Gastrointestinal Anatomy And Physiology

Gastrointestinal Anatomy and Physiology Rowena A. Abante MD Jan. 27, 2009

The

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gastrointestinal system consists of the gastrointestinal tract and associated glandular organs that produce secretions

Physiologic Functions

Topic outline I. Structure and innervation of the GIT II. Regulatory substances in the GIT III. Gastrointestinal motility IV. Gastrointestinal secretion V. Digestion and absorption VI.

Topic outline I. Structure and innervation of the GIT II. Regulatory substances in the GIT III. Gastrointestinal motility IV. Gastrointestinal secretion V. Digestion and absorption VI.

The structure of the GIT varies greatly from region to region, but common features exists in the overall organization of the tissues

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Structure of the GIT

• 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  

Innervation of the GIT The autonomic nervous system of the GI tract comprises both extrinsic and intrinsic nervous system •

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1.Extrinsic innervation  Parasympathetic and sympathetic NS

2.Intrinsic innervation Enteric NS

Innervation of the GIT: Extrinsic • 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

2. ▫ Usually inhibitory on the functions of the GIT

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▫ Fibers originate in the spinal cord between T8 and L2

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▫ Preganglionic sympathetic cholinergic fibers synapse in the prevertebral ganglia

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▫ Postganglionic sympathetic adrenergic fibers leave the prevertebral ganglia and synapse in the myenteric and submucosal plexuses

Innervation of the GIT: Intrinsic • 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

3.

Topic outline I. Structure and innervation of the GIT II. Regulatory substances in the GIT III. Gastrointestinal motility IV. Gastrointestinal secretion V. Digestion and absorption VI.

The functions of the GIT are regulated and coordinated by hormones, paracrine agonists and neurons. 

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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 hormones 1.Gastrin 2.Cholecystokinin (CCK) 3.Secretin 4.Gastric Inhibitory Peptide (GIP)

Regulatory substances: GI hormones Summary of GI hormones Hormones

Site of secretion

Gastrin

G cells of stomach

CCK

Small peptides and amino acids I cells of duodenum and Fatty acids jejunum

Secretin

S cells of duodenum

GIP

Stimulus for secretion Small peptides and amino acids Distention of stomach Vagus Inhibited by H+ in stomach 

H+ in the duodenum Fatty acids in duodenum 

Actions inc gastric H+ secretion Stimulates growth of gastric mucosa 

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 

Inc pancreatic HCO3 secretion Inc biliary HCO3 secretion Dec gastric H+ secretion  

Duodenum and Fatty acids, amino acids, and oral Inc insulin secretion Dec gastric H+ secretion jejunum glucose

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. somatostatin 2. 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

Regulatory substances: Neurocrines 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

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2. GRP

▫ Released from vagus nerves that innervate the G cells ▫ Stimulates gastrin release from G cells

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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

Topic outline I. Structure and innervation of the GIT II. Regulatory substances in the GIT III.Gastrointestinal motility IV. Gastrointestinal secretion V. Digestion and absorption VI.

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 • • •

Gastrointestinal motility • 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

GI motility: slow waves • Are oscillating membrane potentials inherent to the smooth muscle cells of some parts of the GIT

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• Occur spontaneously

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• Originate in the interstitial cells of Cajal, which serves as the pacemaker of GI smooth muscle

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GI motility: slow waves 1. Mechanism of slow wave production 

▫ Is the cyclic activation and deactivation of the cell membrane Na+-K+ pump

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▫ 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.

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▫ Action potentials, produced on the background of slow waves, then initiate contraction of smoth muscle cells

GI motility: slow waves 2. Frequency of slow waves

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▫ Varies along the GIT, but is constant and characteristic for each part of the GIT

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▫ 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

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▫ Sets the maximum frequency of contractions for each part of the GIT

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▫ 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.

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• The swallowing reflex is a rigidly ordered sequence of events that propels food from the mouth to the stomach.

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• This reflex also inhibits respiration and prevents entry of food into the trachea during swallowing

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GI motility: esophageal motility • The esophagus contains a gradient of muscle, from all skeletal at the top to all smooth at the bottom.

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• Innervation: vagus

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• After the food is swallowed, the esophagus functions as a conduit to move the food from the pharynx to the stomach.

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•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

GI motility: esophageal motility • The following sequence of events occurs as food moves into and down the esophagus:

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1. UES relaxation to permit swallowed food to enter the esophagus

2. 3. UES contraction to prevent reflux of food into the pharynx

4. 5. A primary peristaltic contraction moves down the esophagus and propels the food bolus along

6. 7. A second peristaltic contraction clears the esophagus from any remain food

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9. LES relaxation, vagally mediated via VIP

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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 divisionsfundus, body, antrum

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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.

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• 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.

GI motility: gastric motility 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

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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

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GI motility: gastric motility 

3. Gastric emptying

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▫ Caudad region contracts to propel food into the duodenum

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▫ 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.

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▫ Fats inhibits gastric emptying by stimulating release of CCK

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▫ 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: small intestinal motility

GI motility: small intestinal motility

GI motility: small intestinal motility • The SI functions in the digestion and absorption of nutrients.

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• Slow waves set the basic electrical rhythm which occurs at a frequency of 12sw/min.

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• Parasympathetic stimulation increases intestinal smooth muscle contraction; sympathetic stimulation decreases it.

GI motility: small intestinal motility 1.Segmental contractions

2. ▫ 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

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GI motility: small intestinal motility 2. Peristaltic contractions

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▫ 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

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▫ 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: large 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

2.

