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© 2013 Pearson Education, Inc. Surface epithelium Mucosa Lamina propria Muscularis mucosae Oblique layer Circular layer Longitudinal layer Submucosa (contains.

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Presentation on theme: "© 2013 Pearson Education, Inc. Surface epithelium Mucosa Lamina propria Muscularis mucosae Oblique layer Circular layer Longitudinal layer Submucosa (contains."— Presentation transcript:

1 © 2013 Pearson Education, Inc. Surface epithelium Mucosa Lamina propria Muscularis mucosae Oblique layer Circular layer Longitudinal layer Submucosa (contains submucosal plexus) Muscularis externa (contains myenteric plexus) Serosa Layers of the stomach wall Stomach wall Figure 23.15a Microscopic anatomy of the stomach.

2 © 2013 Pearson Education, Inc. Enteroendocrine cell Enlarged view of gastric pits and gastric glands Chief cell Parietal cell Mucous neck cells Surface epithelium (mucous cells) Gastric pits Gastric pit Gastric gland Figure 23.15b Microscopic anatomy of the stomach.

3 © 2013 Pearson Education, Inc. Figure 23.15c Microscopic anatomy of the stomach. Mitochondria Parietal cell Chief cell Enteroendocrine cell Location of the HCl-producing parietal cells and pepsin-secreting chief cells in a gastric gland HCI Pepsin Pepsinogen

4 © 2013 Pearson Education, Inc. Gastric Gland Secretions Parietal cell secretions –HCl  pH 1.5–3.5 denatures protein, activates pepsin, breaks down plant cell walls, kills many bacteria –Intrinsic factor Glycoprotein req for abs of vit B 12 in SI

5 © 2013 Pearson Education, Inc. Gastric Gland Secretions Chief cell secretions –Pepsinogen - inactive enzyme Activated to pepsin by HCl and by pepsin itself (a positive feedback mechanism) and milk protein by rennin in infants –Lipases Digest ~15% of lipids

6 © 2013 Pearson Education, Inc. Homeostatic Imbalance Gastritis –Inflammation caused by anything that breaches mucosal barrier Peptic or gastric ulcers –Erosions of stomach wall Can perforate  peritonitis; hemorrhage –Most caused by Helicobacter pylori bacteria –Some by NSAIDs

7 © 2013 Pearson Education, Inc. Figure Photographs of a gastric ulcer and the H. pylori bacteria that most commonly cause it. A gastric ulcer lesion H. pylori bacteria Bacteria Mucosa layer of stomach

8 © 2013 Pearson Education, Inc. Australia’s Barry Marshall, knew ulcers afflicted 10 % of all adults. In 1981 Marshall discovered the gut could be overrun by hardy, corkscrew-shaped bacteria Helicobacter pylori. Biopsying ulcers and culturing the organisms, Marshall traced not just ulcers but also stomach cancer to this gut infection. The cure, was readily available: antibiotics. But mainstream gastroenterologists were dismissive, holding on to the old idea that ulcers were caused by stress.Helicobacter pylori Unable to make his case in studies with lab mice (because H. pylori affects only primates) and prohibited from experimenting on people, he grew desperate. Finally he ran an experiment on the only human he could ethically recruit: himself. He took some H. pylori, stirred it into a broth, and drank it. As the days passed, he developed gastritis, the precursor to an ulcer: He started vomiting, his breath stunk and he felt sick. Back in the lab, he biopsied his own gut, culturing H. pylori and proving unequivocally that bacteria were the underlying cause of ulcers.underlying cause of ulcers.

9 © 2013 Pearson Education, Inc. Digestive Processes in the Stomach Lipid-soluble alcohol and aspirin absorbed into blood Only stomach function essential to life –Secretes intrinsic factor for vit B 12 abs Pernicious anemia, the body can't make enough RBCs because it doesn't have vit B12 to divide normally and are too large. They may have trouble getting out of bone marrow. You may feel tired and weak. Severe, long-lasting pernicious anemia can damage the heart, brain, and can cause nerve damage, neurological problems (such as memory loss), and digestive problems.

