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Pharmacotherapy I > Exam 4 SLE > Flashcards

Exam 4 SLE Flashcards

1
Q

What is the key characteristic of systemic lupus erythematosis (SLE)?

A

Autoantibodies

Presents with multisystem involvement that varies by patient.

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2
Q

What patient population is at the highest risk of developing SLE?

A

African-american females, usually diagnosed between the ages of 15-45

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3
Q

What three types of factors contribute to developing SLE?

A

Genetic, environmental, and hormonal factors

Estrogens enhance autoimmunity, androgens inhibit

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4
Q

Name some possible triggers of SLE

A

Sunlight/UV light, drugs (OCs), chemicals (hydrazine in tobacco, aromatic amines in hair dyes), diet, viral and bacterial infections

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5
Q

What causes SLE?

A

Autoantibody overproduction, especially to nuclear, cytoplasmic, and surface antigens. These autoantibodies form immune complexes which are the major mechanism of damage. Some antibodies promote coagulation (lupus anticoagulant misnomer). There is also a shift from Th type 1 cells to Th type 2 cells, which enhances B cell activation.

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6
Q

True or false: SLE follows a predictable, downward progression.

A

False. SLE is highly dynamic and unpredictable and occurs in episodes of fluctuations and flare-ups.

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7
Q

What systemic symptoms are commonly associated with SLE?

A

Nonspecific symptoms, including fatigue, malaise, fever, anorexia, and weight loss – hard to diagnose

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8
Q

What musculoskeletal symptoms does SLE often present with?

A

Arthralgias/myalgias, nonerosive polyarthritis, hand deformities, mypopathy, and bone necrosis. Can look like RA but in any joint and shorter flare duration.

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9
Q

How does SLE present cutaneously?

A

Photosensitivity, malar (butterfly) rash, oral painless ulcers, alopecia, discoid rashh, Raynaud’s phenomenon (looks like frostbite)

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10
Q

What hematologic impact does SLE have?

A

Normochromic, normocytic anemia, rarely hemolytic anemia, mild thrombocytopenia during exacerbations

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11
Q

How does SLE impact the lungs?

A

Pleurisy (pain and effusion that compresses lung), coughing, dyspnea

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12
Q

What cardiovascular impact does SLE have?

A

Pericarditis, myocarditis, EKG changes, valvular disease, HTN, CAD (accelerated by immune complexes, must aggressively treat and monitor)

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13
Q

What neurologic symptoms does SLE present with?

A

HA, psychosis, seizures, depression, and anxiety (psychological impact of chronic disease may contribute)

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14
Q

What serious kidney condition does SLE cause?

A

Lupus nephritis – shows up with increased SCr, proteinuria, edema, HTN, and foamy urine.

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15
Q

What symptoms can a patient with SLE have connected to the lupus anticoagulant antibodies?

A

Venous or arterial thrombosis, in about 15% of patients.

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16
Q

What GI symptoms does SLE present with?

A

Nonspecific–dyspepsia, nausea, diarrhea, abdominal pain.

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17
Q

What three factors help us to diagnose SLE?

A

Epidemiologic characteristics, clinical findings, and laboratory abnormalities.

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18
Q

How many of the 11 ACR characteristics are needed to be diagnosed with SLE? What are these criteria?

A

4 of 11 criteria: DOPAMINE RASH
(discoid rash, oral ulcers, photosensitivity, arthralgia, malar rash, immunologic lab phenomenon, neurologic phenomenon, renal disorder, ANA positive, serositis (inflammation of any serosa), hematological phenomena

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19
Q

SLE international collaborating clinic criteria, the more clinically relevant ones, are more to assess the likelihood that someone has SLE rather than to diagnose. How many criteria out of how many possible are required in this tool? What are these criteria divided into?

A

Must have 4 out of 17 possible, and at least one from each category (clinical and lab). OR bioipsy proven lupus nephritis.

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20
Q

What are still the three leading causes of death in SLE, even after improvements in treating them?

A

Renal, infectious, and CAD complications

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21
Q

What non-pharmacological treatments should every SLE patient be counseled on?

A

A balance of rest and exercise to fight fatigue and keep down weight, limiting sun exposure, and smoking cessation.

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22
Q

What five classes of drugs are available to help manage SLE symptoms and decrease flares?

A

NSAIDs, antimalarials, corticosteroids, cytotoxic agents, and biologic agents.

