Gastrointestinal tract Flashcards
GI organs and accessory organs
-oral cavity, esophagus, stomach, small and large intestine
a-salivary glands, liver, gallbladder, pancreas
4 process of GI
digestion
secretion- (endocrine, exocrine, paracrine) from epithelial cells
absorption- moves food from lumen through epithelial cells in blood (transcellular movement)
motility- muscle moves food
layer of the GI tract
mucosal, submucosa, muscularis externa, serosa
mucosa
inside of lumen
mucous membrane -single layer of epithelial cells
submucosa
between mucosa + muscularis externa
has submucosal plexus
muscularis externa
2 layers of smooth muscle
has myenteric plexus
serosa
outer most layer
-protective with mesentery/connective tissue that lines abdominal cavity
enteric nervous system
-autonomous (PSNS +SNS)
-at least 30 diff neurotransmitters
allows for co-ordinate multiple organs
-controls motility of GI using myenteric plexus
-controls secretions of GI using submucosal plexus
oral cavity absorption
minimal
-some drugs and glucose
oral cavity secretion
-saliva from salivary glands 3 each side
-parotid, submandibular, sublingual gland
parotid gland’s saliva
high volume of watery, with salivary amylase and lingual lipase
submandibular gland’s saliva
thicker saliva with more mucus and less salivary amylase and lingual lipase
sublingual gland’s saliva
high in mucus, almost no amylase and lingual lipase
oral cavity digestion
mech- mastication
chem-salivary amylase digest amylose/ complex carb
lingual lipase digests lipids (activated in stomach)
stages of swallowing
voluntary, pharyngeal, esophageal
bolus
food converted into a soft mass
voluntary stage of swallowing
produces bolus through mastication, then pushes in back of oral cavity using tongue
pharyngeal stage of swallowing
involuntary
sensation of bolus at pharynx triggers swallowing
-sensory neurons will activate, closing off nasopharynx by lifting uvula of soft palate. the epiglottis bends over the glottis to prevent food and liquids from entering trachea. upper esophageal sphincter relaxes allow bolus down esophagus
esophageal stage of swallowing
involuntary
-bolus is pushed down esophagus through peristalsis.
lower esophageal sphincter opens
peristalsis vs. secondary peristalsis
contracting + relaxing esophageal circular and longitudinal muscle to move bolus
-if bolus doesn’t make it, a stronger contractions pushes the bolus down
xerostomia
caused inability or reduction in salivary production/ dry mouth
-often has infections in oral cavity
sjogren’s disease
causes xerostomia
-body’s immune system attracts salivary glands. damaging them
stomach absorption
-minimal absorption bc of protective mucus, except small drugs and alcohol
fundus
upper portion of the stomach
-receives bolus
-stretches in response to bolus called receptive relaxation
rugae
folds of mucosa layer which help expand the stomach
4 layers of the stomach
mucosa: secretions by epithelial cells will dictate function
-no other section has acid secreting cells
-thick layer of protective mucus
muscularis externa: has circular longitudinal and oblique layers
rest norm
mucus neck cells
on mucosal layer
secrete mucus and hco3 to protects stomach from hcl
-exocrine in stomach
parietal cells
secrete cells (h and Cl)
intrinsic faction (absorbs b12)
exocrine
in stomach
chief cells
secrete gastric lipase + pepsinogen
exocrine
in stomach
pepsinogen
-zymogen
active becomes pepsin which digests proteins
in stomach
g cells
secrete hormone gastrin
endocrine
in stomach
d cells
secretes somatostatin
endocrine
in stomach
acids role in stomach
HCl activates or inactivates enzymes
in-salivary amylase
act- lingual lipase, pepsin
-aids in denatures of proteins
-destroys microbes
motility of stomach
–receptive relaxation
-gastric emptying
-propulsion
-grinding
-retropulsion
propulsion
smooth muscles push contracts of stomach from upper to lower regions
grinding
vigorous muscular contractions of stomach to make bolus into chyme
retropulsion
movement of chyme back in stomach’s body
-more mixing
gastric emptying
pyloric sphincter opens allowing chyme to enter small intestine
pyloric stenosis
abnormally thick pyloric sphincter
-blocks and narrow opening
-projectile vomiting
treatment: pyloromyotomy
small intestine digestion
uses brush border cells that are on enterocytes membrane
duodenum
-can increase or decrease motility
-does most chem digestion
-villi
Jejunum
2nd portion
villi
-many absorptive epithelial cell with needed transporters
ileum
longest and last segment
-enterocytes to assist in absorption
less villi
b12 and bile salts are mainly absorbed here
layers of small intestine
mucosa layer -no rugae but villi
-has enterocytes
rest similar to stomach
enterocytes
absorptive epithelial cells
have villi and micro villi to increase SA
bushed border/ apical membrane
-basolateral membrane is close to capillary and lymphatic vessels
goblet cells
