Q1

Describe the pathological features of gout.

  • Hyperuricaemia
  • Acute arthritis
    • Precipitation of urate crystals into the joint/s
    • An event (sometimes minor trauma) releases crystals into synovial fluid
    • Cascade occurs resulting in intense inflammatory reaction (complement activated, chemotaxis of neutrophils and macrophages with phagocytosis and activation of lysosymal enzymes, leukotrienes, prostaglandins and free radicals
  • Chronic arthritis and formation of tophi which are urate deposits in synovium and periarticular areas
  • Nephropathy – deposition of urate in kidney as well as formation of uric acid stones

What are the causes of gout?

  • Primary
    • enzyme defect unknown (90%) (overproduction, underexcretion or increased excretion)
    • rare enzyme defect (HGPRT deficiency)
  • Secondary (10%)
    • Increased nucleic acid turnover e.g leukaemias (overproduction and excretion)
    • Chronic renal disease (decreased excretion)
    • Inborn error metabolism (complete HGPRT deficiency – Lesch-Nyhan syndrome) overproduction and excretion

Pass Criteria:

  • Primary PLUS one secondary to pass

 


Q2

What factors lead to osteoarthritis?

  • Genetic & environmental (mechanical)
  • Age – virtually ubiquitous (80-90%) after 65
  • Other exacerbating diseases e.g. Obesity, diabetes, injury, abnormal joints

Describe the pathological changes that occur in an affected joint.

  • Chondrocyte injury
    • Early OA: chondrocytes proliferate (cloning) and secrete inflammatory mediators, collagens, proteoglycans, and proteases which initiates secondary inflammatory changes.
    • Later OA: repetitive injury and chronic inflammation lead to chondrocyte drop out, marked loss of cartilage, and extensive subchondral bone changes

Describe the major clinical features of osteoarthritis.

  • Mostly asymptomatic <50y.o.
    • Deep, achy pain worse with use, morning stiffnesscrepitus, and limited ROM
    • Oligoarthritis 95% ( occas generalized/early)
    • Impingement on spinal foramina by osteophytes results in cervical and lumbar nerve root compression and radicular pain, muscle spasms, muscle atrophy, and neurologic deficits.
  • Common:  hips, knees, lower lumbar and cervical vertebrae, PIP, DIP of the fingers, 1st carpoMC joints, and 1st TarsoMT joints.   Not wrists, elbows, shoulders

 


Q3

Describe the morphology of osteoarthritis affecting a major joint.

  1. Early -1″ chondrocytes, i water, 1 proteoglycans
  2. Fibrillation/cracking/softening
  3. Sloughing, bone exposure
  4. Eburnation
  5. Dislodged cartilage and bone (joint mice)
  6. Fibrous subchondral bone cysts
  7. Osteophytes
  8. Synovium — fibrotic, inflammatory cells

Pass: 4 of 8

Describe the causes of secondary osteoarthritis.

  1. trauma
  2. congenital or acquired deformity
  3. Systemic disease eg diabetes
  4. Obesity

Pass: 2 of 4

 


Q4

Describe the morphology of the joint lesion in Rheumatoid Arthritis.

  1. Joints — perivascular inflammatory infiltration CD4+ helper T cells, plasma cells, Macrophages.
  2. increased vascularity
  3. Organising fibrin, rice bodies
  4. Neutrophil accumulation
  5. Osteoclastic – juxta articular erosion, subchondral cysts, osteoporosis
  6. Pannus
  7. Fibrous ankylosis —> bony ankylosis

Pass: At least 3

What are the extra articular manifestations of RA?

  1. Rheumatoid nodules – 25% forearm/elbow/occiput/lumbosacral.

Less frequent — lungs/spleen/heart/pericardium/valves/aorta.

  1. Fibrinoid necrosis — epithelioid cells/Lymphocytes/ Macrophage.
  2. Vasculitis- ptupura, ulcers, nail bed infarcts Digital – endarteritis (neuropathy/ulcers/gangrene)

Pass: At least 2

 


Q5

Describe the pathogenesis of gouty arthritis.

  1. Purine metabolism — 2 pathways.
  2. Hypoxanthine guanine phosphoribosyltransferase.
  3. Supersaturation — synovial fluid.
  4. Chemotactic, complement activation.

