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10. Digestiv eSystem Part 2

Olivia McKenzie-Allen VNAS 1 level 4 Englisch 126 Karten

10. Digestiv eSystem Part 2

Karten in diesem Stapel (126)

  1. 1what can disturb the balance of microbe substrate, microbes and microbial substrate?change in diet, illness, alteration in hay length fed
  2. 2where is the entrance to the omasum?from the reticulum.
  3. 3how is ingesta moved into the omasum?reticulorumen contractions
  4. 4what is the structure of the omasum?inner surface has long parallel folds of muscle
  5. 5what is the role of the omasum?breaks down food, moves food to abomasum, absorbs remaining VFAs , removes bicarbonates to maintain pH in abomasum, absorbs some water
  6. 6true or false, the omasum has a large role in absorptionfalse
  7. 7how does the abomasum function?the same as the monogastric stomach in other animals
  8. 8how do hindgut fermenters digest cellulose?with symbiotic bacteria in the caecum and colon
  9. 9what are the segments of the large intestine?caecum, ventral colon, dorsal colon, small colon
  10. 10in the equine hindgut where does ingesta move?from small intestine, through ileocaecal sphincter to the caecum
  11. 11what are the parts of the equine caecum?base, main body and apex
  12. 12where is the caecum located?ventral floor of the peritoneal cavity
  13. 13what are haustra?longitudinal bands separating dorsal colon, ventral colon and caecum into a series of lined up sacs
  14. 14what is the caecocolic orifice?the separation of the colon and the caecum
  15. 15how and where is ingesta moved out from the caecum?contractions form the apex and the body of the caecum force ingesta into the right ventral colon
  16. 16how does ingesta move through the equine colon?right ventral colon, through the sternal flexure to the left ventral colon, through the pelvic flexure to the left dorsal colon, through the diaphragmatic flexure to the right dorsal colon, small colon
  17. 17in the equine hindgut, where are areas of potential obstruction and what may this cause?narrow flexures and small colon, as impaction may occur leading to colic
  18. 18what part of the GI tract of the horse isn't good at digesting carbohydrates?small intestine, meaning a significant amount of carbohydrates make it though to the caecum and colon
  19. 19how does protein digestion in the equine small intestine affect nitrogen needs of the horse?less protein nitrogen available to colonic microbes than is available to rumen microbes. the nitrogen needs of the colonic microbes are supplemented by the secretion of urea from the urea into the GI tract
  20. 20in the equine hindgut where and why are VFAs absorbed?in the caecum and colon for the energy requirements of the horse
  21. 21how are acids buffered in the colon and caecum of the horse?secretion of bicarbonate into the colon and caecum
  22. 22why is bicarbonate secretion different in horses compared to ruminants?in ruminants bicarbonate secretion is more important in the saliva, while in horses it is more important in the caecum and colon
  23. 23what is the role of the small colon in the equine hindgut?absorb electrolytes, water, VFAs left over from colon absorption
  24. 24where does fermentation occur in rabbits guinea pigs and chinchillas?the caecum
  25. 25why is the rabbit fermentation system more efficient than that of the equine variety?they have a colonic separation mechanism sorting output into a hard high faecal pellet and a large mucous covered pellet called a caecotroph
  26. 26what happens to Caecotrophs?they are reingested by the anus to be further digested in the stomach and small intestine
  27. 27why are Caecotrophs useful?they provide additional protein and vitamins
  28. 28where is the liver located?in the cranial abdomen caudal to the diaphragm on the left of the stomach
  29. 29what does the liver look like to the naked eye?large, dark red organ with the gall bladder attached
  30. 30what are the lobes of the liver?left lateral and left medial (left division), quadrate and right medial (central division) and right lateral and caudate (right division)
