Conditions for 16/01/23 Flashcards
OA aetiology
- Increased age (takes years to develop)
- Incongruent Jts
- Relationship between stress on articulate cartilage + ability of cartilage to withstand stress
Obesity
OA clinical features
- P starts insidiously + increases slowly over few months
- Aggravated by exertion
- Relieved by rest
- Stiffness usually worse after rest
- Swelling, crepitus, deformity, tenderness, muscle wastage, reduced ROM
OA X-ray findings
- Osteophyte formation
- Jt space narrowing
- Subchondral sclerosis (thickening of bone in affected Jt)
- Cysts
OA pathophysiology
- Softening of cartilaginous surfaces
- Become frayed
- Eventually worn away exposes underlying bone in areas of great stress
- Bone can develop cysts
- Surrounding trabeculae can become thickened
- Ossification produces bony growths
OA cautions
Exercise
Posture
Knees, hips, hands, spine
OA management
- Pharmacological
- Braces/support
- Supplements
- Surgery
- Osteopathy- increased ROM, flexibility
Lumbar spondylosis aetiology
- No specific cause
- Associated with ageing, degeneration of Jts, ligaments, discs, natural wear and tear
Degeneration of intervertebral discs in Jts in lower back- wear + tear
Risks- OA, poor posture, obesity
Lumbar spondylosis clinical features
- P in low back
- Often worse when standing or walking, relieved when sitting or bending forward
- P spread to thighs
- Tight hamstrings
Lumbar spondylosis X-ray finding
- Reactive sclerosis
- Narrowing of intervertebral disc space e
- Deviation or step off signs of SPs
- Degeneration of facet Jt
Lumbar spondylosis pathophysiology
- Occurs as result of new bone formation in areas where annular ligament is stressed
Degen of intervertebral discs + Its in low back
Forms bony spurs, narrowing disc space, which can put pressure on N and cause P
Cautions lumbar spondylosis
- Avoid sitting for more than 30 mins at a time
- Eating diet high in sugar, processed and refined foods (inflammatory)
Lumbar spondylosis management
- Pain relieves
- NSAIDs
- Muscle relaxants
PT- exercises to improve strength + flexibility
Surgery- alleviate pressure on nerves, remove bony spurs
Chronic- requires follow up care
Lumbar facet degeneration aetiology
- Alternate spinal conditions which change the way facets align
- OA leading cause
Lumbar facet degeneration clinical features
- P or tenderness in low back
- Stiffness in surrounding structures
- Difficulty with certain movements, e.g. standing up straight or getting up from a chair
Lumbar facet degeneration X-ray
- Narrowing of disc space
- Subchondral sclerosis
- Osteophytes
Not specific to facet irritation, not all will show these changes
Lumbar facet degeneration pathophysiology
- Facet Jt comprises posterior element of ‘three-Jt complex’
- Intervertebral disc is anterior part
- As disc degenerates more load will shift posteriorly and facet Jt OA will subsequently develop
- Rarely occurs without disc degeneration
Lumbar facet degeneration cautions
Advances age or osteoporosis- increase risk of fracture
Pregnancy- certain treatment not safe
Lumbar facet degeneration management
- Physio and pharmacology (NSAIDs) first line treatment
- Facet Jt injection, medial branch block
Spondylolithesis aetiology
Failure of facet and laminae locking mechanism
Degenerative- wear and tear
Dysplastic- congenital
Isthmic- fracture to pars interarticularis (bone that covers upper + lower facet)- cause forward slip to L5/S1
Pathologic- slip due to weakness of bones
Spondylolithesis clinical features
- Usually painless
- L4/5/S1
- Intermittent back ache, may be exacerbated by exercise or strain
- Step deformity
- Normal ROM in younger Pts
Spondylolithesis X-ray findings
Slippage of vertebra from spinal column
Shows if congenital or acquired
CT/MRI for surrounding structures
Spondylolithesis pathophysiology
- Normal laminae and facet locking mechanism fails
- Causes forward slippage (listheis) of vertebral body
L4/5/S1 most common
Spondylolithesis cautions
Cauda equina- numbness in saddle, los =s of bowel or bladder control
Spondylolithesis management
Conservative- NSAIDs, steroid injection
