GIT Flashcards
Function of the Gastrointestinal Tract (GIT)
Transfers organic nutrients, minerals water from EXT to INT environment
DIGESTION - chemical alteration of food into molecules that can be absorbed
ABSORPTION - movement of digested food from intestine into BLOOD or lymphatic system
EXCRETION - non-absorbable materials (fibre, bacteria intestinal cells, hydrophobic molecules) removed
HOST DEFENCE - continuous with ext of body, inactivate pathogens
Components of submucosa
blood
lymphatic vessels
connective tissue
submucosal plexus - nerve cell bodies (info relay)
Components of mucosa
epithelium - polarized. Basolateral and apical. Tight junctions
lamina propria - connective tissue
muscular muscosa - think layer of smooth muscle. Villi movement
Components of Muscularis Externa
Thick inner layer (circular muscle)
Myenteric nerve plexus (nerves to regulate muscle function)
Thin outer layer of longitudinal muscle - shorten tube
What is the serosa
Thin layer of connective tissue, connecting intestine to the abdominal wall
portal circulation - nutrient rich blood
Intestinal tract –> liver
Blood drains from the intestine, directly to liver
NUTRIENT RICH BLOOD
Liver: removal of harmful substances, process nutrients
What blood/circulation does the liver receive?
"In Series" blood from Hepatic artery, stomach, pancreas, sm/lg intestine. LOW OXYGEN, HIGH NUTRIENTS Hepatic artery (oxygen-rich blood) runs through majors organs first, conglomerate to liver
GI Processes
Secretion and Motility
governed by volume and composition of lumen contents
Reflexes propagated by (3)
Mechanoreceptors
Osmoreceptors (salty)
Chemoreceptors
Intrinsic Neural Regulation
Enteric nervous system (nerve plexi)
Controls activity of SECRETOMOTOR neurons
contained within GIT walls
Dense and complex neural network (10^8)
Brain of the gut - can function independently
Two nerve networks - Myenteric plexus and submucosal plexus
Myenteric plexus
influences SMOOTH MUSCLE
Submucosal plexus
Influences SECRETION
Regulation of Extrinsic Neuronal Regulation
ANS
parasympathetic - Rest and digest (thin saliva), stim peristalsis and secretion
sympathetic - fight or flight - thick saliva, inhibits peristalsis
Influences: Hunger, sight/smell of food, emotional state
4 Chemical Messenger Regulators
Endocrine - hormone - distant target via blood
Neurocrine - neurotransmitter - post-synaptic target cell
Paracrine - diffusion through interstitial fluid
Autocrine - chemical messenger acts on cell that produced it
GI Hormones - all peptides, feedback control system
Secretin
Cholecystokinin (CCK)
Gastrin
Glucose-dependent Insulinotropic peptide (GIP)
CCK - cholecystokinin
Triggered by fatty acids and amino acids in the small intestine (I cells)
STIMULATES:
pancreas increase digestive enzyme secretion
Gall bladder contraction - bile acids break down fat
Fat and AA are absorbed, CCK is removed, stimulation is stopped –> NEGATIVE FEEDBACK
Peristalsis and Segmentation
Peristalsis –> propulsion
contraction on the oral side of food, relaxation on the other side. Moves towards anus. Smoot passage of bolus
Segmentation –> mixing with digestive enzymes
intestinal segments contract and relax, bolus does not move. Small intestine. Slows transit time for more absorption
Phases of GIT control (3)
cephalic (head) - stimulated by sight, smell, taste, chewing, emotions, parasympathetic fibres
gastric (stomach) - receptors stimulated by Distention, Acidity, Amino Acids, Peptides
intestinal - receptors stimulated by Distention, Acidity, Osmolarity, Digestive Products
Hypothalamus affect
Feeding centre in lateral region
Activation –> increased hunger
Satiety centre in ventromedial region
Activation –> feeling of fullness
Factors that influence food intake
