Week 8: MSK Flashcards
1
Q
Explain osteoporosis
A
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
2
Q
What is the cause of osteoporosis?
A
altered metabolism
3
Q
What are some risk factors for osteoporosis and link them to their pathophysiology?
A
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
4
Q
What are the two types of osteoporosis?
A
Generalised → involving major portions of the axial skeleton
regional → involving one segment of the appendicular skeleton
5
Q
What diseases are associated with osteoperosis?
A
- inflammatory bowel disease
- intestinal malabsorption
- kidney disease
- rheumatoid arthritis
- diabetes mellitus
- cirrhosis of the liver secondary to alcoholism
- hyperthyroidism
- hypogonadism
6
Q
What are the complications of osteoperosis?
A
- disability
- pathophysiological fractures (especially in the thoracic and lumbar spine, neck, intertrochanteric region of the femur and wrist)
7
Q
Explain some preventative measures that can be done to reduce the risk of osteoporosis?
A
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
8
Q
Explain the pathophysiology of Osteoperosis
A
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
9
Q
What are some clinical manifestations of osteoperosis?
A
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
10
Q
How is osteoporosis diagnosed?
A
- PMHx
- clinical presentations and recently experinces clinical manifestations
- investigations
11
Q
What are some investigations that may help diagnose osteoporosis?
A
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
12
Q
How can osteoporosis be treated?
A
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
13
Q
What are some key nursing considerations when caring for someone with osteoporosis?
A
- 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
14
Q
What should you assess for a patient with osteoporosis?
A
- 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
15
Q
What education should be provided to someone with osteoporosis?
A
- diet
- lifestyle modification
- exercise advice
- pain management
- injury prevention
- support
16
Q
What are the negative effects of back pain?
A
- 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
17
Q
What are the functions of discs of the spine?
A
- absorb shock
- promote/ facilitate movement
- protect joints
18
Q
What is the pathophysiology of degenerative dics disease?
A
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.
19
Q
What are the risk factors of degenerative disc disease?
A
- ageing → greatest risk
- family history, genetics
- excessive strain → heavy lifting, repetitive movement
- prolonged sitting / poor posture
- modifiable risks → smoking, obesity, sedentary lifestyle
20
Q
What are some complications fo degenerative disc disease?
A
- chronic debilitating pain
- incontinence
- limb weakness
- altered sensation to limbs
- herniated disc
- osteoarthritis
- bone spurs
- spinal canal compression
- spinal stenosis
21
Q
Explain the pathophysiology of degenerative disc disease
A
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
22
Q
Describe a herniated disc
A
a condition that occurs when the spinal intervertebral disc bulges out between the vertebrae
23
Q
What are the classifications of back pain?
A
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
24
Q
What are some common clinical manifestation of DDD?
A
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
25
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
26
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
27
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
28
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
29
Explain arthritis
inflammatory joint disease that can be either infectious or non infectious.
30
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
31
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
32
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
33
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.
34
How is osteoarthritis classified?
- primary or secondary
- localised or generalised
- early/moderate/advanced
35
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
36
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
37
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
38
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
39
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
40
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
41
What is the cause of rheumatoid arthritis?
Unknown
- likely genetic and environmentally triggered
- long term smoking
- positive family history
42
What are some risk factors for rheumatoid arthritis?
```
- advancing age → affects more people in their 60's
smoking
- gender → women more likely to be diagnosed than men
- obesity
- stress
- history of live births
- genetics
- infection
- surgery
```
43
What are the classifications of rheumatoid arthritis?
- number of joints involved
- serology inflammatory markers → CRP and ESR
- duration of symptoms
44
Explain the pathophysiology of rheumatoid arthritis
- affects the synovial membrane first, before spreading to articular cartilage, fibrous joint capsule and surrounding ligaments and tendons
initial immune response to an antigen → triggers formation of abnormal IgG (immunoglobulin G) → autoantibodies (rheumatoid factor [RF]) develop → RF combines with IgG immune complexes → inflammatory response → inflammatory phagocytes (neutrophils, macrophages) ingest immune complexes → release enzymes → cartilage breakdown and thickening of synovial lining → T-helper cells (lymphocytes) activated → produce more RF → synovium digests nearby cartilage → stimulates further inflammatory response
As a result of this ongoing inflammatory response cycle
synovial membrane thickens → increased pressure on surrounding vessels → compromises blood supply and increases cell metabolism → hypoxaemia, metabolic acidosis → stimulates release of enzymes from synovial cells into surrounding tissue → tissue breakdown and erosion of articular cartilage and inflammation of ligaments / tendons → haemorrhage and coagulation of synovial membrane → fibrin deposits on synovial membrane and in synovial fluid → granulation → scar tissue → clinical manifestations such as immobilisation and joint stiffness
45
What are the clinical manifestation of rheumatoid arthritis?
