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GOATED BRS > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Give the definition of a joint

A

Location where 2 bones meet

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2
Q

What are the 2 major divisions of joint disease

A

Inflammatory or Degenerative(OA)

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3
Q

Why does the classification of joint disease matter?

A

Treatment is different

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4
Q

Describe the epidemiology of OA

A

-more prevalent as age increases,
-previous joint trauma (e.g. footballers’ knees)
-jobs involving heavy manual labour

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5
Q

What is the onset of OA like?

A

Slow-gradual

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6
Q

Describe the pathological changes in OA

A

Cartilage loss, bony remodelling

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7
Q

What are the symptoms of OA

A

Joint pain
worse with activity, better with rest
Joint crepitus
creaking, cracking grinding sound on moving affected joint
Joint enlargement
e.g. Heberden’s nodes
Bouchard’s nodes
Limitation of range of motion

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8
Q

What are the typically affected joints of OA

A

Joints of the hand
Distal interphalangeal joints (DIP)
Proximal interphalangeal joints (PIP)
First carpometacarpal joint (CMC)
Spine
Weight-bearing joints of lower limbs
esp. knees and hips
First metatarsophalangeal joint (MTP)

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9
Q

What are the radiographic features of OA?

A

Joint space narrowing
Subchondral bony sclerosis
Osteophytes
Subchondral cysts

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10
Q

What are the 5 hallmarks of inflammation

A
  1. Dolor(Pain)
  2. Calor(Heat)
  3. Rubor(Redness)
  4. Tumor(Swelling)
  5. Loss of function
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11
Q

Physiological changes within an enflamed joint

A

-Increased blood flow
-Migration of white blood cells (leucocytes) into the tissues
-Activation/differentiation of leucocytes
-Cytokine production
E.g. TNF-alpha, IL1, IL6, IL17

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12
Q

What causes of joint inflammation are considered primary causes and what conditions do they commonly cause?

A

Immune-mediated (“autoimmune”)

Rheumatoid arthritis
Seronegative arthritis
Systemic lupus erythematosus (SLE)

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13
Q

What causes of joint inflammation are considered secondary causes(Bodily response due to noxious insult) and what conditions do they commonly cause

A

Infection

Septic arthritis
Tuberculosis

Crystal arthritis

Gout
Pseudogout

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14
Q

What causes of joint inflammation are considered sterile?

A

Crystal arthritis

Gout
Pseudogout

Immune-mediated (“autoimmune”)

Rheumatoid arthritis
Seronegative arthritis
Systemic lupus erythematosus (SLE)

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15
Q

What causes of joint inflammation are considered non-sterile?

A

Infection

Septic arthritis
Tuberculosis

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16
Q

Cause of septic arthritis

A

Bacterial infection of a joint

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17
Q

Risk factors of septic arthritis

A

immunosuppressed, pre-existing joint damage, intravenous drug use (IVDU)

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18
Q

Why is septic arthritis considered a medical emergency?

A

It can rapidly destroy a joint if left untreated

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19
Q

How does septic arthritis present?

A

-Acute red, hot, painful swollen joint
-Usually only 1 joint is affected* (monoarthritis-Can be polyarthritis with gonoccocus)
-Typically fever. Patient often systemically unwell

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20
Q

What organisms are common causes of septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

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21
Q

Treatment of septic arthritis

A

Surgical lavage

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22
Q

What are the 2 main types of crystal arthritis and what’s the difference?

A

Gout

Caused by deposition of monosodium urate (MSU) (aka uric acid) crystals in/around joints
-> inflammation

High uric acid levels (hyperuricaemia) = risk factor for gout

Causes of hyperuricaemia:
Genetic tendency
Increased intake of purine rich foods
Reduced excretion (kidney failure)

Pseudogout

Caused by deposition of calcium pyrophosphate dihydrate (CPPD) crystals
-> inflammation

Risk factors: background osteoarthritis, elderly patients, intercurrent infection

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23
Q

Describe the features of gout

A

Abrupt onset
Usually monoarthritis
Big toe 1st MTPJ (metatarsophalangeal joint) most commonly affected (podagra)
Can also affects other joints: most frequently joints in the foot, ankle, knee, wrist, finger, and elbow

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24
Q

What investigations would you undertake to diagnose gout(bloods+radiographically)?

