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Nursing Science 3 > WEEK 6 - Musculoskeletal Injury > Flashcards

WEEK 6 - Musculoskeletal Injury Flashcards

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1
Q

What are the functions of the musculoskeletal system?

A 
Primary: support & movement.
Secondary:
Protection
Storage (Ca2+)
Formation of blood cells (hematopoiesis)
Heat production
Venous return
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2
Q

What is vargus vs valgus?

A 
Vargus = r = round (bowleggednedd)
Valgus = knock knees
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3
Q

What are the key elements of assessment?

A 
Presenting problem (S&S, function & limitations)
Past Hx (injuries, surgical procedures, illnesses, meds)
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4
Q

What are the key elements of examination?

A 
Inspection
Palpation
Strength testing
ROM
Special tests
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5
Q

What is a closed fracture?

A

No communication between the external environment and the fracture site

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6
Q

What is an open fracture?

A

Communication between the fracture site and external environment
Considered a surgical emergency due to high risk of infection *breach in skin integrity

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7
Q

What is a pathologic fracture?

A

Occurs through an area of bone that has been weakened by disease
Can occur spontaneously with little or no stress with minor trauma.
Eg, bone cysts, cancerous lesions, osteoporosis, Paget’s disease

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8
Q

What is a stress fracture?

A

Results from repeated stress/forces

Common in unconditioned athletes

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9
Q

What is the pathophysiology behind bone healing?

A
  1. Disruption to periosteum & blood vessels in the cortex, marrow and surrounding soft tissues.
  2. Bleeding -> clot formation (haematoma) within medullary cavity. Blood loss can be significant.
  3. Disruption to BF - necrosis of the bone tissue surrounding fracture.
  4. Inflammatory response (vasodilation, extrusion, infiltration by leukocytes and mast cells. Blood flow to bone increases i.e. histamine release. Numerous cytokines released to promote healing. Within 48 hrs vascularisation of # areas - angiogenesis).
  5. Activation of fibroblasts and osteoblasts.
  6. Sub-periosteal procallus (fracture fragments reunited, gap bridged).
  7. Callus formation - collagen & matrix mineralised.
  8. Callus ossification within 2-3 weeks; remodelling
  9. Healing = 4-6 weeks in children, 6-8 weeks in adolescents, 10-18 weeks in adults. Function returns within 6mo.
  10. Bone is unique -> new bone without scar tissue.
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10
Q

What is a dislocation?

A

A complete separation or displacement of the surfaces of a joint.
Simple (no fracture) or complex (assoc fracture).

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11
Q

What is a sublaxation?

A

A partial shift of the surfaces of a joint and some contact remains.

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12
Q

How do dislocations and sublaxations present?

A

Pain & joint swelling due to accumulation of inflammatory exudate into joint/tendon/ligament.
Joint deformity (muscle contractions)
Limitation of movements (effusion, bone displacement)
Investigations & treatment.
Presentation & X-ray

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13
Q

How do you manage dislocations and sublaxations?

A

Immobilise (2-6 weeks) and exercise

Surgery for recurrent dislocations

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14
Q

What is a strain?

A

Tearing of tendon fibres
Occurs due to trauma or when the muscle is overstretched eg. lifting excessive weight (biceps)
Usually no external evidence; pain, stiffness, swelling

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15
Q

What is a sprain?

A

Tearing of ligament fibres.
Can occur at any joint.
Usually occurs when a joint is forced beyond its range of motion.

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16
Q

What is an avulsion?

A

Complete separation of a tendon or ligament from its bony attachment
Young athletes

17
Q

What is the difference between osteoblasts and osteoclasts?

A

Osteoblasts assist in bone formation.
Osteoclasts are involved in bone breakdown.
Both work in bone remodelling.

18
Q

What is the pathophysiology behind soft tissue injuries?

A
  1. Inflammatory exudate between the torn ends
  2. Macrophages & fibroblasts = repair
  3. Capillaries infiltrate the injured area during initial process & supply fibroblasts with nutrients
  4. Collagen formation begins 3-4 days after injury
  5. Increased tensile strength -> organised (mature) collagen; vascular fibrous tissue fuses the new & surrounding tissue into a single mass
  6. Tendon/ligament lack strength for 4-6 weeks

Danger = muscle contractions can pull the injured ends apart

19
Q

How do soft tissue injuries present?

