W9 Muscoloskeletal dysfunction Flashcards

1
Q

Describe the main types of joint and muscle injuries and their common causes.

A

Sprains & strains: forcible mechanical overload, twisting or stretch at joints.
Strains: stretch injury due to mechanical overload of muscle &/or tendon
Sprain: excessive or abnormal movement of join damages ligaments.

Dislocations: displacements or separation of bone ends (joints).
Causes:
- Congenital
- Traumatic
- Pathological 

Most common sites are shoulder and knee sits. Mostly synovial joints + hinge joints.

Degrees of muscle strain

  1. Mild (1st degree) : minor swelling and discomfort, little to no change to muscle strength/movement.
  2. Moderate (2nd degree) strain: Moderate to severe pain, damage to muscle, some loss of strength.
  3. Severe (3rd degree) strain: tear across muscle belly, severe pain & loss of function, surgical intervention required.
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2
Q

Explain how skeletal trauma develops, outlining the risk factors.

A
Skeletal fractures occur when the force applied to a bone exceeds the tensile or compressive strength of the bone.
→ young males (adolecent)
→ elderly
Risk factors:
- Bone disease
- Poor nutrition 

Fracture cause damage to periosteum, blood vessels and other surrounding structures.

Clinical manifestations:

  • Unnatural bone alignment
  • Initial numbness followed by severe pain
  • Impaired sensation
  • Muscle spasm
  • ALtered mobility
  • Tenderness and swelling
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3
Q

PICOutline and describe the types of bone fracture.

A
  • Open (compound)
  • Closed
  • Complete
  • Incomplete
  • Spiral - twisting
  • Comminuted (bone splinting)
  • Longitudinal (runs along length of bone)
  • Segmental fracture
  • Oblique
  • Greenstick
    Avulsion: when a sction of bone at the site of ligamnt is torn away with a fragment of bone attached.
  • Torus: compression and crushing
  • Physeal
  • Pathophysiological
  • Compression
  • Depressed: bone pushed inwards
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4
Q

Describe the stages of fracture repair in healthy bone.

A
  1. Haematoma
    - clot forms in medullary cavity at fracture site.
    - Dead bon at fracture site & other debris stimulates inflamation
  2. Fibrocartilgenous callus formation:
    - Angiogenesis vascular tissue invads fracture site and blood flow ↑
    - Osteoblasts are stimulated and form a procallus - collagen deposition
  3. Ossification:
    - Procallus becomes mineralised → callus
  4. Bone remodelling: osteoblasts and osteoclasts continue to reorganise bone and unnecessary callus is resorbed.
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5
Q

Outline three factors that can affect the process of fracture repair.

A
  1. General health of the person
  2. Nutritional status
  3. Adequacy of initial tx
  4. Age.

ABNORMAL FRAC repair:
Malunion: incorrect healing resulting i a deformity.
Delayed union: failure of fracture to unite within a normal time period.
Nonunion: failure to unite: leads to pain and fracture side mobility, can result in muscle atrophy and loss of range of motion,

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6
Q

Explain the pathogenesis of rhabdomyolysis and its progression to crush syndrome. Learning

A

Compartment syndrome: odemoa and swelling cause increased pressure in muscle compartment.

  • ↓ blood flow - blood vessel occlusion
  • possible muscle and nerve damage
  • Ischemia may cause muscles and nerves to die (limb may need to be amputated.
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7
Q

Define osteomyelitis and briefly explain how this condition may be treated.

A

Acute or chronic infection of the bone due to

  • Direct access via open fracture
  • blood borne
  • skin infections in vascular insufficiency

CAUSE:
_ staphluococcus aureus
- bind to colagen → internalisd osteoblasts.

TX: indentification of infectious organism and tx with parenteral and oral antibiotics, in concert with pain control. May also require surgical debridement and surgical drainage of infection site. Amputation may be required.

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8
Q

Explain how osteoneocrosis may develop and describe the clinical manifestations.

A

Bone death due to interuption of blood supply.

DUE TO:
- Mechanical trauma to vasculator
- THrombosis and embolism
- Vessel dysfunction
- Prior corticosteriod use
RISK FACTORS:
- Long-term use of steroids
- Heavy alcohol intake
- Direct injury to bone or join
- Chemotherapy or radiation
- Organ transplant 
- Diseases

CLINICAL MANIFSTATIONS

  • Insidiois no symptoms
  • Pain when prssir or weight applied to joint
  • Inability to use limb
  • Joint replacement
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9
Q

Define rheumatic disorders and exemplify

A

Characterised by inflammation that affects the connecting or supporting structures of the body - most commonly the joints but sometimes the tendons, ligaments, bones and muscles.
CLASSIFICATION:
Primary - du to systemic autoimmune response.
Secondary - due to degenerative processes with the joint.

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10
Q

Define osteoarthritis and describe its aetiology

A

Osteoarthritis (OA): results from th slow destruction of articular cartilage causes bonee to rub on bone.

CLASSIFICATIONS:

  1. Idopathic OA: wear and teear of joints
    - Can be localisd
    - Generalised affects 3 or morejoints
  2. Secondary OA: metabolic disorder, congenital or trauma.

Risk facts:
Jobs requires hard labor or repetitive motion
- Obesity

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11
Q

Describe the clinical manifestations of osteoarthritis

A
Mild symptoms worsn over time.
- Pain and stiffness associated with joint degeneration
- Worsened by activity and relieved by rest.
Joint enlargement
- Effusion
- Crepitus
- Bone spurs
- Joint instability 

COMMON SITES:

  • Hips
  • Kns
  • Crvical vertebrae
  • Proximal/ distal joint of hands.