A

Bloods:
↑ C-reactive protein (CRP), marker of inflammation
↑ Serum urate

X-rays
-Usually normal initially
-If recurrent attacks/long-standing gout, juxta-articular erosions can develop

Joint aspiration and synovial fluid analysis for definitive diagnosis

25
Q

What is the key investigation required for any septic joint

A

Synovial fluid analysis and aspiration

-Microbiology (gram stain, culture and sensitivities)
-Polarising light microscopy to detect crystals

26
Q

How do you differentiate gout and pseudogout

A
27
Q

What are the 2 main treatment methods of gout

A

Acute attack: reduce inflammation
Non-steroidal anti-inflammatory drugs (NSAIDs)
Glucocorticoids (“steroids”)

Chronic – need to reduce uric acid levels
Lifestyle – avoid purine-rich food, beer
Pharmacological: allopurinol, febuxostat (xanthine oxidase inhibitors)

28
Q

3 main categories of autoimmune joint disease

A

Rheumatoid arthritis
Seronegative inflammatory arthritis
Systemic Lupus Erythematosus (aka SLE or ‘lupus’)

29
Q

What is the primary site of pathology in rheumatoid arthritis?

A

Primary site of pathology is in the synovium
Synovitis = inflammation of the synovial membrane

30
Q

What are the key features of rheumatoid arthritis?

A

Chronic arthritis
Polyarthritis
Early morning stiffness in and around joints
May lead to joint damage and destruction - ‘joint erosions’ on radiographs

Auto-antibodies usually detected in blood

Extra-articular disease can occur
e.g. ocular inflammation, interstitial lung disease, nodules, vasculitis

31
Q

Describe the pattern of joint involvement in rheumatoid arthritis

A

Symmetrical

Affects multiple joints (polyarthritis)

Affects small and large joints, but particularly hands, wrists and feet

Commonest affected joints:
Metacarpophalangeal joints (MCPJs)
Proximal interphalangeal joints (PIPJs)
Wrists
Knees
Ankles
Metatarsophalangeal joints (MTPJs)

32
Q

What is the difference between the synovium in normostasis and rheumatoid arthritis

A

Healthy synovial membrane:
1-3 cell layer that lines synovial joints
Contains:
macrophage-like (type A synoviocyte)
fibroblast-like (type B synoviocyte) cells
type I collagen
Functions: maintenance of synovial fluid

In rheumatoid arthritis:
The synovium becomes a proliferated mass of tissue (pannus) due to:
Neovascularisation
Lymphangiogenesis
Inflammatory cells:
activated B and T cells
plasma cells
mast cells
activated macrophages

Recruitment, activation and effector functions of these cells is controlled by a cytokine network
Excess of pro-inflammatory vs. anti-inflammatory cytokines (‘cytokine imbalance’)

33
Q

What is TNF-a

A

The cytokine tumour necrosis factor-alpha (TNFα) is the dominant pro-inflammatory cytokine in the rheumatoid synovium
Its pleotropic actions are detrimental in this setting

34
Q

Def of pleotropic

A

Having more than one effect

35
Q

What are the actions of TNF-a

A

-Proinflammatory cytokine release
-Hepcidin induction
-PGE2 production
-Osteoclast activation
-Chondrocyte activation
-Angiogenesis
-Leukocyte accumulation
-Endothelial cell activation
-Chemokine release

36
Q

What has been discovered to be the most effective treatment of rheumatoid arthritis

A

Dominant detrimental role of TNFα in rheumatoid arthritis validated by the therapeutic success of TNFα inhibition

TNFα inhibition is achieved via intravenous infusion or sub-cutaneous injection of antibodies or fusion proteins

37
Q

What is the level of CRP in blood cultures of RA, OA and SA?

A

RA: Raised
OA: Normal
SA:Raised
OA is not inflammatory so doesn’t produce CRP

38
Q

Which of RA, OA and SA has a low haemoglobin?

A

RA

39
Q

What are the 2 types of antibodies normally found in the blood of RA patients?