A

Localised & sharp pain
Joint swelling, flexion deformities
Weakness or instability

20
Q

What is the pathophysiology behind osteoporosis?

A

Ageing and hormones = decreased osteoblast activity.
Menopause = decline in oestrogen, triggers rapid bone loss, increased cytokines stimulates osteoclast activity.

Secondary osteoporosis linked to:

  • alcohol abuse (decreases osteoblasts & Ca2+ absorption)
  • endocrine disorders
  • eating disorders
  • medications eg. corticosteroids, anti epileptics

Risk factors:

  • inactivity/lack of exercise increases rate of bone loss
  • poor Ca2+ intake & absorption
  • peak bone mass (determined by genetic factors, Vit D receptor molecule is inherited, race/gender)
21
Q

What are the clinical manifestations of osteoporosis?

A

Depends on bones involved
Early bone loss occurs without symptoms - ‘silent disease’
1. Bone deformity - gradual loss of height, vertebral collapse i.e. kyphosis (hunchback).
2. Spontaneous fractures

22
Q

What is the treatment for osteoporosis?

A

Weight bearing exercise
Ca2+ supplements
Mg2+ - prevents formation of brittle bones & is required for Ca2+ absorption
Calcitonin supplements - slows osteoclast activity
Biphosphonates - inhibit osteoclasts
SERMs - oestrogen like effects
Transdermal oestrogen replacement therapy? - oestrogen blocks osteoclast activity & prolongs life of osteoblasts by suppressing apoptosis but linked to breast cancer

23
Q

What is the pathophysiology behind osteoarthritis?

A

Characterised by significant changes in the composition and mechanical properties of cartilage lining the joint capsule - degeneration & loss of articular cartilage.
Decreased proteoglycan content with ageing & weakening of the collagen network caused by decreased synthesis of collagen due to ageing.
Breakdown of cartilage matrix (collagen, proteoglycans) due to increased enzyme activity (collagenases).
Cytokines stimulate production & release of proteases.
Underlying bone becomes sclerotic.
Cysts form.
Formation of abnormal bony outgrowths.

24
Q

What are the clinical manifestations of osteoarthritis?

A

Pain & stiffness in or around joint/s.
Nocturnal pain in the later stages of disease activity - numbness, tingling, prickling.
Enlargement of joints (swelling) - bone enlargement or proliferation of osteophytes, increased synovial fluid volume.

25
Q

What is the treatment for osteoarthritis?

A

No cure.
Directed toward pain relief & maintenance of mobility & improving function, preserving cartilage.
Exercise & rest - muscle strengthening exercises protect joint & decrease pain.
Weight reduction.
Intra-articular corticosteroid injections
Oral medications to reduce inflammation, swelling, pain.
Transcutaneous electrical nerve stimulation (TENS) for knee pain relief & stiffness.
Paracetamol and short acting NSAIDs - inhibit PG synthesis.

26
Q

What is the pathophysiology behind osteomyelitis?

A

Invading pathogen stimulates an inflammatory response:
- release of inflammatory medicators, vasodilation, oedema
- leucocytes infiltrate the area & phagocytosis starts
- formation of abscesses, small vessel thrombosis
- inflammatory exudate extends into marrow cavity
Infection causes weakness - predisposes bone to pathological fracture

In children: exudate can lift the periosteum off the underlying bone.

27
Q

What are the clinical manifestations of osteomyelitis?

A

Presentation varies with age, site of involvement and infecting organism.
Acute hematogenous occurs predominantly in children & affects long bones - abrupt onset.
Bacteraemia: chills, fever, malaise, pain on movement, elevated WBC & CRP.
Identify causative organism through blood & bone aspiration cultures.

Acute hematogenous in adults has insidious onset
Occurs as result of recent infection or instrumentation.
Vague symptoms: fever, malaise, weight loss, pain.

28
Q

What is the treatment for osteomyelitis for children & adults?

A 
Children: 
Parenteral then oral antimicrobials (6 weeks)
Surgical debridement is rare
Adults:
IV ABx for up to 6 weeks
Immobilise the affected part

Nursing Science 3 (21 decks)

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