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Musculoskeletal > Arthritis > Flashcards

Arthritis Flashcards

1
Q

Define rheumatoid arthritis

A

A chronic systemic inflammatory disease, characterized by potentially deforming symmetrical polyarthritis and extra-articular features

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2
Q

What is the female to male ratio in rheumatoid arthritis?

A

3:1

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3
Q

What are the possible aetiologies of rheumatoid arthritis?

A

Genetic susceptibility (HLA DR4/1), environmental triggers in susceptible individuals (modern world disease). Cigarette smoking, possible infective aetiology

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4
Q

What pathological changes occur in rheumatoid arthritis?

A

Tendon sheath becomes inflamed. Synovium becomes inflamed-laden with macrophages, fibroblasts, multinucleated giant cells (resemble osteoclasts). Synovial membrane expands, actively invades and erodes surrounding bone/cartilage, joint space decreases.

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5
Q

What are the symptoms of rheumatoid arthritis?

A

Joint pain (not DIP), stiffness (esp morning), joint swelling, tenderness, reduced range of movement, deformities, malaise, fatigue, other extra-articular features

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6
Q

What are some extra-articular features of rheumatoid arthritis?

A

Nodules, scleritis, anaemia, pleural effusion, leg ulcers

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7
Q

What is the distribution of joint involvement in rheumatoid arthritis?

A

Symmetrical

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8
Q

What investigations are used in the diagnosis of RA?

A

Anti CCP, Rheumatoid Factor (RF), inflammatory markers- PV, CRP, anaemia of chronic disease, radiology-US, XR

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9
Q

What are some possible late complications of RA?

A

Infection (2y to immobility due to joint damage), cervical myelopathy (atlanto-axial or sub-axial subluxation), ILD and peripheral neuropathy (may both be early)

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10
Q

What are some co-morbidities associated with RA?

A

Serious infection, CV mortality, Lymphoma

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11
Q

What are the principles of treatment of RA?

A

Early initiation of DMARDs with steroids. Review often, with tailoring of treatment against inflammation. Address other systemic risks.

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12
Q

What biologic approaches are used in RA?

A

TNF alpha inhibition (Infliximab), B cell depletion (Rituximab), Disruption of T cell costimulation (Abatacept), IL1 inhibition (Anankira), IL6 inhibition (Tocilizumab), Jak2 inhibitors

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13
Q

What is osteoarthritis?

A

Arthropathy involving articular cartilage failure, subchondral sclerosis, loss of joint space, subchondral cyst formation

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14
Q

What is the pathogenesis of OA?

A

Loss of matrix cartilage, release of cytokines including IL1, TNF,mixed metalloproteinases & prostaglandins by chondrocytes. Fibrillation of cartilage surface and attempted repair with osteophyte formation then occurs

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15
Q

What change in cell morphology is noted in OA?

A

IL1, PGE2 and F-spondin released, along with inflammation and mechanical stress on joint. Different type of proteins form in OA cartilage, cluster formation occurs and cell death

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16
Q

What is Idiopathic OA?

A

Unknown aetiology. Either localised or generalized. Localised-hands, feet, knew, hip and spine. Other joints less commonly effected. Generalised condition- 3 or more sites involved.

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17
Q

What is Secondary OA?

A

OA with known aetiology. Previous injury, RA, genetic elements, acromegaly, calcium crystal deposition disease

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18
Q

What are some risk factors for OA?

A

Age (elderly), F:M ratio (higher in F), obesity, occupation (manual worker), sports activities, previous injury, muscle weakness

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19
Q

What are the symptoms of OA?

A

Pain-typically worse on activity and relieved by rest. May progress. Stiffness- usually morning lasting less than 30 mins-inactivity gelling

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20
Q

What examination findings are there in OA?

A

Crepitus, bony enlargements due to osteophytes, joint tenderness, joint effusion

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21
Q

What joint distribution occurs in OA?

A

Hip, Knee, Foot MTP joints, cervical spine, lumbar spine, Hand-DIP,PIP, 1st IP, 1st MCP, CMC joint

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22
Q

What may be observed regarding the hands in OA?

A

Joint stiffness- DIP, PIP, 1st CMC joints. Bony enlargements may be seen at DIPs (Heberdens nodes) and PIPs (Bouchards nodes), Squaring of thumb

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23
Q

What may be observed regarding the knee in OA?

A

Osteophytes, effusions, crepitus and restriction to movement. Genu varus and valgus deformities, bakers cyst

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24
Q

What may be observed regarding the hip in OA?

A

Pain may be felt in groin or radiating to knee. Pain felt in hip may be radiating from lower back. Hip movements restricted

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25
Q

What may be observed regarding the spine in OA?

A

Cervical – pain and restriction of movement
Osteophytes may impinge on nerve roots

Lumbar – osteophytes can cause spinal stenosis if encroach on spinal canal

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26
Q

What radiological findings may be seen in OA?

