8. Musculoskeletal Conditions Flashcards

1
Q

Arthritis can be classified as:

Give example of each

A

= inflammatory or non-inflammatory

  • Rheumatoid arthritis (inflammatory) is caused by an autoimmune disease, so the body attacks itself causing increased inflammation which causes the joint pain,
  • osteoarthritis (non-inflammatory) is caused by mechanical stress on the joints
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2
Q

Difference between inflammatory and non-inflammatory

A

Inflammatory

  • symptoms aer prominent, including fatigue
  • Onset: Insidious, usually affecting multiple joints
  • morning stiffness: more than an hour
  • Effect on activity: lessen with activity, worse after periods of rest

Non-inflammatory

  • Symptoms: unusual
  • Onset: Gradual, one joint or a few
  • Morning stiffness: less than 30 mins
  • Effect on activity: worsen with activity, lessen with rest
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3
Q

What is Osteoarthritis?

A

= Flexible tissue at the end of bones wears down - progressive

Due to: excessive wear and tear OR non-specific inflammatory change (trauma)

Affects- - synovial joints in hands, hips, knees

-Causes:
loss of cartilage , joint space narrowing, painful, stiff bones, decreased weight baring abilities

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4
Q

Risk factors for OA

A
  • increased age
  • female gender
  • genetic susceptibility
  • nutrition
  • previous damage
  • increasing bone density
  • obesity
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5
Q

Two types of clinical presentation of OA

A

Primary: = most commonly affects all of:
• DIPS and PIP joints of fingers
• Carpometacarpal joint of thumb
• The hip, knee and metatarsophalangeal (MTP) joint of the big toe, and the cervical and lumber spine

Secondary. = occurs in any joint as a sequel to articular injury either
• Acute e.g fracture
• Chronic e.g. occupational overuse of a joint, metabolic disease, hyperparathyroidism or neurologic disorders

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6
Q

Management of OA –> risk Reduction

A
  • Rest inflamed joint, reduce loading, time in use & repetition
  • Use largest muscles and joints to do the job (ie. standing with hips and knees rather than pushing up with hands)
  • Use proper movement and handling techniques
  • Modify home equipment and use gadgets
  • Make exercise part of your every day life
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7
Q

OA management goals

A
  • Pt education about disease and management
  • Pain control
  • Improved function and decreased disability
  • Altering disease process and its consequences
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8
Q

Management Techniques of OA Non pharmacological (3)

A
  1. Exercise and physical therapy
  2. Weight reduction
  3. Thermotherapy -
    • ice packs for acute flares to reduce swelling and inflammation
    • Heat may promote relaxation, joint flexibility and blood flow however it may contribute to inflammation and oedema
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9
Q

Management of OA pharmacotherapy

A
  • Paracetamol (ensure max dose per day, SR-formulations)
  • NSAIDs (relieve pain associated with tissue damage and inflammation, may cause significant GI, renal and CVS issues)
  • Opioids if paracetamol and NSAIDs ineffective
  • Intra-articular corticosteroids (betamethasone, methylprednisolone, triamcinolone in Aus; injected into specific joints to minimise systemic adverse effects)
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10
Q

What is Rheumatoid arthritis?

A
  • Chronic systemic inflammatory autoimmune disorder characterised by inflammation and deformity of synovial joints & inflammations of surrounding tissues such as tendons, ligaments and muscles
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11
Q

Risk factors for RA

A
  • Genetic vulnerability
  • Family history
  • Pregnancy: postpartum period is most common for symptom development
  • Smoking
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12
Q

Early and late presentation of RA?

A

Early

  • Joint pain and stiffness
  • Weakness, fatigue, anorexia and weight loss
  • Low grade fever
  • Soft tissue swelling or effusion of affected joint
  • Accompanying warmth and redness
  • Most commonly affected joints - MCP in hand, Proximal interphalangeal (PIP), Wrist, MTP, Knee, Shoulder

Late stage

  • Joint and tendon destruction
  • Deformity and loss of function (ie. ulnar deviation, boutonniere, swan-neck deformities and hammer toes)
  • Multiple effects of pain, reduced mobility, fatigue and depression
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13
Q

Aim for Management of RA

A
  • Ultimately want to reduce remission, though this may be difficult to achieve
  • Reduce joint swelling, stiffness and pain
  • Preserve range of motion and joint function
  • Improve quality of life
  • Prevent systemic complications
  • Slow destructive joint changes
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14
Q

