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RACP Written Exam 2015 > Rheumatology > Flashcards

Rheumatology Flashcards

0
Q 
In RA which one of the following is associated with disease activity along with CRP and ESR?
RhF
Leukocytosis
Thrombocytosis
Hypoalbuminaemia
Anaemia
A

Thrombocytosis - acute inflammatory marker

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1
Q

In OA of the knee, where is pain experienced most when patient is climbing down stairs?

A

Pain on going downstairs in patella-femoral compartment

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2
Q

How do you differentiate between Spinal Canal Stenosis and peripheral vascular disease / vascular claudication?

A

Spinal claudication

  • patients often find it easier walking down stairs (relieves spinal pressure)
  • can walk further after resting spine / leaning forward
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3
Q

What are the major muscles that contribute to a positive Trendelenburg test?

A

Main thigh adductor is gluteus medius.

“Tensor fascia latae, glut med and min,
adduct the thigh and rotate it in”

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4
Q

Inclusion Body Myositis features

A

most common inflammatory myopathy.

DISTAL myopathy - weakness & atrophy in QUADS!!! (in contrast to DM and PM which cause PROXIMAL weakness)
Affects MEN mostly
CK normal (or only mildly elevated)
Inflammatory myopathy affecting the ENDOMYSIUM

MM Biopsy shows: Inclusion Bodies

Mx: Immunosuppression
Pred, CSA, MMF, CTX, AZA, Rituximab

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5
Q

Fibromyalgia features

A

NON-INFLAMMATORY, chronic pain syndrome

Generalised pain
Continuous with no diurnal variation
MSK bone and joint pain, reproducible on palpation
Frequently includes fatigue, psych issues due to chronic pain

NORMAL ESR, CRP
No investigations are diagnostic

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6
Q

Features of Sjogrens Syndrome

A

Sjogrens is a chronic inflammatory and autoimmune disorder characterised by diminished lacrimal and salivary gland secretion (Sicca complex)

Presents as:
Fatigue
Dry mouth (xerostomia)
Dry eyes (keratoconjunctivitis Sicca)

Diagnosis by positive ANA, ENA SSA/Ro and SSB/La

Treatment is mainly symptomatic

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7
Q

Which is the best antihypertensive for a patient with Gout?

A

Losartan has a hypouricaemic action

“GO LO!” = GOut LOsartan

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8
Q

Rash in hands, how do you differentiate between Lupus rash and Dermatomyositis?

A

SLE = rash affects phalanges, NOT the joints
(also as an aside - Jacouds in SLE - Joints NOT eroded)

Dermatomyositis = rash affects joints

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9
Q

DDx for small- joint arthritis in hands.

How do you differentiate?

A

Are the DIPs affected?

YES -

  • Gout = punched out lesions, erosions
  • Psoriatic = pencil in cup erosions
  • OA = subchondral cysts, L.O.S.S on imaging

NO, THE DIPS are NOT affected –>

  • RA = periarticular erosions
  • Lupus = NO erosions
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10
Q

Criteria for diagnosis of SLE?

A

Need 4/11 criteria of: SOAP BRAIN MD
One clinical plus one immunological criteria.

OR DIAGNOSE SLE if GLOMERULONEPHRITIS + dsDNA
= Class IV: Diffuse proliferative >50% glomeruli affected
(Note Class V = membranous, Class III = focal proliferation)

S - serositis (pleuritis, pericarditis)
O - oral painless ulcers
A - ANA positive
P - Photosensitivity

B - blood = haemolytic anaemia
R - renal
A - arthralgias = NON-erosive (Eg Jacouds), NON-deforming but same hand distribution as RA
I - immunological - dsDNA, anti-Smith, LAC/ACL, HYPOCOMPLEMENTAEMIA
N - Neuro - PRES!!! (Headache, confusion, seizure, visual Dist) psychoses

M - malar rash (includes bridge of nose)
D - discoid rash (scarring)

** LOW VITAMIN D is associated with INCREASED DISEASE ACTIVITY

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11
Q

Radiologic features of OA

A

LOSS of joint space in OA.

L - LOSS of jt space
O - osteophytes
S - subchondral cysts
S - subchondral sclerosis

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12
Q
  1. What cytokines are important in the pathogenesis of RA?

2. What are the main targets for drug blockades in RA?

A

(UNeven cytokines between 1-17 are UNimportant!)

