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2a > Rheum > Flashcards

Rheum Flashcards

1
Q

What XR changes are seen in OA?

A

LOSS
- Loss of joint space
- Osteophytes
- Subchondral sclerosis (increased density along joint line)
- Subchondral cysts (fluid filled holes in the bones)

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2
Q

What hand signs suggest OA?

A
  • Heberden’s nodes (DIP joints)
  • Bouchard’s nodes (PIP joints)
  • Squaring of base of thumb at carbo-metacarpal joint
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3
Q

What is the stepwise management of OA?

A
  1. Lifestyle changes and physiotherapy
  2. Oral paracetamol + topical NSAIDs
  3. Add oral NSAIDs + PPI
  4. Intra-articular steroid injections
  5. Joint replacement
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4
Q

What happens in RA?

A

Chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa

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5
Q

How do patients with RA present?

A
  • Symmetrical distal polyarthropathy
  • Pain and stiffness in small joints
  • Pain improves with activity
  • Pain worse in the morning
  • Systemic symptoms - fatigue, wt loss, flu like illness
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6
Q

What joints are rarely affected by RA?

A

DIP joints

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7
Q

What hand signs suggest RA?

A
  • Z shaped deformity to the thumb
  • Swan neck deformity
  • Boutonnieres deformity (opposite of swan neck)
  • Ulnar deviation of the fingers at the MCP
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8
Q

How do you investigate RA?

A
  • Check RF
  • If ^ negative check anti-CCP antibodies (more sensitive and specific)
  • Inflammatory markers
  • XR hands and feet
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9
Q

What XR changes are seen in RA?

A
  • Joint destruction and deformity
  • Soft tissue swelling
  • Periarticular osteopenia
  • Boney erosions
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10
Q

What is the stepwise management of RA?

A

Manage acute flare with short course of steriods

  1. NSAIDS + PPI
  2. Monotherapy with DMARD (methotrexate, leflunomide, sulfasalazine)
  3. 2 DMARDs in conjunction
  4. Methotrexate + biological therapy (TNF inhibitors)
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11
Q

What do you need to consider when prescribing TNF inhibitors?

A
  • Lead to immunosuppression to patients are prone to serious infections
  • Can lead to reactivation of dormant infections e.g. TB, hep B
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12
Q

What are notable side effects of methotrexate?

A
  • Bone marrow suppression
  • Leukopenia
  • Teratogenic
  • Mouth ulcers
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13
Q

What needs to be prescribed with methotrexate?

A
  • Folic acid 5mg
  • Needs to be taken on different day to methotrexate
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14
Q

What needs to be prescribed with methotrexate?

A
  • Folic acid 5mg
  • Needs to be taken on different day to methotrexate
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15
Q

What happens in gout?

A

Chronically high blood uric acid levels -> urate crystals deposited into joints

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16
Q

What joints are most affected in gout?

A
  • Base of big toe (metatarsophalangeal joint)
  • Wrists
  • Base of thumb (carpometacarpal joints)
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17
Q

What are gouty tophi? Where are they found?

A
  • SC deposits of uric acid
  • Small joint and connective tissue of the hands, elbows and ears
  • DIP most common site
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18
Q

What will joint aspiration show in gout?

A
  • Needle shaped crystals
  • Negatively birefringent
  • Monosodium urate crystals
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19
Q

What will joint XR show in gout?

A
  • Joint spaces maintained
  • Lytic lesions
  • Punched out erosions with sclerotic boarders and overhanging edges
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20
Q

What is the stepwise management of an acute gout flare?

A
  1. NSAIDS
  2. Colchicine
  3. Steroids
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21
Q

When are NSAIDs contraindicated for acute gout?

A

In patients with renal impairment or significant heart disease

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22
Q

What is a side effect of colchicine?

A

GI upset -> diarrhoea

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23
Q

What is used for gout prophylaxis? How does it work? What is key when initiating it?

A
  • Allopurinol
  • Xanthine oxidase inhibitor that reduces uric acid levels
  • Don’t initiate until after the acute attack is settled
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24
Q

What is pseudogout caused by?

A

Calcium pyrophosphate crystals

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25
Q

What joints are commonly affected in pseudogout?

A
  • Knee
  • Shoulders
  • Wrists
  • Hips
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26
Q

What will joint aspiration show in pseudogout?

A
  • Calcium pyrophosphate crystals
  • Rhomboid shaped crystals
  • Positive birefringent
27
Q

What XR finding is pathognomonic of pseudogout?

A
  • Chondrocalcinosis
  • Appears as a thin white line in the middle of the joint space caused by calcium deposition
28
Q

What screening tool should patients with psoriasis complete?

A

Psoriasis epidemiological screening tool (PEST)
- Screens for psoriatic arthritis
- High score triggers referred to a rheumatologist

29
Q

What is arthritis mutilans?

A
  • Most severe form of psoriatic arthritis
  • Osteolysis of the bones around the digit
  • Leads to progressive shortening of the digit
  • The skin folds as this happens and is called ‘telescopic finger’
30
Q

What happens in reactive arthritis?

A

Infection triggers synovitis in the joints

31
Q

What is another name for reactive arthritis?

A

Reiter Syndrome

32
Q

What are features of reactive arthritis?

A
  • Arthritis
  • Bilateral conjunctivitis
  • Anterior uveitis
  • Circinate balanitis (dermatitis of the head of the penis)

Passmed say:
- Oligoarthritis
- Conjunctivitis
- Urethritis

33
Q

What joints are affected in ankylosing spondylitis?

