Presentation on theme: "The Digestive System: Part B"— Presentation transcript:
1The Digestive System: Part B 23The Digestive System: Part B
2Oropharynx and laryngopharynx Allow passage of food, fluids, and airStratified squamous epithelium liningSkeletal muscle layers: inner longitudinal, outer pharyngeal constrictors
3EsophagusFlat muscular tube from laryngopharynx to stomachPierces diaphragm at esophageal hiatusJoins stomach at the cardiac orifice
4Esophageal mucosa contains stratified squamous epithelium EsophagusEsophageal mucosa contains stratified squamous epitheliumChanges to simple columnar at the stomachEsophageal glands in submucosa secrete mucus to aid in bolus movementMuscularis: skeletal superiorly; smooth inferiorlyAdventitia instead of serosa
5(contains a stratified squamous epithelium) Mucosa(contains a stratifiedsquamous epithelium)Submucosa (areolarconnective tissue)LumenMuscularis externa• Longitudinal layer• Circular layerAdventitia (fibrousconnective tissue)(a)Figure 23.12a
6(contains a stratified squamous epithelium) Mucosa(contains a stratifiedsquamous epithelium)(b)Figure 23.12b
8Digestive Processes: Mouth IngestionMechanical digestionMastication is partly voluntary, partly reflexiveChemical digestion (salivary amylase and lingual lipase)PropulsionDeglutition (swallowing)
9Pharyngeal-esophageal phase DeglutitionInvolves the tongue, soft palate, pharynx, esophagus, and 22 muscle groupsBuccal phaseVoluntary contraction of the tonguePharyngeal-esophageal phaseInvoluntaryControl center in the medulla and lower pons
10Figure 23.13 Bolus of food Tongue Uvula Pharynx Bolus Epiglottis TracheaBolusEsophagusUpper esophageal sphincter is contracted. During the buccal phase, the tongue presses against the hard palate, forcing the food bolus into the oropharynx where the involuntary phase begins.1The uvula and larynx rise to prevent food from entering respiratory passageways. The tongue blocks off the mouth. The upper esophageal sphincter relaxes, allowing food to enter the esophagus.2The constrictor muscles of the pharynx contract, forcing food into the esophagus inferiorly. The upper esophageal sphincter contracts (closes) after entry.3Relaxed musclesFood is moved through the esophagus to the stomach by peristalsis.4Relaxed musclesThe gastroesophageal sphincter opens, and food enters the stomach.5Circular muscles contractBolus of foodLongitudinal muscles contractGastroesophageal sphincter closedGastroesophageal sphincter opensStomachFigure 23.13
11Bolus of food Tongue Pharynx Epiglottis Glottis Trachea 1Upper esophageal sphincter is contracted. During the buccal phase, the tongue presses against the hard palate, forcing the food bolus into the oropharynx where the involuntary phase begins.Figure 23.13, step 1
12Bolus3The constrictor muscles of the pharynx contract, forcing food into the esophagus inferiorly. The upper esophageal sphincter contracts (closes) after entry.Figure 23.13, step 3
13Uvula Bolus Epiglottis Esophagus The uvula and larynx rise to prevent food from entering respiratory passageways. The tongue blocks off the mouth. The upper esophageal sphincter relaxes, allowing food to enter the esophagus.2Figure 23.13, step 2
14Food is moved through the esophagus to the stomach by peristalsis. Relaxed muscles4Food is moved through the esophagus to the stomach by peristalsis.Circular muscles contractBolus of foodLongitudinal muscles contractGastroesophageal sphincter closedStomachFigure 23.13, step 4
15The gastroesophageal sphincter opens, and food enters the stomach. 5Relaxed musclesGastroesophageal sphincter opensFigure 23.13, step 5
