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97 Cards in this Set

  • Front
  • Back
Inside gastrointestinal (GI) tract, food is broken down by hydrolysis into molecular monomers
Absorption of monomers occurs in small intestine
disacchride + water =
peptide + water =
amino acid + amino acid
fat + water =
fatty acids + glycerol
Then, inside the cells in the neighborhood….
Each of the digested and absorbed monomers is reconnected to others and built into whatever recipe the DNA in that cell decides it should be
MacDonald’s mystery meat becomes you. Hair, skin, nails, enzymes, hormones, neurotransmitters, and blood, sweat and tears.
Is movement of food through GI tract by means of:
Ingestion--taking food into mouth
Mastication--chewing food & mixing it with saliva
Deglutition--swallowing food
Peristalsis--rhythmic wave-like contractions that move food through GI tract
Includes release of exocrine & endocrine products into GI tract
Exocrine secretions include: HCl, H20, HC03-, bile, families of many enzymes ;lipase, pepsin, amylase, trypsin, elastase, & histamine
Endocrine includes hormones secreted into stomach & small intestine to help regulate GI system
E.g. gastrin, secretin, CCK-PZ, GIP, VIP, & somatostatin
Is the passage of digested end products into blood or lymph through villi walls. (thin with a huge surface area)
Storage and Elimination
Includes temporary storage & subsequent elimination of indigestible components of food
Digestive System is composed of
GI tract (alimentary canal) & accessory digestive organs
GI tract is 30 ft long; extends from mouth to anus
Accessory organs are liver and pancreas – along with some minor ones – salivary glands, Peyer’s patches, gall bladder
Regulation of GI Tract
Parasympathetic effects, arising from vagus & spinal nerves, stimulate motility & secretions of GI tract
Sympathetic activity reduces peristalsis & secretory activity
GI tract contains an intrinsic system that controls its movements--the enteric nervous system
GI motility is influenced by paracrine & hormonal signals
Layers of GI Tract
Are called tunics
The 4 tunics are mucosa, submucosa, muscularis, & serosa
Is the absorptive & secretory layer lining lumen of GI tract
In places is highly folded with microscopic villi to increase absorptive area
Contains lymph nodules, mucus-secreting goblet cells, & thin layer of muscle
Is a thick, highly vascular layer of connective tissue where absorbed molecules enter blood & lymphatic vessels
Contains glands & nerve plexuses (submucosal (Meissner’s)plexus) that carry ANS activity to muscularis mucosae
Is responsible for segmental contractions & peristaltic movement through GI tract
Has an inner circular & outer longitudinal layer of smooth muscle
Activity of these layers moves food through tract while pulverizing & mixing it
Myenteric (Auerbach’s) plexus between these layers is major nerve supply to GI tract
Includes fibers & ganglia from both Symp & Parasymp systems
Is outermost layer; serves to bind & protect
Consists of areolar connective tissue covered with layer of simple squamous epithelium
3 swallowing phases
From Mouth to Stomach
Mastication (chewing) mixes food with saliva which contains salivary amylase
An enzyme that catalyzes partial digestion of starch

Deglutition (swallowing) begins as voluntary activity
Oral phase is voluntary & forms a food bolus
Pharyngeal & esophageal phases are involuntary & cannot be stopped
To swallow, larynx is raised so that epiglottis covers entrance to respiratory tract
A swallowing center in medulla orchestrates complex pattern of contractions required for swallowing

Esophagus connects pharynx to stomach
Upper third contains some skeletal muscle
Middle third contains mostly smooth
Terminal portion contains only smooth
Passes through diaphragm via esophageal hiatus
Peristalsis propels food thru GI tract
= wave-like muscular contractions
After food passes into stomach, the cardiac sphincter constricts, preventing reflux
Not a true sphincter – functions erratically in infants, causing ‘spit ups’. Some animals have an intact cardiac sphincter prohibiting regurgitation – rodents esp. can’t puke up poison
Is enclosed by cardiac sphincter on top & pyloric sphincter on bottom
Is divided into 3 regions:
Is most distensible part of GI tract
Empties into the duodenum
Functions in: mixing & storage of food; initial denaturing of proteins; killing bacteria with high acidity; moving soupy food mixture (chyme) into intestine