secrete s mucus to aid in lubricating
-exocrine
in SI
intestinal gland cells
secretes a watery mucus with hco3 to neutralize chyme
-this protects mucosa layer
-interstitial
in SI
s cells
secrete hormone secretin
in SI
i cells
releases hormone Cholecystokinin/cck
in SI
k cells
secretes hormone glucose dependent insulinotropic peptide/GI
in SI
brush border enzymes
-on the apical membranes of microvilli
-also called disaccharidase
-causes nutrient to be absorbable
lactase
BBE
make lactose into glucose and galactose
sucrase
BBE
sucrose digest into glucose and fructose
maltose
BBE
maltose digest into 2 glucose
alpha-limit dextrinase
BBE
branches polymers of glucose in linear glucose polymers
ex. amylopectin
dipeptidase
protease that digest dipeptide into 2 single AA
aminopeptidase
protease
digest peptide by remove 1 single AA from protein strand
protease
protein digesting enzyme
enterokinase/enteropeptidase
protease
digest peptides
trypsinogen into trypsin
small intestine motility fed state
segmentation
peristalsis
segmentation
localized mixing contractions to help absorption
small intestine motility fasted state
-absent chyme solution
-migrating motility complex/MMC > a type of peristalsis where pushes out any particle of food that remain in stomach or small intestine
-autonomic unlike regular peristalsis
peptic ulcer disease
-open sores within GI tract
-caused by imbalance in mucosa layer or more acidic
-treatments depends on cause
large intestine absorption
finishes absorption
mainly water
large intestine’s layers
-mucosa have haustra
>pocket structures that force lumen contents to churn making chyme expose to mucosa’s surface
norm
large intestine secretions
mainly secretes mucus from goblet cells
-some electrolytes (k, cl)
-no other digestive enzymes are secreted
large intestine motility
-moves slowly
-peristalsis
-haustral churning
-gastrolienal reflex
gastrolienal reflex
presence of new bolus in stomach will stimulate opening of ileocecal valve
large intestine digestion
bacteria break down and salvage undigested nutrients
-produces vitamins (K)
flatus
intestinal gases which is a byproduct of bacteria
-tooting
oral cavity motility
mastication, swallowing and peristalsis
stomach digestion
pepsin breaks down proteins
stomach secretion
mucus, hco3, hormones, HCl
small intestine absorption
very effective
carbs, proteins and lipids
small intestine secretions
mucus, hc03, hormones,
pancreas anatomy
the exocrine secretions from the pancreas move though the body of the pancreas via pancreatic duct
-pancreatic duct joins the common bile duct which connects to gallbladder and liver
-hepatopancreatic sphincter opens to allow secretions to enter duodenum
-accessory pancreatic duct also allows for secretion to enter duodenum
zymogen activation in pancreas
zymogens are secreted by acinar cells then secreted in lumen of small intestine. Then enterokinase activates trypsin. This then activity of trypsin converts zymogen into active enzymes. then the enzymes break down the nutrients
pancreatic amylase
enzyme that digest amylose (starch)
pancreatic lipase
enzyme that digests triglycerides
trypsinogen
zymogen that converts into trypsin to digest proteins
zymogen
inactivate pre cursor of enzymes
Chymotrypsinogen
a zymogen that is converted into the enzyme chymotrypsin, chymotrypsin digests proteins
Procarboxypeptidase
a zymogen that is converted into the enzyme carboxypeptidase, carboxypeptidase digests proteins
Proelastase
a zymogen that is converted into the enzyme elastase, elastase digests proteins
Prophospholipase
a zymogen that is converted into the enzyme phospholipase, phospholipase digests phospholipids
Procolipase
inactive protein that is converted into the coenzyme colipase, colipase helps pancreatic lipase more efficiently digest triglycerides
pancreas secretions
zymogen, enzymes, hco3, water, insulin, glucagon,
acinar cells
secretes many diff enzymes and zymogen
exocrine
pancreas
ductal cells
secrets hco3 and h2o
exocrine
pancreas
liver function
removes waste, makes bile secretions which is stored in gallbladder
-converts nutrients into useable forms/ metabolism
liver’s anatomy
hepatocytes
hepatic ducts
cystic duct and common hepatic duct form common bile duct
connects to gallbladder via cystic duct
-secretions from the pancreatic duct connect to the common bile duct
-hepatopancreatic sphincter opens in allowing secretions in common bile duct then enter duodenum
liver vasculature
-hepatic artery gives blood to liver
-hepatic portal vein gives nutrient rich blood from GI tract to liver
-leaves liver via hepatic vein
liver lobule
-special arrangement of hepatocytes
-hexagonal shape
- a branch of hepatic artery, hepatic portal vein and bile duct
-each lobule has in its center a central vein
-sinusoids
-bile solution collected bile canaliculi
hepatocytes
-cells in liver
exposed to both blood via the sinusoids, and the bile canaliculi.
