Pharm Exam 4: Gout, RA, SLE

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choward04
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Pharm Exam 4: Gout, RA, SLE
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2013-03-15 22:46:12
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  1. What is the only way to diagnose acute gout?
    -Joint aspiration and crystal identification
  2. What are the 4 distinct stages of gout?
    • 1. Asymptomatic hyperuricemia
    • 2. Acute flares
    • 3. Intercritical gout
    • 4. Advance gout
  3. Discuss asymptomatic hyperuricemia.
    -Can take as long as 10yr after increased serum levels for gout to occur
  4. Discuss Acute flares.
    -Acute inflammation, often podagra
  5. T or F. Gout flares in the wrist is a common place.
    False--> pseudogout may effect wrist/knees, not REAL gout
  6. Discuss intercritical gout.
    -Intervals between acute flares
  7. Discuss Advanced gout.
    • -Long term gout with complications, uncontrolled hyperuricemia
    • -may see kidney stones, renal nephritis
  8. What are 6 med treatments for gout?
    • 1. NSAIDs (high doses)
    • 2. Colchine (only PO, be cautious)
    • 3. Oral corticosteriods (higher doses, no taper)
    • 4. Intra-articular corticosteriods (in joint)
    • 5. Parental corticosteriods (IM ACTH)
    • 6. Adrenocorticotropin hormone (ACTH)
  9. What are common S/E of NSAIDs?
    -GI toxicity, impaired platelet fxn, renal/liver tox, hypersensitivity, tinnitus, H/A, aseptic meningitis
  10. What are some commone S/E for colchicine?
    -abdominal pain, N/D, bone marrow suppression, neuromyopathy (chronic use)
  11. What is the driving force for choosing a medication for gout?
    Presence of comorbidities
  12. What patients should NSAIDs be avoided? (2)
    • 1. renal impairment
    • 2. GI bleeding risk
  13. What patients should colchicine use be avoided?
    • -severe liver/renal impairment
    • -Patients on bed rest
  14. What gout medication is great for renal impairment or GI bleeding patients?
    Corticosteroids (esp good if >3 joints effected)
  15. What are 6 situations to consider using uric acid lowering therapy?
    • 1. 2 or > episodes of gout a year
    • 2. Tophaceous gout (absolutely)
    • 3. erosive arthritis on radiographs
    • 4. Urate nephropathy (crystal in kidneys)
    • 5. uric acid nephropathy (crystals in tubules)
    • 6. Uric acid nephrolithiasis (kidney stones)
  16. Where are tophi most commonly seen?
    ear and extensor aspects of joints
  17. What is a major adverse reaction of allopurinol?
    -Toxic dermal exfoliation (SJS?)
  18. Which Uric acid lowering meds should NOT be used in patients w/ kidney stones?
    • Probenecid
    • -Suflinpyrazone
  19. Name 4 urate lowering medications.
    • 1. Allopurinol
    • 2. probenecid
    • 3. sulfinpyrazone
    • 4. febuoxostat
  20. Which urate lowering med is a NON-purine inhibitor of xanthine oxidase?
    -Febuxostat--> good for patients intolerant of allopurinol
  21. What is your target uric acid value?
    <6mg/dl
  22. When should you consider treating asymptomatic hyperuricemia or treat prophylactically?
    • 1. Tumor lysis syndrome (leukemia)
    • 2. Severe hyperuricemia (>12--> risk of gout >95% within the year)
  23. T or F.  Urate lowering meds should be started in acute gout situations?
    FALSE--> but don't stop during acute episodes
  24. What prophylactic therapy should be started with starting urate lowering therapy meds?
    -Can cause a flare initially so start colchicine, NSAIDs, prednisone for 3-12months with urate lowering meds
