Week 8: MSK Flashcards
Explain osteoporosis
a types of metabolic disease which is characterised by abnormal bone structures include;
- decreased bone density
- loss of structural integrity of trabecular (spongy) bone
- cortical (compact) bone becomes weak, thinner and more porous
What is the cause of osteoporosis?
altered metabolism
What are some risk factors for osteoporosis and link them to their pathophysiology?
Genetics → predisposed to low bone mass
Ageing → 65 years → due to endocrine disorders or malignancies → hormones (oestrogen, calcitonin and testosterone) inhibit bone loss
Gender → increased risk with women → 1:2 women, 1:3 men
- due to menopause and loss of oestrogen
Nutrition status → poor intake of calcium and essential vitamins such as D, excessive sodium, low magnesium, high caffeine intake → reduces nutrients for bone remodelling
Physical exercise → bones need stress for bone maintenance
Decreased sun exposure → loss of vitamin D
Lifestyle choices → caffeine, smoking and excessive alcohol consumption → reduce osteogenesis in bone remodelling
Medications → corticosteroids, heparin, thyroid hormone, aluminium containing antacids → affect calcium absorption and metabolism
Comorbidity → obesity, anorexia nervosa, hyperthyroidism, kidney failure → affects calcium absorption and metabolism
What are the two types of osteoporosis?
Generalised → involving major portions of the axial skeleton
regional → involving one segment of the appendicular skeleton
What diseases are associated with osteoperosis?
- inflammatory bowel disease
- intestinal malabsorption
- kidney disease
- rheumatoid arthritis
- diabetes mellitus
- cirrhosis of the liver secondary to alcoholism
- hyperthyroidism
- hypogonadism
What are the complications of osteoperosis?
- disability
- pathophysiological fractures (especially in the thoracic and lumbar spine, neck, intertrochanteric region of the femur and wrist)
Explain some preventative measures that can be done to reduce the risk of osteoporosis?
Lifestyle modification
- balanced diet across the lifespan including high calcium, vitamin D, use of calcium supplements with vitamin C
- regular weight-bearing exercise to improve bone mineral density (BMD)
- avoid excessive alcohol intake
- smoking cessation
- adequate sun exposure
- medical advice regarding medications
- management of comorbidities
Explain the pathophysiology of Osteoperosis
Bone remondeling is altered in a way that;
Bone reabsorption > desposition
osteoclast activity out weights osteoblast activity
Decreased serum Ca2+ triggers the parathyroid gland to release parathyroid hormone which simulates octeoclast activity (bone reabsorption) which puts more calcium in the blood.
Increase serum Ca2+triggers parathyroid gland to release calcatonin which stimulates osteoblast activity and therefore reduces blood Ca2+
the numbers fo the osteoblast cells are controlled by honmones, cytokines and other chemical messsengers (hence why they speed up in puberty and slow down at menopause)
- cytokine binds to osteoclast precursor cell receptors (cells that combine to form osteoclasts) → osteoclast precursor cells multiply and become activated → bone matrix creates a decoy receptor for the cytokine → if cytokine binds to this receptor = no effect on osteoclasts
- balance between amounts of cytokine, number of decoy receptors and the number of osteoclast precursor receptors determine the rate at which bone is resorbed → imbalance → osteoporosis
- rate of bone resorption > rate of bone formation → bone loss → bones become weak, brittle, fragile and progressively porous → clinical manifestations and complications such as fractures
What are some clinical manifestations of osteoperosis?
Most common clinical manifestations:
- pain → joints, bone
- bone deformity
- fractures → most common → long bone fractures, distal radius, ribs, vertebrae
- kyphosis
- diminished height
- low energy, fatigue
Fractured neck of femur → more common with elderly females
Rare clinical manifestations
- fat embolism
- pulmonary embolism
- pneumonia
- haemorrhage
How is osteoporosis diagnosed?
- PMHx
- clinical presentations and recently experinces clinical manifestations
- investigations
What are some investigations that may help diagnose osteoporosis?
