Musculoskeletal Pathophysiology - JOINTS Flashcards

1
Q

What is a Joint?

A

A joint is where 2 or more bones meet

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2
Q

What is the primary function of a joint?

A

To provide stability and mobility to the skeleton

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3
Q

What are the 3 main joint types?

A
  1. Synarthrosis
  2. Amphiarthrosis
  3. Diarthrosis
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4
Q

Main points about Synarthrosis joints

A
  • Formed when the gap bw 2 bones ossify and they become in effect, a single bone
  • Immovable
  • Fibrous
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5
Q

Main points about Aphiarthrosis joints

A
  • When 2 bones are linked by cartilage
  • Slightly movable
  • Cartilaginous
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6
Q

Main points about Diarthrosis joints

A
  • 2 bones are separated by a “joint cavity”
  • aka Synovial
  • Movable
  • Most familiar type of joint
  • Articular cartilage
  • joint cavity
  • Synovial fuid
  • Joint capsule
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7
Q

Types of Synovial Joints

A
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8
Q

Movement

A
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9
Q

Define dislocation

A

The displacement of a bone from its joint

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10
Q

What do you do when a joint is dislocated?

A
  • Joint must be restored to normal position, then joint immobilised for healing of torn ligaments and tendons
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11
Q

Carpal bones

A
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12
Q

What are four disorders of joints?

A
  1. Osteoarthritis
  2. Rheumatoid arthritis
  3. (Ankylosing) Spondylitis
  4. Metabolic joint disease e.g. gout
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13
Q

What is Osteoarthritis?

A

Age related disorder of synovial joints

  • “wear and tear” arthritis
  • fingers, spine, hips, knees
  • rare <40
  • >85% in >70s
  • overweight
  • men>women <55
  • can immobilise hips
  • usually does not cripple
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14
Q

Causes of osteoarthritis

A
  • Trauma - strains, sprains, joint dislocations, fractures
  • Long term mechanical stress - athletics, ballet, obesity
  • Joint instability - due to damaged supporting ligaments, capsule or tendons
  • Neurological disorders
  • Conjenital or aquired skeletal deformities
  • Hematologic or endocrine disorders - hemophilia, hyperthyroidism
  • Obesity
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15
Q

Pathophysiology of osteoarthritis

A
  • Loss of articular cartilage
  • Cartilage becomes thin → underlying bone unprotected
  • Bone becomes sclerotic (dense and hard)
  • Bone spurs can form and break off into synovial cavity → synovitis & joint effusion
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16
Q

Clinical manifestations of osteoarthritis

A
  • Pain
  • Stiffness
  • enlargment/sweling
  • muscle wasting
  • partial dislocation
  • deformity
  • use-related joint pain that is relieved by rest
17
Q

Diagnosis & treatment of osteoarthritis

A

Diagnosis

  • Clinical assessment
  • Radiological studies
  • CT scan
  • Arthroscopy
  • MRI

Treatment

  • Rest, motion exercies, crutches, weight loss, pain relief (analgesic) and anti-inflammatory medication
  • Intra-articular injection of high MW viscosupplements (hyaluronic acid)
  • Surgery - improve joint mvmnt, correct deformity/malignment, create new joint
18
Q

What is Rheumatoid Arthritis?

A

Systemic autoimmune disease associated with swelling and pain in multiple joints

More severe than osteorthritis

Body produces antibodies to fight infection → fails to recognise own tissues → misguided antibody “rheumatoid factor” attacks synovial membrane

19
Q

Rheumatoid arthritis: inflammatory autoimmune disease - Mechanism & what is ankylosis?

A
  • Inflammatory cells accumulate in synovial fluid
  • produce enzymes → degrade articular cartilage, fibrous joint capsule and surrounding tendoms
  • as articular cartilage degrades → joints ossify
  • joints solidly fuse & immobilized → ankylosis
20
Q

Rheumatoid arthritis: Clinical manifestation

A
  • Disease tends to be symmetrical
    • if RHwrist, then LHwrist too
  • Fever, malaise, rash, lymph node/spleen enlargment, Raynaud phenomenon (transient lack of circulation to fingers and toes)

Rheumatoid “hot spots” shown below:

