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Musculoskeletal Flashcards

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1
Q

What is osteoarthritis?

A
  • wear and tear in the synovial joints
  • imbalance between cartilage wearing down and chondrocyte repair leading to structural issues
  • slow onset
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2
Q

What is the pathophysiology behind osteoarthritis?

A
  • chondrocytes release enzymes
  • these break down collagen and proteoglycans
  • exposure of underlying subchondral bone leads to sclerosis
  • reactive remodelling > osteophytes and subchondral cysts
  • joint space lost
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3
Q

What occurs in the joint as OA gets more severe?

A
  • joint space narrows
  • cartilage loss
  • occurrence and growth of osteophytes
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4
Q

What are the causes and risk factors of OA?

A
  • results from genetic factors, overuse, injury
  • RFs: obesity, age, occupation, female, family history
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5
Q

What are the key criteria for diagnosis of OA?

A
  • over 45
  • pain with activity
  • little to no morning stiffness
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6
Q

Which joints are commonly affected in osteoarthritis?

A
  • affects weight bearing joints
  • hip, knee, wrist
  • sacroiliac joints
  • DIPs in hands
  • carpometacarpal joint at base of thumb
  • cervical spine
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7
Q

How does osteoarthritis present?

A
  • joint pain and stiffness worse with activity and at end of day
  • bulky, bony enlargement of joint
  • restricted range of motion
  • crepitus when moving
  • effusions around joint
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8
Q

What signs of OA are seen in the hands?

A
  • Heberden’s (DIP) and Bouchard’s (PIP) nodes
  • squaring at CMC joint
  • weak grip
  • reduced range of motion
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9
Q

What are the signs of OA in the knee?

A
  • occurs in lateral, patellofemoral or medial (most common) compartments
  • occurs without trauma and with slow evolution
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10
Q

What are the 5 key changes seen on X-ray in OA?

A
  • Joint space narrowing
  • Osteophyte formation
  • Subchondral sclerosis
  • Subchondral cysts
  • Abnormalities of bone contour
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11
Q

What is the non-medical management of OA?

A
  • patient advice
  • weight loss: activity and exercise
  • physio, OT, orthotics
  • walking aids: stick/frame
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12
Q

How is OA managed?

A
  • analgesia: paracetamol, NSAIDs (+PPI), opiates
  • intra-articular steroid injection
  • joint replacement last resort
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13
Q

What is systemic sclerosis?

A
  • autoimmune inflammatory and fibrotic connective tissue disease
  • affects skin and internal organs
  • limited cutaneous or diffuse cutaneous
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14
Q

What are the features of limited cutaneous systemic sclerosis?

A
  • Calcinosis
  • Raynaud’s phenomenon
  • oEsophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
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15
Q

What additional problems occur in diffuse systemic sclerosis?

A
  • cardiovascular: htn and coronary artery disease
  • lung: pulmonary htn and fibrosis
  • renal: glomerulonephritis, renal crisis
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16
Q

What is scleroderma?

A
  • hardening of the skin
  • gives shiny, tight appearance without normal folds
  • most notably occurs on hands and face
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17
Q

What is sclerodactyly?

A
  • skin changes in the hands
  • tightening around the joints
  • fat pads on fingers are lost > breaking and ulceration
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18
Q

What is calcinosis and telangiectasia?

A
  • calcinosis: calcium deposits build up under skin (mostly found on fingertips)
  • telangiectasia: small dilated blood vessels in skin - fine, thready appearance
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19
Q

Why does Raynaud’s occur in systemic sclerosis?

A
  • vasoconstriction leads to fingers going white > blue in response to mild cold
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20
Q

Which autoantibodies are found in systemic sclerosis?

A
  • antinuclear antibodies
  • anti-centromere antibodies (limited)
  • anti-Slc-70 antibodies (diffuse)
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21
Q

What is nailfold capillaroscopy?

A
  • where skin meets fingernails is magnified
  • abnormal capillaries, avascular areas and micro-haemorrhages indicate systemic sclerosis
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22
Q

How is systemic sclerosis managed?

A
  • steroids and immunosuppressants
  • Nifedipine for Raynaud’s
  • PPIs and pro-motility meds for GI
  • physiotherapy for healthy joints
  • skin stretching and gentle emollients
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23
Q

What is rheumatoid arthritis?

A
  • autoimmune condition
  • chronic inflammation of synovial lining of joints, tendon sheaths
  • affects multiple symmetrical, peripheral joints
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24
Q

What is the epidemiology of RA?