OREXIGENIC factors - increase intake Neuropeptide Y (NPY) - stimulates hunger Ghrelin - synth and released from endocrine cells in stomach. Stimulate release of NPY
ANOREXIGENIC factors - decrease intake Leptin (adipose) Insulin (pancreas) Peptide YY (intestines) Melanocortin (hypothalamus)
Leptin
ANOREXIGENIC factor - from adipose
Inhibit the release of neuropeptide Y, inhibiting food intake
no apetite regulation
Water intake
Hypothalamus - thirst centre - stimulated by:
- Increased plasma osmolarity - vasopressin (antidiuretic hormone) conserves water at kidney
- Decreased plasma volume - stimulates baroreceptors. Increases thirst due to decreased blood volume
- Dry mouth/throat
- Prevent over-hydration - stimulated by mouth, throat, GIT
Salivary Glands (3) and their secretion
Parotid - watery (serous) secretion
Submandibular - serous/mucous secretion
Sublingual - mucous secretion
Composition of saliva
- Water (hypotonic, slightly alkaline)
- Electrolytes (Rich in K+ and HCO3-, poor in Na+ and Cl-)
- Digestive enzymes (amylase, lipase)
- Glycoproteins (mucin) [mucin + water = mucous]
- other components (anti-microbial)
function of saliva
moisten/lubricate food initiate digestion Dissolve food - diffusion allows for taste antibacterial speech buffering (HCO3- neutralizes acid)
acinar cells
Part of the salivary gland
Important for protein, electrolyte and water secretion
ductal cells
Part of the salivary gland
Important for creating alkaline and hypotonic nature
myoepithelial cells
part of the salivary gland
important for pushing saliva from acinus into duct
smooth muscle and epithelial characteristics
formation of saliva
ACINAR glands secrete initial saliva (isotonic)
water, electrolytes, proteins
MYOEPITHELIAL cells contract, expelling saliva from acinus –> duct
DUCTAL cells modify initial saliva to a hypotonic, alkaline state
loss of Na+ and Cl-
secretion of K+ and HCO3
striated duct
regulation of salivary gland function
Parasympathetic
- smell/taste
- pressure receptors in mouth
- nausea (protection)
- -inhibited by fatigue, sleep, fear, dehydration, drugs
Sympathetic
- increased, thicker*
- increased protein secretion from acing cells
- stimulates myoepithelial cells (increased flow)
Amylase in saliva
Starch digestion in the mouth
– inhibited in the stomach (acidic pH)
Carbohydrates are digested in the small intestine by PANCREATIC AMYLASE
Lingual lipase
Fat breakdown in the mouth
acid stable, active in the stomach
Digestive role of saliva is ______
Minor
“dry mouth” and causes
Xerostomia
congenital
autoimmune process
drug side effect
radiation
Consequences of a dry mouth
dry mouth
decreased oral pH –> tooth decay, esophageal erosion
poor nutrition due to decreased food lubriaction
What initiates swallowing?
Pressure receptors in the walls of the pharynx
liquid/food entering signals pharynx, esophagus, respiratory muscles
Swallowing
- Tongue pushed food to back of PHARYNX
- soft palate elevates to prevent food from entering nasal passages
- -> inhibition of respiration. larynx raises. glottis closes - EPIGLOTTIS covers glottis. prevents liquid or food from entering trachea
- food descends into esophagus
Esophageal phase of swallowing
Transfers food from mouth –> stomach
skeletal muscle on top 1/3, smooth muscle rest
no absorption, past passage via mucous gland help
exposed to rough/abrasive food
Upper and lower sphincter closed except when swallowing, vomiting, burping
- relaxation of upper esophageal sphincter
- peristaltic waves move food down esophagus
- lower sphincter opens, food enters stomach
Stomach
Sac-like organ between esophagus and small intestine
stores food
machanical and chemical breakdown of food
Pepsinogen and HCl in stomach
Pepsinogen - digestion enzymes for PROTEIN
HCl - dissolves food, partial digestion, sterilization
Pernicious Anemia
Stomach doesn’t secrete Intrinsic Factor like normal … Vitamin B12 is not absorbed.
