Rheum Flashcards

(124 cards)

1
Q

Define osteoarthritis

A

Non-inflammatory degenerative disorder of the synovial joints characterised by loss of articular cartilage and new bone formation

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2
Q

Why does prevalence of osteoarthritis increase with age?

A

Cumulative effect of trauma and decrease in neuromuscular function

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3
Q

Give 7 risk factors for osteoarthritis

A
  1. Age
  2. Trauma
  3. Joint hyper-mobility
  4. Other joint conditions - RA
  5. Genetic factors
  6. Obesity
  7. Occupation - heavy manual/sports
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4
Q

Which cells maintain cartilage?

A

Chondrocytes

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5
Q

Where are chondrocytes embedded?

A

Extracellular matrix containing:
Type 2 collagen
Proteoglycans (hyaluronic acid etc.)

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6
Q

How are chondrocytes involved in the pathogenesis of OA?

A

Articular cartilage damage triggers chondrocytes to decrease proteoglycan production and increase type 1 collagen production.

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7
Q

How is the extracellular matrix affected by the increase in type 1 collagen?

A

less elastic, chondrocytes undergo apoptosis

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8
Q

What happens when chondrocytes undergo apoptosis/

A

cartilage weakens and flakes off into the joint space - joint mice

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9
Q

What triggers synovitis?

A
  1. Synovial Type 1 cells attempt to remove joint mice

2. Macrophages and lymphocytes release pro-inflammatory cytokines

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10
Q

What is fibrillation of the articular cartilage?

A

flaking off

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11
Q

What happens as a result of the synovitis and fibrillation?

A
  1. Eburnation of exposed bone due to friction
  2. Subchondral cysts in sclerotic bone
  3. Attempts to reform articular cartilage - calcifies and forms osteophytes.
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12
Q

space

A

space

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13
Q

How is OA treated?

A
  1. Physio and weight loss
  2. Analgesia (NSAIDs)
  3. Intra-articular steroids
  4. Intra-articular hyaluronic acid
  5. Replacement arthroplasty
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14
Q

Which knee deformity can happen as a result of OA in the medial compartment of the knee?

A

Genu varus (bow legged)

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15
Q

What classical findings on XR for OA?

A

LOSS

  1. Loss of joint space
  2. Osteophytes
  3. Subchondral sclerosis
  4. Subchondral cysts
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16
Q

Which inflammatory marker is more likely to be raised in OA?

A

CRP

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17
Q

What conditions can predispose to spinal OA?

A

disc prolapse or degeneration

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18
Q

What conditions can be caused as a result of spinal OA?

A

Spondylolisthesis

Spinal stenosis

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19
Q

What is spondylolisthesis?

A

Displacement of one vertebrae over the other (usually L5-S1)

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20
Q

Which joints of the hand are commonly affected in OA?

A

DIPJ
PIPJ
Carpometacarpal joints

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21
Q

What is the surgical treatment of OA?

A

Fusion
Joint replacement
Osteotomy Bone shortening
Arthroscopy for loose bodies

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22
Q

space

A

space

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23
Q

space

A

space

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24
Q

What does the fibrous joint capsule extend to become?

