Brainscape's Knowledge GenomeTM

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


See full index

MSK > Rheumatoid and other inflammatory arthritis > Flashcards

Rheumatoid and other inflammatory arthritis Flashcards

1
Q

What is arthritis

A

Joint inflammation

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

What are the two major divisions of arthritis

A

Osteoarthritis - degenerative
Inflammatory arthritis

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

Clinical signs of joint inflammation

A

Rubor - redness
Tumour - swelling
Dolor - pain
Calor - heat

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

What are three causes of joint inflammation?

A

Infection,
Crystal Arthritis,
Immune-Mediated (autoimmune)

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

What are two types of infection causing joint inflammation?

A

Septic arthritis
TB

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

What are two types of crystal arthritis?

A

Gout - uric acid crystals
Pseudogout - CPPD (calcium pyrophosphate)

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

Which of the three types are primary inflammation?

A

Autoimmune (others are secondary to toxins)

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

Which of the three is the only non-sterile inflammation?

A

Infection (others are sterile)

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

Distinguishing features of osteoarthritis

A

Very little inflamm
Slow onset
Sterile

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

Distinguishing features of Autoimmune arthritis

A

Inflamm
Subacute onset
Sterile
^ CRP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Distinguishing features of Crystal arthritis

A

2º inflamm to crystals
Rapid onset
Sterile, crystals present in synovial fluid
^ CRP

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

Distinguishing features of Septic arthritis

A

2º inflamm to infection
Rapid onset
Bacteria present
^ CRP
^ WBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the clinical presentation of septic arthritis?

A

Acute, red, hot, painful, swollen monoarthritic joint

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

What is the diagnosis for septic arthritis?

A

Joint aspiration for gram stain and culture

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

What are the common organisms that cause septic arthritis?

A

Staph aureus, strep, gonococcus

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

What is the treatment for septic arthritis?

A

Surgical lavage (wash out) and IV antibiotics

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

What is the primary site of pathology for rheumatoid arthritis?

A

Synovium

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

What is rheumatoid arthritis

A

Chronic autoimmune disease leading to synovial inflammation

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

Where is synovium found?

A

Synovial Joints, Tenosynovium (around tendons), Bursa

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

What are the key features of rheumatoid arthritis?

A

Polyarthritis, Pain, Swelling, Early Morning Stiffness, Extra-articulate manifestations

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

How can you identify RA on an x ray

A

joint erosions due to damage

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

How can you estimate the contribution of genetics vs environment in these conditions?

A

Twin studies - monozygotic/dizygotic twins
If the concordance is greater in monozygotic twins this indicates there is a greater genetic component

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

What are some environmental risk factors for rheumatoid arthritis?

A

Smoking,
Microbiome,
Poor oral health (P. gingivalis)

lead to citrullination of proteins in the lung epithelium which can increase prevalence of ACPA - anti citrullinated protein antibodies

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

What is the strongest genetic risk factor for rheumatoid arthritis?

A

HLA-DR shared epitope
polygenic, cumulative genetic burden rather than any specific locus

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

Implications of HLA class 1 genetic association

A

e.g. HLA-B27 in AnkS, implicates CD8 cells in pathogenesis
It is expressed on all cells and presented to CD8 cells

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

Implications of HLA class 2 genetic association

A

e.g. HLA-DR4 in RA implicates CD4 T cells and B cells
Only expressed on APCs which are presented to CD4 cells
B cells activated by CD4 .: pathogenesis causes prod of autoantibodies

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

What is the pattern of joint involvement for rheumatoid arthritis?

A

Symmetrical,
polyarthritis,
small jts: hands/wrists/feet

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

Rheumatoid vs Osteoarthritis

A

RA - prolonged morning and inactivity stiffness.
- affects PIPJs, MCPJs, wrist
OA - pain worse with activity
- affects PIPJs, DIPJs , thumb CMCJs

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

Common extra articular features of RA due to systemic inflammation

A

Fever
Fatigue
Weight loss

30
Q

extra articular features of RA due to organ specific inflammation

A

subcutaneous nodules,
lung fibrosis/ lung disease
episcleritis,
vasculitis leading to digital ischaemia

31
Q

What is Felty’s syndrome

A

extra-articular presentation of RA
triad incl: splenomegaly, leukopenia, RA

32
Q

Describe the subcutaneous nodules in rheumatoid arthritis

A

Central area of fibrinoid necrosis surrounded by histiocytes (macrophage-like) and connective tissue
present on the hand/ulna

33
Q

What is the pathogenesis of rheumatoid arthritis?

A

Synovium becomes proliferated mass of tissue (pannus) due to neovascularisation, lymphangiogenesis, pro-inflammatory cytokines (TNF-alpha)

synovial inflamm due to autoreactive T/B cells (HLA-DR4) cause compliment activation and raised pro-inflamm cytokines (TNF-a)

34
Q

cellular causes of RA

A

autoreactive T/B cells
cytokine imbalance, more pro-inflammatory cytokines

35
Q

What are some of the roles of TNF-alpha?

