PNB 2265 integrated meal

oral cavity and esophagus

Motility: swallowing, chewing

Secretion: saliva (salivary glands), lipase

Digestion: carbohydrates, fats (minimal)

Absorption: none

stomach

motility: peristaltic mixing and propulsion

Secretion: HCl (parietal cells); pepsinogen and gastric lipase (chief cells); mucus and HCO3- (surface mucous cells); gastrin (G cells); histamine (ECL cells)

Digestion: proteins, fats

Absorption: lipid soluble such as alcohol and aspirin

small intestine

motility: mixing and propulsion by segmentation

secretion: enzymes; HCO3- and enzymes (pancreas); bile (liver); mucus (goblet cells); hormones: CCK, secretin, GIP, and other hormones

digestion: carbohydrates, fats, polypeptides, nucleicacids

absorption: peptides by active transport; amino acids, glucose, and fructose by secondary active transport; fats by simple diffusion ; water by osmosis ions, minerals and vitamins by active transport

large intestine

motility: segmental mixing, mass moment for propulsion

secretion: mucus (goblet cells)

digestion: none (except by bacteria)

absorption: ions, water, minerals, vitamins, and small organic molecules produced by bacteria

cephalic phase means

head

head and esophagus begin digestion

cephalic phase: saliva

digestive and protective

secreted by parotid, sublingual and submandibular glands (autonomic regulation)

Fletcherism

WWI

extract more nutrients from chewing, allow you need to eat less

no evidence of this at all

digestion function of cephalic phase secretions: saliva

salivary amylase

salivary lipse > decreases with age, because we do not use breast milk

protective function of cephalic phase secretions: saliva

lysozyme > breakdown the cell walls of bacteria important microbial role

fluoride > strengthen teeth

HCO3- > neutralize acids in the food that we eat, so contains saliva, water and ions

chewing stimulates

salivate

parasympathetic

3 salivary glands, endocrine

saliva

lubricate food, prevent from chocking

contains amylase

begins chemical digestion, especially carbs

cephalic phase swallowing steps

1. tongue pushes bolus against soft palate and back of mouth, triggering swallowing reflex

2. upper esophageal relaxes while epiglottis closes to get keep swallowed material out of airways

3. food moves downward into esophagus, propelled by peristaltic waves and aided by gravity (still can eat in space)

mouth (bolus) > peristalsis > stomach

pressure gradient created by smooth muscle contraction, phasic contraction

upper esophageal sphincter

skeletal muscle, voluntary, > bolus

bolus

back of throat relaxes upper esophageal pincher allows food to enter esophagus

peristalsis of smooth muscle carry bolus down the esophagus causing lower (smooth) to open allow food to enter stomach

involuntary (except beginning) > swallowing reflex coordinated contraction + relaxation > creates pressure gradient

achalasia

caused by muscle contraction in lower esophagus

high pressure so can not move bolus to that environment

stuff stuck in the throat

could get surgery to fix lower esophagus

esophageal pressure is reduced by

caffeine

alcohol

cigarettes

chocolate

gastroesophageal reflux

caused by changes in pressure

open LES (relaxed SM)

ingestion heartburn

gastroesophageal junction

bolus movement is due to pressure changes down the esophagus

changes in pressure gradient create difficulty swallowing

peristalsis creates low pressure in front

between esophagus and stomach pressure gradient is

lower esophageal spinchter

lower esophageal is greater than pressure inside stomach than

lower esophageal sphincter allows food to enter stomach > begins gastric phase

lower esophageal closes in order to

prevent reflux of stomach acid back in to esophagus

failure of lower esophageal sphincter not closing properly, cause movement of stomach content back up into esophagus when stomach pressure higher > could lead to gastroesophageal reflux

gastric phase summed up

inside stomach when food enters

gastric phase: stomach anatomical divisions

cardia

fundus

body

antrum

pyloric sphincter

gastric phase: stomach functional divisions

proximal (reservoir)

distal (pump, grinder)

tric phase: stomach specializations

rugae

oblique layer

rugae

increase SA of stomach, stretches when stomach increase in volume

specialization of gastric phase: stomach

oblique layer

more muscle, more contraction in muscle externa

important for grading and mechanically digestion

specialization in gastric phase stomach

stretch too much in stomach means

vomit reflex

proximal region in stomach

closet to esophagus

cardiac stomach, fundus, body

food reservoir, store content > expand to accommodate food

distal region of stomach

antrum, pyotric sphincter

closest to smal intestine

active, pumping/ grinding

peristalsis taking place

lumen has a pH of

2

gastric secretion produces a lot of acid due to

parietal cells

gastric secretion region: LES and cardia

LES is part of esophagus

luminal secretion: mucus, HCO3- (in stomach secreted creates a buffer so do not damage tissues)

motility: prevent of reflux, entry of food, regulation of belching

gastric secretion region: fundus and body

luminal secretion: H+, intrinsic factor, mucus, HCO3-, pepsinogen, lipases

motility: reservoir, tonic force due to emptying

gastric secretion region: antrum and pylorus

luminal secretion: mucus and HCO3-

motility: mixing, grinding, sieving, regulation of emptying

gastric secretions by cell type, cells include

chief cells

parietal cells

mucus cells

G cells (inferior)

