SI function & digestion/absorption (Songster) Flashcards
(27 cards)
GIT MOTILITY
5 layers of GIT
- serosa
- longitudinal smoooth muscle
- circular smooth muscle
- submucosa
- mucosa
GIT MOTILITY
Two phases of GIT motility
- Digestive: promotes digestion by mixing contents w/ enzymes and maximizes mucosal contact (for absorption into bloodstream)
- Interdigestive: housekeeping phase. Strong contractions driven by migrating motor complex (electrical waves that migrate in SI that move contents along in response to motilin hormone).
GIT MOTILITY
Segmentation contractions versus peristaltic waves
Segmentation = “chops” the chyme//back-and-forth mixing of chyme w/ secretions
Peristaltic waves = propulsive mixing that move chyme toward ileocolic junction / spread chyme along intestinal mucosa
chyme, a thick semifluid mass of partially digested food and digestive secretions that is formed in the stomach and intestine during digestion. In the stomach, digestive juices are formed by the gastric glands; these secretions include the enzyme pepsin, which breaks down proteins, and hydrochloric acid.
GIT MOTILITY
How are contractions coordinated?
Via intrinsic (enteric) and extrinsic (autonomic – para/symp.) nervous systems
GIT MOTILITY
Two plexuses of enteric nervous sytem and their functions
- Myenteric: motility
- Submucosal: blood flow and GI secretion
GIT MOTILITY
Peptide hormones that enhance SI motility
- gastrin, CCK (digestive phase)
- motilin (interdigestive)
GIT MOTILITY
peptide hormones that inhibit SI motility
secretin & glucagon (GIP)
GIT MOTILITY
CCK (Cholecystokinin)
- cell type of origin/stimulator
- sites of action + major functions
- Stimulated by I cells in the duodenum
- gall bladder contractions++; stimulates pancreatic growth and enzyme secretion (e.g., insulin); inhibits gastric emptying
- stimulated by duodenal fatty acids; amino acids; high levels of duodenal acid
pushes bile from gall bladder into SI –> stomach relaxes
GIT MOTILITY
Secretin
- cell type of origin
- sites of action + major functions
- stimulators
- stimulated by S cells in duodenum/jejunum in response to acid presence
- stimulates secretion of bicarbonate-rich pancreatic fluids and of bile bicarbonate
- relaxes duodenal papilla
GIT MOTILITY
3 Consequences of dysmotility of GIT (hypo- and hypermotility)
- Ileus (hypomotility)
- Diarrhea (either hypo or hypermotility)
- Constipation (hypomotility)
CHO DIGESTION
What species can digest insoluble CHOs and how?
Herbivores (both soluble & insoluble) -> via FERMENTATION insoluble CHOs broken down by host microbes in rumen and/or cecum
True symbiotic rlstp. b/w microbes & insoluble CHOs
CHO DIGESTION
CHO digestion steps (luminal and mucosal phases)
Two phases: LUMINAL phase (part of digestive phase) and MUCOSAL (membranous) phase
- LUMINAL: pancreatic & digestive enzymes
- CHOs get mechanically digested in the stomach
- Chyme from stomach empties into duodenum & mixes with pancreatic juice (pancreatic amylase) -> majority of CHOs digested
- Leftover CHOs (mainly di- and tri-saccharrides) b/c too big to enter enterocytes - MUCOSAL (membranous): only small intestine enzymes
- di/trisacharides too big to enter enterocytes get further digested
- occurs on the BRUSH BORDER (microvili) of the SI
Chyme = the partially digested food expelled by stomach into duodenum
Pancreas and liver both produce “juices” that aid with digestion. The pancreas has a ductal system that drains its pancreatic juices into the duodenum. The liver produces biliary juices (bile) in its tissues (parenchyma) that pass into the biliary ductal system, where its ducts meet to form the common bile duct that then drain into the duodenum. Common bile duct + pancreatic duct drain into duodenum via major duodenal papilla
CHO DIGESTION
How do the products of luminal digestion get absorbed?
PRODUCTS = THE CHOS TOO BIG TO BE ABSORBED IN LUMINAL PHASE -> get absorbed in the MUCOSAL PHASE (in the jejunum) instead:
- enterocytic enzymes (maltase, sucrase, lactase, isomaltase) cleave the di/trisaccharides into monosaccharides via hydrolysis, allowing for their absorption into enterocytes thru active 2º transport or facilitated diffusion
- The monosaccharides within enterocytes then get absorbed into the bloodstream
These enzymes line jejunal walls & form the brush border (chemical barrier which food must pass ino order to be absorbed), and are bound to microvilli
PROTEIN DIGESTION
Describe the GASTRIC luminal phase in protein digestion
STOMACH
- Pepsin + acidic stomach (2-3 pH) break down protein into proteoses (large polypeptides) –> proteoses move into SI
PROTEIN DIGESTION
Describe the enteric luminal phase in protein digestion
- In the Small Intestine
- Pancreatic peptidases break the proteases (large polypeptides) into di/tripeptides, and a few amino acids
- the AAs can be absorbed into the enterocytes, as well as some of the di/tripeptides can be absorbed into them
PROTEIN DIGESTION
Describe the mucosal phase in protein digestion
Occurs in the SI
- Aminopeptidases cleave any remaining polypeptides into absorbale di/tripeptides and/or into absorbable individual amino acids
- Absorbed peptides//AAs then can be absorbed into BOTH the bloodstream and lymphatic circulation
enter both blood and lymph circulation once absorbed
Intracellular proteases: there are also intracellular di/tripeptidases within enterocytes that will further break down any absorbed di/tripeptiddes into individual AAs
- Di and tripeptides can also be absorbed directly into circulation and don’t have to be cleaved into individual AAs!
