Joint pathologies Flashcards
Types of synovial joints
Planar (navicular/cuneiform) Hinge (humerus/ulna) Pivot (radius/ulna) Condyloid (radius/carpals) Saddle (carpal/metacarpal 1) Ball and socket (acetabular/femur)
Synovial joints
Diarthotic
Most moveable joints
Surrounded by capsule, lubricated by synovial fluid.
Cartilage
Avascular CT
No nerve supply
Dense network of collagen and elastic fibres embedded in chondroitin sulfate
Surrounded by perichondrium
Hyaline cartilage
Most abundant but weakest
Fine collagen fibres embedded in gem-type matrix
Provides flexibility and support
Reduces friction and absorbs shock.
Reactions of articular cartilage
Destruction (trauma, compression, corticosteroids, inflammation/infection)
Degeneration (time, premature aging, previous destruction, joint incongruity/irregularity).
Peripheral proliferation (bone spurs, osteoarthritis)
Reactions of Synovial Membrane
Effusion (increased production of synovial fluid)
Thickening of membrane (hypertrophy)
Adhesions post-injury.
Reactions of joint capsules and ligaments.
Joint laxity (post-injury, congenital, pregnancy, infection)
Joint contracture (disuse, congenital, infection, arthritis, muscle contractures)
Joint deformity
Displacement (subluxation, dislocation)
Excessive mobility restricted mobility
Gout
Metabolic arthritis
Monosodium urate (uric acid) crystals deposited in tissues, accompanied by attacks of acute arthritis.
Most common in big toe
Result of urate overproduction or decreased excretion
DDX. Septic arthritis, RA, neoplasm
Pathogenesis of gout
Normally, purines break down into uric acid, which is dissolved, passed through kidneys and excreted.
In gout, uric acid precipates into blood (poor kidney function or overproduction) and deposits in tissue.
- especially articular cartilage.
- triggers inflammatory response. (–> necrosis and proliferation of fibrous tissue).
Types of gout
Primary hyperuricemia (inherited)
Secondary hyperuricemia (secondary to a different metabolic disorder, or cancer/chemo)
Idiopathic
Tophi
Nodular masses of uric acid depositing in soft tissues of the body.
Traumatic Arthritis
Damage to articular cartilage – cartilage replaced by scar tissue – alters how joint works.
Loose bodies
“Joint mice”
Small pieces of bone or cartilage in joint space
Due to trauma, repetitive action, etc.
Hemarthrosis
Bleeding in joint spaces
Acute or chronic
May be complication of anticoagulant treatment.
Infectious arthritis
“Septic arthritis”
Joint inflammation as a result of infection
Most common in adults: staphylococcus aureus.
Medical emergency.
Most common in kids: haemophilia influenza
Most common in those getting lucky: neisseria gonorrhoea
Bacteria adheres to synovium –> breakdown of articular cartilage
Psoriatic arthritis
1/20 people with psoriasis develop psoriatic arthritis
Primarily affects DIPs of fingers and toes. Can also affect spine.
Charcots arthropathy
Charcot joint, Charcot foot, neuropathic arthropathy.
Progressive degeneration of stress bearing portion of foot
Associated with diabetic neuropathy
Pseudogout
Just like regular gout, but crystals formed from calcium pyrophosphate dihedral salt, not uric acid.
Loose Bodies
“Joint Mice”
Small pieces of bone or cartilage in the joint space
Hemathrosis
Bleeding into joint space
Acute or chronic
Can be complication of anticoagulant meds
Infectious Arthritis
“Septic arthritis”
Joint inflammation as a result of infection
Medical emergency. Fast acting.
Most common bacterial pathogens involved in infectious arthritis
Adults: staphylococcus aureus
Kids: haemophilius infulenza
Those getting lucky: neisseria gonorrhoea
Elderly, IV drug users: esherichia coli
Strep, gonococcus
Pott’s Disease
Infectious arthritis of the spine
Caused by m. tuberculosis
Psoriatic arthritis
1/20 people with psoriasis will develop psoriatic arthritis.