A
  • 3x more common in women than in men
  • develops in middle age
  • family history increases risk
  • HLA DR1 and HLA DR4 gene
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25
Which antibodies are found in RA?
- Rheumatoid factor (IgM) is an autoantibody which targets IgG - Cyclic citrullinated peptide antibodies (anti-CCP)
26
How does RA present?
- symmetrical distal polyarthropathy - pain, swelling and stiffness - occurs in small joints of hands and feet - systemic: fatigue, weight loss, flu like, muscle ache
27
Which joints are most commonly affected in RA?
- PIP - MCP - wrist and ankle - metatarsophalangeal joints - cervical spine
28
What signs of RA are seen in the hands?
- Z shaped deformity to thumb - swan neck deformity (hyperextended PIP and flexed DIP) - Boutonnieres deformity (hyperextended DIP and flexed PIP) - ulnar deviation of fingers at knuckle
29
What investigations are done for RA?
- FBC: anaemia and infection - ESR and CRP - RF and anti-CCP - X-ray of hands and feet
30
How is RA managed?
- 1st: methotrexate, leflunomide or sulfasalazine - methotrexate in combination with folic acid - biological therapy can be added (TNF inhibitor) - rituximab
31
What is the pathophysiology of giant cell arteritis?
- no clear margin between media, adventitia and intima - narrowed lumen - activated immune cells infiltrate vessel wall > damage and vascular smooth muscle cell remodelling - leads to weakening and occlusion of vessels - leading to ischaemia, infarction, aneurysm
32
What is the aetiology of vasculitis?
- 1º: idiopathic autoimmune process - 2º: drugs, infection, other autoimmune disease - immune complex or ANCA mediated
33
What are types of large vessel arteritis?
- giant cell arteritis - Takayasu arteritis
34
What are type of medium vessel arteritis?
- Kawasaki disease (coronary in children) - polyarteritis nodosa (adults)
35
What are examples of small vessels ANCA +ve vasculitis?
- small arteries, veins - microscopic polyangitis - Wegner's (granulomatosis with polyangitis) - Churg-Strauss syndrome
36
What are examples of immune complex mediated small vessel vasculitis?
- IgA vasculitis: Henoch-Schonlein purpura (more commonly in children) - Goodpasture's (anti-GBM)
37
What is the general presentation of vasculitis?
- purpura: purple non-blanching spots - joint and muscle pain - peripheral neuropathy - renal impairment - GI disturbance - systemic: fever, weight loss, fatigue
38
How is vasculitis diagnosed?
- CRP and ESR raised - p-ANCA bloods (Churg-Strauss) - c-ANCA bloods (Wegner's)
39
How is vasculitis managed?
- steroids: oral, IV, nasal, inhaled - immunosuppressants: cyclophosphamide, methotrexate, azathioprine, rituximab
40
What is the epidemiology of giant cell arteritis?
- scandanavian - white - peak age: 70-80yrs
41
What is the presentation of giant cell arteritis?
- temporal headache - visual problems - scalp tenderness (when brushing hair) - tongue/jaw claudication - tenderness + thickening of temporal artery
42
What key visual problems occur with giant cell arteritis?
- blurring - veiling - double vision (diplopia) - photopsia - amaurosis fugax - KEY: irreversible visual loss in one eye
43
How is giant cell arteritis investigated?
- 1st line: Raised CRP + ESR - Gold: temporal artery US or biopsy (may be missed due to skip lesions) - PET-CT for extra cranial disease
44
How is giant cell arteritis managed?
- oral prednisolone (40-60mg/day) - IV methylprednisolone - gradual reduction of steroid over 12-18 months
45
Describe polyarteritis nodosa?
- occurs in males and with hep B, age 40-60 - can cause renal impairment, stroke, MI - associated with mottled purple rash: livedo reticularis
46
How does granulomatosis with polyangitis (Wegner's) present?
- epistaxis, crusty nasal secretions - hearing loss and sinusitis - saddle shaped nose due to perforated septum - cough, haemoptysis - glomerulonephritis
47
What is myositis and what is the difference between polymyositis and dermatomyositis?
- autoimmune skeletal muscle inflammation and necrosis - polymyositis: chronic muscle inflammation - dermatomyositis: connective tissue disorder with chronic muscle and skin inflammation
48
What are the possible causes and epidemiology of myositis?
- underlying malignancy - lung, breast, ovarian and gastric cancer - affects females with HLA B8 and HLA DR3 gene