▫ 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

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 Di  stal colon

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▫ ecause most colonic water absorption occurs in the proximal colon fecal

GI motility: large intestinal motility 

3. Rectum, anal canal, and defecation

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▫ Sequence of events:

1.Rectum fills with fecalmaterial, contracts, and then internal anal sphincter relaxes. (rectosphincteric reflex)

2. 3.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 tonicall contracted

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 hen it is convenient to

GI motility: large intestinal motility 4. Gastrocolic reflex

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▫ 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. ▫

Topic outline I. Structure and innervation of the GIT II. Regulatory substances in the GIT III. Gastrointestinal motility IV.Gastrointestinal secretion V. Digestion and absorption VI.

GI secretion: Summary of GI secretions GI secretion

Major characteristics

Stimulated by

Saliva

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High HCO3 High K Hypotonic α αµ ψλ ασε Λ ι ν γ υ αλ λ ι π ασε

PNS SNS

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Gastric secretion

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HCl

Pepsinogen Intrinsic factor

Gastrin PNS Histamine

Inhibited by Sleep Dehydration Atropine  

Dec stomach pH Chyme in duodenum Atropine Cimetidine Omeprazole

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PNS

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Pancreatic secretion

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High HCO3 Isotonic

Pancreatic lipase, amylase,proteases 

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Bile

Bile salts Bilirubin Phospolipids cholesterol

Secretin CCK PNS  

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CCK PNS

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CCK PNS

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Ileal resection

GI secretion: salivary secretion • Functions of saliva ▫ Initial starch digestion by α α µ ψ λ α σ ε (π τ ψ α λ ι ν ) α ν δ ι ν ι τ ι α λ τ ρ ι γ λ ψχ ε ρ ι δ ε δ ι γ ε στ ι ο ν β ψ λ ι ν γ υ αλ λ ι π ασε ▫ 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

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GI secretion: salivary secretion • Formation

▫ Formed by 3 major glands:  Parotid Submaxillary Sublingual

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▫ The acinus produces the initial saliva with a composition similar to that of plasma (isotonic)

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▫ The ducts modify the initial isotonic saliva making it hypotonic

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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 dr mouth

▫ N

  increasing production and growth of salivar glands although effects arer smaller than  N stimulation

▫ thers

ncreased (via N b food in the mouth smells conditioned reflexes and nausea Decreased (via inhibitio of N b sleep dehdration fear anticholinergics

GI secretion: Gastric secretion Gastric mucosa

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▫ Cardiac glandular region

 Mucus secreting

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▫ Oxyntic glandular region Acid secreting

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▫ Pyloric glandular region Gastrin and mucus secreting

GI secretion: Gastric secretion Gastric cell types and their secretion

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• Parietal cells

▫ Located in the body ▫ HCl, IF ▫ Stimuli: gastrin, vagal (ACh), histamine

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• Chief cells

▫ Located in the body ▫ Pepsinogen ▫ Stimulus: vagal (ACh)

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GI secretion: Gastric secretion Gastric cell types and their secretion

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• G cells ▫ ▫ ▫ ▫

Located in the antrum Gastrin Stimuli: vagal (ACh) Inhibited by: somatostatin, H+

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• 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

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• Vagal

▫ Increases H+ secretion by direct and indirect pathway ▫ Direct: Vagus ch parietal cells ▫ Indirect: Vagus G cells gastrin parietal cells ▫ nhibited b tropine via muscarinic receptor

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• 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)

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• Gastrin

▫ Released in response to eating a meal

GI secretion: Gastric secretion Inhibition of gastric acid secretion

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• Negative feedback inhibits the secretion of H+by parietal cells 

• Low pH in the stomach ▫ Inhibits gastrin secretion inhibiting G+ secretion 

• Chyme in the duodenum ▫

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

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GI secretion: Pancreatic secretion

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

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• 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

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• Stimulation of pancreatic secretion ▫ Secretin ▫ CCK ▫ AcH

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GI secretion: Bile secretion and Gallbladder function

• Composition and function of bile ▫

Bile contains bile salts, phospholipids, cholesterol, and bile pigments

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• Formation of bile ▫ ▫

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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 • Primary bile acids

▫ cholic and chenodeoxycholic acids ▫ Synthesized from cholesterol by hepatocytes

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• 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 2oactive 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 GIT II. Regulatory substances in the GIT III. Gastrointestinal motility IV. Gastrointestinal secretion V. Digestion and absorption VI.

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 absorption

Carbohydrates

To monosaccahrides (glucose, galactose, fructose)

SI

To amino acids, dipeptides, tripeptides

SI

To fatty acids, monoglycerides, cholesterol

SI

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Fat-soluble vitamins Water-soluble vitamins Vit B12 Bile acids

SI

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Ca+

SI

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SI

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Proteins Lipids

Fe+

Mechanism of absorption

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Na-dependent co-transport (glucose, galactose) Facilitated Diffusion (fructose) Na-dependent co-transport (amino acids) H+ dependent co-transport (di- and tripeptides)

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 Micelles with bile salts

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Ileum of SI

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Na-dependent co-transport

IF-Vit B12 complex Na-dependent co-transport ; recirculated to liver 

Ileum of SI Fe3+ is reduced to Fe 2+

Vit D-dependent Ca binding protein

Binds to apoferritin in cell Circulates in blood bound to transferrin

GI Digestion and Absorption • Absorption and secretion of water and electrolytes • Electrolytes and water may cross intestinal epithelial cells by either cellular or paracellular •

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Bilirubin Metabolism

senesc ent RBC

heme

a m s a Pl

Macrophages (spleen)

BilirubinAlbumin Adduct

Bilirubin (indirect)

Systemic Circulation Urine (urobilin)

Feces (stercobilin)

Bilirubin Glucuronide

Portal Circ. Urobilin ogen

Intestinal Flora

Bile Duct

Hepatocyte