Pharmacology - Chapter 13

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tscoular
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244781
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Pharmacology - Chapter 13
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2013-11-03 18:50:20
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pharmacology vet tech
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Pharmacology - Dr. Younger
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  1. group of adrenocorticosteroids associated with the antiinflammatory response
    glucocorticoids
  2. cyclooxygenase-produced eicosanoids cause platelets to adhere to each other and thus contribute to the clotting mechanism
    thromboxanes
  3. means "loss of hair" and is a clinical sign of Cushing's disease
    alopecia
  4. type of immunity provided by antibodies
    humoral immunity
  5. combination of NSAID use plus arterial hypotension can produce this kidney condition that can result in kidney failure
    renal papillary necrosis
  6. lipoxygenase produces this eicosanoid
    leukotrienes
  7. diseases caused by the body's own defense mechanisms turning against its own tissues; examples would be lupus or certain hemolytic anemias in which the red blood cells are attacked by the body
    autoimmune reactions
  8. increase in neutrophils
    neutrophilia
  9. effect meaning that tissue is being destroyed or broken down; seen with steroids such as corticosteroids
    catabolic effects
  10. type of cell that produces antibodies against invading pathogens
    B-lymphocytes
  11. refers to the outer part of the adrenal gland (or any gland or organ that has an outer layer)
    cortex
  12. another name for hyperadrenocorticism
    Cushing's syndrome
  13. enzyme that produces prostaglandins and thromboxanes
    cyclooxygenase
  14. the collective term for all the prostaglandins, leukotrienes, and thromboxanes produced by the arachidonic acid pathway
    eicosanoids
  15. means "low numbers of eosinophils"; can be seen on the complete blood count when some species of animals are given corticosteroids
    eosinopenia
  16. condition characterized by clinical signs consistent with insufficient amounts of glucocorticoids
    Addison's disease
  17. the production of glycogen in the liver
    glycogenesis
  18. hormone released from the hypothalamus that stimulates the pituitary to release ACTH
    corticotropin-releasing factor
  19. means "decreased monocytes" and occurs in some species with the use of glucocorticoid drugs
    monocytopenia
  20. means "decreased size"; seen with the muscles and skin in animals with hyperadrenocorticism
    atrophy
  21. means that the animal has an elevated level of either natural cortisol or exogenous corticosteroids
    hyperadrenocorticism
  22. means the patient is exhibiting clinical signs consistent with low levels of corticosteroids
    hypoadrenocorticism
  23. means disease or condition "caused by the veterinarian"
    iatrogenic
  24. hormone released by the adrenal gland; is a mineralocorticoid
    aldosterone
  25. arachidonic acid is acted on by COX and this enzyme to produce the eicosanoids
    lipoxygenase
  26. this group of adrenocorticosteroids affects mainly the electrolytes (sodium and potassium) and water balance in the body with little or no antiinflammatory effect.
    mineralocorticoids
  27. creation of glucose from amino acids (which comes from catabolism of protein)
    gluconeogenesis
  28. a "decrease of lymphocytes in circulation"
    lymphopenia
  29. ibuprofen, ketoprofen, naproxen all belong to the same group of compounds characterized by this chemical structure
    propionic acid
  30. type of body defense mechanism characterized by cells that attack pathogens or foreign proteins (as opposed to the antibody response)
    cell-mediated immunity
  31. thromboxanes and these inflammatory mediators are produced by cyclooxygenase
    prostaglandins
  32. series of enzymes resulting in the production of eicosanoids after an injury
    arachidonic acid pathway
  33. cells involved in cell-mediated immunity; do not produce antibodies
    T-lymphocytes
  34. hormone released by the pituitary gland that stimulates the adrenal gland to produce corticosteroids
    ACTH (adrenocorticotropic hormone)
  35. NSAID that comes in a rapidly disintegrating tablet; not a selective COX-2 inhibitor; called a "dual-pathway NSAID" because it also blocks lipoxygenase
    tepoxalin
  36. chondroprotective agent that is a component of the joint synovial fluid; acts as a lubricant, and increases the viscosity of the fluid; may also suppress production of prostaglandins and scavenge free radicals
    hyaluronic acid
  37. intermediate-acting glucocorticoid that is not a "pred"
    triamcinolone
  38. older NSAID commonly used in equine medicine for relief of inflammation associated with the musculoskeletal system; 99% protein bound; bone marrow suppression has been reported in dogs
    phenylbutazone
  39. first COX-2 selective inhibitor released for veterinary medical use in the United States
    carprofen (Rimadyl)
  40. intermediate-acting corticosteroid; in the active form (does not have to be metabolized to become active)
    prednisolone, methylprednisolone, triamcinolone
  41. antiinflammatory that works differently from NSAIDs or glucocortocoids; scavenges superoxide radicals; stinks
    DMSO
  42. short-acting glucocorticoid; applied topically
    hydrocortisone
  43. besides carprofen, the other three COX-2 selective inhibitors used in veterinary medicine
    etodolac (EtoGesic), deracoxib (Deramaxx), and meloxicam (Metacam)
  44. long-acting glucocorticoid that comes in aqueous solution, alcohol form, and suspension form
    desamethasone
  45. prototype drug for the salicylates; commonly available OTC drug; nonspecific for its COX activity (hits both COX-1 and COX-2); used to reduce the risk for spontaneous clot formation
    aspirin
  46. derivatives of propionic acid; OTC drugs; high incidence of gastric ulcers when given by owner to pet dogs
    ibuprofen, ketoprofen, naproxen
  47. NSAID used primarily in horses for relief from colic; has more analgesic effect than phenylbutazone; thought to provide some protection against endotoxins
    flunixin meglumine
  48. chondroprotective agent that mimics the components of normal joint cartilage; traps water molecules and helps provide springy characteristic that allows the cartilage to tolerate impact; inhibits degrading enzymes in the joint fluid
    PSGAGs
  49. intermediate-acting corticosteroid; must pass through liver to be converted to its active form, prednisolone
    prednisone
  50. nutriceutical chondroprotective agents; precursors for PSGAGs appear to increase the efficiency with which cartilage repairs itself
    glucosamine and chrondroitin sulfate
  51. human OTC drug used to relieve discomfort from pain but is not an NSAID; very toxic to cats; rarely used in dogs
    acetaminophen
  52. True or False