Surgery if grade 3/4, spinal fusion of veterbra to above, laminectomy
Herniated nucleus pulposus aetiology
- Failure of annulus fibrosis integrity
- Makes content pf nucleus protrude into spinal canal
- Trauma, contact sport
Herniated nucleus pulposus clinical features
- Low back P
- Radiculopathy (likely down back of leg, sciatic L4-S3)
Tingling sensation, muscle weakness, bladder control incontinence
Herniated nucleus pulposus further investigations
- Suspected during history/physical exam
- Confirmed from MRI or CT scan- determines location and size
Herniated nucleus pulpous cautions
- Compression on nerve root may cause severe motor deficit
Herniated nucleus pulpous management
- Microdiscectomy- small incision made to remove disc fragment that is impinging nerves
Spinal stenosis aetiology
- Age related- discs become drier and shrink
- Arthritis
Herniated disc
Tumours
Spinal stenosis clinical features
- Lsp- sciatica like symptoms
- Csp- major body weakness, full body paralysis is possible
- Pins and needles, numbness, weakness
- C2 and above is facial symptoms
- C3 or below is paralysis
- Male most common
- Over 50s
Stenosis X-ray
- Narrowed disc space
- Fracture
- Bone spurs
- OA (spondylosis)
CT- degree and location
MRI- spinal canal and neural structures
Stenosis cautions
Surgery should be avoided if suffering with osteoporosis, pregnancy, bleeding disorder
Stenosis pathophysiology
- Narrowing of spinal column that causes pressure on cord or foramina (where N exits)
Stenosis management
- NSAIDs
- Opioids- e.g. oxycodone
- Physical therapy- build strength, maintain flexibility
- Laminectomy- surgery which removes lamina od affected spinal bone, eases pressure on nerves
Arachnoiditis aetiology
- No exact cause
- Rare condition
- Arachnoid can become inflamed because of complications of spinal surgery, direct injury to spine, infection, chronic compression of spinal nerves
Arachnoiditis clinical features
- Headaches
- Shooting P
- Tingling, numbness and weakness in your legs
- Difficulty sitting for too long
- Muscle cramps, spasms
Difficulty with balance + coordination
Arachnoiditis further investigation
- Difficult to diagnose
- Diagnosis based on MRI or CT scan- nerve root thickening, inflammatory mass
MRI preferred imaging test to show changes to arachnoid matter
Arachnoiditis pathology
- Inflammation of arachnoid matter (middle layer of meninges)
- Rare but serious condition
Results in scarring + thickening of membrane which can lead to compression of nerve roots + spinal cord
Arachnoiditis management
- Pain management
- Physical therapy
- Stretching, ROM exercises
- Adaptation- mobility, comfort
Medication- corticosteroid, opioids
Spinal infection aetiology (osteomyelitis)
- Bacterial or fungal in other part of body that has been carried into spine via bloodstream
Most commonly staphylococcus
Spinal infection clinical features
- Point tenderness
- Local P
- Referred P- deep muscle, Jt, throbbing sensation
- Systematic signs of infection- feeling faint, nausea, vomiting
Weakness, numbness, tingling in arms or legs
Infection further investigations
- Blood work- WBC count, erythrocyte sedimentation rate + C-reactive protein count- elevated with spinal infection
- Imaging tests to pin point exact location (MRI or CT)
Spinal fluid extraction to identify bacteria
Infection pathology
Caused by spread of microorganism, such as bacteria to bones and soft tissues of spine
Causes inflammation and damage to bones
Leading to formation of abscesses and/or sepsis
Management of infection
ABS or anti fungal therapy
PT- manage P and weakness
Multiple sclerosis aetiology
- Unknown
- Considered immune mediated disease
- Immune system destroys myelin
- Genetic (gene on chromosome 6p21) and environmental factors contribute
Multiple scelerosis clinical features
- Depend on location and severity
- Some can lose ability to walk or ambulate
- Some may experience periods of remission without new symptoms
- Numbness or weakness in limbs, typically unilateral
- Tingling
- Lack of coordination
- Blurry vision, vertigo
Multiple sclerosis further investigation
Diagnosis of exclusion
