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BRS > MSK - arthritis > Flashcards

MSK - arthritis Flashcards

1
Q

Outline osteoarthritis

A

Chronic

Cartilage deterioration → bones rub together → stiffness, pain, less mobility

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2
Q

Main risk factors of OA?

A 
Age
Weight
Intense sport or forces 
Hereditary 
Female gender and menopause
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3
Q

Explain the cycle of obesity and OA

A 
Obesity increases pressure on knee joints
This leads to joint pain/arthritis 
Limited mobility 
Lack of physical activity 
Obesity
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4
Q

Where are the main sites of OA?

A

Spine
Knees
Fingers
Hips

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5
Q

Signs and symptoms of OA?

A

Pain gets worse throughout day as use increases
Little morning stiffness
Joint instability, bony enlargement, less mobility, crepitus, some swelling

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6
Q

What abnormalities can be seen on an OA radiograph?

A

Osteophytes
Subchondral cysts
Sclerosis
Small space between bones

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7
Q

What are the 3 main types of OA management + examples?

A

Conservative - weight loss, analgesics, physio

Injections - steroids, lubrications gel, platelet plasma

Operative - replace, realign, excise

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8
Q

What are the names of DIP and PIP nodes?

A

Bouchard’s - proximal

Heberdens - distal

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9
Q

What are the 3 functional classifications of joints?

A

Synarthoses - no movement

Amphiarthoses - limited movement

Diarthosese - free movement

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10
Q

What makes up the synovium?

A

Type A synoviocyte - phagocytic
Type B synoviocyte - hyaluronic acid
Type 1 collagen

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11
Q

What are the main components of articulation cartilage?

A

Chondrocytes

ECM:
Type 2 collagen
Proteoglycan, aggrecan
Water

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12
Q

What is a function of aggrecan?

A

Interacts with hyaluronic acid to from proteoglycan aggregates

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13
Q

Why does cartilage heal poorly?

A

It is avascular

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14
Q

What are the two types of arthritis?

A

Osteo, degenerative

Inflammatory

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15
Q

5 manifestations of inflammation?

A 
Redness 
Pain
Heat
Swelling
Loss of function
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16
Q

Pathophysiology of inflammation?

A

Increased blood flow
Leucocytes to tissues
Activation of these
Cytokine produced

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17
Q

What are the 3 main causes of joint inflammation?

A

Infection
Crystals
Autoimmunity

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18
Q

What causes septic arthritis?

A

Infection usually from blood

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19
Q

Septic arthritis risk (3)

A

Intravenous drug use
Immunosuppressed
Pre existing joint damage

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20
Q

What is the usual presentation of SA?

A

Mono arthritis

Acute pain, redness, heat, swelling, fever

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21
Q

How is SA diagnosed and treated?

A

Joint aspiration sent for gram stain and culture

Treatment of surgical lavage and IV antibiotics

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22
Q

What organisms can cause SA?

A

Staphylococcus aureus
Stretococci
Gonococcus

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23
Q

How does gonococcal SA present differently?

A

Usually polyarthritis

Less likely to cause joint destruction

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24
Q

2 types of Crystal arthritis?

A

Gout

Pseudogout

25
Q

What is gout caused by?

A

Deposition of urate crystals

This caused by high uric acid levels

26
Q

What causes hyperuricaemia?

A

Genetics
Increased consumption of purine rich foods
Kidney failure- reduced excretion

27
Q

What causes pseudogout?

A

Deposition of calcium pyrophosphate dihydrate crystals

28
Q

What are 3 risk factors for pseudogout?

A

Osteoarthritis
Elderly
Inter current infection

29
Q

What are the clinical features of gout?

A

Acute rapid onset monoarthritis
Can be in foot, ankle, knee, wrist, finger, elbow
Tophi can also be seen

30
Q

What is the most commonly affected joint on gout?

A

First metatarsophalangeal joint - podagra

31
Q

How can crystal arthritis present on radiography?

A

Rat bite erosions

32
Q

What is the difference between gout and pseudogout aspirations? And how is it analysed?

A

Under microscope using polarised light
G - needle crystals, negative birefringence
PG - rhomboid crystals , positive birefringence

33
Q

How can rheumatoid arthritis be classified?

