Pharm Exam 4: Gout, RA, SLE
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Pharm Exam 4: Gout, RA, SLE
What is the only way to diagnose acute gout?
-Joint aspiration and crystal identification
What are the 4 distinct stages of gout?
1. Asymptomatic hyperuricemia
2. Acute flares
3. Intercritical gout
4. Advance gout
Discuss asymptomatic hyperuricemia.
-Can take as long as 10yr after increased serum levels for gout to occur
Discuss Acute flares.
-Acute inflammation, often podagra
T or F. Gout flares in the wrist is a common place.
False--> pseudogout may effect wrist/knees, not REAL gout
Discuss intercritical gout.
-Intervals between acute flares
Discuss Advanced gout.
-Long term gout with complications, uncontrolled hyperuricemia
-may see kidney stones, renal nephritis
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)
What are common S/E of NSAIDs?
-GI toxicity, impaired platelet fxn, renal/liver tox, hypersensitivity, tinnitus, H/A, aseptic meningitis
What are some commone S/E for colchicine?
-abdominal pain, N/D, bone marrow suppression, neuromyopathy (chronic use)
What is the driving force for choosing a medication for gout?
Presence of comorbidities
What patients should NSAIDs be avoided? (2)
1. renal impairment
2. GI bleeding risk
What patients should colchicine use be avoided?
-severe liver/renal impairment
-Patients on bed rest
What gout medication is great for renal impairment or GI bleeding patients?
Corticosteroids (esp good if >3 joints effected)
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)
Where are tophi most commonly seen?
ear and extensor aspects of joints
What is a major adverse reaction of allopurinol?
-Toxic dermal exfoliation (SJS?)
Which Uric acid lowering meds should NOT be used in patients w/ kidney stones?
Name 4 urate lowering medications.
Which urate lowering med is a NON-purine inhibitor of xanthine oxidase?
-Febuxostat--> good for patients intolerant of allopurinol
What is your target uric acid value?
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)
T or F. Urate lowering meds should be started in acute gout situations?
FALSE--> but don't stop during acute episodes
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
T or F. Urate lowering meds should not be started or stopped during acute attacks
What are the meds of CANT LEAP for meds that cause hyperuricemia?
N- nicotinic acid
A- aspirin (low dose)
What 3 meds may have beneficial effect on serum uric acid?
3. Vit C
**use as adjuncts
T or F. Asymptomatic hyperuricemia rates requires treatment.
T or F. Colchicine is more effective than NSAIDs and corticosteriods in treating acute gout.
FALSE--> all have same efficacy
T or F. Consider uric acid lowering therapy is 2 more attacks/yr
T or F. Uricosurics should not be used in patients with renal stones, tophaceous gout, GFR <50 or who are overproducers.
-Uricosurics--> probenecid & sulfinpyrazones
What population is classic for Rheumatoid arthritis?
Women of child-bearing age
How long should joints symptoms be occuring before considering rheumatoid arthritis?
>6 weeks b/c synovitis viruses can last that long
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
What are 4 positive outcomes of PT/OT on RA?
1. joint protection
2. adaptive aids
3. muscle strengthening
4. safe exercising
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)
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
When should you refer a patient with RA?
Within 3 mo--> most damage by RA is done within the first 2-3yrs
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
What is the role of NSAIDs in the txt of RA?
Symptom control and adjunct to other therapies (NOT SOLE therapy)
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
When a patient in on MTX, how often should labs be checked?
CBC, CMP q 2mo
If a patient is taking Hydroxychloroquine, what exam should be performed yearly?
Eye exam, b/c can cause retinopathy
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)
What is the MOA of hydroxychloroquine?
-Interferes w/ antigen processing, concentrates in lysosomes (anti-inflammatory)
-Anti-inflammatory and antimicrobial effects
-Inhibits purine synthesis via dihydrofolate reductase, decreases T & B cell proliferation
Inhibits dihydroorotate dehydrogenase (blocks pyrimidines-->blocking proliferative lymphocyte response)
-purine analog and immunosupressant (both T & B cell function
What is the major S/E for Hydroxychloroquine.
Hydroxy--> Retinal toxicity
What is the major SE for sulfasalazine?
Neutropenia, hepatic enzymes elevation
What is the major SE MTX?
Hepatic fibrosis, myelosuppression. Caution in rena/liver d/o, Limit ETOH
What are major SE of Leflunomide?
Neutropenia, thrombocytopenia, hepatic liver enzymes
What are major SE of Azathioprine?
Leukopenia, megaloblastic anemia, thrombocytopenia, hepatotoxicity
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
What are the 11 S/S for SLE classification?
1. Malar rash
2. Discord rash
4. Oral ulcers
7. renal disorder
8. neurologic disorder
9. hematologic disorder
10. immunologic d/o
11. antinuclear antibodies (ANA)
What are 5 drug classes used to treat SLE?
4. immunosuppressive agents
What are the goals of SLE treatment of cutaneous disease? (4)
2. pigmentary changes
Are NSAIDs apart of the txt for SLE: cutaneous disease?
-intralesional corticosteriod injections
Which SLE med is used for non-scarring lesions?
Which SLE med is used for scarring lesions?
Are ulcers in the mouth r/t to lupus painful or painless?
Painless, and usually on the palate
When do patients with SLE absolutely need a referral?
with nephritic sediment
What class of renal disease is treatment essential?
Class III--> focal proliferative
Class IV--> diffuse proliferative
** possible Class V (membraneous)
What does txt of SLE: renal disease include (2)?
2. cytotoxic therapy
What is the main txt of SLE: hematolytic disease?
High dose corticosteroids
What are the main txts for SLE: MSK disease?
-add antimalarials--> arthritis
-add MTX--> refractory
What are manifestations of SLE: Cardio disease?
1. pericardial disease
2. valvular heart disease
3. coronary heart disease
6. pulmonary hemorrhage
8. interstitial lung disease
What is the SLE treatment for pericardial disease and myocarditis?
-Pericardial disease--> NSAIDs, low dose corticosteroids
-Myocarditis--> high dose corticosteriods
What focal manifestations of SLE: CNS caused by?
-intravascular occlusion due to antibodies or vasculitis
What are the diffuse manifestation of SLE:CNS caused by?
-Immune mechanism--> immune complexes, vasculitis, and vasculopathies
T or F. Fertility is not usually an issue in SLE?
Which drugs for SLE are class B?
Which drugs for SLE are class C in pregnancy?
Which drug for SLE is class X in pregnancy?
What is the goal of SLE in patients w/ APLA syndrome?
Prevent clots (anticoagulation or immunosuppression agents)