Evoked potentials- measure electrical activity in brain in response to visual, auditory or somatosensory stimuli
Multiple sclerosis pathology
- Immune system attacks myelin sheath and causes communication problems between brain and rest of body
- Can eventually cause permanent damage or deterioration of nerve fibres
Cautions of multiple sclerosis
- May also develop muscle stiffness/spasm, weakness or paralysis, problems with bladder
Wide range of symptoms therefore difficult to predict
Management of multiple sclerosis
- Interferon beta medication- interfere with diseases that attack body and decrease inflammation and increase nerve growth
PT- rehab, help with mobility, balance + coordination
Occupational therapy- help with daily living
Bone info
Bone turnover= removal + replacement of old bone
Cortex- outer shell of bone
Matrix- soft + light inner structure
Phosphorus + calcium protect cortex
Vitamin D controls levels of calcium + phosphorus
Rickets aetiology
Lack of vitamin D or calcium
Lack of sunlight exposure, poor diet
Most common in children
Rickets clinical features
- Thickening of ankles, wrists and knees
- Bowed legs
- Poor growth
- Dental problems
Rickets X-ray
- Fraying- indistinct margins of metaphysis
- Splaying- widening of metaphyseal ends
- X-ray of wrists and ankles usually confirm diagnosis
Rickets pathology
Usually from extreme,e prolonged vitamin D deficiency- failure in mineralisation of bones, softness + weakness
Rare inherited problems can cause rickets
Can cause hormone imbalance of parathyroid hormone, leading to increased bone resorption
Cautions of rickets
Treatable, delay can cause serious complications such as irreversible bone deformities
Management of rickets
- Increase child’s intake of vitamin D and calcium
PT- maintain ROM and strength
Paget’s disease aetiology
- Unknown
- Suggest combination of genetic and environmental factors
- Several genes appear to be linked
Abnormal bone remodelling
More common in adults
Paget’s clinical features
- Most people have no symptoms
- Most common complain is bone P
- Pelvis- hip P
- Skull- overgrowth of bone hearing loss or headaches
- Spine- nerve root compression, P and tingling
- Legs- weaknening bending
Paget’s X-ray
- Areas of bone breakdown
- Enlargement of bone and deformities that are characteristic of disease (e.g. bowing of long bones)
Paget’s pathology
- Interference of bodys normal recycling process
- Causes body to generate new bone faster than normal, rapid remodelling produces bone that’s weaker than normal bone, leading to P, deformities and fractures
- Over time bone become fragile
- Pelvis, skull, spine and legs most affected
- Risk increases with age
Cautions of Pagets
Long term treatment
Paget’s management
- Osteoporosis drugs (bisphosphonates)
- Typically administered through injection, can be taken orally (however can irritate stomach)
Hyperthyroidism aetiology
- Inefficiency in parathyroid gland
- Primary due to- noncancerous growth (adenoma|) on gland, enlargement (hyperplasia) of parathyroid gland, cancerous tumour (very rare cause)
- Secondary- anything condition leading to severe calcium/vit D deficiency, chronic kidney failure
Tertiary- chronic secondary hyperthyroidism
Hyperthyroidism clinical features
- Primary often described before signs and symptoms occur
- Severe- Weak bones that break easily (osteoporosis)
- Kidney stones
- Excessive urination
- Fatigue
- Nausea, vomiting, loss of appetite
Hyperthyroidism further investigation
Blood tests- elevated calcium levels
X-ray bone density loss, bone cysts in rare cases
Hyperthyroidism pathology
Parathyroid gland produces PTH in response to low calcium levels, PTH increases calcium absorption in gut, activates osteoclasts to break down bone, releasing calcium into blood stream
- Where parathyroid gland over produces parathyroid hormone in bloodstream
- Parathyroid healps maintain right balance of calcium in blood stream and tissues
- Especillay important for nerve and muscle function as well as bone health
- Primary- enlargement of parathyroid gland casues overproduction of parathyroid hormone
