GI1- Physiology

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  1. What are the 3 fundamental processes of the GI tract?
    secretion (enzymes, mucus, ions, hormones), absorption (water, ions nutrients), motility
  2. What type(s) of muscle make up the esophagus of dogs, cows, and pigs?
    skeletal
  3. What type(s) of muscle makes up the esophagus of cats, horses, humans, and opossums?
    skeletal--> skeletal and smooth--> smooth
  4. What is the clinical relevance of the differences in types of esophageal muscle in small animal medicine?
    most GI pro-motility drugs have an effect on smooth muscles but not skeletal muscles; therefore, they won't work for a dog with esophageal dysfunction but will work for a cat
  5. Describe the unique features of the LES.
    high pressure zone that is a physiologic sphincter (NOT ANATOMIC)- tonically contracted- anti-reflux
  6. What types of drugs increase the tone of the LES? What are 3 specific drugs in this group?
    acetylcholine/cholinergic drugs: Bethanecol, Metoclopramide, Cisapride
  7. What types of drugs decrease the LES tone? (2)
    anti-cholinergics, most pre-anesthetics
  8. What diseases can predispose to LES relaxation and reflux? (2)
    hiatal hernia, distal esophagitis
  9. What are the secretions of the stomach exocrine glands? (3 glands)
    • mucous cells- alkaline mucus
    • parietal cells- HCl
    • Chief cells- pepsin
  10. What are the secretions of the endocrine glands of the stomach? (2 glands)
    • G- cells- gastrin
    • D- cells- somatostatin
  11. What potions of the autonomic NS coordinates GI functions by receiving signals from the brain?
    enteric nervous system
  12. What part of the enteric NS is responsible for motor control of the GI?
    myenteric plexus/ganglia
  13. What part of the enteric NS is important for control of intestinal secretions through the glandular epithelium, intestinal endocrine cells, and submucosal blood vessels?
    submucous plexus/ganglia
  14. What is the function of acetylcholine in the GI tract? (1)
    promotes most GI functions
  15. What are the functions of dopamine in the GI tract? (2)
    decreased motility, increase pancreatic secretions
  16. What are the functions of opioids in the GI tract? (4)
    decrease secretion and peristalsis, increased segmental contractions, contract sphincters
  17. What are the functions of NE in the GI tract? (3)
    decreased GI blood flow, decreased motility, contract sphincters [fight or flight--> worry about digestion later]
  18. What are the functions of serotonin in the GI tract? (2)
    increased peristalsis, increased blood flow
  19. What is the function of somatostatin in the GI tract? (1)
    decreased secretion
  20. The _________ nerves are part of the sympathetic NS going to the GI; two hormones involved in this pathway are __(2)__.
    splanchnic nerves; NE and epinephrine
  21. The _________ nerve is part of the parasympathetic NS going to the GI tract; the hormone involved here is ____________.
    vagus; acetylcholine
  22. What are the effects of parasympathetic stimulation on salivation, gastric motility, intestinal peristalsis, and GI secretions?
    increases all
  23. What are the effects of sympathetic stimulation on salivation, gastric motility, intestinal peristalsis, and GI secretions?
    decrease all
  24. How would accidentally cutting the vagus nerve during surgery affect GI peristalsis?
    decreased motility
  25. How does an opioid drug affect GI peristalsis?
    decrease peristalsis (but increase segmental contractions)
  26. How would Atropine affect GI peristalsis?
    [anticholinergic] decreased motility
  27. How would toxins, such as organophosphates/carbamates or a drug such as neostigmine affect GI peristalsis and why?
    anticholinesterase activity (Ach not degrades, builds up); increased motility
  28. What is the source of gastrin?
    G cells of gastric antrum
  29. What are the target organs of gastrin? (2)
    stomach and somewhat pancreas
  30. What are the receptors of gastrin? (2)
    CCK-1 and CCK-2
  31. What is the primary effect of gastrin?
    causes gastric parietal cells to secrete acid to lower stomach pH
  32. What are the stimuli of gastrin release? (4)
    luminal protein digestion products, gastric distention, vagal reflexes, luminal pH
  33. What is the feedback control of gastrin?
    negative feedback- decreases its own secretion
  34. How is gastrin cleared from the body?
    through the kidneys
  35. What is a tumor that causes profound release of gastrin, stimulating development of gastric ulcers in dogs? What are clinical signs?
