MSK Joint Pathology Flashcards
Osteoarthritis is the ______ progressive ________ of articular cartilage, resulting in _________.
Osteoarthritis is the CHRONIC progressive DESTRUCTION of articular cartilage, resulting in REDUCED JOINT SPACE.
State 4 common secondary causes of osteoarthritis
- Congenital abnormality
- Avascular necrosis
- Trauma
- Joint diseases
State the common pathological changes of osteoarthritis.
- Eburnation with smooth, polished surface due to constant friction of bone surfaces
- Formation of subchondral cyst
- Formation of osteophytes
- Thickening of subarticular bone
- Reactive thickening of synovium
- Destruction of articular cartilage
- Secondary changes to surrounding tissue
State the two types of osteophytes formed in OA, state their corresponding locations.
Hebedern’s nodes = DIPJ
Bouchard’s nodes = PIPJ
State the common clinical presentations of OA.
- pain
- swelling
- decreased ROM
- formation of osteophytes/bone spurs
- cervical spondylosis spinal nerve compression
State the 2 complications of OA
- deformity of knee (bilateral genus valgus deformity)
- cervical spondylosis and spinal nerve compression
State the 3 types of OA.
- primary generalised OA
- erosive inflammatory OA
- hypertrophic OA
State the difference between erosive inflammatory OA and hypertrophic OA.
erosive inflammatory OA - rapid progression
hypertrophic OA - slow progression
State the common group of individuals that present with primary generalised OA.
menopause women!
Hypertrophic OA is a _____, inflammatory, reparative activity involving _____ cartilage and _____ bone. It has secondary effects on ____, _____ and ____.
Hypertrophic OA is a DEGENERATIVE, inflammatory, reparative activity involving ARTICULAR cartilage and SUBARTICULAR bone. It has secondary effects on SYNOVIUM, MUSCLE and NERVES.
State the 2 common pathological changes associated with hypertrophic OA.
- florid osteophyte formation
- bone sclerosis
State the common causes of hypertrophic OA.
- increased unit load on joint
- degradation of articular cartilage
- biochemical abnormalities (reduction of prosteoglycans, protein synthesis, chondrocyte replication)
- genetic abnormalities (familial mutation of type 2 collagen COL2A1)
State the 2 most important parts of the intervertebral disc.
- nucleus pulposus (inner) = contains water and proteoglycans
- disc annulus (outer) = obliquely oriented collagen fibres and cartilaginous end plate
State some causes of degenerative intervertebral disc.
- age related wear and tear - nucleus pulposus dehydrated, fibrotic and atrophied
- mechanical factors
- genetic predisposition
- nutrition, metabolic, infection
State the stages of disc herniation.
- Degeneration
- Prolapse - weakened annulus, outer layers of annulus still intact
- Extrusion
- Sequestration - part of nucleus pulposus spurts out through a tear in annulus into the spinal foramen
State the common complications of intervertebral disc degeneration. Give 1 example for each complication.
- Posterior compression –> injury to spinal cord (eg: cervical myelopathy)
- Posterolateal compression –> injury to nerve roots (eg: radiculopathy)
State the clinical features of prolapsed intervertebral disc
- lower back pain, worse on activity
- asymmetrical gait
- straight leg test positive = disc pathology + nerve rot irritation
- scoliosis or kyphosis
Rheumatoid arthritis is a _____ chronic ______ ______ disease affecting many tissues but specifically the joints.
Rheumatoid arthritis is a SYSTEMIC chronic INFLAMMATORY AUTOIMMUNE disease affecting many tissues but specifically the joints.
Which parts of the body does RA usually affect?
Joints of hand (PIP, MCP), wrists, elbows, knees
RA is most common in _____.
RA is most common in MIDDLE-AGED WOMEN.
What are the elevated serum markers of RA?
