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The Digestive System: Part B

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1 The Digestive System: Part B
23 The Digestive System: Part B

2 Oropharynx and laryngopharynx
Allow passage of food, fluids, and air Stratified squamous epithelium lining Skeletal muscle layers: inner longitudinal, outer pharyngeal constrictors

3 Esophagus Flat muscular tube from laryngopharynx to stomach Pierces diaphragm at esophageal hiatus Joins stomach at the cardiac orifice

4 Esophageal mucosa contains stratified squamous epithelium
Esophagus Esophageal mucosa contains stratified squamous epithelium Changes to simple columnar at the stomach Esophageal glands in submucosa secrete mucus to aid in bolus movement Muscularis: skeletal superiorly; smooth inferiorly Adventitia instead of serosa

5 (contains a stratified squamous epithelium)
Mucosa (contains a stratified squamous epithelium) Submucosa (areolar connective tissue) Lumen Muscularis externa • Longitudinal layer • Circular layer Adventitia (fibrous connective tissue) (a) Figure 23.12a

6 (contains a stratified squamous epithelium)
Mucosa (contains a stratified squamous epithelium) (b) Figure 23.12b

7 Go to GI Diseases (Esophagus)

8 Digestive Processes: Mouth
Ingestion Mechanical digestion Mastication is partly voluntary, partly reflexive Chemical digestion (salivary amylase and lingual lipase) Propulsion Deglutition (swallowing)

9 Pharyngeal-esophageal phase
Deglutition Involves the tongue, soft palate, pharynx, esophagus, and 22 muscle groups Buccal phase Voluntary contraction of the tongue Pharyngeal-esophageal phase Involuntary Control center in the medulla and lower pons

10 Figure 23.13 Bolus of food Tongue Uvula Pharynx Bolus Epiglottis
Trachea Bolus Esophagus Upper 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. 1 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. 2 The constrictor muscles of the pharynx contract, forcing food into the esophagus inferiorly. The upper esophageal sphincter contracts (closes) after entry. 3 Relaxed muscles Food is moved through the esophagus to the stomach by peristalsis. 4 Relaxed muscles The gastroesophageal sphincter opens, and food enters the stomach. 5 Circular muscles contract Bolus of food Longitudinal muscles contract Gastroesophageal sphincter closed Gastroesophageal sphincter opens Stomach Figure 23.13

11 Bolus of food Tongue Pharynx Epiglottis Glottis Trachea
1 Upper 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

12 Bolus 3 The 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

13 Uvula 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. 2 Figure 23.13, step 2

14 Food is moved through the esophagus to the stomach by peristalsis.
Relaxed muscles 4 Food is moved through the esophagus to the stomach by peristalsis. Circular muscles contract Bolus of food Longitudinal muscles contract Gastroesophageal sphincter closed Stomach Figure 23.13, step 4

15 The gastroesophageal sphincter opens, and food enters the stomach.
5 Relaxed muscles Gastroesophageal sphincter opens Figure 23.13, step 5

16 Figure 23.13 Bolus of food Tongue Uvula Pharynx Bolus Epiglottis
Trachea Bolus Esophagus Upper 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. 1 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. 2 The constrictor muscles of the pharynx contract, forcing food into the esophagus inferiorly. The upper esophageal sphincter contracts (closes) after entry. 3 Relaxed muscles Food is moved through the esophagus to the stomach by peristalsis. 4 Relaxed muscles The gastroesophageal sphincter opens, and food enters the stomach. 5 Circular muscles contract Bolus of food Longitudinal muscles contract Gastroesophageal sphincter closed Gastroesophageal sphincter opens Stomach Figure 23.13

17 Stomach: Gross Anatomy
Cardiac region (cardia) Surrounds the cardiac orifice Fundus Dome-shaped region beneath the diaphragm Body Midportion

18 Stomach: Gross Anatomy
Cardiac region (cardia) Surrounds the cardiac orifice Fundus Dome-shaped region beneath the diaphragm Body Midportion

19 Stomach: Gross Anatomy
Pyloric region: antrum, pyloric canal, and pylorus Pylorus is continuous with the duodenum through the pyloric valve (sphincter) Greater curvature Convex lateral surface Lesser curvature Concave medial surface

20 Cardia Fundus Esophagus Muscularis externa Serosa • Longitudinal layer
• Circular layer Body • Oblique layer Lumen Lesser curvature Rugae of mucosa Greater curvature Pyloric canal Pyloric antrum Duodenum Pyloric sphincter (valve) at pylorus (a) Figure 23.14a

21 Stomach: Gross Anatomy
Lesser omentum From the liver to the lesser curvature Greater omentum Drapes from greater curvature Anterior to the small intestine The 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.