Macrophages –> TNF, IL1, IL6
T cells –> IL2, IFNgamma, IL17

2. Blockades:
Biologics:
TNF
IL1 (not as good)
IL6
B cells (CD20 on B cells)
IL12/23
Jak Kinase (new)

** ALL are targets for blockade EXCEPT CTLA4!!! Etanercept is a CTLA4 fusion Ig which POTENTIATES the function of Treg’s (does NOT block it!) –> enhances the Treg function to turn down the immune system.

non-Biologics:
DNA synthesis (MTX= DHFR, Leflunomide = DHOR)
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13
Q

What is the best parameter for monitoring disease activity in SLE?

A

dsDNA for monitoring!! never use CRP!

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14
Q

Features of Dermatomyositis?

How do you diagnose it?

A

Patients present with WEAKNESS (not pain)
+
Rash (3) - Heliotrope rash, Shawl rash, Gottron’s Papules (over DIp/PIP/MCP joints)
+
Solid Cancer INCREASED RISK (45% assoc with a malignancy!) –> MUST LOOK FOR CANCER with CT Chest/Abdo/Pelvis, Mammogram and Paps
+
Elbow Calcinosis ***, tendon contractures, ILD in the longer term

Diagnosis:
- MRI showing Myositis
- MM BIOPSY- PERIFASCICULAR ATROPHY (ie in PERIFery),
NOT MUCH INFLAMMATORY CELLS
- Histo: (dermatomyositis and Inclusion body Myositis) –> Endomysial inflammation, infiltrating Muscle fibres
- CD8 T cell predominant (» CD4) and complement-mediated
- anti-Jo1

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15
Q

Features of Polymyositis?

How do you diagnose it?

A

Patients present with WEAKNESS (not pain)

Diagnosis:

  • Myositis on MRI
  • Histo: ENDOmysial inflammatory infiltrates, muscle fibre necrosis, atrophy, muscle fibre regeneration. LOTS OF INFLAMMATORY CELLS INSIDE MM FASCICLES
  • CD4 T cell predominant (»CD8) (“4 letters in poly hence CD4”)
16
Q

What is the management for Dermatomyositis and Polymyositis?

A

Mx is the same for both.

steroids –> MTX / AZA / CTX
–> IVIG a

17
Q 
What condition presents with:
Myositis
Interstitial lung disease
Arthropathy
Fever
Raynauds
Mechanics hands
Anti-Jo1 positivity
A

Anti-Synthetase Syndrome

18
Q

What is the management for Scleroderma renal crisis?

A

CAPTOPRIL!!!

Short Half-life, Can dose increment quickly
Start at 6.25mg QID and double dose until renal crisis controlled

19
Q

What is the management for SLE?

A

MANAGEMENT
- HCQ (Plaquenil, an anti malarial that inhibits IFNgamma)
S/E is OCULAR toxicity hence need YEARLY EYE checks.

  • Steroids!!!
- AZA for GN class III (FOCAL proliferative GN) 
and class V (membranous GN)
  • MMF IS THE TREATMENT OF CHOICE FOR LUPUS NEPHRITIS CLASS IV Diffuse proliferative GN (>50% glomeruli affected)
  • CTX (depletes B cells) - use for CNs disease and when all other treatments fail. CTX followed by AZA.
  • BELIMUMAB (anti-BAFF/BLyss, a B cell activating factor) inhibits B cell activation. add on to MTZ / AZA.

(Pregnancy: HCQ and AZA safe)

20
Q

What condition/s have positive Anti-Jo1?

A

Dermatomyositis

Anti-synthetase Syndrome
Myositis, Interstitial lung disease, arthropathy, fever, Raynauds, mechanics hands

21
Q

What are the clinical features of Diffuse Systemic Sclerosis (Scleroderma)?

A

CREST “PLUS”
Calcinosis, Raynauds, Oesophageal dysmotility, Sclerodactyly (with ulceration, digital pitting), capillary loop drop-out
(Telangiectasia also includes GAVE - if telangiectasia in mouth, likely also in the stomach)

PLUS
PULMONARY HTN
fibrosis, alveolitis
Hypertensive Crisis

22
Q

What is the management for Diffuse Systemic Sclerosis?

A

Treat the symptoms
- Mx Raynauds (see other card, basically non-pharm methods, then CCBs Nifedipine/Amlodipine +/- GTN nitrate patch. 2nd line Alprostadil IV.

