SLE - Block 1 Flashcards

1
Q

What is systemic lupus erythematosus (SLE)?

A

An autoimmune dx that is associated with the production of autoantibodies

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2
Q

What are the predisposing factors of SLE?

A
  1. Genetic influences
  2. Epigenetic regulation of gene expression: inhibition of DNA methylation (hydralazine, procainamide) -> DI-lupus
  3. Environmental factors: Medications
  4. Hormones
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3
Q

What are 2 common drugs that can induce lupus?

A

Hydralazine and procainamide

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4
Q

Anti-arrhythmic that cause lupus?

A
  1. Procainamide
  2. Quinidine
  3. Amiodarone
  4. Mexiletine
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5
Q

Anti-thyroid that induce lupus?

A

Methimazole
Propylthiouracil

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6
Q

Anti-HTN that indue lupus?

A

Hydralazine
Methyldopa

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7
Q

Anti-infective that induce lupus?

A

Doxycycline, minocycline, tetracycline, isoniazid, nitrofurantoin

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8
Q

TNFa inhibitors that induse lupus?

A
  1. Adalimumab
  2. certolizumab pegol
  3. etanercept
  4. golimumab
  5. infliximab
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9
Q

Anti-siezure that induce lupus?

A

Carbamazepine, ethosuximide, lamotrigine, phenobarbital, phenytoin, zonisamide

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10
Q

Anti-psychotics that induce lupus?

A

Clozapine, chloropromazine, fluphenazine, perphenazine, thioridazine, thiothixene, trifluoperazine

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11
Q

PPIs that induce lupus?

A

Dexlansoprazole, esomeprazole, lansoprazole, omeprazole, pantoprazole, rabeprazole

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12
Q

How do you diagnose drug-induced lupus?

A

Symptom onset of at least 1 month after initiation & symptom improvement within days to months after drug discontinuation

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13
Q

What are the characteristics of SLE?

A
  1. Dysfunction of the innate and adaptive immune system
  2. Altered activation and signaling of T and B lymphocytes
  3. Reduces clearance of apoptotic cellular debris -> stimulation of immune system
  4. Increases risk for infection
  • Certain autoantibodies can be present for years prior to the clinical presentation of SLE
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14
Q

What are the complications of having autoantibodies to blood cells? Phospholipids?

A

Cytopenia; thrombosis and fetal loss

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15
Q
A
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16
Q

Stimulates B-cell production, along with autoantibodies, in renal cells, which can cause skin & join symptoms associated with SLE?

A

IL-10

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17
Q

Increased production from T cells, which is associated with disease activity & kidney/tissue damage?

A

IL-17

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18
Q

Important for T-regulatory cell function & inhibition of IL-17 and decreases concnetration in SLE?

A

IL-2

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19
Q

Secreted from plasmacytoid dendritic cells?

A

Type 1 interferon and interferon-γ

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20
Q

Interferon associated with mucocutaneous inflammation?

A

High concentrations of type 1 interferon

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21
Q

Interferon associated with nephritis and arthitis?

A

High concentrations of interferon-γ

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22
Q

increase B-cell survival & differentiation?

A

BLyS

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23
Q

Increases antibody production?

A

IL-6

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24
Q

What is the most common sign of lupus? Others?

A

Arthritis
Rash
Fever
Raynaud’s phenomenon

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25
Q

What is the most common sx of lupus? Others?

A

Fatigue
Joint pain/stiffness

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26
Q

T/F: Presence of ANA means a patient has SLE?

A

False: used as a screening test, but NOT specific for SLE

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27
Q

Examples of diagnostic tests for lupus?

A

Serology: autoantibodies, antiphospholipis antibodies, complement
Inflammatory markers: CRP, ESR

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28
Q

What is the 1st sign of systemic dx?

A

Skin manifestations via cutaneous lupus

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29
Q

What are the types of cutaneous lupus?

A
  1. Acute cutaneous lupus erythematosus (malar rash or butterfly rash)
  2. Subacute cutaneous lupus erythematosus
  3. Chronic cutaneous lupus erythematosus
  4. Intermittent cutaneous lupus erythematosus
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30
Q

Lupus nephritis are more common to what populations? Most prevelant in?

A

African American, Hispanic, Asian patients

More prevalent in men

31
Q

Patients with lupud nephritis may also have ___ and are at risk for ____?

A

other cormorbities (HTN); accelerated atherosclerosis

32
Q

What are the general approaches to treating SLE?

