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FRACP Exam > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What antibodies cause neonatal CHB in lupus?

A

Anti-ro/La

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2
Q

What is Anti-La ass with?

A

Sjogren’s syndrome

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3
Q

What is the most specific antibody for lupus?

A

Anti-Sm (renal and CNS disease)

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4
Q

What is Anti-U1RNP/RNP associated with?

A

Myositis, mixed connective tissue

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5
Q

What is ds-DNA associated with?

A

If elevated - marker of disease activity in lupus

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6
Q

What is spared in a malar rash?

A

nasolabial folds

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7
Q

Whats the most common cardiac manifestation of SLE?

A

Pericarditis

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8
Q

Autoimmune hepatitis from lupus is rare, what marker is it associated with?

A

Ribosomal P

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9
Q

Whats the main side effect/concern with long term hydroxychloroquine use?

A

Retinal toxicity.
Should be screened basline then annually after 5 years with fundoscopy

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10
Q

What happens to RA and lupus in pregnancy ?

A

RA - goes into remission

Lupus - Commonly flares

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11
Q

When does congenital heart block most commonly occur in SLE pregnancy?

A

between 16-26 weeks - irreversible once establoished

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12
Q

What autoimmune condition is infliximab contraindicated in?

A

MS - cannot be used in family members of people with MS

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13
Q

Why cant you use TNF inhibitors in MS?

A

Can cause demyelination + precipitate MS in susceptible individuals

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14
Q

What are some side effects of tocilizumab?

A

Cannot be used in patients with dierticulosis due to risk of bowel perforation
It does not need to be used WITH methotrexate
It has interactions with other CYP3A4 drugs

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15
Q

Nailfold capilloroscopy showing a relative paucity of capillary loops with enlarged and distorted loops with background of raynauds indicates what?

A

Raynauds from connective dissue disorder e.g polymyositis

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16
Q

What HLA subtypes are associated with increased risk of SLE?

A

HLA-A1, HLA-B8, and HLA-DR3

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17
Q

What are the histological findings of polyarteritis nodosa?

A

characterized by segmental transmural inflammation of muscular arteries

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18
Q

What do you give to patients in scleroderma renal crisis?

A

Ace inhibitors!

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19
Q

What conditions lead to primary urate over production?

A

Accelerated synthesis ( PRPPP synthase enzyme hyperactivity)
Imparired purine salvage HGPRT1 deficiency
G6PD deficiency

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20
Q

What conditions lead to secondary urate over production?

A

Anything that leads to increased RBC turnover

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21
Q

How is urate excreted?

A

ABCG2 transporter in the gut
Renal: Prox tubule - OAT1, and ABCG2

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22
Q

What meds increase gout?

A

Diuretics, low dose aspirin, pyrazinamide, ciclosporin

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23
Q

What proinflammatory receptors signal when monosodium urate crystals precipitate in the joint?

A

TLR 2 and 4 on chrondrocytes.

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24
Q

What does light microscopy of gout show?

A

intra-cellular needle shaped, negatively birefringent crstals. When the light is parallel - yellow, when the light is perpendicular - blue

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25
Q

What does gout XR show?

A

Bone erosions - cortical breakdown
“punched-out” erosions with sclerotic margins in a marginal and juxta-articular distribution
Preserved joint space

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26
Q

What is the Moa of probenecid in gout?

A

Uricosuric agent - promotes urinary excretion of uric acid
Contraindicated in people with nephrolithissis

27
Q

whats the urate target?

A

0.36

28
Q

what is the consideration for febuxostat?

A

inc CVD risk

29
Q

HLA5801 does what?

A

inc risk hypersensitivity to allopurinol (SJS reaction)

30
Q

what are the important drug interactions with allopurinol?

A

Azathioprine, mercaptopurine, theophylline.

31
Q

what conditions are associated with cppd?

A

joint trauma, Hypomag, hyperPTH, haemochromatosis, hypophosphatasi

32
Q

joint most commonly affected by cppd?

A

knee

33
Q

what are xr findings of cppd?