```
fever
fatigue
malaise
rash
anorexia
weight loss
generalised aching and stiffness
spleen enlargement
lymphadenopathy
```
After many weeks of experiencing these initial systemic symptoms, there will be a gradual onset of localised clinical manifestations:
- joint pain and tenderness → caused by pressure in the joint, pain increases with movement
- joint stiffness → especially following activity
- warm joints
- swollen and deformed finger joints (metacarpal-phalangeal and peripheral interphalangeal joints) → joint subluxation, dislocations, ulnar drift, swan neck and boutonniere deformities - see the following images for deformities, typical deformities of RA
- loss of dexterity → difficulty grasping objects
- disability
- fever, malaise, anorexia
- elevated serum leukocyte levels
- elevated serum fibrinogen levels
46
What are some complications of rheumatoid arthritis
- osteoporosis
- rheumatoid nodules
- dry eyes / mouth
- infections
- carpal tunnel
- lung disease
- cardiac disease → premature heart disease
47
Explain the psoriatic arthritis
- a chronic, immune-mediated inflammatory joint disorder
- typically affects large joints, mostly of the lower extremities, and fingers / toes, back and pelvis
- affects men = women
48
Explain psoriasis
- a chronic autoimmune disorder
Characterised by;
- the rapid build up of skin cells that form patches of scaly, itchy, dry skin
- patches will be red or silvery found mostly on the knees, elbows, torso and the scalp
triggers include infections, stress and cold weather
49
What is the cause of psoriatic arthritis?
- exact cause is unknown
| - string genetic link with immune and environmental factors (trauma, bacterial infections)
50
What are the risk factors for psoriatic arthritis?
- psoriasis
- age
- obesity
- trauma
- smoking
- infections
- stress
- weather extremes
51
What are some types of psoriatic arthritis?
Symmetric
- similar to RA
- affects joints on both sides of the body at the same time
- 50% of cases
Asymmetric
- usually mild
- affects one side of the body at a time
- 30% of cases
Distal
- inflammation and stiffness to the ends of the fingers and toes, including nails
- causes nail pitting, white spots and lifting from the nail bed
Spondylitic
- pain and stiffness of the spine and neck
- affects men > women
Arthritis mutilans
- most severe
- deformities of small joints
- 5% of cases
52
Explain the pathophysiology of Psoriatic arthritis
It is not fully understood
53
Explain the clinical manifestations of Psoriatic arthritis
- joint inflammation → swollen, stiff, painful, erythematous, hot joints → worse in the morning
- swollen fingers / toes → like sausages
- skin changes → skin plaques from psoriasis
- ridging and pitting of the nails
- lower back pain
- onycholysis → separation of nail
p dactylitis → inflammation and swelling of full digit
- enthesitis → inflammation and pain of point where tendon joins bone → example - heel
54
Explain some complications of Psoriatic arthritis
- 'pencil in a cup' deformity of the distal joints in fingers
- conjunctivitis
- inflammation of the aorta
- amyloidosis → amyloid deposits around the body
- depression / anxiety / mood changes
- anaemia
- chronic fatigue
- hypertension
- hypercholesterolaemia
- Type 2 Diabetes Mellitus
- Obesity
55
Explain gout
- a complex, recurring inflammatory arthritis
- a metabolic disorder
Characterised by;
- an acute exacerbation with long periods of remission
- can progress to chronic gout
- disruption of bodys control of uric acid production or excertion.