Macrophage free radical, leukotrienes, lysosomal enzymes. Hagemann.

  1. Acute arthritis — cartilage, joint damage

Pass: At least 3

What are the risk factors for primary gout?

  1. Age
  2. Genetic predisposition
  3. Alcohol
  4. Obesity
  5. Drugs
  6. Lead toxicity

Pass: At least 4

 


Q6

Describe pathogenesis of osteomyelitis.

PROMPT – What organisms cause osteomyelitis?

  • Local bone injury and organism entry, blood borne organisms, neighbouring source entry.
  • Organisms
    • Staphylococcus aureus >80% of pyogenic ones
    • Others: Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa from IVDU and GU, Haemophilus influenzae, Group B streptococcus
    • 50% no organisms found

Pass Criteria:

  • Bold + 1 other organism to pass

What changes occur to the bone?

  • Acute inflammation
  • Necrosis
  • Abscess
  • Sclerosis
  • Involucrum and sequestrum
  • Lytic focus and surrounding necrosis – periosteal elevation

Pass Criteria:

  • Bold to pass

What are the pathological sequelae of osteomyelitis?

  • Chronic – up to 25%
  • Resolve
  • Deformity and bone destruction
  • Severe sepsis
  • Pathological fracture
  • Endocarditis
  • SCC
  • Sarcoma

Pass Criteria:

  • Bold to pass

 


Q7

A 60 year old woman presents with severe jaw pain following a dental extraction a month earlier and is given IV morphine. Her X-ray reveals evidence of bony destruction in the mandible. Describe the pathogenesis of osteomyelitis.

PROMPT – How would this patient have suffered a bony infection of his jaw?

  • Local infection related to extraction of tooth
  • Blood borne
  • Spread from neighbouring gingival source

Pass Criteria:

  • 2/3

What organisms cause osteomyelitis?

  • Staphylococcus aureus majority >80% pyogenic
  • Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, from genitourinary tract or IV drug use
  • Haemophilus influenzae and GBS in neonates
  • Viruses, fungi, parasites, tuberculosis, syphilis
  • About 50% no organisms found.

Pass Criteria:

  • Staph aureus and 1 other

What changes occur in the bone?

  • Acute inflammation and necrosis, abscess formation
  • Sclerosis and involucrum formation
  • Deformity and sequestrum formation, Draining sinus
  • Characteristic lytic focus surrounded by zone of necrosis on X-ray, lifting of periosteum
  • 5-25% become chronic inflammation

Pass Criteria:

  • Bold to pass

What are the clinical consequences of osteomyelitis?

  • Resolution after treatment with IV antibiotics and drainage
  • Conversion to chronic osteomyelitis
  • Deformity and bony destruction
  • Severe sepsis syndrome, ARF

Pass Criteria:

  • 2 to pass

 


Q8

Describe the steps in fracture repair process.

  1. Haematoma fills fracture gap – provides fibrin mesh framework (hours)
  2. Influx of inflammatory cells, fibroblasts, new vessels (days)
  3. Haematoma organising –> Procallus
  4. Osteoprogenitors despoti trabeculae of woven bone – ossification –> bony callus (2-3 weeks)
  5. Callus matures, remodelling (6 weeks)

Pass Criteria:

  • 4 of 5 steps
  • Logical sequence

How does remodelling of callus occur?

  • Initial large volume of callus – portions not physically stressed are resorbed, reducing callus size/altering contour

Pass Criteria:

  • Physical stress
  • Resorption

What factors can impede the healing of a fracture?

  • Inadequate immobilisation
  • Marked displacement/soft tissues
  • Vascular compromise
  • Infection (open fractures/foreign bodies)
  • Systemic factors (nutrition, osteoporosis, smoking…)

Pass Criteria:

  • 2 bold and 1 other

How are fractures classified?

  • Complete/incomplete
  • Open/Closed
  • Comminuted
  • Displaced
  • Pathologic
  • Stress

Q9

Q9 MSK Path

Describe the abnormality.

  • Spiral/oblique fracture mid-shaft left humerus with displacement

Pass Criteria:

  • Bold

Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 18162

What structure may be injured in this fracture?

  • Radial nerve

Pass Criteria:

  • Bold