10 © 2013 Pearson Education, Inc. Regulation of Gastric Secretion Neural and hormonal mechanisms Gastric mucosa  up to 3 L gastric juice/day Vagus nerve stimulation  secretion  Sympathetic stimulation  secretion  Hormonal control largely gastrin –   Enzyme and HCl secretion –Most SI secretions - gastrin antagonists

11 © 2013 Pearson Education, Inc. Regulation of Gastric Secretion Three phases of gastric secretion –Cephalic (reflex) phase – conditioned reflex triggered by aroma, taste, sight, thought –Gastric phase – lasts 3–4 hours; ⅔ gastric juice released Stimulated by distension, peptides, low acidity, gastrin (major stimulus) Enteroendocrine G cells stimulated by caffeine, peptides, rising pH  gastrin

12 © 2013 Pearson Education, Inc. HCl Formation Parietal cells pump H + (from carbonic acid breakdown) into stomach lumen –K + goes into cells to balance charge –HCO 3 – from carbonic acid breakdown  blood (via Cl – and HCO 3 – antiporter)  blood leaving stomach more alkaline  Alkaline tide –Cl – (from blood plasma via antiporter) follows H +  HCl

13 © 2013 Pearson Education, Inc. HCI Parietal cell Interstitial fluid HCO 3 − - Cl − antiporter Alkaline tide H + -K + ATPase Stomach lumenChief cell Gastric gland H+H+ K+K+ CO 2 H2OH2O H 2 CO 3 + HCO 3 − H+H+ K+K+ Carbonic anhydrase HCO 3 − Blood capillary Cl − Figure Mechanism of HCl secretion by parietal cells.

14 © 2013 Pearson Education, Inc. Figure Deglutition (swallowing). Slide 4 Grinding: The most vigorous peristalsis and mixing action occur close to the pylorus. 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. 2 Propulsion: Peristaltic waves move from the fundus toward the pylorus. 1 3 Pyloric valve closed Pyloric valve closed Pyloric valve slightly opened

15 © 2013 Pearson Education, Inc. Regulation of Gastric Emptying As chyme enters duodenum –Receptors respond to stretch and chemical –Enterogastric reflex inhibit gastric secretion and duodenal filling Carb-rich chyme moves quickly through Fatty chyme remains duodenum 6 hrs or more

16 © 2013 Pearson Education, Inc. Presence of fatty, hypertonic, acidic chyme in duodenum Duodenal entero- endocrine cells Chemoreceptors and stretch receptors SecreteTarget Enterogastrones (secretin, cholecystokinin, vasoactive intestinal peptide) Via short reflexes Via long reflexes Duodenal stimuli decline Enteric neurons CNS centers sympathetic activity; parasympathetic activity Contractile force and rate of stomach emptying decline Initial stimulus Stimulate Inhibit Figure Neural and hormonal factors that inhibit gastric emptying. Physiological response Result

17 © 2013 Pearson Education, Inc. Homeostatic Imbalance Vomiting (emesis) caused by Extreme stretching Intestinal irritants, e.g., bacterial toxins, excessive alcohol, spicy food, certain drugs Chemicals/sensory impulses  emetic center of medulla Excessive vomiting  dehydration, electrolyte and acid-base imbalances (alkalosis)

18 © 2013 Pearson Education, Inc. Small Intestine: Gross Anatomy Major organ of digestion and absorption 2-4 m long; from pyloric sphincter to ileocecal valve (TI) Subdivisions –Duodenum (retroperitoneal) –Jejunum (attached posteriorly by mesentery) –Ileum (attached posteriorly by mesentery)

19 © 2013 Pearson Education, Inc. Duodenum Curves around head of pancreas; shortest part – 25 cm Bile duct and main pancreatic –Join at hepatopancreatic ampulla –Enter duodenum at duodenal papilla –Entry controlled by hepatopancreatic sphincter

20 © 2013 Pearson Education, Inc. Figure The duodenum of the small intestine, and related organs. Right and left hepatic ducts of liver Common hepatic duct Bile duct and sphincter Accessory pancreatic duct Tail of pancreas Pancreas Jejunum Main pancreatic duct and sphincter Head of pancreas Hepatopancreatic ampulla and sphincter Duodenum Mucosa with folds Gallbladder Major duodenal papilla Cystic duct

21 © 2013 Pearson Education, Inc. Jejunum and Ileum Jejunum –Extends from duodenum to ileum –About 2.5 m long Ileum –Joins large intestine at ileocecal valve –About 3.6 m long

22 © 2013 Pearson Education, Inc. Structural Modifications Increase surface area for nutrient abs –Circular folds (plicae circulares) –Villi - Microvilli (brush border) – contain enzymes for carbs and protein dig

23 © 2013 Pearson Education, Inc. Figure 23.22a Structural modifications of the small intestine that increase its surface area for digestion and absorption. Vein carrying blood to hepatic portal vessel Muscle layers Circular folds Villi Lumen

24 © 2013 Pearson Education, Inc. Microvilli (brush border) Absorptive cells Villus Lacteal Goblet cell Blood capillaries Mucosa- associated lymphoid tissue Intestinal crypt Muscularis mucosae Duodenal gland Enteroendocrine cells Venule Lymphatic vessel Submucosa Figure 23.22b Structural modifications of the small intestine that increase its surface area for digestion and absorption.