A
  1. Rheumatoid factor
  2. Antibodies to citrulinnated protein antigen (ACPA)
40
Q

What are rheumatoid factor antibodies types Ig_?

A

Usually IgM that bind to the Fc region of IgG

41
Q

Why is testing for rheumatoid factor bad for diagnosing RA?

A
  1. Only pos in 80% of patients
  2. Is present in other conditions
42
Q

What is citrullination?

A
43
Q

What is the clinical test used to detect ACPAs?

A

anti-cyclic citrullinated peptide antibody ‘anti-CCP antibody’

44
Q

What is different in testing for anti-CCP antibodies rather than rheumatoid factor?

A

-anti-CCP antibodies are more commonly associated with RA than RF is
-anti-CCP antibodies are also more commonly associated with more erosive/aggressive disease

45
Q

What are the radiographic features of RA?

A

Soft tissue swelling
Peri-articular osteopenia
Bony erosions

Erosions occur only in established disease.
The aim of modern therapy is to treat EARLY before erosions (permanent damage) has occurred

46
Q

Apart from X-ray, give 2 other imaging methods used to detect RA and give the radiographic signs of RA in one of them

A

Ultrasound (US) is a much better test for detecting synovitis. US changes in RA:

Synovial hypertrophy (thickening)
Increased blood flow (seen as doppler signal)
May detect early erosions not seen on plain X-ray

US (usually of hands and wrists) can be performed alongside clinical assessment in a dedicated early arthritis clinic

MRI can also be used but expensive and time-consuming

47
Q

Give the main 3 principles of RA treatment

A

Early recognition of symptoms, referral and diagnosis

Prompt initiation of treatment: joint destruction = inflammation * time

Aggressive pharmacological treatment to suppress inflammation

48
Q

What are DMARDs?

A

Disease-modifying anti-rheumatic drugs

Immunomodulatory drugs that halt or slow the disease process

Methotrexate, Hydroxychloroquine, Sulphasalazine

49
Q

What are NSAIDs?

A

(non-steroidal anti-inflammatory drugs)
e.g. ibuprofen, naproxen, diclofenac
Historically used but increasingly less relevant

Can provide partial symptom relief but do not prevent disease progression

Unfavourable long-term side-effect profile

50
Q

What is first and second line treatment for RA?

A
51
Q

Why are glucocorticoids less commonly used in long term treatment of RA?

A

Poor side effect profile

52
Q

Outline the overarching differences between OA and RA

A
53
Q

What is seronegative arthritis and give a few examples

A

Family of conditions with overlapping clinical features and pathogenesis

Unlike rheumatoid arthritis, RF and CCP antibodies not present in blood (“seronegative”)
BUT they are immune-mediated

54
Q

What is psoriatic arthritis and give its hallmarks

A

Psoriasis is an autoimmune disease affecting the skin
Scaly red plaques on extensriaor surfaces (eg elbows and knees)

~10% of psoriasis patients also have joint inflammation

Varied clinical presentations:
-Classically asymmetrical arthritis affecting IPJs
(interphalangeal joints)

But also can manifest as:
-Symmetrical involvement of small joints (rheumatoid pattern)
-Oligoarthritis of large joints
-Spinal and sacroiliac joint inflammation

55
Q

What is reactive arthritis?

A

Sterile inflammation in joints following infection elsewhere in the body

56
Q

Give the common infections causing reactive arthritis

A

urogenital (e.g. Chlamydia trachomatis)
gastrointestinal (e.g. Salmonella, Shigella, Campylobacter infections)

57
Q

What is the symptomalogy/aetiology of reactive arthritis

A

Important extra-articular manifestations include:
Enthesitis (tendon inflammation)
Skin inflammation
Eye inflammation

Reactive arthritis may be first manifestation of HIV or hepatitis C infection

Commonly young adults with genetic predisposition (e.g. HLA-B27) and environmental trigger (e.g. Salmonella infection)
Symptoms follow 1-4 weeks after infection and this infection may be mild

Reactive arthritis NOT the same as infection in joints (septic arthritis)

58
Q

How can you differentiate between reactive and septic arthritis?

A
59
Q

Give the overall classifications of joint diseases

A

GOATED BRS (57 decks)

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