Clinical (Weeks 1+2) Flashcards Preview

Year 2 - Musculoskeletal (DP) > Clinical (Weeks 1+2) > Flashcards

Flashcards in Clinical (Weeks 1+2) Deck (183)
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1

What genes are associated with a susceptibility to RA?

HLA DR4
HLA DR1

2

What cells invade the synovium in RA?

Macrophages
Fibroblasts
Multinucleated giant cells

3

What is the basic process behind RA?

1. Synovial expansion
2. Invasion of bone
3. Erodes bone and cartilage

4

Articular symptoms of RA?

Joint pain
Morning stiffness
Joint swelling

5

Extra-articular manifestations of RA

Respiratory:
- Effusions
- Fibrosis
- Nodules
Rheumatoid nodules on extensor surfaces
Ocular involvement:
- Keratoconjunctivitis
- Episcleritis
- Uveitis
- Nodular scleritis
Increased CVS morbidity and mortality

6

What hand joint is not affected by RA?

DIP

7

What pattern of joint involvement is seen in RA?

Symmetrical

8

How is RA defined by the EULAR/ACR Classification?

Synovitis in >/=1 joint
Absence of better diagnosis
Achievement of >/=6/10 of:
- Number and site of affected joints (0-5)
- Serological abnormality (0-3)
- Increased CRP/ESR (0-1)
- Symptom duration (0-1)

9

What is the best autoantibody to test for to aid in the diagnosis of RA?

Anti-CCP (Cycli citrullinated peptide) Antibody

10

Does a patient need to be Rheumatoid Factor positive (RhF) to have RA?

No

11

What chronic haematological change may be seen in RA?

Anaemia

12

What x-ray changes are seen in RA?

Osteopaenia:
- Loss of joint space
- Periarticular erosions
Soft tissue swelling

13

What late complications can be seen in RA?

Infection
Cervical myelopahy secondary to:
- Atlanto-axial/Subaxial subluxation
ILD
Peripheral neuropathy

14

What comorbidities is RA associated with?

Severe infections
CVS mortality
Lymphoma

15

What genetic factor is a poor prognostic factor in RA?

HLA DR4 positive

16

How soon must treatment be begun in RA to prevent irreversible damage?

Within 3 months

17

What are the principles of RA treatment?

DMARDs
Steroids to cover lag phase
Frequent reviews

18

Give examples of DMARDs and when they might be used?

1st line - Methotrexate
2nd line and in pregnancy - Sulphasalazine
Hydroxychloroquine
Leflunamide

19

What four approaches to biologic therapy can be used in RA and give examples of drugs in each class?

TNF-alpha inhibition:
- Infliximab
- Adalimumab
- Etanercept
B cell depletion:
- Rituximab
Disruption of T cell co-stimulation:
- Abatecept
Interleukin inhibition:
- Anankira (IL-1)
- Tocilizumab (IL-6)
(Jak-2 inhibitors)

20

What is the pathogenesis of OA?

Loss of matrix (Collagen ii with chondrocytes embedded)
Cytokine release:
- IL-1
- TNF-alpha
- Metalloproteinases
- Prostaglandins from chondrocytes
Surface fibrosis and attempted repair -> Oestophytes

21

How are localised and generalised idiopathic OA defined

Localised:
- Hands
- Feet
- Knee
- Hip
- Spine
Generalised is >/= 3 sites involved

22

What are some secondary causes of OA?

Previous injury
RA
Genetic
Acromegaly
Crystal arthropathy
Perthes
SUFE

23

Risk factors of OA

Age
Female
Obesity
Job
Injury/Sports

24

When is pain typically present in OA?

During exercise

25

How long does morning stiffness last in OA?

Less than 30 minutes

26

What might be found on examination of a patient with OA?

Crepitus
Bony enlargements
Joint tenderness and effusion

27

What can lumbar spine OA result in?

Spinal stenosis

28

Where does hip OA pain radiate to?

Groin/back

29

OA at what site can result in genu valgum and a Baker's cyst?

Knee

30

What are some features of OA in the hand?

Heberden's nodes (DIP OA)
Bouchard's nodes (PIP OA)
Thumb base squaring (CMC OA)