Brainscape's Knowledge GenomeTM

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


See full index

GOATED BRS > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Give the definition of a joint

A

Location where 2 bones meet

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

What are the 2 major divisions of joint disease

A

Inflammatory or Degenerative(OA)

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

Why does the classification of joint disease matter?

A

Treatment is different

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

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

What is the onset of OA like?

A

Slow-gradual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the pathological changes in OA

A

Cartilage loss, bony remodelling

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

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

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

What are the radiographic features of OA?

A

Joint space narrowing
Subchondral bony sclerosis
Osteophytes
Subchondral cysts

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

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

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

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

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

What causes of joint inflammation are considered non-sterile?

A

Infection

Septic arthritis
Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cause of septic arthritis

A

Bacterial infection of a joint

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

Risk factors of septic arthritis

A

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

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

Why is septic arthritis considered a medical emergency?

A

It can rapidly destroy a joint if left untreated

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

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

What organisms are common causes of septic arthritis?

A

Staphylococcus aureus, Streptococci, Gonococcus

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

Treatment of septic arthritis

A

Surgical lavage

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 (56 decks)

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