A

Loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes

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27
Q

How is a diagnosis of OA made?

A

History, exam, X-ray. No specific lab tests

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28
Q

What history would you expect from a patient with OA?

A

Small hand joints- over a 2y period pain improves, swelling becomes more marked. Knees- 1/3 symptoms each improve, stay stable, deteriorate. Hips- 10% will come off surgical waiting list due to improved symptoms

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29
Q

What is the management for OA?

A

Physiotherapy, weight loss exercise etc. Analgesia, NSAIDs, pain modulators-tricyclics, anti-convulsants. Intra-articular-steroids, hyaluronic acid. Surgical-Arthroscopic washout, loose body, soft tissue trimming, Joint replacement.

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30
Q

What is Gout?

A

Inflammation in the joint triggered by uric acid crystals

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31
Q

What sex have a higher prevalence of gout?

A

Men

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32
Q

What is the uric acid metabolism which leads to gout?

A

Overproduction and under excretion of uric acid occurs. Leads to hyperuricaemia-results in crystallization (encouraged by low temp in synovial fluid-32’)

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33
Q

What are some causes of increased urate production leading to hyperuricaemia?

A

Inherited enzyme defects, myeloproliferative/lymphoproliferative disorders, psoriasis, haemolytic disorders, alcohol (beer, spirits), high dietary purine intake (red meat, seafood, corn syrup)

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34
Q

What are some causes of reduced urate excretion leading to hyperuricaemia?

A

Chronic renal impairment, volume depletion (e.g. HF), hypothyroidism, diuretics, cytotoxics e.g. cyclosporin

35
Q

How does acute gout present?

A

Usually monoarthropathy:- 1st MTP > ankle > knee
Settles in about 10 days without treatment
Settles in about 3 days with treatment
Abrupt onset, often overnight
May have normal uric acid during acute attack

36
Q

What drug is often associated with gout?

A

Diuretics

37
Q

What may be found in a case of chronic tophaceous gout?

A 
Chronic joint inflammation 
Often diuretic associated
High serum uric acid
Tophi-painless white accumulations of uric acid in soft tissues which erupt through skin
May get acute attacks
38
Q

What investigations are involved in diagnosing gout?

A 
Serum uric acid raised (may be normal during acute attack)
Raised inflammatory markers
Polarised microscopy of synovial fluid
Renal impairment (may be cause or effect
Xrays
39
Q

What is the treatment of acute gout?

A

NSAIDs, Colchicine, Steroids

40
Q

What is the prophylactic treatment in gout?

A

Allopurinol, Febuxostat, start 2-4 weeks after attack. Requires cover with NSAID etc

41
Q

Describe calcium pyrophosphate deposition disease(pseudogout)

A

Related to OA. Chondrocalcinosis (deposition of crystals in cartilage and soft tissues without inflammatiion) increases with age. Affects fibrocartilage-knees, wrists, ankles

42
Q

What are acute attacks of CPPD due to?

A

Calcium pyrophosphate crystals (pseudogout)

43
Q

Describe calcium pyrophosphate crystals

A

Envelope shaped, mildly +vely birefringent

44
Q

What conditions are associated with CPPD?

A

Hyperparathyroidism, Familial Hypocalciuric Hypercalcaemia, Haemochromatosis, Haemosiderosis, Hypophosphatasia, Hypomagnesia, Hypothyroidism, Gout, Neuropathic joints, Ageing, Amyloidosis, Trauma

45
Q

What is the treatment of CPPD?

A

NSAIDs, Colchicine, Steroids, Rehydration

46
Q

Where can hydroxyapatite deposition commonly occur, and what is this called?

A

Shoulder- Milwaukee shoulder

47
Q

What occurs in Milwaukee shoulder?

A

Release of collagenases, serine proteinases and IL1. Acute/rapid deterioration. Affects females, 50-60yo

48
Q

What is the treatment of Milwaukee shoulder?

A

NSAIDs, Intra-articular steroid injection, Physiotherapy, Partial/Total arthroplasty

49
Q

What is soft tissue rheumatism?

A

General term to describe pain that is caused by inflammation/damage to ligaments, tendons, muscles or nerve near a joint rather than either the bone or cartilage

50
Q

What is neck joints pain likely attributable too?

A

Muscular, usually self limiting. Consider OA of cervical spine, occipital migraine etc

51
Q

What is shoulder joint pain likely attributable too?

A 
Commonest area for soft tissue pain. Adhesive Capsulitis
Rotator cuff tendinosis
Calcific tendonitis
Impingement 
Partial rotator cuff tears
Full rotator cuff tears
52
Q

What is elbow joint pain likely attributable too?

A

Medial and lateral epicondylitis

- Cubital tunnel syndrome

53
Q

What is wrist joint pain likely attributable too?

