Lp 14 digestive system 2009

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Lp 14 digestive system 2009

  1. 1. Digestive System VTT 235/245 Anatomy & Pathology Lab
  2. 2. Introduction The digestive system consists of:  **A tube that runs from the mouth to the anus.  Accessory digestive organs that aid in the process of digestion and absorption of nutrients.  The accessory organs are:  Salivary glands  The liver  The pancreas
  3. 3. Functions Prehension (grasping of food) Mastication Chemical digestion Absorption of nutrients and water Elimination of wastes
  4. 4. Oral Cavity Mechanical digestion- chewing, breaking food down into smaller particles to increase the surface area available for exposure to enzymes involved in chemical digestion.
  5. 5. Oral Cavity… Digestive enzymes are proteins that promote (catalyze) the chemical reactions that split complex food molecules into simpler compounds. The addition of saliva helps moisten, soften, and shape food into a form that is more easily swallowed. Salivary amylase breaks down amylose, a sugar component of starch. Lipase, an enzyme that digests lipids (fats) can also be found in the saliva of some species.
  6. 6. Oral Cavity… The salivary glands are controlled by the autonomic nervous system. Stimulation of the parasympathetic division results in increased salivation.
  7. 7. Peristalsis The contents of the digestive tract are moved and mixed by two types of smooth muscle contractions:  Peristaltic- move contents along the digestive tract.  They consist of circular muscle contractions that propel contents.  Segmental- cause back-and-forth mixing movements.
  8. 8. Esophagus A muscular tube that extends from the pharynx to the stomach. Its function is to conduct swallowed material to the stomach. The esophagus enters the stomach at the cardia.  Made of smooth muscle,  Which helps with peristalsis.
  9. 9. Gastroesophageal Reflux & Esophagitis Inflammation of the esophageal wall most often associated with contact of irritants with the mucosa of the esophagus. Acids, alkalis, drugs, toxins, and hot materials can produce lesions of varying severity. Once inflammatory damage occurs, lower esophageal sphincter function becomes abnormal, perpetuating the problem.
  10. 10. Megaesophagus Esophageal paralysis or hypomotility. A dilation of the esophagus Due to a vascular ring anomaly or an unknown cause May be secondary to systemic disease (hypothyroidism) Primary sign- regurgitation (begins at weaning if congenital)
  11. 11. Esophageal Obstruction Bones and small toys commonly enlodge at the thoracic inlet, cardiac base, or distal esophagus. The degree of damage to the esophagus depends on:  The size of the object  The shape  The time spent in contact with the mucosal lining
  12. 12. Spirocera lupi Can cause neoplasia of the esophagus.
  13. 13. Stomach… Divisions-  Cardia- the area immediately surrounding the opening from the esophagus.  Associated with the cardiac sphincter.  Fundus- the section that forms a blind pouch that expands as more food is swallowed.
  14. 14. Stomach… Divisions-  Body- also a distensible section in the “middle” of the stomach.  ***Pylorus- the distal part of the stomach that grinds up swallowed food and regulates hydrochloric acid (HCl).  **The glands of the pylorus contain endocrine cells called G cells which secrete the hormone gastrin.
  15. 15. Stomach… The body & fundus are both rich in glands containing 3 key cells-  Parietal cells- which produce HCl.  Chief cells- which produce pepsinogen.  Mucous cells- which produce protective mucus. Mucous- adjective Mucus- noun
  16. 16. Stomach… Inside the stomach, multiple folds called rugae can be observed.
  17. 17. Gastric Motility Swallowing of food stimulates vigorous mixing, grinding, and propulsive contractions that move food toward the pylorus. The smooth muscle in the wall of the stomach responds to several hormones, peptides, and nervous system controls.  Stimulation of the vagus nerve causes the fundus to relax (so it can fill), while increasing the contractions in the body and pylorus for mixing and peristaltic movements.
  18. 18. Gastric Secretions Pepsinogen is secreted by chief cells and is a precursor for the enzyme pepsin. The proteins broken down by pepsin form chains of amino acids (polypeptides & peptides). The presence of peptides in the pylorus stimulates the G cells to release more gastrin, which stimulates more HCl and pepsinogen release.