RBC deficiency
Fundus and body (stomach)
Upper 2/3 of stomach
thin layer of smooth muscle
Secretion of mucus, pepsinogen, Hal
Antrum (stomach)
bottom 1/3 of stomach
Thick smooth muscle layer
Secretion of mucus, pepsinogen, gastrin
Major and Minor secretions of stomach
Chemical messengers secreted into ducts, then to epithelial surface
does not enter blood
Endocrine:
Mucus - prevents self digestion
HCl - hydrolysis of protein, sterilization
Pepsinogen - digestion of proteins
minor:
Intrinsic Factor (B12)
Gastrin (Endocrine - stimulates HCl production, stomach motility)
Histamine (Paracrine - HCl production)
Somatostatin (Paracrine - HCl production)
Parietal Cell
found in gastric glands in fundus/body region
oxyntic cell
secretes HCl and Intrinsic Factor
CANALICULI increase surface area of cells, maximize secretion into stomach lumen
[canaliculus - actively secreting cell]
lost of mitochondria (energy needed for acid secretion)
Gastric glands
Chief cell - all regions
secrete pepsinogen
- precursor of pepsin
- accelerates protein digestion
Enteroendocrine cell - antrum (G-cell)
secretes gastrin
- HCl production
- GI motility
Enterochromaffin-like cells - all regions
secrete histamine
- HCl release
D-cells - all regions
secretes somatostatin
- HCl secretion
SOMATOSTATIN
secreted by D-cells
NEGATIVE regulator of HCL secretion
Acidification of Stomach Lumen
- H+/K+ ATPase - H+ into lumen in exchange for K+ into cell. ACTIVE transport, electroneutral
- -> regulated by Gastrin (gastric molecule), Acetylcholine (NT), Histamine (paracrine), and somatostatin (paracrine)
- Carbonic Anhydrase (CA) - formation of H2CO3 from H2O and CO2
- Cl-/HCO3- exchanger - OH- is effluxes from cell in exchange for Cl-. neutral cellular pH
- K+ channels - K+ enters stomach lumen via diffusion thru a channel
- Cl- channels - Cl- enters stomach lumen via diffusion thru a channel
Cl-/HCO3- exchanger
Stomach:
EXCESS BASE
Cl-/HCO3- exchanger - OH- is effluxes from cell in exchange for Cl-
neutral cellular pH
Pancreatic:
ducts secrete watery all secretion to neutralize gastric acid
Pepsinogen Secretion and Activation
Secreted by chief cells (inactive precursor)
- stimulated by enteric nervous system
- parallels release of HCl
Cleaved and activated by pepsin (via acidic pH in stomach)
ADVANTAGE OF INACTIVE PRECURSOR:
irreversibly inactivated when it enters small intestine - prevents auto digestion
Phases of Gastric Secretion
- Cephalic phase (parasympathetic)
- ACh release by parietal cells
- anticipatory, excitatory
- via Vagus nerve - Gastric phase
- major phase
- excitatory
- via gastrin - Intestinal phase
- inhibitory due to presence of acid, fat, digestion products
- hypertonic solutions in duodenum (stomach slows down, ingestion)
Regulation of gastric secretion
3 Stimulators:
- Acetylcholine, gastrin, histamine
- directly increase acid secretion by parietal cell
1 Inhibitor:
- Somatostatin
- decreased acid secretion by parietal cell
Once acid secretion is at a high rate:
- PS input (cephalic phase) is reduced
- Negative feedback occurs
Gastric Motility
Consumption of meal –> smooth muscle relaxation –> stomach volume increases to 1.5 L without added pressure
Relaxation - PS nerves to ENS
Arrival of food causes peristaltic waves - weak contraction in body of stomach, strong in antrum