produces and secretes bile solutions and help with absorbing lipids
sinusoids
leaky capillary bed that has hepatic portal vein, hepatic artery
gallbladder
-under liver that made of smooth muscle
-connected to liver via cystic duct
-stores and concentrates bile solution from liver
-when chyme enters duodenum, gallbladder will contract to push bile through cystic duct, down common bile duct in duodenum when hepatopancreatic sphincter opens
path of bile salts
idk i think
-hepatocytes, bile canaliculi, common hepatic duct, cystic duct
bile solution
-helps metabolism lipids and excretes waste
-has bile salts > amphipathic (hydrophobic and philic, function as detergents to solubilize lipids
-secreted in duodenum from common bile duct
-stored in gallbladder
gall stone
small crystals from hyper concentrated solutions in bile
-painful
-if blockage is in common bile duct, it can prevent liver secretions from entering duodenum
cholecystectomy
removal of gallbladder
ANS in GI tract
SNS, PSNS
enteric nervous system, can share and receive info from SNS and PSNS
Sensory neurons of ENS
part of submucosal plexus
3 diff types of sensory neurons
mechoreceptors in GI tract
sensory neurons that detect stretching in GI organ, if there is a contents, detect if solid or liquids
chemoreceptors
sensory neurons detect contents including nutrients density and types of macronutrients
nociceptors
sensory neurons can transmit pain, identifying damages like injury or inflammation
gastrin
peptide hormone secreted by g cells of stomach
-triggered for release bc of activation of ACh, stretching of stomach bc of bolus or AA in bolus
cholecystokinin (CCK)
stimulates enzyme secretion from pancreas, causing gallbladder to contract and releasing bile in small intestine
-peptide hormone secreted by I cell of small intestine
-released bc protein or lipids in chyme
somatostatin
peptide hormone secreted by D cells of stomach
-released bc of low pH
inhibits gastrin
secretin
peptide hormones released by s cells of small intestine
-released bc low pH
- stimulates hco3 from pancreas and liver
Glucose dependent insulinotropic GIP
-stimulates the release of insulin
-peptide hormone secreted by k cells of small intestine
-released when there is carbs, lipids and proteins in chyme
hepatic ducts
collects bile in liver
bile canaliculi
bile collecting vessels
-bile solution collected by small vessels
short loop reflex and their effects
Local reflexes can begin and end within the wall of the GI tract
Can increase motility
Sensory neurons detect lumen contents, k detect stretching of GI tract, if f protein AA, or lipid in bolus/chyme are presence, consistency of contents.
Induces secretes enzyme, and acid
-no CNS
long loop reflex
-Any reflex that is integrated in the CNS
ex/
when bolus enters stomach, CNS detects it bc stretching of stomach bc vagus nerve
salivary gland regulation
SNS and PSNS stimulate salivary secretion
SNS saliva- increase mucus and less enzymes
each gland is innervation by spinal nerve t1-t3
PSNS saliva- increase volume of saliva
-parotid gland innervated by glossopharyngeal
nerve
-submandibular and sublingual by facial nerve
MMCs
Migrating Motility Complex
-types of peristalsis
ensure that no remaining meal contents remain
- empties contents towards the large intestine, preparing the fed state of motility.
Regulation of stomach motility
Has interstitial cells cause smooth muscle contraction by self basal electrical rhythms
-When no bolus, MMC initiates and goes through the stomach, and small intestine.