16Figure 23.13 Bolus of food Tongue Uvula Pharynx Bolus Epiglottis TracheaBolusEsophagusUpper esophageal sphincter is contracted. During the buccal phase, the tongue presses against the hard palate, forcing the food bolus into the oropharynx where the involuntary phase begins.1The uvula and larynx rise to prevent food from entering respiratory passageways. The tongue blocks off the mouth. The upper esophageal sphincter relaxes, allowing food to enter the esophagus.2The constrictor muscles of the pharynx contract, forcing food into the esophagus inferiorly. The upper esophageal sphincter contracts (closes) after entry.3Relaxed musclesFood is moved through the esophagus to the stomach by peristalsis.4Relaxed musclesThe gastroesophageal sphincter opens, and food enters the stomach.5Circular muscles contractBolus of foodLongitudinal muscles contractGastroesophageal sphincter closedGastroesophageal sphincter opensStomachFigure 23.13
17Stomach: Gross Anatomy Cardiac region (cardia)Surrounds the cardiac orificeFundusDome-shaped region beneath the diaphragmBodyMidportion
18Stomach: Gross Anatomy Cardiac region (cardia)Surrounds the cardiac orificeFundusDome-shaped region beneath the diaphragmBodyMidportion
19Stomach: Gross Anatomy Pyloric region: antrum, pyloric canal, and pylorusPylorus is continuous with the duodenum through the pyloric valve (sphincter)Greater curvatureConvex lateral surfaceLesser curvatureConcave medial surface
21Stomach: Gross Anatomy Lesser omentumFrom the liver to the lesser curvatureGreater omentumDrapes from greater curvatureAnterior to the small intestineThe omenta have fat deposits and lots of lymph nodes. The immune cells and macrophages in the omenta police the peritoneal cavity. The omenta can wall off peritoneal infections.
27Liver (cut) Diaphragm Inferior vena cava Esophagus Celiac trunk Common hepaticarteryLeft gastricarteryHepatic arteryproperStomachSplenic arteryGastroduodenalarteryLeftgastroepiploicarteryRight gastric arteryGallbladderSpleenPancreas(major portion liesposterior to stomach)RightgastroepiploicarteryDuodenumSuperiormesentericAbdominal aorta(b) The celiac trunk and its major branches. The left half of the liver has been removed.Figure 19.24b
28The Ligamentum Teres Hepatis is the remnant of the umbilical vein Falciform ligamentLiverGallbladderSpleenStomachLigamentum teresGreater omentumSmall intestineCecum(a)The Ligamentum Teres Hepatis is the remnant of the umbilical veinFigure 23.30a
29Stomach: Microscopic Anatomy Four tunicsMuscularis and mucosa are modifiedMuscularis externaThree layers of smooth muscleInner oblique layer allows stomach to churn, mix, move, and physically break down food
31(a) Layers of the stomach wall (l.s.) SurfaceepitheliumMucosaLamina propriaMuscularismucosaeSubmucosa(contains submucosalplexus)Oblique layerMuscularis externa(contains myentericplexus)Circular layerLongitudinallayerSerosaStomach wall(a) Layers of the stomach wall (l.s.)Figure 23.15a
32Stomach: Microscopic Anatomy MucosaSimple columnar epithelium composed of mucous cells – they produce a cloudy two layer coat of alkaline mucus which the surface layer consists of a viscous-insoluble mucus that traps bicarbonate-rich fluid beneath itThe smooth lining is lined with dotted Gastric pits that lead into gastric glands that produce the various gastric juices
33The cells forming the walls of the gastric pits are primarily mucous cells – but the gastric gland cells differ in the different regions of the stomach.Cardia (entrance) and pylorus (exit) are primarily mucus secreting cellsPyloric Antrum produce mucus and hormones (enteroendocrine cells)Fundus and body – where most chemical digestion occurs produce the majority of stomach secretions
34(b) Enlarged view of gastric pits and gastric glands Surface epithelium(mucous cells)GastricpitMucous neck cellsParietal cellChief cellGastricglandEnteroendocrine cell(b) Enlarged view of gastric pits and gastric glandsFigure 23.15b