    pancreatic gastrinoma- vomiting, diarrhea, melena, anorexia, depression, anemia, abdominal pain
  36. Why are animals with kidney failure at risk for gastric erosions and ulcers?
    gastrin is usually inactivated in the kidney--> elevated gastrin--> increased gastric acid
  37. What is the source of cholecystokinin?
    I-cells in the upper small intestine
  38. What are the target organs of CCK? (4)
    pancreas, gall bladder, somewhat stomach and SI
  39. What are the receptors for CCK? (2)
    CCK-1 and CCK-2
  40. What are the primary effects of CCK? (2)
    pancreatic enzyme secretion (for digestion), gallbladder contraction (bile release to duodenum)
  41. What are the stimuli for CCK release? (2)
    long chain fatty acids and AAs in the proximal SI
  42. What is the feedback control of CCK release?
    self-limiting
  43. What is the source of secretin?
    S-cells of the upper SI
  44. What are the target organs of secretin? (2)
    pancreatic ducts, bile ducts
  45. What is the primary effect of secretin? (2)
    stimulate pancreatic fluid and bicarb secretion (neutralizes gastric acid in duodenum)
  46. What is the stimulus for secretin secretion?
    acid in upper SI
  47. What is the feedback control of secretin secretion?
    negative feedback
  48. What are the muscarinic (parasympathetic) signs of toxicity?(6)
    SLUDDE- salivation, lacrimation, urination, defecation, dyspnea, emesis
  49. What are slow waves?
    Smooth mm. of the GI (distal to proximal stomach) has spontaneous rhythmic fluctuations in membranes, called slow waves or "Basic Electrical Rhythm" (BER); BER is initiated by interstitial cells of Cajal (intestinal pacemaker cells).
  50. What is the relationship between slow waves and spike potentials?
    slow waves are NOT action potentials and do not elicit muscle contractions; spike potentials ARE action potentials that induce peristalsis; spike potentials result when slow waves pass over an area that has already been primed by neurotransmitters (Ach) from the enteric NS.
  51. What are the components of salivary secretions? (5)
    water, electrolytes (Na, K, Cl), bicarb, mucus, enzymes
  52. ____________ NS stimulates salivation; ____________ NS inhibits salivation.
    Parasympathetic; sympathetic
  53. What are the functions of saliva? (6)
    lubrication, solubilize dry food, oral hygiene, starch digestion (herbivores), alkaline buffering, evaporative cooling
  54. What are stimuli for salivation? (3)
    resting salivation, oral (food in mouth, irritation in mouth), psychological (thought or smell of food)
  55. What are the components of gastric secretions? (4)
    bicarb-rich mucus, HCl, proteases (pepsinogen, chymosin), hormones
  56. What molecules increase gastric parietal cell secretion of acid? (3)
    acetylcholine, histamine, gastrin
  57. What is a molecule that inhibits gastric acid secretion from parietal cells? (1)
    prostaglandin E2
  58. What are the functions of GI motility? (3)
    mix food with enzymes, disperse nutrient molecules for maximum contact with epithelium, move chyme downstream
  59. What are the 2 patterns of small intestinal motility?
    peristalsis, segmental contractions
  60. What pattern of small intestinal motility actually slow the progression of ingesta?
    segmental contractions
  61. Describe the composition of a diet that would promote gastric emptying in a dog. (4)
    liquid/canned diet, low fat, more alkaline, decreased protein
  62. How do opioids affect small intestinal motility?
    opioids increase segmental contractions and decrease intestinal secretions
  63. What are the effects of the following on acid secretion by the gastric parietal cell:
    Acetylcholine
    Histamine
    Gastrin
    Prostaglandins
    Somatostatin
    Histamine-receptor antagonist
    Anticholinergic drugs
    • Acetylcholine-increase
    • Histamine- increase
    • Gastrin- increase
    • Prostaglandins- decrease
    • Somatostatin- decrease
    • Histamine-receptor antagonist- decrease
    • Anticholinergic drugs- decrease
  64. What stimulates myenteric reflex?
    gut wall is stretched by luminal contents
  65. What is myenteric reflex?
    circular contraction behind the luminal contents and relaxation in front of it
  66. The myenteric reflex is independent of ____________ but is influenced by __(2)__ input.
    extrinsic innervation; sympathetic or parasympathetic
  67. Describe the act of swallowing.
    initiated voluntarily and then becomes a reflex movement from the pharynx downward
