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Y2 LCRS Musc Fwong HR > 3. Pathogenesis of autoimmune disease > Flashcards

3. Pathogenesis of autoimmune disease Flashcards

1
Q

Upon which cells is HLA 1 and 2 presented?

A

HLA 1 = all cells

HLA 2 = APCs

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2
Q

What sort of antigens are presented by MHC 1 and 2

A 
MHC1 = endogenous
MHC2 = exogenous
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3
Q

What class of T cells is involved in recognising MHC1 and 2?

A 
MHC1 = CD8+
MHC2 = CD4+
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4
Q

Recall the general pathogenesis of AID

A

Ag binds HLA to trigger disease

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5
Q

Recall the HLA association of anklyosing spondylitis

A

HLA-B27

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6
Q

Recall the HLA association of rheumatoid arthritis

A

HLA-DR4

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7
Q

Recall the HLA association of SLE

A

HLA-DR3

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8
Q

What class of HLA are HLA-B molecules?

A

Class 1

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9
Q

What class of HLA are HLA-DR molecules?

A

Class 2

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10
Q

What sort of auto-antibody is associated with rheumatoid arthritis?

A

Anti-CCP

RF

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11
Q

What is ankylosing spondylitis?

A

Chronic spinal inflammation, leading to spinal fusion and deformity

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12
Q

What is enthesitis?

A

Inflammation where a tendon inserts into the bone

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13
Q

What antibodies are associated with ankyloing spondylitis?

A

None - it is seronegative

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14
Q

Recall 2 extra-articular associations of ankylosing spondylitis

A

Psoriatic arthritis

IBD + enterpathic synovitis

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15
Q

What if the main form of inflammation in ankylosing spondylitis?

A

Enthesitis

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16
Q

What is the main driver of inflammation in SLE?

A

Immune complexes

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17
Q

Which autoantibodies are present in SLE?

A

ANA

anti-dsDNA

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18
Q

Where does SLE cause inflammation?

A

Connective tissue

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19
Q

Recall the site of production and effect(s) of gamma-IFN

A

T cells:

Activates macrophages

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20
Q

Recall the site of production and effect(s) of IL1

A

Macrophages:
Activates T cells
Pyretic
Pro-inflammatory

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21
Q

Recall the site of production and effect(s) of IL2

A

T cells:

Activates T and B cells

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22
Q

Recall the site of production and effect(s) of IL6

A

T cells:

Activates B cells

23
Q

Recall the site of production and effect(s) of TNF alpha

A

Similar to IL1 but more destructive
Activates T cells
Pyretic
Pro-inflammatory

24
Q

Which cytokine is particularly important for bone destruction in rheumatoid arthritis?

A

RANK-L

25
Q

By what sort of cells is RANK-L produced?

A

T cells

Synovial fibroblasts

26
Q

What is the effect of RANK-L binding to RANK?

A

Osteoclast activation

27
Q

What is the most important inflammatory mediator in rheumatoid arthritis?

A

TNF-alpha

28
Q

What is the effect of TNF-alpha on bone?

A

It activates macrophages, which damage bone and cartilage

29
Q

Recall 2 treatments for rheumatoid arthritis?

A

Anti-TNF-alpha

PG blockade

30
Q

How do glucocorticoids affect the prostaglandin production pathway?

A

Inhibit PLA2, the enzyme that liberates arachdionic acid from cell membranes

31
Q

Recall a virus that may be associated with SLE development

A

EBV

32
Q

Summarise the known pathogenesis of SLE

A

Apoptosis
Nuclear antigens translocated to cell surface
ANA produced
Clearance impaired = stimulus to mount immune response–> B cell-auto-immunity
Complement and cytokine activation
Tissue damage

33
Q

What class of Ig is ANA

A

IgG

34
Q

Recall 3 specific non-sinister features of SLE

A

“Butterfly” erythematous rash
Arthralgia
Raynaud’s

35
Q

Recall 2 more sinister features of SLE

A

Vital organ inflammation

Accelerated atherosclerosis

36
Q

Recall 4 initial features of SLE

A

Weight loss
Fatigue
Fever
Lymphadenopathy

37
Q

Describe the pattern of ANA staining in SLE

A

Homogenous nuclear staining

38
Q

Recall 3 specific antibodies for SLE diagnosis, and which of these is definitively diagnostic

A

Anti-dsDNA
Anti-Smith (def)
Anti-Ro

39
Q

Recall one specific danger associated with Anti-Ro antbodies

A

Can cross placenta –> heart block in foetus

40
Q

How can you test the activity level of SLE

A

Complement consumption

41
Q

How does a complement test differ in rheumatoid arthritis and SLE?

A

In RA, complement = high

In SLE, complement CONSUMPTION is high so would be low

42
Q

Recall 2 haematological conditions that SLE patients are at high risk of contracting

A

AIHA

Thrombocytopenia

43
Q

Why is a urine dipstick test used in SLE diagnosis?

A

Looking for proteinuria to assess renal inflammation

44
Q

Recall 2 important non-antibody lab markers used in SLE diagnosis

A

ESR is high whilst CRP is low

45
Q

How is mild SLE treated?

A

Paracetemol and NSAID

46
Q

How is mild SLE defined?

A

Only joint and skin involvement

47
Q

how is moderate SLE defined?

A

More than just skin and joint involvement - add in inflammation of heard/lungs/kidney:
Pleuritis
Pericarditis
Nephritis

48
Q

Recall the management of moderate SLE

A

Paracetemol and NSAID like mild, in addition:
Corticosteroid: suppresses disease, titre this down as disease is managed
Immunological therapy: azothioprine - these have a synergistic effect with steroids

49
Q

How is severe SLE defined?

A

Sever inflammation in vital organs

50
Q

Recall 4 features of severe SLE

A

Myocarditis
Severe nephritis
AIHA/ thrombocytopenia

51
Q

Recall 2 approaches to treatment of severe SLE

A

Immunomodulatory drugs

Biologics

52
Q

Recall an example of an immunomodulatory therapy used in severe SLE and one advantage and disadvantage of this drug

A

Mycophenalate mofetil
Ad: doesn’t impair fertility like cyclophosphamide
Dis: Doesn’t protect renal function so well

53
Q

Recall an example of an immunoodulatory therapy used in moderate SLE, and one drawback of its use

A

Cyclophosphamide

Impairs fertility

Y2 LCRS Musc Fwong HR (8 decks)

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