36(c) Location of the HCl-producing parietal cells and PepsinogenPepsinHClMitochondriaParietal cellChief cellEnteroendocrinecell(c) Location of the HCl-producing parietal cells andpepsin-secreting chief cells in a gastric glandFigure 23.15c
37Gastric Gland Secretions Glands in the fundus and body produce most of the gastric juiceParietal cell secretionsHCl pH 1.5–3.5 denatures protein in food, activates pepsin, and kills many bacteriaIntrinsic factorGlycoprotein required for absorption of vitamin B12 in small intestine
38Gastric Gland Secretions Chief cell secretionsInactive enzyme pepsinogenActivated to pepsin by HCl and by pepsin itself (a positive feedback mechanism)Chief cells also secrete insignificant amounts of gastric lipase
39Gastric Gland Secretions Enteroendocrine cellsSecrete chemical messengers into the lamina propriaParacrinesSerotonin and histamineHormonesSomatostatin and gastrin
40Mucosal BarrierLayer of bicarbonate-rich mucusTight junctions between epithelial cellsDamaged epithelial cells are quickly replaced by division of stem cells – that reside where the gastric pits join the gastric glands.The surface epithelia are replaced every three to six days
41Homeostatic Imbalance Gastritis: inflammation caused by anything that breaches the mucosal barrierPeptic or gastric ulcers: erosion of the stomach wallMost are caused by Helicobacter pylori bacteriaGo to GI Diseases PowerPoint
42(a) A gastric ulcer lesion (b) H. pylori bacteria Mucosalayer ofstomach(a) A gastric ulcer lesion(b) H. pylori bacteriaFigure 23.16
43Digestive Processes in the Stomach Physical digestionDenaturation of proteinsEnzymatic digestion of proteins by pepsin (and rennin in infants)Secretes intrinsic factor required for absorption of vitamin B12Lack of intrinsic factor pernicious anemiaDelivers chyme to the small intestine
44Regulation of Gastric Secretion Gastric Secretion has three phases – (1) Cephalic (2) Gastric and (3) Intestinal.Some are more stimulatory – Cephalic and Gastric and one is more inhibitory – Intestinal PhaseNeural (vagus and enteric plexus) and hormonal mechanisms control the secretionsCephalic (reflex) phase: last just a few minutes prior to food entry into the stomach. It occurs even if you don’t actually get the food – if you desire the food and are not depressed or have a lack of appetite
45Gastric PhaseLasts approximately 3–4 hours after food enters the stomachStimuli for this phase is gastric distention, peptides, and low acidityGastric Distention activates stretch receptors and initiates both local (myenteric) reflexes and vagovagal – both stimulate acetylcholine release
46Gastrin (1)Gastrin is secreted by G-cells in the Pyloric Antrum in accordance with chemical stimuli and neural stimuliThe chemical stimuli for Gastrin secretion are partially digested proteins, caffeine, and rising alkaline pH. High acidity less than a pH of 2 inhibits Gastrin secretionGastric stimulates release of enzymes, also Histamine from the enterochromaffin cells – but its main targets are the Parietal cells in body of the stomach that secrete HCl- prodding them to secrete increased amounts of HCl
47Gastrin (2)When protein products enter the stomach, the pH generally rises due to the proteins buffering H+.The rising pH stimulates Gastrin which causes HCl to spew out thus denaturing the proteins. The more proteins the more Gastrin.As proteins are decomposed the acidity rises and Gastrin is inhibited
48Gastrin (3)In addition to G-cells being stimulated chemically – they are also stimulated neurally. The parasympathetic turns on secretion via acetylcholine from the Vagus and Sympathetic turns it offThe vagus was activated in the Cephalic Phase and Gastric Phase due to stomach distentionEmotional upset, fear, anxiety, and anything that triggers the fight and flight response turns off Gastric secretion.
