Ch. 18 Day 2 Flashcards
Ability of bile salts to emulsify fat
conversion of hydrophobic cholesterol into amphipathetic bile acids
–occurs in liver
PRO and CHO water-soluble, fat isn’t water-soluble
Digestion and Absorption of Fats
Digestion begins in duodenum: bile stabilizes fat emulsion and lipase (from pancreas) breaks it down into fatty acids and glycerol
Phospholipase A (from pancreas) digests phospholipids into fatty acids and lysolecithin
Fat Emulsification and Digestion
Digestion products of fat (free fatty acids) incorporated into micelles, producing mixed micelles; these diffuse into absorptive surface and fatty acids pass into cells
In micelles, hydrophilic parts sticking out, hydrophobic parts sticking in
Absorption and Transport of Fats
Fatty acids, monoglycerides, and lysolecithin move into bile micelles and are transported to brush border
Fat molecules then leave micelles and diffuse into epithelial cells of villi
Inside epithelial cells, they are regenerated into triglycerides, cholesterol, and phospholipids and combined with proteins to form Chylomicrons
Chylomicrons are secreted by exocytosis into the central lacteal of villus
What is the Central Lacteal?
Main collection point for lymph; eventually chylomicrons secreted int there will be returned to blood at thoracic duct at subclavian vein
Fluid and electrolyte secretion and absorption
Oral fluid intake = 2,000 mL/day; digestive secretions = 7,000 mL/day; all but 100mL is reabsorbed, mainly in small intestine but also in large intestine
Mostly water and ions (Na+, K+, Cl-, HCO3-, H+).
Secreted ions are reabsorbed, water follows osmotic gradients created by solute transfer
Where is most of the water coming into the gut coming from?
The GI tract itself and accessory organs
–some comes from food
Most of water being secreted by GI tract going to be reabsorbed
Control of digestive function occurs at each level of the GI tract. What are the 3 phases?
- Cephalic phase
- -stimulation of gastric activity - Gastric phase
- -stimulation of gastric activity - Intestinal phase
- -inhibition of gastric activity, stimulation of digestion in intestine
Cephalic Phase
Short duration, prepares stomach for arrival of food
Mechanism: neural - reflex signals from medulla oblongata via vagal preganglionic fibers to synapses in submucosal plexus
Actions:
- 1: direct neural stimulation of acid, mucus, enzyme secretion
- 2: indirect via stimulation of gastrin release from G cells, gastrin stimulates motility and acid secretion
- 3: indirect via stimulation of histamine release from ECL cells
Vagal signals stimulate acid secretion via 3 mechanisms occurring simultaneously in both fundus and antrum:
- -a) direction signal via ACh
- -b) indirect via histamine
- -c) indirect via gastrin
Gastric Phase
Duration: 3-4 hours, enhances secretion, mix, acidify, and increase surface area of chyme, begin hydrolysis of protein
Mechanisms:
- 1: neural reflexes triggered by stretch, rising pH
- 2: hormonal (gastrin) release triggered by vagal signals, peptides, AA’s
- 3: local release of histamine (stimulates acid secretion) triggered by stretch
Actions: increased production and secretion of acid and pepsinogen, increased motility and mixing waves
Gastric Emptying
Chyme metered out into duodenum as stomach empties
Emptying is regulated by intestinal signals to prevent “dumping”
Liquids empty fastest, solids slowest, nutrient-specific control (sensing of physiochemical properties, e.g. H+, fat)
Intestinal Phase
Duration: hours, acts to control gastric emptying rate, to limit gastric acid secretion, and to optimize conditions for enzymatic digestion in intestinal lumen
Mechanisms:
- 1: neural - short reflex (enterogastric reflex) triggered by distention of duodenum
- 2: hormonal - stimulation of secretin, CCK, GIP, by presence of H+, CHO, AAs, lipids