49
What is the importance of CK in myositis?
- creatine kinase: enzyme released in muscle inflammation - usually less than 300U/L but is >1000 in disease - can also be caused by: rhabdomyolysis, AKI, MI, strenuous exercise
50
How does myositis present?
- muscle pain, fatigue and weakness - bilaterally, affects proximal muscles - affects shoulder and pelvic girdle - onset over weeks
51
How does dermatomyositis present?
- Gottron lesions on knuckles, elbows, knees - photosensitive erythematous rash (back, shoulders, neck) - purple rash on face + eyelids - periorbital oedema - calcinosis
52
Which autoantibodies are seen in myositis?
- Anti-Jo-1: polymyositis - Anti-Mi-2 antibodies: dermatomyositis - Anti-nuclear antibodies: dermatomyositis
53
How is myositis diagnosed?
- clinical presentation - elevated CK + LDH - autoantibodies - electromyography - muscle biopsy is definitive
54
How is myositis treated?
- 1st line: corticosteroids - immunosuppressants (azathioprine) - IV immunoglobulins - biological therapy (infliximab)
55
What is ankylosing spondylitis?
- inflammatory condition of the spine causing progressive stiffness and pain - part of seronegative spondyloarthropathy conditions - relates to HLA B27 gene
56
How does ankylosing spondylitis present?
- lower back pain and stiffness - sacroiliac pain in buttock - pain is worse with rest and improves with movement - worse at night, improves in morning (30+ mins activity
57
How is ankylosing spondylitis investigated?
- CRP and ESR raised - HLA B27 raised - X-ray of spine and sacrum - spinal MRI shows bone marrow oedema
58
What is seen on X-ray of ankylosing spondylitis?
- Bamboo spine - squaring of vertebral bodies - subchondral sclerosis and erosion - Syndesmyophytes (bone growth at ligaments) - ossification of ligaments, discs, joints - fusion of joints
59
How is ankylosing spondylitis managed?
- NSAIDs for pain - steroids - Anti-TNF: etanercept/infliximab - Secukinumab (monoclonal antibody against interleukin-17)
60
What complications is ankylosing spondylitis associated with?
- anterior uveitis - enthesitis - dactylitis - heart block - restrictive lung disease - aortitis
61
What is psoriatic arthritis?
- inflammatory arthritis associated with psoriasis - occurs in 10-20% of patients with psoriasis
62
What is arthritis mutilans?
- occurs in phalanxes - osteolysis of bones around joints in digits - leads to progressive shortening of finger (telescopic)
63
What are signs of psoriatic arthritis?
- plaques of psoriasis - pitting of nails - onycholysis - dactylitis - enthesitis - inflamed DIP joints
64
What X-ray changes are seen in psoriatic arthritis?
- periosititis: thickened and irregular outline of bone - ankylosis: joint stiffening - osteolysis: destruction of bone - dactylitis: appears as soft tissue swelling - pencil-in-cup appearance: central erosions of bones causes one to sit in another
65
How is psoriatic arthritis managed?
- NSAIDs - DMARDS: methotrexate - Anti-TNF (etanercept, infliximab) - Ustekinumab targets interleukin 12 and 23
66
What is reactive arthritis?
- synovitis occurs in joints as reaction to an infective trigger - presents as acute monoarthritis usually in lower limb/knee
67
What is the aetiology of reactive arthritis?
- triggered by infection: gastroenteritis, chlamydia - c. jejuni, salmonella, shigella - linked to HLA B27
68
What is the presentation of reactive arthritis?
- Reiter's triad: can't pee, can't see, can't climb a tree: urethritis, arthritis, conjunctivitis - uveitis - enthesitis
69
How is reactive arthritis managed?
- aspiration to exclude septic arthritis - NSAIDs - Steroid injections into affected joints - systemic steroids if multiple affected
70
What is the difference between osteoporosis and osteopenia?
- osteoporosis: reduction in bone density: bone is weaker and more prone to fracture - osteopenia: less severe reduction in bone density
71
What are the risk factors for osteoporosis?
- Steroid use - Hyperthyroidism - Alcohol - Thin (low BMI) - Testosterone (low) - Early menopause - Renal/liver failure - Erosive/inflammatory bone disease - Dietary low calcium
72
What is the epidemiology of osteoporosis?
- older age - female - post-menopausal - oestrogen is protective
73
What is the pathophysiology behind osteoporosis?
