Digestive System

Intro

-how long

-accessory organs

-where is the lumen technically

-digestion

-30 feet in cadavers; shorter in living body due to muscle tone

-Accessory organs: not part of digestive tract but secrete substances into it; ex=pancreas, liver

-Lumen is technically outside the body (*some things never absorbed; imp barrier bc don’t want gut bacteria to mix)

-Digestion: breaking down food into simpler chemicals that can be absorbed/utilized by the body (*ex: protein → AA)

secretion vs absorption

-secretion: blood → lumen

-absorption: lumen → blood

where does most digestion happen?

small intestine (first half)

-mouth: mechanical break down and saliva

-stomach: holding take, some digestion with HCl and pepsin

-SI: most digestion in first half, bile and pancreatic secretions, most useful things absorbed by end of SI

-LI: some absorption, water and electrolytes

*liver: main organ of nutrient balance

average secretions

Average amounts of solids and fluid ingested, secreted, absorbed, and excreted from the gastrointestinal tract daily; most reabsorbed

-salivary secretions: in mouth

-gastric secretions: gastrin, pepsin

-pancreatic secretions

-LI: recovers a lot of water not reabsorbed earlier

-only 100mL water lost

Structure of the Gastrointestinal Tract Wall

same throughout GI, but customized to dif organs; outer → inner…

Serosa

-connective tissue, separates and encloses

Muscularis externa

-Myenteric plexus: in between muscle layers and nerve that coordinates contraction

-usually 2 layers of muscle (stomach=3); contract together to create peristalsis

• longitudinal: schrunch up and shorten

• circular: ring, narrow diameter to break up content

Submucosa

-Submucosal plexus: nervous tissue, controls secretion from mucosal cells

-majority blood and lympathic vessels

Mucosa

-in contact with digestive contents; ex=esophagus

-Muscularis mucosa: anchor point, resistance and strength

-lamina propria

-small vessels

-epithelium: single-layer absorb important things, more layers if mechanical

receptors if GI tract + plexuses

Receptors in GI tract can sense:

-Acidity

-Nutrient concentrations

-Distension

Plexuses

-Myenteric plexus neurons: generally stimulate muscle contraction

-Submucosal plexus neurons: generally stimulate glands

*stim=emotional states/hunger; long reflexes=use ANS PSNS; short reflexes=don’t need brain

chewing + saliva

-Chewing: breaks apart food; increases surface area that can be acted upon by acid and digestive enzymes (*mechanical)

Saliva:

-Contains amylase which begins the digestion of starch (*complex carb; most in SI)

-Dissolves food which allows for taste (*tastebuds work in aq envionrment)

-Helps to form a bolus that can be swallowed

*more hydrated so easier to move food bolus

upper and lower esophageal sphincters

-Upper: prevents air from entering esophagus (*bc negative pressure in chest; after trachea)

-Lower: prevents stomach contents from entering esophagus; decline in this function is gastroesophageal reflux

-Swallowing causes relaxation of sphincters

-Peristaltic waves propel food toward stomach – swallowing works even upside down or in zero gravity

stomach

-High acidity denatures proteins, which makes enzyme sites accessible (*pH ~1-2 bc high HCl)

-Also kills most bacteria

-Stomach is lined with mucus for protection (*bc high acid)

-Peristaltic waves mix and break up food

-Not much absorption: digestion is only beginning to occur; also large volume relative to surface area (*mainly holding and mixing tank)

gastric glands cell types

-Parietal cells:

• Secrete hydrochloric acid (HCl)

• Secrete intrinsic factor that is used for Vitamin B12 absorption

-Chief cells: secrete pepsinogen, precursor form of pepsin (digests proteins)

-G cells: produce gastrin, a hormone (*switch on majors stomach processes)

secretion of HCL by parietal cells

*takes energy so use “proton pump”; “proton pump inhibitor” drugs slow down stomach acid secretion

*if vomit a lot, lose acid and increase HCO3- ratio so get alkalosis

*HCO3- out

regulation of HCl secretion

-brain or local reflexes

-stimulus=think about food; increase acid production rate when eating a meal

-gastrin, histamine, ACh: increase acid secretion (common drug to block histamine, not as powerful at decreasing acid secretion as proton pump blocker)

-block H+ acid secretion if proton pump inhibitor

-gastric phase stimuli: food in stomach, local reflex increases H+ secretion and gastrin

pepsin secretion

-first step of protein digestion, NOT AA but into smaller peptides

-pepsinogen → pepsin; protective so make sure left cell before activate, bc not specific

-chief cell; activate with HCl

3 stages of stomach digestion: cephalic phase

-controlled and activated by brain; “cephalic”=head; signals from brain

-sight, smell, taste, or thoughts of food

-vagus nerve (CN X)

-get stomach ready for digestion: increase mucus so protected, increase pepsinogen, increase HCl

-gastrin reinforces

3 stages of stomach digestion: gastric phase

-mainly local reflexes

-stretch receptors, chemoreceptors (detect higher pH, signal production more acid) → stimulate plexuses

-muscle layers contract and create mixing waves; stomach 3 layers, transverse layer further enhance mixing and provide structural support as stretch

3 stages of stomach digestion: intestinal phase

-negative feedback SI to stomach (inhibit upstream); create chyme

-CCK=cholecystokinin: need to shift focus to digestion and signal satiety; brain, pancreas, liver