RA management Non-pharmacological

A
  • Diet PUFA rich diet, Standard changes to help reduce CV risk factors, limit alcohol intake
  • Weight If overweight, try and lose weight
  • Smoking cessation
  • Multidisciplinary team management (OT, PT)
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15
Q

RA management Pharmacological management - 3 main drug groups used

A
  1. Analgesics (important to educate pt that analgesia is not an alternative to DMARDs)
    o Paracetamol
    o NSAIDs mainly in early stages of disease
    o Sometimes opioids
  2. Corticosteroids
    - Used to rapidly and effectively control severe inflammation in early disease or active flares
    - Oral (mainly prednisolone) used in 3 ways:
    i. Initial ‘bridging therapy’ until DMARDs take effect
    ii. Management of acute flares
    iii. Combination with DMARDs when DMARD is suboptimal
  3. Disease modification anti-rheumatic drugs (DMARDs) including biological DMARDs
    - Mainstay therapy in RA due to ability to limit disease progression and relatively favourable toxicity profile
    - Preserve joint function, reduce symptoms, induce clinical remission while maintaining reasonable long-term safety
    - Response should be apparent in 12 weeks
    - Early DMARD use decreases rates of joint damage and appears to make disease easier to control compared to delayed DMARD use
    - Well tolerated and very safe when used correctly
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16
Q

What is Osteoporosis?

A

Osteoporosis = Disease characterised by low bone mass and micro architectural deterioration of bone tissue, leading to enhanced bone fragility and consequent increased fracture risk

17
Q

Risk factors of OP

A
  • Low body weight
  • oral glucocorticoid therapy
  • increased risk of falls
  • smoking
  • age
  • female
  • early menopause
18
Q

What is Glucocorticoid- induced osteoporosis (GIO)

A

= osteoporosis due to steroids

  • risk of GIO related to systemic steroid use

drugs of concern

  • thyroid hormones
  • PPIs
19
Q

Bone Remodelling in osteoporosis?

A

2 main cells are involved in bone remodelling
- Osteoclasts which carry out resorption of old bone
- Osteoblasts which build new bone
Bone remodelling occurs under the influence of various factors such as endocrine, humoral, nutritional, mechanical or genetic
- Abnormalities in one or more of these factors underlie the development of osteoporosis

20
Q

First line of treatment OP non-pharmacological?

A
  • Addressing modifiable risk factors
    o Smoking – aim for cessation/reduction
    o Diet
    o Exercise to increase bone mass by 1-3%
  • Review drugs that increase risk of #, ie. are there appropriate alternatives to drugs that
    o Decrease bone mass density
    o Increase falls risk
21
Q

First line management Pharmacological OP?

A
  • calcium
  • Vitamin D
  • Bisphosphonates
22
Q

Practice points for pharmacological OP management?

A

To promote optimal absorption:

  • dosing half an hour before food
  • minimise adverse effects
  • calcium supplements if required
23
Q

What is gout?

A

Gout refers to acute attacks ‘gouty arthritis’, occurrence of these attacks indicates chronic hyperuricaemia (ie. raised level of serum uric acid - SUA). Occurs when monosodium urate crystals form in synovial fluid of joints (most commonly MTP joint in foot – big toe)

24
Q

Cause of GOUT?

A

result from:

  • increased production of uric acid
  • reduced renal elimination of uric acid
25
Q

Risk factors of gout?

A
  • Obesity
  • Family history of gout
  • Renal disease
  • Excessive alcohol intake
  • Acute infection
  • Excessive meat & seafood intake
  • Drugs: diuretics, cytotoxic agents
26
Q

Management of GOUT aims:

A
  • Treatment of acute attacks to resolve symptoms
  • Prevention of recurrent attacks
  • Prevention/reversal of hyperuricaemic complications
27
Q

Pharmacological treatment of GOUT for acute attack - rapid

A

Anti-inflammatory therapy to terminate attack

  • NSAIDs to treat pain and inflammation (first line) – eg indomethacin 50mg
  • Various inc COX-2s
  • Colchicine to reduce inflammation –
  • Corticosteroids when NSAID or colchicine is contraindicated ie. due to significant renal impairment
28
Q

Pharmacological treatment GOUT chronic attacks

A
  • Xanthine oxidase inhibitors
    o Eg. Allopurinol (first line), febuxostat
    o Chronic urate lowering therapy (ULT) begun in between acute attacks
  • Probenecid: lowers SUA by increasing renal clearance (not as effective as xanthine oxidase inhibitors)
    o Usually used in intolerance/hypersensitivity to XO inhibitors