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MD2 Rheumatology > Rheumatological Red Flags > Flashcards

Rheumatological Red Flags Flashcards

1
Q

What are the usual clinical features suggestive of systemic inflammation?

A

Fatigue (disproportionate to the patient’s usual tiredness) in the presence of adequate sleep

Lethargy (not as productive as usual)

Insidious onset (rare for inflammatory conditions to present overnight)

Sometimes weight loss with or without anorexia or a low grade fever are associated

May be associated rashes, arthralgia

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2
Q

What is vasculitis? What is the mechanism of the clinical features seen in vasculitis?

A

Inflammation in the walls of the blood vessels (arteries and veins of all sizes)

Clinical features are a mixture of inflammatory and ischaemic/infarction organ dysfunction +/- damage as the lumen of affected vessels become narrowed when the walls become thickened

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3
Q

Which organs are typically involved in vasculitis?

A

Some syndromes manifest in one organ only (e.g. skin, kidney) but MOST involve multiple organs

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4
Q

What symptoms are common in a vasculitis with a multiple organ syndrome?

A

Limb girdle ache/stiffness in the mornings (especially around the shoulders)

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5
Q

Common large vessel vasculitides

A

GCA

Takayasu

NB Probably the same condition in different age groups (histopathologically similar)

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6
Q

List 2 medium vessel vasculitides

A

Kawasaki

Polyarteritis nodosa

(Medium vessel vasculitides are rarer)

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7
Q

79 year old woman, 4-week Hx of recurrent headaches (gradual onset)

No PHx of headaches

Associated features: jaw pain when chewing and talking on the phone, vision normal, 5 kg LOW, fatigue

Severe shoulder and hip stiffness (worse in the morning, i.e. inflammatory joint pain)

I.e. there are some systemic inflammatory symptoms and some localised ischaemic symptoms involving masseter muscles and scalp skin and muscles

DDx? Ix?

A

Polymyalgia rheumatica (PMR) with GCA

RA (but no arthritis)

Polymyositis (unlikely)

Hypo or hyperthyroidism (may present with myopathy)

Malignancy (may present with paraneoplastic syndrome)

Trigeminal neuralgia

Ischaemic cardiac pain

Ix: CRP, ESR

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8
Q

When should you suspect GCA?

A

Caucasian men and women (>55 years; almost exclusively Caucasian)

New headache

Jaw claudication

Unexplained fever, ESR >100mm/hr

PMR-type symptoms (i.e. limb girdle stiffness) In any patient with a Dx of PMR, esp when ESR remains elevated despite treatment with low dose steroids

Sudden monocular blindness (anterior ischaemic optic neuropathy, AION; can be transient initially)

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9
Q

Describe the symptom complex seen in GCA

A

Superficial headache, scalp tenderness, jaw and tongue claudication (common; ask if it hurts when brushing their hair)

Polymyalgia rheumatica with shoulder and hip girdle pain and morning stiffness (very common)

Fever and fatigue LOW AION, retinal artery occlusion (risk less than 1%)

Upper limb claudication (rare)

Cough, sore throat (very rare)

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10
Q

How common is it for a patient with GCA to have a visibly enlarged temporal artery?

A

Extremely rare; most patients with GCA have no obvious signs (although opthalmologists may observe blood vessel changes on careful fundoscopy)

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11
Q

List 9 complications of GCA by the vessels involved

A

Opthalmic/long ciliary arteries: blindness

Subclavian: arm claudication, absent pulses

Renal: renovascular HTN (angiotensin 2 mediated)

Aorta, esp ascending and thoracic: aortic valve incompetence, aneurysm rupture (late)

Coronary: angina pectoris, MI ICA: TIA, stroke

Vertebral: TIA, stroke Iliac: leg claudication

Mesenteric: bowel ischaemia

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12
Q

DDx for acute monoarthritis

A

Bacterial septic arthritis

Crystal arthritis (e.g. gout, pseudogout)

Subchondral bone lesion (e.g. #, osteonecrosis, osteomyelitis)

Haemarthrosis (e.g. trauma, haemophilia, anti-coag therapy)

Palindromic rheumatism

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13
Q

22 year old woman presents with 2/7 Hx of spotty rash over lower legs and buttocks

No fever or headache but has bouts of pain in her muscles, knees and ankles

O/E: palpable, purpuric rash over lower legs, afebrile, neck supple, knees and ankle joints normal, peripheral sensation normal, muscle strength and reflexes normal

Ix: urinalysis (dipstick) shows trace of protein (+1) and no blood

DDx?