Inner surface of stomach is highly folded into rugae
Contractions of stomach churn chyme, mixing it with gastric secretions
Eventually these will propel food into small intestine

Gastric mucosa has gastric pits in its folds
Cells that line folds deeper in the mucosa, are exocrine gastric glands
Gastric glands contain cells that secrete different products that form gastric juice
Goblet cells secrete mucus
Parietal cells secrete HCl & intrinsic factor (necessary for B12 absorption in intestine)
B12 is required for the maturation of RBCs
Chief cells secrete pepsinogen (precursor for pepsin)
Enterochromaffin-like cells (ECL) secrete histamine & serotonin
G cells secrete gastrin
HCl in Stomach
Is produced by parietal cells which actively transport H+ into stomach lumen via an H+/ K+ pump (pH ~1.2)
Cl- is secreted by facilitated diffusion
H+ comes from dissociation of H2CO3
Cl- comes from blood side of cell in exchange for HC03-

Is secreted in response to the hormone gastrin; & ACh from vagus
These are indirect effects since both stimulate release of histamine which causes parietal cells to secrete HCl

Makes gastric juice very acidic which denatures proteins to make them more digestible
Converts pepsinogen into pepsin
Pepsin is more active at low pHs
Digestion & Absorption in Stomach
Proteins partially digested by pepsin
Carbohydrate digestion by salivary amylase is soon inactivated by acidity
Alcohol, aspirin and water are only the commonly ingested substances absorbed in the stomach
Protective Mechanisms of Stomach
Impermeability of parietal & chief cells to HCl
A layer of alkaline mucus containing HC03-
Tight junctions between adjacent epithelial cells
Rapid rate of cell division (entire epithelium replaced in 3 days)
Prostaglandins (PGs) inhibit gastric HCl secretions
Which is why PG blockers such as NSAIDs can cause ulcers
Small Intestine (SI)
Is longest part of GI tract

Spit starts chemical digestion, then everything stops in the stomach
Duodenum=ph shift juices enter
Jejunum-main digestion and absorption

Majority of digestion occurs in the SI
Absorption of digested food occurs in SI
Facilitated by long length & tremendous surface area
Beginning of SI is lined with Brunner’s Glands – secrete alkaline mucus.
Brunner’s Gland secretion is inhibited by symp. stim.

Surface area increased by foldings & projections
Large folds are plicae circulares
Microscopic finger-like projections are villi
Apical hair-like projections are microvilli
Each villus is covered with columnar epithelial cells interspersed with goblet cells
Epithelial cells at tips of villi are exfoliated & replaced by mitosis in crypts of Lieberkuhn
Inside each villus are lymphocytes, capillaries, & central lacteal
A carpet of hair-like microvilli project from apical surface of each epithelial cell
Create a brush border
Intestinal Enzymes
Attached to microvilli are brush border enzymes that are not secreted into lumen
Enzyme active sites are exposed to chyme
Intestinal Contractions and Motility
2 major types of contractions occur in SI:
Peristalsis is weak & slow & occurs mostly because pressure at pyloric end is greater than at distal end
Segmentation is major contractile activity of SI
Is contraction of circular smooth muscle to mix chyme
Intestinal Contractions & Motility
Occur automatically via endogenous pacemaker activity
Contractions are driven by graded depolarizations called slow waves
Slow Waves
Rhythmical changes in membrane potential caused by variations in sodium conductance -

Fixed frequency -
Interstitial cells of Cajal - pacemaker cells
Dictates max. frequency of SM contraction
Independent of nervous / hormonal stimuli

Variable amplitude -
Affected by nervous / hormonal stimuli
↑ amplitude → ↑ spike potential frequency →
↑ strength of contraction
Spike Potentials
True action potentials
Occur when slow waves reach threshold (-40 mV)
Cause SM contraction

Voltage dependent calcium channels
Ca++ entry → contraction

Affected by nervous / hormonal stimuli
↑ frequency → stronger contraction
↑ frequency of stim. does not ↑ max. frequency of contraction
Propulsive Movements - Peristalsis
Stimuli that initiate peristalsis -
Distention - orad contraction with downstream receptive relaxation = “Law of the Gut”
Irritation of gut epithelium
Parasympathetic nervous system