Primarily affects distal joints; can affect spine
Charcots arthopathy
Charcot joint, Charcot foot, neuropathic arthropathy.
Progressive degeneration of the stress bearing portion of a joint.
Most commonly associated with diabetic neuropathy.
Osteoarthritis
“Degenerative joint disease”
Most common joint disorder
Prevalence increases with age
Gradual loss of articular cartilage, with thickening of subchondral bone, osteophytes at joint margins, and mild nonspecific synovial inflammation.
Idiopathic, unless secondary.
How normal cartilage ages:
Glycosamnioglycans (GAGs) shorten and are replaced by less efficient types. Associated proteoglycans change, and cartilage’s ability to retain water is decreased. Biomechanical nature of the joint is changed.
Fissures may develop in cartilage mostly stress fractures of collagen network.
Three abnormalities of osteoarthritis
Reduced joint space
Formation of osteophytes
Sclerosis of subchondral bone.
Stages of OA pathogenesis
Phase 1. Edema and microcracks
Phase 2. Fissuring and Pitting
Phase 3. Erosion
Phase 1 of OA pathogenesis
Edema and microcracks
- edema of ECM
- cartilage loses its smooth appearance and develops micro cracks.
- cartilage softens and thins; loss of joint space
- Focal loss of chondrocytes (thus unable to repair).
Phase 2 of OA pathogenesis
Fissuring and Pitting
- microcracks deepen perpendicularly; along collagen fibres
- vertical clefts form in cartilage above subchondral bone
Phase 3 of OA pathogenesis
Erosion
- Fissures cause fragments of cartilage to detach, causing
- -> osteocartilaginous loose bodies
- synovial inflammation (more focal than rheumatoid synovitis) –> synovial hypertrophy and capsular thickening
- -> uncovering subchondral bone
- sclerosing of subchondral bone; subchondral cysts; osteophyte formation
Symptoms of OA
Pain, usually relieved with rest.
Morning stiffness – less than 30 minutes
Commonly located at hand; knee (high association with obesity); spine; hip
Heberden’s nodes at DIPs; Bouchard’s nodes at PIPs.
Rheumatoid Arthritis
Systemic inflammatory autoimmune disease that predominantly manifests as chronic progressive synovial inflammation and destruction of joint architecture.
Results in hyperplasia, edema, fibrin exudation of synovial fibroblasts and structural damage of cartilage, bone and ligaments.
Extra-articular manifestation can affect a variety of organs and is a significant factor in morbidity and mortality
Damage usually symmetrical and uniform
3:1 women:men
Pannus formation
Pannus – abnormal layer of fibrovascular or granulation tissue
In RA, the synovial membrane hypertrophies and extends into (and destroys) surrounding cartilage and bone (=pannus formation)
Tenosynovitis
Inflammation of synovium around a tendon.
Common in RA
Swan neck
Hand deformity seen in RA
PIP hyperextended; DIP flexed
Boutonniere Deformity
In hand. Seen in RA
PIP flexed; DIP hyperextended
Baker’s Cyst
“Popliteal Cyst”
Seen in RA
Deformities associated with RA
Valgus knee Swan neck Boutonniere Baker's Cyse Ulnar drift
Ankylosing Spondylitis
Systemic disorder characterized by inflammation of the axial skeleton.
Enthesitis central feature.
ankylosis – immobility and fixation of a joint
spondylitis – inflammation of vertebrae
Male dominant.
Insidious.
Onset 20-40
May result in fusion of joint.
Seronegative spondyloarthopathy
seronegative – test negative for rheumatoid factor (RF)
Include ankylosing spondylitis, psoriatic, reactive and enteropathic arthropathies.
Enthesitis
Inflammation of the enthesis ( connection between tendon/ligament and bone)
Key feature of AS
Inflammation of ligament –>fibrosis, bony erosions and reactive bone growth and spurring
Signs and symptoms of AS
Fixed, flattened chest
Pain diminishes as vertebrae fuse
Muscle wasting, fatigue
Possible osteoporosis, stenosis
Bamboo spine (fused vertebrae) Dagger sign -- SPs fuse