-When bolus enters the stomach
-BER halt
-propulsion, grinding and retropulsion are triggered by neurotransmitters on smooth muscles cells
- gastrin, reinforces muscular contractions .
regulation of stomach’s acid secretions
maximum HCl causes by 3 stimuli
ACh, histamine, gastrin
gastrin: released if there are AA by G cells or gastrin releasing peptide from neural stimulation
-stimulates parietal or ECL cells
Histamine: released by gastrin binding to ECL cell or neural stimulation
-stimulates parietal or ECL cells
ACh: released by long loop reflex triggered by thinking of food
-or by short loop reflex triggered by bolus entering stomach
-stimulates parietal or ECL cells
How to stop stomach acid secretions
-if pH is too low, somatostatin is released stopping gastrin release
Regulation of gastric emptying
-increase vagus nerve activity and gastrin, opening pyloric sphincter more
-increase sympathetic nerve activity and CCK, less open the pyloric sphincter will
regulation of small intestine motility
absence of chyme results in slow, waves of contractions moving down the small intestine, due to the MMC from stomach
-when bolus enters stomach, motility patterns change to segmentations and peristalsis
-MMC stops
regulation of pancreatic secretions
-CCK stimulates secretions from acinar cells and secretin
secretin will increase hco3 and h2o by ductal cells stimulation
-both acinar and ductal cells are activated by efferent neurons from vagus nerve
regulation of bile secretions
neural and hormonal inputs regulate bile from liver
-CCK stimulates gallbladder to contract and relax hepatopancreatic sphincter, stimulation secretions from hepatocytes
-secretin stimulation secretions of hco3 and h2o from ductal cells that line common bile duct
phases of GI tract
cephalic phase, gastric phase, intestinal phase
Cephalic phase
Stimulus: taste, thought and smell of food
-medulla oblongata activates submucosal and myenteric plexus neuron
-response is increase salivary and acid secretions, increase intestine mucus, increase motility of stomach and small intestine
Gastric phase
stimulus: bolus stretching stomach and presence of AA
-medulla oblongata activates submucosal and myenteric plexus neuron
-hormonal regulation by G cells releasing gastrin
-increase hcl, intestine mucus, stomach’s motility, and opening of pyloric sphincter
Intestinal phase
-hormonal regulation of secretion, CCK, GIP
-stimulus: chyme in intestine
-medulla oblongata activates submucosal and myenteric plexus neuron
-increase intestine mucus, increase hco3, digestive enzymes, insulin from pancreas, increase motility of intestine, gallbladder contraction
-decrease hcl, stomach’s motility and gastric emptying
ECL cell
enterochromaffin like cell
basal electrical rhythms
self generate electrical signals
order of energy sources
carbs, triglycerides, aa
chemical digestion of carbs
not monosaccharide as they are absorbs
oral cavity: salivary amylase (starch (amylose + amylopectin) > maltose)
stomach: salivary amylase stops working
SI: lactase (lactose > glucose + galactose)
Maltase (maltose > 2 glucose)
sucrase (sucrose > glucose + fructose)
Pancreas: pancreatic amylase (starch (amylose + amylopectin) > maltose)
carb absorption
enterocytes (SI) bc it has monosaccharide transporters
-glucose and galactose move in absorptive cells by Na symporter on apical membrane, while fructose moves in bcc of fructose uniporter
-monosaccharides move out basolateral membrane by, monosaccharide uniporter into interstitial fluid > blood
lactose intolerance
-GI discomfort
-caused by loss of lactase so lactose can’t be absorbed
-bacteria in LI can metabolism lactose but produces gases
-not allergy
proteins
composed of 20 diff AA
-denature by low pH
-also called polypeptide
di- 2 AA, tri- 3 AA, peptide 4-50, poly >51
one end of a protein is called amino terminus and other carboxy terminus
protein chemical digestion
oral cavity: n/a
stomach: pepsin (polypeptides > peptides)
SI: aminopeptidase (polypeptides > polypeptides + single AA)
dipeptidase (dipeptides > 2 single AA)
pancreas: trypsin, chymotrypsin, elastase (polypeptides > peptides)
carboxypeptidase (polypeptides > peptides)
exopeptidase
enzyme that recognizes either end of a polypeptide
ex. aminopeptidase removes last AA on amino terminus
carboxypeptidase removes last AA on carboxy terminus
endopeptidase
proteases cut peptides based on AA sequence
ex. trypsin cuts carboxy side of lysine or arginine if it isn’t followed by proline
protein absorption
-works best with single AA
-apical Na/AA symporter moves many AA across apical membrane
-DI and tri peptides can cross by apical H symporter
-in cell, cytosolic peptidase can digest single AA for basolateral membrane
-AA uniporter moves AA through basolateral membrane
lipids
mostly triglycerides
-difficult bc enzymes are hydrophilic while lipids phobic
-enzymes only act on surface of fat droplet
lipid chemical digestion
oral cavity: lingual lipase (inactive)
stomach: lingual + gastric lipase (triglycerides > monoglycerides + fatty acids)
Liver: bile
Pancreas: pancreatic lipase (triglycerides > monoglycerides + fatty acids)
phospholipase ( phospholipids > fatty acids)
triglyceride and lipase vs. biglyceride and lipase
lingual, gastric and pancreatic lipase removes 1 fatty acid making di glyceride
lipase removes 1 fatty acid making mono glyceride
bile salts
amphipathic to make lipid droplets soluble
-they cover smaller lipid droplets so they stop getting bigger + stay soluble called emulsification and droplets called micelles
lipid absorption
free fatty acids and monoglycerides from micelles diffuse across apical membrane of enterocytes by protein carrier
-then they are moved to smooth ER and recombined into triglycerides, packaged into proteins called chylomicron.