Function -
Myenteric plexus required
Atropine (blocks Ach receptors) - ↓ peristalsis
Congenital absence of plexus - no peristalsis
Intestinal Contractions & Motility
Slow waves are produced by non-neuronal interstitial cells of Cajal (ICC)
Conducted to smooth muscle via gap junctions
Slow waves spread from 1 smooth muscle cell to another thru nexuses
Intestinal Contractions & Motility
When slow waves exceed threshold, trigger APs in smooth muscle by opening V-gated Ca2+ channels
Influx of Ca2+ produces depolarization phase of AP & stimulates contraction
Repolarization via K+ efflux
Contractions are modified by ANS activity
ACh from Parasymp increases amplitude & duration of slow waves
NE & Epi from Symp decrease activity of intestines
Large Intestine (LI) or Colon
Has no digestive function but absorbs H20, electrolytes, B & K vitamins, & folic acid
Internal surface has no villi or crypts & is not very elaborate
Contains large population of microflora
LI bacteria produce folic acid & vitamin K & ferment indigestible food to produce fatty acids

Extends from ileocecal valve at end of SI to anus
Outer surface bulges to form pouches (haustra)
Chyme from SI enters cecum, then passes to ascending colon, transverse colon, descending colon, sigmoid colon, rectum, & anal canal
Fluid & Electrolyte Absorption in LI
SI absorbs most water but LI absorbs 90% of water it receives
Begins with osmotic gradient set up by Na+/K+ pumps
Water follows by osmosis
Salt & water reabsorption stimulated by aldosterone
LI can also secrete H20 via AT of NaCl into intestinal lumen
After electrolytes & water have been absorbed, waste material passes to rectum, creating urge to defecate
Defecation reflex begins with stimulation of internal anal sphincter allowing feces to enter rectum
Longitudinal rectal muscles contract to increase rectal pressure; external anal sphincter relaxes
Elimination is aided by contractions of abdominal & pelvic muscles which push feces from rectum
Structure of Liver
Liver largest internal organ
Hepatocytes form hepatic plates that are 1–2 cells thick
Plates separated by sinusoids which are fenestrated & permeable even to proteins
Hepatic Portal System
Food absorbed in SI is delivered 1st to liver
Capillaries in digestive tract drain into hepatic portal vein which carries blood to liver
Hepatic vein drains liver
Liver also receives blood from hepatic artery
Liver Lobules
Are functional units formed by hepatic plates
In middle of each is central vein
At edge of each lobule are branches of hepatic portal vein & artery which open into sinusoids

Bile is secreted by hepatocytes in bile canaliculi
Empty into bile ducts which flow into hepatic ducts that carry bile away from liver
Enterohepatic Circulation
Is recirculation of compounds between liver & intestine
Many compounds are released in bile, reabsorbed in SI, & returned to liver to be recycled
Liver excretes drug metabolites into bile to pass out in feces
major categories of liver function
detoxificatino of blood
carb metabolism
lipid metabolism
protien syntheisis
secretion of bile
Bile Production and Secretion
Amounts to 250–1500 ml/day
Bile pigment (bilirubin) is produced in spleen, bone marrow, & liver
Is a derivative of heme groups (minus iron) from Hb
Carried in blood attached to albumin
Free bilirubin combines with glucuronic acid to form conjugated bilirubin that is secreted into bile
Converted by intestinal bacteria to urobilinogen
30-50% of urobilogen is absorbed by intestine & enters hepatic vein
Thus enters enterohepatic circulation to be recycled or filtered by kidneys & excreted in urine
Bile Acids
Are formed in major breakdown pathway for cholesterol
Are mostly cholic & chenodeoxycholic acids
Form bile salts by combining with glycine or taurine
Bile salts aggregate as micelles
95% of bile acids are absorbed by ileum
Detoxification of Blood
Liver can remove hormones, drugs, & other biologically active molecules from blood by:
Excretion into bile
Phagocytosis by Kupffer cells
Chemical alteration of molecules
E.g. ammonia is produced by deamination of amino acids in liver
Liver converts it to urea which is excreted in urine

