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What are the four layers of the digestive system
Mucosa, submucosa, serosa, muscularis externa
Explain the three layers of the mucosa
Mucosal membrane – epithelial cells that come in contact with food. Endocrine cells that secrete hormones into the blood and exocrine cells that secrete juices into the lumen
Lamina propria – connective tissue and lymphatic tissue (macrophages and lymphocytes)
Muscular mucosa – layer of smooth muscle
Explain the submucosa
Second layer – Connective tissue, blood vessels, lymph vessels, lymphoid tissue
plexus of Meisner - network of nerves that control secretions and peristalsis
What type of muscle does the muscularis external have?
Circular, smooth muscle and long smooth muscle
Which plexus does muscularis externa have
Myentric Plexus– controls the frequency and strength of contractions
Saliva contains
Water, electrolytes, mucus, enzymes, and antibacterial proteins
Explain the serosa
– Continuous with the peritoneum
– Connective tissue (outer cover that protects the G.I. tract)
What neural and hormonal system prevents gastroesophageal reflux?
The tonic pressure of the sphincter is higher than the intragastric pressure that keeps it closed
What are the functions of the gastric juice
convert pepsinogen to pepsin
denaturing proteins
release nutrients/minerals for absorption
bactericide agent
explain the enzymes in gastric juice
pepsin: protease (hydrolyze protein) and endopeptidase (hydrolyze peptide bonds in proteins)
gastric lipase (hydrolyze fatty acids from glycerol)
a-amylase (starch breakdown)
explain the first phase of gastric secretions
stimulation: eating, tasting, thinking, seeing, smelling food
submucosal plexus: acetylcholine secretes and enhances release of gastric from g cells —>
acetylcholine triggers paracrine histamine and HCl secretes
chief cells release enzymes
explain the second phase of gastric secretions
stimulation: food
distension and protein presence enhances gastric secretions (by submucosal plexus, gastrin, parasym NS
explain the third phase of gastric secretions
stimulation: food in small intestine
reduced chyme and pH gastric juice triggers somatostatin in pancreas, antrum, duodenum
presence of chyme in duod: release of secretin and CCK (reduce gastric juice, peristalsis, gastric emptying
parts of the small intestine
kerckring folds
villi: has enterocytes, capillaries, lacteal vessels for nutrient transport
microvilli: has glycocalyx (hydrolyze partially dig nutr)
crypts of lieberkuhn: stem cells for enterocytes
explain the absorptive process
either diffusion, facilitated diffusion, active transport, or pinocytosis
nutrients absorbed on brush border to basolateral membrane OR through tight junctions
depends on solubility/ electric gradient/ size
what does the colon do for absorption
liquid content get mixed by contractions
proximal colon mucosal cells absorb Na, Cl, water.
sodium absorbed by active transport and ADH
what are colonic secretions
goblet cells secrete mucus (lubricant for feces and protect mucus cells from gut bacteria)
bicarbonate secreted and trades with Cl (which is absorbed)
provide alkaline environment that helps neutralize acids produced by gut microbiome
what is the role of the pancreas in digestion
islets of langerhans:
a cells: glucagon
b cells: insulin
d cells: somatostatin
acinar exocrine cells produce and package digestive enzymes and alkaline rich juice to buffer chyme (water, cations and anions, bicarb)
stimuli for release of pancreatic juice and enzymes are
secretin: in response to acidic chyme
cholecystokinin: presense of fat and partial digested proteins
what is bile made of
made in the liver, it has bile acids, salts, cholesterol, phospholipids, bile pigments dissolved in alkaline juice
why is bile important
it emulsifies large fat globules into small micelles for easy lipid absorption
how are gallstones formed
when bile becomes super saturated with cholesterol and crystallizes
explain hypercholesterolemia and how to treat it
def: high blood cholesterol concentations
resin medication binds to bile and excretes it from the body
plant stanols/sterols can also bind bile and excrete it WHICH CAUSES decreased recirculation of bile and absorption of cholesterol so the body uses cholesterol to make more bile, decreasing the concentration
peptic ulcer disease
caused by H pylori, alcoholism, NSAIDS (pain meds_. treated by H2 receptor blockers (pepcid)
pancreatitis
occur with alcoholism, hypertriglyceridemia, duct blockage,
Zymogens become activated and digest pancreatic tissue
patients need lipase or partially hydrolyzed nutrients
what are some regulatory hormones that control digestion/absorption
gastrin (stimulate HCl and Pepsin)
CCK (bile release into small intestine)
secretin (pancreatic juice to neutralize)
peptide YY (fat causes decrease appetite and gastric acid/emptying)
motilin (stim by acetylcholine, controls motility bwn meals)
what are some regulatory paracrines that control digestion/absorption
somatostatin: inhibit gastrin, gastric empty
histamine: stimulate parietal cells to secrete HCl
glucagon like peptides: release insulin and inhibit glucagon
insulin like growth factor 1: increase proliferation of GI