A

Radiographic chondrocalcinosis is common and frequently asymptomatic
- Involvement at sites uncommon for primary OA
Prominent oseteophyte formation, hook osteophytes of the MCPJ

34
Q

Anti-SRP assiciated with what?

A

Immune mediated necrotising myopathy, also Anti-HMGCR

35
Q

What are the antibodies in dermatomyositis?

A

Anti-IFH1 antibody, MDA-5 in amyopathic DM, Anti-Mi2, TIF gamma, MJ

36
Q

What myositis is associated with malignancy?

A

Dermatomyositis

37
Q

What antibodies are involved in inclusion body myositis?

A

Anti-cN1A

38
Q

What antibodies ass with antisynthetase syndome?

A

Anti-ARS, anti-Jo1, anti-PL7, anti-PL112

39
Q

What antibodu is associated with mixed connective tissue disease?

A

URNP

40
Q

What are clinical manifestations of antisynthetase syndrome?

A

Myositis/proximal weakness, pain, ILD (UIP pattern), athritis, raynauds, mchanics hands

41
Q

What are clinical features of dermatomyositis?

A

Heliotrope rash with periorbital/infraorbital oedema. Gottrons papules and mechanic hands.
1/5 will be amyopathic

42
Q

What are RF antibodies targeted against?

A

The Fc portion of human IgG

43
Q

In RA which patients have higher risk of ILD?

A

Anti-CCP positive patients, UIP pattern for RA-ILD

44
Q

What are XR findings in RA?

A
  • Periartiicular soft tissue swelling
    • Juxta-articular osteoporosis
    • Marginal erosions
    • Joint space narrowing
      Symmetrical involvement
45
Q

What using TNFi in RA can you stop MTX?

A

No additiv ebenefit is in combination with MTX
All biologics are better with methotrexate, with the exception of JAKi which can be used as monotherapy

46
Q

What is abatacept?

A

CTLA4 mimic - T-cell co-stimulator inhibitor - response similar to TNFi

47
Q

What is felty syndrome>

A

Seropositive RA + Splenomegaly + neutropenia

48
Q

How do people with Felty syndrome present?

A

They are at increased risk of bacterias infection - present with infection + neutropenia

49
Q

How do you treat Felty syndrome?

A

Treat the underlying disease with DMARD, GCSF for neutropenia, and if refractory to treatment and ongoing recurrent infections then splenectomy.
DMARD - methotrexate then if refractory add Ritux, avoid TNF

50
Q

Can patients taking tofacitinib have live vaccines?

A

No

51
Q

What are adverse outcomes of tofacitinib?

A

MACE and cancer risk increased.

52
Q

What marker shows that a cell is a T-reg cell?

A

FoxP3

53
Q

What does tofacitinib block?

A

JAK1/3

54
Q

What does baricitinib block?

A

JAK1/2

55
Q

Which TNFi is least likely to cause drug induced lupus?

A

Etanercept

56
Q

whats the most common clinical feature of AxSpa?

A

Sacroiliitis inflammation occurs both first and most commonly

57
Q

what % of patients with AxSpa have normal inflamatory markers?

A

25%

58
Q

when dont you use ertanercept in axspa?

A

(less effectvie if uveitis and IBD),

59
Q

What biologic therapy can cause flares of IBD in axSpa?

A

IL-17 inhibitors - secukinumba, ixekinumab
They are very effective if overlapping psoriasis however

60
Q

What is the HLA associated with scleroderma?

A

HLADRB1

61
Q

What scleroderma antibody is associated with scleroderma renal crisis?

A

RNA polymerase III antibody, speckled ANA pattern

62
Q

What is the treatment for scleroderma renal crisis?

A

ACEi for rapid BP control - ARBS not proven to help
ACEi + plasma exchange better survival if MAHA present
AVOID B-blockers

63
Q

What do you do in scleroderma renal crisi if normal BP?

A

Still give ACEi

64
Q

What are the nailfold capilloroscopy findings in secondary raynauds>

A

Drop outs, megacapilladies, disorganisation, microhaemorrihages

FRACP Exam (15 decks)

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