  25. T or F.  Urate lowering meds should not be started or stopped during acute attacks
    True
  26. What are the meds of CANT LEAP for meds that cause hyperuricemia?
    • C-cyclosporine
    • A-alcohol
    • N- nicotinic acid
    • T- Thiazides
    • L- lasix
    • E-ethambutol
    • A- aspirin (low dose)
    • P-pyrazinamide
  27. What 3 meds may have beneficial effect on serum uric acid?
    • 1. fenofibrate
    • 2. Losartan
    • 3. Vit C
    • **use as adjuncts
  28. T or F.  Asymptomatic hyperuricemia rates requires treatment.
    True
  29. T or F.  Colchicine is more effective than NSAIDs and corticosteriods in treating acute gout.
    FALSE--> all have same efficacy
  30. T or F.  Consider uric acid lowering therapy is 2 more attacks/yr
    True
  31. T or F. Uricosurics should not be used in patients with renal stones, tophaceous gout, GFR <50 or who are overproducers.
    • True
    • -Uricosurics--> probenecid & sulfinpyrazones
  32. What population is classic for Rheumatoid arthritis?
    Women of child-bearing age
  33. How long should joints symptoms be occuring before considering rheumatoid arthritis?
    >6 weeks b/c synovitis viruses can last that long
  34. What are the 4 goals of RA therapy?
    • 1. Preservation of joint structures
    • 2. Eradication of pain & inflammation
    • 3. Maintenance of pre-morbid quality of life
    • 4. Control of systemic complications
  35. What are 4 positive outcomes of PT/OT on RA?
    • 1. joint protection
    • 2. adaptive aids
    • 3. muscle strengthening
    • 4. safe exercising
  36. What are 3 groups of meds used for RA?
    • 1. Anti-inflammatory--> NSAIDs, corticosteriods
    • 2. DMARDs (MTX)
    • 3. Biologic response modifiers (TNF & IL-1 inhibitors)
  37. What should you be wary about when starting a patient on biologic response modifiers?
    -Long term effects have not been studies, so be wary about starting in younger populations that will need it long term
  38. When should you refer a patient with RA?
    Within 3 mo--> most damage by RA is done within the first 2-3yrs
  39. What risk factors should aggressive treatment be initiated in? (6)
    • 1. > 20joints affected
    • 2. Extra-articular disease
    • 3. RF or CCP +
    • 4. Erosions on xrays
    • 5. <11 grade education
    • 6. HLA-DR4 positivity
  40. What is the role of NSAIDs in the txt of RA?
    Symptom control and adjunct to other therapies (NOT SOLE therapy)
  41. When should corticosteriods be use in management of RA?
    • 1. Low dose--> symptom control, dx modifying
    • 2. bridge therapy (starting MTX)
    • 3. Intra-articular corticosteriods--> rapid control in specific joints
    • 4. High-dose--> severe extra-articular, pneumonitis
    • 5. AVOID long term
  42. When a patient in on MTX, how often should labs be checked?
    CBC, CMP q 2mo
  43. If a patient is taking Hydroxychloroquine, what exam should be performed yearly?
    Eye exam, b/c can cause retinopathy
  44. What are the 4 meds and how often is monitoring for DMARD therapy in RA?
    • 1. MTX, (CBC, CMP, Hep baseline-CBC/CMP q 2mo)
    • 2. Hydrochloroquine- annual eye
    • 3. Sulfasalazine (G6PD, CBC, CMP, monitor q 3mo)
    • 4. Feflunomide (like MTX)
  45. What is the MOA of hydroxychloroquine?
    -Interferes w/ antigen processing, concentrates in lysosomes (anti-inflammatory)
  46. MOA: Sulfazalazine
    -Anti-inflammatory and antimicrobial effects
  47. MOA: MTX
    -Inhibits purine synthesis via dihydrofolate reductase, decreases T & B cell proliferation
  48. MOA: Leflunomide
    Inhibits dihydroorotate dehydrogenase (blocks pyrimidines-->blocking proliferative lymphocyte response)