- RF (rheumatoid factor)
- ACPA (anticitrullinated protein antibody)
State the pathogenesis of RA
(hint: very very long)
Step 1:
- genetic predisposition = HLA-DR4
-> unregulated lymphocyte activation
-> loss of immune tolerance - environmental factors (infection, smoking) = formation of autoantibodies against CCP
-> citrullination of self-proteins - recognised as foreign
Step 2: T and B lymphocyte response to self-Ag present in joint tissues
- Th17 -> secrete IL-17 -> activates other immune cells to inflame joint
- Th1 -> secrete cytokines (IL-1, TNF-a) -> promote inflammatory response
- B lymphocyte -> secrete RF and ACPA -> form immune complexes
Step 3: Proliferation of chondryocytes, synovial cells, fibroblasts
Step 4: Release of elastase, stromelysin, collagenase, PGE2
Step 5: Pannus formation, ankylosis, fibrosis, desturction of bone and cartilage
State the common pathological features of RA
- Pannus formation - composed of granulation tissue that grows and destroys articular cartilage -> fibrosis across joint -> ankylosis
- Synovial inflammation - swelling and villous formation of synovium
- Destruction of adjacent bone - joint deformity
- Formation of rheumatoid nodules
Is RA or OA systemic?
RA is a systemic disease!!
- 25% of patients have subcutaneous rheumatoid nodules (has central zone of fibrinoid nodules)
- found in other organs
- presents with…
1. necrotising vasculitis of small vessels (affects GIT, lung, heart, kidneys)
2. amyloidosis
How do we differentiate OA and RA?
Morning stiffness:
RA >30 minutes, OA <30 minutes
Serum markers:
RA - RF and ACPA, OA none
Pannus:
RA - present, OA - absent
Nature:
RA - inflammatory and autoimmune, OA - non-inflammatory and degenerative
Cause:
RA - autoimune attack on synovium, OA - wear and tear of cartilage
Affected joints:
RA - small joints (PIP, MCP, wrists, elbow, knees) , OA - weight-bearing joints (knees, hips, spine)
Findings:
RA - synovial hyperplasia with dense inflammation, pannus, eroding cartilage, bony and fibrous ankylosis, subchondral cyst
OA - synovium with mild inflammation, osteophytes, thinned (destruction) of cartilage, subchondral cyst, subchondral sclerosis, no ankylosis
Systemic symptoms:
RA - yes, OA - no
Gender preference:
RA - older females, OA - none
State two other types of inflammatory arthritis.
- Seronegative spondyloarthropathies
- Autoimmune arthritis - SLE, RF, systemic sclerosis
State some unique features of seronegative spondyloarthropathies.
- lacks RF (since seronegative)
- high incidence of HLAB27
- either axial location (vertebrae, sacr-iliac joint) or asymmetric involvement of the peripheral joints in digits
- USE MRI OVER SACRO-ILIAC JOINT
- hip pain -> sacroiliac -> lumbar -> thoracic (with some cervical pain)
- pathology found in ligamentous attachments instead of synovium
State the 3 commoner types of seronegative spondyloarthropathies.
- ankylosing spondylitis = destruction of vertebral column and sacroiliac joint
- psoriatic arthropathy (@DIPJ)
- reactive arthritis (post infection of conjunctivitis, polyarthritis, urethritis)
State the common clinical presentation and determining factor for ankylosing spondylitis.
- commonly presents with inflammatory back pain
- patient is unable to bend on any axis due to stiff axial skeleton (uniquely cannot bend sideways)
State the presentation fo ankylosing spondylitis on x-ray.
X-RAY OF SACRO-ILIAC SPINE + LUMBAR SPINE
- joint space narrowing and calcaification of ligaments
- sauaring of vertebrae + loss of lumbar lordosis
- syndesmosis and fusion of posterior elements
- diffuse idiopathic skeletal hyperostosis
- syndesmophytes in cervical spine
State 2 common inflammatory joint pathologies related to infection.
- Septic arthritis
- Osteomyelitis
Septic arthritis is the _______ inflammation of the _____ and ________ _______ due to ______.
Septic arthritis is the SUPPURATIVE inflammation of the SYNOVIUM and JOINT STRUCTURES due to INFECTION.
State the common clinical presentations of septic arthritis
- acute onset of severe joint pain
- warm and swollen joints (AT HIP AND KNEE)
- fever
- systemic symptoms
State the common sources of infection for septic arthritis. State the common causative agents.
