Week 4 Flashcards
Arthritis (21 cards)
definition of osteoarthritis (OA)
the clinical and pathological outcome of a range of disorders that results in structural and functional failure of synovial joints
OA features include
pattern of joint involvements: weight-bearing joints, Distal interphalangeal joints DIP, and proximal interphalangeal joints PIP
systemic features: none
synovial fluid: non-inflmamatory
radiological features: bony spurring, cartilage disruption
OA primary or secondary
- occupational, sports trauma, other injury
-underlying cause for damaged joints:
1. inflammatory arthritis; RA
2. crystal arthropathy
3. congenital hip dysplasia
4. slipped capital femoral ephiphyses
5. Paget’s
6. AVN
-underlying metabolic disease or endocrinopathy
1. Haemochromatosis, acromegaly
-primary/familial OA
OA pathogenesis
- final common pathway of a number of pathological processes
- cartilage irregularities (fibrillation, clefts) –> ulceration of cartilage surface —> frank cartilage loss
-biochemically: low glycosaminoglycan content, high water content and high MMP activity
-traditionally considered a disease of cartilage: newer concept is as whole joint problem:
1. cartilage, menisci, ligaments, synovial capsule, periarticular muscles, subchondral bone
2. failure in any area can lead to common end product of OA
OA pathological/radiological characteristics
- focal damage to load bearing articular cartilage asymmetric joint space loss
- new bone formation at joint margins : osteophytes
- subchondral bone changes: subchondral sclerosis and subchondral cysts
- variable degrees of synovitis and joint capsule thickening
OA risk fcators
- Age
- women
- obesity, particularly for knees
- occupation, sports activities, previous injury
- genetic contribution
- muscle weakness and proprioceptive deficits
- calcium crystal deposition disease
- acromegaly
- lack of osteoporosis
OA genetic factors
may involve
-connective tissue defect e.g. mutations in type 2 collagen in some rare, familial forms
-alterations in cartilage or bone metabolism
-genetic influence on a known risk e.g. obesity
OA symptoms and signs
- pain:
insidious onset, usually mild to moderate intensity, worsens with use, relieved by rest, may be intermittent with self-limited flares, may be worsen in cold weather
-morning or after rest stiffness in affected large joints, usually lasts less than 30 minutes
-reduced function
-signs localised to affected joints; crepitusm locking, tenderness at joint margins, defroming body enlargement, deforming bony enlargement, decreased rande of motion, misalignment
OA Joints involved
- common;
1. cervical and lumbar spine
2. hands: first carpometacarpal joint (aka base of thumb), proximal interphalangeal joint ( Bouchard’s nodes), distal interphalangealjoint (Heberden’s nodes)
3. hip, knee, subtalar joint
4. first metarsophalangeal joint
-“atypical” OA
1. shoulder, wrist, elbow, metacarpophalangeal joint
2. evaluate for underlying cause/secondary OA
-generalised OA
1. 3 or more joints
2. may associate with nodal OA
3. often in middle aged or older women
OA radiology
clinical diagnosis generally confirmed with x-rays correlation between severity of symptoms and radiological severity.
Classic OA features are:
1. asymmetrical joint space narrowing
2. osteophytes at joint margins
3. subchondral bone sclerosis
4. subchondral bone cysts
OA other investigations
- blood tests
1. screening for associated/underlying/inflammatory conditions
2.monitoring for complications of therapy
3. e.g. renal and liver functions tests, Hb, inflammatory markers, uric acid etc
-synovial fluid analysis “non-inflammatory”
1. clear fluid with normal viscosity
2. WCC ( greater than 20,000 inflammatory, greater than 70,000 usually infection )
overview of mono - and oligo- arthropathies
mono-arthropathy affects a single joint, while oligo-arthropathy involves a few joints (typically 2-4). conditions that fall into these categories include osteoarthritis, crystaline arthropathies ( like gout and pseudogout) and septic arthritis.
OA
aetiology: often due to wear and tear on joints with age, or risk factors like obesity, joint, injury or genetics
pathogenesis: involves the degeneration of joint cartilage and changes in the underlying bone, leading to reduced joint space, osteophytes ( bone outgroeths), an inflammation in later stages,
clinical features: joint pain that worsens with activity, stiffness, and decreased mobility. commonly affects knees, hips, and hands.
diagnosis: diagnosed through history, physical exam, and imaging (x-rays shows joint space narrowing and osteophytes)
complications: can lead to significant disability and chronic pain
Gout (crystalline arthropathy)
aetiology: caused by high levels of uric acid in the blood, which crystallises in joints
pathogenesis: uric acid crystals accumulate in the joint space, triggering intense inflammatory responses.
clinical features: sudden and severe pain, redness, swelling, often starting in the big toe (podagra)
diagnosis: diagnosis is confirmed by synovial fluid analysis, showing urate crystals under polarised light microscopy,, along with blood tests for uric acid levels
complications: can lead to chronic joint damage and the formation of tophi (uric acid deposits)
Pseudogout ( calcium pyrophosphate deposition disease - CPPD)
overview: simialr to gout but caused by calcium pyrophosphate crystals. often affects larger joints, like the knee.
diagnosis: identified through synovial fluid analysis showing CPPD crystals.
septic arthritis
overview: a joint infection caused by bacteria, often following an injury or surgery
clinical features: sudden pain, fever, swelling, and warmth in the affected joint
diagnosis: requires joint fluid aspiration and culture, along with blood tests for infection markers
synovial fluid analysis
purpose: used to differentiate between types of arthritis ( e.g., gout, pseudogout, septic arthritis) by analysing fluid for cell count, presence of crystals, and culture for infection
overview of poly-arthropathies
these affect five or more joints and often involve systemic symptoms. examples include rheumatoid arthritis, spondyloarthropathy,a nd connective tissue diseases.
rheumatoid arthritis (RA)
Aetiology: autoimmune condition where the immune system attacks the synovium ( joint lining)
pathogenesis: chronic inflammation leads to synovial hypertrophy an djoint destruction. RA is also associated with systemic effects such as cardiovascular risks
clinical features: symmetrical joint pain, morning stiffness lasting over an hour, joint swelling, and deformity in advanced stages.
Diagnosis: blood tests for rheumatoid factor (RF) and anti-CCP antibodies, imaging for joint erosion, and synovial fluid analysis.
complications: can lead to joint deformity, disability, and systemic involvement ( e.g., lungs, and heart)
connective tissue diseases
overview: includes lupus and scleroderma, which can cause polyarthritis as part of broader systemic symptoms
diagnosis: blood tests for specific antibodies ( e.g., ANA, anti-dsDNS for lupus)
spondyloarthropathies
overview: a group of diseases, including ankylosing spondylitis, that primarily affects the spine and may cause peripheral arthritis
diagnosis: HLA-B27 gene testing is relevant, and imaging shows sacroiliac joint inflammation