- Secondary- result of another disease
Cautions of hyperthyroidism
Avoid high calcium diet- such as dairy
Avoid Vit D supplements
Hyperthyroidism management
Primary- surgery to remove parathyroid gland
Secondary- treat underlying condition, phosphate binders
Severe- IV fluids, diuretics, steroids used to remove excess calcium from blood + reduce symptoms
Regular monitoring of blood tests to confirm normalisation of calcium levels
Hypothyroidism aetiology
- Acquired- Removal or injury to parathyroid gland
- Autoimmune disease- attacks parathyroid gland
Idiopathic- no cause
Hypothyroidism clinical features
- Twitching facial muscles
- Muscle P or cramps
- Fatigue or weakness
- memory loss
Hypothyroidism further investigation
Blood test
X-ray- increased bone density + calcification of soft tissue
Urine analysis
Hypothyroidism pathology
- Uncommon
- Body produces abnormally low levels of parathyroid hormone
- Difficulty regulating calcium and phosphorus
Low blood calcium leads to formation of membrane and muscle spams, nerve damage
Cautions of hypothyroidism
Avoid low calcium diets
Cautions of vit D and calcium supplements if HX of kidney stones/renal failure as this increases risk
Hypothyroidism management
- Supplements can bring calcium and phosphorus levels to normal range
Regular blood tests to check levels
Parkinson’s aetiology
- Breakdown of neurons
- Mainly due to loss of neurons that produce dopamine in brain
- When dopamine levels decrease, it causes atypical brain activity, leadsing to impaired movement and other symptoms of Parkinson’s
Parkinson’s acronym
TRAP
Tremor, rigidity, akinesia/bradikinesia (stopping starting/stopping), posture
1. resting tremor first sign
2. bradikinesia (generalised slowness of movement)- difficulty with daily activities
3. muscle rigidity- muscle tone increases
Parkinson’s clinical features
- Symptoms start slowly
- First symptoms barely noticeable
- Tremors are common
- Early stage- little expression on face, arms may not swing when walking, speech may become slurred
- Loss of automatic movements
- Swoop posture
Man, aged 70
Parkinson’s further investigation
- No specific test to diagnose
- Neurologist will diagnose Parkinson’s based on medical history, review signs and symptoms, and a neurological and physical examination
Normal X-ray
Parkinson’s pathology
- Progressive disorder which affects nervous system and parts of body controlled by the nerves
- Genes and environmental factors
Basal ganglia in middle of brain responsible for movements such as walking and looking around
Substantia nigra in basal ganglia produces NT dopamine
Dopamine essential for basal ganglia function
Parkinson’s= decrease in dopamine
Parkinson’s management
- Medication- levodopa- absorbed by nerve cells in brain and turned into dopamine, which transmits messages between parts of the brain and nerves that control movement
PT- improve mobility, manage non-motor symptoms, improve QOL
Gout aetiology
- Obesity
- Kidney disease
- Drinking too much alcohol
Build up of uric acid in Jts- leads to formation of crystals which deposit in Jts and cause inflammation
Gout clinical features
- Acute attacks 1-2 weeks
- Spontaneous- may be precipitated by minor trauma, operation, excessive alcohol
- Most common site- metatarsopharyngeal Jt of hallux, ankle, olecranon bursa + finger Jt
- Skin looks red, shiny, swollen, hot and tender
Gout further investigation
- Dual-energy computerised tomography (DECT)- detects urate crystals in Jts
- Blood tests- uric acid levels
- X-ray to rule out other potentials- normal on acute attacks
Chronic shows tophi- large lumps of crystals in JTs
Gout pathology
- Characterised by presence of crystals in Jt, bursa and tendons
- Consequences of these deposits may be inert + asymptomatic may include acute inflammatory reaction, may result in slow destruction of tissue
Cautions of gout
Long term management
Serious complications lead to Jt damage and kidney stones
Gout management
- NSAIDs
- Colchicine- anti-inflammatory drug that effectively reduces gout P
- Corticosteroids- e.g. prednisone, controls inflammation and P
