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What is the only way to diagnose acute gout?
-Joint aspiration and crystal identification
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What are the 4 distinct stages of gout?
- 1. Asymptomatic hyperuricemia
- 2. Acute flares
- 3. Intercritical gout
- 4. Advance gout
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Discuss asymptomatic hyperuricemia.
-Can take as long as 10yr after increased serum levels for gout to occur
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Discuss Acute flares.
-Acute inflammation, often podagra
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T or F. Gout flares in the wrist is a common place.
False--> pseudogout may effect wrist/knees, not REAL gout
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Discuss intercritical gout.
-Intervals between acute flares
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Discuss Advanced gout.
- -Long term gout with complications, uncontrolled hyperuricemia
- -may see kidney stones, renal nephritis
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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)
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What are common S/E of NSAIDs?
-GI toxicity, impaired platelet fxn, renal/liver tox, hypersensitivity, tinnitus, H/A, aseptic meningitis
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What are some commone S/E for colchicine?
-abdominal pain, N/D, bone marrow suppression, neuromyopathy (chronic use)
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What is the driving force for choosing a medication for gout?
Presence of comorbidities
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What patients should NSAIDs be avoided? (2)
- 1. renal impairment
- 2. GI bleeding risk
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What patients should colchicine use be avoided?
- -severe liver/renal impairment
- -Patients on bed rest
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What gout medication is great for renal impairment or GI bleeding patients?
Corticosteroids (esp good if >3 joints effected)
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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)
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Where are tophi most commonly seen?
ear and extensor aspects of joints
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What is a major adverse reaction of allopurinol?
-Toxic dermal exfoliation (SJS?)
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Which Uric acid lowering meds should NOT be used in patients w/ kidney stones?
- Probenecid
- -Suflinpyrazone
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Name 4 urate lowering medications.
- 1. Allopurinol
- 2. probenecid
- 3. sulfinpyrazone
- 4. febuoxostat
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Which urate lowering med is a NON-purine inhibitor of xanthine oxidase?
-Febuxostat--> good for patients intolerant of allopurinol
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What is your target uric acid value?
<6mg/dl
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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)
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T or F. Urate lowering meds should be started in acute gout situations?
FALSE--> but don't stop during acute episodes
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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
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T or F. Urate lowering meds should not be started or stopped during acute attacks
True
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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
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What 3 meds may have beneficial effect on serum uric acid?
- 1. fenofibrate
- 2. Losartan
- 3. Vit C
- **use as adjuncts
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T or F. Asymptomatic hyperuricemia rates requires treatment.
True
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T or F. Colchicine is more effective than NSAIDs and corticosteriods in treating acute gout.
FALSE--> all have same efficacy
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T or F. Consider uric acid lowering therapy is 2 more attacks/yr
True
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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
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What population is classic for Rheumatoid arthritis?
Women of child-bearing age
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How long should joints symptoms be occuring before considering rheumatoid arthritis?
>6 weeks b/c synovitis viruses can last that long
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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
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What are 4 positive outcomes of PT/OT on RA?
- 1. joint protection
- 2. adaptive aids
- 3. muscle strengthening
- 4. safe exercising
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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)
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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
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When should you refer a patient with RA?
Within 3 mo--> most damage by RA is done within the first 2-3yrs
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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
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What is the role of NSAIDs in the txt of RA?
Symptom control and adjunct to other therapies (NOT SOLE therapy)
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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
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When a patient in on MTX, how often should labs be checked?
CBC, CMP q 2mo
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If a patient is taking Hydroxychloroquine, what exam should be performed yearly?
Eye exam, b/c can cause retinopathy
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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)
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What is the MOA of hydroxychloroquine?
-Interferes w/ antigen processing, concentrates in lysosomes (anti-inflammatory)
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MOA: Sulfazalazine
-Anti-inflammatory and antimicrobial effects
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MOA: MTX
-Inhibits purine synthesis via dihydrofolate reductase, decreases T & B cell proliferation
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MOA: Leflunomide
Inhibits dihydroorotate dehydrogenase (blocks pyrimidines-->blocking proliferative lymphocyte response)
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MOA: Azathiprine
-purine analog and immunosupressant (both T & B cell function
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What is the major S/E for Hydroxychloroquine.
Hydroxy--> Retinal toxicity
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What is the major SE for sulfasalazine?
Neutropenia, hepatic enzymes elevation
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What is the major SE MTX?
Hepatic fibrosis, myelosuppression. Caution in rena/liver d/o, Limit ETOH
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What are major SE of Leflunomide?
Neutropenia, thrombocytopenia, hepatic liver enzymes
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What are major SE of Azathioprine?
Leukopenia, megaloblastic anemia, thrombocytopenia, hepatotoxicity
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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
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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)
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What are 5 drug classes used to treat SLE?
- 1. NSAIDS
- 2. Antimalarials
- 3. corticosteroids
- 4. immunosuppressive agents
- 5. biologics
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What are the goals of SLE treatment of cutaneous disease? (4)
- Prevent:
- 1. Telangectasias
- 2. pigmentary changes
- 3. alopecia
- 4. scarring
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Are NSAIDs apart of the txt for SLE: cutaneous disease?
- NO
- -topical corticosteriods
- -antimalarials
- -immunosuppressives
- -intralesional corticosteriod injections
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Which SLE med is used for non-scarring lesions?
Anti-malarials
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Which SLE med is used for scarring lesions?
Immunosuppressive agents
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Are ulcers in the mouth r/t to lupus painful or painless?
Painless, and usually on the palate
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When do patients with SLE absolutely need a referral?
with nephritic sediment
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What class of renal disease is treatment essential?
- Class III--> focal proliferative
- Class IV--> diffuse proliferative
- ** possible Class V (membraneous)
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What does txt of SLE: renal disease include (2)?
- 1. immunosuppressives
- 2. cytotoxic therapy
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What is the main txt of SLE: hematolytic disease?
High dose corticosteroids
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What are the main txts for SLE: MSK disease?
- Analgesics/NSAIDs--> arthralgias
- -add antimalarials--> arthritis
- -add MTX--> refractory
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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
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What is the SLE treatment for pericardial disease and myocarditis?
- -Pericardial disease--> NSAIDs, low dose corticosteroids
- -Myocarditis--> high dose corticosteriods
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What focal manifestations of SLE: CNS caused by?
-intravascular occlusion due to antibodies or vasculitis
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What are the diffuse manifestation of SLE:CNS caused by?
-Immune mechanism--> immune complexes, vasculitis, and vasculopathies
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T or F. Fertility is not usually an issue in SLE?
true
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Which drugs for SLE are class B?
NSAIDs, glucocorticosteroids
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Which drugs for SLE are class C in pregnancy?
- Azathioprine
- cyclophosphamide
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Which drug for SLE is class X in pregnancy?
MTX
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What is the goal of SLE in patients w/ APLA syndrome?
Prevent clots (anticoagulation or immunosuppression agents)
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