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NSAIDs - pharmacology 2

Gelöschter Nutzer Der Nutzer hat seine Fachbereichs-Information gelöscht. Englisch 105 Karten

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  1. 1What is aspirin?Acetylsalicylic acid, a nonsteroidal anti-inflammatory agent, a salicylate ester of acetic acid
  2. 2In vivo, what is ASA hydrolyzed to?Salicylate and acetate
  3. 3What is ASA's Pka?3.5, acidic
  4. 4Which enzyme is irreversibly acetylated and inactivated by ASA?Cyclooxygenase 1
  5. 5What is the purpose of cyclooxygenase 1?-Catalyzes the formation of prostaglandin synthesis precursors from arachidonic acid
  6. 6If ASA is inhibiting prostaglandin synthesis, what are effects?anti-inflammatory
  7. 7What does ASA do to bleeding time? In which population is it worst?prolong bleeding time by several minutes; longer in children and patients with bleeding disorders
  8. 8Why are platelets affected by ASA?The inactivation of cyclooxygenase-1 prevents thromboxane A2 synthesis preventing platelet aggregation and release reaction
  9. 9ASA irreversible effect on platelets' and megakaryocytes last how long?4-7 days the life of a typical platelet bc cox-1 is not resynthesized
  10. 10Why are ASA and salicylates rapidly absorbed in GI after oral ingestionThey are nonionized in low pH
  11. 11What factors affect the bioavailability of ASA?dosage form, the presence of food, gastric emptying time, gastric pH, the presence of antacids
  12. 12What is the rate-limiting step in the absorption of ASA? What can help?Dissolution; higher pH (addition of buffers to ASA tablets)
  13. 13What is the downside of increasing pH for dissolution of ASA?decrease absorption due to increased degree of ionization
  14. 14The pH of stomach is 1.5, pka of ASA is 3.5, so what state is ASA in?nonionized
  15. 15How does ASA move to gastric mucosol cells and why does it stay there?passive diffusion; then ASA become ionized in new pH and cannot reenter lumen of stomach
  16. 16Where is ASA distribution? Which barriers can it pass?In most bodily tissues, it can readily cross placental barrier and blood-brain barrier
  17. 17What does ASA do in the plasma?Bind to albumin, this concentration dependent cause drug interaction
  18. 18What is the initial route of metabolism for ASA and salicylates?Conversion to salicylic acid
  19. 19How is ASA excreted in the urine?As Salicyclic acid
    - as salicyluric acid (with glycine)
    - Glucuronide ether and ester (w/ glucuronic acid)
  20. 20How is excretion done? dependent on?By the kidney; pH of urine
  21. 21What increases the excretion (renal clearance) of urinary pH?more basic urine (alkalinization) from
    pH 5 to 8
  22. 22What are the GI disturbances associated withdyspepsia, heartburn
    epigastric distress, nausea
    vomiting anorexia
    abdominal pain
  23. 23Which salicylate has more GI disturbances?ASA
  24. 24What percentage of patients taking analgesic or antipyretic have GI disturbances?2-10 %
  25. 25What percentage of patients taking high doses ASA have GI disturbances10- 30 %
  26. 26What percentage of patients with preexisting peptic ulcers have GI disturbances30 - 90%
  27. 27What can minimize the GI effects of ASAfood and large volumes of water or milk, enteric coated tablets
  28. 28When can occult bleeding happen with ASA?usual dosages, specifically with ulcers (painless)
  29. 29How much blood loss can uncoated aspirin cause? What can it lead to?2-8 ml daily blood loss; iron deficient anemia
  30. 30What type of damage is common in long-term ASA therapy?Gastric mucosal damage
  31. 31What might ASA reactivate?Latent gastric/ duodenal ulcers
  32. 32What kind of effect does ASA have with alcohol? What do they cause?Synergistic effect; GI bleeding
  33. 33What can prostaglandins do to the stomach? How?Protect the stomach by lowering gastric acid productions
  34. 34What is misoprostol (lytotec)? What effect does it have?prostaglandin E1 analogue; anti-ulcer effect for patient' s on long term ASA
  35. 35What otic effects can large doses of ASA have? What should ASA be discontinued with these symptomsTinnitus/ hearing loss; they are indicative of chronic salicylate intoxication
  36. 36Reversible tinnitus is observed at 200 ug/ml what does that mean?adequate concentrations for anti-inflammatory effects have been reached
  37. 37Hepatic function must be monitored in ASA bc?Reversible hepatotoxicity develops after 1-4 wks of therapy when concentration exceeds 200 mg/ ml