22 Greater and Lesser Omentums

23 ANS nerve supply to stomach
Sympathetic via splanchnic nerves and celiac plexus Parasympathetic via vagus nerve

24 Blood supply to Stomach
Celiac trunk – branches go to liver, stomach, spleen, pancreas Veins of the hepatic portal system

25 (c) The hepatic portal circulation.
Inferior vena cava (not part of hepatic portal system) Gastric veins Hepatic veins Spleen Inferior vena cava Liver Splenic vein Right gastroepiploic vein Hepatic portal vein Inferior mesenteric vein Superior mesenteric vein Small intestine Large intestine Rectum (c) The hepatic portal circulation. Figure 19.29c

26 Celiac Trunk Figure 19.24a Abdominal aorta L. gastric artery Inferior
Diaphragm Abdominal aorta L. gastric artery Inferior phrenic arteries R. gastric artery Common hepatic artery Hepatic artery proper L Celiac Trunk Celiac trunk Gastro- duodenal artery Splenic artery R R. gastroepiploic artery Middle suprarenal arteries L. gastroepiploic artery Middle colic artery Intestinal arteries Superior mesenteric artery R. colic artery Renal arteries Ileocolic artery Gonadal arteries Sigmoidal arteries Inferior mesenteric artery L. colic artery Superior rectal artery Lumbar arteries Median sacral artery (a) Schematic flowchart. Common iliac arteries Figure 19.24a

27 Liver (cut) Diaphragm Inferior vena cava Esophagus Celiac trunk
Common hepatic artery Left gastric artery Hepatic artery proper Stomach Splenic artery Gastroduodenal artery Left gastroepiploic artery Right gastric artery Gallbladder Spleen Pancreas (major portion lies posterior to stomach) Right gastroepiploic artery Duodenum Superior mesenteric Abdominal aorta (b) The celiac trunk and its major branches. The left half of the liver has been removed. Figure 19.24b

28 The Ligamentum Teres Hepatis is the remnant of the umbilical vein
Falciform ligament Liver Gallbladder Spleen Stomach Ligamentum teres Greater omentum Small intestine Cecum (a) The Ligamentum Teres Hepatis is the remnant of the umbilical vein Figure 23.30a

29 Stomach: Microscopic Anatomy
Four tunics Muscularis and mucosa are modified Muscularis externa Three layers of smooth muscle Inner oblique layer allows stomach to churn, mix, move, and physically break down food

30 Liver Gallbladder Lesser omentum Stomach Duodenum Transverse colon
Small intestine Cecum Urinary bladder (b) Figure 23.30b

31 (a) Layers of the stomach wall (l.s.)
Surface epithelium Mucosa Lamina propria Muscularis mucosae Submucosa (contains submucosal plexus) Oblique layer Muscularis externa (contains myenteric plexus) Circular layer Longitudinal layer Serosa Stomach wall (a) Layers of the stomach wall (l.s.) Figure 23.15a

32 Stomach: Microscopic Anatomy
Mucosa Simple 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 it The smooth lining is lined with dotted Gastric pits that lead into gastric glands that produce the various gastric juices

33 The 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 cells Pyloric 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) Gastric pit Mucous neck cells Parietal cell Chief cell Gastric gland Enteroendocrine cell (b) Enlarged view of gastric pits and gastric glands Figure 23.15b

35 Gastric Glands Cell types
Mucous neck cells (secrete thin, acidic mucus) Parietal cells Chief cells Enteroendocrine cells

36 (c) Location of the HCl-producing parietal cells and
Pepsinogen Pepsin HCl Mitochondria Parietal cell Chief cell Enteroendocrine cell (c) Location of the HCl-producing parietal cells and pepsin-secreting chief cells in a gastric gland Figure 23.15c

37 Gastric Gland Secretions
Glands in the fundus and body produce most of the gastric juice Parietal cell secretions HCl  pH 1.5–3.5 denatures protein in food, activates pepsin, and kills many bacteria Intrinsic factor Glycoprotein required for absorption of vitamin B12 in small intestine

38 Gastric Gland Secretions
Chief cell secretions Inactive enzyme pepsinogen Activated to pepsin by HCl and by pepsin itself (a positive feedback mechanism) Chief cells also secrete insignificant amounts of gastric lipase

39 Gastric Gland Secretions
Enteroendocrine cells Secrete chemical messengers into the lamina propria Paracrines Serotonin and histamine Hormones Somatostatin and gastrin