D cells

ECL cells

mucous neck cells (posterior)

goal is to regulate acid

gastric pits

other than mucus, speciaization of epithelial layer of the gastric mucosa

deep down to form lateral pit > where secretory cellar located

bypass stomach

decrease intrinsic factor, can not absorb as much B12

chief cells

pepsinogen (pepsin precursor)

secrete inactive enzyme

regulate protein digestion

pepsin is a endopeptidase

gastric secretion

parietal cell

HCl also called gastric acid (catalyst, antimicrobial)

intrinsic factor secrete (B12 absorption)

acide production

gastric secretion

mucus cells

mucus

gastric secretions

G cells

gastrin

gastic secretion

D cells

somatostatin > peptide messenger

gastric secretion

ECL cells

histamine

gastric secretion

secretions: Hydrochloric acid (HCl)

parietal cells of gastric glands

apical membrane proton pump > rate limiting step

acid production (increase or decrease proton amp)

factor is ATP hydrolysis

phosphorylation kinase

regulation of proton pump, activating it

histamine > increases cAMP

histamine is released by ECL > has receptors on basolateral membrane, Gs coupled

ACh and Gastrin > increase Ca 2+ > protein kinase C so increase acid production

gastrin released by G cell into bloodstream, bind basolateral membrane of parietal cells

Ca2+ Gq

regulation of protein pump

on parietal cells, no MLCK

protein kinase A

cyclic AMP dependent

protein kinase C

calcium dependent

when you increase protein kinase A and C then

leads to phosphorylate pump, so increase acid production

feedback and regulation of acid secretion consists of

direct vagal secretion

local activation

negative feedback

direct vagal stimulation

innervated by parasympathetic which this stimulates everything

release Ach G cell turn it on as well as partial, enterochromaffin, Ach

local activation

ECL > receptors here as well also stimulate parietal cell

parietal cell > goal to activate protein pump here so activation G cell > gastrin > basolateral > increase Ca 2+ > acid production > protein digestion

gastrin good acid production directly and indirectly

increase acid production caused by local pathways

all cells except neurons in

gastric pit

negative feedback

D cell decrease cyclic AMP, turn off PKA, turn proton pump, slow down production acid pump

acid > high H+ ions, so more protons, more acidic, so build H+, activate D cell

acide in the antrum stimulates somatostatin release to inhibit meal stimulated gastrin secretion

local regulation

response of the cells in the gastric mucosa to contents your stomach that are in the lumen

motor function of stomach > storage

fundus and body

relaxation receptive and adaptation

mixing motor function of the stomach

occurs in antrum > distal, happen a lot

peristalsis > forward motion, pyloric sphincter < usually closed so crash against so mix with pepsin, helps with mechanical digestion

before stretch tissue which

have stretch receptors > send afferent info to NS to get efferent back inhibit smooth muscle in stomach > causing to relax

receptive relaxation

food in esophagus (preemptive)

stomach prepare for meal going to expand a little

adaptive releaxation

food in stomach

stretch wall itself

gastric motility

movements are under neural control (vagovagal reflexes)

regulated by secretions from small intestine as well

small intestine

segmentation

when active inhibit movement of stomach

mechanical stimuli

distention (stretch)

stretching receptors important for gastric emptying

chemical stimuli

digestive products present (proteins)

gastric secretion > gastrin > hormone trigger gastric emptying into small intestine, increase contraction inside stomach

absorption in stomach

quickly

stomach tissue wall is not specialized for absorption

no SA, villi, brush border

food is not simple enough to be absorbed he3re

asprin and alcohol are absorbed here (eat to reduce speed, but hard since membrane permeable)

gastri ulcers

caused by infection with helicobacter pylori

protection of the stomach wall

alkaline mucus protects against HCl

rapid replacement of gastric epithelia via mitosis

impacted by chemotherapy (e.g)

