carbohydradase
- Paneth Cells= Found @ bottom of villi and Secrete [antimicrobial peptides & enzymes like ribonuclease]
- SOME G-cells and D-cells still exist in small intestine BUT MOST OF THEM ARE IN THE STOMACH
Note: Goblet Cells (secrete [Mucin glycoprotein]) are found in small intestinal Villi and INCREASES in # as you move thru Small Intestine
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DIGESTION
A: Digestive Enzymes are secreted in salivary / gastric / Pancreatic Juices / present in apical intestinal epithelial
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B: There are 2 ways for ABSORPTION to occur
1) Cellular = substances enter intestinal epithelial cells via apical membrane and are extruded to enter blood
2) ParaCellular= Substances move across tight junctions thru lateral interspaces to enter blood
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A: Carbohydrates make up 50% of our diet.
ONLY MONOSACCHARIDES ARE ABSORBED THRU INTESTINAL EPITHELIAL CELLS soo Carbs have to be broken down into Monosaccharides
B: The Major dietary carbohydrate is STARCH which is a mix of Straight AND Branched-chain glucose polymers
ºAmylose = Straight-chain glucose polymers
C: The 3 Disaccharides IN FOOD DON’T REQUIRE [Alpha-Amylase] and are…
*Trehalose—> 2 molecules of Glucose
- Sucrose–> 1 Fructose and 1 Glucose
- Lactose–> 1 Galactose and 1 Glucose
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A: Monosaccharides are absorbed in [Intestinal Epithelial cells]
1. [galactose & glucose] both use [SGLT1 (Na-Sugar) symporter] and transports them against their gradient ACTIVELY in the [apical brush border]. They then Extrude across basolateral membrane into blood via [GLUT2] facilitated diffusion
- ## fructose uses [GLUT5 Transporter] apically and DOESN’T NEED Na+ help. This is FACILITATED DIFFUSION for BOTH [apical brush border] [GLUT5] AND basolateral [GLUT2] sidesB: Lactose Intolerance occurs when you LACK LACTASE in the [apical brush border] of intestine. This is a normal developmental decline in production of lactase by enterocytes. Lactose remains undigested in the intestinal lumen—>INC osmotic gradient—>Osmotic Diarrhea
B3: CONGENITAL Lactose Intolerance is RARE and occurs when pts lack [jejunal lactase] specifically
C: [Glucose-galactose mal-absorption] occurs due to [SGLT1 Na-Sugar Symporter] mutation! It is ALSO RARE and causes severe diarrhea. Tx= Fructose diet replacement
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A: Of the 20 [Amino Acids AA], Essential AA can NOT be made by the body and have to be obtained thru diet. They are
-His and Lys = BASIC
- Val / Leu / iLE = Aliphatic Uncharged
- Phe / Try = Aromatic Uncharged
- Thr = Hydroxyl Uncharged
B: Protein digestion STARTS in stomach with PEPSIN(produced from Pepsinogen by Chief Cells when converted from low pH) but occurs MOSTLY in small intestine with brush-border proteases such as trypsin
C: 2 Classes of Proteases
1) ENdopeptidases = Hydrolyzes interior peptide bonds
[ex: pepsin / trypsin / chymotrypsin / elastase]
2) EXOpeptidases= Hydrolyzes 1 AA at a time from C-terminal end
[ex: Carboxypeptidases A & B]