PROTEIN DIGESTION
Exocrine Pancreatic Insufficiency (EPI – malabsorption)
- pathogenesis
- clinical signs
- etiology
- Pathogenesis: Failure of production of normal pancreatic enzymes –> proteins and carbs cannot be digested like normal -> therefore, the lack normal nutritional subunits that would typically get absorbed by enterocytes (malabsorption)
- Clinical signs: weight loss/emaciated even though presence of ravenous appetite; very laege/soft stool with tan/yellow color due to excessive fat in stool
- Etiology: atropy of the pancreas, often genetic or autoimmune condition
german shepherds; rough-coated collies
Tx = life-long via supplementing the missing pancreatic enzymes
FAT DIGESTION
Enteric Fat Digestion
Describe the secretion of bile into the duodenal lumen + its role in fat digestion, and describe the roles of CCK and Secretin
BILE BREAKS DOWN FAT (TRIGLYCERIDES) INTO FATTY ACIDS via emulsification
- Bile is made in liver, stored in gallbladder, and secreted into duodenum via common bile duct
- Presence of fat + AAs in duodenum -> signal release of CCK -> CCK stimulates gallbladder contractions -> bile (acid + salts) gets released into lumen of SI//duodenum
- Secretin acts on pancreas to open up the duodenal papillae to allow for relase of bile into duodenum
bile salts = BA but with taurine or glycine attached, lowering PKA
lower pka allows for bile salts to be more soluble in water
FAT DIGESTION
Emulsification
Required to transform insoluble triglycerides into soluble forms for absorption
- occurs in the LUMEN of the duodenum, under the influence of bile
- bile salts break the large fat globules down into smaller particles: fat droplets // soluble triglycerides
bile salts = BA but with taurine or glycine attached, lowering PKA; lower pka allows for bile salts to be more soluble in water
FAT DIGESTION
Steps of fat absorption:
- Once emulsification occurs in duodenal lumen, the emulsified fat droplets (soluble triglycerides) are hydrolized (via pancreatic lipase) into fatty acids and monoglycerides in a micelle formation in the jejunum
- The micelle components (all bile components except for bile acids) are absorbed into enterocytes, then reassembled BACK into insoluble triglycerides
- The insoluble triglycerides are transported out of the enterocyte via combining with cholesterol & phospholipids -> transport vehicle (chylomicron)
- The chylomicrons are transported out into lymphatic circulation (never bloodstream!)
PANCREATIC LIPASE ACT ON MICELLES IN THE JEJUNUM!!
Micelles = in jejunal LUMEN
Chylomicron = in enterocyte
FAT DIGESTION
Steps for the Bile Acids test
- Fast for 12 hours
- Obtain a pre blood sample
- Feed a fatty meal
- Obtain a post blood sample 2 hours later (after gallbladder has been able to contract/secrete bile into duodenum)
if liver is not functioning properly, will have high bile acids
Normal liver function: reabsorbs bile acids in distal ileum vasculature via portal circulation (enterohepatic circulation)
Abnormal liver function: Bile acids accumulate in portal circulation, spill over into systemic circulation -> high bile acids
FAT DIGESTION
Bile composition
bile acids, water, electrolytes, choelsterol, phospholipids, proteins, fatty acids, bilirubin
synthesized by hepatocytes from cholesterol; stored in gallbaldder
FAT DIGESTION
What stimulates gallbladder contraction in the interdigestive phase versus the post-prandial phase?
Interdigestive phase: GI contractions occur in response to the gallbladder’s response to the migrating motor complex (MMC) via motilin –> induces
Post-prandial: vagal stimulation (stomach distends with food), CCK, and Secretin (–> relaxtion of duodenal papilla)
Neuroendocrine controls GB contraction in post-prandial state especially
FAT DIGESTION
Micelle
- are smaller than emulsified fat droplets
- are water-soluble -> CAN move thru watery SI luminal contents
- diffue to apical surface of enterocytes (all components of bile MINUS bile acid)
bile acid gets reabsorded in distal ileus