- resulting in high levels of serum uric acid
- severity can range from infrequent, mild episodes to multiple severe exacerbations (>12 per year)
- affects men > women
- peak age 40 - 60 years for men, later years for women
56
How is gout classified
primary
- 90% of cases → hereditary → dysfunction of purine metabolism → overproduction or retention of uric acid
secondary
- related to other risk factors
Acute
- sudden onset of symptoms
- usually of a peripheral joint
- symptoms occur usually at night, peaking within several hours and resolving in 2-10 days (regardless of being treated or untreated)
- 1 - 4 joints involved (monoarticular arthritis = 1 joint)
- exacerbation of great toe most common (50% of cases) → great toe is prone to chronic strains due to waking
- wrist, finger, elbow, knee, ankles, mid-tarsal, olecranon bursae
Chronic
- multiple joints involved
- visible deposits of sodium urate crystals called tophi
- can be found in synovium, subchondral bone, olecranon bursae, vertebrae, along tendons, skin, cartilage
- the ear helix is the most common area for tophi to be noted
57
Causes of gout
Gout is caused by defects in uric acid metabolism attributed to one or more of the following:
1. increase in uric acid production → enough to crystallise
2. decrease in uric acid excretion
3. increase in consumption of food / drinks containing high levels of purine eg seafood, shellfish, alcohol, sugary drinks
58
What are ricks of gout?
Medications
- those that increase cell death → chemotherapy
- thiazide diuretics
- aspirin
- immunosuppressants
obesity
systemic infection
trauma → surgery, injury
anorexia nervosa → prolonged starvation
postmenopausal women
comorbidities
hypertension, diabetes mellitus, hyperlipidaemia, sickle cell anaemia, renal disease, atherosclerosis, cancer
excessive alcohol consumption → increases production of keto acids → inhibits uric acid excretion
diet → high consumption in of purine-rich foods can trigger an exacerbation of gout → seafood, shellfish, spinach, beef, pork, lentils
exposure to lead
59
Explain the pathophysiology of gout
Closely related to purine metabolism and kidney function
Purine
- natural chemical compounds found in food and produced in the body
- examples include adenine and guanine
- used for the production of ATP and nucleic acids
- uric acid is the major end product of purine metabolism → excreted in the kidneys
- urate is filtered at the glomerulus → reabsorbed or excreted in urine
Those with a history of gout will have either:
- accelerated purine synthesis
- breakdown or poor uric acid secretion in the kidneys
Pathophysiology is closely related to the cause (see above)
cause → in conjunction with increased urate reabsorption or sluggish urate excretion by the kidneys → monosodium urate crystals are deposited in renal interstitial tissues→ impaired urine flow → accumulation of crystals in connective tissue (ear lobes, kidneys, heart, joints), synovial membrane, cartilage → inflammatory response → neutrophils die and release additional crystals → tissue damage and further inflammation
- exact pathophysiological process of how crystals are deposited in joints and how it then causes gout is unknown
- there are known
Aggravating mechanisms for crystal deposition
- low body temperature → build up of monosodium urate peripherally → decreased body temperature reduces solubility of monosodium urate
- decreased albumin or glycosaminoglycan levels → decrease urate solubility
changes in ion concentration → enhance urate solubility
- changes to pH → enhance urate solubility
- trauma → promotes urate crystal precipitation most aggravating
60
What are the stages of gout?
asymptomatic hyperuricaemia → serum urate is elevated but arthritic symptoms, tophi and renal complications are not present
acute gouty arthritis → exacerbation of symptoms with elevated serum urate concentration, occurs with sudden or sustained increase in urate level, can also occur with medications, alcohol or trauma
tophaceous gout → chronic stage → occurs as early as 3 years post initial gout episode, or as late as 40 years → progressive inability to excrete uric acid → tophi appearance in cartilage, synovial membrane, tendons and soft tissue
61
What are the clinical manifestations fo gout?
Acute
- dusky apperance
- excruciating pain
- hot to touch
- decreased range of movement
- difficulty weight bearing
- systemic sings of inflammation
- low grade fever
- lymphadenopathy → enlarged, swollen lymph nodes
- elevated inflammatory markers
Chronic
- lingering joint discomfort
- limited range of movement
- slowly progressive disability
- chronic joint inflammation
- cartilage destruction → osteoarthritis
- joint deformity
62
What are some complications of gout?
kidney dysfunction
- acute kidney injury
- kidney stones
- pyelonephritis
tophi
- grotesque deformities are usually painless but can lead to additional complications
- large clumps may perforate through the overlying skin → wound infections
- progressive stiffness and movement limitations
- persistent aching
- nerve compressions → carpal tunnel
63
Explain septic arthritis
an infection caused by the invasion of bacteria into the joint cavity.
- usually effects single joints
- most commonly large joints such as knees (50% of cases), elbows, hips, shoulders
Medical emergency due to high risk and serous complications
Haematogenous seeding= bacteria travels though the body and deposites into the joint cavity
64
What causes septic arthritis?