A

DDx: infection (most likely due to very short Hx; possible Dx includes meningococcal infection), allergic drug reaction (e.g. OCP, Abx), vasculitis (LCP classically, or HSP)

If fingers or toes were involved, it could suggest an embolic phenomenon (micro-emboli)

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14
Q

Which vessels are typically affected in Takiyatzu’s vasculitis vs GCA?

A

Takiyatsu’s: aorta

GCA: temporal

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15
Q

What is the mechanism of the weight loss and fever?

A

IL-1, IL-6, TNF-a

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16
Q

Give 7 examples of small vessel vasculitides

A

ANCA-associated: GPA (granulomatosis with polyangiitis; Wegener), MPA (microscopic polyangiitis), EGPA (eosinophilic granulomatosis with polyangiitis; Churg-Strauss)

Immune complex: cryoglobulinaemic, IgA (Henoch-Schonlein purpura), HUV (hypocomplementaemic urticarial vasculitis), anti-GBM

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17
Q

What organs are of greatest concern RE involvement in vasculitis?

A

Kidney

Lungs

Cerebral (rare)

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18
Q

Give 2 examples of variable vessel vasculitides

A

Behcet

Cogan

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19
Q

ANCA

A

Anti-neutrophil cytoplasmic Ab

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20
Q

Describe the findings

A

Pathological specimen: inflamed vessel

Findings include red cell extravasation, lumen obliterated with thrombus, fibrinoid material deposited in the wall of the vessel (fibrinoid-type necrosis), and evidence of inflammation (inflammatory infiltrate)

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21
Q

Describe the findings and give a DDx

A

Lung granuloma with macrophages, giant cells and eosinophils

DDx: some forms of vasculitis (classically ANCA-associated), TB, sarcoidosis (rare)

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22
Q

What is the mechanism of jaw claudication in GCA?

A
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23
Q

Temporal artery biopsy in GCA: describe the findings

A

Segmental destruction of internal elastic lamina (arrow), and granulomatous vessel inflammation with giant cells (small arrows); inflammatory exudate extends into the intima, where there is fibrosis

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24
Q

Is temporal artery biopsy always positive in GCA?

A

No; can be negative as lesions can be patchy

If there is a good story for GCA but the biopsy is negative, patient should be treated anyway

25
Q

Describe the relationship between GCA and PMR

A

Both are diseases of elderly Caucasians

Frequently occur synchronously or sequentially in same individual

PMR in >50% of GCA patients; 25% of PMG patients have co-existent GCA

Histological temporal arteritis has been documented in patients with no headache and clinically normal temporal arteries (very tricky!)

PET imaging shows increased aortic uptake in many patients with PMR who have no headache

26
Q

Mx of GCA

A

Have a low index of suspicion (because there is a high risk of blindness!)

Commence prednisolone 40-60mg daily immediately and arrange temporal artery biopsy (changes will still be present within a week of treatment)

Decide what to do if biopsy is negative - usually steroids are rapidly tapered and stopped unless the pre-test probability of GCA is very high

Taper corticosteroids according to ESR or CRP

Provide fracture prevention therapy

Be alert to early (infection) and late (fractures, aortic aneurysms, hyperglycaemia) complications

27
Q

When should “steroid sparing” drugs (e.g. methotrexate) be used for treatment of GCA?

A

If patients have been taking prednisolone 15mg daily for 6/12, consider steroid-sparing agents

Consider commencing steroid-sparing agents from onset if patient is diabetic

28
Q

63 year old woman with a PHx of knee OA presents with 2/7 of severe R knee pain, swelling and redness

She is unable to sleep or walk due to the pain

O/E: febrile (38.5 degrees), resists passive movement of R knee, R knee has tense effusion

DDx?

Ix?

A

DDx: bacterial septic arthritis, crystal arthritis (gout, pseudogout), subchondral bone lesion (e.g. fracture, osteonecrosis, osteomyelitis), haemarthrosis (e.g. trauma, haemophilia, anticoagulation, therapy), palindromic rheumatism

Ix: arthrocentesis

29
Q

63 year old woman with a PHx of knee OA presents with 2/7 of severe R knee pain, swelling and redness

She is unable to sleep or walk due to the pain

O/E: febrile (38.5 degrees), resists passive movement of R knee, R knee has tense effusion

Purulent synovial fluid is aspirated from the R knee joint and microscopy shows 60,000 neutrophils/mm, 2000 RBCs/mm, Gram positive cocci

Likely causative organism?