  49. MOA: Azathiprine
    -purine analog and immunosupressant (both T & B cell function
  50. What is the major S/E for Hydroxychloroquine.
    Hydroxy--> Retinal toxicity
  51. What is the major SE for sulfasalazine?
    Neutropenia, hepatic enzymes elevation
  52. What is the major SE MTX?
    Hepatic fibrosis, myelosuppression. Caution in rena/liver d/o, Limit ETOH
  53. What are major SE of Leflunomide?
    Neutropenia, thrombocytopenia, hepatic liver enzymes
  54. What are major SE of Azathioprine?
    Leukopenia, megaloblastic anemia, thrombocytopenia, hepatotoxicity
  55. Wh⇑

    at are the major SE of TNF inhibition? (4)
    • 1. Disseminated infections (MOST WORRISOME)--> ⇑ risk of viral infections, bacteria less common, screen for latent TB
    • 2. Malignancy risk (avoid in skin cancers)
    • 3. Demyelinating disorders
    • 4. Class III/IV heart failure
  56. What are the 11 S/S for SLE classification?
    • 1. Malar rash
    • 2. Discord rash
    • 3. Photosensitivity
    • 4. Oral ulcers
    • 5. arthritis
    • 6. serositis
    • 7. renal disorder
    • 8. neurologic disorder
    • 9. hematologic disorder
    • 10. immunologic d/o
    • 11. antinuclear antibodies (ANA)
  57. What are 5 drug classes used to treat SLE?
    • 1. NSAIDS
    • 2. Antimalarials
    • 3. corticosteroids
    • 4. immunosuppressive agents
    • 5. biologics
  58. What are the goals of SLE treatment of cutaneous disease? (4)
    • Prevent:
    • 1. Telangectasias
    • 2. pigmentary changes
    • 3. alopecia
    • 4. scarring
  59. Are NSAIDs apart of the txt for SLE: cutaneous disease?
    • NO
    • -topical corticosteriods
    • -antimalarials
    • -immunosuppressives
    • -intralesional corticosteriod injections
  60. Which SLE med is used for non-scarring lesions?
    Anti-malarials
  61. Which SLE med is used for scarring lesions?
    Immunosuppressive agents
  62. Are ulcers in the mouth r/t to lupus painful or painless?
    Painless, and usually on the palate
  63. When do patients with SLE absolutely need a referral?
    with nephritic sediment
  64. What class of renal disease is treatment essential?
    • Class III--> focal proliferative
    • Class IV--> diffuse proliferative
    • ** possible Class V (membraneous)
  65. What does txt of SLE: renal disease include (2)?
    • 1. immunosuppressives
    • 2. cytotoxic therapy
  66. What is the main txt of SLE: hematolytic disease?
    High dose corticosteroids
  67. What are the main txts for SLE: MSK disease?
    • Analgesics/NSAIDs--> arthralgias
    • -add antimalarials--> arthritis
    • -add MTX--> refractory
  68. What are manifestations of SLE: Cardio disease?
    • 1. pericardial disease
    • 2. valvular heart disease
    • 3. coronary heart disease
    • 4. costochondritis
    • 5. pneumonitis
    • 6. pulmonary hemorrhage
    • 7. mycarditis
    • 8. interstitial lung disease
  69. What is the SLE treatment for pericardial disease and myocarditis?
    • -Pericardial disease--> NSAIDs, low dose corticosteroids
    • -Myocarditis--> high dose corticosteriods
  70. What focal manifestations of SLE: CNS caused by?
    -intravascular occlusion due to antibodies or vasculitis
  71. What are the diffuse manifestation of SLE:CNS caused by?
    -Immune mechanism--> immune complexes, vasculitis, and vasculopathies
  72. T or F.  Fertility is not usually an issue in SLE?
    true
  73. Which drugs for SLE are class B?
    NSAIDs, glucocorticosteroids
  74. Which drugs for SLE are class C in pregnancy?
    • Azathioprine
    • cyclophosphamide
  75. Which drug for SLE is class X in pregnancy?
    MTX
  76. What is the goal of SLE in patients w/ APLA syndrome?
    Prevent clots (anticoagulation or immunosuppression agents)

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