40 Mucosal Barrier Layer of bicarbonate-rich mucus Tight junctions between epithelial cells Damaged 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

41 Homeostatic Imbalance
Gastritis: inflammation caused by anything that breaches the mucosal barrier Peptic or gastric ulcers: erosion of the stomach wall Most are caused by Helicobacter pylori bacteria Go to GI Diseases PowerPoint

42 (a) A gastric ulcer lesion (b) H. pylori bacteria
Mucosa layer of stomach (a) A gastric ulcer lesion (b) H. pylori bacteria Figure 23.16

43 Digestive Processes in the Stomach
Physical digestion Denaturation of proteins Enzymatic digestion of proteins by pepsin (and rennin in infants) Secretes intrinsic factor required for absorption of vitamin B12 Lack of intrinsic factor  pernicious anemia Delivers chyme to the small intestine

44 Regulation 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 Phase Neural (vagus and enteric plexus) and hormonal mechanisms control the secretions Cephalic (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

45 Gastric Phase Lasts approximately 3–4 hours after food enters the stomach Stimuli for this phase is gastric distention, peptides, and low acidity Gastric Distention activates stretch receptors and initiates both local (myenteric) reflexes and vagovagal – both stimulate acetylcholine release

46 Gastrin (1) Gastrin is secreted by G-cells in the Pyloric Antrum in accordance with chemical stimuli and neural stimuli The chemical stimuli for Gastrin secretion are partially digested proteins, caffeine, and rising alkaline pH. High acidity less than a pH of 2 inhibits Gastrin secretion Gastric 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

47 Gastrin (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

48 Gastrin (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 off The vagus was activated in the Cephalic Phase and Gastric Phase due to stomach distention Emotional upset, fear, anxiety, and anything that triggers the fight and flight response turns off Gastric secretion.

49 Figure 23.17 Stimulatory events Inhibitory events Sight and thought
of food 1 Cephalic phase Cerebral cortex Lack of stimulatory impulses to parasym- pathetic center Cerebral cortex Loss of appetite, depression 1 Conditioned reflex Stimulation of taste and smell receptors 2 Hypothalamus and medulla oblongata Vagus nerve Stomach distension activates stretch receptors 1 Vagovagal reflexes Medulla Vagus nerve Gastrin secretion declines G cells Excessive acidity (pH <2) in stomach 1 Gastric phase Local reflexes Overrides parasym- pathetic controls Sympathetic nervous system activation Emotional upset 2 Food chemicals (especially peptides and caffeine) and rising pH activate chemoreceptors 2 G cells Gastrin release to blood Stomach secretory activity Entero- gastric reflex Local reflexes Distension of duodenum; presence of fatty, acidic, hypertonic chyme, and/or irritants in the duodenum 1 Presence of low pH, partially digested foods, fats, or hypertonic solution in duodenum when stomach begins to empty 1 Intestinal (enteric) gastrin release to blood Vagal nuclei in medulla Brief effect Intestinal phase Pyloric sphincter Release of intestinal hormones (secretin, cholecystokinin, vasoactive intestinal peptide) Distension; presence of fatty, acidic, partially digested food in the duodenum 2 Stimulate Inhibit Figure 23.17

50 Regulation and Mechanism of HCl Secretion
Three chemicals (ACh, histamine, and gastrin) stimulate parietal cells through second-messenger systems All three are necessary for maximum HCl secretion Antihistamines block H2 receptors and decrease HCl release

51 Secondary 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.

52 Alkaline tide Inter- fluid
Blood capillary Chief cell Stomach lumen CO2 CO2 + H2O H+-K+ ATPase Carbonic anhydrase H2CO3 H+ H+ K+ K+ HCO3– HCI Alkaline tide Parietal cell HCO3– Cl– Cl– Cl– l HCO3–- Cl– antiporter Inter- stitial fluid Figure 23.18

53 Regulation 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 inhibitory As 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.

54 The 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 reflex The 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.

55 Response of the Stomach to Filling
Stretches to accommodate incoming food Reflex-mediated receptive relaxation Coordinated by the swallowing center of the brain stem and mediated by the vagus nerves acting on Serotonin and Nitric Oxide releasing enteric neurons Gastric accommodation Plasticity (stress-relaxation response) of smooth muscle

56 Small rippling waves in the body and fundus of stomach where good (food storage) chemical digestion occur Waves 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.