Dual-energy x-ray absorptiometry (DEXA) scan → results are presented as a T-score, for every reduction in T-score, the risk of a fracture occurring doubles
Laboratory studies → calcium, phosphate, vitamin D, phosphate, thyroid function, haematocrit, erythrocyte sedimentation rate (ESR), sex hormones → to determine risk of low bone density
X-Rays → to exclude other possible medical diagnoses
Bone mineral density (BMD) testing → to determine risk of fracture by comparing a person’s current degree of loss of bone density with the ‘typical’ bone density of a young adult
- normal bone density → osteopenia (low bone density) → osteoporosis → severe osteoporosis
How can osteoporosis be treated?
The aim of treatment:
- slow down the rate of calcium and bone loss
- prevent deterioration
Includes:
- increasing dietary intake of calcium to 1500mg / day
increase vitamin D with supplements → enables intestinal absorption of calcium
- decrease intake of phosphorus → can neutralise calcium
- increase intake of magnesium → increases bone growth by stimulating cytokine activity in the bone
- postmenopausal women may be given oestrogen and progestins to prevent bone loss but this is high risk for the development of breast cancer, stroke and pulmonary embolism
- implementation of weight-bearing exercises → slows down bone loss and reverse demineralisation, increased bone strength decreases risk of falls
What are some key nursing considerations when caring for someone with osteoporosis?
- promoting knowledge, understanding and education about osteoporosis and the treatment options
- management of pain to promote and improve quality of life → pharmacological and non-pharmacological
- injury preventions - falls
- support
What should you assess for a patient with osteoporosis?
- family history of osteopenia and osteoporosis
- previous fractures and recent injuries, trauma or falls → the patient may have a pathological fracture without trauma
- lifestyle factors
- onset of menopause
- use of steroids, caffeine, smoking and alcohol
What education should be provided to someone with osteoporosis?
- diet
- lifestyle modification
- exercise advice
- pain management
- injury prevention
- support
What are the negative effects of back pain?
- mental health impact → anxiety and depression
- leading cause of activity limitation and absence from work
- the right treatment is often difficult to find
- leading cause of health system expenditure
What are the functions of discs of the spine?
- absorb shock
- promote/ facilitate movement
- protect joints
What is the pathophysiology of degenerative dics disease?
Cause= structural degeneration
The drying/aging of the soft gel like insides of the discs coupled with the thinning of the harder outer layer causes a rupture hich is very painful.
DDD occurs as a result of normal ageing processes combined with the deterioration and herniation of the intervertebral discs.
Can involve the cervical, thoracic and lumbar spinal regions.
What are the risk factors of degenerative disc disease?
- ageing → greatest risk
- family history, genetics
- excessive strain → heavy lifting, repetitive movement
- prolonged sitting / poor posture
- modifiable risks → smoking, obesity, sedentary lifestyle
What are some complications fo degenerative disc disease?
- chronic debilitating pain
- incontinence
- limb weakness
- altered sensation to limbs
- herniated disc
- osteoarthritis
- bone spurs
- spinal canal compression
- spinal stenosis
Explain the pathophysiology of degenerative disc disease
DDD results in the intervertebral discs losing elasticity, flexibility and shock-absorbing properties due to progressive degeneration, repeated stress or as a result of trauma to the spine.
The nucleus pulposus (gel like disc in centre) starts to dry and shrink-> limits intervertebral discs to absorb and distribute pressure loads between the vertebrae-> the load is transferred to the other annulus fibrosus-> degredation of this structure-> nucleus pulposus seeps/herniates though the toen annulus fibrosis= herniated disc
->this places pressure on near by nerves as those that emerge from spinal cord through verterbral foraemen. are pressed against= radiculopathy and altered sensation in limbs
Describe a herniated disc
a condition that occurs when the spinal intervertebral disc bulges out between the vertebrae
What are the classifications of back pain?
Localised → pain occurs when area palpated
Diffuse → spread over a large area, generated from deep tissue
Radicular → irritation of the nerve root, often caused by a herniated disc e.g. sciatica
Referred → pain felt in one area but originates in another e.g. kidneys, abdomen, bladder, ovaries
What are some common clinical manifestation of DDD?