PT- ROM, strength, avoid Jt damage
Reduce purine intake
Combination of meds and lifestyle changes needed to prevent future gout attacks
Pseudo-gout aetiology
- Presence of calcium pyrophosphate dihydrate crystals within affected Jt
- Appear in nearly half the population older than 85
- Not all develop pseudogout
Predisposed- Jt damage, OA, hyperthyroidism
Pseudo-gout clinical features
- Most commonly affects knees
- Swollen, warm and severely painful- sudden + severe
Accompanied by fever and chills
Pseudo-gout further investigation
- Arthrocentesis- withdraw sample of fluid with needle
- X-ray can reveal Jt damage + crystal deposits in Jt cartilage
Jt fluid analysis and blood tests confirm diagnosis- detect calcium pyrophosphate dehydrate in Jt fluid
Pseudo-gout pathology
- Form of arthritis
- Aka calcium pyrophosphate deposition disease (CPPD)
- Crystal deposits form in Jt (different to usual gout)
Calcium pyrophosphate crustals cause inflammation
Cautions of pseudo gout
Risk increases with age
Chronic therefore requires long term treatment
Management of pseudo gout
- Colchicine daily as preventative measure
- Corticosteroids
- NSAIDs- relive P, reduce inflammation
Lifestyle- lose weight
Surgery may be needed to remove crystals
Reactive arthritis aetiology
- Bacteria spreads it
- Chlamydia, salmonella, shigella
Reactive arthritis clinical features
- Usually targets knees, ankles and feet
- Signs and symptoms often occur 1-4 weeks after exposure to triggering infection
- P and stiffness
- Eye inflammation (conjunctivitis)
- Urinary problems
- Swollen toes or fingers
- Low back P which rends to be worse in the morning
Further investigations of reactive arthritis
Changes in Jts typically not as severe as OA- X-ray
Osteopenia- no osteophytes or Jt space narrowing
Blood tests- to determine cause of infection
Reactive arthritis pathology
- Jt P and swelling triggered by an infection in another part of the body- most often intestines, genitals and urinary tract
- Numerous bacteria can cause reactive arthritis
Immune system overreacts to infection, causing inflammation
Reactive arthritis management
- DMARDs- disease-modifying anti-rheumatic drugs
- NSAIDs
Manage underlying condition
If lasts longer than 6 months management approach is different
Osteomalacia
Softening + weakness of bones
Symptoms of osteomalacia
Bone P in legs, groin, upper thighs and knees
Muscle weakness/stiffness
Fractures which can lead to full breaks
Affects anyone with Vitamin D deficiency
Osteomalacia aetiology
Vit D deficiency, essential for absorption of calcium and formation of strong bones
Inadequate light exposure, dietary intake
Osteomalacia clinical features
Muscle weakness + P, particularly in low back, hips, thighs, pelvis
Bone P
Difficulty standing from seated
Tenderness to touch over bone
Osteomalacia x-ray
Bone demineralisation
Early stages may be norma
Blood tests- identify fit D, phosphorus, calcium deficiency
Osteomalacia patho
Decreased vitamin D
Decreased absorption of calcium in gut and decreased bone mineralisation
Bones become less dense
Unable to support weight of body, muscle weakness + P
Vitamin D affects muscle function- cramping, weakness and P
Osteomalacia cautions
Hx of kidney stones or hyperglycaemia
Medication which interacts with vitamin D
Osteomalacia management
VItamin D supplements
Adequate sun exposure
Regular exercise, healthy diet
Polymyalgia rhematica aetilogy
Unknown
Thought to be autoimmune
Most common in women over 50s
Polymyalgia clinical features
muscle P and stiffness in neck, shoulders and hip
Fatigue, fever, weight loss
Stiffness usually worse in mornings or after periods of rest
Polymyalgia further investigations
Erythrocyte sedimentation rate + c-reactive proteins to confirm diagnosis and monitor effectiveness of treatment
Polymyalgia patho
Chronic inflammation of muscles and tendons
Polymyalgia causions
Chronic condition requiring long term treatment
Polymyalgia management
Corticosteroids to reduce inflammation + P
Treatment typically at a high dose, gradually tapered over several months
PT- maintain Jt ROM and strength