  19. 19. Gastric Secretions… Once the pepsin moves from the acidic pH of the stomach to the more alkaline pH of the duodenum, it is inactivated by the change in pH and stops functioning. The mucus produced by the gastric glands provides a protective coating of the stomach. Mucins are complex molecules produced by the goblet cells in the gastric glands and are the main constituents of the coating. Bicarbonate ion is also secreted onto the surface making it more alkaline.
  20. 20. Gastric Secretions… The parietal cells in the gastric glands secrete hydrogen and chloride ions separately into the stomach. Once these ions are secreted, they combine to produce the HCl that accounts for the stomach’s acidic pH. The parietal cells have 3 receptors that regulate acid production.
  21. 21. Gastric Secretions… These receptors are for:  Gastrin  Acetylcholine  Histamine Stimulation of all receptors results in the optimum amount of hydrogen and chloride secretion.
  22. 22. Gastric Secretions… When the pH of the stomach contents drops below 3, gastrin release is inhibited. When gastrin is inhibited, hydrogen and chloride production is terminated, and HCl production declines. Selectively blocking any one of these receptors decreases the production of stomach acid.  This is the way antacid drugs work.
  23. 23. Mechanism of Vomiting Vomiting occurs due to the stimulation of the emetic center in the brain.  Visual, vestibular, toxins… Color and content of the vomit can assist in a diagnosis.  Flecks of blood- recent hemorrhage in the esophagus or stomach.  Coffee grounds- digested blood  Yellow-green- bile
  24. 24. Acute Gastritis Causes include:  Diet- spoiled food, change in diet, food allergy, or food intolerance.  Infection- bacterial, viral, or parasitic.  Toxins- chemicals, plants, drugs, or organ failure. Ingestion of foreign objects may also result in gastritis. Once the mucosa is damaged, inflammation occurs and clinical symptoms develop.
  25. 25. Gastric Ulcers Commonly a result of drug therapy.  NSAID’s  Aspirin, ibuprofen…  Disruption of the normal gastric mucosal barrier, resulting in ulceration.
  26. 26. GDV Diet and exercise have been indicated in the development of GDV. As the stomach fills with air, food, and/or fluid, the outflow tracts become occluded. Further distension results in a simple dilation (air-filled stomach), or the air- filled stomach may twist along its longitudinal axis (volvulus).
  27. 27. GDV… The pylorus usually passes under the stomach. The enlarged stomach presses against the diaphragm, making breathing difficult and blocking venous return. The spleen may also be involved.
  28. 28. GDV
  29. 29. Pyloric Stenosis Hypertrophy of circular smooth muscle fibers of the pyloric sphincter This causes an obstructive narrowing and projectile vomiting
  30. 30. Pathology… Hemorrhagic Gastroenteritis- (HGE)  Acute onset of bloody diarrhea Malabsorption Syndrome- the small intestine is unable to deliver nutrients to the circulation (EPI)
  31. 31. SmallIntestine Function: Digestion and absorption
  32. 32. Small Intestine Where the majority of nutrients are absorbed into the bloodstream. Divided into 3 segments-  Duodenum- first short section leaving the stomach.  Jejunum- longest portion, makes up the majority of the small intestine.  Ileum- enters the colon at the ileocecal sphincter.
  33. 33. Small Intestine… Ileocecal sphincter- regulates movement of materials from the small intestine to the colon. The parasympathetic nervous system provides stimulation for small intestinal motility, secretions, & blood flow.
  34. 34. Structure The mucosa is adapted to provide a large surface area for absorbing nutrients through folds in the intestinal wall and millions of villi. Each villus contains thousands of microvilli called the brush boarder. These cells have many digestive enzymes and carrier molecules embedded in their cell membrane for digestion and absorption of nutrients, vitamins, and minerals.
  35. 35. Motility Has peristaltic waves, which mix the intestinal contents and slow their movement through the length of the intestine. The churning motion brings digested material into contact with the surface for absorption. Slowing the movement also allows enough time to contact with the intestinal wall long enough to be absorbed. Peristaltic movements are stimulated by reflexes to dilation.