25 © 2013 Pearson Education, Inc. Homeostatic Imbalance Chemotherapy targets rapidly dividing cells –Kills cancer cells –Kills rapidly dividing GI tract epithelium  nausea, vomiting, diarrhea

26 © 2013 Pearson Education, Inc. Mucosa Peyer's patches protect against bacteria B lymphocytes leave intestine, enter blood, protect intestinal with IgA Duodenal glands of duodenum secrete alkaline mucus to neutralize acidic chyme

27 © 2013 Pearson Education, Inc. Intestinal Juice 1-2 L secreted d in response to distension or irritation of mucosa Slightly alkaline Largely water; enzyme-poor (enzymes of small intestine only in brush border); contains mucus

28 © 2013 Pearson Education, Inc. The Liver and Gallbladder Accessory organs Liver –Many functions; only digestive function  bile production Bile – fat emulsifier Gallbladder –Chief function  bile storage

29 Attorney General John Ashcroft was in intensive care after what he thought was a bout of stomach flu turned out to be a severe case of a pancreatic ailment. After complaining of stomach pain Ashcroft, 61, was taken to the ER His condition was diagnosed as ''a severe case'' of gallstone pancreatitis, which is an inflammation of the pancreas. The department did not specify which type the attorney general had, but gallstone pancreatitis is usually considered the less serious variety. © 2013 Pearson Education, Inc.

30 Physician Ron Shemenski 59, passed a gallstone and had pancreatitis. Subsequently the NYAir National Guard was mobilized for a medevac. Flights to the South Pole base are normally halted winter because of extreme cold with temp up to 75 degrees below zero.. But rescuers are worried that Dr Shemenski's condition could worsen in the coming months when an airlift would be virtually impossible. In October 1999, Dr Jerri Nielsen, the lone physician at the Amundsen-Scott Station was evacuated after she discovered a breast tumor that was diagnosed as cancerous. © 2013 Pearson Education, Inc.

31 Figure 23.25a–b Microscopic anatomy of the liver. Lobule Central vein Connective tissue septum

32 © 2013 Pearson Education, Inc. Liver: Microscopic Anatomy Liver sinusoids - leaky capillaries between hepatic plates Kupffer cells (hepatic or stellate macrophages) in liver sinusoids remove debris & old RBCs

33 © 2013 Pearson Education, Inc. Interlobular veins (to hepatic vein) Central vein Sinusoids Plates of hepatocytes Portal vein Stellate macrophages in sinusoid walls Bile canaliculi Bile duct (receives bile from bile canaliculi) Fenestrated lining (endothelial cells) of sinusoids Bile duct Portal venule Portal arteriole Portal triad Figure 23.25c Microscopic anatomy of the liver.

34 © 2013 Pearson Education, Inc. Liver: Microscopic Anatomy Hepatocytes – increased rough & smooth ER, Golgi, peroxisomes, mitochondria Hepatocyte functions –Process bloodborne nutrients –Store fat-soluble vitamins –Perform detoxification –Produce ~900 ml bile per day

35 © 2013 Pearson Education, Inc. Liver Regenerative capacity –Restores full size in 6-12 m after 80% removal –Injury  hepatocytes  growth factors  endothelial cell proliferation

36 © 2013 Pearson Education, Inc. Hepatitis –Usually viral infection, drug toxicity, wild mushroom poisoning Cirrhosis –Progressive, chronic inflammation from chronic hepatitis or alcoholism –Liver  fatty, fibrous  portal hypertension

37 © 2013 Pearson Education, Inc. Bile Yellow-green, alkaline solution containing –Bile salts - cholesterol derivatives that function in fat emulsification and absorption –Bilirubin - pigment formed from heme Bacteria break down in intestine to stercobilin  brown color of feces –Cholesterol, neutral fats, phospholipids, and electrolytes

38 © 2013 Pearson Education, Inc. Bile Enterohepatic circulation –Recycles bile salts –Bile salts  duodenum  reabsorbed from ileum  hepatic portal blood  liver  secreted into bile

39 © 2013 Pearson Education, Inc. The Gallbladder Stores and conc bile by abs water Muscular contractions release bile via cystic duct, which flows into bile duct

40 © 2013 Pearson Education, Inc.


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