Pyloric sphincter closes - small amount of stomach content released to duodenum
mix contents with enzymes and acid
PACEMAKER CELLS in smooth muscle layer
Vomiting
Vomiting centre - medulla
Caused by:
- psychogenic (smell, sight)
- GIT disturbances (infection, distension)
- Motion sickness, inner ear infection
- Chemoreceptors (Brain or GIT, influenced by alcohol, toxins)
- Pressure on CNS
Glottis closes off trachea
diaphragm and ab muscles contract
reverse peristalsis
Stomach contents move up through esophagus, out the mouth
Benefit and Negatives of Vomiting
Benefits:
- removal of harmful substances (bacteria, toxins)
- prevents re-consumption in the future
Negative:
- dehydration
- electrolyte imbalance
- metabolic alkalosis (loss of H+)
- acid erosion on enamel
Ulcers
damaged/eroded area of the GIT mucosa, in acidic regions
Imbalance between aggressive factors (acid, pepsin) and protective factors (HCO3-, mucus)
Helicobacter pylori –> bacterial infection
Non bacterial factors - NSAIDS - decrease prostaglandin (stomach lining protection)
Treatment:
Abx
H+/K+ ATPase inhibitor
Pancreas
EXOcine and ENDOcrine gland
Exocrine –> digestion (apical surface)
- secretions that go into guts
- source of enzymes
- produced in excess
- HCO3- secretion
Duct cells - secrete H2O and HCO3- to neutralize acid
Endocrine –> regulation hormones (Ductless glands)
What are Pancreatic Juices
Isotonic, alkaline, 1-2L/day
contains electrolytes
–> high HCO3-, low Cl-
–> Na+, K+ same as in plasma
–> HCO3- and H2O secreted by duct cells
–> HCO3- neutralizes gastric acid in duodenum
Digestive enzymes - secreted by acinar cells
Proteolytic enz stored and secreted in inactive forms (prevent auto digestion)
CFTR - Cystic Fibrosis Transmembrane Conductance Regulator
Cystic Fibrosis - thick mucous in pancreas
Ductular cell secretion
- Chloride channel opens (CFTR)
- Cl- in lumen is exchanged for HCO3-
- H2O and Na+ paracellularly response to electrochemical gradient
- Neutral pH of cytosol is maintained by exchange of H+ (exported from cell) for Na+ (imported)
ducts secrete watery all secretion to neutralize gastric acid
Alkaline tide
After big meal:
Parietal cells in stomach produce a lot of acid
–> large amount of HCO3- is pumped across the basolateral surface into blood stream
HCO3- (stomach) and H+ (pancreas) meet in portal vein
Two processes balance each other to maintain acid base balance
Acid tide
After big meal:
Duct cells in pancreas produce and secrete HCO3-
–> large amount of H+ is pumped across the basolateral surface into blood stream
HCO3- (stomach) and H+ (pancreas) meet in portal vein
Two processes balance each other to maintain acid base balance
Digestive function of Pancreas
source for majority of enzymes for meal digestion
Acinar cells synthesize and pack pro-enzymes into zymogen granules, stored in the apical pole of cell
neurohormonal input results in the exocytosis into lumen of duct
Proteases
Digestion of PROTEINS into PEPTIDES and AMINO ACIDS
Amylolytic enzymes
Digestion of STARCH into SUGARS
Lipases
Digestion of TRIGLYCERIDES into FREE FATTY ACIDS and MONOGLYCERIDES
pancreatic lipase is water soluble, only works on the surface of lipid droplets
Nucleases
Digestion of NUCLEIC ACIDS into free nucleotides
Where are enzymes activated? How?
