Gastrointestinal Anatomy and Physiology Rowena A. Abante MD Jan. 27, 2009
Gastrointestinal Anatomy and PhysiologyRowena A. Abante MDJan. 27, 2009
The
gastrointestinal
system consists
of the
gastrointestin
al tract and
associated
glandular
organs that
produce
secretions
Physiologic Functions
Topic outline
I. Structure and innervation of the GITII. Regulatory substances in the GIT
III.Gastrointestinal motilityIV. Gastrointestinal secretionV. Digestion and absorption
Topic outline
I. Structure and innervation of the GITII. Regulatory substances in the GIT
III.Gastrointestinal motilityIV. Gastrointestinal secretionV. Digestion and absorption
The structure of the GIT varies greatly from region to region, but common features exists in the overall organization of the tissues
• Mucosa Consists of an epithelium, the lamina propia, and
muscularis mucosae Epithelial cells are specialized for secretion or
absorption Contraction of the muscularis mucosae causes a
change in surface area for secretion or absorption
Structure of the GIT
• Submucosa Consists largely of loose connective tissue with
collagen and elastin fibers Glands may be present in some regions
Structure of the GIT
• Muscularis externa Inner circular , outer longitudinal Contraction of the circular muscle causes a decrease
in diameter of the lumen of the GIT Contraction of the longitudinal muscle causes
shortening of a segment of the GIT
Structure of the GIT
• Serosa Consists mainly of connective tissue covered with a
layer of squamous mesothelial cells
Structure of the GIT
Innervation of the GIT
The autonomic nervous system of the GI tract comprises both extrinsic and intrinsic nervous system
1. Extrinsic innervation Parasympathetic and sympathetic NS
2. Intrinsic innervation Enteric NS
•Afferent fibers carry sensory information from chemoreceptors and mechanoreceptors in the GI tract to the brain stem and spinal cord
•Efferent fibers carry information from the brainstem and spinal cord to the GI tract
Innervation of the GIT: Extrinsic
1. Parasympathetic NS
▫Usually excitatory on the functions of the GIT
▫Innervation of the GIT down to the level of the transverse colon is provided by the vagus nerve
▫The remainder of the colon, the rectum, and the anus receive from fibers of the pelvic nerves
Innervation of the GIT: Extrinsic
1. Sympathetic NS
▫Usually inhibitory on the functions of the GIT
▫Fibers originate in the spinal cord between T8 and L2
▫Preganglionic sympathetic cholinergic fibers synapse in the prevertebral ganglia
▫Postganglionic sympathetic adrenergic fibers leave the prevertebral ganglia and synapse in the myenteric and submucosal plexuses
Innervation of the GIT: Extrinsic
•Coordinates and relays information from the PNS and SNS to the GI tract
•Uses local reflexes to relay information within the GI tract
•Controls most functions of the GIT, especially motility and secretion, even in the absence of the extrinsic innervation
Innervation of the GIT: Intrinsic
1. Myenteric plexus▫ Auerbach’s plexus▫ Primarily controls the motility of the GI
smooth muscle
2. Submucosal plexus▫ Meissner’s plexus▫ Primarily controls the secretion and blood flow▫ Receives sensory information from
chemoreceptors and mechanoreceptors in the GI tract
Innervation of the GIT: Intrinsic
Topic outline
I. Structure and innervation of the GITII. Regulatory substances in the GIT
III.Gastrointestinal motilityIV. Gastrointestinal secretionV. Digestion and absorption
The functions of the GIT are regulated and coordinated by hormones, paracrine
agonists and neurons.