- active infection anywhere in the body.
e. g. cellulitis, UTI, URTI, LRTI, osteomyelitis
- trauma
- surgical incision/procedure
- IV drug use
65
What are risk factors for septic arthritis?
- immunocompromised people
- recent infection
- cellulitis, skin ulcer, bacteremia
- medications → corticosteroids, immunosuppressants
- pre-existing joint disease → rheumatoid arthritis
- previous joint replacement / prosthesis
- comorbidities → cardiovascular disease, diabetes mellitus, cancer, HIV, chronic renal failure
- age → >80 years most common
- IV drug use
66
Explain the pathophysiology of septic arthritis
- directly related to the cause= the pathogen enters the patients and the patient immune response acts
cause → bacterial colonisation → rapid bacterial proliferation → synovial membrane is well vascularised and allows easy entry of bacteria into the joint → bacteria seeds in the closed joint space → low fluid conditions enable bacterial adherence → joint infection → additional colonisation of the bacteria → onset of clinical manifestations → induction of an acute inflammatory response → cytokines and interleukins are released into the joint fluid by synovial cells → influx of inflammatory cells into the synovial membrane → phagocytosis of the bacteria by macrophages → release of additional inflammatory cytokines → activation of immune response
67
Explain come clinical manifestations of septic arthritis
- single joint with severe pain, worse with movement
- poor range of movement
- effusion
- symptoms of inflammation → erythematous and swollen joint that is hot to touch
- symptoms of infection → fever, rigours, lethargy, myalgia, tachycardia, anorexia
68
What are some complications associated with septic arthritis?
Sepsis= death
Irreversible cartilage damage within 8 hrs.
```
unstable vital signs changes
increased / uncontrolled pain
avascular necrosis
osteoarthritis
osteomyelitis
bony erosion
fibrous ankylosis
permanent joint dysfunction
```
69
How is arthritis diagnosed?
| Explain each types diagnosis
- patient history
- clinical presentation
- assessment
- diagnostics
```
Osteoarthritis
Imaging to identify early changes or for staging of joint damage → detects loss of joint space, bony sclerosis, osteophyte formation
- Xray
- CT scan
- MRI
- Bone scan
```
Rheumatoid arthritis
- blood pathology: rheumatoid factors, immune complexes, inflammatory markers
- synovial fluid analysis
- imaging (xray, bone scans, MRI)
Diagnosis will be based on the patient having at least 4 of the following factors for longer than 6 weeks;
- morning stiffness lasting > 1 hour
- arthritis > 3 joints, including the hands
- symmetric arthritis
- rheumatoid nodules over bony prominences
- serum rheumatoid factor
- xray changes
Gout
- presence of tophi (tone-like deposits of monosodium urate in the soft tissues, synovial tissues, or in bones near the joints)
- blood pathology
- serum uric acid → in gout, levels will be > 0.45mmol / L → not used as a sole diagnostic for gout
- inflammatory markers
- 24 hour urine collection → urine uric acid levels
- aspiration of joint (arthrocentesis)
- synovial fluid tested for presence of crystals
- xrays are not useful in acute exacerbations but can be helpful to rule out other causes of joint pain
- can be used to determine chronic gout as tophi can appear in eroded areas of the bone
Septic arthritis
- arthrocentesis (aspirate tested for crystals gout) sent for MCS
- Blood pathology (ultures to test for both aerobic and anaerobic organisms (two sets of cultures are always collected)
- Imagine
Psoritic arthritis
- diagnosis is made based on clinical presentation and history of clinical manifestations → skin / nail changes related to psoriasis
- xray → will resemble RA with widened joint spaces with bone erosion
- blood pathology → RF negative, ACPA (anti-citrullinated protein antibodies) negative
70
What is the treatment for
Goal: improve functional capacity and prevent disability
symptom management= stop inflammation, minimise pain
- improve mobility / function
- limit exacerbations
- preventing complications= joint contractures, loss of joint function, development of comorbidities, muscle atrophy
- health promotion
Treatment includes:
- balance of rest with exercise → resting with exacerbations then, when symptoms allow → cardiovascular and aerobic exercise with lower extremity strength training
- weight loss → to decrease load on the affected joints
- orthotics → wedged insoles, braces, splints
- walking aids with occupational and physical therapy assessment
- dietary changes → low-purine
71
What are some non pharmacological managements for arthritis?