    A long-acting glucocorticoid drug combined with acetate, diacetate, pivalate, or valerate would identify it as an aqueous solution.
    • False. Acetate, diacetate,
    • pivalate, or valerate extensions on drugs such as dexamethasone identify it as
    • suspension formulation. Although an aqueous solution drug can be given IV, a
    • suspension must never be given IV.
  53. True or False

    Vaccines should not be given to a dog that has been on prednisone for allergic skin reactions because the immune system will not be able to adequately respond.
    False. B-lymphocyte responses are not suppressed by normal doses of glucocorticoids. B-lymphocytes are responsible for producing antibodies.
  54. True or False

    In hypoalbuminemic animals the dose of NSAIDs may have to be increased to achieve the same effect on the tissues.
    False. Less blood protein means less protein for the NSAIDs to bind to in the blood. Thus more of the NSAID molecules are available in the free form to distribute to the tissues. If anything, the dose would have to be decreased to compensate for a greater percentage of the drug being able to get to the target tissues.
  55. True or False

    The two most common target organs for NSAID toxicity are the liver and the kidney.
    False. Kidney (renal papillary necrosis) and GI tract (ulcerations). Although the liver is listed as a target organ for some COX-2 selective toxicities, these are fairly rare incidences.
  56. True or False

    NSAIDs should be able to provide enough analgesia to allow an animal with a broken leg to be positioned for a radiograph of the leg without using anesthesia.
    False. NSAIDs are not true analgesics in that they do not reduce the perception of pain at the brain level to any great degree. An opioid analgesic is needed for this type of procedure.
  57. associated with glucocorticoid effects?

    increased retention of sodium
    No. that would be a mineralocorticoid effect.
  58. associated with glucocorticoid effects?