  • Mx Pulmonary HTN
  • -> Bosentan (also reduces new ulcers), Sildenafil (also improves Raynauds)
  • Mx Interstitial Lung disease / Fibrosis / Alveolitis
  • -> CTX SIGNIFICANTLY IMPROVES LUNG FUNCTION AND SKIN MANIFESTATIONS
  • Scleroderma Hypertensive crisis
  • -> Captopril
23
Q

Management for Raynauds Phenomenon.

A

First line: non-pharmacological.

  • Warming of hands
  • stop smoking
  • avoid beta blockers

Pharmacological:

  • Dihydropyridine (“–dipine”) CCBs! - Nifedipine, Amlodipine
  • Nitrates - GTN patch

2nd line drugs for severe digital ISCHAEMIA:
- ALPROSTADIL - a Prostacycline, potent vasodilator

24
Q

What are the key features of Spondyloarthropathies?

What genes are involved?

A
  • Enthesitis (where ligaments/tendons insert to bone)
  • -> ACHILLES TENDITINIS
  • -> PLANTAR FASCIITIS
  • -> axial and pelvic girdle involvement
  • Inflammatory back pain (nocturnal, worse with rest, morning stiffness)
  • Oligoarthritis (>4 joints) - DISEASE ACTIVITY ASSESSED BY SWOLLEN JT COUNT, ESR, CRP
  • -> asymmetric
  • -> lower limbs usually
  • Dactylitis
  • IBD association
  • ANTERIOR UVEITIS - UNILATERAL, acute, eye pain, blurred vision, photophobia
  • Psoriaform rash
  • HLA B27, ERAP1 gene (**new, trims peptides and reduces IL1, IL6, TNFa)
25
Q

DISH - what is this condition?

What is the difference between AS and DISH?

A

Diffuse Idiopathic Skeletal Hyperostosis.

  • NOT INFLAMMATORY
  • Ossification/CALCIFICATION of ANTERIOR LONGITUDINAL LIGAMENTS –> candle wax appearance, vertebral corners not involved
  • NOT associated with HLAB27
  • Associated with Diabetes and is likely polygenic
  • Mx: NSAIDS

Ankylosing Spondylitis

  • inflammatory back pain
  • Spinal X-RAY: SYNDESMOPHYTES (CALCIFICATION of ANNULUS FIBROSIS –> “shiny corners”, sclerosis develops East-west, then North to South (whereas osteophytes go north-South)
  • posterior facet joints also involved
26
Q

What are the features of Ankylosing spondylitis?

What is the strongest predictor of POOR OUTCOME?
What is the earliest and most sensitive test for spinal immobility?

A

“I “GUESS” you have Ank Spond, based on these features”

G - genes HLAB27, ERAP1
U - uveitis
E - enthesitis
S - sacroiliitis and inflammatory arthritis
S - syndesmophytes on X-RAY (calcification of ligaments)

Need Sacroilitis plus 1 clinical feature for diagnosis,
OR
Need gene positive HLAB27 plus 2 clinical features.

Also

  • Onset in young, aged less than 45
  • duration of symptoms > 3 months
  • positive Schober test > 5cm
  • LUNG FIBROSIS, upper lobes
  • AORTIC REGURGITATION

Strongest predictor of poor outcome = HIP ARTHRITIS

First/ MOST SENSITIVE sign of SPINAL IMMOBILITY = reduced Lateral spinal flexion (normal is >10cm)

27
Q

What is the Management for Ank Spond?

A

Mainstay of treatment is NSAIDS NSAIDS NSAIDS and Physiotherapy.

Then, if failure of 2x NSAIDS after 3 months
–> ANTI-TNFs (INFLIXIMAB, ADA, GOLIMUMAB)
(do not use Etanerept in IBD)

–> PERIPHERAL DISEASE, can use SZP (but NOT for spinal disease)

  • INCREASED OSTEOPOROSIS RISK with AS hence manage OP

** Need to show improvement in BASDAI score.
BASDAI (Bath AS Disease Activity index) evaluates Disease Activity

28
Q

Psoriatic arthritis.

What are the radiological features and treatment?

A

Imaging:

  • “Pencil in cup” deformity = FUSION at DIPJ
  • evidence of joint erosions and bony proliferation:
  • -> PERIOSTITIS (fluffy joint margins)
  • -> OSTEOLYSIS (wide joint space)
TREATMENT IS EXACTLY AS PER RA.
NSAIDS
Steroids
Methotrexate / SZP
Leflunomide

Then Biologics if failed treatment for 6 months
Anti TNFs etc

29
Q

What is the management for Enteropathic Arthritis (IBD associated PERIPHERAL arthritis)?