- rest for inflamed joints → avoid weight bearing with exacerbations
- heat → for stiffness
- ice → for pain
- complementary therapies → acupuncture, yoga, massage, nutritional supplements
- guided exercises → joint strength
- adequate hydration → to improve excretion of wastes
72
What are some pharmacological managements for arthritis?
Analgesics for pain
Antiinflammatories
- NSAIDS
- cortocisteroids
Consider a multi modal approach
73
Explain some surgical managements for arthritis
- total joint replacement surgery; an option for severe joint dysfunction associated with all types of arthritis
- arthrodesis → fusion of two bones = joint becomes immobile
- arthroplasty → repair of joint
- osteoarthritis → arthroscopy no longer recommended due to potential to exacerbate OA
- rheumatoid arthritis → synovectomy to decrease inflammation and effusions
- septic arthritis → incision and drainage with a washout
74
What may you refer someone with arthritis to for an intercollabrative approach?
```
GP
Specialist
Rheumatologist → rheumatoid arthritis
Orthopaedic Surgeon → joint function management
Occupational therapist
Social worker
Exercise physiologist / physiotherapist
Podiatrist
Dietician
Nursing team
Pharmacist
```
75
What are some nursinf can considerations that should be taken for someone with arthritis?
- determine patients history with targeted health history questions
- current strategies in place for managing clinical manifestations → effectiveness of each
- ability to complete ADLs
- any history of falls
- mental health response to chronic pain and disability, impaired social / work roles
76
What is involved in a focused assessment for someone with arthritis?
Focused assessment
- full joint assessment → comparing left with right (contralateral joint) → swelling, tenderness, range of movement, crepitation
- if any erythema → a surgical pen is used to mark the boarder of the erythema → this allows for the accurate reassessment of the joint → determines infection / inflammation trend
- if any swelling → a tape measure is used to assess the area of swelling → ensuring that contralateral assessment is completed
- neurovascular observations
Additional assessments
- risk assessment → falls, assess if mobility aids required
- pain assessment
- close observation of vital signs; to identify deterioration
77
Explain the nursing management of someone with arthritis
- assist with ADLs
- ensure room is clutter free= safe
- manage pain
- pharmacological management
- non pharmacological management
e. g. heat/ice packs, bandage, joint support, if septic= immobilise the joint
- ensure patient and family are educated
- lifestyle modification (referal if neccessary) e.g. educate on diet, alcohol reduction
Document
78
Describe fractures
- break in the continuity of bone
- occurs when the force exerted on the bone exceeds what the bone can absorb
- highest occurance → young males and the elderly
79
What is the cause of fractures?
- trauma
- overuse
- pathological → disease processes
80
What are risk factors of fractures?
- age related factors (younger population = sustain more trauma related injuries, older population = muscle deterioration, general frailty)
- comorbidities → conditions that produce decreased cerebral arterial perfusion, osteoporosis, diabetes mellitus, rheumatoid arthritis, celiac disease, inflammatory bowel disease
- lifestyle → smoking, excessive alcohol, obesity
- medications → steroids
- family history
81
What are some complications of fractures?
Direct
- osteomyelitis → infection to the bone
- delayed union / nonunion / malunion
- permanent disability → loss of strength, compromised range of movement, uneven limbs
- avascular necrosis
Indirect → associated with damage to nerves, blood vessels and surrounding tissue
- soft tissue injury → scarring, infection
p adverse reaction to internal fixation devices
- complex regional pain syndrome (CRPS)
- compartment syndrome
- rhabdomyolysis
- amputation
- deep vein thrombosis
- pulmonary embolism
- sarcoma
- fat embolism
- hypovolaemic shock → large bone fracture e.g. femur, pelvis
death → can results from damage to underlying organs / vascular structures or, from complications of the fracture or immobility
82
How can fractures be prevented?
- consume adequate amounts of calcium and vitamin D
- life style changes= high vitamin diet, exercise to increase stress and therefore no osteoblast stimulation, cease smoking
- avoid missadventure
- regular reviews with GP
(bone mineral density tests, general wellness, preventative measures, medications to slow bone loss and reduce fracture risks, vision tests)
83
Explain some clinical manifestations of fractures
- immediate localised pain / tenderness
- swelling
- paraesthesia → damaged nerves
- bruising → ecchymosis
- deformity → not always present
- muscle spasms → irritation of tissues and protective responses to the injury, can displace the fracture further
- loss of function → strength, range of movement, inability to weight bear
- crepitation → crunching and grating together of bony fragments, producing palpable / audible crunching
- guarding → a person with a fracture will usually guard the injury against movement, protecting against further injury
84
How are fractured classified?
