27 digestion 2
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Transcript of 27 digestion 2
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Digestion 2: Mouth through Stomach
Chapter 20; pages 570 - 581
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Salivary Glands: Fig 20.9
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Salivary Glands
• Parotid
– amylase (ptyalin)
– 1 - 4 hexose linkages
• Submaxillary & Sublingual
–mucin (protein for lubrication)
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Fig 5.3: Review of Sugar Structure
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– linkage
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Starch: 1 – 4 & 1 – 6 linkages
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Cellulose: 1 – 4 linkages
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Salivary Glands
Acinus type glands:
Primary secretion by secretory cells and then modified by duct cells as saliva passes through on the way to the oral cavity
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Accessory Gland Structure: Fig 20.8
Na+
K+ <--
Cl-
<-- HCO3-
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Saliva
• As saliva flows down duct:
–[Na+] and [Cl-] decrease
–[HCO3-] and [K+] increase
– also decreases - hypotonic• As flow rates increase, this exchange is
less complete
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Salivary pH
• Saliva pH is basic (vs. plasma pH)
• WHY?? (i.e., for what purpose?)
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Excitatory Signal Molecules
• ACh from Parasympathetic NS onto muscarinic receptors
• VIP from enteric NS
• Increased blood flow in response to kininogen activation
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Kininogen Activation
• Glands release Kallikrein when activated – acts on a kininogen, a plasma globulin
• Results cleavage forming a peptide --> bradykinin
• Bradykinin ---> local vasodilation (10X increase in BF)
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Other Components of Saliva
• Muramidase --> cleave muramic acid in bacterial cell walls
• Lactoferrin --> binds Fe++
• Epidermal growth factor --> stimulates mucosal cell growth
• IgA• Lingual lipase (small amounts)• ABO antigens (secreters)
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Salivary Secretion
• Cephalic Phase–Thought or sensory input
• Gastric Phase–Distention
–Secretagogues
–Vagal - Vagal reflex
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Fig 20.29Fig 20.29
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Stomach; Figure 20.4
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Stomach Mucosal Surface:
Folds are called
Rugae gastricae
Achalasia: failure to open esophageal sphincter
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History Lesson:
Alexis St. Martin
and
William Beaumont
http://www.james.com/beaumont/dr_life.htm
http://www.guineapigzero.com/AlexisStMartin.html
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Dr. William Beaumont
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Beaumont & St. Martin
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Stomach; Figure 20.4
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Oxyntic Glands
• Surface Epithelium - insoluble mucous
• Neck Cells - soluble mucous
• G cells - gastrin
• Parietal (or oxyntic) Cells - HCl & Intrinsic Factor
• Chief Cells - pepsinogen
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Gastric Acid Secretion: Fig 20.22
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Postprandial
Alkaline Tide
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http://en.wikipedia.org/wiki/File:Control-of-stomach-acid-sec.png
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Histamine
• From enterochromafin-like cells (ECL cells) in the gastric mucosa
• produce, store, & release histamine
• activated by ACh, gastrin, & secretagogues
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Treatment of Hyperacidity
• Atropine
•Antihistamine (H2 antagonists)–Cimetidine
•Proton pump inhibitors–Nexium
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Pepsin
• Pepsinogen ---> pepsin in acidic conditions of stomach
• It is a family of endopeptidases
• pH optima 1.8 - 3.5
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Activation of Pepsin; Fig 20.14Activation of Pepsin; Fig 20.14
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Three Different Pepsins
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Vitamin B12
• aka, cyanocobalamin• required for nucleic
acid synthesis • is very labile in acid
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Haptocorrin & Intrinsic Factor
• Haptocorrin (transcobalamin) made in salivary glands
• binds Vitamin B12 very tightly
• protects it from gastric acid digestion
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Haptocorrin
http://en.wikipedia.org/wiki/Haptocorrin
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Haptocorrin
• Haptocorrin is digested by pancreatic proteolytic enzymes in the duodenum
• Vit B12 now binds to Intrinsic Factor (IF)
• The B12 – IF complex is taken up by endocytosis in the duodenum
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Intrinsic Factor
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Secretagogues
• caffeine and theophylline
• peptides
• spices
• Alcohol
• aspirin
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Digestion Review:
• ANS and enteric nervous system
• Smooth muscle structure - function
• Saliva and regulation of flow
• Stomach secretions
• On to regulation of gastric secretion and motility (emptying)…….
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Table 20.2 Gastrointestinal Hormones
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Hormones: GastrinHormone Site of secretion Stimuli Actions
Gastrin Stomach Protein digestion products in stomach, distention, and parasympathetic input
Stimulates gastric secretion & motility, relaxes ileocecal sphincter, stimulates mass movement of colon
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Hormones: Cholecystokinin (CCK)
Hormone Site of secretion Stimuli Actions
CCK Duodenum and jejunum
Fat or protein digestion products in Duodenum
Inhibits gastric secretion & motility, potentiates secretin action, stimulates pancreatic enzyme secretion, stimulates bile secretion, and contracts bile duct and gall bladder
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Hormones: SecretinHormone Site of secretion Stimuli Actions
Secretin Duodenum and jejunum
Acid in duodenum
Inhibits gastric secretion & motility, stimulates pancreatic HCO3
- secretion, potentiates actions of CCK, and stimulates bile secretion by liver
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Hormones: GIP(glucose-dependent insulinotropic peptide)
Hormone Site of secretion Stimuli Actions
GIP Duodenum and jejunum
Glucose, fats or acid in duodenum and distention of the duodenum
Inhibits gastric secretion & motility, stimulates insulin secretion by the pancreas
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Contol of G.I. Function: Fig. 21.21
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GASTRIN
• Peptide hormone
• From G cells (stomach)
• Increases HCL & pepsinogen secretion
• Increases gastric motility and emptying into duodenum
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Gastric Acid Secretion:Cephalic Phase Fig 20.23a
• Thought of food, smell, chewing, swallowing
• Vagus nerve to parietal cells (ACh)
• Vagus nerve (ACh) onto G cells & thus causes gastrin release
• See TABLE 20.2 !!!!!
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Fig 20.23aCephalic Phaseof GastricSecretion
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Fig 20.23bGastric Phaseof GastricSecretion
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Gastric Acid Secretion:Intestinal Phase
• Stimulus - digested peptides, peptides in duodenum, distention
• G cells (gastrin)
• distention -->Intestinal endocrine cells release CCK, Secretin, & GIP
• see Table 20-2
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Inhibition of Gastric Secretion
• Important for protection of duodenum
• Acid in duodenum ---> secretin & CCK---> inhibits gastric secretion and motility
See Table 20.2 for sure !!!
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Inhibition of Gastric Secretion
• Acid, fats, hyper-osmotic solutions in the duodenum ---> release of enterogastrones ---> inhibit gastric motility and secretion
• Gastric Inhibitory Peptide or Glucose-dependent Insulinogenic Peptide (GIP) from duodenum ---> inhibits parietal cell function– Decreases release of acid, motility, & secretion– Increases release of insulin from pancreas
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• Ulcers - page 576
–Peptic & Duodenal–Role of Helicobacter pylori
• Vomit reflex - page 599
–Note sympathetic symptoms