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Digestive System Part 3 Honors Anatomy & Physiology Chapter 23
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© 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 small intestine secretions - gastrin antagonists
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© 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
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© 2013 Pearson Education, Inc. Stimuli of Gastric Phase Gastrin enzyme and HCl release Low pH inhibits gastrin secretion (as between meals) Buffering action of ingested proteins rising pH gastrin secretion Three chemicals - ACh, histamine, and gastrin - stimulate parietal cells through second-messenger systems All three are necessary for maximum HCl secretion
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© 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
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© 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 23.18 Mechanism of HCl secretion by parietal cells.
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© 2013 Pearson Education, Inc. Regulation of Gastric Secretion Intestinal phase Stimulatory component Partially digested food enters small intestine brief intestinal gastrin release Inhibitory effects ( enterogastric reflex and enterogastrones) Chyme with H +, fats, peptides, irritating substances inhibition
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© 2013 Pearson Education, Inc. Enterogastric Reflex Three reflexes act to Inhibit vagal nuclei in medulla Inhibit local reflexes Activate sympathetic fibers tightening of pyloric sphincter no more food entry to small intestine Decreased gastric activity protects small intestine from excessive acidity
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© 2013 Pearson Education, Inc. Intestinal Phase Enterogastrones released Secretin, cholecystokinin (CCK), vasoactive intestinal peptide (VIP) All inhibit gastric secretion If small intestine pushed to accept more chyme dumping syndrome Nausea and vomiting Common in gastric reduction for weight loss
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© 2013 Pearson Education, Inc. Figure 23.17 Neural and hormonal mechanisms that regulate release of gastric juice. Lack of stimulatory impulses to parasym- pathetic center Gastrin secretion declines Overrides parasym- pathetic controls Sympathetic nervous system activation Cerebral cortex G cells Emotional stress Excessive acidity (pH < 2) in stomach Loss of appetite, depression Entero- gastric reflex Local reflexes Pyloric sphincter Vagal nuclei in medulla Distension of duodenum; presence of fatty, acidic, or hypertonic chyme; and/or irritants in the duodenum Release of enterogastrones (secretin, cholecystokinin, vasoactive intestinal peptide) Distension; presence of fatty, acidic, partially digested food in the duodenum Intestinal (enteric) gastrin release to blood Brief effect Gastrin release to blood Vagus nerve Vagus nerve Conditioned reflex Local reflexes Vagovagal reflexes G cells Presence of partially digested foods in duodenum or distension of the duodenum when stomach begins to empty Stimulate Inhibit Hypothalamus and medulla oblongata Cerebral cortex Medulla Stomach distension activates stretch receptors Food chemicals (especially peptides and caffeine) and rising pH activate chemoreceptors Stimulation of taste and smell receptors Sight and thought of food 1 1 2 1 2 1 2 1 2 1 Stimulatory events Inhibitory events Cephalic phase Gastric phase Intestinal phase Stomach secretory activity
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© 2013 Pearson Education, Inc. Gastric Contractile Activity Peristaltic waves move toward pylorus at rate of 3 per minute Basic electrical rhythm (BER) set by enteric pacemaker cells (formerly interstitial cells of Cajal) Pacemaker cells linked by gap junctions entire muscularis contracts Distension and gastrin increase force of contraction
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© 2013 Pearson Education, Inc. Gastric Contractile Activity Most vigorous near pylorus Chyme is either Delivered in ~3 ml spurts to duodenum, or Forced backward into stomach
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© 2013 Pearson Education, Inc. Figure 23.19 Deglutition (swallowing). Slide 1 Grinding: The most vigorous peristalsis and mixing action occur close to the pylorus. The pyloric end of the stomach acts as a pump that delivers small amounts of chyme into the duodenum. Retropulsion: The peristaltic wave closes the pyloric valve, forcing most of the contents of the pylorus backward into the stomach. 2 Propulsion: Peristaltic waves move from the fundus toward the pylorus 13 Pyloric valve closed Pyloric valve slightly opened Pyloric valve closed
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© 2013 Pearson Education, Inc. Regulation of Gastric Emptying As chyme enters duodenum Receptors respond to stretch and chemical signals Enterogastric reflex and enterogastrones inhibit gastric secretion and duodenal filling Carbohydrate-rich chyme moves quickly through duodenum Fatty chyme remains in duodenum 6 hours or more
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© 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 23.20 Neural and hormonal factors that inhibit gastric emptying. Physiological response Result
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© 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)
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© 2013 Pearson Education, Inc. Intestinal Juice 1-2 L secreted daily in response to distension or irritation of mucosa Slightly alkaline; isotonic with blood plasma Largely water; enzyme-poor (enzymes of small intestine only in brush border); contains mucus Facilitates transport and absorption of nutrients
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Large Intestine “colon” larger in diameter but shorter than small intestine (which it “frames”) functions: 1. dry out indigestible food residue by absorbing water 2. elimination
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Parts of the Large Intestine Cecum Appendix Colon Ascending Transvere Descending Rectum Anal Canal
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Cecum sack-like 1 st part of large intetine site of ileoceal valve: empties chyme into large intestine from small intestine
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Appendix Vermiforme appendix vestigial organ easily twists small amounts food & bacteria get trapped appendicitis
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Signs of Appendicitis
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Appendicitis
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Appendectomy
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Colon
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Colonoscopy
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Colon Descending colon enters pelvis in LLQ where it becomes S-shaped = sigmoid colon
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Rectum
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Wall of the Colon muscularis externa’s longitudinal layer in 3 bands called teniae coli “ribbons of the colon” are normally partially contracted colon wall puckers forming haustra
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Histology of Colon no villi (absorption mostly in small intestine) many Goblet cells mucus (aids movement of feces)
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Rectum storage area for feces
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Anal Canal 2 sphincters: 1. external sphincter skeletal muscle (voluntary) 2. internal sphincter smooth muscle (involuntary)
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