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95 Cards in this Set
- Front
- Back
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Mastication (Chewing)
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Mastication (chewing)
• Breaks food into smaller pieces o Mixes food with salina o Brings food into contact with taste receptors and releases odors • Taste buds on tongue and soft palate contain gustatory cells • Olfactory nerves of olfactory bulb (CN I, cribriform plate) provides smell |
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Saliva
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* Secreted by the parotid, sublingual and submandibular glands
* 0.5-1L.day |
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Saliva Content
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* Enzymes (ex. alpha amylase, lipase)
* Electrolytes * Proteins (ex. mucin) |
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Saliva Control
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Secretion controlled by autonomic nerves:
* Parasympathetic discharge: large volume of watery saliva with high [electrolytes] and low [protein] * Sympathetic discharge: small volume, thick fluid, high [mucus] |
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Saliva Control continued...
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Stimulated by: conditioning, food, nausea, smell
Inhibited by: dehydration, fear, sleep, anticholinergic drugs * Anticholinergic drugs (ex. atropine) inhibit parasympathetic Ach release and thus causes the side effect of dry mouth |
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Deglutition (Swallowing) - Oral phase
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* Oral (voluntary) phase
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Deglutition - Pharyngeal phase
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Pharyngeal phase
* Nasopharynx is closed by the soft palate and uvula * Glottis and vocal cords close * Epiglottis moves down over larynx and closes airway |
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Deglutition - Esophageal phase
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Esophageal phase
* Food bolus is propelled into the stomach by peristalsis * Peristalsis is controlled by vagal fibers |
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GI Tract - Mucosa Layer
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CT lined with epithelial cells (enterocytes) that perform secretion and absorption
enterocytes - columnar epithelial cells that line the gi tract and are secretory |
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GI Tract - Muscularis Mucosa Layer
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Thin smooth muscle later that contracts to alter surface area for secretion and absorption
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GI Tract - Circular Muscle Layer
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Decrease GI tract lumen diameter
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GI Tract - Longitudinal Muscle Layer
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Causes shortening of GI tract segments
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GI Tract - Submucous (Meissner's) and Myenteric (Auerbach's) Plexus
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Enteric nervous system
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GI Tract Innervation - Intrinsic control
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Enteric nervous system:
Coordinates input from ANS Provides local and regional control |
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GI Tract Innervation - Extrinsic Control
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ANS:
Provides overall gross stimulation or inhibition |
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Intrinsic Innervation (enteric nervous system)
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Myenteric (Auerbach's) Plexus
* Lies btwn circular and longitudinal muscles * Primarily controls motility Submucous (Meissner's) Plexus * Lies btwn circular muscle and mucosa * Primarily controls secretion and blood flow |
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Extrinsic Innervation - Parasympathetic nervous system
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Vagus and pelvic nerves discharges increase motility
Vagus innervates: esophagus, stomach, pancreas, small intestine, and proximal large intestine Pelvic nerves innervate: distal large intestine, rectum and anus |
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Extrinsic Innervation - Sympathetic nervous system
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Decrease motility
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Esophagus
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• Upper esophageal sphincter (cricopharyngeal muscle) is a true anatomic sphincter
• Proximal 1/3 is striated muscle • Distal 2/3 is smooth muscle • Lower esophageal (Cardiac) sphincter (LES) is NOT a true anatomic sphincter o Opens during peristalsis |
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Stomach - Fundus
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Enlarges to store 1-2L of food
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Stomach - Body (corpus)
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In the presence of food peristalsis and retropulsion is increased
(retropulsion - propels food backwards to keep circulating movement |
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Stomach - Antrum
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Secretes gastrin
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Stomach - Pylorus and Pyloric Sphincter
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Separates stomach and duodenum
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Stomach - Gastric mucosa
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Mucosal barrier that protects stomach from autodigestion
Major component is mucus (a thick viscous alkaline secretion) Mucosal cells have a high turnover rate and the entire mucosa is replaced in 1-3 days |
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Stomach - Digestion and Absorption
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Minimal in the stomach
Major function: break food into smaller bit and mix it with secretions (chyme - food particles. bile, fluids...) |
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Gastric Motility - Peristalsis