  36. 36. Structure… Goblet cells are also present. They produce mucus that helps protect the intestinal mucosa from the flow of ingestion as it passes over the intestinal lining.
  37. 37. Digestion Electrolytes and vitamins can be absorbed intact into the small intestine wall while carbohydrates, proteins and fats must be chemically digested. Chemical digestion has 2 steps-  By enzymes in the lumen of the intestine.  By enzymes associated with the brush boarder.
  38. 38. Mechanism of Diarrhea Osmotic-  or poor absorption of contents.  Dietary overload, maldigestion or malabsorption Secretory- hyper secretion of the valley portion of the villi.  More secretion than absorption.  Ex. Parvo, bacterial Abnormal Motility- abnormal transit time, usually a hypomotility.  Hypomotility allows for bacterial overgrowth and rotting ingesta. Yummy!
  39. 39. Small vs. Large Intestine DiarrheaSigns Small Intestine Large IntestineFrequency Normal to  Volume Large SmallUrgency Absent PresentStraining Absent PresentMucus Presence Absent PresentBlood Presence Coffee grounds Very redVomiting Present AbsentWeight Loss Present Absent
  40. 40. Small Intestine Pathology… Enteritis  Inflammation of the small intestine.  Can be infectious or inflammatory.  The diarrhea usually contains digested blood. Volvulus-  Rotation of the bowel. Perforations-  Penetration of the small intestine wall.  Causes: ulcers, foreign bodies, necrosis IIº to obstruction, herniation or external penetration.  This causes painful peritonitis!
  41. 41. Parvo Parvo virus affects the lining of the small intestine. It invades/wipes out the simple columnar tissue which exposes blood vessels causing “bloody diarrhea”. The intestinal response is to become inflamed-  Increased peristaltic activity- cramps  Propels chyme through rapidly- diarrhea!
  42. 42. Intussusception The cause is usually idiopathic but can be the result of:  Parasite infection  Foreign bodies  Infections  Neoplasia
  43. 43. Intussusception… The telescoping of the proximal intestine into the distal intestine. It produces a partial to complete blockage and compromises blood supply to the segments causing bowel necrosis.
  44. 44. Mesentery Mesentery- Clear, suspends the intestines from the roof of the abdomen.  Prevents intestine entanglement  Supplies blood to the intestines (small & large) Omentum-  Part of the mesentery.  Helps prevent a torsion.  Attached at the greater curvature of the stomach.
  45. 45. Large IntestineWater absorption and bacterial digestion
  46. 46. Anatomy Review “Colon”  Ascending  Transverse  Descending
  47. 47. Colitis Acute-  Chronic-  Sudden onset of  Long-term, non-specific inflammation of the colon.  Often in dogs. inflammation of the colon.  Frequent defecation,  Causes include: idiopathic, small amounts. FIV+, FIP+  Causes: garbage ingestion,  Signs include: diarrhea stress, parasites:  Trichuris, Coccidia with slow, progressive  Bacteria: Salmonella weight loss. All cause a change in motility!
  48. 48. Megacolon An abnormally dilated colon or segment of the colon. Seen frequently in cats. The presenting symptom is straining to defecate. These cats are usually dehydrated and may be vomiting. The cause of this disorder has been thought to involve a defect in the neurostimulation mechanism that promotes colon evacuation.
  49. 49. Megacolon… Other causes include:  Hypothyroidism  Pelvic deformities Severe prolonged colon distension for any reason can disrupt normal motility and result in megacolon.
  50. 50. Constipation True constipation is uncommon. The presence of foreign objects, tumors, pelvic injury, anal sac abscesses, urinary obstruction, and dehydration can result in the failure to pass feces.
  51. 51. Inflammatory Bowel Disease (IBD)- A group of GI diseases characterized by similar signs with unknown causes. Diagnosis is made when an excessive number of inflammatory cells are found in mucosal samples of the GI system. Colonic inflammation disrupts mucosal integrity and results in decreased absorption of sodium and water. Inflammation also results in hypermotility, resulting in more frequent defecation.