if protection of the stomach wall is specialized then

there is al tea that covers mucosa of the stomach at the top of the gastric pit

release secreting cells

barrier between gastric juice that have HCL and fragile underlying tissue

protection of the stomach wall impacted by chemotherapy in depth

have load GI side effects like diarrhea, vomiting, ulcerations

cancer arise rapid dividing epithelia ells

increase in digestion so unintentionally targeted on chemotherapy

mucus barrie then gets depleted over time, now acid supposed to underlying tissue, causing side effects

food empties leading to

intestinal phase

specialization of small intestine

villi > created by smooth muscle contraction, muscularis is mucosa, increase SA (giving more membrane space), give brush border, secretion, absorption

lacteal

small intestine anatomy

duodenum

jejenum

illeum

jejenu, and ileum both have more SA for absorption, and optimization

duodenum

connects to stomach

mixing and chemical digestion

secretions from accessory organs come into digestive system

jejunum

absorption and digestion

ileum

connects to large intestine

illiocecal value (to LI)

mostly absorption

gastric dumping syndrome

loos of feedback control

excess simple (refined) sugars lead to water retention (distention)

pain, cramping, malabsorption, fast heart rate, sweating, nausea, diarrhea or vomiting

intense swells causing cramps and pain

sugary food leaves the stomach to quickly

interfere with nutrient digestion and absorption in small intestine

too much stuff in duodenum, intestine full

associated with gastric bypass surgery > reduce size of stomach > stomach empty faster due to stretching promoting gastric emptying

gastric emptying

factors decrease gastric motility

small intestine active or secretion standpoint inhibit gastric emptying

enterogasterones (secretin, CCK, GIP)

enterogasterones

inhibit gastric emptying

secretions from all intestine inhibit the stomach

secretin

enterogasterone

brings bicarbonnate in to small intestine to neutralize that stomach acid

pH > released due to low pH in duodenum due to stomach pH of 2

so stomach can stop sending gastric juice down till small intestine can deal with it

CCK (cholecystokinin)

enterogasterone

fat

important for starting fat digestion in the small intestine

Gastric inhibitory peptide (GIP)

enterogastrones

carbs

triggers insulin release

helps body use sugars once4 they absorbed into bloodstream

regulation of gastric emptying is increased by

gastric volume and content (lipid, high protein)

neural control (on pyloric sphincter) gastrin

regulation of gastric emptying

pyloric sphincter relax, door is open

everything moving by pressure gradients

pressure in intestine > stomach means that pyloric sphincter is open

things moe from intestine into stomach (wrong direction)

empty stomach release neurotransmitter called VIP (vasoactive intestinal peptide > causes pyloric sphincter to relax, while other stimuli, produce contractions and emptying (Ach, histamine, sodium) of smooth muscle in stomach

How can smooth muscle relaxation and contraction occur simultaneously

strong peristaltic waves

increased tone in gastric reservoir

opening of the pyloric sphincter > o9w things move out, inhibit contraction so it relaxes, (sphincter is smooth muscle and tonic), release histamine at pyloric sphincter, contraction there too on top of stomach

inhibition fo duodenal segmental contractions > nervous system important, innervate specific cell populations

sending stomach contents to duodenum < proximal segment of small intestine

motility in small intestine consists of

primarily segmentation contractions

infrequent peristalsis

primarily segmentation contractions of small intestine

mixing > back and forth

slow propulsion (frequency gradient) > due to little forward movement

proximal and distal at same time

infrequent peristalsis of motility in small intestine

response to fasting

migrating motor cortex (MMC) > peristaltic wave passed through intestine, allows no contractions, loud stomach growl, squeezing on tube ultimately moist and empty

stimulation: motion (fasting) > activate peristaltic wave

inhibition: feeding

water enema

flush intestine with water claim to get rid of toxins

hydrotherapy does not help at all

secretions into SI: pancreas

regions

pancreatic acini (acinus) > exocrine enzyme

pancreatic islet > endocrine > hormones

pancreatic acini (acinus) exocrine

ENZYMES

• amylase

• lipase

• HCO3-

• precursors (trypsinogen, chymotrypsinogen, procarboxypeptidase)

through pancreatic duct (common bile duct)

accessory organs

secretions not from small intestine itself

pancreas have a close relationship to

duodenum

protein digestion continues here since

pancreas secrete peptidase

amylase

produce disaccharides > then can be attacked by disaccharides here at brush border

lipase

fat digestion start in small intestine (start here basically)

trypsinogen

become trypsin (endopeptidase)

saliva cephalic phase

bulb region connect to duct

secretions in pancreas regulated in large part

by enterogasterones

secretin can stimulate pancreatic duct > to neutralize stomach

bicarbonate produced in duct while

enzymes produced in assignor bulb