secreted in INACTICE form
activated in the DUODENUM
Cleavage of trypsinogen –> trypsin (protease that activates other proteases)
Pancreas prevention of auto digestion
Storage –> inactive form (until it reaches small intestine)
Trypsin inhibitors antagonize prematurely activated trypsin
Trypsin can degrade itself if activated before small intestine is reached
Endopeptidases
Hydrolyze interior peptide bonds from protein and polypeptides
Exopeptidases
Hydrolyze bonds at C-terminal end
Regulation of Pancreatic HCO3- Secretion
Acid enter duodenum from stomach
Reduced pH triggers secretin from cells in small intestine into blood
Circulating secretin stimulates:
- Pancreas (Duct cells) to increase HCO3-secretion
- Liver (Duct cells) to increase HCO3- secretion
CCK
Triggered by fatty acids and amino acids in the small intestine
Circulating CCK stimulates:
- pancreas increase digestive enzymes
- gall bladder contraction (bile acids break down fat)
Negative feedback control system
–> fats and amino acids are absorbed and CCK stimulation is stopped
phases of Pancreatic Secretion
- Cephalic Phase (via PS nerves)
- Gastric Phase (via PS nerves)
- Intestinal Phase
Components of Liver and Biliary System
Bile Duct (from liver)
Sphincter of Oddi (controls content release into small intestine)
Gallbladder
COMMON HEPATIC DUCT
COMMON BILE DUCT
Pancreas
HEPATIC PORTAL VEIN - 75% blood volume, rich in nutrients, poor in oxygen
CENTRAL VEIN - blood back to inferior vena ceva
Lobule
Hexagonal structure with:
- central vein running through the centre
- portal trains at each corner (composed of hepatic artery, portal vein, bile duct)
What forms bile ducts
Hepatocytes
Bile Duct epithelial cells
BILE CANALICULI
Portal triad
Composed of:
- hepatic artery
- portal vein
- bile duct
bathed in blood, filters
hepatic sinusoid
functions of liver
Exocrine gland (formation and secretion of bile)
Metabolism and storage of nutrients (liver matches supply to demand)
Deactivation and detoxification (drugs, hormones, waste products, toxins)
Production of circulating proteins (blood coagulation factors, lipoproteins)
Constituents of Bile (secreted by liver)
- Bile Acids
- synthesized within hepatocyte from cholesterol
- amphipathic
- Cholesterol
- slightly amphipathic
- Salts and Water
- Na+, K+, HCO3-
- Phospholipids
- phosphatidylcholine (amphipathic)
- Bile Pigments
- bilirubin
- Trace Metals
Emulsification
Mechanical disruption to make lipid droplets small
Emulsifying agent prevents droplets from re-forming
what is a micelle? how is it formed?
Soluble cluster of amphipathic molecules - holding station for small insoluble molecules
- non polar groups in the middle
- polar groups on the outer layer
Formed by emulsification via bile acids
product of lipase digestion
Formation of bile
Hepatocytes: produce and secrete bile, phospholipids, cholesterol, bile pigments,
Bile Duct: adds HCO3-, salts, H2O to bile
Gallbladder: stores and concentrates bile between meals, releases into duodenum after a meal
Enterohepatic circulation of bile acids
Steps for bile acid recycling
- Bile acids are released by the liver/gallbladder into duodenum for fat digestion
- Bile acids are reabsorbed across the small intestine (ileum) into portal circulation
- Bile acids are transported back into hepatocytes
Regulation of Heoatobiliary secretion
Bile Salts - as ileum absorbed bile salts, more is produced. reduced when enteropathic circulation is working
Secretin - produced and released by S-cells. Increased HCO3- secretion by bile duct cells
Cholectstokinin -
Gallstones
Cholesterol stones
high concentration of cholesterol results in precipitation
Consequences:
Location - obstruction, infection impacting gall bladder, liver, pancreas
pain, nausea, jaundice, malabsorption
Pigment stones
Result of excessive hemolysis
pigments form precipitates with Ca2+
Gallstone treatment
Cholecystectomy (remove gall bladder) - reduce fat in diet
Remove stones
Drugs to dissolve stones
Location and sections of Small Intestine
Between stomach and large intestine
- duodenum
- jejunum
- ileum
Major function of Small intestine
digestion and absorption of protein, fat, carbohydrate, electrolytes, water, minerals, vitamins