Liver conjugates steroid hormones & xenobiotics with groups that make them anionic
Which can be transported into bile or urine by multispecific organic anion transport carriers & excreted
Cytochrome P450 enzymes are involved in hepatic metabolism of steroids & drugs
Secretion of Glucose, Triglycerides & Ketones
Liver helps regulate blood glucose by removing it from blood or releasing it to blood
Removes it via glycogenesis & lipogenesis
Or produces it via glycogenolysis & gluconeogenesis
Can convert free fatty acids into ketone bodies (ketogenesis) that can be used for energy during fasting
Production of Plasma Proteins
Albumin & most of plasma globulins are produced by liver
Albumin makes up 70% of total plasma protein & contributes most to colloid osmotic pressure of blood
Globulins transport cholesterol & hormones, inhibit trypsin, & are involved in blood clotting
Constitute many of the clotting factors
Is a sac-like organ attached to inferior surface of liver
Stores & concentrates bile continuously produced by liver
When SI is empty, sphincter of Oddi in common bile duct closes & bile is forced into gallbladder
Expands as it fills with bile
When fatty food is in SI, sphincter of Oddi opens, gall bladder contracts, & bile is ejected thru cystic duct into common bile duct then to duodenum
Is located behind stomach
Has both endocrine & exocrine functions
Endocrine function performed by islets of Langerhans
Secretes insulin & glucagon
Exocrine secretions include bicarbonate solution & digestive enzymes
These pass in pancreatic duct to SI
Exocrine secretory units are acini
Pancreatic Juice
Contains water, bicarbonate, & digestive enzymes
Digestive enzymes include amylase for starch, trypsin for proteins, and lipase for fats
Brush border enzymes are also required for complete digestion

Most pancreatic enzymes are produced in inactive form (zymogens)
Trypsin is activated by brush border enzyme, enterokinase
Trypsin activates other zymogens
digests starch to maltose and short chains fo glucose mlecules
cleaves fatty acids from glycerol
Neural and Endocrine Regulation
Neural & endocrine mechanisms modify activity of GI system
Vagus nerve is heavily involved in regulating & coordinating digestive activities
GI tract is both an endocrine gland & target for action of hormones
Hormones include secretin, gastrin, CCK, & GIP
Chemistry of GI Peptides
Two structurally related families -

Gastrin and CCK
5 C-terminal AA identical
Produce all effects of each other at high doses

Secretin, GIP, VIP, glucagon
some effects are shared

GIP = Gastric Inhibitory Peptide
VIP = Vasoactive Intestinal Peptide
GI Hormones identified in:
Secretin - 1902

Gastrin 1905

Cholecystokinin (CCK) 1928

Gastric Inhibitory Peptide (GIP) - 1969

Motilin - 1970
Chemistry of GI Peptides
Two structurally related families -

Gastrin and CCK
5 C-terminal AA identical
Produce all effects of each other at high doses

Secretin, GIP, VIP, glucagon
some effects are shared

GIP = Gastric Inhibitory Peptide
VIP = Vasoactive Intestinal Peptide
Gastrin - Chemistry
Molecular forms - G-17, G-34, G-14
G-34 is not a dimer G-17
All share same AA sequence

Biological activity -
All effects can be produced by 4 C-terminal AA
G-34 and G-17 are equipotent
Pentagastrin - 5 AA synthetic product
Gastrin - Distribution and Release
Released from G cells in antrum and duodenum
Stimuli - protein digestion products
- nervous, physical distention
- (calcium, decaf coffee,and wine)
Inhibition - acidification of antrum

Response to meal -
Large amounts of G-17 released from antrum
Small amounts of G-34 released from duodenum
Gastrin - Physiological Effects
Gastric acid secretion
1,500x more potent than histamine

Trophic activity
Stimulates growth of oxyntic mucosa of stomach, duodenal mucosa, and colon mucosa
Surgical removal of antrum causes atrophy of mucosa
Patients with gastrin secreting tumors have mucosal hyperplasia and hypertrophy
Gastrinoma - Zollinger-Ellison syndrome
Gastrin secreting tumor
Non-beta cell tumor of pancreas (80%) or G-cell tumors in duodenum (10-15%)
Continually secretes gastrin into blood