57 Gastric 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.

58 The 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.

59 Gastric Contractile Activity
Most vigorous near the pylorus Chyme is either Delivered in ~ 3 ml spurts to the duodenum, or Forced backward into the stomach

60 Propulsion: Peristaltic waves move from the fundus toward the pylorus.
Pyloric valve closed Pyloric valve closed Pyloric valve slightly opened Propulsion: Peristaltic waves move from the fundus toward the pylorus. 1 Grinding: The most vigorous peristalsis and mixing action occur close to the pylorus. 2 Retropulsion: The pyloric end of the stomach acts as a pump that delivers small amounts of chyme into the duodenum, simultaneously forcing most of its contained material backward into the stomach. 3 Figure 23.19

61 Regulation 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 more The 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 duodenum Receptors respond to stretch and chemical signals Enterogastric reflex and enterogastrones inhibit gastric secretion and duodenal filling Carbohydrate-rich chyme moves quickly through the duodenum Fatty chyme remains in the duodenum 6 hours or more

62 Gastric Emptying Carbohydrate-rich chyme moves quickly through the duodenum Fatty chyme remains in the duodenum 6 hours or more

63 Presence of fatty, hypertonic, acidic chyme in duodenum
Duodenal entero- endocrine cells Chemoreceptors and stretch receptors Secrete Target Enterogastrones (secretin, cholecystokinin, vasoactive intestinal peptide) Via short reflexes Via long reflexes Enteric neurons CNS centers sympathetic activity; parasympathetic activity Duodenal stimuli decline Contractile force and rate of stomach emptying decline Initial stimulus Physiological response Stimulate Result Inhibit Figure 23.20

64 Vomiting 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.

65 Gastroparesis Gastroparesis, 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.

66 Causes Gastroparesis 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.

67 Small Intestine: Gross Anatomy
Major organ of digestion and absorption 2–4 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) Subdivisions Duodenum (retroperitoneal) 10 inches Jejunum (attached posteriorly by mesentery) 8 feet Ileum (attached posteriorly by mesentery) 12 feet

68 The 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

69 Parotid gland Mouth (oral cavity) Sublingual gland Salivary glands
Tongue Submandibular gland Pharynx Esophagus Stomach Pancreas (Spleen) Liver Gallbladder Transverse colon Duodenum Descending colon Small intestine Jejunum Ascending colon Ileum Cecum Large intestine Sigmoid colon Rectum Vermiform appendix Anus Anal canal Figure 23.1

70 The bile duct and main pancreatic duct
Duodenum The bile duct and main pancreatic duct Join at the hepatopancreatic ampulla Enter the duodenum at the major duodenal papilla Are controlled by the hepatopancreatic sphincter

71 Bile duct and sphincter Accessory pancreatic duct
Right and left hepatic ducts of liver Cystic duct Common hepatic duct Bile duct and sphincter Accessory pancreatic duct Mucosa with folds Tail of pancreas Pancreas Gallbladder Jejunum Major duodenal papilla Main pancreatic duct and sphincter Hepatopancreatic ampulla and sphincter Duodenum Head of pancreas Figure 23.21

72 Structural Modifications
Increase surface area of proximal part for nutrient absorption Circular folds (plicae circulares) 1 cm tall – permanent folds of mucosae and submucosa Villi – 1 mm high Microvilli

73 Structural Modifications
Circular folds Permanent (~1 cm deep) Force chyme to slowly spiral through lumen

74 Vein carrying blood to hepatic portal vessel Muscle layers Lumen
Circular folds Villi (a) Figure 23.22a

75 Structural Modifications
Villi (gives a velvety look) Motile fingerlike extensions (~1 mm high) of the mucosa Villus epithelium Simple columnar absorptive cells (enterocytes) Goblet cells In the core of each villus is a dense capillary bed and a wide lymph capillary called a lacteal.

76 The 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.

77 Structural Modifications
Microvilli Projections (brush border) of absorptive cells Bear brush border enzymes – these enzymes complete the digestive process

78 Histology of Intestinal Wall
Epithelium of the villus is largely simple columnar absorptive cells bound by tight junctions and richly endowed with microvilli. Goblet cells Between the villi are intestinal pits that lead into tubular glands called intestinal crypts – also known as the crypts of Lieberkühn.

79 Intestinal 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 chyme Enteroendocrine 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 cytokines Release cytokines that kill infected cells Paneth cells – release defensins and lysozyme Stem cells – can differentiate – become specialized absorptive cells, goblet cells, and enteroendocrine cells.

80 The 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 base The crypts decrease in number along the length of the small intestine, but the goblet cells become more abundant.