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Initiated by pacemaker cells in the greater curvature
Peristaltic wave velocity increases as it approaches antrum and pylorus Chyme: propelled into the duodenum via pyloric sphincter |
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Gastric Emptying Regulation - Local Reflexes
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Excitatory impulses from antral expansion increase gastric motility
Food with high or low osmolality or pH and fat or protein digestion products causes gastric reflex inhibition |
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Gastric Emptying Regulation - Migrating Motor (Myoelectric) Complex
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Peristaltic wave beginning in esophagus and travels thru entire GI tract every 60-90 min btwn digestive periods
Removes remaining food in GI tract |
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Gastric Emptying Regulation Hormones - Gastrin
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Antral distention causes gastrin release by G cells
Increases gastric motility |
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Gastric Emptying Regulation Hormones - Cholecystokinin (CCK)
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Released by duodenal and jejunal I cells in response to fat or protein digestion
Decreases gastric motility |
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Gastric Emptying Regulation Hormones - Secretin
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Released bu duodenal S cells in response to acid
Decreases gastric motility |
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Gastric Emptying Regulation Hormones - Glucose dependent insulinotropic peptide (gastric inhibitory peptide - GIP)
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Released by duodenal/jejunal K cells
Decrease HCl secretion Increase insulin secretion |
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Aberrant Gastric Emptying - Vomiting (Emesis)
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Forceful expulsion of food from the stomach
Triggered by activation of: * Vomiting center in the medulla * Chemoreceptor trigger zone within the floor of the 4th ventricle |
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Aberrant Gastric Emptying - Vomiting Center
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Activated by
* Gagging * Irritation secondary to injury * Increased intracranial pressure All can cause projectile vomiting without nausea |
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Aberrant Gastric Emptying - Chemoreceptor Trigger Zone (CTZ)
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Activated by:
* Afferent nerves from GI tract (ex. pancreatitis or appendicitis) * Circulating emetic agents (ex. morphine) All can cause vomiting with nausea |
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Gastric Secretions
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Approx 2L/day
Increased by thought, sight, taste or smell of food and stomach distention |
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HCl
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Functions:
* Secreted by parietal cells * Breaks down proteins * Provides pH optimum for pepsin * Decrease growth of pathogenic bacteria |
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HCl Secretion
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K+ and Cl- transported out of parietal cells into gastric lumen
H+ exchanged for K+ by the H+-K+-ATPase pump Parietal cell H+ comes from dissociation of H2CO3 HCO3- is reabsorbed by the ECF in exchange for Cl - ("alkaline tide" - increased blood pH during acid production) |
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HCl Formation
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Stimulated by:
* Ach (vagus nerve) * Gastrin * Histamine (produced by enterochromaffin-like cells - ELC) * Ingested protein, ETOH, caffeine and NSAIDs |
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HCl Formation
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Inhibited by:
* Prostaglandins (ingest or given in a med) * Somatostatin * Gastric Inhibitory Peptide (GIP) |
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HCl Formation - Pharmacological Inhibition
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H2-receptor antagonists (ex. cimetidine and ranitidine)
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HCl Formation - Pharmacological Inhibition
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Proton-pump inhibitors (ex. omeprazole - Prilosec)
* irreversibly blocks H+-K+ ATPase pump |
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HCl Formation - Pharmacological Inhibition
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Prostaglandins (ed. misoprostol - Cytotec)
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HCl Formation - Pharmacological Inhibition
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Acetazolamide - a carbonic anhydrase inhibitor (not really used clinically)
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Pepsinogen
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Secreted by chief cells
Converted to pepsin in acidic pH Begins: protein digestion |
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Gastrin
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Secreted by G cells
Stimulates HCl Secretion Increases gastric and intestinal motility Increases pancreatic secretions (gastrinoma = increase acid production, erosion, gastritis) |
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Intrinsic Factor
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Glycoprotein produced by parietal cells (in the antrum)
Required for ileum absorption of Vitamin B12 (cyanocobalamin) |
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"Gut-Brain Axis"
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Neurohormonal pathways that balance homeostasis and behavior
Control satiety |
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Leptin
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Produced by adipose tissue and binds to receptors in the hypothalamus
Binds to "satiety" center and this regulates energy intake and expenditure [Leptin] is proportional to body fat |
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Small Intestine
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Major site of digestion and asborption of CH2O, proteins and fats