A

De-Quervains tenosynovitis

- Carpal tunnel syndrome

54
Q

What is pelvic joint pain likely attributable too?

A

Trochanteric, Iliopsoas, Ischiogluteal bursitis and stress

55
Q

What is foot joint pain likely attributable too?

A

Plantar fascitis

56
Q

What investigations are involved in soft tissue rheumatism?

A

Usually unnecessary
X-ray - calcific tendonitis
MRI if fails to settle
Identify precipitating factors

57
Q

What treatment is involved in soft tissue rheumatism?

A

Pain control, rest and ice compressions, PT, steroid injections, surgery

58
Q

Describe joint hypermobility syndrome

A

Hypermobility of joints. Present in rare genetic syndromes- Marfans, Ehlers Danlos. Females>males. General or localized. Usually presents in childhood -20s. Treat using physiotherapy, explanation

59
Q

How is a modified beighton score calculated?

A

> 10º hyperextension of the elbows
Passively touch the forearm with the thumb, while flexing the wrist.
Passive extension of the fingers or a 90º or more extension of the fifth finger
Knees hyperextension ≥ 10º)
Touching the floor with the palms of the hands when reaching down without bending the knees.

Hypermobility if ≥ 4/9

60
Q

What are the seropositive arthridies?

A

RA, lupus, scleroderma, vasculitis, sjogren’s

61
Q

What are the seronegative arthridies?

A

Ankylosing spondylitis, psoriasis arthritis, reactive arthritis, IBD arthritis

62
Q

What is the classic site of disease for Gout?

A

1st MTP joint - known as Podagra. Ankle and knee other most affected

63
Q

What is vasculitis?

A

Inflammation of blood vessels-results in vessel wall thickening, stenosis, and occlusion with subsequent ischaemia.

64
Q

What is large vessel vasculitis?

A

Primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its major branches

65
Q

What are the two major categories of large vessel vasculitis?

A

GCA, takayasu arteritis.

66
Q

Who does TA commonly affect?

A

Often young women in teens/20s. Overall

67
Q

What are the early features of large vessel vasculitis?

A

Non-specific features such as low grade fever, malaise, night sweats, wt loss, arthralgia, fatigue. Claudicant symptoms in upper and lower limbs.

68
Q

What can occur if large vessel arteritis is untreated?

A

Vascular stenosis and aneurysms

69
Q

What are the serological features of large vessel arteritis?

A

ESR, PV, CRP elevated

70
Q

What is the treatment for large vessel arteritis?

A

Corticosteroids- prednisolone. Methotrexate and azathioprine can be added

71
Q

What are the ANCA +ve small vessel vasculitis’?

A

Wegener’s granulomatosis, microscopic polyangiitis, renal limited vasculitis, Churg Strauss Syndrome

72
Q

What features may be seen in small and medium vessel vasculitis’?

A 
Fever and weight loss 
A raised, non blanching purpuric rash 
Arthralgia/arthritis 
Mononeuritis multiplex 
Glomerulonephritis 
Lung opacities on x-ray
73
Q

What symptoms are common in granulomatosis with polyangiitis (GPA) or Wegeners?

A

ENT syntoms-nose bleeds, deafness, recurrent sinusitis, nasal crusting, over time nose collapse. Resp symptoms such as haemoptysis, caviting lesions on XR

74
Q

What serological findings are associated with GPA?

A

cANCA, PR3

75
Q

What is eosinophilic granulomatosis with polyangiitis (EGPA) characterised by?

A

Late onset asthma, rhinitis and raised peripheral blood eosinophil count. Neuro symptoms such as mononeuritis multiplex common

76
Q

What is the most important complication of microscopic polyangiitis?

A

Glomerulonephritis

77
Q

What are the non-ANCA associated vasculitis’?

A

Henoch schonlein purpura, Cryoglobulinaemia, other non ANCA (e.g. IBD vasculitis)

78
Q

What investigations are required in ANCA associated vasculitis’?

A

ANCA- ESR,PV, CRP raised. Anaemia common, U+E, Urinalysis (renal vasculitis), CXR, biopsy infected area.

79
Q

What is the management of ANCA associated vasculitis?

A

IV steroids and cyclophosphamide, other options considered dependent on presentation

80
Q

What is Henoch-Schonlein purpura(HSP)?

A

Acute IgA mediated disorder characterised by generalised vasculitis involving small vessels of skin, GIT, kidneys, joints, rarely lungs and CNS.

81
Q

Who does HSP commonly affect?

A

Children, often history of URTI predates symptoms by few wks

82
Q

What are the cimmon symptoms of HSP?

A

Purpuric rash over buttocks and lower limbs, abdo pain, vomiting, joint pain

83
Q

What treatment is required for HSP?

A

Usually self limiting, requiring no specific treatment

Musculoskeletal (16 decks)

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