- location
- displacement of fracture lines
- appearance of the limb → dinner fork deformity
- which part of the bone is fractured
- fracture pattern → anatomical alignment of bone fragments
- severity of overall injury → stable / unstable
85
What are the two main categories of fractures?
Displaced/non displaced
(bone breaks in two or more parts and shifts so that the ends do not align/bones still align)
Open/closed
(breaks through skin)
86
Explain some subtypes of fractures
greenstick → bone is bent but does not separate into two pieces (children only)
buckle → also known as a torus fracture, results from compression of two bones driving into each other (children only)
growth plate fracture→ fracture through the joint which can impact bone growth → shorter bone length (children only)
comminuted → bone breaks into 3 or more fragments, usually results from high-impact trauma
oblique → break is on an angle through the bone, results from a sharp blow from an angle
spiral → spiral break around the bone, often long bones impacted, caused by twisting injury
transverse → also known as a linear fracture, fracture line is perpendicular to the bone shaft, caused by trauma such as a fall
compression → bones are crushed resulting in flatter, wider bones, occur most often in the spine
impacted → broken ends of the bone are driven together by the force of the injury
pathological → caused by disease that weakens the bone
stress → fatigue & insufficiency cause a hairline crack, results from repetitive motion such as running
avulsion → bone fragment is pulled off the bone by a tendon or ligament, often occurs to the ankles or fingers / wrist
87
Explain hip fractures
A hip fracture is a break occurring at the upper third (proximal) of the femur, which extends 5 cm below the lesser trochanter.
NOF- neck of femur
extracapsular → of the trochanteric region
intracapsular → of the neck of femur → increased risk of complications due to potential damage to the vascular system that supplies blood to the head and neck of the femur → if blood supply is compromised, avascular necrosis or non-union of the femoral head may occur.
88
What are some complications of hip fractures?
- delerium with up to 25% of patients experiencing at least one episode during the initial stages post fracture
delirium can occur due to;
- shock
- pain
- hypovolaemia → either due to blood loss and / or dehydration
```
delirium will lead to decreased function post fracture and increased mortality / morbidity
to prevent the occurrance of delirium
- interprofessional team approach
- adequate pain management (analgesia)
- multimodal approach
- nerve block
- nutritional support
- correcting electolyte imbalances
- rehydration
- minimising delay in treatment
```
89
Explain the pathophysiology of fractures
Force exceeds what the bone can absorb (bone strength) e.g. falling onto an outstretched hand (FOOSH)
normal force is exerted on a bone that has not developed correctly e.g. osteogenesis imperfecta
normal bone is weakened secondary to deterioration from structural changes e.g. osteoporsis
normal bone is fatigued secondary to repeated force on a bone e.g. runners
90
What are the three phases of bone remodeling called?
- inflammatory phase
- reparative phase
- remodeling phase
91
Explain the e phases of bone remodeling after a fracture
1. Inflammatory phase (0-2 wks)
- immediatley at time of fracture
- bleeding occurs= formation of a fracture haematoma between the medullary canal and beneath the periosteum
- fractured ends of bones seal
- damaged blood vessels disrupts oxygen supply resulting in bone tissue death immediately adjacent to the fracture
- inflammatory response is triggered
- vasodilation, increased permeability, exudation of plasma, infiltration of inflammatory mediators such as leukocytes and mast cells
- decalicfy the fractured bone ends
- procallus formation
2. reparative phase (2-6 wks)
- A capilliary network forms within the haematoma from surrounding soft tissue and the marrow cavity into the fractured area
- increase in blood flow to the area
- phagocytes start cleaning up debris
- Granulation tissue develops
- fibroblasts (collagen-forming cells create fibrocartilaginous callus) and osteobalsts (bone-forming cells = create bone matrix) create a bridge of spongy bone between the bone ends
- osteoblasts migrate inwards to mineralise new bone
- bone callus
3. Remodelling phase 6 weeks- several months
- Gradual spread of the callus
- creation of compact and cancellous bone structures (over several months to 2 years)
- osteoclast cells absorb fragments of dead bone tissue and unnecessary callus
- bone's internal and external structure is reformed
92
What factors that affect bone healing post fractures
```
- complexity / type of fracture
(displacement, comminuted, compound)
- genetics
- advancing age
- lifestyle (high alcohol consumption, smoking, illicit drug use, medications → steroids, exercise, poor nutrition
- endogenous factors (comorbidities, hormones, inflammation / infection, blood supply to area
- immobilisation
- internal fixation devices
```
93
Explain the progression of a fracture healing
48 hours → angiogenesis occurs → new blood vessels formed
3 weeks → new bone is splinted but not strong enough to withstand pre-injury strength
6 weeks → most fractures have healed and the new bone can support movement and normal function
larger bones / complex fractures such as compound or comminuted fractures, can take up 4 to 6 months to regain strength and function
94
What factors affect a bones ability to heal?