  52. 52. Inflammatory Bowel Disease (IBD)… Signs include:  Diarrhea with little weight loss.   frequency of defecation and  fecal volume.
  53. 53. Rectum & Anus Rectum- the part of the colon running through the anal cavity. Anus-  Anal sphincter- a muscular ring that controls the passage of feces out of the body.  What type of muscle?  Smooth!
  54. 54. Anatomy Perianal Glands- sebacous glands located in the skin, encircling the anus. Anal Glands- located in the submucosa, at the anocutaneous junction.  Where are the ducts?
  55. 55. Anal Gland Impaction Retention of anal sac secretions If left untreated, they may abscess Anal sac rupture is secondary to obstructions
  56. 56. Perianal Adenoma Usually in intact male dogs. Bengin, hormone dependant tumor that arises from the perianal gland.  Which hormone?  Testosterone
  57. 57. Perianal Fistulae Multiple ulcerative, smelly draining tracts surrounding the anus Caused by dogs with a low tail carriage and/or a broad tail base (which retains fecal film) ex. GSD
  58. 58. Hepatic Anatomy
  59. 59. The Liver The largest gland in the body. A digestive gland of substantial importance in metabolism.
  60. 60. The Liver… Functions:  Detoxification of drugs and toxins.  Formation and secretion of bile.  Metabolism of carbohydrates and fats.  Plasma protein production.  Urea formation.
  61. 61. Anatomy The liver consists of six lobes.  HEPATOCYTES.
  62. 62. Blood Supply The liver has a unique venous system referred to as the Hepatic Portal System, which receives both oxygenated and deoxygenated blood. All products of digestion are filtered through the liver and approximately 80% of the blood that flows into the liver enters through the portal vein and originates from the stomach and intestines.
  63. 63. Blood Supply… The hepatocytes are nourished by this blood which is rich in nutrients but not in oxygen. As blood enters the lobules, it flows across the hepatocytes and filters into the central vein. The blood then travels from the central vein into the hepatic vein and eventually the caudal vena cava.
  64. 64. Blood Supply… As the blood is filtered through the liver, it passes through Kupffer cells, which help remove bacteria. The hepatic artery supplies the remaining 20% of blood to the liver.  This blood, which is rich in both oxygen and nutrients, supports the high metabolic activity of the hepatocytes.
  65. 65. Hepatocytes The hepatocytes also secrete hormones and bile, a green digestive hormone liquid. The bile is carried through channels to the gallbladder where it is stored and the common bile duct, which leads to the duodenum, where bile is released.
  66. 66. Physiology
  67. 67. Bile Bile plays an important role in digestion, and bile production is one of the main functions of the liver. Bile consists primarily of bile salts, water, and bile pigments such as bilirubin. One of the most important functions of bile is to emulsify fat so it can be broken down by digestive enzymes in the gut.
  68. 68. Carbohydrate Metabolism In a process called glycolysis, the liver metabolizes carbs by converting excess glucose into glycogen for storage. The process is reversed when energy is needed. The entire cycle is known as glycogenolysis and is under the influence of the hormone glucagon.
  69. 69. Deamination Amino acids are broken down by the removal of an amino group. The discarded amino group is converted into ammonia and then into urea or uric acid, which is excreted through renal filtration.  Animals with liver failure may have increased levels of ammonia.
  70. 70. Synthesis The liver synthesizes both alpha and beta globulins, which transport lipids and fat-soluble vitamins throughout the body. Prothrombin is one of the most important alpha globulins produced by the liver.
  71. 71. Pathology Cirrhosis- scarring of the liver, which is replaced with connective tissue. 70% of the liver can be destroyed before problems occur. Jaundice- A build-up of bilirubin in the body. Hepatitis- inflammation of the liver causing damage to the hepatocytes. Cholecystitis- inflammation of the gallbladder.
  72. 72. Infectious Canine Hepatitis Caused by Canine Adenovirus I and has long been recognized as a cause of hepatic necrosis in dogs. Infection occurs via the oronasal route. Viral replication occurs in the tonsils and lymph nodes.
