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PR3152 > SLE > Flashcards

SLE Flashcards

1
Q

causes of SLE

A
  1. genetic factors
  2. drug-induced
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2
Q

patho of genetic SLE

A

disorders of the innate and adaptive immune system
1. T and B lymphocyte activation and signaling are altered in SLE
2. abnormal clearance of apoptotic debris containing nuclear material which can stimulate immune responses
3. When the body is unable to clear the apoptotic debris fast, the body recognised it as foreign body and hence this stimulates immune response
4. number of plasma cells increased in active SLE and these cells produce autoantibodies, causing tissue damage
5. These autoantibodies are directed against nuclear proteins and nucleic acids
6. a multisystem disease as autoantibodies travel around the body to target apoptotic debris fast

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3
Q

patho of drug-induced lupus

A

Mostly idiosyncratic reactions precipitated by interplay of generic and environment. One possible MOA:
Drugs are small molecules that can induce an immune response by binding to larger molecules like proteins

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4
Q

what are the possible drugs that cause drug-induced lupus?

A

Drugs with highest risks: Procainamide, Hydralazine (high chance of getting lupus), Quinindine
Others: minocycline, isoniazid, methyldopa, carbamazepine

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5
Q

primary treatment to treat drug-induced lupus?

A

stop and consider symptomatic treatment

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6
Q

clinical presentation of lupus (8)

A
  1. Mouth and nose ulcers
  2. Skin - butterfly rash and red patches
  3. Blood - Anemia, High blood pressure, Low blood count Rbc, wbc low –> prone to infections
  4. Heart - Endocarditis, Atherosclerosis, Inflammation of the fibrous sac, pericarditis, myocarditis
  5. Muscle and joints - Pain and arthritisaches, Swollen joints
  6. lupus nephritis
  7. Lungs - Pleuritis, Pneumonitis, Pulmonary emboli, Pulmonary hemorrhage
  8. neuropsychiatric lupus - stroke (cerebrovascular disease), anxiety, seizures, cognitive dysfunction, confusion, peripheral neuropathy, psychosis
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7
Q

clinical presentation (labs of lupus)

A
  1. full blood count low –> hemolytic anemia [low rbc], wbc, lymphocytes, platelets ALL low
  2. immunologic
    - ANA, dsDNA, anti-Sm, anti-RNP is high,
    - low complement (C3, C4, CH50)
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8
Q

goal of therapy for lupus

A
  1. Remission, but achieving low disease activity might be more realistic
  2. Designed to prevent flares and other organs, slow disease activity, reduce use of steroids, improve QOL, while minimising adverse effects
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9
Q

treatment for genetic lupus

A
  1. need to evaluate and treat for any other comorbidities such as heart, kidney and brain
  2. lifestyle and support group eg Advise patients to stop smoking
  3. Only drugs approved by the FDA for treatment of SLE are aspirin, prednisone, hydroxychloroquine and belimumab
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10
Q

what is the drug that is needed for ALL sle patients, including pregnant women?

A

hydroxychloroquine

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11
Q

benefits of hydroxychloroquine

A

long term survival: anti-inflammatory, immunomodulatory, anti-thrombotic effects

minimal ADR

but takes about 4-8 weeks to have effects

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12
Q

what are the rest of the off-label drugs for SLE

A

NSAIDs, steroids, biologics (belimumab, rituximab), immunosuppressants (cyclophosphamide IV/PO, mycophenolate, azathioprine)

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13
Q

function of NSAIDs in SLE patients

A

acute symptoms like pain

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14
Q

caution when using NSAIDs

A
  1. worsening lupus nephritis (NSAID is nephrotoxic, hence giving this will worsen kidney function)
  2. increase cardiac risk
  3. GI bleed
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15
Q

benefits of steroids

A
  1. Monotherapy or adjunctive to control flares and maintain low disease activity (helps with inflammation)
  2. Rapid onset
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16
Q

ADR of steroids (10)

A
  1. Immunosuppressed and hence increased risk and number of infections
  2. Myopathy (muscle issue)
  3. Osteonecrosis/Osteoporosis
  4. Neuropsychiatric symptoms - Anxiety, Depression, Changes in mood
  5. Metabolism - Weight gain/obesity, Buffalo bump, Moon face, Fluid retention/edema, Impaired glucose metabolism, Insulin resistance, B cells dysfunction
  6. Cushing syndrome ( a disorder that occurs when your body makes too much of the hormone cortisol over a long period of time.)
  7. Stomach - Gastric ulcer (If concomitant NSAIDs)
  8. Skin - Skin thinning, Hirsutism where women have thick, dark hair on their face, neck, chest, tummy, lower back, buttocks or thighs
  9. Eyes - Cataract, Glaucoma
  10. Cardiovascular system - Increased cardiovascular risk, Hypertension
17
Q

benefits of biologics

A

targets and disrupts functioning of B cells

18
Q

benefits of immunosuppressants

A

steroid-sparing

19
Q

ADR of cyclophosphamide

A

severe organ involvement

20
Q

associated syndrome you would get with SLE

A

antiphospholipid syndrome (APS)

21
Q

What is APS?

A
  • Antiphospholipid antibody (lupus anticoagulant, anticardiolipin, anti-beta2 glycoprotein I) positive
  • High risk of clotting and pregnancy morbidity
22
Q

general treatment of APS (primary and secondary)

A

Patients who never had clots before: Primary thromboprophylaxis –> hydroxychloroquine + aspirin
Patients with clots before: Secondary thromboprophylaxis –> warfarin

23
Q

evaluation of therapeutic outcomes of SLE (lab, what to look out for)

A

monitor lab - (1) urinalysis/renal function - improving means good because lupus nephritis (2) C-reactive protein (CRP) –> inflammatory marker, cannot be too high or low (3) full blood count –> increase means good (4) liver function tests improve means ok (5) complement C3, C4 –> target to increase (5) anti-dsDNA –> to go as low as possible
ANA, anti-Sm and anti-RNP do not need to be repeated at each visit as levels do not fluctuate with disease

24
Q

evaluation of therapeutic outcomes

A
  1. Look at symptoms
  2. Look at labs
  3. Adverse drug reactions
  4. Development of comorbidities
  5. Measures of disease activity:
    - Regular labs every 1-3 months with active disease; 6-12 months if stable
    - Look at trends

PR3152 (7 decks)

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