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Arthritis Flashcards

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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
What may be observed regarding the spine in OA?
Cervical – pain and restriction of movement Osteophytes may impinge on nerve roots Lumbar – osteophytes can cause spinal stenosis if encroach on spinal canal
26
What radiological findings may be seen in OA?
Loss of joint space, subchondral sclerosis, subchondral cysts, osteophytes
27
How is a diagnosis of OA made?
History, exam, X-ray. No specific lab tests
28
What history would you expect from a patient with OA?
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
29
What is the management for OA?
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.
30
What is Gout?
Inflammation in the joint triggered by uric acid crystals
31
What sex have a higher prevalence of gout?
Men
32
What is the uric acid metabolism which leads to gout?
Overproduction and under excretion of uric acid occurs. Leads to hyperuricaemia-results in crystallization (encouraged by low temp in synovial fluid-32')
33
What are some causes of increased urate production leading to hyperuricaemia?
Inherited enzyme defects, myeloproliferative/lymphoproliferative disorders, psoriasis, haemolytic disorders, alcohol (beer, spirits), high dietary purine intake (red meat, seafood, corn syrup)
34
What are some causes of reduced urate excretion leading to hyperuricaemia?
Chronic renal impairment, volume depletion (e.g. HF), hypothyroidism, diuretics, cytotoxics e.g. cyclosporin
35
How does acute gout present?
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
What drug is often associated with gout?
Diuretics
37
What may be found in a case of chronic tophaceous gout?
``` 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
What investigations are involved in diagnosing gout?
``` 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
What is the treatment of acute gout?
NSAIDs, Colchicine, Steroids
40
What is the prophylactic treatment in gout?
Allopurinol, Febuxostat, start 2-4 weeks after attack. Requires cover with NSAID etc
41
Describe calcium pyrophosphate deposition disease(pseudogout)
Related to OA. Chondrocalcinosis (deposition of crystals in cartilage and soft tissues without inflammatiion) increases with age. Affects fibrocartilage-knees, wrists, ankles
42
What are acute attacks of CPPD due to?
Calcium pyrophosphate crystals (pseudogout)
43
Describe calcium pyrophosphate crystals
Envelope shaped, mildly +vely birefringent
44
What conditions are associated with CPPD?
Hyperparathyroidism, Familial Hypocalciuric Hypercalcaemia, Haemochromatosis, Haemosiderosis, Hypophosphatasia, Hypomagnesia, Hypothyroidism, Gout, Neuropathic joints, Ageing, Amyloidosis, Trauma
45
What is the treatment of CPPD?
NSAIDs, Colchicine, Steroids, Rehydration
46
Where can hydroxyapatite deposition commonly occur, and what is this called?
Shoulder- Milwaukee shoulder
47
What occurs in Milwaukee shoulder?
Release of collagenases, serine proteinases and IL1. Acute/rapid deterioration. Affects females, 50-60yo
48
What is the treatment of Milwaukee shoulder?
NSAIDs, Intra-articular steroid injection, Physiotherapy, Partial/Total arthroplasty
49
What is soft tissue rheumatism?
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
What is neck joints pain likely attributable too?
Muscular, usually self limiting. Consider OA of cervical spine, occipital migraine etc
51
What is shoulder joint pain likely attributable too?
``` Commonest area for soft tissue pain. Adhesive Capsulitis Rotator cuff tendinosis Calcific tendonitis Impingement Partial rotator cuff tears Full rotator cuff tears ```
52
What is elbow joint pain likely attributable too?
Medial and lateral epicondylitis | - Cubital tunnel syndrome
53
What is wrist joint pain likely attributable too?
De-Quervains tenosynovitis | - Carpal tunnel syndrome
54
What is pelvic joint pain likely attributable too?
Trochanteric, Iliopsoas, Ischiogluteal bursitis and stress
55
What is foot joint pain likely attributable too?
Plantar fascitis
56
What investigations are involved in soft tissue rheumatism?
Usually unnecessary X-ray - calcific tendonitis MRI if fails to settle Identify precipitating factors
57
What treatment is involved in soft tissue rheumatism?
Pain control, rest and ice compressions, PT, steroid injections, surgery
58
Describe joint hypermobility syndrome
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
How is a modified beighton score calculated?
>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
What are the seropositive arthridies?
RA, lupus, scleroderma, vasculitis, sjogren's
61
What are the seronegative arthridies?
Ankylosing spondylitis, psoriasis arthritis, reactive arthritis, IBD arthritis
62
What is the classic site of disease for Gout?
1st MTP joint - known as Podagra. Ankle and knee other most affected
63
What is vasculitis?
Inflammation of blood vessels-results in vessel wall thickening, stenosis, and occlusion with subsequent ischaemia.
64
What is large vessel vasculitis?
Primary vasculitis that causes chronic granulomatous inflammation predominantly of the aorta and its major branches
65
What are the two major categories of large vessel vasculitis?
GCA, takayasu arteritis.
66
Who does TA commonly affect?
Often young women in teens/20s. Overall
67
What are the early features of large vessel vasculitis?
Non-specific features such as low grade fever, malaise, night sweats, wt loss, arthralgia, fatigue. Claudicant symptoms in upper and lower limbs.
68
What can occur if large vessel arteritis is untreated?
Vascular stenosis and aneurysms
69
What are the serological features of large vessel arteritis?
ESR, PV, CRP elevated
70
What is the treatment for large vessel arteritis?
Corticosteroids- prednisolone. Methotrexate and azathioprine can be added
71
What are the ANCA +ve small vessel vasculitis'?
Wegener's granulomatosis, microscopic polyangiitis, renal limited vasculitis, Churg Strauss Syndrome
72
What features may be seen in small and medium vessel vasculitis'?
``` Fever and weight loss A raised, non blanching purpuric rash Arthralgia/arthritis Mononeuritis multiplex Glomerulonephritis Lung opacities on x-ray ```
73
What symptoms are common in granulomatosis with polyangiitis (GPA) or Wegeners?
ENT syntoms-nose bleeds, deafness, recurrent sinusitis, nasal crusting, over time nose collapse. Resp symptoms such as haemoptysis, caviting lesions on XR
74
What serological findings are associated with GPA?
cANCA, PR3
75
What is eosinophilic granulomatosis with polyangiitis (EGPA) characterised by?
Late onset asthma, rhinitis and raised peripheral blood eosinophil count. Neuro symptoms such as mononeuritis multiplex common
76
What is the most important complication of microscopic polyangiitis?
Glomerulonephritis
77
What are the non-ANCA associated vasculitis'?
Henoch schonlein purpura, Cryoglobulinaemia, other non ANCA (e.g. IBD vasculitis)
78
What investigations are required in ANCA associated vasculitis'?
ANCA- ESR,PV, CRP raised. Anaemia common, U+E, Urinalysis (renal vasculitis), CXR, biopsy infected area.
79
What is the management of ANCA associated vasculitis?
IV steroids and cyclophosphamide, other options considered dependent on presentation
80
What is Henoch-Schonlein purpura(HSP)?
Acute IgA mediated disorder characterised by generalised vasculitis involving small vessels of skin, GIT, kidneys, joints, rarely lungs and CNS.
81
Who does HSP commonly affect?
Children, often history of URTI predates symptoms by few wks
82
What are the cimmon symptoms of HSP?
Purpuric rash over buttocks and lower limbs, abdo pain, vomiting, joint pain
83
What treatment is required for HSP?
Usually self limiting, requiring no specific treatment

Musculoskeletal (16 decks)

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