A

pro-inflamm cytokine

Leukocyte accumulation,
Osteoclast activation - bone absorption
Chondrocytes activation (cartilage destruction MMP prod)

36
Q

How does TNF-a cause pannus formation

A

Inflamm cell recruitment
angiogenesis
lymphangiogenesis

37
Q

How does TNF-a cause cartilage loss

A

Matrix metalloprotease

38
Q

How does TNF-a cause bone loss

A

Osteoclast activation
leads to osteopenia, erosions

39
Q

RA bloods presentation

A

^ESR,
^CRP
^Platelets

RF - rheumatoid factor (not a standalone indicator)
Anti-CCP, specific and associated with aggressive disease

40
Q

What are the three methods of imaging in rheumatoid arthritis?

A

X-Rays, USS, MRI

41
Q

What features can X-Rays pick up?

A

Soft tissue swelling,
peri-articular osteopenia - dark areas around jts
bony erosions

42
Q

What can ultrasound see?

A

Synovitis - synovial hypertrophy,
increased blood flow using doppler,
erosions (more detail)

43
Q

What are the disadvantages of MRIs?

A

Expensive and time-consuming

44
Q

What is the treatment objective for rheumatoid arthritis?

A

Prevent joint damage

45
Q

How can we prevent joint damage in RA

A

Early diagnosis,
prompt aggressive pharmacological treatment,
MDT input (physio, OT)

46
Q

What is the first line treatment regime for rheumatoid arthritis?

A

IM or oral glucocorticoids (steroids),
DMARD therapy (disease-modifying anti-rheumatic drugs)

47
Q

What are some examples of DMARDs?

A

Methotrexate, Hydroxychloroquine

47
Q

What is the second line treatment for rheumatoid arthritis?

A

if the disease is still active
Biological therapies, targeting sp molecules
Janus Kinase (JAK) inhibitors

47
Q

What are DMARDs

A

disease-modifying anti-rheumatic drugs
Immunomodulatory drugs that halt or slow the disease process

47
Q

What are NSAIDs

A

Non-steroid anti inflammatory drugs
e.g. ibuprofen, naproxen
Provide partial symptom relief but do not prevent disease progression

47
Q

What is the mechanism of glucocorticoids?

A

Bind to glucocorticoid receptor in cytoplasm, complex acts as transcription factor

47
Q

Methods of steroid admin

A

oral
intramuscular
intravenous
intra-articular

48
Q

Side effects of glucocorticoids

A

Cushing’s disease
T2DM
Weight gain
Infection risk

48
Q

What do biological therapies usually target?

A

Inflammatory cytokines

48
Q

How do you measure progression of disease

A

DAS28, swollen/tender jts
If not suppressed rq treatment escalation

48
Q

What are four different biological therapies?

A

Inhibition of TNF-alpha,
IL 6 inhibition
B cell depletion,
T cell modulation,

48
Q

What are examples of an anti-TNF drug?

A

Infliximab, Adalimumab

49
Q

What is an example of an IL-6 inhibitor?

A

Tocilizumab

49
Q

What is an example of a b cell depletion drug?

A

Rituximab

50
Q

What antibody does rituximab target?

A

CD20

51
Q

What is an example of a T cell modulator drug?

A

Abatacept
CTLA4-Ig

52
Q

What are four examples of seronegative arthritis?

A

Psoriatic arthritis,
reactive arthritis,
ankylosing spondylitis,
IBD-associated

53
Q

What is seronegative arthritis

A

Immune mediated but w/o antibodies in the blood

54
Q

What are the clinical features of psoriatic arthritis?

A

Scaly red plaques on elbows and knees, (extensor surfaces)
joint inflammation,
asymmetrical arthritis affecting mainly IPJs
enthesitis

55
Q

What is the main pathogenic pathway in psoriatic arthritis?

A

IL-17, IL-23

56
Q

Nail changes in psoriatic arthritis

A

Pitting
Onycholysis

57
Q

What is reactive arthritis?

A

Sterile inflammation from infections elsewhere in body (urogenital, gastrointestinal)
may be the first manifestation of HIV/Hep C

58
Q

What are the extra-articular manifestations of reactive arthritis?

A

Enthesitis, Skin inflammation, eye inflammation

59
Q

What is a genetic predisposition to reactive arthritis?

A

HLA-B27

60
Q

What is an environmental trigger for reactive arthritis?

A

Salmonella infection

61
Q

Septic arthritis vs Reactive arthritis

A

SA - positive culture RA - negative culture
AB therapy No AB
joint lavage No lavage

MSK (7 decks)

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