  38. 38What dosage can cause hepatic damage? how is it shown?overdosage; marked reduction in creatinine clearance or acute tubular necrosis with renal failure
  39. 39What does inhibition of COX-2 (renal prostaglandin) cause in renal damage?Renal medullary ischemia; renal fucntion should be monitored
  40. 40How do salicylates cause moderate to serve noncardiogenic pulmonary edema? How is risk higherIncreasing alveolar-capillary membrane permeability; long-term salicylate therapy and smoking
  41. 41What type of content should be avoided for CHF patientshigh buffered (high sodium)
  42. 42What are the hematologic effects of daily ASAdecrease hematocrit; iron concentration and erythematous life span
  43. 43In what event, should ASA therapy be discontinued? Why?5-7 days before surgery to prevent excessive perioperative bleeding
  44. 44What types of patients is ASA counter indicativepatients with bleeding disorders like hemophilia
  45. 45What is the hypersensitive response involving IgE antibodies? What type is it?Urticaria/ angioedema; type 1 hypersensitivity reactions
  46. 46In asthma patients, what does aspirin sensitivity look like? What is it called?bronchospasm related to nasal polyps; aspirin triad
  47. 47When children have varicella infections (chicken pox) or influenza-like diseases, they are at risk of what?Reye's syndrome (vomiting, HA, belligerence, delirium, and coma)
  48. 48What can be used instead of ASA in children/ teens with suspected varicella?Acetominophen
  49. 49ASA is not approved for safe use during pregnancy specifically?during the last 3 months of pregnancy unless potential benefits justify possible risks to fetus like prevention of preeclampsia (high BP)
  50. 50What is the possible risk to focus?hemorrhagic complications
  51. 51Due to risk of platelet function, what should long term salicylate therapy mother's not do?Breastfeed bc salicylates are secreted into mother's milk
  52. 52What is chronic salicylate intoxication called? What does it result from?Salicylism; therapy with high dosages
  53. 53How much ASA causes death in adults? Children?10- 30 g; 4g
  54. 54When does plasma salicylate cause analgesic? Anti-inflammatory, tinnitus and intoxication0-10, 0- 20, 50, and 100 mg/ dl
  55. 55What are the most common manifestations of chronic intoxicationsTinnitus and hearing loss
  56. 56What are principle manifestations of salicylate OD?acid-base and electrolyte disturbances
    dehydration
    hyperpyrexia (high fever)
    hyper or hypoglycemia
  57. 57when should OD treatment start? what does it consist of?immediately; removal from GI tract (Ipecac syrup induced emesis) prevention of absorption by activated charcoal (with in 2 hours)
  58. 58How do you enhance salicylate elimination?IV sodium bicarbonate to alkalinize urine to pH 7.5 to enhance excretion (loop direutic)
  59. 59Why would NSAIDS not be used with other NSAIDSsynergistic effects increase GI effects and combination has not been established to be more efficacious
  60. 60Which is ASA used for? In prevention of?-mild to moderate pain, fever and inflammatory disease
    -Arterial/ venous thrombosis
  61. 61ASA is salicylate of the first choice for anti-inflammatory and analgesic effects, when is it used as an initial long-term treatmentRheumatoid arthritis, juvenile arthritis and osteoarthritis
  62. 62what is the normal dose for arthritis required patients?2.4 - 3.6 g in divided doses daily, but more maybe
  63. 63What is diflunisal (Dolobid)?Diflurorphenyl derivate of salicylic acid
  64. 64How is diflunisal different from ASA?- not hydrolyzed to salicylate
    - little antipyretic activity
    - reversibly inhibits cyclooxygenase enzyme
  65. 65diflunisal also rapidly absorbed in GI tract but its half-liferanges from 8 to 12 hours which is 3 to 4 times greater than ASA
  66. 66What properties do NSAIDS have (acetic acid derivatives)analgesic and antipyretic properties
  67. 67What is the main mechanism of action of NSAIDS? Results? (not ASA)Reversible cyclooxygenase 1 & 2 enzyme inhibition; reduction of production of prostaglandins/ thromboxane B2
  68. 68Most NSAIDs are used for RA and osteoarthritis except?Ketorolac & mefenamic acid
  69. 69Which NSAIDS are used for JRA?Tolmetin & naproxen
  70. 70What is the speed of NSAID absorption and what can delay it?Rapidly and completely; food delays absorption but drug is still absorbed
  71. 71What are NSAIDs bound to?protein
  72. 72What are NSAID half-lives like and pka?1.5 to 86 hours; pka is acidic 3.5 to 6.3
  73. 73Where are NSAIDs metabolized and excreted (as what)?liver; kidney (metabolites)