- reduction in bone density - osteoclast activity is higher than osteoblast activity causing large spaces in brittle bone - usually occurs due to trauma or a fall - force applied to bone > strength of bone
74
What 2 scoring systems can be used to grade osteoporosis?
- DEXA scan: measures bone mineral density with T score of hip - FRAX score: 10 year probability of major osteoporotic fracture
75
Describe DEXA scoring
- Normal: T ≥ -1.0 - Osteopenia -2.5 < T < -1.0 - Osteoporosis T ≤ -2.5 - Severe osteoporosis T ≤ -2.5 plus a fracture
76
How should osteoporosis be investigated?
- FRAX on women > 65 and men > 75, younger patients with risk factors - If intermediate risk: offer DEXA, if high then offer treatment
77
How is osteoporosis managed?
- avoiding falls - calcium supplementation with vit D - glucocorticoids - 1st line: bisphosphonates e.g. zoledronic acid - 2nd line: Denosumab
78
What lifestyle advice is given for osteoporosis?
- exercise - maintain healthy weight - stop smoking - reduce alcohol - avoid falls
79
How do bisphosphonates work and what are the side effects?
- interfere with osteoclasts and reduce their activity - prevents reabsorption of bone - side effect: osteonecrosis of jaw and auditory canal - reflux and oesophageal erosion
80
How does Denosumab work?
- blocks osteoclast activity by binding to the RANK-ligand
81
What is gout?
- crystal arthropathy - chronically high blood uric acid levels - urate crystals deposition causing hot, swollen, painful joints
82
What is the aetiology of gout?
- high purine foods: beer, shellfish, offal, red meat, fructose - low dose aspirin, diuretics and ketones impair renal ability to excrete uric acid
83
What are the risk factors for gout?
- male - obesity - high purine diet (meat) - alcohol - existing CVD/renal disease - family history
84
How is gout managed acutely?
- 1st line: NSAIDs - 2nd line: colchicine - 3rd line: steroid
85
How is gout managed in the long-term?
- allopurinol: xanthine oxidase inhibitor which reduces uric acid levels - lifestyle changes: losing weight, staying hydrated, minimising consumption of high purine foods
86
What does fluid aspiration from gout show?
- no bacterial growth - needle shaped crystals - negatively birefringent of polarised light - monosodium urate crystals
87
What do joint X-rays in gout show?
- joint space maintained - lytic lesions - punched out erosions with sclerotic borders and overhanging edges
88
Which joints does gout typically affect?
- base of big toe (metatarso-phalangeal) - DIP joints in hands - wrist - base of thumb
89
How does gout present?
- gouty top: subcut deposits of uric acid - affects small joints and connective tissues in hand, ears, elbows - single acute hot, swollen, painful joint
90
What is the pathophysiology of gout?
- purines are converted to uric acid by xanthine oxidase - it is normally in the form of monosodium urate in the blood - most cases occur if there is impaired excretion (kidneys), not from uric acid overproduction
91
What is pseudogout and what is the epidemiology?
- crystal arthropathy caused by calcium pyrophosphate crystals - mostly in elderly women
92
What is the pathophysiology behind pseudogout?
- chondrocytes are the main cell involved in formation and deposition of CPP - excess pyrophosphate production leads to CPP over saturation - the excess CPP takes the form of crystals - this stimulates a pro inflammatory response leading to activation of neutrophils and phagocytes
93
How does pseudogout present?
- older adults - hot, swollen, stiff, painful knee, shoulder, wrist or hip - chronic - can be asymptomatic and picked up on X-ray
94
How is pseudogout diagnosed?
- aspiration for synovial fluid - calcium pyrophosphate crystals - rhomboid shaped - positive birefringent of polarised light
95
What is chondrocalcinosis?
- thin white line in the middle of the joint space - caused by calcium deposition - appears on X-ray - Gold standard diagnosis for pseudogout
96
How is pseudogout managed?
- usually resolves spontaneously - NSAIDs, colchicine, joint aspiration - steroids - arthrocentesis if severe
97
What is the key differential diagnosis to be excluded from the crystal arthropathies?
- septic arthritis also presents with an acute, hot, swollen and painful joint
98
What is SLE?
- inflammatory autoimmune connective tissue disease - presents with non-specific symptoms - relapsing-remitting course
99