49Figure 23.17 Stimulatory events Inhibitory events Sight and thought of food1CephalicphaseCerebral cortexLack ofstimulatoryimpulses toparasym-patheticcenterCerebralcortexLoss ofappetite,depression1Conditioned reflexStimulation oftaste and smellreceptors2Hypothalamusand medullaoblongataVagusnerveStomachdistensionactivatesstretchreceptors1VagovagalreflexesMedullaVagusnerveGastrinsecretiondeclinesG cellsExcessiveacidity(pH <2)in stomach1GastricphaseLocalreflexesOverridesparasym-patheticcontrolsSympatheticnervoussystemactivationEmotionalupset2Food chemicals(especially peptides andcaffeine) and rising pHactivate chemoreceptors2G cellsGastrinreleaseto bloodStomachsecretoryactivityEntero-gastricreflexLocalreflexesDistensionof duodenum;presence offatty, acidic,hypertonicchyme, and/orirritants inthe duodenum1Presence of lowpH, partially digestedfoods, fats, orhypertonic solutionin duodenum whenstomach begins toempty1Intestinal(enteric)gastrinreleaseto bloodVagalnucleiin medullaBriefeffectIntestinalphasePyloricsphincterRelease of intestinalhormones (secretin,cholecystokinin, vasoactiveintestinal peptide)Distension;presence offatty, acidic,partiallydigested foodin theduodenum2StimulateInhibitFigure 23.17
50Regulation and Mechanism of HCl Secretion Three chemicals (ACh, histamine, and gastrin) stimulate parietal cells through second-messenger systemsAll three are necessary for maximum HCl secretionAntihistamines block H2 receptors and decrease HCl release
51Secondary Messenger Systems for HCl release Acetylcholine and Gastrin increase intracellular Calcium levels.Histamine released by the enterochromaffin-like cells in response to Gastrin and to a lesser extent by Ach acts through the cyclic AMP system.
53Regulation of Gastric Secretion Intestinal phase: brief stimulatory effect as partially digested food enters the duodenum, followed by inhibitory effects (enterogastric reflex and enterogastrones)Some actions are excitatory and some are inhibitoryAs partially digested foods fill the initial part of the small intestine (duodenum). This action stimulates the release of intestinal Gastrin. This stimulates the stomach to continue its secretory activity. However, this action is brief.
54The action is brief due to the fact that as the intestines fill with chyme containing large amounts of H+, fats, partially digested proteins and various irritating substances, the inhibitory component is triggered in the form of the enterogastric reflexThe enterogastric reflex is a trio of reflexes that (1) inhibit the vagal nuclei in the medulla (2) inhibit local reflexes and (3) activate sympathetic fibers that cause the pyloric sphincter to tighten and prevent further food entry.The purpose of this inhibitory action is to not fill the duodenum with excess acidity and match the small intestines processing time.Additionally there is a release of several intestinal hormones – termed enterogastrones (Secretin, Cholecystokinin, and Vasoactive Intestinal Peptide). All are inhibitory on the stomach.
55Response of the Stomach to Filling Stretches to accommodate incoming foodReflex-mediated receptive relaxationCoordinated by the swallowing center of the brain stem and mediated by the vagus nerves acting on Serotonin and Nitric Oxide releasing enteric neuronsGastric accommodationPlasticity (stress-relaxation response) of smooth muscle
56Small rippling waves in the body and fundus of stomach where good (food storage) chemical digestion occurWaves get stronger in pyloric antrum. The pyloric region which holds about 30 cc of chyme acts as a dynamic filter that allows only liquids and small particles to pass through the barely open pyloric valve during the digestive process.Normally each peristaltic wave reaching the pyloric muscle squirts only 3 cc or less of chyme into the small intestines. Because the contraction also closes the pyloric valve, which is normally partially relaxed, the rest (27 cc) goes back into the stomach to be better mixed.
57Gastric Contractile Activity The intensity of peristaltic waves can be changed but the rate is constant – about 3 waves per minute.Pacemaker cells (cells of Cajal) located in the longitudinal muscle layer – automatically depolarize and repolarize setting the cyclic slow waves – also known as the Basic electrical rhythm (BER)The smooth muscle cells are connected by gap junctions to the rest of muscularis – the waves are efficiently transmitted.
58The pacemakers set the maximum rate of contraction, but they do not initiate the contractions or regulate the force.They generate subthreshold depolarization waves, which are then ignited (enhanced by further depolarization and brought to threshold) by neural and hormonal factors.Factors that increase the strength of contractions are the same factors that enhance stomach secretions.
