Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

FINALS REVISION > Rheum > Flashcards

Rheum Flashcards

1
Q

Define osteoarthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Why does prevalence of osteoarthritis increase with age?

A

Cumulative effect of trauma and decrease in neuromuscular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which cells maintain cartilage?

A

Chondrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where are chondrocytes embedded?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

less elastic, chondrocytes undergo apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens when chondrocytes undergo apoptosis/

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What triggers synovitis?

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

2. Macrophages and lymphocytes release pro-inflammatory cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is fibrillation of the articular cartilage?

A

flaking off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

space

A

space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Genu varus (bow legged)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What classical findings on XR for OA?

A

LOSS

  1. Loss of joint space
  2. Osteophytes
  3. Subchondral sclerosis
  4. Subchondral cysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What conditions can predispose to spinal OA?

A

disc prolapse or degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Spondylolisthesis

Spinal stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is spondylolisthesis?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which joints of the hand are commonly affected in OA?

A

DIPJ
PIPJ
Carpometacarpal joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the surgical treatment of OA?

A

Fusion
Joint replacement
Osteotomy Bone shortening
Arthroscopy for loose bodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

space

A

space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

space

A

space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does the fibrous joint capsule extend to become?

A

Periosteum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is fibrous capsule lined by?

A

Synovium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What cells are present in the synovium and what is their function?

A

Synoviocytes
Type A - remove debris (macrophagic)
Type B - produce synovial fluid (fibroblastic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the three types of joints?

A

Synovial
Fibrous
Cartilaginous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which joints are affected in RA?

A

Synovial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Describe the disease process in RA.

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the two pathological characteristics of pannus?

A
  1. Inflammation - chronic inflammatory reaction with macrophage, lymphocyte, and plasma cell infiltration
  2. Proliferation - tumour like mass which grows over cartilage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the role of RANKL in RA?

A

RANKL binds to RANK and stimulates osteoclasts to break down bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the role of RF and anti-CCP in RA?

A

bind to their targets and form immune complexes in the joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is RF?

A

rheumatoid factor

IgM antibody which binds to constant Fc portion of alterred IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is anti-CCP?

A

binds to citrullinated proteins (citrullinated vimentin and type 2 collagen)

amino acid arginine is converted to citrulline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the role of immune complexes in RA?

A

Immune complexes activate the complement system and cause inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the three different ways that RA can cause bone loss?

A

Focal erosions
Periarticular osteoporosis
Generalised osteoporosis in skeleton

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does cartilage loss occur in RA?

A

inflammatory cytokines (ILs and TNFa) stimulate the production of proteases which break down cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe the pathophysiology of RA (up to pannus formation)

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is bone eroded in RA?

A

T cells are stimulated to display RANK-Ligand, which binds to RANK on osteoclasts.
Stimulates osteoclasts to break down bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How is cartilage broken down in RA?

A

Activated synovial cells secrete proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are immune complexes formed by in RA?

A

RF and anti-CCP bind to their targets and form immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the role of immune complexes in RA?

A

Activate the complement system and cause inflammation of the joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is RF?

A

Rheumatoid factor = IgM antibody which binds to Fc (constant portion) in altered IgG antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is citrullination in RA?

A

Amino acid arginine is changed into citrulline in certain proteins such as vimentin and type 2 collagen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does anti-CCP bind to?

A

citrullinated peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What sites (joints) are commonly affected in RA?

A

Hands, knees, feet, ankles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the signs of RA in the hands?

A
  1. Boutonniere
  2. Swan neck
  3. Z-thumb
  4. Ulnar deviation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Where can RA present (extra-articular)?

A
  1. Neuro
  2. Lungs
  3. Heart
  4. Kidneys
  5. Skin
  6. Eyes
  7. Haem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the neuro manifestations of RA?

A
  1. Peripheral neuropathies
  2. Entrapment neuropathies
  3. Cervical instability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What can occur as a result of cervical instability in RA?

A
  1. Atlanto-axial subluxation

2. Cervical myelopathy

51
Q

Give two entrapment neuropathies

A

Carpal tunnel

Tarsal tunnel

52
Q

What are the RA manifestations in the lungs?

A
  1. Pleural effusion
  2. Interstitial lung disease
  3. Caplan’s syndrome
  4. Rheumatoid nodules
  5. Small airways disease
53
Q

What are the RA manifestations in the heart?

A

Pericardial rub
Pericardial effusion
Pericarditis

54
Q

What are the RA manifestations in the kidney?