Regulatory substances: GI hormones
•Released from endocrine cells in the GI mucosa into the portal circulation, enter the general circulation, and have physiologic functions on target cells
•GI hormones1. Gastrin2. Cholecystokinin (CCK)3. Secretin4. Gastric Inhibitory Peptide (GIP)
Summary of GI hormonesHormones Site of
secretionStimulus for secretion Actions
Gastrin G cells of stomach
•Small peptides and amino acids•Distention of stomach•Vagus •Inhibited by H+ in stomach
• inc gastric H+ secretion•Stimulates growth of gastric mucosa
CCK I cells of duodenum and jejunum
•Small peptides and amino acids•Fatty acids
•Stimulates contraction of gallbladder and relaxation of the sphincter of Oddi•Inc pancreatic enzyme and HCO3- secretion•Inc growth of exocrine pancreas/gallbladder•Inhibits gastric emptying
Secretin S cells of duodenum
•H+ in the duodenum•Fatty acids in duodenum
•Inc pancreatic HCO3 secretion•Inc biliary HCO3 secretion•Dec gastric H+ secretion
GIP Duodenum and jejunum
•Fatty acids, amino acids, and oral glucose
•Inc insulin secretion•Dec gastric H+ secretion
Regulatory substances: GI hormones
Regulatory substances: Paracrines •Released from endocrine cells in the GI
mucosa
•Diffuse over short distances to act on target cells located in the GI tract
1. somatostatin2. histamine
Regulatory substances: Paracrines 1. Somatostatin
▫ Secreted by cells throughout the GI tract in response to H+ in the lumen
▫ Secretion is inhibited by vagal stimulation▫ Inhibits the release of ALL GI hormones▫ Inhibits H+ secretion
2. Histamine ▫ Secreted by mast cells of the gastric mucosa▫ Inc gastric H+ secretion directly and by
potentiating the effects of gastrin and H+ secretion
Regulatory substances: Neurocrines
•Synthesized in neurons of the GIT, moved by axonal transport down the axon, and released by action potentials in the nerves
•Then diffuse across the synaptic cleft to a target cell
1. Vasoactive intestinal polypeptide (VIP)2. Gastrin-releasing peptide (GRP)3. Enkephalins
1. VIP▫ Homologous to secretin▫ Released from neurons in the mucosa and smooth muscle of the
GIT▫ Produces relaxation of GI muscle , including the LES
2. GRP▫ Released from vagus nerves that innervate the G cells▫ Stimulates gastrin release from G cells
3. Enkephalins▫ Secreted from nerves in the mucosa and smooth muscle of the GIT▫ Stimulate contraction of GI smooth muscle (LES, pyloric, ileocecal
sphincters)▫ Inhibits intestinal secretion of fluid and electrolytes
Regulatory substances: Neurocrines
Topic outline
I. Structure and innervation of the GITII. Regulatory substances in the GIT
III.Gastrointestinal motilityIV. Gastrointestinal secretionV. Digestion and absorption
Gastrointestinal motility
•Contractile tissue of the GIT is almost exclusvely unitary smooth muscle, with the exception of the pharynx, upper 1/3 of the esophagus, and external anal sphincter, all of which are striated muscles
•Depolarization of circular muscle leads to contraction of a ring of smooth muscle and a decrease in the diameter of that segment of the GIT
•Depolarization of longitudinal muscle leads to contraction in the longitudinal direction and a decrease in length of that segment of the GIT
Gastrointestinal motility
• Phasic contractions occur in the esophagus, gastric antrum, and small intestine
• Tonic contraction occur in the LES, orad stomach, and ileocecal and internal anal sphincters
Gastrointestinal motility
GI motility: slow waves
• Are oscillating membrane potentials inherent to the smooth muscle cells of some parts of the GIT
• Occur spontaneously
• Originate in the interstitial cells of Cajal, which serves as the pacemaker of GI smooth muscle
GI motility: slow waves1. Mechanism of slow wave production
▫ Is the cyclic activation and deactivation of the cell membrane Na+-K+ pump
▫ Depolarization during each slow waves brings the membrane potential of smooth muscle cells closer to threshold and, therefore, increases the probability that action potentials will occur.
▫ Action potentials, produced on the background of slow waves, then initiate contraction of smoth muscle cells
GI motility: slow waves2. Frequency of slow waves
▫ Varies along the GIT, but is constant and characteristic for each part of the GIT
▫ Not influenced by hormonal nor neural input, in contrast, the frequency of the action potentials that occur on top of the slow waves is modified by neural and hormonal influences
▫ Sets the maximum frequency of contractions for each part of the GIT
▫ Is lowest in the stomach (3sw/min), and highest in the duodenum (12sw/min)
GI motility: Chewing
•Lubricates food by mixing it with saliva
•Decreases the size of food particles to facilitate swallowing and to begin the digestive process
GI motility: Swallowing
•The swallowing reflex is coordinated in the medulla.
•Fibers in the vagus and glossopharyngeal nerves carry information between the GIT and the medulla
GI motility: Swallowing • Swallowing can be
initiated voluntary, but thereafter it is almost entirely under reflex control.
• The swallowing reflex is a rigidly ordered sequence of events that propels food from the mouth to the stomach.
• This reflex also inhibits respiration and prevents entry of food into the trachea during swallowing
• The esophagus contains a gradient of muscle, from all skeletal at the top to all smooth at the bottom.
• Innervation: vagus
• After the food is swallowed, the esophagus functions as a conduit to move the food from the pharynx to the stomach.
GI motility: esophageal motility
• Sphincters at either end of the esophagus prevent air from entering the upper esophagus and gastric acid from entering the lower esophagus.