59Gastric Contractile Activity Most vigorous near the pylorusChyme is eitherDelivered in ~ 3 ml spurts to the duodenum, orForced backward into the stomach
60Propulsion: Peristaltic waves move from the fundus toward the pylorus. PyloricvalveclosedPyloricvalveclosedPyloricvalveslightlyopenedPropulsion: Peristalticwaves move from thefundus toward thepylorus.1Grinding: The mostvigorous peristalsis andmixing action occurclose to the pylorus.2Retropulsion: The pyloricend of the stomach acts as apump that delivers smallamounts of chyme into theduodenum, simultaneouslyforcing most of its containedmaterial backward into thestomach.3Figure 23.19
61Regulation of Gastric Emptying The stomach usually empties completely within 4 hours after a meal.The larger the meal (more stomach distention) and the more liquid the meal is – the faster it empties.Fluids pass quickly through the stomach.Solids take longer in that they need to be processed moreThe rate of gastric emptying depends not only on the stomach but just as much on the small intestines processing time. Too much release into the small intestine (too much stretch) initiates the enterogastric reflex.As chyme enters the duodenumReceptors respond to stretch and chemical signalsEnterogastric reflex and enterogastrones inhibit gastric secretion and duodenal fillingCarbohydrate-rich chyme moves quickly through the duodenumFatty chyme remains in the duodenum 6 hours or more
62Gastric EmptyingCarbohydrate-rich chyme moves quickly through the duodenumFatty chyme remains in the duodenum 6 hours or more
63Presence of fatty, hypertonic, acidic chyme in duodenum Duodenal entero-endocrine cellsChemoreceptors andstretch receptorsSecreteTargetEnterogastrones(secretin,cholecystokinin,vasoactive intestinalpeptide)Via shortreflexesVia longreflexesEntericneuronsCNS centerssympatheticactivity;parasympatheticactivityDuodenalstimulideclineContractile force andrate of stomachemptying declineInitial stimulusPhysiological responseStimulateResultInhibitFigure 23.20
64Vomiting and Gastroparesis Vomiting is caused by many factors – with the most common being extreme stretching of the stomach and/or intestines. Other factors are bacterial toxins, excessive alcohol, spicy foods, and certain drugs.Both bloodborne molecules and sensory impulses going to the emetic center in the medulla initiate the events for vomiting.
65GastroparesisGastroparesis, also called delayed gastric emptying, is a medical condition consisting of a paresis (partial paralysis) of the stomach, resulting in food remaining in the stomach for a longer period of time than normal. Normally, the stomach contracts to move food down into the small intestine for digestion. The vagus nerve controls these contractions. Gastroparesis may occur when the vagus nerve is damaged and the muscles of the stomach and intestines do not work normally. Food then moves slowly or stops moving through the digestive tract.
66CausesGastroparesis may be chronic or transient; transient gastroparesis may arise in acute illness of any kind, with the use of certain cancer treatments or other drugs which affect digestive action, or due to anorexia nervosa, bulimia and other abnormal eating patterns.Chronic gastroparesis is frequently due to autonomic neuropathy. This may occur in people with type 1 diabetes or type 2 diabetes. The vagus nerve becomes damaged by years of high blood glucose, resulting in gastroparesis. Gastroparesis has also been associated with various autoimmune diseases and syndromes, such as fibromyalgia and Parkinson's disease, and may occur as part of a mitochondrial disorder.