A

Chronic
Auto immune
Inflammatory

34
Q

What are 3 main signs of RA?

A

Polyarthritis - often hands and wrists
Symmetrical
Early morning joint stiffness

35
Q

What can be detected in the blood of RA patients?

A

Rheumatoid factor - an autoantibody against IgG

36
Q

What is the main site of pathology in RA?

A

Synovium- synovitis, tenosynovitis, bursitis

37
Q

What are some extra articular features of RA?

A

Fever, weight loss, subcutaneous nodules

Vasuculitis
Episcleritis
Neuropathies
Feltys syndrome
Lung disease
Amyloidosis
38
Q

What is Felty’s syndrome?

A

Triad of splenomegaly, leukopenia, RA

39
Q

What are the subcutaneous nodules in RA?

A

Centre of fibrinogen necrosis surrounded by histiocytes and connective tissue
Approx 30% patients

40
Q

Explain the pathogenesis of RA in regards to the synovium

A

Synovium becomes a mass of tissue (pannus) due to :
Neovascularisation
Lymohangiogenesis
Imflammatiry cells excess due to an excess of pro inflammatory cytokines

41
Q

What is the dominant pro inflammatory cytokine in RA and what is it produced from?

A

TNF-a produced by activated macrophages

42
Q

Name a treatment for RA

A

TNFa inhibitors

43
Q

What are the 2 antibodies in RA?

A

Rheumatoid factor (IgM antibody against IgG)

Antibodies to citrullinated protein antigens (ACPA) - highly specific to RA

44
Q

What is the citrulliantion of peptides and what enzyme is involved?

A

Arginine → citrulline

Peptidyl arginine deaminases (PADs)

45
Q

What are the treatment options for RA?

A

DMARDs

1st: methotrexate with hydroxychloroquine/salfasalazine
2nd: biological therapies, Janus Kinase inhibitors

Glucocorticoids (prednisolone)

46
Q

Give 4 examples of biological therapies for RA?

A

Anti TNFa
B cell depletion, rituximab
Modulation of T cell co stimulation
Inhibition of IL6 signalling , tocilizumab

47
Q

Outline some of the differences in presentation between OA and RA

A

RA : 30-50yrs, rapid onset, bilateral symmetric, better with movement, morning stiffness, PIP & MCP joints, wrist ankle elbow, systemic symptoms, red warm joint swelling, serum positive, high CRP & ESR

OA : >50yrs, slow onset, assymetric, worse with movement, no morning stiffness, DIP & CMC joints, bony joint swelling , serum negative

48
Q

Radiological differences between OA and RA?

A

RA : osteopenia, bony erosions

OA : subchondral sclerosis, osteophytes

Both have joint space narrowing

49
Q

What is one difference between RA and psoriatic arthritis?

A

PA is seronegative , no rheumatoid factors

50
Q

How can psoriatic arthritis present?

A

Asymmetrical arthritis in IPJs
Symmetrical involve,ent of some small joints (rheumatoid pattern)
Spinal and sacroiliac joint inflammation (spondyloarthritis)
Oligoarthritis of large joints
Arthritis mutilans

51
Q

What is reactive arthritis and when does it normally occur?

A

Sterile inflammation of joints

Follows urogenital or gastrointestinal infections , 1-4 weeks after

52
Q

What 2 conditions can reactive arthritis present in?

A

HIV and hepatitis C

53
Q

What are 3 extra articular manifestations of reactive arthritis?

A

Skin inflammation
Eye inflammation
Enthesitis

54
Q

What is a risk factor for reactive arthritis?

A

Young adults with genetic predisposition with environmental trigger

55
Q

Differences between septic and reactive arthritis?

A

SA : positive synovial fluid culture, antibiotic therapy, joint lavage

RA : negative culture, no ab therapy, no joint lavage

56
Q

What is systemic lupus erythematous?

A

Autoimmune disease affecting multiple organs

57
Q

What do the autoantibodies in SLE attack?

A

Nucleus - nucleic acids and proteins

58
Q

What are the 2 autoantibodies in SLE and their differences?

A

Antinuclear antibodies - high SLE sensitivity but not specific

Anti-double stranded DNA antibodies - high specificity for SLE

BRS (7 decks)

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