Duodenal ulcers, diarrhea, steatorrhea, hypokalemia

Hypergastrinemia causes hypersecretion of acid
Increased parietal cell mass
Constant stimulation of hyperplastic mucosa
Cholecystokinin - Chemistry
Molecular form - 8-AA, 33-AA, 38-AA, 59-AA
Synthesized as preprohormone, then cleaved to form family of peptides
5 C-terminal AA identical to gastrin

Biological activity -
Minimal active fragment - 7 C-terminal AA
Tyrosine, 7 residues from C-terminal must be sulfated for full activity at physiological levels
Produces all effects of gastrin at high doses.
CCK - Distribution and Release
Released from I-cells in duodenum and jejunum

Stimuli for release
Fatty acids or monoglycerides (not triglycerides)
peptides and single AA
Acid (weak)
CCK - Physiological Effects
Emptying of gallbladder -
contracts gallbladder, relaxes sphincter of Oddi

Pancreatic exocrine
Potent stimulator of enzyme secretion
Weak stimulator of bicarbonate secretion (but can potentiate secretin effects)

Inhibits gastric emptying

Trophic effects - exocrine pancreas and gallbladder mucosa
Secretin - Chemistry
Molecular form - 27-AA peptide
Synthesized as a preprohormone
14 AA identical to glucagon in kind and position

Biological activity -
No active fragments - entire molecule is required
Active form is α-helix - tertiary structure requires all AA
Released from S-cells of duodenal mucosa

Stimuli for release
Acid in duodenum (pH <4.5)
Fatty acids in duodenum

Physiological effects - “Nature’s Antacid”
Inhibits gastric acid secretion (enterogastrone)
Stimulates pancreatic and bile bicarbonate secretion
Stimulates pepsin secretion
Trophic effect on exocrine pancreas
Gastric Inhibitory Peptide (GIP)
Chemistry - Member of secretin family
9 AA identical to secretin in kind and position

Stimuli / release -
Released from duodenum and proximal jejunum
All major foodstuffs - fat must be hydrolyzed
Oral glucose but not i.v. glucose

Physiological effects -
Stimulates insulin release (also called glucose-dependent insulinotrophic peptide - GIP)
Inhibits gastric acid secretion (enterogastrone)
Chemistry - linear 22 AA peptide - unrelated to other hormones

Stimuli / release -
Released from duodenum and proximal jejunum during fasting at 100 min intervals
Release is under neural control

Physiological effects -
Stimulates upper G.I. motility
Accounts for the migrating motility complex, “housekeeping contractions”
only I homone in antrum
only 2 GI homones in Illeum
secretin and CCK
Somatostatin (peptide) from D cells
Found in gastric / duodenal mucosa and pancreas
Release - stimulated by acid, inhibited by Ach
Inhibits release of all gut hormones
Directly inhibits parietal cell acid secretion
Mediates acid induced inhibition of gastrin release

Histamine – from EnteroChromaffinLike cells (argentaffin)
Gastrin and Ach cause release from cells in stomach
Stimulates acid secretion
Histamine H2 receptor blockers → ↓ Acid secretion
Cimetidine (Tagamet), Ranitidine (Zantac)
Neural Control of GI Tract
Intrinsic Control - Enteric nervous system
Myenteric (Auerbach’s) plexus
Submucosal (Meissner’s) plexus

Extrinsic Control - Autonomic nervous system
Parasympathetic - mainly stimulates (Ach)
Sympathetic - mainly inhibits (NE)
Enteric Nervous System (ENS)
Location - gut wall from esophagus to anus

Composition - cell bodies, axons, dentrites, nerve endings

Innervation - gut cells, sensory nerves, other neurons

Integration - can occur entirely within ENS.
- can function independent of ANS

Transmitters - many. - excitatory and inhibitory
ENS - Myenteric Plexus
Location -
Esophagus to anus
Between longitudinal and circular SM layers

Function - controls GI motility
Stimulatory influences -
↑ tonic contraction (tone)
↑ contraction frequency / intensity (↑ propulsion)
Inhibitory influences
Decreased Sphincter tone (relax) - pyloric sphincter, ileocecal sphincter,
ENS - Submucosal Plexus
Location - Mucosal layer from esophagus to anus

Function - Local control
Contraction of muscularis mucosa
Parasympathetic Innervation
Cranial Division - (Vagus N.) - first half of gut