  31. 31how is blood supplied to the liver?by one artery (aorta) and two veins (caudal vena cava and the hepatic portal vein)
  32. 32what is the microscopic appearance of the liver?made of hepatocytes, arranged into hexagonal lobules surrounded by connective tissues. sinusoids allow blood to flow from external sources and bile canaliculi collect bile produced in the liver
  33. 33where does oxygenated blood flow first in the body?to the liver
  34. 34how does blood reach the liver?hepatic portal vein
  35. 35what is the job of the liver?it is a factory which manufactures, reprocesses and produces waste
  36. 36how do products of protein digestion, carbohydrate digestion and fats reach the liver?products of protein and carbohydrate digestion, in the blood while fats reach the liver indirectly through lacteals and lymphatic vessels
  37. 37what are Kupffer cells?specialised phagocytic cells lining the sinusoids of the liver to phagocytose abnormal or foreign cells and play a role in activation of t cells as a part of the immune response
  38. 38—
  39. 39what is the appearance and purpose of the gall bladder?small green organ attached to the liver which stores bile entering from the liver via hepatic ducts
  40. 40how does the bile in the gall bladder get used?bile leaves via the common bile duct into the duodenum at the duodenal papilla to maintain a constant pH in the duodenum, not the acidic pH from the stomach
  41. 41what are the 11 functions of the liver?-carbohydrate metabolism
    -protein metabolism
    -fat metabolism
    -destruction of old red blood cells
    - formation of new red blood cells
    -formation of bile
    storage of vitamins
    - storage of iron
    -regulation of body temperature and production of heat
    -detoxification of drugs and alcohol
    -detoxification and conjugation of steroid hormones
  42. 42from what part of the diet does most of the glucose for energy come from?carbohydrates
  43. 43what happens to excess glucose in the liver?converted into glycogen to be stored in the liver through glycogenesis
  44. 44how is glycogen used in the body?glycogen is broken back down into glucose through glycogenolysis
  45. 45what organs are involved in glucose homeostasis?liver and pancreas
  46. 46what are important roles in protein metabolism?urea production, regulation of amino acids, and formation of plasma proteins
  47. 47what are the roles of the following plasma proteins? 1.albumin 2.globulins 3.fibrinogen, prothrombin etc 4. angiotensinogen1. maintains fluid balance
    2. part of the immune system
    3. blood clotting mechanism
    4. blood pressure regulation
  48. 48how does the body regulate amino acid presence?proteins are formed from amino acids so it is vital for the body to make more useful amino acids from those less used by transamination. mediated by growth hormone
  49. 49how is urea produced and excreted?surplus amino acids in the liver produce ammonia then to urea by deamination. this occurs in the ornithine cycle and then urea is excreted in urine
  50. 50what are fatty acids and glycerol made into in the liver?phospholipids to be used in cell membranes, cholesterol for bile salts, fat for an energy store
  51. 51what vitamins are stored in fat saved in the liver?fat soluble, A,D,E,K
  52. 52where is vitamin D activated?liver
  53. 53what causes fatty liver disease?too much fat stored in the liver
  54. 54what is bile made up of?bile acids, cholesterol and bilirubin
  55. 55what is bilirubin?green pigment from the breakdown of red blood cells
  56. 56what is bile important for and what triggers its release into the duodenum?important in digestion of fats and is released under the influence of cholecystokinin
  57. 57how does bile aid fat digestion?allows fat to be emulsified and increases surface area for enzymes to act as well as activating lipases
  58. 58what is extra medullary haematopoiesis and when does it occur?only occurs in foetuses and is the production of red blood cells