67Small Intestine: Gross Anatomy Major organ of digestion and absorption2–4 m (20 feet long in cadaver but feet long in living person); extends from pyloric sphincter to ileocecal valve – approximately 200 square meters of surface area (doubles tennis court)SubdivisionsDuodenum (retroperitoneal) 10 inchesJejunum (attached posteriorly by mesentery) 8 feetIleum (attached posteriorly by mesentery) 12 feet
68The Ligament of Treitz (named after Václav Treitz) connects the duodenum of the small intestines to the diaphragm. It contains a slender band of skeletal muscle from the diaphragm and a fibromuscular band of smooth muscle from the horizontal and ascending parts of the duodenum. When it contracts, the suspensory muscle of the duodenum widens the angle of the duodenojejunal flexure, allowing movement of the intestinal contents
70The bile duct and main pancreatic duct DuodenumThe bile duct and main pancreatic ductJoin at the hepatopancreatic ampullaEnter the duodenum at the major duodenal papillaAre controlled by the hepatopancreatic sphincter
71Bile duct and sphincter Accessory pancreatic duct Right and lefthepatic ductsof liverCystic ductCommon hepatic ductBile duct and sphincterAccessory pancreatic ductMucosawith foldsTail of pancreasPancreasGallbladderJejunumMajor duodenalpapillaMain pancreatic ductand sphincterHepatopancreaticampulla and sphincterDuodenumHead of pancreasFigure 23.21
72Structural Modifications Increase surface area of proximal part for nutrient absorptionCircular folds (plicae circulares) 1 cm tall – permanent folds of mucosae and submucosaVilli – 1 mm highMicrovilli
73Structural Modifications Circular foldsPermanent (~1 cm deep)Force chyme to slowly spiral through lumen
75Structural Modifications Villi (gives a velvety look)Motile fingerlike extensions (~1 mm high) of the mucosaVillus epitheliumSimple columnar absorptive cells (enterocytes)Goblet cellsIn the core of each villus is a dense capillary bed and a wide lymph capillary called a lacteal.
76The villi are large and leaflike in the duodenum and gradually narrow and shorten along the length of the small intestine.A slip of smooth muscle in the villus core allows it to alternatively shorten and lengthen.The pulsations (1) increase the contact between the villus and contents of the intestinal lumen making better absorption and (2) milk lymph along the lacteals.
77Structural Modifications MicrovilliProjections (brush border) of absorptive cellsBear brush border enzymes – these enzymes complete the digestive process
78Histology of Intestinal Wall Epithelium of the villus is largely simple columnar absorptive cells bound by tight junctions and richly endowed with microvilli.Goblet cellsBetween the villi are intestinal pits that lead into tubular glands called intestinal crypts – also known as the crypts of Lieberkühn.
79Intestinal Crypts Intestinal crypt epithelium Primarily composed of secretory cells that produce intestinal juice – a watery mixture containing mucus that serves as a carrier fluid for absorbing nutrients from chymeEnteroendocrine cells – source of the enterogastrones (Secretin and CCK)Intraepithelial lymphocytes (IELs) – these are T-cells that do not need priming – upon encountering antiges they immediately release killing cytokinesRelease cytokines that kill infected cellsPaneth cells – release defensins and lysozymeStem cells – can differentiate – become specialized absorptive cells, goblet cells, and enteroendocrine cells.
80The stem cells migrate up to become the epithelial cells – the existent epithelial cells undergo apoptosis and are shed from the villus tips, renewing the villus epithelium every two days.but when the stem cells differentiate into Paneth cells – they stay at the baseThe crypts decrease in number along the length of the small intestine, but the goblet cells become more abundant.