A
  1. ANti-malarial med (hydroxychloroquine)
  2. Lifestyle modifications (counseling, aerobic exercise, weight loss, sun protection, smoking cessation)
  3. Evalute and treat other comorbidies
33
Q

What are the approaches of using NSAID for lupus?

A
  1. Are not disease modifying agents
  2. Onyl used to relieve sx control
  • Low dose aspirin (81 mg PO QD) for patients with antiphospholipid antibodies
34
Q
A
34
Q

What are the approaches of using CS for lupus?

A

Monotherapy or adjunct therapy
High doses: pulse IV regimens
Maintenance doses: low as possible for SLE flares
* Assess for ADRs: ↑ BP/BG, glaucoma, cataracts, weight gain, osteoporosis, mood changes
* Evalutate patients with SLE for prevention and tx of GC-induced osteoporosis

Prednisone, Methylprednisolone

35
Q

What is the preferred medication for all patients with SLE especially for pregnancy and lactation?

A

Hydroxychloroquine

36
Q

Hydroxychloroquine

Therapeutic Effects, ADR, RF, Monitoring

A

Therapeutic effects:
* Improvements in SLE manifestations -> 2 – 8 weeks
* Maximum clinical efficacy -> 3 – 6 months

ADR: Retinal toxicity
RF for retinal tox:
* Therapy duration > 5 years
* daily doses > 5mg/kg ABW
* concurrent use of tamoxifen
* past medical history of renal dysfunction or macular disease

Monitoring for eye exams:
* Baseline testing -> within 1-2 months of initiation
5 years of therapy -> annual testing, except for high-risk patients (monitored annually earlier)

37
Q

Belimumab

ADR, CI

A

CI:
* Don’t give with DMARD or live vaccines
* Pregnancy caution
* Africican America patients have a low response rate

ADR:
* Depression and suicidal ideation
* Infusion or hypersensitivity rx (anti-pyretic, anti-histamine agents

38
Q

Rituximab

ADR, Caution

A

ADR: Infusion related rx
Caution:
* Don’t give with DMARD or live vaccines
* Screen High risk patients for HBC and HCV before initiating therapy
* Consider pre-medication with steroid, acetaminophen, & antihistamine before initiating therapy.

39
Q

Cyclophosphamide

ADR, Counseling

A

ADR: hemorrhagic cystitis from increased concnetrations of acrolein
Counseling:
* Administer with IV fluids before drug
* Administer mesna to decrease bladder toxicity (binds to acrolein)

40
Q

Mycophenolate mofetil

ADR, Counseling

A

ADR: GI complaints
Counseling:
* Undergoes enterohepatic recycling to convert to active form
* Consider a dose reduction or switch to enteric-coated form (Myfortic) to decrease sx

41
Q

Azathioprine

CI

A

Recommended to screen patients for TPMT deficiency prior to initiating therapy

TPMT deficiency -. myelosuppression

42
Q

How does mercaptopurine undergo metabolism?

A

Inactivated by thiopurine methytransferase (TPMT)

43
Q

Methotrexate

Dosing, Counseling

A

Dosing: QW
Counseling: Administer w/ folic acid to reduce toxicities

44
Q

What is the recommended daily dosae of VD3?

A

1000-2000 IU PO QD

45
Q

What is the first line for lupus nephritis?

A

Hydroxychloroquine

46
Q

What are the antibodies that can increase the antiphospholipid syndrome and promote clotting and pregnancy morbidity?

A
  1. Anti-cardiolipin
  2. Anti-β2-glycoprotein
  3. Lupus anticoagulant
47
Q

How do you diagnose antiphospholid syndrome?

A

One laboratory feature:
* Presence of antiphospholipid antibodies on two (2) separate occasions, separated by 12 weeks
*High risk: presence of lupus anticoagulant, combination of 2-3 antiphospholipid antibodies, or presence of persistently elevated antiphospholipid antibody titers
*Low risk: positive anticardiolipin or anti-β2-glycoprotein I at low-medium titers

One clinical feature:
* Vascular events
* Obsteric complication

48
Q

What is the tx for Thromboprophylaxis in Patients with SLE and Antiphospholipid Antibodies?

A

Low-dose aspirin (81mg PO daily) for both high and low risk

49
Q

When would aspirn be switched to warfarin?

A

Patient has first VTE (INR goal 2-3)

50
Q

What is the INR target range?

A

2-3

51
Q

What do you do it INR is ≥6?

A

Refer to Vitamin K policy

52
Q

Tx for Class I & II (minimal mesangial & mesangial proliferative) lupus nephritis?