-then the chylomicron exocytosis across basolateral membrane and absorbed in small lymphatic vessel then enter venous blood
h2o soluble vitamin absorption
B and C
-absorbed by protein carriers in plasma membrane of absorptive intestinal cells
fat soluble vitamin absorption
A, D, E, K
-transport in large lipid droplets and micelles
-when they are near plasma membrane of intestinal cells, vitamins cross without protein carrier then exported by chylomicrons for distribution
metabolism
process of enzymes converting biomolecules into other forms
-makes ATP
-result of catabolism
building blocks for carbs
glucose is biomolecule in production of ATP or creates glycogen
building blocks for proteins
aa is biomolecule in production of ATP or creates new proteins
building blocks for lipids
fatty acids and glycerol can be metabolized to make ATP or new lipids
cellular respiration
36 atp= 1 glucose, by product co2+h2o
1)glycolysis (in cytosol)
glucose > pyruvate using 2 atp and enzymes
-anaerobic
2)pyruvate biotransformation (mito)
pyruvate > acetyl coenzyme A
3)citric acid cycle (mito with acetyl coenzyme A)
-aerobic
-2 atp produced
4)electron transport chain (mito)
aerobic
produces 34 atps
lactic acid
-low o2
-pyruvate > lactic acid (less atp than usually)
reversible
-produced by skeletal muscles
rxt that is not reversible
pyruvate> acetyl coenzyme A
what happens to monosaccharide
glucose mainly absorbs
galactose > glucose by hepatocytes
fructose> glycogen by hepatocytes and enterocytes
fed state: carbs
1) glycolysis: glucose > glucose-6-phosphate, makes ATP
2) glycogen synthesis: glycogenesis
glucose 6-phosphate > glycogen
3) triglyceride synthesis: excess AA will concert into triglycerides
glucose>glycerol >
»»»»»»»»»»triglyceride
glucose>pyruvate>Acetyl coenzymes A > fatty acids
4)AA synthesis:
subset of AA > acetyl coenzyme A >
»»»»»»»»» fatty acids
subset of AA > pyruvate>
fasted state: carbs
1)glycogen breakdown: glycogen in hepatocytes >glucose-6-phosphate which finishes off glycolysis to produce ATP
glycogen (skeletal) > glucose 6-phosphate> (liver)> glucose
2) gluconeogenesis
-triglycerides get catabolized > glycerol
-catabolism of proteins > glucose
-lactic acid > glucose
mostly by liver
fed state: lipids
used to produce ATP, phospholipids and myelin sheaths
-triglycerides are stored adipose tissues for energy source
fasted state: lipids
-lipolysis
-gluconeogenesis
-ketogenesis
lipolysis
-produce ATP by catabolized triglycerides > acetyl coenzymes A when glycogen is low
-in hepatocytes
ketogenesis
2 acetyl coenzyme A can form a ketone
-in hepatocyte
can reverse ketone> 2 acetyl coenzyme A >citric acid cycle
-heart muscles and renal cortex prefer ketones for ATP production
fed state: proteins
protein anabolism
lipogenesis
Fasted state: proteins
-protein catabolism
gluconeogenesis
what controls the regulation of metabolism
insulin and glucagon
hormone produced in fed state vs. fasted state
insulin
glucagon
what is regulated by insulin
- increase glucose uptake
-increase glycogenesis
-increase lipogenesis
-increase protein anabolism
what is regulated by glucagon
-increase glycogenolysis
-increase lipolysis
-increase gluconeogenesis
-increase ketogenesis
Glycogenesis
glucose> glycogen
Lipogenesis
production of lipids from non-lipids
protein anabolism + catabolism
-forms new proteins
-breaks down proteins to make ATP
gluconeogenesis
-triglycerides get catabolized > glycerol
-catabolism of proteins > glucose
-lactic acid > glucose
-making glucose from non carb sources