A

Staph aureus (shows preferential joint localisation)

Beta-haemolytic Streptococci

Gram negative bacilli (including E. coli)

Streptococcus pneumoniae

Polymicrobial

N. gonorrhoea

NB Septic arthritis with bacteria such as these typically affect single and usually large joints (50% of cases are knee, other common sites include hip, shoulder, ankle, wrist, elbow)

30
Q

What is palindromic rheumatism?

A

Rare episodic form of inflammatory arthritis; between attacks, the symptoms disappear and the affected joints go back to normal, with no lasting damage

31
Q

RFs for joint sepsis

A

Very young or advanced age

Recent joint aspirate/injection, or penetrating injury

Portals for bacteraemia

Previous joint damage (e.g. OA, RA)

Corticosteroid therapy

DM

Chronic renal or liver disease

Immunodeficiency (e.g. hypogammaglobulinaemia, CLL, any cancer)

Prosthetic joints (don’t stick a needle into a prosthetic joint!!)

32
Q

List 5 possible portals for bacteraemia

A

Skin ulcers

Bowel inflammation (e.g. diverticulitis)

Colonic biopsy

Dental work

UTI

Lower urinary tract instrumentation

33
Q

What does a polyarticular arthralgia +/- tenosynovitis suggest about the aetiology of the presentation?

A

Suggests immune complex response to systemic infection (e.g. rubella, parvovirus, hepatiti B)

NB This is very rare and the patient will be very, very sick (ICU on inotropes sick)

34
Q

Sick young adult (20-35), multiple joints infected, casual sexual activity and rash

Dx?

A

Possibility of disseminated N. gonorrhoea (disseminated gonococcal infection - DGI)

Infection of multiple joints contemporaneously is other quite rare; think immunosuppression (and disseminated MAC) or damaged joints

35
Q

MAC

A

Mycobacterium avium complex

36
Q

List 8 clinical features of septic arthritis

A

Fever, “septic” appearance

Joint pain (with no diurnal or activity variation)

Joint swelling

Heat over the affected joint

Erythema overlaying the joint

Loss of function

Pain on attempted joint motion (passive or active)

Rapidly progressive joint destruction on XR (within days or 1-2 weeks)

37
Q

What conditions might staphylococcal joint sepsis co-exist with?

A

Endocarditis

Deep abscess (e.g. epidural space)

38
Q

List some important diagnostic steps in a case of suspected septic arthritis

A

Always obtain synovial fluid for analysis ASAP

A low synovial WCC or the absence of a fever does not exclude infection, especially if the patient is immunosuppressed

Plain radiographs should be performed as a baseline and repeated at 1/52 if no Dx

MRI scan may be performed (sensitive and relatively specific)

FBE (neutrophilia is not specific)

Blood cultures are useful (50% of patients with non-gonococcal septic arthitis have positive blood cultures)

CRP is non-specific but useful if elevated

39
Q

What features are diagnostic of septic arthritis on XR?

A

Demineralisation

Rapid articular cartilage loss

NB This is critical if cultures are negative!

40
Q

Outline one hypothesis explaining Staph. aureus’ preferential joint localisation

A

Cna gene may determine adhesion to collagen

41
Q

Mx of septic arthritis

A

Maintain high index of suspicion

Choose effective Abx based on age, clinical situation and Gram stain

Joint drainage is critical: closed needle drainage is rarely adequate, arthroscopic washout is preferred (and is mandatory for hip and shoulder joints, prosthetic joints and damaged joints in RA), and remember that yield of cultures is significantly reduced if Abx are given beforehand!

Analgesia (opioids usually required)

Initial rest followed by joint mobilisation

Consider associated infection (e.g. endocarditis)

42
Q

Before cultures from arthrocentesis in septic arthritis become positive, which empirical Abx should be chosen and how long should they be continued?

A

6/52 broad spectrum (e.g. flucloxacillin)

43
Q

Give 6 examples of ANCA-negative SVVs

A

Hypersensitivity vasculitis (many causes including drug reaction)

HSP

Rheumatic disorders (e.g. SLE, RA, Sjogren’s disease)

Mixed cryoglobulinaemia (hep C, rarely HIV or cancer)

Infection (hep C, hep B)

Malignancy (leukaemia, lymphoma, myelodysplastic syndromes)

44
Q

Describe the clinical spectrum of Sx which may be seen in small vessel vasculitides

A

Constitutional: fevers, night sweats, malaise

Myalgias, arthralgias and/or arthritis

Rashes: palpable purpura (more specific), non-palpable purpura (less specific), urticaria

Nail-fold or digital infarcts

Mononeuropathy multiplex (e.g. foot drop; due to small vessel ischaemia of nerves, can be irreversible if not treated promptly)

Upper respiratory tract: sinusitis, epistaxis

Lungs: haemoptysis, diffuse alveolar haemorrhage

Haematuria (may look “smoky” in colour), microhaematuria or proteinuria on dipstick (glomerulonephritis) - can affect kidneys quickly and progress to ESKD within days!

