Rheumatoid Arthritis
Chronic progressive inflammation causing joint destruction
Increases morbidity and mortality
Epidemiology
Onset aged 30-60
40-50 people per 100,000
2:1 F:M (world) and 3:1 F:M (UK)
Aetiology
Infection, viral, immune system, diet, smoking and genetics
Pathophysiology
Greatest impact of synovial joints (hands and feet)
Symmetrical effect
Synovium – protective fluid layer around joint
Synoviocytes – macrophages or fibroblasts
Symptoms:
Increased blood flow – heat/redness
Proliferation of synovial membrane – swelling
Increased synovial fluid – swelling
Muscle loss – loss of function
1. Synovitis - inflammation of the synovial membrane causing swelling and
reduced fluid
2. Pannus formation – bone and cartilage erodes and inflamed tendon
3. Fibrous ankylosis – fibrous connective tissue forms with loss of bone causing
immobility (less inflammation)
4. Bony ankylosis – no pain or swelling as bones fuse with connective tissue and
leading to osteoporosis
Clinical Features
Pain
Stiffness (prolonged in morning)
Loss of function
Fever, sweating and malaise
Diagnosis
MCP or MTP squeeze test – pain suggests inflammation
Bloods – raised ESR and CRP
Rheumatoid factor (RF)
Anti-CCP
Decreased platelet and FBC
X-ray, MRI and ultrasound
ACR/EULAR criteria (>6) – joint involvement, serology (RF and ACCP), acute
phase reaction (CRP/ESR) and duration (>6 weeks)
DAS (>2.6) – assess 28 joints, ESR, CRP and patient feeling
Management
, Refer for specialist appointment
Analgesics – not NSAIDs (no effect on disease)
NSAIDs
Only effect pain not inflammation
Mode of action – inhibit COX stopping conversion of arachidonic acid to PGG 2
COX 1 – promotes renal blood flow, maintain stomach lining and alter platelet
aggregation
Prostaglandins:
PGI2 – dilates vascular smooth muscle, decreases platelet aggregation and causes
pain
TXA2 – constricts vascular smooth muscle and increases platelet aggregation
PGF2 – constricts respiratory smooth muscle
PGD2 – dilates vascular smooth muscle and decreases platelet aggregation
PGE2 – dilates vascular smooth muscle and increases pain
Issues:
CV risk – HT, HF and MI
GI risk – inhibit gastro-protective prostaglandins
Renal risk – increased sodium reabsorption (weight gain and oedema),
hyperkalaemia and acute renal failure
COX 2:
Advantages – reduced GI SEs
Issues – withdrawing from market as increased thrombotic risk
Rheumatoid Arthritis II
Chronic progressive inflammation causing joint destruction
Increases morbidity and mortality
Epidemiology
Onset aged 30-60
40-50 people per 100,000
2:1 F:M (world) and 3:1 F:M (UK)
Aetiology
Infection, viral, immune system, diet, smoking and genetics
Pathophysiology
Greatest impact of synovial joints (hands and feet)
Symmetrical effect
Synovium – protective fluid layer around joint
Synoviocytes – macrophages or fibroblasts
Symptoms:
Increased blood flow – heat/redness
Proliferation of synovial membrane – swelling
Increased synovial fluid – swelling
Muscle loss – loss of function
1. Synovitis - inflammation of the synovial membrane causing swelling and
reduced fluid
2. Pannus formation – bone and cartilage erodes and inflamed tendon
3. Fibrous ankylosis – fibrous connective tissue forms with loss of bone causing
immobility (less inflammation)
4. Bony ankylosis – no pain or swelling as bones fuse with connective tissue and
leading to osteoporosis
Clinical Features
Pain
Stiffness (prolonged in morning)
Loss of function
Fever, sweating and malaise
Diagnosis
MCP or MTP squeeze test – pain suggests inflammation
Bloods – raised ESR and CRP
Rheumatoid factor (RF)
Anti-CCP
Decreased platelet and FBC
X-ray, MRI and ultrasound
ACR/EULAR criteria (>6) – joint involvement, serology (RF and ACCP), acute
phase reaction (CRP/ESR) and duration (>6 weeks)
DAS (>2.6) – assess 28 joints, ESR, CRP and patient feeling
Management
, Refer for specialist appointment
Analgesics – not NSAIDs (no effect on disease)
NSAIDs
Only effect pain not inflammation
Mode of action – inhibit COX stopping conversion of arachidonic acid to PGG 2
COX 1 – promotes renal blood flow, maintain stomach lining and alter platelet
aggregation
Prostaglandins:
PGI2 – dilates vascular smooth muscle, decreases platelet aggregation and causes
pain
TXA2 – constricts vascular smooth muscle and increases platelet aggregation
PGF2 – constricts respiratory smooth muscle
PGD2 – dilates vascular smooth muscle and decreases platelet aggregation
PGE2 – dilates vascular smooth muscle and increases pain
Issues:
CV risk – HT, HF and MI
GI risk – inhibit gastro-protective prostaglandins
Renal risk – increased sodium reabsorption (weight gain and oedema),
hyperkalaemia and acute renal failure
COX 2:
Advantages – reduced GI SEs
Issues – withdrawing from market as increased thrombotic risk
Rheumatoid Arthritis II