Radiculopathy
- results from constant pressure on the nerve endings in the involved region of the spine → altered sensation and motor responses
- cervical radiculopathy → pain felt in shoulders, arms or hands
- lumbar radiculopathy → pain felt in hips, buttocks or down the posterior region of the legs
- usually described as continuous mild to moderate pain, but can be severe debilitating pain
- pain can be sharp, sudden onset, intense, stabbing, hot
- pain eases with position changes
- pain increases with prolonged sitting and activities that involve bending or twisting, heavy lifting
spinal instability → sensation of spine ‘giving out’ or locking up and feeling that the spine is unable to provide basic support
- altered lower limb sensation
- decreased lower limb motor function → strength, weight-bearing, range of movement
- loss of spinal flexibility
- bone spurs
- muscle spasms / tension
- spinal deformity
How is DDD diagnosed?
Diagnosis can be made on a combination of:
Past medical / surgical history
Clinical presentation including recent / current clinical manifestations
Imaging → to determine the location of structural defects, severity and localised damage
- x rays
- CT scan
- MRI
Explain the treatment of DDD
Treatment for DDD is usually conservative with the majority of people with DDD recovering and includes:
supportive care
- enhance quality of life
- limitation of spinal movement until symptoms subside
- spinal brace, corset, belt - improve mobility
- exercises to increase back and core strength → at least twice a week
pharmacological management → aimed to reduce pain, reduce inflammation and improve movement
- NSAIDs
- corticosteroids
- analgesia - for example, tramadol
- opioids - short term only
- muscle relaxants
- tricyclic antidepressants → amitriptyline
- anticonvulsants → gabapentin
surgery
- viewed as the last option
- is rarely required because it is not always successful and may exacerbate the symptoms
- in extreme cases of severe DDD (nerve root or spinal cord damage) with failed conservative management, surgery may be the only option and can include:
- microdiscectomy
- laminectomy,
- hemilaminectomy or laminotomy
- discectomy or foraminotomy
What should be includied in the fofoced part of anursing assessment for someone with DDD?
straight leg raising test → patient is unable to perform a straight leg raise when lying supine → positive result for DDD → indicates nerve root irritation
from sitting position on edge of bed (without feet resting on floor), ask the patient to raise one leg at a time and flex their foot at 90⁰ → back / leg pain will be reproduced with DDD
other causes of back pain will not result in pain with this movement
dermatome assessment → to assess for paraesthesia
neurovascular assessment → to assess for motor function i.e. limb weakness
Additional Assessments
- pain assessment
- falls risk assessment
- skin integrity check
What is the nursing management of someone with DDD?
Non-pharmacological management
- heat pack
- ice pack
- assistance with ADLs as directed by patient
- massage
Education
- explanation of condition and management plan
- dietary advice - high-fibre diet, increase water consumption
- symptom management
- medication regimen
- lifestyle modification - weight loss, cessation of smoking, minimise alcohol consumption
Support
- psychological
Explain arthritis
inflammatory joint disease that can be either infectious or non infectious.
Who is arthritis more prevalent in?
- inflammatory joint disease
- affects >15% of the population
- rate increases with age → prevalence will increase with our ageing population
- majority of cases diagnosed are women > 75 years
- there are >100 different types of arthritis
- most common → osteoarthritis, rheumatoid arthritis and gout
What are the risk factors for arthritis?
- socioeconomic status → living in low socioeconomic areas increases the risk of developing arthritis
- modifiable risks → obesity, smoking, excessive alcohol intake, poor diet, sedentary lifestyle, stress
- age
- genetics → family history
- occupation
- endocrine disorders
Further explain the two types of arthritis
Infectious
- invasion of the joint by bacteria, mycoplasma, viruses, fungi, protozoa → inflammation
- invasion occurs through traumatic wound, invasive procedure (contaminated needle, surgery) or transferred in bloodstream from site of infection elsewhere in the body (bones, heart, blood vessels)
e. g. septic arthritis
non-infectious
- inappropriate immune response → rheumatoid arthritis, psoriatic arthritis
- deposition of urate crystals in the synovial fluid → gout
Explain osteoarthritis
A chronic, slow and progressive, non-inflammatory disorder of a synovial joint → cartilage destruction and joint degeneration
process rather then specific illness
Effects women > men
- the most prevelant and disabling of all joint disorders.