Function of Duodenum
mixing of pancreatic digestive enzymes and bile with food
absorption of nutrients, iron, calcium
release endocrine hormones secretin and CCK
Function of jejunum
digestion and absorption
function of Ileum
digestion and absorption
bile acids and vitamin B12
Folds in small intestine
Folds of Kerckring/Circular folds
increase surface area
villus - protrudes
crypt - invagination
4 cells derived from stem cells
- Absorptive cell (enterocyte)
absorption
brush border enzyme
- Goblet cell
lubricate food
protect from stomach acid
- Enteroendocrine cell (I or S cells)
- Paneth cell
antimicrobialBrush Border Enzyme
small projections (microvilli) of epithelial cells covers villi of small intestine absorptive sufrace
BBE: enzyme anchored to brush border, catalytic activity in lumen
breaks down carbohydrates and peptides into sugars and amino acids before transporting across the enterocyte
Carbohydrate digestion
Starch (amylose and amylopectin) broken down into maltose, maltotriose, and alpha-limit dextrin
cleavage of alpha1,4 and alpha1,6 bonds
sucrose —> glucose + fructose
lactose —> glucose + galactose
Protein digestion and absorption
Proteins broken down may pepsin (sm int) and pancreatic proteases (trypsin and chymotrypsin)
Free amino acids are abs by 2° active transport
Fat Digestion and absorption
lipid droplets are emulsified via mechanical disruption and bile acids
release free fatty acids and monoglycerides
products are incorporated into micelles (breakdown of triglycerides)
Breakdown of micelles results in the diffusion of fatty acids and monoglycerides across intestine epithelium
Extracellular fat droplets - “chylomicrons”
Chylomicron
contains triglycerides, phospholipids, fat soluble vitamins. cholesterol
Lipoprotein lipase on endothelial cell of blood vessels release triglycerides from chylomicrons as monoglycerides and free fatty acids (energy)
absorption of iron
Fe2+ actively transported into enterocyte and incorporated into ferritin –> storage
Transferrin - plasma protein - transport through blood
Iron-Deficiency Anemia
reduced number and size of RBC
tired, light headed, headaches
Not enough iron (diet), iron loss, poor absorption, intestine disease
Water and Electrolyte Abs and Secretion
Absorption - villi
Secretion - crypts
Osmotic gradient
ABS - Na+ gradient
SEC - Cl- gradient
Water transport and electrolyte transport
MMC (motility sm intestine)
MIGRATING MYOELECTRIC COMPLEX
pushes any undigested material from the small intestine to large intestine
prevents bacteria from remaining in the small intestine
Regulated by motilin
feeding inhibits motilin
Lactose intolerance
Lactose - milk sugars
lactate (BBE) digests lactose into glucose and galactose
loss of lactase expression after weaning
decreased water abs in gut, bacteria in lg intestine digest lactose (gas, diarrhea)
Monosacchraides in lactose
lactose —————-> glucose + galactose
via lactase
Vibrio cholera
vomiting and excessive diarrhea
increases cAMP production in crypto of small intestine
activates Cl- channel, water follows (diarrhea)
Anus sphincters
Ileocecal valve
between cecum and ileum
closed when lg int is distended
cecum/appendix
Ascending/transverse/decending/sigmoidal colon
reabs water
reservoir for storage of waste
rectum - hold feces
anus - control defecation
Colon crypt cell types
ONLY CRYPTS, no villi
ABSORPTIVE CELLS/ENTEROCYTES
GOBLET CELLS
PANETH and ENDOCRINE
bacteria - metabolize fibre, produce vitamins (Vit K), gas production
Water absorption in large intestine depends on:
Na+ gradients (ABS)
Cl- gradients (SEC, NKCC1)
Components of GIT
Mouth (chopper)
Pharynx
Esophagus
Stomach (blender, acid sterilizer, reservoir)
Small Intestine - duodenum (run vessel), jejunum, ileum (catalytic & absorptive)
Large intestine (residue combusted, desiccator, pelleter)
Accessory organs - pancreas (enz supplier, neutralizer), liver, gallbladder
Paracellular transport
Across epithelium - BETWEEN CELLS
Limited by tight junction seal
Water and small ions diffuse through
Transcellular pathway
THROUGH CELL
two steps:
transport protein on apical and basolateral cell surface
Defecation
feces - water, undigested food, bacteria old cells
REFLEX - contraction, peristalsis,