Actions: feedback inhibition of gastric acid/pepsinogen secretion, gastric motility, promotion of intestinal/pancreatic/biliary secretion, intestinal motility
Gastrin (KNOW FOR EXAM)
Secreted by stomach
Effects:
- -stimulates parietal cells to secrete HCl
- -stimulates chief cells to secrete pepsinogen
- -maintains structure of gastric mucosa
Secretin (KNOW FOR EXAM)
Secreted by small intestine
Effects:
- -volume and HCO3- secretion from pancreas: raises pH of incoming chyme –> allows pancreatic enzymes to be active
- -promotes favorable environment for enzymatic digestion
CCK (KNOW FOR EXAM)
Secreted by small intestine
Effects:
- -1) pancreatic enzyme secretion
- -2) bile secretion via stimulation of gallbladder contraction - responsible for enzymatic digestive activity, fat emulsion stability, and absorption of digestion products of fat
Regulation of pancreatic juice and bile secretion
When chyme enters duodenum, 2 hormones produced:
- a) secretin is produced in response to drop in pH (production stops w/ rise in pH)
- b) cholecystokinin (CCK) is produced in response to presence of partially digested proteins and fats in chyme (production stops when food leaves small intestine)
Pancreatic enzyme production of trypsin, lipase, and amylase is stimulated by ACh from vagus nerve and CCK
Pancreatic bicarbonate production is stimulated by secretin
Liver produces bile continuously, but arrival of food into duodenum stimulates increased bile production
Happens when:
- -bile acids are returned to liver after intestinal absorption via enterohepatic circulation (so we don’t have to continually make bile salts)
- -secretin and CCK stimulate increased bicarbonate secretion into bile
- -CCK (in response to presence of fat in chyme) stimulates gallbladder contraction
Enterohepatic Circulation
Recycling of bile salts regulates hepatic synthesis of bile acids from cholesterol, and therefore, controls plasma cholesterol levels
–can “exploit” this process to reduce plasma cholesterol levels to help patients w/ higher levels
~5% of bile salts lost in feces, rest are reabsorbed
Bile acid-binding resins:
- -Questran (cholestryamine)
- -Welchol (colesnvelam)
- -Colestipid/Colestid (colestipol)
- -disrupt enterohepatic circulation, reduce cholesterol levels
Pancreatic and Biliary Secretion
Control by both vagal stimulations and intestinal hormones
Pancreatic Exocrine Secretion:
- -acid in duodenum –> secretin –> stimulates secretion of HCO3- by pancreas
- -fat, AA’s in duodenum –> CCK –> stimulates secretin of enzymes by pancreas
Biliary Secretion:
–fat in duodenum –> CCK –> stimulation of bile secretion by gallbladder and relaxation of Sphincter of Odi
Pancreatic Exocrine Secretion
Enzymes from acing cells: trypsinogen, chymotrypsinogen, lipase, amylase; HCO3- form ductal cells
Proteases secreted as inactive, zymogen form - activated ONLY in lumen of gut
What is a Zymogen?
aka proenzyme
Inactive enzyme precursor. Requires a biochemical change (such as hydrolysis reaction releasing active site, or changing configuration to reveal active site) for it to become an active enzyme
Pancreatic Enzymes
most are inactive (zymogens) until they reach small intestine:
- -enteropeptidase activates trypsinogen –> trypsin (to digest protein)
- -trypsin activates other enzymes
Enteropeptidase is also called enterokinase; expressed w/in brush border
What are the fat soluble vitamins?
A, D, E, and K vitamins (“ADEK” vitamins)
–absorbed w/ fat
What are the water soluble vitamins?
Vitamin C and most B vitamins
–carrier mediated transport
Vitamin B12
Requires gastric secreted Intrinsic Factor (IF), uptake by enterocytes in terminal ileum
IF is produced and secreted into stomach by parietal cells - the SAME cells which secrete gastric acid
Thus, if anything which affects acid secretion is going to similar affect IF secretion –> absorption of vitamin B12 is affected
Vitamin B12 deficiency manifests as anemia
