Rheumatology: RA + OA

Question 1

Whats the incidence of RA

Answer 1

Increased in middle aged females :M -3:1
FHx
HLA DRA associated

Question 2

Diagnostic pointers for RA

Answer 2

1. Morning stiffness >1 hour for a duration of >6 weeks
2. > 3 joints affected, > 6 weeks
3. Involves joints of hands & wrists
4. Symmetrical
5. Rh Nodules e.g. Lungs
6. Serum Rh Factor (RF) +ve
7. X-Ray changes

Question 3

General Signs & Symptoms of RA

Answer 3

Pain
Early morning  stiffness
Joint swelling, 
fever, 
wt loss, 
Anemia- chronic disease, NSAIDs causing blood loss, DMARDs causing marrow supression and Feltys syndrome causing splenomegaly. 
Rheumatoid nodules 

C-spine: atlantoaxial subluxation- care in anaesthesia

Feet: hammer toes
Hallux valgus

Question 4

Hand & Wrist signs & symptoms of RA

Answer 4

Symmetrical joint tenderness, redness, swelling
Sausage shaped fingers
Loss of valleys around knuckles
Loss of function
Wasting of inteinsic hand muscles
Swan neck deformity- hyperextension at the PIP and flexion of the DIP joint
Boutonniere deformity- flexion of PIP joint, hyperxtension of DIP joint
Z-thumbs
Wrist subluxation
Carpal tunnel syndrome
Palmar erythema
Radial deviation of wrist
Ulnar deviation of fingers

Question 5

Extra articular manifestations of RA

Answer 5

Eyes- dry eyes (Sjogrens syndrome), scleritis,
Skin- vasculitis, rheumatoid nodules, pyoderma gangrenosum,
CVS- pericarditis, myocarditis
Resp- Pulmonary fibrosis (from methotraxate) pulmonary nodules, pleural effusion
Neuro- cord compression, carpal tunnel syndrome
Felty’s syndrome- splenomegaly, ⬇️WCC, RA
Rheumatoid nodules- present on elbow, achilles tendon, pleura, pericardium, sclera.

Question 6

How would you investigate RA?

Answer 6

FBC- anaemia of chronic disease, thrombocytosis
ESR/CRP ⬆️⬆️
RF (IgM Abs against Fc portion of IgG Abs)
Antinuclear antibodies (ANA) + Anti- CCP Abs
XR of joint
Synovial fluid aspiration- ⬆️ neutrophils, sterile!!
CXR- heart & lung involvment.

Question 7

What are the X-Ray characteristics of RA?

Answer 7

1. Soft tissue swelling
2 joint soace narrowing
3. Secondary osteoporisis
4. Erosions of joint margins
May: peri-articular osteopenia

Question 8

Tx of RA

Answer 8

🔹Physiotherapy✔
️🔹NSAIDS- Diclofenac- they dont hault disease progression + PPIs (gastric muscosa protection)
🔹Steroids- oral or intra-articular injections - only short term use ❌
DMARDs- slow progression of disease, reduce inflammation & erosions. (Max effect reached >6 M)
1. Diagnosis– Methotraxate + another DMARD.
MONITOR- effective: CRP

DMARDs- often start methotraxate or sulphalazine.
Anti- TNF a inhibitors (biological drugs) only if 2 drugs have failed( 1 of them to be methotraxate)

Surgery- if worsening joint function, deformity, persistent oain

Question 9

Medications that can be used for RA & common SE

Answer 9

Methotraxate- 1st line- contraindicated in pregnancy cz its an anti-folate.
SE: bone marrow supression, pulmonary fibrosis, RF, hepatotoxicity
Sulphasalazine: SE: hepatotoxicity, bone marrow supression (BMS) , oligosperimia
Azathioprine : SE- hepatotoxicity, BMS
Penicillamine: SE: nephrotic syndome
Gold- oral or IM injection. Rarely used, SE: nephrotic, skin rcxts
Leflunomide: HTN, hepatotoxicity, teratogenic (FUCK)
Anti TNF a inhibitors- infliximab, SE: anaphylaxis, reactivation of TB, blood dyscrasias.

Question 10

So many medications… What do you need to monitor?

Answer 10

FBC, LFTs, U+Es, eyes (Hydroxychloroquine), BP (Leflunomide) , PFTs(methotraxate), urine for proteinuria.

Question 11

Define Rheumatoid arthritis

Answer 11

Systemic autoimmune inflammatory disease
Symmetric polyarthritis
Numerous extra articular symptoms
Characterised by joint pain & morning stiffness > 20-30 mins (OA

Question 12

Whats OA characterised by?

Answer 12

Cartilage loss
Peri-articular bone rcts of joints

Most common joint disorder
Progresses slowly
Often elderly +- early life due to injury
NOT life threatening.
Can cause severe pain + loss of mobility + independance.

Question 13

Epidemiology of OA

Answer 13

3-6% general population
15% by 55 asymptomatic
WOMEN MORE SEVERE :(

Question 14

Whats the pathogenesis of OA?

Answer 14

🔹Affects entire joint, esp cartilage. 
🔹Cartilage degradation
1. Initiated by abnoramal biochemical forces on the joint
2 OR cartilage abnormalities,-> 
🔹process mediated by enzymes
1. Metalloproteases
2. Cytokines

1. Superficial cartilage layer becomes abnormal with deep fissures
2. Hypertrophy of bone causes subchondral sclerosis and osteophyte formation
3. Joint space narrowing.

Question 15

RFs of OA

Answer 15

Genetic- nodal and generalised
Altered joint surfaces e.g. Epiphyseal dysplesia
Previous trauma e.g. Fracture through joint
Obesity: hip n knee
Age
Occupational- farmer- hip OA, hamds of cotton wool workers
Gender: polyarticular OA in post menopausal women.

Question 16

Some clinical features of OA

Answer 16

DIP, hips, knees, pain om exertion or moevement
Relieved by rest, if too bad, pain at rest too

O/E 
Bony swellings in carpal joints
Heberden's nodes: DIP
Bouchards nodes: PIP
Joint deformities
Crepitus: grating/ creeping sensation upon movement of jnt
Stress pain
Restricted joint movement

Question 17

Those with bony swellings are more at risk of developing what?

Answer 17

hip, knee and spine arthritis

Question 18

Invx of Osteoarthritis

Answer 18

🔴LAB Inx NOT helpful
Xray- joint space narrowing 
Hypertrophy of bone causes: 
🔹Subchondral sclerosis
🔸Osteophyte formation

Question 19

Managment of oa

Answer 19

Non- pharmacological
Education on joint protection- walking stick? 
Wt loss
Exercise to strenghten muscles
No effective medical treatment 

Complementary treatments

1. Glucosamine
2. Chonrotim supplements- improve modility of OA in knee.

Paracetamol & NSAIDs - pain relief.

Question 20

Surgical management of OA

Answer 20

Joint replacement
Fusion

Offer complete pain relief
Limited to knee amd hips (large)
Only in severe( risks and benefits) - last 10 years… Then need anotherone..should be last resort.. Not 50/60s..