How is osteoarthritis classified?
- primary or secondary
- localised or generalised
- early/moderate/advanced
What causes osteoarthritis
Usually by a known event or condition e.g. Post inflammation disorder - rheumatoid arthritis - Septic joint
Trauma
- fracture/dislocation
- ligament/meniscus injury
- cumulative occupational or recreational trauma
Mechanical stress
- repeated activity
Inflammation
- release of enzymes in response to inflammation can affect cartilage and cause degradation
Anatomic or bone disorders
- hip dysplasia
- avascular necrosis
- paget’s disease
Metabolic disorders
- calcium crystal deposition (gout), acromegaly, Wilson’s disease
menopause
- due to low oestrogen
What are some risk factors for osteoarthritis?
- increased age
- modifiable risks
- obesity → hip and knee OA
- limited exercise - previous joint damage or trauma → anterior cruciate ligament (ACL) injury from quick movement changes with football / netball
- repetitive use → “wear and tear” occupations → carpet layer, plumber
- anatomical deformity → malalignment
- metabolic conditions
- genetic predisposition → congenital hip dysplasia, biochemical abnormalities in collagen and bone formation → structural damage to cartilage
Explain the pathophysiology of osteoarthritis
OA is multifaceted with a combination of articular cartilage degradation, bone stiffening and reactive inflammation of the synovium.
- the collagen matrix becomes disorganised and proteoglycan content within the cartilage is lost.
risk factor-> cause -> joint changes occur
Progressive loss of articular cartilage → new joint tissue forms in response to cartilage destruction → cartilage becomes dull, yellow, granular, soft and less elastic (less able to resist wear with heavy use) → cartilage repair cannot keep up with cartilage destruction → fissuring / erosion of articular surfaces → osteophytosis (new bone formation of the joint margin) → subchondral bone changes → variable degree of synovitis (early stiffness and pain) → clinical manifestations develop as a result of contact between exposed bony joint surfaces → thickening of the joint capsule caused by constant friction of the two bone surfaces
Explain the clinical manifestations of osteoarthritis
- pain
- mild discomfort to severe disability
- can be referred to groin, buttock, medial side of thigh / knee
- due to synovium inflammation, joint capsule or ligament stretching, irritation of the nerve endings in the periosteum over osteophytes, microfracture of the trabecular, intraosseous hypertension, bursitis, tendinitis and muscle spasm
- early stages → rest relieves pain
- later stages → pain with rest, sleep is disturbed, mobility impaired with difficulty sitting down and getting back up
- joint stiffness → most commonly experienced in the morning for less than 30 minutes and worse after periods of inactivity / static inactivity
- crepitus with movement
- asymmetry of joints
- joint effusions
- functional impairment
- joint deformity → specific to involved joint e.g. bowed legs, altered gait, one leg shorter than the other
Further, explain inflammatory arthritis
a group of diseases that results in joint inflammation, swelling, stiffness, decreased range of movement
- have potentially disabling clinical manifestations
- symptoms worsen with age
Multiple types of inflammatory arthritis exist, each with a different cause;
- wear and tear
- infections
- underlying disease
- overactive immune response
- deposit of urate crystals in the synovial fluid
- can affect a single joint or multiple joints simultaneously
Explain rheumatoid arthritis
- a chronic systemic, autoimmune disease
- inflammation of the connective tissue in synovial joints
- affects multiple joints bilaterally
Characterised by;
- periods of remission with exacerbations
- prevalence increases with age
- more common in women
- worse in colder climates
- most commonly affects fingers, wrists, elbows, feet, ankles, knees
- can also affect other tissues in the body such as lungs, heart and eyes
What is the cause of rheumatoid arthritis?
Unknown
- likely genetic and environmentally triggered
- long term smoking
- positive family history