A

Do NOT require immunosuppressive agents

53
Q

Tx for Class III & IV (focal & diffuse) lupus nephritis?

Duration

A

Treat with immunosuppressive therapy & glucocorticoids.
* Caucasian & Asian patients -> recommend IV cyclophosphamide for induction therapy
* African American & Hispanic patients -> recommend mycophenolate mofetil for induction therapy

Duration of induction therapy -> 6 months

54
Q

Tx of Class V mixed with Class III & IV lupus nephritis?

Duration

A

Recommend same treatment for patients with Class III & IV lupus nephritis:
* Caucasian & Asian patients -> recommend IV cyclophosphamide for induction therapy
* African American & Hispanic patients -> recommend mycophenolate mofetil for induction therapy

Duration of induction therapy -> 6 months

55
Q

For lupus nephritis what does induction tx look like?

A

Start maintencance therapy (mycophenolate mofetil or azathioprine)

56
Q

How long does lupus nephritis maintenance therapy go for?

A

Continue 3-5 years in complete renal remission

57
Q

When can non-live vaccines be administered in patients with SLE?

A

2 weeks before initiating immunosuppressive therapies

58
Q

When can live vaccines be administered in patients with SLE?

A

Administer at least 4 weeks before initiating immunosuppressive therapies

59
Q

Can rZoster be given to SLE patients?

A
  • Can be administered while on immunosuppressive therapies
  • Avoid use in pregnancy!
60
Q

Tx for Pure Class V (membranous) lupus nephritis?

A
  • Recommend induction therapy with mycophenolate mofetil & glucocorticoids for 6 months.
  • Improvement after induction therapy -> recommend mycophenolate mofetil or azathioprine
  • Duration of maintenance therapy -> continue for 3 – 5 years in complete renal remission
61
Q

Tx for Class VI (advanced sclerosing) lupus nephritis?

A

Consider renal replacement therapy.

62
Q

When would we use ACEI/ARB?

A

proteinuria (≥ 0.5g/day) to delay dx progression and maintain BP of <130/80

63
Q

When would be use statin therapy?

A

LDL > 100mg/dL for prevention of accelerated atherosclerosis

64
Q

What is first line for cutaneuous lupus?

A

Topical CS

65
Q

How do we select topical CS?

A

Low potency: thin skin regions on face & groin
Moderate potency: skin on trunk & extremities
High: thick-skin areas (scalp, soles, palms)

Use the lowest effective potency & shortest duration of therapy

66
Q

What is the 1st line for severe, disseminated cutaneous lupus?

A

Hydroxychloroquine

67
Q

What are medications that can bring about fertilitity issues while with SLE?

A
  1. Cyclophosphamide
  2. Estrogen-containing oral contraceptives
  3. Mycophenolate
68
Q

What kinds of contraceptives are suitible for SLE women?

A
  1. COC
  2. Vaginal ring
  3. POP
  4. Progestin-IUD
69
Q

What kinds of contraceptives are suitible for women with SLE and antiphospholid antibody (+)?

A

Avoid COC

70
Q

What the approaches for SLE women wanting to get pregnant?

A
  1. Avoid attempting pregnancy within 6 months of a severe SLE flare
  2. Pregnancy has best outcomes in patients with inacitve SLE for at least 6 mpnths
  3. DC teratogenic meds
    * Methotrexate & thalidomide: DC 1-3 months before conception, DC thalidomide 4 weeks before conception
    * Mycophenolate: Discontinue > 6 weeks before conception (women).
    * Cyclophosphamide: Discontinue 3 months before conception (men & women).
    * Leflunomide: Initiate oral cholestyramine elimination procedure (8 grams PO TID for 11 days).
    * Avoid fluorinated CS: dexamethasone, betamethasone
    * NSAIDS: Avoid use in 1st trimester due to risk of miscarriage, Avoid use in 3rd trimester due to risk of premature closure of ductus arteriosus.
    * HTN: DHP-CCB, beta-blockers, a2-agonists (Avoid ACEI/ARBs)

Hydroxychloroquine can be used during pregnancy

71
Q

What is the difference between non-live/recombinant vs line-attenuated vaccines?

A

Non-live: safe for immunocompromised patients
Live: safe for immunocompromised patients

72
Q

Are B-cell depleting therapies (rituximab) safe with immunizations?

A
  • Decreases humoral immune response to vaccines.

Administer vaccines at least 6 months after & 4 weeks before next course of B-cell-depleting therapies