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Flashcards in Arthritis Deck (83):
1

Define rheumatoid arthritis

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

2

What is the female to male ratio in rheumatoid arthritis?

3:1

3

What are the possible aetiologies of rheumatoid arthritis?

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

4

What pathological changes occur in rheumatoid arthritis?

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.

5

What are the symptoms of rheumatoid arthritis?

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

6

What are some extra-articular features of rheumatoid arthritis?

Nodules, scleritis, anaemia, pleural effusion, leg ulcers

7

What is the distribution of joint involvement in rheumatoid arthritis?

Symmetrical

8

What investigations are used in the diagnosis of RA?

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

9

What are some possible late complications of RA?

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

10

What are some co-morbidities associated with RA?

Serious infection, CV mortality, Lymphoma

11

What are the principles of treatment of RA?

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

12

What biologic approaches are used in RA?

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

13

What is osteoarthritis?

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

14

What is the pathogenesis of OA?

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

15

What change in cell morphology is noted in OA?

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

16

What is Idiopathic OA?

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.

17

What is Secondary OA?

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

18

What are some risk factors for OA?

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

19

What are the symptoms of OA?

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

20

What examination findings are there in OA?

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

21

What joint distribution occurs in OA?

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

22

What may be observed regarding the hands in OA?

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

23

What may be observed regarding the knee in OA?

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

24

What may be observed regarding the hip in OA?

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

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