    maintain integrity of capillaries
    yes
  59. associated with glucocorticoid effects?

    decreased fibroblast activity
    yes
  60. associated with glucocorticoid effects?

    decreased T-lymphocyte activity
    Yes. This is why fungal diseases and other pathogens normally killed or suppressed by cell-mediated immunity can get worse when on glucocorticoid drugs.
  61. associated with glucocorticoid effects?

    decreased scar tissue formation
    Yes. Decreased fibroblasts decrease the amount of scar tissue laid down.
  62. associated with glucocorticoid effects?

    increased B-lymphocyte activity
    No. it affects primarily T-lymphocyte activity and cell-mediated immunity; much less so for antibody formation.
  63. associated with glucocorticoid effects?

    lymphocytosis
    Lymphocytosis is an increased number of lymphocytes. Glucocorticoids cause lymphopenia.
  64. associated with glucocorticoid effects?

    increased eosinophils and monocytes
    No. glucocorticoids cause eosinopenia and monocytopenia.
  65. associated with glucocorticoid effects?

    increased neutrophils
    yes
  66. associated with glucocorticoid effects?

    muscle wasting and atrophy
    yes
  67. What effect do NSAIDs have on the following?
    a.    Stomach and intestinal mucus production
    b.    Production of sodium bicarbonate by the GI tract wall
    c.    Repair of the GI epithelial cells
    Prostaglandins increase mucus production, increase sodium bicarbonate secretion, and increase the rate at which GI epithelial cells turn over and the GI tract wall repairs itself; thus NSAIDs that block these prostaglandins will decrease mucus and bicarbonate secretion and slow healing of the GI tract wall. This is what predisposes the GI tract to ulcers when nonselective COX inhibiting NSAIDs are used.
  68. You have heard the veterinarian talk about being cautious about using glucocorticoids in animals that are diabetics. What is the connection between a lack of insulin and glucocorticoid effects.
    Glucocorticoids increase gluconeogenesis (increased amino acid conversion to glucose), which can increase the amount of glucose in the blood. In diabetics, there is a decreased amount of insulin hormone present, and without insulin glucose cannot move from the blood into the cells (with the exception of nervous system cells). Thus more glucose in the blood from glucocorticoid drugs could increase the blood glucose in a diabetic animal. This increase may not necessarily be clinically significant with short-term use of intermediate-acting glucocorticoids.
  69. If an animal has an adrenal cortex tumor that is producing glucocorticoids, what would the clinical condition be called? Would levels of natural cortisol be higher or lower than normal? What about CRF and ACTH levels?
    The tumor is producing glucocorticoids regardless of whether the adrenal gland is being stimulated to do so. Thus the adrenal gland is expected to produce massive amounts of cortisol. Because the cortisol levels are so high, there is a significant amount of negative feedback on the hypothalamus and pituitary to stop secretions of CRF and ACTH. Thus CRF and ACTH levels would be very low. This condition is either hyperadrenocorticism or Cushing’s syndrome
  70. An animal has been on dexamethasone tablets for 5 weeks to control severe allergies. He is showing signs of hyperadrenocorticism. If you were to check concentrations of ACTH, CRF, and natural cortisol, would they be higher or lower than normal? What would this clinical condition be called? Should the dexamethasone be stopped immediately to prevent worsening of clinical signs?
    This is hyperadrenocorticism caused by administration of the dexamethasone. The administration of drug results in cortisol-like effects and thus the clinical signs of  iatrogenic Cushing’s are seen. This condition would be called iatrogenic hyperadrenocorticism because it is caused by the physician or the medication and not by a tumor on the adrenal gland. Like natural cortisol, dexamethasone also suppresses the activity of the pituitary and hypothalamus. Therefore, CRF and ACTH would both be decreased below normal. Although this animal is showing signs of iatrogenic Cushing’s, dexamethasone should not be stopped immediately because the animal may be thrown into a state of hypoadrenocorticism because of atrophy of the adrenal gland. The atrophy of the adrenal gland is caused by ACTH release being suppressed by the dexamethasone and thus blocking any ACTH stimulation of the adrenal gland. Without stimulation, the adrenal gland atrophies. If dexamethasone is stopped immediately, the levels of dexamethasone would decrease but the atrophied adrenal gland would not be able to respond to the increased need for natural cortisol to take its place. The net effect would be below-normal level of glucocorticoids. This is Addison’s disease or hypoadrenocorticism. Instead of stopping the dexamethasone immediately, the dose of dexamethasone needs to be tapered off over 2 to 3 weeks until the animal is weaned completely off the drug.