A
  • Sacroiliac joints
  • Joints of the vertebral column
34
Q

How does ankylosing spondylitis present?

A
  • Lower back pain and stiffness
  • Sacroiliac pain in the buttock region
  • Slow onset >3 months
35
Q

What special test is useful for diagnosing ankylosing spondylitis?

A
  • Schober’s test
  • Distance less than 20cm when bending forward supports a diagnosis of AS
36
Q

What is SLE?

A
  • Systemic lupus erythematosus
  • Inflammatory autoimmune connective tissue disease
37
Q

How and when does SLE typically present

A
  • Non specific symptoms
  • Red malar rash
  • Arthralgia
  • Myalgia
  • Hair loss
  • Mouth ulcers
  • Raynaud’s phenomenon
  • Lymphadenopathy
  • Relapsing and remitting course
  • More common in women and Asians
  • Presents young to middle age
38
Q

What is the initial step in testing for SLE? What autoantibodies are specific to SLE?

A
  • Anti-nuclear antibodies - present in 85% of patients with SLE
  • Anti-double stranded DNA
39
Q

How is SLE diagnosed?

A
  • Using specific criteria
  • Involves confirming the presence of antinuclear antibodies and establishing a number of clinical features of SLE
40
Q

What are 2 key complications of SLE?

A
  • CVD - leading cause of death, chronic inflammation in blood vessels -> HTN and CAD
  • Infection - more common in patients with SLE and secondary to immunosuppressants
41
Q

What are first line treatments for SLE?

A
  • NSAIDs
  • Steroids
  • Hydroxychloroquine (mild DMARD)
42
Q

What is fibromyalgia?

A

A syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites

43
Q

What are features of fibromyalgia?

A
  • Chronic pain
  • Lethargy
  • Cognitive impairment (‘fibro fog’)
  • Sleep disturbance, headaches, dizziness are common
44
Q

What is the management of fibromyalgia?

A

Lack of evidence + guidelines
- Explanation
- Aerobic exercise
- CBT
- Meds - pregabalin, duloxetine, amitriptyline

45
Q

How does Polymyalgia Rheumatica present?

A
  • Rapid onset muscle stiffness
  • Stiffness is worse in the morning
  • Affects proximal limb muscles
  • Weakness is not a feature
  • Can also present with mild polyarthralgia, lethargy. low grade fever, night sweats
46
Q

What age group is affected by PMR?

A

Typically patients are >60 yrs

47
Q

What would investigations show in Polymyalgia rheumatica?

A
  • Raised inflammatory markers (ESR >40)
  • CK and EMG normal
48
Q

What is the management of PMR?

A
  • Prednisolone
  • Pts typically respond dramatically to steroids - failure may indicate different dx
49
Q

What is antiphospholipid syndrome?

A

An autoimmune disorder caused by antiphospholipid antibodies

50
Q

What do antiphospholipid antibodies do?

A

Target proteins that bind to phospholipids on the cell surface -> inflammation and increasing the risk of thrombosis

51
Q

What are the antiphospholipid antibodies?

A
  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies
52
Q

What are clinical features of antiphospholipid syndrome?

A
  • Livedo reticularis - purple lace-like rash that gives the skin a mottled appearance
  • Libmann-Sacks endocarditis - non-bacterial endocarditis
  • Thrombocytopenia
53
Q

What are complications of antiphospholipid syndrome?

A
  • VTE
  • Arterial thrombosis
  • Pregnancy related complications
  • Catastrophic antiphospholipid syndrome (rare complication with rapid thrombosis in multiple organs)
54
Q

What is the management of antiphospholipid syndrome?

A
  • Long term warfarin to prevent thrombosis
  • LMWH + aspirin in pregnancy
55
Q

What do polymyositis and dermatomyositis present with?

A
  • Gradual onset proximal muscle weakness
  • May be muscle pain
  • Dermatomyositis also presents wit skin changes - gottron lesions, heliotrope rash
56
Q

What are causes of polymyositis and dermatomyositis?

A

Both are autoimmune disorders

Possible causes include:
- Underlying cancers (making them paraneoplastic syndromes)
- Viral infection (HIV, coxsackie A)

57
Q

What is a key investigation in polymyositis and dermatomyositis?

A

CK - often in the thousands (normal is <300)

58
Q

What antibody is specific to polymyositis?

A

Anti-Jo-1 antibody

59
Q

What is the management of polymyositis and dermatomyositis?

A
  • Physio
  • Corticosteroids - first line
  • Immunosuppressants
  • IV immunoglobulins
60
Q

What antibodies are associated with Sjogrens syndrome?

A
  • Anti-SS-A (Anti-Ro)
  • Anti-SS-B (Anti-La)
61
Q

What is Behçet’s disease?

A
  • Complex inflammatory condition that affects blood vessels and tissues
  • Main feature are recurrent oral and genital ulcers
62
Q

What can trigger hyper inflammatory syndrome?

A
  • Autoimmune disease
  • Cancer
  • Infection - esp coronavirus
63
Q

What causes hyper inflammatory syndrome?

A

Immune dysregulation - immune system doesn’t ‘switch off’ once trigger is removed. This leads to:
- Macrophage (haemo)phagocytosis
- Cytokine release -> uncontrolled T cells -> cytokine storm

64
Q

What are the characteristics of hyper inflammatory syndrome?

A

3 Fs
- Fever (cytokine storm)
- Falling counts (haemophagocytosis)
- Ferritin highly elevated

2a (12 decks)

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