VIVA: Pathology - Musculoskeletal Flashcards
Name and describe the different types of fractures
4 to pass:
- Simple: overlying skin intact
- Compound: bone communicates with skin surface
- Comminuted: bone is fragmented
- Displaced: ends of bone at fracture site are not aligned
- Stress: slowly developing fracture that follows increased physical activity in which the bone is subjected to repetitive loads
- Greenstick: extending only partially through bone, common in children
- Pathologic: involving bone weakened by underlying disease process (e.g. tumour)
Describe the steps and timeframe in fracture healing
3/5 to pass:
1. Within hours:
- Haematoma fills fracture site and provides a fibrin mesh
2. Within days:
- Influx of inflammatory cells
- Ingrowth of fibroblasts and capillary buds
3. Within 0-2 weeks:
- Organising haematoma and procallus formation
- Inflammatory cells release growth factors which activate osteoprogenitor cells
- Activated osteoclasts and osteoblasts form a soft tissue callus
4. Within 2-3 weeks:
- Cartilage and bony callus formation
- Osteoblasts deposit trabeculae of woven bone
- Chondroblasts make cartilage which undergoes endochondral ossification to form bony callus
5. >3 weeks:
- As callus matures the portions that are not stressed are resorbed/remodelled
What factors affect fracture healing?
Local*:
- Inadequate immobilisation
- Significant displacement
- Infection (increased risk with open fractures, foreign body)
Systemic*:
- Diabetes
- Vascular insufficiency
- Systemic infection
- Malnutrition
- Osteoporosis
- Osteomalacia
- Smoking
- Corticosteroid use
- Age
*2 examples from each to pass
How does remodelling of callus occur?
Initial large volume of callus -> portions not physically stressed are resorbed, reducing callus size and altering contour
What are the causes of gout?
Hyperuricaemia*:
1. Primary gout (90%):
- Often idiopathic
- Overproduction (e.g. due to diet, unknown enzyme defects)
- Reduced filtration/excretion with normal production
2. Secondary gout (10%):
- Overproduction with increased excretion (e.g. leukaemias, tumour lysis, psoriasis, inborn errors of metabolism)
- Reduced excretion (e.g. chronic renal disease)
*needed to pass + 1 primary and 1 secondary cause
Describe the pathogenesis of acute gouty arthritis
- Hyperuricaemia
- Precipitation of urate crystals into joints* (in synovium/cartilage)
- Release of crystals into synovial fluid* (? trauma)
- Inflammatory response initiated*:
- Crystals phagocytosed by macrophages and neutrophils
- Release of inflammatory mediators by macrophages (ILs including IL-1B, cytokines) results in further neutrophil chemotaxis
- Neutrophils also release inflammatory mediators (free radicals, LTB4, lysosomal enzymes)
- Releases in acute arthritis
*needed to pass
What factors contribute to the conversion of asymptomatic hyperuricaemia into gout?
- Age
- Duration of hyperuricaemia
- Genetic predisposition
- EtOH
- Obesity
- Drugs (e.g. thiazides)
- Lead toxicity
Describe the pathogenesis of osteomyelitis
2/3 to pass:
- Haematogenous spread of organism to bone
- Extension from a contiguous site
- Local bone injury and direct organism entry
What organisms cause osteomyelitis?
- Staphylococcus aureus* (>80% of pyogenic osteomyelitis)
- E. coli
- Klebsiella pneumoniae
- Pseudomonas aeruginosa (especially IVDU or from genitourinary tract)
- Haemophilus influenzae
- Group B streptococcus (in neonates)
*needed to pass + 1 other
What pathological changes occur to the bone in osteomyelitis?
- Acute inflammation* (predominantly neutrophilic)
- Abscess* (sub-periosteal / surrounding soft tissue)
- Necrosis* (dead bone i.e. sequestrum)
- Involucrum (fibrous tissue and reactive bone deposition) forms around devitalised infected bone
*needed to pass
What are the possible sequelae of osteomyelitis?
- Resolution* after treatment with IVAbx and drainage
- Chronic (up to 25%)*:
- Acute flare-ups
- Pathological fracture
- Endocarditis
- Severe sepsis, AKI
- SCC in draining sinus tracts
- Sarcoma in infected bone
*needed to pass + 1 chronic complication
What is the pathogenesis of rheumatoid arthritis?
- Triggered by exposure of genetically susceptible host to an arthritogenic antigen resulting in chronic inflammatory change
- Continuing autoimmune reaction with activation of CD4 helper T cells and release of inflammatory mediators and cytokines, resulting in destruction of the joint
- Genetic susceptibility (association with HLA-DRB1 alleles)
- Environmental arthritogens (unclear what; various microbial agents implicated but none proven)
- Autoimmunity*: once inflammatory synovitis is initiated, autoimmune reaction with T cells results in chronic destruction
*needed to pass + 1 other
What are the extra-articular manifestations of rheumatoid arthritis?
2 to pass:
- Rheumatoid nodules (elbows, forearms, lumbar)
- Fibrinoid necrosis of lymphocytes
- Vasculitis (purpura, neuropathy, ulcers)
What are the long term complications of rheumatoid arthritis?
- Joint destruction
- Renal failure
Which organisms may cause septic arthritis?
- Staphylococcus*
- Streptococcus*
- Neisseria gonorrhoeae
- H. influenzae
- Gram negative bacilli (E. coli, Salmonella, Pseudomonas)
*needed to pass