  74. 74Due to problem with fluid retention and peripheral edema which patients should be cautious with NSAIDScompromised cardiac function
    hypertension
    predisposition to fluid retention
  75. 75Which NSAID cause strong HAs? Which of the two is also associated with psychiatric distrubances?indomethacin/ ketorolac; indomethacin
  76. 76Why would NSAIDS cause CNS side effects like dizziness, HA and somnolescence/ dizzinessability to cross BBB
  77. 77Which population has increased adverse reaction to NSAIDSpt's older than 65
  78. 78What are major problems of GI with NSAIDSGastric and duodenal ulcer with gross bleeding and perforation
  79. 79Autoimmune hemolytic anemia is a type II drug allergy caused by? How do you stop it?Use of Tolmetin after 12 months or longer; effect is reversible with discontinuation of Tolmetin
  80. 80What has been reported with hepatic abnormalitieshepatitis, jaundice and toxic hepatitis
  81. 81What can hypersensitivity manifest as?asthma, anaphylaxis, acute respiratory distress, rapid fall in BP, angioedema, dyspnea, angitis
  82. 82When does ibuprofen have severe reactions?In patients with systematic lupus erythematous or other collagen disease
  83. 83What hypersensitivity does Tolmetin causeautoimmune hemolytic anemia
  84. 84Why is there a precaution for nursing mothers?Most NSAIDS are secreted in breast mile with potential effect on infant's cardiovascular system
  85. 85What can NSAIDS metabolites progressively cause?Renal impairment; (its COX-2) decreased renal prostaglandin product might lead to renal decomposition
  86. 86What are the renal effects? What fixes it?Hyperkalemia, hypernatremia, and papillary necrosis (irreversible); discontinuation of NSAIDs leads to recovery
  87. 87What dangerous event occurs in pregnancy? WHy?Premature closure of fetal ductus arteriosus; bc of inhibition of prostaglandin E2 synthesis (should be avoided in 3rd trimester)
  88. 88What FDA labeled NSAIDs are used for closure of patent (open) ductus arterious in premature infantsIndomethacin & Ibuprofen
  89. 89How does celecoxib (celebrex) inhibit prostaglandin synthesisInhibition of the cyclooxygenase-2 (cox -2) in kidney and neuron; does not inhibit COX-1
  90. 90What metabolites celecoxibcytochrome p450 2C9, metabolites are inactive
  91. 91Celecoxib should not be given to patients;s who have allergic type reactions to? Why?Sulfonamides; its chemically bexene sulfamide
  92. 92What is another name for acetaminophen?N-acetyl-p-aminophenol or paracetamol
  93. 93What us acetaminophen's active metabolitephenacetin
  94. 94what does acetaminophen act on to increase dissipation of body heat? How?Hypothalmic heat regulating center; vasodilation and sweating
  95. 95How is acetaminophen different from NSAIDSonly weakly inhibits COX-1 and COX-2 enzymes
  96. 96What are Acetaminophen metabolites? Are they activate?Acetaminophen sulfate and acetaminophen glucuronide; not active
  97. 97What is acetaminophen deactivated by?hepatic microsomal enzymes and in smaller amounts cytochrome p450
  98. 98What is bad about cytochrome p450 metabolism? What makes it worse?Its metabolites are N-acetyl-p- benzoquinoneimine are highly reactive to cellular proteins and causes toxic to both liver and kidney; in large amounts, they can be inactivated by GSH (glutathione sulfhydryl)
  99. 99What is the most serious reaction?Hepatoxicity - fatal hepatic centrilobular necrosis in high doses
  100. 100what is a specific antidote for acetaminophen toxicity? What does it restore?oral N-acetylcysteine (Mucomyst); restore glutathione levels
  101. 101Acetaminophen is good substitute for ASA as analgesic-antipyretic agent butanti-inflammatory effects are weaker
  102. 102What disease is acetaminophen used for?osteoarthritis
  103. 103What is conventional dose of acetaminophen and cannot exceed325- 500 mg four times daily; 4000 mg
  104. 104What is the max dose of acetaminophen for alcoholics2000 mg/ day
  105. 105What is the common daily dose of adults/ children depending on age and weight?1000 mg; 40 - 480 mg

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Der Nutzer hat seine Fachbereichs-Information gelöscht. Karteikarten am NSAIDs - pharmacology 2, erstellt von Gelöschter Nutzer am 22/10/2017.
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Gelöschter Nutzer · Okt 2017
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22 Okt 2017
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  • Erstellt von Jen Orellana · 22 Okt 2017
  • Kopiert von Jen Orellana · 22 Okt 2017
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