GI motility: esophageal motility
• The following sequence of events occurs as food moves into and down the esophagus:
1. UES relaxation to permit swallowed food to enter the esophagus
2. UES contraction to prevent reflux of food into the pharynx
3. A primary peristaltic contraction moves down the esophagus and propels the food bolus along
4. A second peristaltic contraction clears the esophagus from any remain food
5. LES relaxation, vagally mediated via VIP
6. Receptive relaxation- or the relaxation of the orad region of the stomach
GI motility: esophageal motility
GI motility: esophageal motility
GI motility: gastric motility
• The stomach has 3 layers of smooth muscle- the usual longitudinal and circular and a third oblique layer
• The stomach has 3 anatomical divisions- fundus, body, antrum
GI motility: gastric motility• The orad region includes
the fundus and the proximal body. ▫ This region contains the
oxyntic glands and is responsible for receiving the ingested meal.
• The caudad region icludes the antrum and the distal body. ▫ This region is responsible
for contractions that mix food and propel it into the duodenum.
1. Receptive relaxation▫ A vagovagal reflex that is initiated by distention of the
stomach and is abolished by vagotomy▫ Orad region relaxes to accomodate the ingested meal▫ CCK participates by increasing distensibility of the
stomach
2. Mixing and digestion▫ Caudad region contracts to mix the food with gastric
secretion and begins the process of digestion▫ The size of food particles are reduced
GI motility: gastric motility
3. Gastric emptying
▫ Caudad region contracts to propel food into the duodenum
▫ The rate of gastric emptying is fastest when the stomach contents are isotonic. If the stomach contents are hypotonic or hypertonic, gastric emptying is slowed.
▫ Fats inhibits gastric emptying by stimulating release of CCK
▫ H+ in the duodenum inhibits gastric emptying via direct neural reflexes
GI motility: gastric motility
• Regulation of gastric emptying
▫ Chyme entering the duodenum activates intestinal receptors.
▫ This leads to increased contraction of the duodenum and decreased contraction of the stomach (Delayed Gastric Emptying)
▫ Secretin, CCK, and GIP (enterogastrone) are released by the duodenum and feed back on the stomach to slow down.
GI motility: gastric motility
GI motility: small intestinal motility
GI motility: small intestinal motility
• The SI functions in the digestion and absorption of nutrients.
• Slow waves set the basic electrical rhythm which occurs at a frequency of 12sw/min.
• Parasympathetic stimulation increases intestinal smooth muscle contraction; sympathetic stimulation decreases it.
GI motility: small intestinal motility
1. Segmental contractions
▫ Mix the intestinal contents▫ a section of the intestine contracts sending the
chyme in both orad and caudad directions▫ This back-and-forward movement produced by
segmentation contraction causes mixing without net forward movement of the chyme
GI motility: small intestinal motility
2. Peristaltic contractions
▫ Highly coordinated, and propel the chyme through the SI toward the LI
▫ Contraction behind the bolus, and simultaneous relaxation in front of the bolus cause the chyme to be propelled caudally.
GI motility: small intestinal motility
3. Gastroileal reflex
▫ mediated by the extrinsic NS and possibly by gastrin▫ The presence of food in the stomach triggers peristalsis
in the ileum and relaxation of the ileocecal sphincter.
GI motility: small intestinal motility
GI motility: large intestinal motility
•Fecal material moves from the cecum to the colon, to the rectum, and then to the anal canal
•Haustra, or sac-like segments, appear after contractions of the large intestines
GI motility: large intestinal motility
1. Cecum and proximal colon
▫ When the proximal colon is distended with fecal material, ileocecal sphincter contracts to prevent reflux into the ileum.
▫ Segmentation contractions in the proximal colon mix the contents
▫ Mass movements occur 1-3x/day and cause the colonic content to move distally for long distances (e.g. From the transverse colon sigmoid colon)
2. Distal colon
▫ Because most colonic water absorption occurs in the proximal colon, fecal material in the distal colon becomes semisolid and moves slowly
GI motility: large intestinal motility
3. Rectum, anal canal, and defecation
▫Sequence of events:1. Rectum fills with fecal material, contracts, and then
internal anal sphincter relaxes. (rectosphincteric reflex)
2. Once rectum is filled with 25% of its capacity there is an urge to defecate, however, defecation is prevented because the external anal sphincter is tonically contracted
3. When it is convenient to defecate, the external anal sphincter is relaxed voluntarily. The smooth muscle of the rectum contracts, forcing the feces out.
GI motility: large intestinal motility
4. Gastrocolic reflex
▫The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements
▫It has a rapid parasympathetic component taht is initiated when the stomach is stretched by food.
