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MSK - my cards > SLE (connective tissue disease) > Flashcards

SLE (connective tissue disease) Flashcards

1
Q

What causes inflammation and tissue damage in SLE?

A

The immune system attacking the body’s cells.
(autoimmune)
Antibody-immune complexes precipitate and cause a further immune response.

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2
Q

Is SLE more common in males or females?

A

Females (9:1)

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3
Q

Which races is SLE most common in IN THE UK/US?

A

Asians, Afro-Americans, Afro-Caribbeans, Hispanic Americans (more than americans of european decent)

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4
Q

What hormonal factors are thought to increase incidence of SLE?

A

Incidence increased in those with higher oestrogen exposure. (those who develop early, those on oestrogen containing contraceptive, those on HRT)

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5
Q

What environmental factors are thought to increase risk of SLE?

A

Viruses (e.g. epstein-barr virus)

UV light exposure (stimulating skin cells to secrete cytokines, stimulating B ells)

Silca dust (in cleaning powders, cigarette smoke and cement)

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6
Q

Outline some of the main points in the pathogenesis of SLE:

A

Loss of immune regulation

Increased and defective apoptosis

Necrotic cells release nuclear material (which act as potential auto-antigens) (autoimmunity probable results from the extended exposure to nuclear and intracellular auto-antigens)

B and T cells stimulated

Autoantibodies are produced

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7
Q

What constitutional symptoms can be present in SLE?

A 
Fever
Malaise
Poor appetite
Weight loss
Fatigue
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8
Q

What mucocutaneous features can be present in SLE?

A 
Photosensitivity
Malar rash
Discoid lupus erythematosus (may scar)
Subacute cutaneous lupus
Mouth ulcers (painless)
Alopecia non-scarring)
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9
Q

What musculoskeletal features can be present in SLE?

A

Non-deforming polyarthritis/polyarthralgia
Deforming arthropathy 0 Jaccoud’s arthritis
Erosive arthritis (RARE)
Myoathy - weakness, myalgia and myositis

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10
Q

What type of distribution does non-deforming polyarthritis have?

A

Same distribution as Rheumatoid Arthritis but no radiological erosion

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11
Q

What renal features can be present in SLE?

A

Proteinuria of .500mg in 24 hours

Red cell casts

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12
Q

What is serositis?

A

Inflammation of the serous membrane

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13
Q

What can serositis in SLE cause?

4

A

Pericarditis
PLeurisy
Pleural effusion
Pericardial effusion

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14
Q

What neurological features can be present in SLE?

A 
Depression, psychosis ( not always related to disease activity)
Migrainous headache
Seizures
Cranial or peripheral neuropathy
Mononeuritis multiplex
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15
Q

What is mononeuritis multiplex (seen in SLE)?

A

A form of damage to one or more peripheral nerves (nerves outside brain and spinal cord)

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16
Q

What haematological features can be present in SLE?

A

Lympadenopathy
Leucopenia (a reduction in the number of white cells in the blood)
Lymphopenia (low level of lymphocytes in blood)
Haemolytic anaemia
Thrombocytopenia (deficiency of platelets)

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17
Q

How many patients with SLE will have lymphadenopathy during their course of illness?
(%)

A

Approx. 25%

18
Q

What is anti-phospholipid syndrome?

A

A disorder of the immune system that causes an increased risk of blood clot

19
Q

What other name is used for anti-phospholipid syndrome?

A

Hughes Syndrome

20
Q

What happens in anti-phospholipid syndrome?

A 
Increased risk of blood clots.
Venous and arterial thrombosis.
Recurrent miscarriage.
Livido reticularis (skin appearance)
Thrombocytopenia
Prolongued APTT (activated partial thromboplastin time)

Association with other autoimmune conditions, especially SLE)

21
Q

What is livido reticularis?

A

A common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by small blood clots.
(Anti-phospholipid syndrome)

22
Q

Why are people with SLE particularly susceptible to infection?

A 
Intrinsic factors:
Low complements
Impaired cell mediated immunity
Defective phagocytosis
Poor antibody response to certain antigens

Extrinsic Factors:
Steroids
Other immunosuppressive drugs
Nephrotic syndrome (kidney disease)

23
Q

In what titre is ANA positive in in almost all SLE patients (95%)?

A

Positive in titire of 1:160 or greater

titres less than 1:160 are present in up to 20% of healthy population

24
Q

Other than SLE, what conditions is ANA found in?

A

RA, HIV, Hep C, other autoimmune conditions

25
Q

How many patients with SLE does anti-double stranded DNA antibody occur in?

A

Approx. 60% of patients with SLE

Highly specific for SLE
(Titre correlates with disease activity)
(May be associated with lupus nephritis)

26
Q

Is anti-double stranded DNA antibody highly specific for SLE?

A

Yes

27
Q

Is ANA highly specific for SLE?

A

No
(in titres <1:160, present in about 20% of healthy population)
(Can also be found in other conditions such as Hep C, HIV, Rheumatoid Arthritis and other autoimmune conditions)

28
Q

What is lupus nephritis?

A

Inflammation of the kidney caused by SLE

29
Q

When should a positive ANA test be taken seriously (as an indicator of SLE?

A

If other antinuclear antibodies are positive (Anti-dsDNA, anti-Sm, anti-Ro, Anti-RNP)
When the patient presents with connective tissue disease features

30
Q

What is Anti-Ro associatd with?

A

Associated with cutaneous manifestations
(usually associated with anti-La)

(60%)

31
Q

Is Anti-Sm specific?

A

Yes, very.

(Probable association with neurological involvement)

(10-20%)

32
Q

Is Anti-Sm sensitive?

A

No

specific but low sensitivity
(if positive - likely to be SLE)
(if negative, doesn’t rule out)

33
Q

Are Anti-Ro, Anti-La and Anti-RNP specific?

A

No, may be seen in SLE but may also be seen in other conditions

34
Q

What happens to C3/4 levels in SLE?

A

Levels are lower when SLE active, especially renal disease

35
Q

Why is urinalysis does in SLE?

A

To look for evidence of glomerulonephritis

36
Q

Which anti-phospholipid antibodies may be positive in SLE?

A

Anti-cardiolipin antibody
Lupus anticoagulant
Anti-beta 2 glycoprotein

(Must be positive on 2 occasions, 12 weeks apart)

37
Q

What is monitored to monitor disease activity in a patient with SLE after diagnosis?

A

Anti-dsDNA (positivity correlates with activity)

(C3/4 levels negatively correlate with disease activity)

(clinical assessment (incl. BP), urine examination incl. protein, cells and casts, FBC, blood biochemistry)

38
Q

What is the drug management of SLE?

A

NSAIDs and simple analgesia
Hydroxychloroquine (Anti-malarials) - (Useful for arthritis, cutaneous manifestations and constitutional symptoms)
(May reduce systemic complications)
Steroids (useful but associated wih numerous side-effects)

39
Q

When (and in what doses) would you give steroids (prednisolone) for SLE?

A

Small doses - for skin rashes, arthritis, serositis

Moderate doses - for resistant serositis, haematologic abnormalities and class V glomerulonephritis

High doses - for severe/resisitant haematologic changes, diffuse glomerulonephritis and major organ involvement

40
Q

Name 4 immunouppressives that are used in SLE:

A

Azathioprine
Cyclophosphamide
Methotrexate
Mycophenolate mofetil

(all cause bone marrow suppression)
(all can cause increased succeptibility to infection
(ptentially teratogenic)

41
Q

Which (2) Biologics may be used in SLE?

A

Anti-CD20 (Rituximab)

Anti-Blys (Belimumab)

MSK - my cards (13 decks)

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