  59. 59what are the results of destruction of old red blood cells?haemoglobin excreted as bilirubin in bile, bile reabsorbed (enterohepatic circulation) and gives colour to faeces and urine
  60. 60what happens to iron from broken down haemoglobin?either stored in spleen or liver macrophages, or combined with plasma proteins to form transferrin to create new haemoglobin in bone marrow
  61. 61what type of drugs tend to be detoxified in the liver and why?fat soluble drugs, as all the water soluble toxins tend to be excreted via the kidneys
  62. 62where in the liver does detoxification occur?in the microsome of the smooth endoplasmic reticulum in hepatocytes
  63. 63what is the name of the enzyme involved in detoxification in the liver?cytochrome P450
  64. 64why is detoxification in the liver clinically important to understand?- metabolism may be altered in the cases of different diseases
    - drug interactions may change rate of metabolism
    - species/individual differences may occur
    - substances can effect metabolism (cigarettes increase metabolism, grapefruit decreases metabolism)
  65. 65where is the pancreas?an l shape to the right of the duodenum and next to the greater curvature of the stomach
  66. 66where does the pancreas empty into?into the duodenum via one or two pancreatic ducts
  67. 67why is the pancreas describes as an extrinsic gland?it isn't essential to the GI tract
  68. 68what does the pancreas look like?pale pink and lobular
  69. 69what are the exocrine functions of the pancreas?secretes digestive enzyme and bicarbonate into duodenum via pancreatic ducts
  70. 70what are the endocrine functions of the pancreas?produces hormones from islets of Langerhans, areas of hormonal tissue containing alpha beta and delta cells (insulin production etc)
  71. 71what triggers pancreatic secretion?autonomic nervous system, gastrointestinal hormones (gastrin, secretin and cholecystokinin
  72. 72what does pancreatic juice contain?bicarbonate, lipase, amylase and protease
  73. 73what are pancreatic proteases released as and why?inactive precursors to the enzymes to inhibit autodigestion of the pancreas
  74. 74in the pancreas, where is insulin produced and why?produced from beta cells in the pancreas when blood glucose is high to increase uptake of glucose by cells by promoting glycogenesis
  75. 75in the pancreas where is glucagon produced and why?in alpha cells in response to low blood glucose and raises blood glucose by glycogenolysis
  76. 76what is the purpose of somatostatin produced in the pancreas?regulates glucagon secretion to prevent large swings in glucose levels by decreasing gut motility and secretion of other digestive juices
  77. 77what are some serious consequences of diarrhoea and vomiting?fluid and electrolyte loss (hypovolaemia and dehydration), acid base and electrolyte disturbances, malnutrition, aspiration pneumonia, pain and discomfort
  78. 78how is vomiting triggeredbrain stem and chemoreceptor trigger zones
  79. 79what are the three phases of vomiting?nausea, retching and emesis
  80. 80how is the act of vomiting completed?reverse peristalsis forces ingesta out of the stomach cranially
  81. 81what is diarrhoea?an increase in frequency of volume of defacation
  82. 82what are the 4 types of diarrhoea?osmotic, secretory, infectious and deranged motility
  83. 83when does osmotic diarrhoea occur?if excess solutes remain in the intestinal lumen so water is drawn into bowel by osmosis
  84. 84what typically causes osmotic diarrhoea?ingestion of poorly absorbed solutes (e.g. sorbitol and lactulose), malabsorption (lactose intolerance)
  85. 85how is osmotic diarrhoea resolved?if patient fasts or stops ingesting problem solute
  86. 86what causes secretory diarrhoea?when secretion of fluid into intestine exceeds absorption of fluid
  87. 87why does secretory diarrhoea occur?bacterial toxins or drugs
  88. 88what is the cause of inflammatory diarrhoea and what does this lead to?caused by disruption of epithelial barrier due to bacterial, viral, parasitic infections. leads to exudation of serum into lumen and damage to absorptive epithelium, as well as resulting in poor water reabsorption.