-hormones inhibit acid, enzymes, and peristalsis

-GIP cause insulin secretion

regulation of gastric emptying

-slow down stomach to tell brain full

-enterogastrones: intestinal hormones that signal stomach and intestine

small intestine segments

-Duodenum: first ~25cm (*mix chyme from stomach, bile from liver, and pancreatic secretions)

-Jejunum: longest segment, majority of absorption

-Ileum: third segment, normally most absorption completed by this point

*all 3 designed to be efficient and capture most nutrients

structure of SI

long length, and high SA bc of structural adaptions…

-Circular folds: largest; not smooth and creates turbulent flow so mix things around

-Villi: finger-life projections

-Microvilli: smallest; mediate absorption

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-Lacteal: lympathic vessels, absorb lymphatic fats

-Goblet cells: mucous

-Capillary network: absorb other stuff

-simple columnar epithelium: mediate absorption

-enteroendorcine cells: secrete hormones

where do the liver, gallbladder, and pancreas all meet?

-Duodenum is a “mixing bowl” for chyme and secretions from liver, pancreas

*gallbladder: stores bile

*common bile duct

*pancreas: endocrine (ex=insulin) and exocrine (=digestion)

*sphincter of Oddi/Hepatopancreatic sphincter: liver and pancreas → SI

control of pancreatic enzyme secretion

-slow down stomach and release bile and pancrease secretions

-stimuli=chyme, chemoreceptor

pancreatic enzymes

-Pancreas secretes enzymes that digest the major classes of molecules in food: carbohydrates, fats, proteins, nucleic acids (DNA/RNA)

-Many pancreatic enzymes are activated once they reach the lumen of the small intestine

-Brush-border enzymes: produced by intestinal epithelial cells; activate pancreatic enzymes and perform digestion (*final stage of digestion)

• pancreatic amylase=starch

• lipase=fats

• protease=protein (*ex=enterokinase)

• nucleas=nucleic acids

*before: salivary amylase and pepsin, so relatively undigested; proteins and carbs complex, lipid digestion more simple

different brush border enzymes (enzyme, location, substrate)

-Pepsin: stomach, protein

-Amylse: saliva or pancreas, starch

• ex: startch → (amaylse) → matlose/2xglucose → (maltase) → glucose

-Proteases: pancreas brush border, protein

-Lipase: pancrease, fat

liver structure and function

-Most significant digestive function is bile production

-Bile aids in digestion by emulsifying fats (*break apart globs of fat)

-Bile also serves as a path for excretion of metabolic waste and excess cholesterol through the feces (*that can’t be filtered by kidneys easily)

enterohepatic circulation of bile salts

-bile salts intestine → hepatic portal vein + hepatic artery → liver → bile duct

-recycle bile salts, only 5% lost in feces; bile salts made of cholesterole

-liver: processes nutrients and detoxes; control regulation of nutrients and metabolism

regulation of bile flow + gallstones

-liver secretes bile continuously but espically when lot of fat; CCK when feed/fat in SI; can constrict so bile goes to gallbladder

-gallstone: salts in bile percipiate out; “gallbladder attack” bc increase CCK signal and increase contraction of gallbladder

bile sal

-bile’s 4-ring structure looks similar to cholesterol

-nonpolar side inward and polar side outwards

-phopholid lipid helps bile salt emuslify fat so get emulsification droplet

fat digestion and absorption

triglycerides → (lipase) → FFA → rebuild triglyceride in cells

carbohydrates

-Most carbohydrates in the diet are consumed as disaccharides or polysaccharides: Sucrose (table surgar), Lactose (dairy), Maltose (2 glucose, intermediate startch breakdown), Starch (plant, long-chain glucose), Glycogen (animal, long-chain glucose), Cellulose (non-digestible carb, dietary fiber)

-Only monosaccharides are absorbed by the intestinal cells for use in the body (*glucose, lactose, galactose)

-Disaccharides and polysaccharides must be digested to monosaccharides before they can be absorbed

carb digestion and absorption

startch → (pancreatic amylase) → maltose → (BBE maltase) → monosaccharides → dif transporters (SGLT active transport using Na+)

segmentation

-coordinated contraction from myenteric plexus

-mix stuff

large intestine: anatomy

-ascending, transverse, descending, sigmoid: absorb

-rectum: store fecal

absorption in the large intestine

-Less than 10% of total nutrient absorption (*less than SI)

-Reabsorption of water: reduces about 1500 ml of material down to 200 ml

-Reabsorption of bile salts

-Absorption of vitamins produced by bacteria, most significant is vitamin K (*bacteria also make FFA)

*”large” bc bigger diameter

composition of feces + why color and smell

-75% water, 5% bacteria

-Remainder is indigestible material (e.g. fiber), and dead epithelial cells

• epithelial cells have short lifespans so undergo constant renewable cycle

-Color due to urobilins and stercobilins – pigments that are bilirubin metabolites (*waste products that give brown/yellow colors; bilirubin=old RBC and Hb, if build-up=gnondis)

-Smell is mainly due to compounds produced by bacteria (e.g. hydrogen sulfide, which smells like rotten eggs)

Movements of material through the GI tract: different reflexes

-Gastroileal reflex: opens ileocecal valve in response to stretch in stomach (*between SI and LI)

-Stretch also causes mass movements, powerful peristaltic contractions that move material through the colon (gastrocolic reflex) (*why a meal triggers bowel movement)

-Defecation reflex triggered by stretch in rectum