A

Amyloidosis (presents with proteinuria)

Analgesic nephropathy

55
Q

What is amyloid?

A

Acute phase protein

56
Q

What are the soft tissue manifestations in RA?

A
  1. Rheumatoid nodules
  2. Bursitis
  3. Muscle wasting
  4. Tenosynovitis
57
Q

What are the haematological manifestations of RA?

A
  1. Felty syndrome

2. Anaemia

58
Q

What is Felty syndrome?

A

seropositive RA + neutropaenia + splenomegaly

59
Q

What anaemias can occur as a result of RA?

A
  1. Normocytic normochromic (chronic disease)
  2. Iron deficiency anaemia
  3. Haemolytic anaemia (rare)
  4. Anaemia occurring as part of a pancytopaenia
60
Q

What are the eye manifestations of RA?

A

Scleritis
Episcleritis
Necrotising scleritis
Sicca, sjogren’s

61
Q

What are some consequences of RA vasculitis?

A
  • Nailbed infarcts

- Mononeuritis multiplex

62
Q

What can occur as a result of mononeuritis multiplex in RA?

A

wrist drop

foot drop

63
Q

How is RA treated?

A

Methotrexate
Steroids
Cyclophospamide
Mycophenolate

NSAIDs

Biologics:
Infliximab
adalimumab
tocilizumab

64
Q

What are the XR findings in RA?

A

LESS

Loss of joint space
Erosions
Soft tissue swelling
Soft bones

65
Q

How is RA treated?

A
  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
Q

Give 3 examples of a TNF-a blocker

A

Infliximab
Etanercept
Adalimumab

67
Q

Give an example of a B cell blocker

A

Rituximab (CD20)

Stops production of RF

68
Q

Give two examples of IL blockers

A

Tocilizumab

Anakinra

69
Q

Give an example of a T cell activation blocker

A

Abatacept

Blocks T cells
no activation of macrophages and B cells

70
Q

Who does ank spond mainly affect

A

men 20-30s

71
Q

how does ank spond present

A
  • lower back/buttock pain and stiffness, worse in morning, relieved by exercise
  • back pain at night, relieved by waking up
72
Q

what would you see on clinical examinaton of ank spond

A
  • reduced lateral flexion
  • reduced forward flexion - schober’s test, <5cm extension
  • reduced chest expansion
73
Q

What are the other features of ank spond (A features)?

A
  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
Q

what is a key complication of ank spond

A

vertebral fractures

75
Q

what are some other symptoms of ank spond aside from arthritis

A 
aortitis
enthesitis
dactylitis
anaemia
heart block
76
Q

what investigations for ank spond

A
  • ESR, CRP might be raised, neg does not exclude
  • XRay spine and sacrum - sacroillitis, bamboo
  • MRI Spine - may show bone marrow oedema
77
Q

what Xray changes would you see in ank spond

A
  • sacroillitis
  • squaring of vertebral bodies
  • subchondral sclerosis and erosions
  • syndesmophytes
  • ossification of ligaments, tendons, and joints
  • fusion of facet, sacroiliac, and costovertebral joints
78
Q

how is ank spond managed

A
  • encourage regular exercise, swimming, physiotherapy
  • NSAIDs first line
  • steroids during flares to control symptoms
  • anti-TNF - etanercept/infliximab
  • secukinumab - anti IL17
79
Q

what type of anti interleukin is secukinumab against

A

anti-IL17

80
Q

what might spirometry show in ank spond

A

restrictive picture:

  • pulm fibrosis
  • kyphosis
  • ankylosis of costovertebral joints
81
Q

what are some additional treatments for ank spond’s other features

A

stop smoking

bisphosphonates for osteoporosis

82
Q

What scoring for ank spond

A

BASDAI

83
Q

what is olecranon bursititis

A

inflammation of bursa, thickening of synovial membrane and increased synovial fluid production - leading to swelling

84
Q

what causes bursitis

A
  • friction from repetitive movements or leaning on the joint
  • trauma
  • inflammatory conditions - gout, RA
  • infection - septic bursitis
85
Q

how does bursitis present

A

swollen
warm
tender
fluctuant - fluid filled

86
Q

what is an important differential diagnosis of bursitis

A

septic arthritis

87
Q

how would septic arthritis differ from bursitis in presentation

A

septic arthritis - inflammation of whole joint, limited range of movement

88
Q

how is bursitis investigated

A

aspiration of fluid if infection suspected

89
Q

what do different bursa fluid colours indicate

A

pus - infection
straw-coloured - infection less likely
blood stained - trauma, inflammatory causes, infection
milky - gout/pseudogout

