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BPT > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Catastrophic Antiphospholipid Syndrome

A

Rare, life threatening form of APS
Characterised by micro and macrovascular thrombosis of multiple organs that develop either simultaneously or in short succession

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2
Q

Mechanism of Obstetric Antiphospholipid Syndrome

A

Direct trophoblast inhibition

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3
Q

Overarching rule for Antiphospholipid Syndrome testing

A

Persistent positivity required

(positive result on two tests done at least 3 months apart)

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4
Q

When are the different antiphospholipid syndrome antibodies significant?

A

Cardiolipin >40
Anti-Beta2 Glycoprotein >40 or >99th percentile
Lupus Anticoagulant: positive

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5
Q

Risk stratification for Antiphospholipid Syndrome

A

High: Positive Lupus Anticoagulant, any Cardiolipin or Beta2-Glycoproteinresult

Moderate: Negative Lupus Anticoagulant, moderate to high Beta2 glycoprotein and/or Cardiolipin

Low: Negative Lupus Anticoagulant, low titre Cardiolipin and/or Beta2 glycoprotein

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6
Q

Who needs primary thromboprophylaxis in Antiphospholipid Syndrome?

A

High risk aPL profile, low risk aPL profile but have SLE, history of obstetric antiphospholipid syndrome

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7
Q

Management of Thrombosis in Antiphospholipid Syndrome

A

Warfarin indicated, DOAC inferior. Target INR 2.5-3.5, increasing to 3-4 if recurrent on therapy.

Lifelong if unprovoked, recurrent or high risk aPL profile, otherwise as per usual guidelines

Recurrence: lifelong, increase INR target, add Aspirin, consider change to LMWH

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8
Q

Management of Antiphospholipid Syndrome during pregnancy

A

High risk aPL but no history of thrombosis or pregnancy complications: Aspirin monotherapy

History of obstetric APS but no thrombosis (≥3 recurrent spontaneous miscarriages prior to 10 weeks, history of foetal loss)
- Aspirin + prophylactic dose heparin during pregnancy

History of thrombosis: therapeutic dose heparin, which needs to be continued for 6 months post partum

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9
Q

Diagnosis of Sjogren’s

A

Schirmer test <5mm wetting in 5 minutes = dryness
ANA, Ro/La (SSa/SSb)

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10
Q

Primary Lymphoma type associated with Sjogren Syndrome

A

Mucosal Associated Lymphoid Tissue Lymphoma

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11
Q

Clinical features of SJogren’s associated with higher lymphoma risk

A

Lymphadenopathy
Recurrent parotid swelling
Monoclonal gammopathy
Depressed C4
Decreased RF (if elevated at baseline)

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12
Q

What population needs additional testing prior to starting Allopurinol, and what testing is this?

A

Four South East Asian patients, need to check HLAB58*01

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13
Q

HLA associated with Behcet’s?

A

HLA B51

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14
Q

Etanercept

A

TNF Inhibitor

Shouldn’t be used for IBD → increases risk of bowel perforation

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15
Q

Infliximab

A

TNF Inhibitor

First line biologic for IBD, good for fistulas, perianal disease

Risk of anti-drug antibodies

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16
Q

Adalimumab

A

TNF Inhibitor

Risk of anti drug antibodies

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17
Q

Certolizumab

A

TNF Inhibitor

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18
Q

Golimumab

A

TNF Inhibitor

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19
Q

Anakinra

A

IL-1 Inhibitor

Less effective for inflammatory arthritis, so not used much. Can be used for gout, TRAPS, Familial Mediterranean Fever

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20
Q

Tocilizumab

A

IL-6 Inhibitor

In GCA: Reduces flares by 40%, faster steroid wean.
Drops CRP drastically as IL-6 drives acute phase reactant production
GIACTA Trial key

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21
Q

Secukinumab

A

IL-17 Inhibitor

Used for Psoriasis, PsA, AS, Axial Spondyloarthritis

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22
Q

Ixekizumab

A

IL-17 Inhibitor

Only really used for PsA/Psoriasis

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23
Q

Ustekinumab

A

IL-12/23 Inhibitor

Good for joints, less so skin

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24
Q

Guselkumab

A

IL-23 Inhibitor

Good for joints, less so skin

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25
Q

Abatacept

A

T cell costimulation blockade. Blocks CD28 from binding to CD80/86 → reduced Treg suppression and limitation of T effector cell activity

In a sense is a CTLA-4 analogue. SO downregulated T cell activity overall.

Similar efficacy to TNF Inhibitors in RA

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26
Q

Rituximab

A

Anti CD20 → depletes B cells, blocks formation of new antibodies

Can cause hypogammaglobulinaemia

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27
Q

Belimumab

A

Inhibits B cell activation

Can be used in Lupus

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28
Q

Tofacitinib

A

JAK Inhibitor: Reduced DNA transcription in lymphocytes

High risk of cardiovascular disease, stroke, VTE, cancer in older patients and smokers

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29
Q

Upadacitinib

A

JAK Inhibitor: Reduced DNA transcription in lymphocytes

High risk of cardiovascular disease, stroke, VTE, cancer in older patients and smokers

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30
Q

Baricitinib

A

JAK Inhibitor: Reduced DNA transcription in lymphocytes

High risk of cardiovascular disease, stroke, VTE, cancer in older patients and smokers

31
Q

Lofgren Syndrome

A

Pathognomic presentation of sarcoid

Fever plus triad of:
- Migratory polyarthritis
- Erythema nodosum
- Bilateral hilar lymphadenopathy

70-80% experience spontaneous remission, and biopsy is not required to confirm diagnosis

32
Q

Biopsy in Sarcoid

A

Gold standard for diagnosis. Skin lesions a good option as easily accessible

Noncaseating granulomas containing
- Giant cells
- Asteroid bodies
- Schaumann bodies

33
Q

Indications for Immunosuppression in Sarcoidosis

A
  • Symptomatic, progressive disease
  • Persistent pulmonary infiltrates
  • Progressive decline in lung function
34
Q

Sarcoidosis staging

A
  1. Bilateral Hilar Lymphadenopathy, no pulmonary infiltrates
  2. Pulmonary infiltrates, No Bilateral Hilar lymphadenopathy
  3. Both bilateral hilar lymphadenopathy and pulmonary infiltrates
  4. Substantial pulmonary fibrosis
35
Q

Sarcoidosis Pathology

A

Granulomas produced following macrophage activation → Th1 cell activation → IFN-gamma release → epithelioid cell and multinucleated giant cell formation

Epithelioid cells produce ACE and recruit fibroblasts leading to fibrosis

Alveolar macrophages increase calcitriol leading to hyperphosphataemia, hypercalcaemia, renal failure. Driven by 1-alpha hydroxylase

36
Q

Mitochondrial Myopathy

A

Maternal inheritance

External ophthalmoplegia, Ptosis, exertional muscle weakness. However also subtypes such as MELAS (encephalopathy, myopathy, lactic acidosis, stroke like episodes)

Lactic acidosis, CK normal

Muscle Biopsy shows: Ragged red fibres but no inflammatory cells or necrosis

37
Q

Risk Factors for RA

A

Smoking is key risk factor. 25% of all RA and 35% of seropositive RA attributable to smoking

Obesity, silica, shared epitope all increase risk

Moderate alcohol intake reduces risk slightly

38
Q

Key HLA for Rheumatoid Arthritis

A

HLA-DRB1

Concept of shared epitope

Around 60% heritable

PTPN22 SNP is other key gene

39
Q

Most specific test for Rheumatoid Arthritis

A

Anti-CCP

40
Q

DAS-28

A

Key tool for monitoring RA
<2.6 = remission
>5.1 = active

41
Q

Poor prognostic factors for Rheumatoid Arthritis

A

Low socioeconomic/education
Female
Advanced age at onset
Increased DAS28
Presence or high tires of RF and/or ACPA (i.e. seropositive does worse)
Presence of erosions
Smoking
Delayed diagnosis/treatment

42
Q

How much do TNF Inhibitors increase infection risk?

A

~5%

43
Q

Key extra-articular manifestations and complications of RA

A
  • Scleritis
  • Sicca
  • Atherosclerosis
  • Pulmonary: ILD, pleural effusion
  • Renal amyloid (a-a)
44
Q

MPO-ANCA

A

Microscopic Polyangitis
ANCA present >90%

Necrotising GN +/- pulmonary capillaritis

45
Q

PR3-ANCA

A

Granulomatosis with polyangitis
ANCA present >80%

Respiratory involvement core feature
Can have a pauci-immune GN

46
Q

EGPA

A

Eosinophil rich granulomatous inflammation of respiratory tract
Often also have Atopy
40% ANCA positive, more common if have GN as well as lung involvement. MPO typical

47
Q

Most common presenting feature (or at least first clinical feature) of GPA/EGPA?

A

ENT involvement

48
Q

ILD patterns in ANCA

A

pANCA (MPO, MPA): UIP
cANCA (PR3, GPA): NSIP

49
Q

What infection is commonly ANCA positive?

A

Infective Endocarditis (c-ANCA)
Cystic Fibrosis, esp. Pseudomonas aeruginosa

50
Q

What drugs can induce ANCA?

A

Hydralazine
Carbimazole/Propylthiouracil
Minocycline
Penicillamine

51
Q

What is Avacopan, and when might it be used?

A

C5a receptor inhibitor
Used for ANCA vasculitis
Reduces cumulative corticosteroid exposure

52
Q

Mepolizumab

A

IL-5 Inhibitor
Can be used in non-severe/refractory EGPA

53
Q

What is the biggest risk factor for GCA/PMR?

A

Age
Essentially does not occur in those <50

54
Q

When should Aspirin be used in GCA?

A

Critical/flow limiting cerebral artery disease. However some bosses will use in all

55
Q

Which antibody is associated with Scleroderma Renal Crisis?

A

RNA polymerase III

Abrupt onset moderate to severe hypertension
Urine sediment often normal, or mild proteinuria
Progressive renal failure
Steroids can precipitate, also very hard to wean them if it occurs.

56
Q

Which Rheumatologic condition is associated with GAVE?

A

Scleroderma

57
Q

U1-RNP

A

Mixed Connective Tissue Disease

58
Q

Nucleolar ANA

A

Diffuse SSC

59
Q

Centromere ANA pattern

A

Limited SSc

60
Q

Anti Scl-70

A

Diffuse SSc

61
Q

PMSCL 100/75

A

Myositis/Scleroderma overlap

62
Q

First line treatment for SSc related inflammatory arthritis

A

MTX

Second line: Glucocorticoids

63
Q

Treatment for SSc related skin disease

A

MTX first line for mild disease, MMF if not responding
MMF first line if severe
3rd line IV cyclophosphamide

64
Q

Treatment for SSc related ILD

A

MMF first line for induction and maintenance
IV CYC 2nd line for induction, RTX 3rd line
AZA 2nd line for maintenance, CYC 3rd line

65
Q

Treatment for SSc related PAH

A

Mild:
- 1st: PDE5i (sildenafil, tadalafil)
- 2nd: add ERA (Bosentan, Ambrisentan)
- 3rd line: Prostanoid

Moderate:
- Start with prostanoid
- 2nd line ERA + PDE5i
- 3rd line: ERA + prostanoid

66
Q

Treatment for SSc related Myocarditis

A

1st line MMF or high dose steroids
In conjunction with normal CCF treatment
2nd line: IV CYC or RTX

67
Q

Poor Prognostic Factors in SSC

A
  • Increasing age
  • Sclerdoderma renal crisis
  • PAH
  • Pulmonary Fibrosis
  • Rapid onset/progression
  • Associated malignancy
68
Q

Poor prognostic factors and SLE

A
  • Age: onset >50, or <30 with organ involvement
  • Haemolytic anaemia
  • Male
  • Renal lupus within 1 year of presentation
  • Neuropsychatric lupus
69
Q

What gene mutation is associated with SLE pathogenesis

A

PTP-N22

70
Q

Immunopathogenesis of SLE

A

Increased apoptosis → excess antigen → CRP and C1q overwhelmed

Formation of neutrophil extracellular trans (NETs) → NETosis

Immune complexes important in nephritis

71
Q

Stages/Classes of Lupus Nephritis

A

I. Minimal change (Excellent prognosis)
II. Mesangial LN (Excellent prognosis)
III. Focal proliferative (Variable prognosis)
IV. Diffuse proliferative (Variable prognosis)

72
Q

Anti sm antibodies

A

Renal and Neurological Lupus

73
Q

Drug Induced Lupus Causes

A

6-12% of lupus is drug induced

High Risk (5-20%)
- Procainamide)
- Hydralazine

Low Risk: Anti TNF, PPI, Statins, Chemo, ACEi, Propylthiouracil, Minicycline, Methyldopa, D-penicillamine

74
Q

Antibodies in Drug Induced Lupus

A

100% ANA positive
Anti-histone antibodies classic
dsDNA, esp in TNFi
ANCA (MPO): Hydralazine, minocycline, PTU

BPT (20 decks)

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