  71. The veterinarian has just prescribed a COX-2 selective NSAID for Mrs. Jones’ German shepherd with arthritic hips. Mrs. Jones is grumbling about the high cost of the medication and finally asks you why she cannot use aspirin because it is much cheaper. What is the medical reason for using the more expensive and newer COX-2 inhibitors over aspirin drugs?
    A COX-2 inhibitor is more selective for decreasing the production of inflammatory prostaglandins than a drug such as aspirin that suppresses both COX-2 and COX-1 enzymes. The COX-1 enzyme produces prostaglandins that are required for normal functions such as maintaining local blood flow (kidneys) or for maintaining the normal health of the stomach and intestinal wall. Because aspirin blocks both COX-1 (enzyme that produces helpful eicosanoids) and  COX-2 (enzyme that produces  prostaglandins that are associated with inflammation), the aspirin may compromise the health of the GI tract and increase the risk for ulcer formation. Although they are more expensive, selective COX-2 inhibitors tend to be safer at normal doses than aspirin because they block inflammatory prostaglandin formation while still allowing the healthy prostaglandins to be formed by COX-1 enzymes.
  72. The owner of an animal that is being discharged from the hospital after orthopedic surgery wants to know why a drug is given for pain before the surgery. “That doesn’t make any sense,” she says. “And according to the doctor, it was an aspirin-like drug! Who takes aspirin before having bone surgery?” What do you say to explain this?
    The use of NSAIDs or other analgesics before surgery is to decrease the amount of pain signals being sent up the spinal cord to the brain from the pain receptors around the site of the surgical procedure and bone manipulation. When many pain signals are sent up the spinal cord, the neurons in the spinal cord change and over time will more readily send pain signals to the brain with less stimulation from the pain receptors. This is the process called wind-up and it contributes significantly to the pain felt after the surgical procedure. By using NSAIDs (the aspirin-like compound) to decrease inflammation, decrease pain receptors depolarizing, and decrease the wind-up process, the perception of pain by the brain after surgery can be significantly reduced
  73. What precautions should you take when working with DMSO?
    DMSO can penetrate the skin and also carry toxins or other chemicals into the skin with it. Always wear good-quality gloves when applying this compound topically.
  74. A client is surprised to find out from you that acetaminophen (Tylenol) is so toxic to cats. “So, aspirin must be poisonous, too, since they are really the same thing, aren’t they?” Answer her and explain why acetaminophen is so poisonous to cats.
    This client needs to understand that aspirin is not Tylenol, which is not ibuprofen, which is not Aleve, and so forth. This is a common misperception by the public. The only safe one of these drugs for use in the cat is aspirin. Aspirin has to be used at a lower dose than for dogs because of the slow metabolism of cats, but it can still be safely used at the “baby” aspirin dose every 2 days. Acetaminophen, on the other hand, is converted by the cat liver into a toxic substance. Unfortunately, the cat’s liver does not have much of the necessary compound available to convert the toxic substance into a nontoxic substance. Thus cats can die from accumulation of the toxic metabolite of acetaminophen
  75. What signs are seen with acetaminophen toxicosis in the cat? What is the treatment
    of choice?
    Typically the acetaminophen metabolite causes changes in the red blood cells that result in hemolysis and changes in the hemoglobin so that the mucous membranes appear chocolate-colored. The urine also turns black because of the hemolysis of the red blood cells and excretion of the methemoglobin. The face of a cat with acetaminophen toxicosis will often swell. Treatment is acetylcysteine, which provides the materials the liver needs to convert the toxic metabolite to a nontoxic metabolite.

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