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23
Q

How are NSAIDs used to treat SLE?

A

Used at anti-inflammatory doses in mild disease.

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24
Q

What adverse effects of NSAIDs are unique in SLE patients?

A

Higher incidence of hepatotoxicity, associated with aseptic meningitis.
Monitor baseline SCr, UA, CBC (Hgb esp), AST/ALT, annual SCr, CBC.

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25
Q

How are antimalarials used to treat SLE?

A

Used as long-term management for mild disease, especially good for cutaneous manifestations, arthralgias, pleuritis, anemia, fatigue, and fever.

26
Q

How do antimalarials help with SLE?

A

Not certain, but may interfere with T cell activation or inhibit cytokines. Also decrease photosensitivity and increase anti-inflammatory and anti-HLD activity. Steroid-sparing effect?

27
Q

Which antimalarial is considered safer and is considered 1st line? Which antimalarial has a shorter onset time of 1-3 months?

A

Hydroxychloroquine is 1st line, max effect 6-12 months. Dosed 200-400mg PO daily.
Chloroquine higher incidence retinal toxicity, response 1-3 months. Dosed 250-500mg PO daily.

28
Q

What adverse effects come with the antimalarials hydroxychloroquine and chloroquine?

A

Retinal toxicity (potentially irreversible – monitor baseline, q12mos HCQ, q3mos chloroquine), CNS effects (HA, nervousness, insomnia), rashes, pigment changes, GI upset.

29
Q

How are topical corticosteroids used to treat SLE?

A

Second step (after non-PCOL), advantage = not systemic but may not provide adequate clearing of rashes when used alone.

30
Q

Where should a high potency corticosteroid like clobetasol be used? What about a mild potency agent like triamcinolone or betamethasone? Low potency agent like fluocinolone or hydrocortisone?

A

High – soles and palms
Mild – trunk and extremeties
Low – face

31
Q

What adverse effects and clinical pearls should we counsel patients about their topical corticosteroids?

A

ADE: skin atrophy, telangiectasis, rosacea so limit duration
Use creams/ointments on body and non-hairy areas
Use foams or solutions on scape
Can use topical calcineurin inhibitors (tacrolimus, pimecrolimus)

32
Q

When should we use systemic corticosteroids?

A

In mild disease unresponsive to NSAIDS/antimalarials or severe disease (nephritis, pneumonitis, myositis, vasculitis, CNS symptoms)
Goal: suppress active disease and maintain remission with lowest dose

33
Q

How are systemic corticosteroids dosed for SLE?

A

Maintenance: Prednisone 10-20mg/day for mild/remission, 1-2mg/kg PO daily for severe or active flare (can divide doses)
Pulse therapy: methylprednisolone IV 500-1000mg daily x3-6 days THEN prednisone 1-1.5mg/kg PO daily tapered down.

34
Q

What should we monitor in long-term corticosteroid therapy?

A

Baseline BP, bone mineral density, basic metabolic panel, fasting lipid panel
Routine BMP q6mos, FLP and bone marrow density q12mos

35
Q

When are cytotoxic agents used for SLE?

A

In severe disease, especially if life-threatening or refractory organ complications.
Includes cyclophosphamide, azathioprine, and mycophenolate mofetil

36
Q

What is cyclophosphamide (Cytoxan) especially good for? How does it work?

A

Cyclophosphamide is especially good for lupus nephritis and life-threatening/refractory organ complications. It works by crosslinking DNA, preventing cell division.

37
Q

How is cyclophosphamide dosed?

A

Oral: 1-3 mg/kg daily
IV: 0.5-1 g/m2 of body surface area, given monthly for 6-7 months, then q3mos for 2 years or 1 year after nephritis remission

38
Q

What concerning adverse effects are associated with cyclophosphamide? How can we minimize them?

A

Myelosuppression, opportunistic infections, infertility, bladder cancer and hemorrhagic cystitis (toxic metabolite may persist in renal failure especially)
Monitor: baseline CBC, urinalysis, plt, monthly CBC/urinalysis, yearly urine cytology and PAP
Minimize toxicity by administering in pulse doses, hydrating patient with IV fluids, and giving mesna at dose 20% of cyclophosphamide before, 4, and 8 hours after therapy (binds metabolite)

39
Q

How is azathioprine used for SLE? How does it work?

