Conditions for 16/01/23 Flashcards
(138 cards)
1
Q
OA aetiology
A
- Increased age (takes years to develop)
- Incongruent Jts
- Relationship between stress on articulate cartilage + ability of cartilage to withstand stress
Obesity
2
Q
OA clinical features
A
- 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
3
Q
OA X-ray findings
A
- Osteophyte formation
- Jt space narrowing
- Subchondral sclerosis (thickening of bone in affected Jt)
- Cysts
4
Q
OA pathophysiology
A
- 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
5
Q
OA cautions
A
Exercise
Posture
Knees, hips, hands, spine
6
Q
OA management
A
- Pharmacological
- Braces/support
- Supplements
- Surgery
- Osteopathy- increased ROM, flexibility
7
Q
Lumbar spondylosis aetiology
A
- 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
8
Q
Lumbar spondylosis clinical features
A
- P in low back
- Often worse when standing or walking, relieved when sitting or bending forward
- P spread to thighs
- Tight hamstrings
9
Q
Lumbar spondylosis X-ray finding
A
- Reactive sclerosis
- Narrowing of intervertebral disc space e
- Deviation or step off signs of SPs
- Degeneration of facet Jt
10
Q
Lumbar spondylosis pathophysiology
A
- 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
11
Q
Cautions lumbar spondylosis
A
- Avoid sitting for more than 30 mins at a time
- Eating diet high in sugar, processed and refined foods (inflammatory)
12
Q
Lumbar spondylosis management
A
- Pain relieves
- NSAIDs
- Muscle relaxants
PT- exercises to improve strength + flexibility
Surgery- alleviate pressure on nerves, remove bony spurs
Chronic- requires follow up care
13
Q
Lumbar facet degeneration aetiology
A
- Alternate spinal conditions which change the way facets align
- OA leading cause
14
Q
Lumbar facet degeneration clinical features
A
- 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
15
Q
Lumbar facet degeneration X-ray
A
- Narrowing of disc space
- Subchondral sclerosis
- Osteophytes
Not specific to facet irritation, not all will show these changes
16
Q
Lumbar facet degeneration pathophysiology
A
- 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
17
Q
Lumbar facet degeneration cautions
A
Advances age or osteoporosis- increase risk of fracture
Pregnancy- certain treatment not safe
18
Q
Lumbar facet degeneration management
A
- Physio and pharmacology (NSAIDs) first line treatment
- Facet Jt injection, medial branch block
19
Q
Spondylolithesis aetiology
A
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
20
Q
Spondylolithesis clinical features
A
- Usually painless
- L4/5/S1
- Intermittent back ache, may be exacerbated by exercise or strain
- Step deformity
- Normal ROM in younger Pts
21
Q
Spondylolithesis X-ray findings
A
Slippage of vertebra from spinal column
Shows if congenital or acquired
CT/MRI for surrounding structures
22
Q
Spondylolithesis pathophysiology
A
- Normal laminae and facet locking mechanism fails
- Causes forward slippage (listheis) of vertebral body
L4/5/S1 most common
23
Q
Spondylolithesis cautions
A
Cauda equina- numbness in saddle, los =s of bowel or bladder control
24
Q
Spondylolithesis management
A
Conservative- NSAIDs, steroid injection
Surgery if grade 3/4, spinal fusion of veterbra to above, laminectomy
25
Herniated nucleus pulposus aetiology
- Failure of annulus fibrosis integrity
- Makes content pf nucleus protrude into spinal canal
- Trauma, contact sport
26
Herniated nucleus pulposus clinical features
- Low back P
- Radiculopathy (likely down back of leg, sciatic L4-S3)
Tingling sensation, muscle weakness, bladder control incontinence
27
Herniated nucleus pulposus further investigations
- Suspected during history/physical exam
- Confirmed from MRI or CT scan- determines location and size
28
Herniated nucleus pulpous cautions
- Compression on nerve root may cause severe motor deficit
29
Herniated nucleus pulpous management
- Microdiscectomy- small incision made to remove disc fragment that is impinging nerves
30
Spinal stenosis aetiology
- Age related- discs become drier and shrink
- Arthritis
Herniated disc
Tumours
31
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
32
Stenosis X-ray
- Narrowed disc space
- Fracture
- Bone spurs
- OA (spondylosis)
CT- degree and location
MRI- spinal canal and neural structures
33
Stenosis cautions
Surgery should be avoided if suffering with osteoporosis, pregnancy, bleeding disorder
34
Stenosis pathophysiology
- Narrowing of spinal column that causes pressure on cord or foramina (where N exits)
35
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
36
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
37
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
38