21
Q

Rheumatoid arthritis: Incidence

A
  • 1-2% adults (>30yrs)
  • f:m = 3:1
22
Q

Rheumatoid arthritis: Diagnosis & treatment

A

Diagnosis:

  • Physical examination
  • Xray of joint
  • Serological tests for RF & circulating immunr complrxities
  • Diagnosis criteria (requires 4+)
    • Morning stifness >1hour
    • Arthritis >3 joint areas
    • Arthritis of hand joints
    • Symmetric arthritis
    • Rheumatoid nodules
    • Abnormal levels of serum RF present
    • Radiographic changes

Treatment

  • Rest, hot/cold packs, physical therapy
  • Antineoplastic medicaton, anti-inflam drugs, immunosuppressants, disease modifying antirheumatic drugs, corticosteroids
  • ↑calorie and vitamin diet
  • Surgical syneovectomy (early disease)
    • correct deformality/mechanical resistance
  • Arthroplasty/joint relplacement (late disease)
23
Q

What is Ankylosing Spondylitis?

A

The stiffening and fusion (ankylosis) of the spine and sacroiliac joints

  • An inflammatory joint disease
  • m:f = 3:1
  • Begins late adolecence/early adulthood (peak at ~20)
24
Q

How can you clinically diagnose Ankylosing spondylitis?

A
  • Low back pain/stiffness worse after prolonged rest
  • Pain eases with activity
  • Normal convex curve of lower back diminishes
  • Concavity of the upper spine increases
  • Thoratic-spine becomes rounded
  • Head and neck helf forward on shoulders
  • Hips are flexed
  • Pleuritic chest pain
  • Restricted chest movement
  • Pelvic tenderness
  • Tenderness in heals
  • Unable to sit on hard surfaces
  • Fibrotic changes in lungs
  • Cardiomegaly
  • Aortic incompetence
  • Amyloidosid
  • Achilles tendinitis
  • Fatigue
  • Weight loss
  • Low-grade fever
  • Hypochronic anemia
25
Q

Ankylosing spondylitis: Evaluation and treatment

A

Evaluation/diagnosis:

  • History & physical examination
  • X-ray
  • MRI
  • Serum analysis (HLA-B27)
  • Erythrocyte sedimentation
  • ↑ alikaline phosphatase

Treatment:

  • Physical therapy to maintain skeletal mobility
  • NSAIDs
  • Analgesic medication (supress pain and stiffness)
  • Symptom relief
26
Q

What is Gout?

A
  • A syndrome caused by an inflammatory response to uric acid production or excretion - hyperuricemia*
  • Leads to increased uric acid in synovial joint
27
Q

Gout: Risk factors

A
  • Age
  • Genetic predisposition
  • Excessive alcohol
  • Obesity
  • Certain drugs (e.g. thiazides)
  • Lead toxicity
28
Q

Pathophysiology of Gout

A
  • Most uric acid (protein metabolism) eliminated from body via kidneys
  • Crystalization in synovial tissue
    • Lower body temperatures → ↓solubility
    • Changes in pH → ↓solubility
    • Trauma → ↑crystal pptn
  • Leads to inflammatory response in the joints → tissue damage
29
Q

What is the incidence/time of onset of gout?

A
  • Rare in children, premenopausal women, and men <30
  • Males peak at ~40-50 yrs
  • Females, later than M
30
Q

Clinical manifestations/symptoms of Gouts

A
  • ↑ serum uric acid conc.
  • recurrent monoarticular arthritis attacks
  • urate crystal deposits around joint
  • renal disease → renal stones
  • trauma is aggrevating
  • abrupt attacks
  • primary symptom: severe pain, night, affected area hot, red, tender, swollen
  • 50% initial attacks in metatarsalophalangeal joint
  • 50% elbow, heel, ankle, knee, wrist
31
Q

How would you treat gout?

A
  • Antiinflammatory drugs
  • NSAIDs
  • Xanthine oxidase inhibitors
    • allopurinol
    • febuxostat
  • Ice may relieve pain
  • Hydrocortisone injection at joint
  • Antihyperuricemeid drugs
  • Low protein diet
32
Q

What is Arthroplasty?

A

The replacement of diseased joint with artificial device called prosthesis

Avaliable for:

  • finger
  • shoulder
  • elbow
  • hip
  • knee