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Small Intestine - Motility
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Smooth muscle contraction mixes chyme with digestive juices and bile
Propels chyme from duodenum to colon (2-4hrs) |
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Small Intestine - Duodenum
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Superior, descending, inferior and ascending portions
Retroperitoneal Structure Ligament of Treitz: anatomic cut-off point for upper vs. lower GI bleeding |
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Small Intestine - Ligament of Treitz
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Suspensory muscle of the duodenum
Upper GI bleeding: hematemesis and melena Lower GI bleeding: hematochezia |
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Small Intestine - Jejunum
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Contains large and thickened circular folds (plica circularis)
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Small Intestine - Ileum
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Contains "M(G)ALT": Mucosa (Gut)-Associated Lymphoid Tissue
Peyer's patches: aggregations of lymph nodes |
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Small Intestine - Villi
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Luminal surface covered with villi
Villus contains: * Arteriole becomes a capillary bed at the tip of the villus * Venule eventually drains into portal vein carries absorbed nutrients to the liver * Lymphatic branch (lacteal) extends from villus tip and carries absorbed fats to the thoracic duct |
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Small Intestine - Villi
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Each villus is covered with enterocytes (intestinal epithelium)
Enterocytes project microvilli into the lumen brush border Microvilli contain: peptides and disaccharidases (brush border enzymes) Enterocytes also secrete water and electrolytes to aid in digestion |
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Small Intestine - Stem Cell Niche
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Microenvironments contain stem cells for lifelong need of differentiated cells
Stem cells regenerate entire villus every 3-5 days |
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Small Intestine - CH2O Digestion
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To be absorbed, CH2Os must be digested to monosaccharides
Digestive enzymes include: * alpha-amylase * brush border enzymes |
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Small Intestine - Protein Digestion
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To be absorbed, proteins must be digested to amino acids, di/tri-peptides
Digestive enzymes include: * Pancreatic proteases * Peptidases * Pepsin |
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Small Intestine - Lipid Digestion
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Bile acids emulsify fats
* Increase surface area for digestion Lipids are digested into FA, monoglycerides and cholesterol |
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Small Intestine - Lipid Digestion
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Digestive enzymes include:
Pancreatic lipase Cholesterol ester hydrolase Phospholipase A2 |
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Small Intestine - Fatty Acids (FA)
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FA are absorbed thru intestinal enterocyte with help of bile salts
FA converted to TG and packaged into chylomicrons |
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Small Intestine - Chylomicrons
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Chylomicrons are secreted from enterocytes into lacteals
Chylomicrons deliver: * Dietary TG to peripheral tissues * Dietary cholesterol to liver |
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Small Intestine - Electrolyte Transport
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Cl- channels are located in crypts
* Increase Cl- secretion with increased water loss (ex. diarrhea from vibrio cholerae infxn) Ca++ is absorbed in small intestine and requires Vitamin D Fe++ is absorbed in small intestine |
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Small Intestine - Vitamin Absorption
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Fat-soluble vitamins (A,D, E, K) are absorbed with other lipids
Water soluble vitamins are absorbed by Na+-dependent cotransport * Vit B12 is absorbed by ileum and requires intrinsic factor |
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Large Intestine - Functions
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Absorbs some nutrients
Proximal portion passively absorbs most of the remaining stool water (Max water absorption is 2-3L/day) |
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Large Intestine - Electrolyte Transport
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K+ is secreted
Diarrhea causes increased K+ secreted and may cause hypokalemia |
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Large Intestine - Motility
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Haustra - bowel segmentations that help move chyme distally
Mass movement: peristaltic wave that rapidly moves fecal material into rectum (occurs 3-4x's/day) |
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Large Intestine - Defecation
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Urge occurs when rectum is 25% occupied (dilated)
Internal and anal sphincter (smooth muscle) relaxes When the external anal sphincter (skeletal muscle) relaxes, it prompts rectal smooth muscle contraction and fecal expulsion |
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Pancreas - Endocrine
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Cells are arranged in small islets (Islets of Langerhans)
Secretes insulin, glucagon, somatostatin and pancreatic polypeptide |
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Pancreas - Exocrine
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Cells are organized into acini and ducts
Secretes: * Peptidases that digest proteins * Lipases hydrolyze fats * Amylases hydrolyzes glycogen and starch disaccharides * Nucleases digest nucleic acids |
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Pancreas - Enzymes
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Lack of pancreatic enzymes lead to malabsorption syndromes