  68. What are the stages of normal swallowing?
    • 1- oropharyngeal phase
    •       a- oral stage
    •       b- pharyngeal stage
    •       c- pharyngoesophageal stage
    • 2- esophageal phase
    • 3- gastroesophageal phase
  69. What is the voluntary stage of swallowing?
    oropharyngeal phase - prehension, mastication, bolus formation, delivery to pharynx
  70. What is the order of a substance's likelihood of stimulation a swallow from the pharynx (from most to least)? (3)
    solid bolus>>>> liquids>>>>> oils
  71. What anatomic structures are associated with the oropharyngeal stage of swallowing? (5)
    teeth, tongue, hard palate, bone, mm. of mastication
  72. What anatomic structures are associated with the pharyngeal and pharyngoesophageal stages of swallowing? (3)
    pharyngeal muscles, soft palate, cricopharyngeal muscle (UES)
  73. Why SHOULDN'T you give cats mineral oil for hairballs?
    oils don't really stimulate a swallow response at the pharynx and can therefore be aspirated--> aspiration pneumonia
  74. Primary peristalsis of the esophageal phase of swallowing is initiated in the __________; secondary peristalsis is perpetuated by ____________.
    pharynx; local esophageal distention
  75. Why are softer foods given to animals with esophageal motility problems?
    liquids require a lesser peristaltic contraction
  76. Coordinated motor function for the esophageal phase of swallowing requires intact ________________.
    extrinsic innervation from the vagus n.
  77. Without the GES, what would happen to ingesta?
    the pressure gradient (thorax has negative pressure, abdomen has positive pressure) would allow food to flow freely from the stomach back into the thoracic esophagus
  78. Gastric emptying of liquids is determined by... (4)
    volume in stomach, tonic contraction of proximal stomach, pressure gradient b/w stomach and duodenum, pyloric resistance
  79. Gastric emptying of solids is determined by... (7)
    peristaltic contractions, particle size must be <2mm, antral motility, pyloric resistance, high fat content, increased parasympathetic stim increases emptying, sympathetic stim decreases emptying
  80. What are recommendations for patients with delayed gastric emptying? (3)
    low fat diet, liquid/canned food, small frequent meals
  81. What are the events that take place as part of colonic motility? (4)
    segmentation, mass movement of materials, defecation, gastrocolic reflex
  82. What is the interdigestive migrating motor complex (MMC)?
    "housekeeper function"- cycles of motor activity that occur during the fasting state, moving undigested debris from the stomach through the intestinal tract
  83. What is the major regulator of interdigestive MMC in dogs?
    motilin
  84. Why is erythromycin used as a pro-motility drug in dogs?
    it causes motilin release
  85. What are possible stimulators of the vomiting reflex? (4)
    peripheral input (GI tract- duodenal distention), vestibular center, CRTZ, cerebral cortex (less in animals)
  86. What are the efferent pathways involved int he vomiting reflex? (3)
    vagal and phrenic nerves (diaphragmatic and GI contractions), parasympathetic nerves to salivary glands (hypersalivation before vomiting), somatic motor nerves to abdominal muscles (abdominal contractions)
  87. What is the CRTZ?
    chemoreceptor trigger zone- area in the brain the detects toxins and leads to a vomiting reflex
  88. How does apomorphine work in dogs?
    stimulates vomiting by stimulating dopamine receptors in the CRTZ
  89. What is the first choice drug to stimulate vomiting in cats? Why isn't it the same a dogs?
    xylazine; cats lack the dopamine receptor in the CRTZ (apomorphine in dogs)
  90. What are 4 antiemetics?
    phenothiazines (CRTZ), metaclopramide (CRTZ), ondansetron (CRTZ), maropitant (vomiting center)
  91. What is the most likely pathway for stimulation of the vomiting reflex in the following situations:
    Uremia
    Digitoxin toxicity
    Apomorphine
    Hepatotoxins
    Endotoxemia
    CRTZ
  92. What is the most likely pathway for stimulation of the vomiting reflex in the following situations:
    Motion sickness
    Vestibular disease
    Vestibular apparatus
  93. What is the most likely pathway for stimulation of the vomiting reflex in the following situations:
    Duodenal obstruction
    Gastric ulcer
    Peritonitis
    afferents from the GI tract
  94. What is the most likely pathway for stimulation of the vomiting reflex in the following situations:
    Oral hydrogen peroxide
    Chemotherapy
    CRTZ?????
  95. What is the most important receptor and neurotransmitter to stimulate the vomiting center in dogs and cats? What drug blocks this receptor?
    substance P (neurotransmitter) binding Neurokinin-1 receptor in the vomiting center; Cerenia (maropitant)
Author:
Mawad
ID:
313959
Card Set:
GI1- Physiology
Updated:
2016-01-25 01:25:19
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vetmed GI1
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vetmed GI1
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