Sacral Division - (Pelvic N.) - second half of gut

Neurons - preganglionic - long
- postganglionic - short, entirely in ENS
Synapse with ENS neurons (mainly)

Stimulation - Excites ENS (in general)

Parasympathetic nerves also contain afferent sensory fibers
Sympathetic Innervation
Preganglionic Neurons (long) - Originate at T5-L2 (cell bodies). Synapse in prevertebral ganglia

Postganglionic Neurons (long)
Originate in ganglia (cell bodies)
Innervate entire gut. Terminate in ENS (mostly)

Inhibitory influences (mostly) by (a) decreasing activity of ENS. (b) Direct effect to inhibit SM

Sympathetic nerves also contain afferent sensory fibers
Neurotransmitters (Neurocrines)
Preganglionic efferent neurons - acetylcholine

Postganglionic efferent neurons
PNS - acetylcholine
SNS - norepinephrine

Enteric nervous system (many others)
Excitatory - acetylcholine, substance P
Inhibitory – Vasoactive Inhibitory P, NO
Sensory Afferent Neurons
Stimulation of afferent neurons
Distention of gut wall
Non-specific irritation of gut mucosa
Specific chemical stimuli

Stimulation - can excite or inhibit
Intestinal movements
Intestinal secretions
Regulation of Gastric Function
Gastric motility & secretion occur automatically
Waves of contraction are initiated spontaneously by pacesetter cells & secretion occurs in absence of hormonal & neural input
ANS & hormonal effects are superimposed on automatic activity
Extrinsic control of gastric function is divided into cephalic, gastric, & intestinal phases
Cephalic Phase
Refers to control by brain of vagus activity
Stimulated by sight, smell, & taste of food
Activation of vagus:
Stimulates chief cells to secrete pepsinogen
Directly stimulates G cells to secrete gastrin
Directly stimulates ECL cells to secrete histamine
Indirectly stimulates parietal cells to secrete HCl
Continues into 1st 30 min of a meal
Gastric Phase
Arrival of food in stomach stimulates gastric phase
Gastric secretion stimulated by distension of stomach & chemical nature of chyme
Gastric Phase continued
Short polypeptides & amino acids stimulate G cells to secrete gastrin & chief cells to secrete pepsinogen
Gastrin stimulates ECL cells to secrete histamine which stimulates parietal cell secretion of HCl
This is a positive feedback mechanism: As more HCl & pepsinogen are secreted, more polypeptides & amino acids are formed

Secretion of HCl is also regulated by a negative feedback mechanism:
HCl secretion decreases if pH < 2.5; at pH 1 gastrin secretion stops
D cells stimulate secretion of somatostatin which inhibits gastrin secretion
Intestinal Phase
Begins with inhibition of gastric activity when chyme enters SI
Arrival of chyme in SI is detected by sensory neurons of vagus
This causes a neural reflex that inhibits gastric motility & secretion
Fat in chyme stimulates SI to secrete enterogasterones--hormones that inhibit gastric motility & secretion
Enterogasterones include somatostatin, CCK-PZ
Enteric Nervous System
For peristalsis:
ACh & substance P stimulate smooth muscle contraction above bolus
NO, VIP, & ATP stimulate smooth muscle relaxation below bolus
Paracrine Regulators of Intestine
ECL cells release serotonin & motilin in response to pressure & chemical stimuli in SI
Serotonin stimulates intrinsic afferents which activate motor neurons in intrinsic NS
Motilin stimulates contraction in duodenum & stomach antrum
Guanylin, from ileum & colon, stimulates production of cGMP which inhibits absorption of Na+& causes secretion of Cl- & H20
Gastrointestinal Reflexes
Local (within ENS)
Afferent fibers from gut terminate in ENS
Affect (+ or -) secretion, peristalsis, mixing movements

Long loop
Gut → Aff. N. → prevertebral ganglia → Eff. N. → gut
Reflexes: gastrocolic, enterogastric, colonoileal
Gastrointestinal Reflexes (cont’d)
Vagovagal Reflexes
Stomach / duodenum → Aff. N. → brain stem → Eff. N. → stomach / duodenum
Controls gastric motor and secretory activity

Defecation Reflexes
Colon / rectum → Aff. N. → spinal cord → Eff. N. → colon / rectum