GI motility: large intestinal motility
Topic outline
I. Structure and innervation of the GITII. Regulatory substances in the GIT
III.Gastrointestinal motilityIV. Gastrointestinal secretion
V. Digestion and absorption
GI secretion:Summary of GI secretions
GI secretion Major characteristics Stimulated by Inhibited by
Saliva •High HCO3•High K•Hypotonic• amylase•Lingual lipase
PNSSNS
•Sleep•Dehydration•Atropine
Gastric secretion •HCl •Gastrin•PNS•Histamine
•Dec stomach pH•Chyme in duodenum•Atropine•Cimetidine•Omeprazole•Pepsinogen
•Intrinsic factor•PNS
Pancreatic secretion •High HCO3•Isotonic
•Secretin•CCK•PNS
•Pancreatic lipase, amylase,proteases
•CCK•PNS
Bile •Bile salts•Bilirubin•Phospolipids•cholesterol
•CCK•PNS
•Ileal resection
•Functions of saliva▫Initial starch digestion by amylase
(ptyalin) and initial triglyceride digestion by lingual lipase
▫Lubrication of ingested food by mucus▫ protection of the mouth and esophagus by
dilution and buffering of ingested foods
GI secretion: salivary secretion
• Composition▫Characterized by:
High volume High K+ and HCO3 conc Low Na and Cl conc Hypotonicity Presence of amylase, lingual lipase, and kallikrein
▫At lowest flow rates, saliva has the lowest osmolarity and lowest Na, Cl, and HCO3 conc, but has the highest K conc.
▫At the highest flow rates (up to 4ml/min), the composition is closest to that of plasma
GI secretion: salivary secretion
• Formation▫ Formed by 3 major glands:
Parotid Submaxillary Sublingual
▫ The acinus produces the initial saliva with a composition similar to that of plasma (isotonic)
▫ The ducts modify the initial isotonic saliva making it hypotonic
GI secretion: salivary secretion
• Regulation of salivary production
▫ Salivary formation is unique in that it is increased by both parasympathetic and sympathetic activity. Parasympathetic activity, however is more important
▫ PNS- CN VII and IX By increasing the transport process in the acinar and ductal cells and by
causing vasodilatation Anticholinergics inhibit production dry mouth
▫ SNS By increasing production and growth of salivary glands, although effects
arer smaller than PNS stimulation▫ Others:
Increased (via PNS) by food in the mouth, smells, conditioned reflexes, and nausea
Decreased (via inhibitio of PNS) by sleep, dehydration, fear, anticholinergics
GI secretion: salivary secretion
GI secretion: Gastric secretionGastric mucosa
▫ Cardiac glandular region Mucus secreting
▫ Oxyntic glandular region Acid secreting
▫ Pyloric glandular region Gastrin and mucus
secreting
Gastric cell types and their secretion
• Parietal cells▫ Located in the body▫ HCl, IF▫ Stimuli: gastrin, vagal
(ACh), histamine
• Chief cells▫ Located in the body▫ Pepsinogen▫ Stimulus: vagal (ACh)
GI secretion: Gastric secretion
Gastric cell types and their secretion
• G cells▫ Located in the antrum▫ Gastrin▫ Stimuli: vagal (ACh)▫ Inhibited by: somatostatin,
H+
• Mucus cells▫ Located in the antrum▫ Mucus, pepsinogen▫ Stimulus: vagal (ACh)
GI secretion: Gastric secretion
Physiology
• Cholinergic input via the vagus nerve and histaminergic input from local gastric sources are the principal contributors to basal acid secretion.
• Stimulated gastric acid secretion occurs primarily in three phases based on the site where the signal originates (cephalic, gastric, and intestinal).
