Pathology - MSK Flashcards
How are fractures classified
complete/incomplete
simple/compound (open)
comminuted
displaced/undisplaced
stress
pathological
Describe the steps in fracture healing
1) immediate rupture of blood vessels, HAEMATOMA fills the gaps and provides a fibrin mesh within hours
2) influx of inflammatory cells and fibroblasts, angiogenesis within days
3) soft PROCALLUS forms within 1 week, characterised by organisation of the haematoma
4) OSSIFICATON into BONY CALLUS at 2 weeks, characterised by woven bone oriented perpendicular to cortical axis
5) REMODELLING occurs at 6 weeks, characterised by woven bone becoming lamellar bone
What factors impede fracture healing?
INADEQUATE IMMOBILISATION
Marked displacement
Soft tissue and vascular compromise
INFECTION (open fracture/foreign bodies)
Systemic factors (malnutrition, osteoporosis, smoking)
(think about AO principles on fracture management: anatomical reduction, stable fixation, preservation of blood supply, early and safe mobilisation)
How does remodelling of callus occur?
-woven bone is initially orientated perpendicular to cortical axis
-remodelling occurs along lines of weight bearing, converting woven bone to lamellar bone
(Wolff’s law: bone remodels to increase mechanical strength to resist stress forces. Role of osteoclasts and osteoblasts to restore the Haversian canals.)
What are the causes of osteomyelitis
-most common = staph aureus
-IVDU = e coli, klebsiella, pseudomonas
-sickle cell = salmonella
What is the pathogenesis of osteomyelitis
-infection of bone/marrow due to haematogenous spread, extension from local infection or trauma
-bacteria proliferate and induce a neutrophil inflammatory reaction
-entrapped bone undergoes necrosis, dead bone is called sequestrum
-bacteria lift off the periosteum, leading to rupture and abscess formation
-involucrum develops, with new bone encasing an inflammatory focus
What are the outcomes of osteomyelitis
resolution
development of chronic infection (pathological fracture, acute flare up, severe sepsis)
What are the causes of osteoarthritis
risks include age, inflammation, genetics, mechanical stress, joint injury
-primary OA = no obvious initiating cause
-secondary OA = systemic disease (diabetes), mechanical stress (obesity), congenital deformity, previous trauma
Pathogenesis of osteoarthritis
3 phases
1) chondrocyte injury = due to genetic and environmental factors
2) early = chondrocytes proliferate and secrete inflammatory mediators/collagen/proteoglycan, causing remodelling
3) late = repetitive injury and inflammation causes chondrocyte drop out and loss of cartilage
Morphology and clinical features of osteoarthritis
Morphology:
1. early - increased chondrocytes and water, decreased proteoglycans
2. fibrillation/cracking/softening
3. sloughing, bone exposure
4. eburnation (sclerosis)
5. dislocated cartilage and bone (loose bodies)
6. fibrous subchondral bone cysts
7. osteophytes
8. synovium fibrosis and inflammation
Clinical: mostly asymptomatic in < 50 yo
1. slowly progressing disease, deep aching pain, worse with use, morning stiffness, crepitus, limited ROM
2. oligoarthritis 95%
3. hands and knees worse in women, hips in men
4. in spine, foraminal stenosis resulting in radiculopathy
What are the causes of rheumatoid arthritis
chronic systemic inflammatory disease, mainly attacks joints, autoimmune - type 3 hypersensitivity
pathogenesis: triggered by exposure of genetically susceptible host to arthritogenic antigen
leads to loss of self tolerance and immune response (CD4+ T helper cells, IL-1, macrophages)
risks: EBV, genetics (HLA-DRB1 genes)
Morphology of rheumatoid arthritis
symmetric arthritis, mostly small joints of hands and feet, inflammatory infiltration of joints (microscopic and macroscopic changes)
- joints - perivascular inflammatory infiltration of CD4 helper T cells, plasma cells, macrophages, accumulation of neutrophils
- increased vascularity
- organising fibrin, rice bodies
- juxta-articular erosion, cyst formation, osteoporosis
- pannus formation, proliferative synovium with inflammatory cells, fibroblasts, granulation tissue
- fibrosing ankylosis, pannus forms a bridge between opposing bones that eventually ossifies -> bony ankylosis
Extra-articular manifestations and long term complications of RA?
extra-articular manifestations: rheumatoid nodules (elbows/forearm/occiput/lumbosacral), vasculitis (purpura, ulcers, nail bed infarcts, digital gangrene), fibrinoid necrosis
long term complications: joint destruction, renal failure, systemic amyloidosis, opportunistic infections
What organisms cause septic arthritis, what are pre-disposing conditions
organisms:
gonococcus, staphylococcus, streptococcus, h influenzae, salmonella
predisposition:
immunosuppression, joint trauma, surgery, chronic arthritis, IVDU
Name 2 different species of staphylococcus and give examples of infections they cause
-staph aureus = skin (impetigo), pneumonia, osteomyelitis, TSS, endocarditis in IVDU
-staph epidermidis = endocarditis in prosthetic valves
-staph saprophyticus = UTI