- complexity / type of fracture (displacement, comminuted, compound)
- genetics
- advancing age
- lifestyle
- high alcohol consumption
- smoking
- illicit drug use
- medications → steroids
- exercise
- poor nutrition
- endogenous factors (comorbidities, hormones, inflammation / infection, blood supply to area.
- immobilisation
- internal fixation devices
95
Explain sprains and strains
- muscle → attached to bone by tendons → made up of fibres that shorten and lengthen to produce movement of a joint
- tendon → tough bone of slightly elastic connective tissue that connect muscle to bone.
- ligament → strong bands of inelastic connective tissue that connect bone to bone
other soft tissues include fascia, fibrous tissue, blood vessels, nerves, synovial membranes, fat
```
Strain= muscle + tendon
Sprain= ligaments
```
96
Explain a sprain
the tear or stretch of a ligament
Cause: fall or external force that displaces the surrounding joint from its normal alignment
97
Explain a strain
occurs in reaction to a tear, twist, or excessive stretch of a muscle, its muscle sheath and / or its tendon.
- can be sever or moderate
- mostly occurs in large muscle groups
Cause: over exertion, trauma or repetitive movement
98
What are some risk factors for both strains and sprains?
- advancing age
- obesity
- poor physical fitness → sedentary lifestyle
- smoking
- medications → steroids
- poor posture
- comorbidities that result in muscle fatigue / tightness / imbalance
- not warming up before activity
99
What are some complications of strains and sprains?
- ligament pulls of the bone= avulsion fracture
- immobility
- joint weakness
- dislocation
- chronic instability
- loss of function / strength
- chronic pain and swelling
- arthritis
- muscle atrophy
- muscle firbosis
- compartment syndrome
100
How can you prevent a strain or sprain?
- adequate warm up and streaching
- correct technique during movement
- taping or protection
- balanced nutrition
- maintain a healthy weight
regular exercise
- avoid playing sports / exercising when fatigued or in pain
- avoid traumatic injuries → be aware of falling hazards
- maintain strength
- warm up and stretch before exercise / sports
- wear good fitting and good quality shoes
- wear protective braces / equipment during sports
101
What are the clinical manifestations of a sprain or strain?
- pain / tenderness
- swelling / oedema
- ecchymosis (bruising)
- loss of function → limited / decreased range of movement, loss of strength
- difficulty weight bearing
- antalgic gait
- contusion
- altered sensation with severe oedema
- muscle spasms
102
Explain the pathophysiology of a sprain or strain and how they are measured
graded according to how badly the ligament has been damaged and whether or not the joint has been made unstable
Grade I - mild stretching of the ligament (only a few fibres torn) without joint instability.
Grade II - partial tear (rupture) of the ligament but without joint instability (or with mild instability).
Grade III - a severe sprain: complete rupture of the ligament with instability of the joint.
103
Explain the bodys reaction to a tor ligament or tendon
→ torn tendon or ligament
→ inflammatory process triggered
→ inflammatory fluids accumulate at the ends of the damaged tissue
→ inflammatory cells such as macrophages (remove damaged tissue), fibroplasts (make collagen) capilliary buds (new vessel production) and prostaglandins (lipids that sustain homeostasis and balance processes such as the formation of new tissue), grow inwards from surrounding tissue to begin repair process
→ 4-5 days later, new collagen has formed
→ new collagen begins to be organised and associate with existing tendon fibres new and sourrounding tissue fuse into single mass
→ 4-5 weeks post injury, healing tendon or ligament will have adequate enough strength to withstand strong pull
104
How are sprains and strains treated?
RICER