GI secretion: Gastric secretion
GI secretion: Gastric secretion
Stimulation of gastric acid secretion
• Vagal▫ Increases H+ secretion by direct and indirect pathway▫ Direct: Vagus Ach parietal cells▫ Indirect: Vagus G cells gastrin parietal cells▫ Inhibited by: Atropine via muscarinic receptor
• Histamine▫ Released from mast cells in the gastric mucosa▫ Stimulates H+ secretion by activating H2 receptors on the parietal cell
membrane▫ Inhibited by: H2 blockers ( Cimetidine)
• Gastrin ▫ Released in response to eating a meal▫ Stimulates the parietal cells
GI secretion: Gastric secretion
Inhibition of gastric acid secretion
•Negative feedback inhibits the secretion of H+ by parietal cells
•Low pH in the stomach▫Inhibits gastrin secretion inhibiting H+
secretion
•Chyme in the duodenum
GI secretion: Gastric secretion
GI secretion: Pancreatic secretion
GI secretion: Pancreatic secretion• Contains high conc of HCO3 the purpose is to
neutralize the acidic chyme that reaches the duodenum
• Contains enzymes essential for the digestion of protein, carbohydrate, and fat
• Regulates whole body metabolism via▫ Insulin▫ Glucagon▫ Somatostatin
GI secretion: Pancreatic secretion
• Composition of pancreatic secretion▫ High volume▫ Virtually the same conc of Na and K as plasma▫ Much higher HCO3 conc than plasma▫ Isotonic▫ Pancreatic lipase, amylase, and proteases
• At low flow rates, it secretes an isotonic fluid that is composed mainly of Na and Cl
• At high flow rates, it secretes an isotonic fluid that is composed mainly of Na and HCO3
• Regardless of the flow rates, it secretes isotonic fluid
GI secretion: Pancreatic secretion
• Formation of pancreatic secretion▫ Acinar cells
Produce a small volume of initial pancreatic secretion, which is mainly Na and Cl
▫ Ductal cells Modify the initial pancreatic secretion by secreting HCO3 and
absorbing Cl via Cl-HCO3 excahnge mechanism in the luminal membrane
Because the pancreatic ducts are permeable to water, H2O moves into the lumen to make the pancreatic secretion isotonic
• Stimulation of pancreatic secretion▫ Secretin▫ CCK▫ AcH
GI secretion: Pancreatic secretion
• Composition and function of bile▫ Bile contains bile salts, phospholipids, cholesterol, and bile pigments
• Formation of bile▫ Bile is produced continuously by hepatocytes▫ Bile drains into the hepatic ducts and is stored in the gallbladder for subsequent
release.
GI secretion: Bile secretion and Gallbladder function
GI secretion: Bile secretion and Gallbladder function• Primary bile acids
▫ cholic and chenodeoxycholic acids▫ Synthesized from cholesterol by hepatocytes
• In the intestines, bacteria convert a portion of each of the primary bile acids to secondary bile acids ( deoxycholic acid and lithocholic acid
GI secretion: Bile secretion and Gallbladder function
GI secretion: Bile secretion and Gallbladder function• Most bile acids are
taken up by distal ileum epithelial cells by 2o active transport when they are no longer needed for digestion.
• They travel to the liver via the portal vein and are taken up by hepatocytes through the for recycling.
• They re-enter the bile canaliculus through the BSEP (bile salt exchange pump)
Topic outline
I. Structure and innervation of the GITII. Regulatory substances in the GIT
III.Gastrointestinal motilityIV. Gastrointestinal secretion
V. Digestion and absorption
GI Digestion and Absorption
•Carbohydrates, proteins, and lipids are digested and absorbed in the small intestines
•The surface area for absorption in the SI is greatly increased by the presence of brushborders
Summary of digestion and absorption
Nutrient Digestion Site of absorpti
on
Mechanism of absorption
Carbohydrates
To monosaccahrides (glucose, galactose, fructose)
SI •Na-dependent co-transport (glucose, galactose)•Facilitated Diffusion (fructose)
Proteins To amino acids, dipeptides, tripeptides
SI •Na-dependent co-transport (amino acids)•H+ dependent co-transport (di- and tripeptides)
Lipids To fatty acids, monoglycerides, cholesterol
SI •Micelles form with bile salts in intestinal lumen•Diffusion of fatty acids, mono glycerides, and cholesterol into cell•Reesterification in cell to TG and phospholipids•Chylomicrons form in cell (requires apoprotein) and are transferred to lymph
Fat-soluble vitamins
SI •Micelles with bile salts
Water-soluble vitamins•Vit B12
Ileum of SI
•Na-dependent co-transport •IF-Vit B12 complex
Bile acids Ileum of SI
Na-dependent co-transport ; recirculated to liver
Ca+ SI •Vit D-dependent Ca binding protein
Fe+ Fe3+ is reduced to Fe 2+
SI •Binds to apoferritin in cell•Circulates in blood bound to transferrin
•Absorption and secretion of water and electrolytes
•Electrolytes and water may cross intestinal epithelial cells by either cellular or paracellular
GI Digestion and Absorption
Thank you!
Bilirubin Metabolismsenescent RBC
Macrophages (spleen)
Bilirubin (indirect)
Bilirubin-AlbuminAdduct
Plasmaheme
Hepatocyte
Bilirubin Glucuronide
Bile DuctUrobilinogen
Intestinal Flora
Feces(stercobilin)
Urine(urobilin)
Portal Circ.
Systemic Circulation