Some Px can develop giant cell arthritis- requires prompt diagnosis and treatment
Osteoporosis aetiology
Unknown
Thought to be result of genetic + teratogens
Female, over 50s
smoking, excessive alcohol
Osteoporosis x-ray
X-ray cannot detect until significant amount of bone density has been lost
Decreased size of bone, fractures, decreased space between bones
Osteoporosis further investigation
Dual-energy x-ray absorptiometry- measures bone density
Ultrasound bone density testing
Osteoporosis patho
Interruption of new bone formation and old bone reabsorption is disrupted, leading to rapid loss of bone density
Bone density decreases with age
Osteoporosis features
Silent- unaware until fracture
Symptoms of advanced- back P from collapsed vertebra, reduced height, stoop posture, fractures from little to no trauma
Osteoporosis management
Bisphosphonates- medication can slow bone loss and increase density
Regular exercise
Calcium and vit D supplements
Regular check ups to monitor
RA aetiology
Cause unknown
Foreign antigen sets off chain reaction
HLA-DR4 gene
Smoking, exposure to toxins
RA presentation
Symmetrical
Morning stiffness
Women affected 3x more than men
Early stage- swelling, stiffness, warmth, tenderness
Progression- restriction
Later stage- deformity, ulnar deviation, values knees, claw toes
RA further investigations
X-ray- Jt space narrowing, erosion
May take time to see changes on x-ray
Blood tests- C-reactive proteins, erythrocyte sedimentation rate
RA cations
Some medication has serious side effects, e.g. increased risk of infection
Higher risk of CV disease, important to monitor risk factors such as high blood pressure
RA patho
Stage 1- preclinical- well before signs arise, immune pathology begins. increased erythrocyte, c-reactive proteins, rheumatoid factors
2- synovitis- inflammation of synovial membrane, P and swelling in Jts, potentially reversible
3- destruction- persistent Jt inflammation causes destruction, articular cartilage erodes
4- deformity- combination of articular destruction, capsular stretching + tendon rupture leading to progressive instability + deformity
RA management
DMARDs
PT- maintain Jt function and prevent muscle weakness
Reactive arthritis aetiology
After infection (urinary, GI, genitals)
Most caused by salmonella, shigella, chlamydia
Reactive arthritis clinical features
Jt P, swelling
Particularly in knees, ankles and feet
Some may develop skin rash called keratoderma blenorrhagica
Reactive arthritis further investigations
No osteophyte or Jt space narrowing
Osteopenia
Reactive arthritis patho
Immune response to infection
Overreacts causing inflammation in Jts and other parts of body
Reactive arthritis cautions
Any age, more common in young/middle aged
Reactive arthritis management
Manage underlying infection
ABs
Improvement once infection treated
NSAIDs reduce inflammation + P
PT for increasing ROM, strength
DMARDs- prevents Jt damage
Spina bifida aetiology
Combination of genetic and environmental e.g. lack of folate acid during pregnancy, exposure to radiation
Spina bifida detail
Neuralisation- produces CNS
Ectoderm thickens, forming neural plate
Neural plate folds inwards forming neural fold + crest
Day 22- neural crest fuses forming neural tube
Anterior end becomes brain + rest becomes spinal cord
Closure reliant on adequate folic acid- failure= spina bifida
Clinical features of spina bifida
Depends on size and location
Weakness/paralysis of legs
Scoliosis
Hairy patch
Further investigation for spina bifida
Abnormalities of vertebra, defects of spinal column, scoliosis, absence of curve
MRI detects brain and spinal cord impairment
Cautions of spina bifida
Avoid medication that closure to failure of neural tube closure during embryonic development
Careful handling of baby
Spina bifida management
Surgery to cover exposed neural tissue
Types of spina bifida
Occulta- vertebral fail to close properly, bones don’t fuse, predisposing back P
Meningocele- neural tube closes but meninges frequently herniate through vertebra
Myelomeningecele- neural tube failed to close leading to exposure of neural tissue- can’t carry nerve impulse= paralysis