90
Q

how is bursitis managed

A 
rest
ice 
compression
analgesia - nsaids/paracetamol
aspiration of fluid to relieve pressure
steroid injections
91
Q

how is septic bursitis managed

A

fluclox, clarithromycin second line

92
Q

explain the pathophys of gout

A

deposition of monosodium urate crystals in synovium due to chronic hyperuricaemia

93
Q

what can predispose to gout (decreased excretion of uric acid)

A
  • diuretics
  • CKD
  • lead toxicity
94
Q

what can predispose to gout (increased production of urate)

A
  • purine-rich diet - gout and seafood, some alcohols
  • cytotoxic drugs
  • severe psoriasis
  • myeloproliferative/lymphoproliferative disease
95
Q

what x-linked recessive condition can predispose to gout

A

lesch-nyhan syndrome

96
Q

how does gout present

A

painful, swollen, warm, erythematous joint

97
Q

what can repeated untreated gout do to a joint

A

damage

98
Q

what other risk factors for gout?

A

being male
obesity
alcohol
family history

99
Q

what investigations for gout

A
  • joint aspiration
  • negatively birefringent needle-shaped crystals under polarised light

uric acid
- 2 weeks after acute flare

X ray joint

100
Q

what would xray of gout look like

A
  • 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
Q

what is a common side effect of colchicine

A

diarrhoea, dose dependent

102
Q

what management of gout in acute flare

A

nsaids and colchicine, intra-articular or oral steroids can be used

103
Q

when to start allopurinol for gout

A

after acute attack has settled, but should continue use throughout the attack

104
Q

how does radiograph of gout differ to RA?

A

no periarticular osteopaenia in gout

105
Q

what prophylaxis for gout

A

lifestyle mods - lose weight, hydration, decrease purine rich foods (meat seafood, yeast)
allopurinol
febuxostat
uricase

106
Q

what medication can be given in htn and gout, and has a specific uricosuric action

A

losartan

107
Q

which vitamin may decrease uric acid levels in serum

A

vit C

108
Q

what are the extra-articular manifestations of RA

A
  • 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
Q

what xr changes in ra

A 
less
loss of joint space
erosions
soft tissue swelling
soft bones (osteopaenia)
110
Q

what side effects of DMARDs

A

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
Q

what mgmt of ra in preg

A

hydroxychloroquine or sulfasalazine

112
Q

what mgmt of RA

A
  • dmards, steroids as bridging to help induce remission
  • steroids oral, IM for flares
  • 2 dmards combined
  • methotrexate + antiTNF (infliximab etanercept adalimumab
  • methotrexate + rituximab
113
Q

what are some ocular manifestations of RA

A
  • keratoconjunctivitis sicca
  • scleritis, episcleritis
  • keratitis
  • corneal ulceration

iatrogenic:

  • steroid induced cataracts
  • chloroquine retinopathy
114
Q

what investigation on joint fluid in suspected septic arthritis

A
  • gram staining
  • microscopy and culture and sensitivities
  • crystal microscopy
115
Q

what differentials in septic arthritis

A
  • reactive arthritis
  • gout
  • pseudogout
  • haemarthrosis
116
Q

what are the complications of SLE

A
  • 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
Q

what type of hypersensitivity is lupus?

A

SLE = type 3 hypersensitivity

118
Q

what type of hypersensitivity is antiphospholipid

A

anti-phospholipid = type 2 hypersensitivity

119
Q

what are two complications of discoid lupus

A

development of SLE

squamous cell carcinoma

120
Q

how does discoid lupus present

A

photosensitive rash
inflamed dry, scaly, crusty, patchy erythematous rash
hypo/hyperpigmented scars
alopecia if on scalp

121
Q

how is discoid lupus diagnosed

A

skin biopsy

122
Q

how is discoid lupus treated

A

suncream
topical steroids
intralesional steroid injections
hydroxychloroquine

123
Q

what are the RFs for pseudogout

A 
wilson's
haemochromatosis
hyperparathyroidism
hypomagnesaemia, hypophosphataemia
acromegaly
124
Q

what treatment for pseudogout

A

nsaids, colchicine
intraarticular, IM, PO steroids
joint wash out (arthrocentesis) if severe

FINALS REVISION (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions