Topic 4 Musculoskeletal Conditions Flashcards by Chloe Harris

3 bone cells

Osteoblasts
Osteoclasts
Osteocytes

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Role of Osteoblasts

Make bone in response to growth factors and mechanical stress on the bone

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Role of Osteoclasts

Make and secrete digestive enzymes that break up or dissolve the bone tissue. Related to monocytes/macrophages

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Role of Osteocytes

Derive from osteoblasts, or bone-forming cells, and are essentially osteoblasts surrounded by the products they secreted. Live in the Lacuna.

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Bone remodelling process

Activation by a stimulus
Resorption by osteoclasts
Formation by osteoblasts in successive layers
Whole process takes 3-4 months

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Bone repair process

Stage 1: Inflammation / haematoma formation
Stage 2: Procallus formation
Stage 3: Callus formation
Stage 4: Callus replacement

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Types of fractures

Transverse - Horizontal break

Linear - Vertical break

Oblique - Fracture at oblique angle

Greenstick - Break in only one cortex of the bone

Impacted - One end wedged into opposite end of inside fractured fragment

Compound - Skin broken

Spiral - Curves around cortices and may become displaced by twist

Comminuted - With two or more pieces or segments

Pathological - Transverse, oblique or spiral fracture of bone weakened by tumour pressure

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What is rhabdomyolysis

Breakdown of muscle tissue that releases a damaging protein into the blood

Excess myoglobin in urine. Muscle damage disrupts sarcolemma, releasing myoglobin acting as a nephrotoxin which can cause acute renal failure.

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What is compartment syndrome

Pressure build-up from internal bleeding or swelling of tissues. The pressure decreases blood flow, depriving muscles and nerves of required nourishment

Restriction of outward swelling caused by a collection of blood in injured tissue resulting in increased pressure.

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What is osteomyelitis

Inflammation of bone caused by infection, generally in the legs, arm or spine.

Exogenous: caused by open fractures, surgery or contiguous spread from infected local tissue.

Endogenous: caused by pathogens carried in the blood from sites of infection elsewhere in the body

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What is osteomalacia

Softening of the bones

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Aetiology of osteomalacia

Caused by impaired bone metabolism due to inadequate levels of phosphate, calcium, and vitamin D or because of resorption of calcium. Does not involve loss of bone matrix.

Vitamin D deficiency causes the decrease in [plasma calcium] -> increased synthesis and secretion of parathyroid hormone -> increased concentration and renal clearance of plasma phosphate -> decrease bone [phosphate] -> mineralisation cannot precede normally -> trabeculae in spongy bone become thinner and fewer -> Haversian systems in compact bone develop large channels and are irregular -> abnormal quantities of osteoid build up leading to deformities of long bone, pelvis, spine and skull.

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CM of osteomalacia

Diffuse skeletal pain
Tenderness
Pain in hips
Low back pain
Hesitancy to walk
Muscle weakness
Waddling gait
Uraemia
Psuedofractures

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Dx of osteomalacia

Blood test for serum Ca, serum phosphate (over 1.8mmol/L) and Vit D
Bone biopsy
Urinalysis (low phosphate)

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Tx of osteomalacia

Adjust serum Ca and Phosphate levels to normal
Suppress secondary hyperthyroidism
Renal dialysis
Renal transplant
Medications: calcium carbonate, vitamin D

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What is osteoporosis

Decreased bone density and demineralisation of bones.

Aetiology of osteoporosis

Imbalance between new bone formation and old bone resorption. Body fails to form enough new bone or too much old bone may be reabsorbed.

Bone matrix creates decoy receptor for cytokine -> cytokine binds to decoy -> no effect on osteoclast -> imbalance occurs in amount of cytokine, number of receptors on osteoclast precursors and number of decoy receptors -> imbalance leads to osteoporosis

CM of osteoporosis

Pain
Bone deformity
Fractures
Kyphosis

Dx of osteoporosis

X-ray
Bone mineral density test
Radiological examiniation
DEXA
Ultrasound
CT
Serum and urinary biomarkers

Tx of osteoporosis

Increase dietary Ca, Vit D, and magnesium
Oestrogen/progestin supplements
Raloxifene
Alendronate

What is arthritis

Inflammatory joint disease

Types of arthritis

Osteoarthritis: characterised by inflammatory damage or destruction in the weight bearing joints

Rheumatoid Arthritis: systemic, inflammatory auto-immune disease associated with swelling and pain in multiple joints.

CM of osteoarthritis arthritis

Asymptomatic
Aching pain
Referred pain
Stiffness
Swelling
Decreased ROM

Dx of osteoarthritis arthritis

H&amp;P
Clinical assessment
Radiological studies
CT scan
MRI
Arthroscopy

Tx of osteoarthritis arthritis

Resting inflamed joint Analgesia and anti-inflammatory drug therapy Weight loss if patient obese

CM of rheumatoid arthritis

``` Inflammation Fever Fatigue Weakness Anorexia Weight loss Aching Stiffness Painful/tender/stiff joints Joint deformities ```

Dx of rheumatoid arthritis

H&P Physical examination X-ray of joint Serological tests for rheumatoid factor

Tx of rheumatoid arthritis

``` Resting inflamed joint Hot and cold packs Physical therapy Patient education Anti-rheumatic drugs Corticosteroids Anti-inflammatory drugs Surgery used to correct deformity NSAIDs DMARDs: disease-modifying anti-rheumatic drugs ```

Aetiology of osteoarthritis arthritis

Structural damage to cartilage caused by genetic influences and other risk factors -> alteration in chondrocyte function -> stimulating enzyme release with degradation of collagen and proteoglycans -> cytokine release stimulates synovial inflammation and bone remodelling -> promoting muscle weakness

Aetiology of rheumatoid arthritis

Inflammatory autoimmune disease, cartilage damage caused by neutrophil and other cell activation in synovial fluid, cytokines stimulating release of pro inflammatory compounds causing chondrocytes to attack cartilage, synovium digests nearby cartilage.

What is gout

Syndrome caused by defects in uric acid metabolism characterised by inflammation and pain in the joints

Aetiology of gout

Excessive excretion of uric acid by the kidneys causes hyperuricemia. When high levels of uric acid in the blood and other body fluids accumulates, uric crystals form on connective tissue of joints throughout the body Slow urate excretion by kidney -> decrease glomerular filtration of urate, increased urate reabsorption -> monosodium urate crystals deposited in renal interstitial tissues -> impaired urine flow -> monosodium urate crystals form in the synovial fluid or membrane -> stimulate inflammatory response -> neutrophils attracted out of circulation -> phagocytosis of crystals -> neutrophils die releasing both the crystals and lysosomal enzymes causing tissue damage and stimulating further inflammation

CM of gout

``` Severe pain Redness and swelling in joints Pain in the joints, ankle, foot, knee, or toe Joint lumps, stiffness, or swelling Physical deformity Increase [serum urate] Renal disease ```

Dx of gout

H&P | Blood test

Tx of gout

``` NSAIDs Glucocorticoids Colchicine Uricosuric drugs Behavioural modification - diet, exercise, decrease alcohol Ice ```