A

Peripheral arthritis is usually NON-DEFORMING and SELF-LIMITED.

DO NOT USE NSAIDS as risk of flare of IBD!!!

Treatment is as per IBD,
SZP, Steroid
Infliximab

30
Q

Match these antibodies to their conditions.

Anti-Centromere
Anti-Scl-70 Ab
SSA / Ro
SSA / La
** Anti- Histone Ab
dsDNA
Anti U1-RNP (with negative dsDNA)
Anti-Sm (Smith)
** ribosomal P
Anti Jo1
A

Anti-Centromere = CREST (think anti-CRESTomere antibody!)

Anti-Scl-70 Ab = Diffuse Scleroderma, highly specific

SSA / Ro = Sjogrens & NEONATAL LUPUS & FOETAL HEART BLOCK & Subcutaneous Lupus (75%)

SSA / La = Sjogrens

** Anti- SSA stands for “Anti- Sjogrens Syndrome related Antigen A or B” **

Anti- “HE IS STONED” = DRUG INDUCED (“stoned”) LUPUS

dsDNA = SLE, RENAL DISEASE especially
Monitors disease activity in SLE

Anti U1-RNP (with negative dsDNA) = MCTD

Anti-Sm (Smith) = SLE - very specific marker for SLE but only present I. 25%
** CNS LUPUS**

ribosomal “PSYCHO” = PSYCHOSIS & Depression in SLE

Anti Jo1 = Dermatomyositis

31
Q

What are the indicators of CURRENT activity in RA?

A

CRP
ESR
Swollen joint count

32
Q

What are the different treatment options available for RA?

A 
Main sites of Blockades:
Biologics:
TNF
IL1 (not as good)
IL6
B cells (CD20 on B cells)
IL12/23
Jak Kinase (new)
CTLA4
non-Biologics:
DNA synthesis (MTX= DHFR, Lefluno = DHOR)
  1. start with NSAIDS / Steroids
  2. then add non-Biologics
    - MTX = In RA: inhibits T cell activation and suppresses ICAM. In cancer: acts as a DHFR inhibitor, interferes with Purine synthesis. If toxicity, needs Folinic acid rescue WEEKLY PO 20mg.
  • Leflunomide = a DHOR inhibitor, interferes with pyrimidine synthesis. If toxicity, needs cholestyramine washout then recheck levels,
  • can combine MTX + SZP + HCQ, or MTX + Lefluno
  • CsA
  1. add on Biologics (only use one Biologic at a time)
    - TNFs = Etanercept, Infliximab, Adalimumab, Golimumab, Certilumab.
    NO DIFFERENCE IN EFFICACY BETWEEN ANTI-TNF BIOLOGIC AGENTS
  • B cell/CD20 = Rituximab (SLOOOOWWW B CELL DEPLETION, Takes 3 MONTHS to take effect.
    Does not deplete early pre-B or plasma cells (ie CD20 not expressed on the very early or very late stages of B cells, hence Rituximab has no effect on these –> No fall in Ig in early treatment)
  • IL6 = Tocilizumab (IL6 Receptor blocker. S/E are deranged LFTs, cholesterol. But surprisingly reduced CV risk and lowers CRP in RA)
  • IL1 = AnakinRA (receptor antagonist. Not as good as others)
  • CTLA4-Ig = Abatacept = a CTLA4 Ig fusion protein
  • Jak Kinase 1 & 3 = Tofacitinib = blocks Jak Kinase and therefore all its downstream cytokines

OTHER MANAGEMENT:

  • Bone protection
  • Infection / Immunosuppression
  • Control CV risks
  • Toxicity of drugs (eg MTX or Leflunamide rescues)
33
Q

What urate level defines hyperuricaemia?

A

Hyperuricaemia is arbitrarily defined as
>0.36 mmol/L in females
>0.42 mmol/L in males

(eTG)

34
Q

Lupus Nephritis.

What is the best treatment for Class IV Lupus Nephritis?

A

MMF (MYCOPHENOLATE) IS THE TREATMENT OF CHOICE FOR LUPUS NEPHRITIS CLASS IV Diffuse proliferative GN

(all other classes use AZA)

RACP Written Exam 2015 (14 decks)

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