45
Q

List 3 ANCA-associated SVVs

A

Microscopic polyangiitis (MPA)

Granulomatosis with polyangiitis (GPA; Wegener’s)

Churg Strauss syndrome (CSS)

46
Q

Can you have an ANCA-negative ANCA-associated vasculitis? How?

A

Yes; right story but ANCA-negative

Happens in GPA in particular - patient should have biopsy if there is a convincing story

47
Q

How can meningococcus present dermatologically?

A

Meningococcaemia may present with purpuric rash in absence of fever or symptoms and signs of meningitis

48
Q

How can staphylococcal bacteraemia present dermatologically?

A

Palpable purpura may occur in staphylococcal septicaemia, usually associated with deep infection (e.g. endocarditis, septic arthritis, vertebral osteomyelitis, epidural abscess, etc)

49
Q

How can subacute bacterial endocarditis present dermatologically?

A

Palpable purpura, splinter haemorrhages

50
Q

List 5 other SVV mimics

A

Thrombocytopaenia purpura

Arterial thromboembolism

Cholesterol microemboli (rarer)

Malignancy (rarer)

Calciphylaxis (rarer)

51
Q

What is thrombocytopaenia purpura?

A

Very low platelet count (<10,000)

Usually due to immune-mediated platelet destruction (ITP)

52
Q

How can arterial thromboembolism mimic SVV?

A

Showers of tiny emboli

May be due to proximal arterial aneurysm, atherosclerosis or anti-phospholipid syndrome

53
Q

How can cholesterol microemboli mimic SVV?

A

Older patients with atherosclerotic vascular disease, occur downstream from plaque dislodged during angiography

54
Q

What malignancies can mimic SVV?

A

Myxoma

Myelodysplastic syndrome

Cancers with paraneoplastic syndrome

55
Q

What is calciphylaxis?

A

HyperPTH in ESKD

56
Q

What is the gold standard Ix for Dx of a vasculitide?

A

Tissue sample: biopsy!!

57
Q

Suspected vasculitide: important Ix and their rationales?

A

FBE: normocytic anaemia and/or thrombocytosis suggests inflammatory process, thrombocytopaenia suggests ITP

Blood film: look for fragmented RBCs and high RDW suggesting intravascular haemolysis

Acute phase reactants (ESR, CRP)

Albumin: negative acute phase reactant (can fall quickly)

UEC

Septic workup: blood cultures, MSU, CXR, multiplex PCR for meningococcus/pneumococcus

MSU microscopy: “glomerular” or dysmorphic RCC, red cell casts suggest glomerulonephritis (consider renal biopsy)

MSU culture: urinary sepsis

Echocardiogram: essential for any febrile patients with heart murmur, prosthetic valves or PPMs

Skin (punch) biopsy: select fresh lesions for Gram stain, culture and H&E immunostaining (usual pattern is LCP; can get IgA deposits in HSP; immune complexes are absent in AAV)

Ix for systemic involvement (based on likelihood of organ involvement): tissue biopsy (provides direct evidence; choose biopsy site based on clinical involvement and lowest risk of complications, with common sites including skin, kidney and liver), angiography (useful if clinical suspicion of medium vessel vasculitis e.g. PAN), lung CT or pulmonary function tests, nerve conduction tests for neuropathy

58
Q

Mx of suspected vasculitis (e.g. pt presents with palpable purpura)

A

Consider infection early

Obtain Hx of drug exposure

Rapid assessment important to avoid organ damage

Tissue usually required to establish Dx

Treatment involves removal or treatment of triggering cause (e.g. hep C, drugs)

Reserve high dose corticosteroids and immunosuppression for systemic/extensive disease (if there is evidence of end organ damage, consider methylprednisolone)

59
Q

Rituximab

A

Monoclonal Ab against the protein CD20, which is primarily found on the surface of immune system B cells

MD2 Rheumatology (5 decks)

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