Pain Reflexes - overall inhibition of GI tract

Remember the gastrocholic-somoach full=increased motility of the colon
Integration of Nervous and Endocrine Systems
Nervous and hormonal influences do not function independently
Neural activity → release of hormones
Hormones → neural activity
Simultaneous effects

Source of stimuli
Within body
Intestinal Reflexes
Can be mediated by enteric NS & paracrines; & regulated by ANS & hormones
Gastroileal reflex refers to increased motility of ileum & movement of chyme thru ileocecal sphincter in response to increased gastric activity
Ileogastric reflex decreases gastric motility in response to distension of ileum
Intestino-intestinal reflex causes relaxation of rest of intestine when any part is overdistended
Secretion of Pancreatic Juice
Secretion of pancreatic juice & bile is stimulated by secretin & bile
Secretin is secreted in response to duodenal pH < 4.5
Stimulates release of HC03- into SI by pancreas & into bile by liver
CCK is secreted in response to fat & protein content of chyme in duodenum
Stimulates production of pancreatic enzymes
Enhances secretin
Stimulates contraction of sphincter of Oddi
Digestion & Absorption of Carbohydrates
Most carbohydrates are ingested as starch-- a polymer of glucose
Salivary amylase begins starch digestion
Pancreatic amylase converts starch to oligosaccharides
Oligosaccharides hydrolyzed by SI brush border enzymes
Digestion & Absorption of Protein
Begins in stomach when pepsin digests proteins to form polypeptides
In SI, endopeptidases (trypsin, chymotrypsin, elastase) cleave peptide bonds in interior of polypeptides
SI exopeptidases (carboxypeptidase, aminopeptidase) cleave peptide bonds from ends of polypeptides

Protein digestion in SI results in free amino acids, dipeptides, & tripeptides
Which are transported into SI cells where di- & tripeptides are broken down to amino acids
Which are secreted into blood
Digestion & Absorption of Lipids
Occurs in SI
Arrival of lipids in duodenum causes secretion of bile
Fat is emulsified by bile salt micelles
Forms tiny droplets of fat dissolved in bile salt micelles
Greatly increases surface area for fat digestion

Pancreatic lipase hydrolyzes triglycerides to free fatty acids & monglycerides
Phospholipase A breaks down phospholipids into fatty acids & lysolecithin

Products of fat digestion dissolve in micelles forming mixed micelles which move to brush border

Free fatty acids, monoglycerides, & lysolecithin leave micelles & enter epithelial cells
Inside epithelial cells, they are resynthesized into triglycerides & phospholipids

Triglycerides & phospholipids combine with a protein to form small particles called chylomicrons
Which are secreted into central lacteals of SI villi
Transport of Lipids
In blood, endothelial lipoprotein lipase hydrolyzes triglycerides to free fatty acids & glycerol for use in cells
Cholesterol-containing remnants are taken up by liver

Cholesterol & triglycerides from liver form VLDLs which are secreted & take triglycerides to cells
Once triglycerides are removed, VLDLs become LDLs
LDLs transport cholesterol to organs & blood vessels
HDLs transport excess cholesterol back to liver
High ratio of HDL-cholesterol to total cholesterol is believed to confer protection against atherosclerosis
Gastric and Peptic Ulcers
Peptic ulcers are erosions of mucous membranes of stomach or duodenum caused by action of HCl
In Zollinger-Ellison syndrome, duodenal ulcers result from excessive gastric acid in response to high levels of gastrin
Helicobacter pylori infection is associated with ulcers
Antibiotics are useful in treating ulcers
Acute gastritis is an inflammation that results in acid damage due to histamine released by inflammation
Why histamine receptor blockers such as Tagamet & Zantac can treat gastritis
Common GI Problems
Gastroesophageal Reflux Disease (GERD)
Colorectal Cancer
Viral Liver Disease
Alcoholic Liver Disease
Inflammatory Bowel Disease
Irritable Bowel Syndrome
Food Intolerance
Digestive Diseases
Affects 70-95 million Americans
>10 million hospitalized each year
Colorectal cancer - 2nd deadliest cancer in US
Diarrhea is the 3rd leading cause of death worldwide
Total health care costs exceeds $40 billion
Total cost to nation exceeds $90 billion