- Haematogenous dissemination (most common)
- Direct inoculation through skin
- Contiguous infective spread from adjacent soft tissue abscess or osteomyelitis
Common causative agents:
- Staph aureus
- Grp B strep
- Pseudomonas
- Gram negative bacilli
State the laboratory tests used to investigate septic arthritis and the histological features seen under microscopy,
State the most appropriate treatment for patients with septic arthritis.
Laboratory tests:
- gram stain and culture
- high wcc count with predominance of neutrophils
- joint aspiration for histological and microbiological analysis
Histology
- acute inflammation, purulent exudate
- destruction of synovium and stroma
Treatment:
- joint washout and antibiotics for 2-6 weeks
Osteomyelitis is a bone infection involving _____, ____ and ____.
Osteomyelitis is a bone infection involving MEDULLA, CORTEX and PERIOSTEUM.
State the clinical presentations of osteomyelitis and their common sites of presentation.
Clinical presentation:
- fever
- swelling
- pain
- constitutional symptoms
Sites of presentation:
- Children - long bones and jaw
- Adults - small bones, femur, vertebral spine (lumbar > thoracic > cervical)
State the main causative agent of osteomyelitis and modes of transport into bone.
Main causative agent = Staph aureus
Modes of transport:
1. Direct implantation - trauma with open wound/ wound and surgery
2. Bloodborne spread (more common in children)
3. Extension from contiguous site
State the investigations used in osteomyelitis.
State the appropriate treatment needed for osteomyelitis.
Investigations:
- MRI > CT > X-ray
- Tissue culture or CT guided biopsy > wound swab
- If blood culture is positive and clinical signs fit -> immediately diagnose
Treatment:
- Avoid empirical antibiotic treatment to increase chances of growing causative pathogens from tissue sampling
- Treat for 6 weeks minimally
- Surgery to remove necrotic tissue or bone or manage neurological emergency
State the presentation of OM on x-ray
- radiolucencies in cortex
- lytic medullary canal
State the progression of OM.
- Healed OM -> resolution or healing with scarring
- Complicated OM (acute OM -> chronic/subacute OM)
State the complications of OM.
- Pathological fracture with deformities
- Spread of infections -> skin-cellulitis, endocarditis, blood-septicaemia
- Bone abscess (brodie’s abscess)
- Necrosis of bone (sequestrum)
- Proliferative periostitis and involucrum over sequestrum
- Sinus
- Secondary amyloidosis
- Malignant transformation to bone (osteosarcoma) and skin (SCC)
State everything you know about suppurative OM
- Active on chronic suppurative OM
- Bacteria proliferates in bone -> induces acute inflammation and cell death (bone necrosis)
- If infection extends to joints or synovium -> septic arthritis
Histology:
- neutrophils
- necrosis
Progression
- suppurative injury causes tissue destruction
- elevation of periosteum -> inflammation leads to sizable subperiosteal pus or abscess -> causes further bone necrosis
- rupture of periosteum -> leads to inflammation and abscess in surrounding skin and soft tissue (cellulitis) and eventual formation of draining sinus
State everything you know about non-suppurative OM
- chronic OM
- lacking/minimal pus, mainly chronic inflammation and fibrotic/scar
Histology:
- diffuse or focal sclerosing
- proliferative periostitis
State everything you know about chronic OM
- 5-25% acute OM progresses to chronic OM
- causes:
1. delay in diagnosis and treatment
2. extensive bone necrosis
3. incomplete surgical debridement of necrotic bone
4. weakened immunity - complications:
1. pathological fractures and deformity
2. secondary amyloidosis
3. sepsis
4. malignant transformation
State everything you know about Garre’s Sclerosing OM.
CHRONIC OM WITH PROLIFERATIVE PERIOSTITIS
- presentation: mild irritation, dental infection, trauma
- involves jaw -> new bone formation obscuring underlying native bone structure
- mainly affects children and adolescents
- easily misdiagnosed as malignant (osteosarcoma, chondrosarcoma0
State everything you know about Tuberculous OM
CHRONIC OM
- mainly affects very young or very old, immunosuppressed, lower SES with MTB infection
- blood borne or lymphatic drainage
- involves vertebral spine (thoracic and lumbar)
- highly destructive with extensive necrosis -> difficult to treat
- Histology:
1. epitheloid granulomas
2. caseating necrosis
- Complications:
1. compression fracture
2. severe deformities (scoliosis, kyphosis)
3. neurological deficits due to cord and nerve compression
Crystal arthropathies is the ______ of ____ in joints and soft tissues.