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
39
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
40
Arachnoiditis management
- Pain management
- Physical therapy
- Stretching, ROM exercises
- Adaptation- mobility, comfort
Medication- corticosteroid, opioids
41
Spinal infection aetiology (osteomyelitis)
- Bacterial or fungal in other part of body that has been carried into spine via bloodstream
Most commonly staphylococcus
42
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
43
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
44
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
45
Management of infection
ABS or anti fungal therapy
PT- manage P and weakness
46
Multiple sclerosis aetiology
- Unknown
- Considered immune mediated disease
- Immune system destroys myelin
- Genetic (gene on chromosome 6p21) and environmental factors contribute
47
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
48
Multiple sclerosis further investigation
Diagnosis of exclusion
Evoked potentials- measure electrical activity in brain in response to visual, auditory or somatosensory stimuli
49
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
50
Cautions of multiple sclerosis
- May also develop muscle stiffness/spasm, weakness or paralysis, problems with bladder
Wide range of symptoms therefore difficult to predict
51
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
52
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
53
Rickets aetiology
Lack of vitamin D or calcium
Lack of sunlight exposure, poor diet
Most common in children
54
Rickets clinical features
- Thickening of ankles, wrists and knees
- Bowed legs
- Poor growth
- Dental problems
55
Rickets X-ray
- Fraying- indistinct margins of metaphysis
- Splaying- widening of metaphyseal ends
- X-ray of wrists and ankles usually confirm diagnosis
56
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
57
Cautions of rickets
Treatable, delay can cause serious complications such as irreversible bone deformities
58
Management of rickets
- Increase child’s intake of vitamin D and calcium
PT- maintain ROM and strength
59
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
60
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
61
Paget's X-ray
- Areas of bone breakdown
- Enlargement of bone and deformities that are characteristic of disease (e.g. bowing of long bones)
62
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
63
Cautions of Pagets
Long term treatment
64
Paget's management
- Osteoporosis drugs (bisphosphonates)
- Typically administered through injection, can be taken orally (however can irritate stomach)
65
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
66
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
67
Hyperthyroidism further investigation
Blood tests- elevated calcium levels
X-ray bone density loss, bone cysts in rare cases
68
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
69
Cautions of hyperthyroidism
Avoid high calcium diet- such as dairy
Avoid Vit D supplements
70
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
71
Hypothyroidism aetiology
- Acquired- Removal or injury to parathyroid gland
- Autoimmune disease- attacks parathyroid gland
Idiopathic- no cause
72
Hypothyroidism clinical features
- Twitching facial muscles
- Muscle P or cramps
- Fatigue or weakness
- memory loss
73
Hypothyroidism further investigation
Blood test
X-ray- increased bone density + calcification of soft tissue
Urine analysis
74
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
75
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
76
Hypothyroidism management
- Supplements can bring calcium and phosphorus levels to normal range
Regular blood tests to check levels
77
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
78
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
79
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
80
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
81
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
82
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
83
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
84
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
85
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
86
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
87
Cautions of gout
Long term management
Serious complications lead to Jt damage and kidney stones
88
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
89
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
90
Pseudo-gout clinical features
- Most commonly affects knees
- Swollen, warm and severely painful- sudden + severe
Accompanied by fever and chills
91