Ductal cells secrete 1-1.5L/day Secretions contain increased [HCO3-] that neutralize HCl and regulate pH |
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Pancreas - CCK
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Released by endocrine cells in duodenum and jejunum
Stimulates: * Gallbladder contractions * Sphincter of Oddi relaxation * Pancreatic enzyme secretion |
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Pancreas - Secretin
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Released by endocrine cells in duodenum and jejunum
Stimulates secretion of HCO3- from pancreas |
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Liver - Hepatic Portal Circulation
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Portal vein carries venous blood from small intestine to the liver
Pancreas venous drainage (containing insulin and glucagon) also flows into portal vein Portal blood flow = low hydrostatic pressure (10mmHg) |
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Liver Functions - CH2O metabolism
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After meals, the liver takes up glucose and synthesizes glycogen (glycogenesis)
During fasting, the liver produces glucose (glycogenolysis and gluconeogenesis) Maintains stable blood glucose |
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Liver - Protein Synthesis
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Liver manufactures many plasma proteins:
* Albumin * Clotting factors * Binding proteins * Some hormones and precursors |
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Liver - Oxidative deamination and transamination
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Allows AA's to enter metabolic pathways
Site of urea cycle * Allows nitrogen to be excreted as urea * Loss of this function causes increased [NH3] and can lead to AMS |
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Liver - Lipid Metabolism
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Makes 80% of body's cholestreol from acetly-CoA
Synthesizes, stores and exports TG's Site of keto-acid production (FA oxidation enters the Kreb cycle) |
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Liver - lipid regulation
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Hepatocytes synthesize apolipoproteins (solubilizes lipids so that exogenous lipids are made available to tissues)
Liver controls: [TG] by assembling, secreting and taking up various lipoprotein particles |
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Liver - lipid regulation
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Rate limiting step for cholesterol synthesis is catalyzed by HMG-CoA reductase
HMG-CoA reductase inhibitors decrease [cholesterol] - ex. "statins" like atorvastatin (Lipitor) |
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Liver - lipid regulation: VLDL and LDL
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VLDL: delivers hepatic TG to peripheral tissues
(peripheral VLDL is converted to LDL, by lipoprotein lipase secreted by periphreal tissues, and then returns to the liver) LDL: delivers hepatic cholesterol to peripheral tissues |
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Liver- lipid regulation: HDL
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Synthesized and secreted by liver and intestine and scavenges excess cholesterol and TG from blood and other tissues
Returns them to liver for excretion |
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Detoxification and Excretion
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Most enzymes that carry out detoxification of drugs and other substances are located in hepatocyte ER (ex. Cytochrome P450 isoenzymes)
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Detoxification and Excretion
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Metabolism usually involves biotransformation of lipophilic substances into hydrophilic substances that can be excreted via urine or bile
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Detoxification and Excretion - Phase I
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Redox rxns where an oxygen-containing functional group is added to the substance
May convery mildly toxic drugs to more toxic reactive intermediates which are processed by phase II enzymes |
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Detoxification and Excretion - Phase II
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Covalent attachment of drug to a water-soluble carrier (ex. glucuronic acid or glutathione)
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Bile Synthesis and Recirculation
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Bile is produced by hepatocytes and secreted into bile canaliculi
Bile then drains into hepatic ducts and is store in the gallbladder |
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Bile composition
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Bile salts
Phospholipids Cholesterol Bilirubin |
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Bile Synthesis and Recirculation - Primary Bile Acids
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Primary bile acids are made from cholesterol
They are conjugated (to increase solubility) by hepatocytes into bile salts Bile is released into duodenum following a meal to emulsify fats |
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Bile Synthesis and Recirculation - Secondary Bile Acids
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Bile remains with intestine until deconjugated and dehydroxylated by intestinal bacteria into secondary bile acids
Secondary bile acids are reabsorbed by the ileum (site of b12 absoprtion via IF) and then transported back to the liver via portal circulation for reuse |
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Bilirubin
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Product of heme metabolism (hemoglobin breakdown)
Actively taken up by hepatocytes and secreted into bile Increased [bili] leads to jaundice |
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Bilirubin - Numerical Values
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Total: 0.1-1.2mg/dL
Direct (conjugated): 0.1-0.4mg/dL Indirect (unconjugated): 0.1-0.7mg/dL |
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Gallbladder
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Stores and concentrates bile (20-50mL) btwn digestion periods
During digestion, CCK causes gallbladder contraction and relaxes the sphincter of Oddi |