  89. 89what is inflammatory diarrhoea complicated by?often occurs in conjunction with secretory diarrhoea and is complicated by osmotic diarrhoea
  90. 90what is the cause of deranged motility diarrhoea?accelerated transit of ingesta causing reduced time for nutrient and water absorption
  91. 91what is the biggest problem with deranged motility diarrhoea?cause and effect aren't always apparrent
  92. 92how are diarrhoea and vomiting usually managed?dependant on finding and managing the underlying cause, so fluid therapy is vital as well as managing electrolyte and acid base disturbances. nutrition must be considered
  93. 93what animal does megaoesophagus normally effect?dogs
  94. 94what is megaoesophagus?abnormal functioning of the oesophagus resulting in reduced motility and lack of peristalsis, and dilation with pooling of fluid and food in oesophagus
  95. 95what is the normal result of mega oesophagus?regurgitation of undigested food
  96. 96what are the possible causes of megaoesophagus?muscular disease, neurological disease, toxicity, infectious disease, idiopathic causes
  97. 97what are the increased risks associated with megaoesophagus?aspiration pneumonia and oesophagitis
  98. 98how is megaoesophagus treated?no effective treatment but can be managed with postural feeding, small meals and tactical symptomatic medication
  99. 99what is exocrine pancreatic insufficiency?when exocrine pancreatic secretions don't meet the needs of the animal
  100. 100what is exocrine pancreatic insufficiency usually secondary to?pancreatic atrophy or pncreatitis
  101. 101what is the normal cause of exocrine pancreatic insufficiency?genetic as some breeds are predisposed
  102. 102what are problems caused by exocrine pancreatic insufficiency?reduced enzyme and bicarbonate production leads to interfered digestion of protein, fat and carbohydrates
  103. 103how is exocrine pancreatic insufficiency treated?managed with pancreatic supplements and careful feeding regime
  104. 104what is gastric dilation/volvulus?stomach condition in deep chested dogs (mostly)
  105. 105what does volvulus cause?stomach twisting causing obstruction to outflow, gastric distention leading to pressure on diaphragm, pressure on major veins, increased rick of ischemia and tearing of gastric arteries
  106. 106what are the severe consequences of volvulus?shock, rapid deterioration (death), severe acid base/electrolyte disturbances
  107. 107what treatment is needed for volvulus?rapid surgical correction of stomach torsion or death is definite
  108. 108what is colic?severe abdominal pain with sudden onset
  109. 109what can cause colic?intestinal obstruction, intestinal spasm, intestinal ischemia and other catastrophes in the abdomen
  110. 110what is the small animal equivalent of colic?acute abdomen
  111. 111how is colic treated?emergency surgery to resolve cause
  112. 112what are the internal causes of liver disease?hepatitis (inflammation of liver parenchyma), cholangitis (inflammation of biliary tract) or colangiohepatitis (inflammation of both)
  113. 113what can cause liver disease externally?infections, toxins, tumours,
  114. 114what are the common signs of liver disease?lethargy, anorexia, depression, vomiting, polydipsia, polyurea, icterus, abdominal pain, hepatic encephalopathy and bleeding tendency
  115. 115what is icterus?jaundice
  116. 116what is meant by jaundice?yellowing of whites of eyes, mucous membranes, skin and plasma
  117. 117what is the reason for jaundice?excess bilirubin build up moving from blood to tissues
  118. 118what are the causes of jaundice?hepatic failure, excess destruction of red blood cells or blocked bile ducts
  119. 119what is hepatic encephalopathy?toxic effect of liver failure/ malfunction of the central nervous system and neuromuscular system
  120. 120what is the cause of hepatic encephalopathy?ammonia and other neurotoxic compounds not being detoxified in the liver
  121. 121what are the signs of hepatic encephalopathy?anorexia, vomiting, hypersalivation, bizarre behaviour, head pressing, circling, aimless wandering, blindness, seizures
    , coma
  122. 122what animals is hepatic encephalopathy common in?animals with a portosystemic shunt
  123. 123what is a portosystemic shunt?a condition in which portal blood from the intestines bypasses the liver going directly into systemic circulation usually via the caudal vena cava
  124. 124what are the results of a portosystemic shunt?essential nutrients being wasted and toxins not being removed from blood
  125. 125what is normal of congenital portosystemic shunts?usually 1 vessel with an abnormality, can be intra or extrahepatic, can be surgically treated
  126. 126what is normal of acquired portosystemic shunts?usually effect multiple vessels, develops secondary to liver diseases and cant easily be managed

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level 4 VNAS 1 Karteikarten am 10. Digestiv eSystem Part 2, erstellt von Olivia McKenzie-Allen am 16/12/2019.
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