81 Microvilli (brush border) Absorptive cells Lacteal Goblet cell Blood
capillaries Vilus Mucosa associated lymphoid tissue Enteroendocrine cells Intestinal crypt Venule Muscularis mucosae Lymphatic vessel Duodenal gland Submucosa (b) Figure 23.22b

82 Submucosa Typical areolar connective tissue Contains individual and aggregated lymphoid follicles Peyer’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

83 Submucosal Duodenal Glands
Duodenal (Brunner’s) glands of the duodenum secrete alkaline mucus The glands help neutralize acidic chyme moving in from the stomach When this protection is absent or insufficient – duodenal ulcers can occur The 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

84 Intestinal Juice Normally secrete 1 to 2 ml of intestinal juice daily – that facilitates transport and absorption of nutrients Secreted in response to distension or irritation of the mucosa by hypertonic or acidic chyme. Slightly alkaline (7.4 – 7.8) and isotonic with blood plasma Largely 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

85 Liver Largest gland in the body Four lobes—right, left, caudate, and quadrate

86 Round ligament (ligamentum teres)
Liver Falciform ligament Separates the (larger) right and (smaller) left lobes Suspends liver from the diaphragm and anterior abdominal wall Round ligament (ligamentum teres) Remnant of fetal umbilical vein along free edge of falciform ligament

87 Sternum Bare area Nipple Falciform Liver ligament Left lobe of liver
Right lobe of liver Round ligament (ligamentum teres) Gallbladder (a) Figure 23.24a

88 Sternum Nipple Liver Bare area Lesser omentum (in fissure)
Caudate lobe of liver Left lobe of liver Sulcus for inferior vena cava Porta hepatis containing hepatic artery (left) and hepatic portal vein (right) Hepatic vein (cut) Bile duct (cut) Right lobe of liver Quadrate lobe of liver Gallbladder Ligamentum teres (b) Figure 23.24b

89 Liver: Associated Structures
Lesser omentum anchors liver to stomach Hepatic artery and vein at the porta hepatis Bile ducts Common hepatic duct leaves the liver Cystic duct connects to gallbladder Bile duct formed by the union of the above two ducts

90 Bile duct and sphincter Accessory pancreatic duct
Right and left hepatic ducts of liver Cystic duct Common hepatic duct Bile duct and sphincter Accessory pancreatic duct Mucosa with folds Tail of pancreas Pancreas Gallbladder Jejunum Major duodenal papilla Main pancreatic duct and sphincter Hepatopancreatic ampulla and sphincter Duodenum Head of pancreas Figure 23.21

91 Liver: Microscopic Anatomy
Liver lobules Hexagonal structural and functional units Filter and process nutrient-rich blood Composed of plates of hepatocytes (liver cells) Longitudinal central vein

92 (a) (b) Lobule Central vein Connective tissue septum Figure 23.25a, b

93 Liver: Microscopic Anatomy
Portal triad at each corner of lobule Bile duct receives bile from bile canaliculi Portal arteriole is a branch of the hepatic artery Hepatic venule is a branch of the hepatic portal vein Liver sinusoids are leaky capillaries between hepatic plates Kupffer cells (hepatic macrophages) in liver sinusoids

94 Hepatic macrophages in sinusoid walls
Interlobular veins (to hepatic vein) Central vein Sinusoids Bile canaliculi Plates of hepatocytes Bile duct (receives bile from bile canaliculi) Fenestrated lining (endothelial cells) of sinusoids Bile duct Hepatic macrophages in sinusoid walls Portal venule Portal triad Portal arteriole Portal vein (c) Figure 23.25c

95 Liver: Microscopic Anatomy
Hepatocyte functions (see MS Word Liver Functions for complete list) Process bloodborne nutrients Store fat-soluble vitamins Perform detoxification Produce ~900 ml bile per day Stores glycogen

96 Liver Regeneration The 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.

97 Yellow-green, alkaline solution containing
Bile Yellow-green, alkaline solution containing Bile salts: cholesterol derivatives that function in fat emulsification and absorption Bilirubin: pigment formed from heme Cholesterol, neutral fats, phospholipids, and electrolytes

98

99 Enterohepatic circulation
Bile Enterohepatic circulation Recycles bile salts Bile salts  duodenum  reabsorbed from ileum  hepatic portal blood  liver  secreted into bile

100 The Gallbladder Thin-walled muscular sac on the ventral surface of the liver Stores and concentrates bile by absorbing its water and ions Releases bile via the cystic duct, which flows into the bile duct


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