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
92
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
93
Cautions of pseudo gout
Risk increases with age
Chronic therefore requires long term treatment
94
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
95
Reactive arthritis aetiology
- Bacteria spreads it
- Chlamydia, salmonella, shigella
96
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
97
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
98
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
99
Reactive arthritis management
- DMARDs- disease-modifying anti-rheumatic drugs
- NSAIDs
Manage underlying condition
If lasts longer than 6 months management approach is different
100
Osteomalacia
Softening + weakness of bones
101
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
102
Osteomalacia aetiology
Vit D deficiency, essential for absorption of calcium and formation of strong bones
Inadequate light exposure, dietary intake
103
Osteomalacia clinical features
Muscle weakness + P, particularly in low back, hips, thighs, pelvis
Bone P
Difficulty standing from seated
Tenderness to touch over bone
104
Osteomalacia x-ray
Bone demineralisation
Early stages may be norma
Blood tests- identify fit D, phosphorus, calcium deficiency
105
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
106
Osteomalacia cautions
Hx of kidney stones or hyperglycaemia
Medication which interacts with vitamin D
107
Osteomalacia management
VItamin D supplements
Adequate sun exposure
Regular exercise, healthy diet
108
Polymyalgia rhematica aetilogy
Unknown
Thought to be autoimmune
Most common in women over 50s
109
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
110
Polymyalgia further investigations
Erythrocyte sedimentation rate + c-reactive proteins to confirm diagnosis and monitor effectiveness of treatment
111
Polymyalgia patho
Chronic inflammation of muscles and tendons
112
Polymyalgia causions
Chronic condition requiring long term treatment
113
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
114
Osteoporosis aetiology
Unknown
Thought to be result of genetic + teratogens
Female, over 50s
smoking, excessive alcohol
115
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
116
Osteoporosis further investigation
Dual-energy x-ray absorptiometry- measures bone density
Ultrasound bone density testing
117
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
118
Osteoporosis features
Silent- unaware until fracture
Symptoms of advanced- back P from collapsed vertebra, reduced height, stoop posture, fractures from little to no trauma
119
Osteoporosis management
Bisphosphonates- medication can slow bone loss and increase density
Regular exercise
Calcium and vit D supplements
Regular check ups to monitor
120
RA aetiology
Cause unknown
Foreign antigen sets off chain reaction
HLA-DR4 gene
Smoking, exposure to toxins
121
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
122
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
123
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
124
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
125
RA management
DMARDs
PT- maintain Jt function and prevent muscle weakness
126
Reactive arthritis aetiology
After infection (urinary, GI, genitals)
Most caused by salmonella, shigella, chlamydia
127
Reactive arthritis clinical features
Jt P, swelling
Particularly in knees, ankles and feet
Some may develop skin rash called keratoderma blenorrhagica
128
Reactive arthritis further investigations
No osteophyte or Jt space narrowing
Osteopenia
129
Reactive arthritis patho
Immune response to infection
Overreacts causing inflammation in Jts and other parts of body
130
Reactive arthritis cautions
Any age, more common in young/middle aged
131
Reactive arthritis management
Manage underlying infection
ABs
Improvement once infection treated
NSAIDs reduce inflammation + P
PT for increasing ROM, strength
DMARDs- prevents Jt damage
132
Spina bifida aetiology
Combination of genetic and environmental e.g. lack of folate acid during pregnancy, exposure to radiation
133
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
134
Clinical features of spina bifida
Depends on size and location
Weakness/paralysis of legs
Scoliosis
Hairy patch
135
Further investigation for spina bifida
Abnormalities of vertebra, defects of spinal column, scoliosis, absence of curve
MRI detects brain and spinal cord impairment
136
Cautions of spina bifida
Avoid medication that closure to failure of neural tube closure during embryonic development
Careful handling of baby
137
Spina bifida management
Surgery to cover exposed neural tissue
138
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