A

Azathioprine is used for long term suppressive therapy for renal flares and to reduce doses of corticosteroids. It blocks purine synthesis and is incorporated into DNA and halts replication

40
Q

How is azathioprine dosed for SLE?

A

1-3 mg/kg/day, often with corticosteroids in severe disease

Test thiopurine methyltransferase (TPMT) before initiation – absence might increase half life

41
Q

What side effects are associated with azathioprine?

A

Myelosuppression, opportunistic infections (herpes zoster), hepatotoxicity, ovarian failure (sterility)
Monitor baseline CBC, plt, AST/ALT, yearly LFTs and PAP, CBC q1-3mos if stable, q1-2 weeks during dose change.

42
Q

How is mycophenolate mofetil used in SLE? How does it work?

A

Good for lupus nephritis, arthritis, cutaneous, hematologic manifestations. It inhibits proliferation of B and T cells via inhibiting IMPDH.

43
Q

How is mycophenolate mofetil dosed in SLE?

A

1-3g PO daily, often in combination with CS

Often works better in african-american patients

44
Q

What adverse effects are associated with mycophenolate?

A

N/V/D, myelosuppression, hepatotoxicity, oncogenic potential
Monitor: Baseline CBC, LFTs, renal function tests
CBC monitored weekly for 1st month, biweekly for next two months, and monthly for the first year.

45
Q

What biologic agents can we use in SLE to reduce B cells?

A

Belimumab (Benlysta) and rituximab (Rituxan)

46
Q

How does belimumab work to help SLE?

A

It binds to BLyS, cytokine important for B cell functions. Good for autoantibody positive active SLE, but no benefit in african-american patients.

47
Q

How is belimumab dosed?

A

10mg/kg q2weeks for 3 doses, then q4 weeks

48
Q

How does rituximab help in SLE?

A

A chimeric antibody that targets CD20, it depletes B cells and is effective in lupus nephritis and more effective in african-american patients.

49
Q

How is rituximab dosed in SLE?

A

375 mg/m2 BSA IV weekly x 4 OR 500-1000mg IV on days 1 and 15

50
Q

Name other alternative immunosuppressive agents that may help in SLE.

A

Methotrexate (especially if cutaneous, arthritis), adalimumab, etanercept, infliximab, tacrolimus

51
Q

In the treatment of lupus nephritis, what is the first step of treatment in african-american or hispanic patients? In other patients?

A

Mycophenolate mofetil plus pulse of prednisone for african-american/hispanic patients.
Cyclophosphamide plus prednisone pulse in other patients.

52
Q

If the first step of mycophenolate or cyclophosphamide + steroids is not working in 6 mos, what options do you have?

A

Can try azathioprine, but reserve rituximab, calcineurin inhibitor, and long term corticosteroids for last-line.

53
Q

What positive lab value indicates increased risk of thrombotic events and spontaneous abortion?

A

Anti-phospholipid antibodies

54
Q

What complications are SLE patients at higher risk for?

A

Preeclampsia, preterm labor, fetal growth retardation, spontaneous abortion, maternal mortality.
Exacerbation less likely if disease has been in remission for at least 6 MOS prior to conception.

55
Q

How many months before conception should a patient stop teratogenic drugs like cyclophosphamide, mycophenolate, and methotrexate?

A

3 months prior to conception

56
Q

What is our SLE maintenance drug of choice for pregnancy?

A

Hydroxychloroquine

However, NSAIDs, corticosteroids, and azathioprine are safe as well.

57
Q

If a patient with no prior fetal losses is trying to conceive and positive for antiphospholipid antibodies, what can we do prophylactically? What if the patient has had recurrent fetal losses?

A

No prior fetal losses: aspirin 81mg daily
Recurrent fetal losses: low dose heparin or LMWH +/- aspirin 81mg
AVOID warfarin–teratogenic

58
Q

What drugs can induce reversible lupus?

A

Procainamide, chlorpromazine, hydralazine, isoniazid, methyldopa, minocycline, quinidine, TNF-a inhibitors (adalimumab, etanercept, infliximab)

59
Q

How does drug-induced lupus most commonly present?

A

Musculoskeletal symptoms, fever, fatigue, pericarditis, pleurisy. Skin manifestations are rare.

60
Q

How do we treat drug-induced lupus?

A

Stop the drug!
Topical or systemic corticosteroids
NSAIDs for myalgias

Pharmacotherapy I (15 decks)

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