A

Periosteum

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25
What is fibrous capsule lined by?
Synovium
26
What cells are present in the synovium and what is their function?
Synoviocytes Type A - remove debris (macrophagic) Type B - produce synovial fluid (fibroblastic)
27
What are the three types of joints?
Synovial Fibrous Cartilaginous
28
Which joints are affected in RA?
Synovial
29
Describe the disease process in RA.
Inflammation and thickening of the synovium with infiltration of lymphocytes and macrophages with IL-1, IL-6, and TNF-a production. Stimulates proliferation of pannus and angiogenesis. Pannus erodes into cartilage and bone.
30
What are the two pathological characteristics of pannus?
1. Inflammation - chronic inflammatory reaction with macrophage, lymphocyte, and plasma cell infiltration 2. Proliferation - tumour like mass which grows over cartilage
31
What is the role of RANKL in RA?
RANKL binds to RANK and stimulates osteoclasts to break down bone
32
What is the role of RF and anti-CCP in RA?
bind to their targets and form immune complexes in the joint
33
What is RF?
rheumatoid factor | IgM antibody which binds to constant Fc portion of alterred IgG
34
What is anti-CCP?
binds to citrullinated proteins (citrullinated vimentin and type 2 collagen) amino acid arginine is converted to citrulline
35
What is the role of immune complexes in RA?
Immune complexes activate the complement system and cause inflammation
36
What are the three different ways that RA can cause bone loss?
Focal erosions Periarticular osteoporosis Generalised osteoporosis in skeleton
37
How does cartilage loss occur in RA?
inflammatory cytokines (ILs and TNFa) stimulate the production of proteases which break down cartilage
38
Describe the pathophysiology of RA (up to pannus formation)
1. T-cells enter the joint and recruit macrophages. 2. Macrophages secrete TNF-a, IL1, IL6 3. Cytokines stimulate synovial proliferation and pannus formation and angiogenesis (allows more inflammatory cells/markers into joint) 4. Pannus erodes into bone and cartilage
39
How is bone eroded in RA?
T cells are stimulated to display RANK-Ligand, which binds to RANK on osteoclasts. Stimulates osteoclasts to break down bone
40
How is cartilage broken down in RA?
Activated synovial cells secrete proteases
41
What are immune complexes formed by in RA?
RF and anti-CCP bind to their targets and form immune complexes
42
What is the role of immune complexes in RA?
Activate the complement system and cause inflammation of the joint
43
What is RF?
Rheumatoid factor = IgM antibody which binds to Fc (constant portion) in altered IgG antibodies
44
What is citrullination in RA?
Amino acid arginine is changed into citrulline in certain proteins such as vimentin and type 2 collagen
45
What does anti-CCP bind to?
citrullinated peptides
46
What sites (joints) are commonly affected in RA?
Hands, knees, feet, ankles
47
What are the signs of RA in the hands?
1. Boutonniere 2. Swan neck 3. Z-thumb 4. Ulnar deviation
48
Where can RA present (extra-articular)?
1. Neuro 2. Lungs 3. Heart 4. Kidneys 5. Skin 6. Eyes 7. Haem
49
What are the neuro manifestations of RA?
1. Peripheral neuropathies 2. Entrapment neuropathies 3. Cervical instability
50
What can occur as a result of cervical instability in RA?
1. Atlanto-axial subluxation | 2. Cervical myelopathy
51
Give two entrapment neuropathies
Carpal tunnel | Tarsal tunnel
52
What are the RA manifestations in the lungs?
1. Pleural effusion 2. Interstitial lung disease 3. Caplan's syndrome 4. Rheumatoid nodules 5. Small airways disease
53
What are the RA manifestations in the heart?
Pericardial rub Pericardial effusion Pericarditis
54
What are the RA manifestations in the kidney?
Amyloidosis (presents with proteinuria) | Analgesic nephropathy
55
What is amyloid?
Acute phase protein
56
What are the soft tissue manifestations in RA?
1. Rheumatoid nodules 2. Bursitis 3. Muscle wasting 4. Tenosynovitis
57
What are the haematological manifestations of RA?
1. Felty syndrome | 2. Anaemia
58
What is Felty syndrome?
seropositive RA + neutropaenia + splenomegaly
59
What anaemias can occur as a result of RA?
1. Normocytic normochromic (chronic disease) 2. Iron deficiency anaemia 3. Haemolytic anaemia (rare) 4. Anaemia occurring as part of a pancytopaenia