82SubmucosaTypical areolar connective tissueContains individual and aggregated lymphoid folliclesPeyer’s patches (aggregated lymphoid follicles) – increase in number as go towards end of small intestine. They protect distal part against bacteria since normal flora increases there.Also contains proliferating lymphocytes that leave the intestine enter blood stream and then return to home in the submucosa to produce IgA
83Submucosal Duodenal Glands Duodenal (Brunner’s) glands of the duodenum secrete alkaline mucusThe glands help neutralize acidic chyme moving in from the stomachWhen this protection is absent or insufficient – duodenal ulcers can occurThe muscularis of the small intestine is bilayered and except for the duodenum which is retroperitoneal and has an adventitia, the external intestinal surface is covered by a visceral peritoneum
84Intestinal JuiceNormally secrete 1 to 2 ml of intestinal juice daily – that facilitates transport and absorption of nutrientsSecreted in response to distension or irritation of the mucosa by hypertonic or acidic chyme.Slightly alkaline (7.4 – 7.8) and isotonic with blood plasmaLargely water, enzyme-poor, due to the fact that enzymes are limited to the intestinal enzymes bound to brush border. It does contain contains mucus – secreted by goblet cells and duodenal glands
85LiverLargest gland in the bodyFour lobes—right, left, caudate, and quadrate
86Round ligament (ligamentum teres) LiverFalciform ligamentSeparates the (larger) right and (smaller) left lobesSuspends liver from the diaphragm and anterior abdominal wallRound ligament (ligamentum teres)Remnant of fetal umbilical vein along free edge of falciform ligament
87Sternum Bare area Nipple Falciform Liver ligament Left lobe of liver Right lobeof liverRound ligament(ligamentumteres)Gallbladder(a)Figure 23.24a
88Sternum Nipple Liver Bare area Lesser omentum (in fissure) Caudate lobeof liverLeft lobe of liverSulcus forinferiorvena cavaPorta hepatiscontaining hepaticartery (left) andhepatic portal vein(right)Hepatic vein(cut)Bile duct (cut)Right lobe ofliverQuadrate lobeof liverGallbladderLigamentum teres(b)Figure 23.24b
89Liver: Associated Structures Lesser omentum anchors liver to stomachHepatic artery and vein at the porta hepatisBile ductsCommon hepatic duct leaves the liverCystic duct connects to gallbladderBile duct formed by the union of the above two ducts
90Bile duct and sphincter Accessory pancreatic duct Right and lefthepatic ductsof liverCystic ductCommon hepatic ductBile duct and sphincterAccessory pancreatic ductMucosawith foldsTail of pancreasPancreasGallbladderJejunumMajor duodenalpapillaMain pancreatic ductand sphincterHepatopancreaticampulla and sphincterDuodenumHead of pancreasFigure 23.21
91Liver: Microscopic Anatomy Liver lobulesHexagonal structural and functional unitsFilter and process nutrient-rich bloodComposed of plates of hepatocytes (liver cells)Longitudinal central vein
92(a)(b)LobuleCentral veinConnectivetissue septumFigure 23.25a, b
93Liver: Microscopic Anatomy Portal triad at each corner of lobuleBile duct receives bile from bile canaliculiPortal arteriole is a branch of the hepatic arteryHepatic venule is a branch of the hepatic portal veinLiver sinusoids are leaky capillaries between hepatic platesKupffer cells (hepatic macrophages) in liver sinusoids
94Hepatic macrophages in sinusoid walls Interlobular veins(to hepatic vein)Central veinSinusoidsBile canaliculiPlates ofhepatocytesBile duct (receivesbile from bilecanaliculi)Fenestratedlining (endothelialcells) of sinusoidsBile ductHepaticmacrophagesin sinusoid wallsPortal venulePortal triadPortal arteriolePortal vein(c)Figure 23.25c
95Liver: Microscopic Anatomy Hepatocyte functions (see MS Word Liver Functions for complete list)Process bloodborne nutrientsStore fat-soluble vitaminsPerform detoxificationProduce ~900 ml bile per dayStores glycogen
96Liver RegenerationThe regenerative ability of the liver is exceptional. It can regenerate to its former size even if 70% is removed.Liver cells secrete VEGF (Vascular Endothelial Growth Factor) which binds to specific receptors on endothelial cells lining the sinusoids.The endothelial cells proliferate and release other growth factors, such as hepatocyte growth factor (HGF) and interleukin 6.
97Yellow-green, alkaline solution containing BileYellow-green, alkaline solution containingBile salts: cholesterol derivatives that function in fat emulsification and absorptionBilirubin: pigment formed from hemeCholesterol, neutral fats, phospholipids, and electrolytes
99Enterohepatic circulation BileEnterohepatic circulationRecycles bile saltsBile salts duodenum reabsorbed from ileum hepatic portal blood liver secreted into bile
100The GallbladderThin-walled muscular sac on the ventral surface of the liverStores and concentrates bile by absorbing its water and ionsReleases bile via the cystic duct, which flows into the bile duct