DIAGNOSIS:
- x-ray, MRI, ultrasound.

TX: analgesics

  • anti-inflammatory drugs
  • chondroprotective injections

NON-DRUG: heat and cold application

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12
Q

Describe the manifestations, diagnostic and tx of osteoporosis

A
Diagnosis:
DEXA scan
- Not diagnosd until fracture happens itself.
PREVENTION: 
- Smoking cessation
- Reduction of cola-cased bevs
- ↑ calcium vit D 
TREATMENT:
Drugs to prevent/slow bone resorption
- gonadal hormones
- Calcitonin
- fluroides
- bisphosphonates 

BISPHOSPHONATES:

  • Inhibit digestion of bon by encouraging osteoclasts to ndeergo apoptosis, thus slowing bone loss.
  • Side effect: osteonecrosis > 2 years
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13
Q

Define rheumatoid arthritis and describe its aetiology

A

Theumatoid arthritis: autoinmmune disorder involving a chronic inflammatory response. SEEN IN BOTH JOINTS. Bilateral involvement of joints. The cause of the chronic inflammation uncrtain.

  • Chronic systemic autoimmun disordre,
  • most common form of autoimmune arthritis
  • Cause is unknown
  • Various factors may b involved
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14
Q

Explain the pathogenesis of rheumatoid arthritis

A

Involves the early changes occuring within the synovium and disease progression that leads to erosion and the formation of pannus.

  1. Antibodies in RA bind with other proteins and tissues.
  2. Create immune complexes that cause inflammation
  3. Enzymes cause further joint tissue degradation
  4. Pannus forms
  5. Osteoclasts cause underlying bone to demineralize
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15
Q

Describe the clinical manifestations of rheumatoid arthritis

A

The most commonly affects joints are fingers, feet, wrists, elbows, ankles & knees.
Inflammation causes pain, tenderness, swelling, stiffness, warmth, joint deformity and loss of function.
Loss of function is followed by muscle atrophy
- Dislocation of joints can occur.

EXTRA-ARTICULAR SYSTEMIC MANIFESTATIONS OF RA:

  • Fatiguee, anorexia, wight loss, generalised aching, low grade fever
  • Anamia
  • Rheumatoid nodules
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16
Q

Outline the diagnosis and treatment methods currently employed to treat rheumatoid arthritis

A
DIagnosis:
- BLood tests
- Anti-cyclic citrullinated peptid (CCP) tst
- Examination of synovial fluid
TX: → aims to control symptoms
Pharmacological tx:
- NSAIDs
- ↓ dos oral corticostroids
- Disease-modifying antihumatic drugs (DMARDs)
- Intra-articular steroid injction
17
Q

Define DMARDs and explain the mechanism of action of three subgroups.

A

GENETIC + ENVIROMENTA. Disease-modifying antirheumatic drugs comprise a group of immunosuppressant/anti-inflammatory drugs that target the cellular responses involved in rheumatoid arthritis. Stopping inflammation at cytokine level.

Most common:

  • Methotrxat
  • Leflunomid
  • Sulfasalazin
18
Q

Define ankylosing spondylitis and outline its clinical manifestations.

A

(Spondyloarthropathies: group of inflammatory disorders affecting primarily the axial skeleton)
Ankylosing spondylitis: chronic, systemic, inflammaatory erosion of tendon and ligament attachment sites at joints of axial skeleton. Results in bone bridges forming betwene adjacent bone. Inflxibility,
PRODUCES: pain, stiffness, loss of motion in vertebral colum

Extraskletal manifestations: wight loss, fever, fatigue.

TX:
Control pain
Reduce inflammation

Drives inflammation via mast cells etc. Changes osteoclasts

19
Q

Outline treatment aims for the four common pharmacological agents used to treat gout.

A

NSAIDs:
- Drug of preference - indomethacin
- Low does asprin should not b eused due to retention of uric acid.
Colchicine:
anti-inflammatory effects due to inhibition of microtubules formation which then prevents leukocyte migration and phagocytosis. Also inhibits leukotriene B production.
Uricosuric agents: affect proximal renal tubule to ↓ uric acid reabsorption.
Allopurinol: inhibits xanthin oxidas → ↓ synthsis of uric acid

20
Q

Explain how muscular dystrophy is inherited and describe its clinical manifestations.

A

DYstrophy: Most common is Duchenne.
X-linked recessive disorder, thereforee males are affected. The Mutation in dystrophin gene.
Muscle cells unable to maintain structural integrity. No cur.

MANIFESTATIONS: Muscle is rplacd by fat and CT.
- Weakness starts in pelvis girdel

21
Q

Define rickets and describe its causes, manifestations and tx.

A

Caused by a lack of vit D, calcium or phosphorus. Can occur as a result of having dark skin, lack of xposure to sun light, nutritional deficiencies and disorders of the liver, kidny and small intestine.

CLINICAL MANIFSTATIONS: rducd longitudinal growth, widening of epiphyseal regions, lower limb deformities, joint swlling, tooth malformation, dental caries.

TX: sunlight, vit D.

22
Q

Define gout and outline it’s clinical manifestations

A

Gout is a form of arthritis that results from the deposition of uric acid crystals within joints and other structures. Elevated serum uric acid. Uric acid is the end product of purine mtabolism. Its a weak acid that is ionisd

Unable to get rid of uric acid via h renal system, therefore accumulates.

CLINICAL MANIFESTATIONS: ↑ in serum urate concerntration
Gouty toph