60
What are the eye manifestations of RA?
Scleritis Episcleritis Necrotising scleritis Sicca, sjogren's
61
What are some consequences of RA vasculitis?
- Nailbed infarcts | - Mononeuritis multiplex
62
What can occur as a result of mononeuritis multiplex in RA?
wrist drop | foot drop
63
How is RA treated?
Methotrexate Steroids Cyclophospamide Mycophenolate NSAIDs Biologics: Infliximab adalimumab tocilizumab
64
What are the XR findings in RA?
LESS Loss of joint space Erosions Soft tissue swelling Soft bones
65
How is RA treated?
1. DMARDs - Methotrexate is gold standard 2. NSAIDs for pain 3. Steroids while waiting for DMARDs to work 4. Biologics a. TNF-a blockers are first line Infliximab, etanercept, adalimumab b. Rituximab c. IL-blockers Tocilizimab, anakinra d. T cell activation blockers Abatacept
66
Give 3 examples of a TNF-a blocker
Infliximab Etanercept Adalimumab
67
Give an example of a B cell blocker
Rituximab (CD20) | Stops production of RF
68
Give two examples of IL blockers
Tocilizumab | Anakinra
69
Give an example of a T cell activation blocker
Abatacept Blocks T cells no activation of macrophages and B cells
70
Who does ank spond mainly affect
men 20-30s
71
how does ank spond present
- lower back/buttock pain and stiffness, worse in morning, relieved by exercise - back pain at night, relieved by waking up
72
what would you see on clinical examinaton of ank spond
- reduced lateral flexion - reduced forward flexion - schober's test, <5cm extension - reduced chest expansion
73
What are the other features of ank spond (A features)?
1. Apical fibrosis 2. Anterior Uveitis 3. Aortic regurgitation 4. Achilles Tendonitis (enthesitis) 5. AV node block 6. Amyloidosis 7. And Cauda Equina 8. Arthritis (peripheral, more common in females)
74
what is a key complication of ank spond
vertebral fractures
75
what are some other symptoms of ank spond aside from arthritis
``` aortitis enthesitis dactylitis anaemia heart block ```
76
what investigations for ank spond
- ESR, CRP might be raised, neg does not exclude - XRay spine and sacrum - sacroillitis, bamboo - MRI Spine - may show bone marrow oedema
77
what Xray changes would you see in ank spond
- sacroillitis - squaring of vertebral bodies - subchondral sclerosis and erosions - syndesmophytes - ossification of ligaments, tendons, and joints - fusion of facet, sacroiliac, and costovertebral joints
78
how is ank spond managed
- encourage regular exercise, swimming, physiotherapy - NSAIDs first line - steroids during flares to control symptoms - anti-TNF - etanercept/infliximab - secukinumab - anti IL17
79
what type of anti interleukin is secukinumab against
anti-IL17
80
what might spirometry show in ank spond
restrictive picture: - pulm fibrosis - kyphosis - ankylosis of costovertebral joints
81
what are some additional treatments for ank spond's other features
stop smoking | bisphosphonates for osteoporosis
82
What scoring for ank spond
BASDAI
83
what is olecranon bursititis
inflammation of bursa, thickening of synovial membrane and increased synovial fluid production - leading to swelling
84
what causes bursitis
- friction from repetitive movements or leaning on the joint - trauma - inflammatory conditions - gout, RA - infection - septic bursitis
85
how does bursitis present
swollen warm tender fluctuant - fluid filled
86
what is an important differential diagnosis of bursitis
septic arthritis
87
how would septic arthritis differ from bursitis in presentation
septic arthritis - inflammation of whole joint, limited range of movement
88
how is bursitis investigated
aspiration of fluid if infection suspected
89
what do different bursa fluid colours indicate
pus - infection straw-coloured - infection less likely blood stained - trauma, inflammatory causes, infection milky - gout/pseudogout
90
how is bursitis managed
``` rest ice compression analgesia - nsaids/paracetamol aspiration of fluid to relieve pressure steroid injections ```
91
how is septic bursitis managed
fluclox, clarithromycin second line
92
explain the pathophys of gout
deposition of monosodium urate crystals in synovium due to chronic hyperuricaemia
93
what can predispose to gout (decreased excretion of uric acid)