  73. 73. Infectious Canine Hepatitis… Signs include:  Petechial hemorrhages  Lethargy  Fever >103°F  Depression  Pale MM  Abdominal pain  Anorexia  Bloody diarrhea  Hepatomegaly
  74. 74. Feline Hepatic Lipidosis “Fatty Liver Disease” Severe accumulation of fat in the liver Secondary to diabetes mellitus in obese cats, malnutrition, drugs, toxins, or idiopathic. Complete anorexia in obese cats CBC- non-regenerative anemia, stress neutrophilia, lymphopenia. ↑ALP (20x normal), ↑ALT (10x normal), hyperbilirubinemia, hypoalbuminemia,  bile acids.
  75. 75. Hepatic Lipidosis Signs-  Hepatoencephalopathy  V/D  Icterus  Sporadic vomiting  Anorexia  Obesity  Melena (black, tarry stools)
  76. 76. Portosystemic Shunts Portal Systemic Shunts The blood by-passes the liver due to a congenital defect or acquired by chronic hepatitis. This leaves the blood unfiltered as it returns to the heart. Ammonium biurate crystals in the urine can be an indicator.
  77. 77. Shunts Causes:  Congenital- a vascular anomaly  Acquired- IIº to chronic active hepatitis or serosis, (portal vein non- functional) Signs:  CNS- hepatoencephalopathy d/t ammonia build-up in the brain.
  78. 78. Shunts Signs-  Anorexia  Depression  Ataxia  Head-pressing  Circling, pacing, blindness  Seizures  Hypersalivation
  79. 79. Pancreas: Anatomy Review
  80. 80. Pancreatic Function An endocrine and exocrine gland. The primary organ supplying digestive enzymes. Helps regulate glucose levels. 4 Secretions-  Sodium bicarbonate  Trypsin  Amylase  Lipase
  81. 81. Pancreatic Function No secretion: starvation due to nutrients not digested. Oversecretion: over digestion, autodigestion of the pancreas.
  82. 82. Anatomy Located along the greater curvature of the stomach. Venous drainage of the pancreas to the portal vein, (filtered by the liver), and then returned to circulation.  Hepatitis is common with acute pancreatitis.
  83. 83. Pancreatic Anatomy… Pancreatic secretions pass from secreting cells in the pancreas into small ducts. The small ducts ultimately unite to form the ducts that carry secretions to the small intestine. The pancreas is made up of small clusters of glandular epithelial cells.
  84. 84. Pancreatic Anatomy… About 99% of the cells are arranged in clusters called acini and constitute the exocrine portion of the organ. The cells within the acini secrete a mixture of fluid and digestive enzymes called pancreatic juice. The remaining 1% of cells are organized into clusters called pancreatic islets. They form the endocrine portion of the pancreas that secrete the hormones insulin and glucagon.
  85. 85. Pancreatitis Inflammation of the pancreas. May be acute or chronic. Develops when digestive enzymes are activated within the gland, resulting in autodigestion. Once autodigestion develops, the gland becomes inflamed, resulting in tissue damage, multisystemic involvement, and often death. More prevalent in obese animals.
  86. 86. Pancreatitis… Diets high in fat may predispose animals to the disease. Most commonly a post-holiday disease.  Feeding scraps from turkey, ham, or roast drastically increases an animal’s dietary fat, resulting in acute signs of the disease.
  87. 87. Pancreatitis… Clinical signs-  Depression  Anorexia  Vomiting  Dehydration  Abdominal pain
  88. 88. Exocrine Pancreatic Insufficiency (EPI) Develops with a progressive loss of acinar cells followed by inadequate production of digestive enzymes. Clinical signs may not develop until 85%-90% of the secretory ability has been lost. Lack of normal secretions affects the mucosal lining of the small intestine and decreases its absorptive power. Disruption of the normal acinar structure may affect insulin production, leading to glucose intolerance.
  89. 89. Exocrine Pancreatic Insufficiency & EPI… Clinical signs-  Mild to marked weight loss  Polyphagia, copraphagia  Diarrhea, fatty stool  Flatulence

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