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97 Cards in this Set
- Front
- Back
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Inside gastrointestinal (GI) tract, food is broken down by hydrolysis into molecular monomers
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Absorption of monomers occurs in small intestine
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disacchride + water =
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monosacchride
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peptide + water =
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amino acid + amino acid
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fat + water =
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fatty acids + glycerol
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Then, inside the cells in the neighborhood….
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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. |
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Motility
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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 |
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Secretion
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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 |
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Absorption
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Is the passage of digested end products into blood or lymph through villi walls. (thin with a huge surface area)
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Storage and Elimination
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Includes temporary storage & subsequent elimination of indigestible components of food
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Digestive System is composed of
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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 |
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Regulation of GI Tract
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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 |
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Layers of GI Tract
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Are called tunics
The 4 tunics are mucosa, submucosa, muscularis, & serosa |
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Mucosa
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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 |
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Submucosa
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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 |
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Muscularis
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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 |
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Serosa
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Is outermost layer; serves to bind & protect
Consists of areolar connective tissue covered with layer of simple squamous epithelium |
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3 swallowing phases
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buccal
pharyngeal esophogeal |
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From Mouth to Stomach
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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 |
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Peristalsis propels food thru GI tract
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= 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 |
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Stomach
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Is enclosed by cardiac sphincter on top & pyloric sphincter on bottom
Is divided into 3 regions: Fundus Body Antrum |
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Stomach
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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 |
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Gastric glands contain cells that secrete different products that form gastric juice
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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 |
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HCl in Stomach
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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 |
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Digestion & Absorption in Stomach
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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 |
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Protective Mechanisms of Stomach
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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 |
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Small Intestine (SI)
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Is longest part of GI tract
Duodenum Jejunum Ileum 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 |
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Intestinal Enzymes
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Attached to microvilli are brush border enzymes that are not secreted into lumen
Enzyme active sites are exposed to chyme |
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Intestinal Contractions and Motility
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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 |
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Intestinal Contractions & Motility
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Occur automatically via endogenous pacemaker activity
Contractions are driven by graded depolarizations called slow waves |
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Slow Waves
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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 |
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Spike Potentials
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True action potentials
Occur when slow waves reach threshold (-40 mV) Cause SM contraction Voltage dependent calcium channels Ca++ entry → contraction Frequency Affected by nervous / hormonal stimuli ↑ frequency → stronger contraction ↑ frequency of stim. does not ↑ max. frequency of contraction |
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Propulsive Movements - Peristalsis
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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 |
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Intestinal Contractions & Motility
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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 |
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Intestinal Contractions & Motility
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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 |
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Large Intestine (LI) or Colon
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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 |
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Fluid & Electrolyte Absorption in LI
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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 |
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Defecation
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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 |
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Structure of Liver
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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 |
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Hepatic Portal System
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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 |
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Liver Lobules
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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 |
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Enterohepatic Circulation
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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 |
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major categories of liver function
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detoxificatino of blood
carb metabolism lipid metabolism protien syntheisis secretion of bile |
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Bile Production and Secretion
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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 |
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Bile Acids
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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 |
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Detoxification of Blood
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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 |
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Secretion of Glucose, Triglycerides & Ketones
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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 |
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Production of Plasma Proteins
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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 |
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Gallbladder
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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 |
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Pancreas
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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 |
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Pancreatic Juice
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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 |
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amylase
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digests starch to maltose and short chains fo glucose mlecules
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lipase
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cleaves fatty acids from glycerol
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Neural and Endocrine Regulation
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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 |
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Chemistry of GI Peptides
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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 |
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GI Hormones identified in:
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Secretin - 1902
Gastrin 1905 Cholecystokinin (CCK) 1928 Gastric Inhibitory Peptide (GIP) - 1969 Motilin - 1970 |
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Chemistry of GI Peptides
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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 |
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Gastrin - Chemistry
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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 |
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Gastrin - Distribution and Release
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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 |
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Gastrin - Physiological Effects
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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 |
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Gastrinoma - Zollinger-Ellison syndrome
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Gastrin secreting tumor
Non-beta cell tumor of pancreas (80%) or G-cell tumors in duodenum (10-15%) Continually secretes gastrin into blood Symptoms Duodenal ulcers, diarrhea, steatorrhea, hypokalemia Hypergastrinemia causes hypersecretion of acid Increased parietal cell mass Constant stimulation of hyperplastic mucosa |
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Cholecystokinin - Chemistry
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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. |
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CCK - Distribution and Release
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Released from I-cells in duodenum and jejunum
Stimuli for release Fatty acids or monoglycerides (not triglycerides) peptides and single AA Acid (weak) |
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CCK - Physiological Effects
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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 |
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Secretin - Chemistry
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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 |
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Secretin
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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 |
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Gastric Inhibitory Peptide (GIP)
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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) |
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Motilin
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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” |
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only I homone in antrum
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gastrin
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only 2 GI homones in Illeum
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secretin and CCK
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Paracrines
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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) |
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Neural Control of GI Tract
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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) |
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Enteric Nervous System (ENS)
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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 |
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ENS - Myenteric Plexus
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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, |
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ENS - Submucosal Plexus
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Location - Mucosal layer from esophagus to anus
Function - Local control Secretion Absorption Contraction of muscularis mucosa |
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Parasympathetic Innervation
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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 |
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Sympathetic Innervation
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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 |
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Neurotransmitters (Neurocrines)
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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 |
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Sensory Afferent Neurons
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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 |
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Regulation of Gastric Function
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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 |
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Cephalic Phase
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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 |
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Gastric Phase
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Arrival of food in stomach stimulates gastric phase
Gastric secretion stimulated by distension of stomach & chemical nature of chyme |
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Gastric Phase continued
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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 |
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Intestinal Phase
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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 |
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Enteric Nervous System
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For peristalsis:
ACh & substance P stimulate smooth muscle contraction above bolus NO, VIP, & ATP stimulate smooth muscle relaxation below bolus |
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Paracrine Regulators of Intestine
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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 |
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Gastrointestinal Reflexes
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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 |
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Gastrointestinal Reflexes (cont’d)
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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 |
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Integration of Nervous and Endocrine Systems
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Nervous and hormonal influences do not function independently
Neural activity → release of hormones Hormones → neural activity Simultaneous effects Source of stimuli Environmental Within body |
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Intestinal Reflexes
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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 |
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Secretion of Pancreatic Juice
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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 |
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Digestion & Absorption of Carbohydrates
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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 |
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Digestion & Absorption of Protein
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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 |
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Digestion & Absorption of Lipids
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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 |
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Transport of Lipids
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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 |
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Gastric and Peptic Ulcers
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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 |
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Common GI Problems
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Gastroesophageal Reflux Disease (GERD)
Ulcers Colorectal Cancer Gallstones Viral Liver Disease Hemorrhoids Constipation Diarrhea Alcoholic Liver Disease Inflammatory Bowel Disease Irritable Bowel Syndrome Food Intolerance Flatus Pancreatitis |
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Digestive Diseases
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Pandemic
Affects 70-95 million Americans >10 million hospitalized each year Deadly Colorectal cancer - 2nd deadliest cancer in US Diarrhea is the 3rd leading cause of death worldwide Costly Total health care costs exceeds $40 billion Total cost to nation exceeds $90 billion |