- diuretics - CKD - lead toxicity
94
what can predispose to gout (increased production of urate)
- purine-rich diet - gout and seafood, some alcohols - cytotoxic drugs - severe psoriasis - myeloproliferative/lymphoproliferative disease
95
what x-linked recessive condition can predispose to gout
lesch-nyhan syndrome
96
how does gout present
painful, swollen, warm, erythematous joint
97
what can repeated untreated gout do to a joint
damage
98
what other risk factors for gout?
being male obesity alcohol family history
99
what investigations for gout
- joint aspiration - negatively birefringent needle-shaped crystals under polarised light uric acid - 2 weeks after acute flare X ray joint
100
what would xray of gout look like
- joint effusion - punched out erosions with sclerotic margins in a juxta-articular distribution, with overhanging edges - lytic lesions in bone - soft tissue tophi may be seen
101
what is a common side effect of colchicine
diarrhoea, dose dependent
102
what management of gout in acute flare
nsaids and colchicine, intra-articular or oral steroids can be used
103
when to start allopurinol for gout
after acute attack has settled, but should continue use throughout the attack
104
how does radiograph of gout differ to RA?
no periarticular osteopaenia in gout
105
what prophylaxis for gout
lifestyle mods - lose weight, hydration, decrease purine rich foods (meat seafood, yeast) allopurinol febuxostat uricase
106
what medication can be given in htn and gout, and has a specific uricosuric action
losartan
107
which vitamin may decrease uric acid levels in serum
vit C
108
what are the extra-articular manifestations of RA
- rheumatoid nodules - CV disease - pulmonary fibrosis and nodules (caplan syndrome) - bronchiolitis obilterans - felty - RA neutropaenia splenomegaly - secondary sjogren - anaemia of chronic disease - scleritis episcleritis - lymphadenopathy - carpal tunnel syndrome - amyloidosis
109
what xr changes in ra
``` less loss of joint space erosions soft tissue swelling soft bones (osteopaenia) ```
110
what side effects of DMARDs
methotrexate - bone marrow suppression and leukopaenia, teratogenic hydroxychloroquine - nightmares, retinopathy sulfasalazine - reduced sperm count leflunomide - HTN and peripheral neuropathy biologics - reactivation of TB, Hep B rituximab (CD20) - thrombocytopaenia, night sweats
111
what mgmt of ra in preg
hydroxychloroquine or sulfasalazine
112
what mgmt of RA
- dmards, steroids as bridging to help induce remission - steroids oral, IM for flares - 2 dmards combined - methotrexate + antiTNF (infliximab etanercept adalimumab - methotrexate + rituximab
113
what are some ocular manifestations of RA
- keratoconjunctivitis sicca - scleritis, episcleritis - keratitis - corneal ulceration iatrogenic: - steroid induced cataracts - chloroquine retinopathy
114
what investigation on joint fluid in suspected septic arthritis
- gram staining - microscopy and culture and sensitivities - crystal microscopy
115
what differentials in septic arthritis
- reactive arthritis - gout - pseudogout - haemarthrosis
116
what are the complications of SLE
- CV disease - infection - anaemia of chronic disease - pericarditis - pleuritis - interstitial lung disease - pulm fibrosis - lupus nephritis - neuropsychiatric - depres,anx, seizures, psychosis - recurrent miscarriage - VTE due to antiphospholipid syndrome
117
what type of hypersensitivity is lupus?
SLE = type 3 hypersensitivity
118
what type of hypersensitivity is antiphospholipid
anti-phospholipid = type 2 hypersensitivity
119
what are two complications of discoid lupus
development of SLE | squamous cell carcinoma
120
how does discoid lupus present
photosensitive rash inflamed dry, scaly, crusty, patchy erythematous rash hypo/hyperpigmented scars alopecia if on scalp
121
how is discoid lupus diagnosed
skin biopsy
122
how is discoid lupus treated
suncream topical steroids intralesional steroid injections hydroxychloroquine
123
what are the RFs for pseudogout
``` wilson's haemochromatosis hyperparathyroidism hypomagnesaemia, hypophosphataemia acromegaly ```
124
what treatment for pseudogout
nsaids, colchicine intraarticular, IM, PO steroids joint wash out (arthrocentesis) if severe