Crystal arthropathies is the DEPOSITION of CRYSTALS in joints and soft tissues.
State the presentation of crystal arthropathies.
State the investigations common to crystal arthropathies.
- Acute pain
- Swelling
- Erythema at joints (foot and big toe)
Investigation:
Joint fluid analysis (gram stain and culture)
Gout is characterised by increased serum _____ ____ and _____ ____ deposition.
Gout is characterised by increased serum URIC ACID and URATE CRYSTALS deposition.
State the primary and secondary causes of gout.
Primary causes:
- obesity
- alcohol
- HTN
- fatty diet
Secondary causes:
CONDITIONS THAT PROMOTE HYPERURICEMIA
- renal failure
- familial juvenile hyperuricaemic nephropathy
- congenital enzyme defects
State the pathogenesis of gout.
State the lab observations of gout.
Problems of purine metabolism -> increased uric acid production and decreased uric acid elimination
- overproduction of purines (high purine diet)
- increased catabolism of nucleic acids due to high cell turnover (infection or cancer)
- decreased uric acid excretion by kidneys
Lab: strongly birefringent needle shaped crystals
Recap: purine is the precursor for uric acid
State the presentation of gout and its associated complications.
Presentation: deposition of urate crystals -> erythematous inflammation
Complications
- gouty tophi
- deformities
- erosions of joints
- interstitial nephritis
- kidney disease and kidney stones
State the pathogenesis of acute gouty arthritis.
- urate crystals are phagocytosed by macrophages
- activation of inflammaotey mediators that release IL-1
- IL-1 recruit neutrophils -> release of cytokines (TNF-A) -> free radicals and proteases
- neutrophils phagocytose crystals which together with macrophages damage the membranes of the lysosomes leading to release of enzyme
Pseudogout is the deposition of _____ _____ ______ in joints.
Pseudogout is the deposition of CALCIUM PYROPHOSPHATE DIHYDRATE in joints.
State the common causes of pseudogout.
State the presentation of pseudogout.
State the lab findings of pseudogout.
Common causes:
1. Idiopathic - trauma association
2. Hyperparathyroidism
3. Haemochromatosis
Presentation:
- mostly asymptomatic
- acute, subacute or chronic arthritis
Lab: crystals are rhomboid-shaped and positively birefringent under polarised light
State the presentation of prosthetic joint infections
Acute infection = <6 months post surgery
Chronic infection = 6 months-2 years post surgery
Presents as…
1. fever
2. joint pain
State the causative agents of prosthetic joint infections.
State the investigations of prosthetic joint infections.
Causative agents:
- >70% due to staph, can be due to any skin flora related bacteria
- CONS (coagulative negative staph) - insidious presentation
- Staph aureus - acute presentation
Investigations:
- DO NOT DO NOT DIAGNOSE WITH GRAM STAIN
- Multiple (>3,6) intraoperative tissue or pus culture
- DO NOT USE WOUND SWAB
State the appropriate way to treat prosthetic joint infection.
- antibiotic usage is guided by culture results
- use antibiotics with ability to penetrate biofilm (rifampicin, ciprofloxacin)
- combination antibiotic therapy preferred
- start with IV antibiotics -> switch to PO provided antibiotics with excellent bioavailability
Acute infection
- local debridement with retention of prosthesis and prolonged antibiotics (>6 weeks)
- chances of cure without removal of prosthesis is pessimistic especially for bacterias (staph, enterococci, pseudomonas)
Infected prosthesis
1. one stage exchange arthroplasty = remove infected prosthesis, insert new prosthesis during the same operation with antibiotic loaded cement
2. two stage approach = remove infected prosthesis, install antibiotic loaded cement to stabilise bone -> treat with weeks or months of antibiotics -> insert new prosthesis after prolonged course of antibiotics