What is the epidemiology of SLE?
- more common in: - women - Asians - presents in young to middle aged adults
100
What is the pathophysiology behind SLE?
- characterised by anti-nuclear antibodies - antibodies to proteins within the person's cell nucleus - this causes an autoimmune response
101
How does SLE present?
- fatigue - weight loss - photosensitive malar rash (butterfly shaped across nose and cheeks - worsens with sunlight) - shortness of breath - lymphadenopathy and splenomegaly - glomerulonephritis - Raynaud's
102
What investigations can be done for SLE?
- FBC: normocytic anaemia - decreased C3 and C4 levels - raised CRP and ESR - raised immunoglobulins - autoantibodies
103
Which autoantibodies are commonly seen in SLE?
- anti-nuclear antibodies +ve in 85% patients - Anti-dsDNA - Anti-ENA
104
How is SLE treated?
- 1st line: NSAIDs, corticosteroids, hydroxychloroquine - methotrexate, leflunomide, azathioprine - avoid sunlight and use suncream
105
What complications can occur from SLE?
- CVD - infection - anaemia of chronic disease - pericarditis or pleuritis - lupus nephritis
106
What is antiphospholipid syndrome?
- Blood becomes prone to clotting and patient is in hyper-coagulable state - associated with antiphospholipid antibodies
107
The presence of which antibodies are used to diagnose antiphospholipid syndrome?
- lupus anticoagulant - anticardiolipin antibodies - Anti-β-2 glycoprotein I antibodies
108
What conditions is antiphospholipid syndrome associated with?
- DVT and PE - stroke, MI and renal thrombosis - miscarriage, stillbirth and pre-eclampsia - Libmann-Sacks endocarditis
109
What signs and symptoms are common in antiphospholipid syndrome?
- livedo reticularis: purple lace like rash giving mottled appearance - thrombocytopenia
110
How is antiphospholipid syndrome managed?
- long term warfarin with INR range of 2-3 - pregnant women in LmwH and aspirin
111
What is Sjrogen's?
- autoimmune condition affecting exocrine glands - 1º occurs in isolation, 2º related to SLE/RA
112
Which antibodies are found in Sjrogen's?
- anti-Ro and anti-La
113
What symptoms are caused by Sjrogen's?
- leads to dry mucous membranes: - dry eyes, mouth, vagina
114
How is Sjrogen's diagnosed?
- Schirmer test - inset folded piece of filter paper under lower eyelid - tears should travel 15mm in 5 mins - <10mm is significant
115
How is Sjrogen's managed?
- artificial tears, saliva - vaginal lubricants - hydroxychloroquine to halt progress
116
What is fibromyalgia?
- non-specific muscular disorder - primarily affects insertions of tendons, associated soft tissues - potentially hyper excitability of pain fibres - more common in women with onset 40-50
117
What is the presentation of fibromyalgia?
- pain worse with stress, cold weather and activity - morning stiffness - pins and needles in hands and feet - poor sleep
118
How is fibromyalgia diagnosed?
- widespread bilateral joint pain above and below the hips - pain on > 11 of the 18 palpable sites for at least 3 months
119
How is fibromyalgia managed?
- manage pain: amitriptyline - avoid opioids - improve sleep - exercise - local heat application
120
What are examples of types of bone tumours?
- chondrosarcoma - osteosarcoma (in children) - Ewing sarcoma (bone marrow) - giant cell tumour of bone (benign)
121
What are risk factors for bone tumours?
- previous radiotherapy - previous cancer - Paget's disease - benign lesions
122
How do bone malignancies present?
- common in long bones - worse at night, resistant to analgesia - bony/soft tissue swelling - easy bruising - mobility issues - joint stiffness, reduced range of motion
123
What investigations are done for bone tumours?
- 1st line: X-ray - Gold: bone biopsy - Bloods: FBC, ESR, Ca, U&Es
124
How are MSK malignancies managed?
- chemo/radiotherapy - surgical resection: limb sparing or sacrificing
125
From where do tumours most commonly metastasise to bone?
- Breast (Sclerotic/Mixed) - Lung (Lytic / Mixed) - Thyroid (Lytic) - Kidney (Lytic) - Prostate (Sclerotic/Mixed)
126
What is polymyalgia rheumatica?
- inflammatory condition causing pain and stiffness in shoulders, neck and pelvic girdle - strong association with giant cell arteritis
127
What is the epidemiology of polymyalgia rheumatica?
- female - age 50+ - more common in caucasians
128
How does PMR present?
- bilateral shoulder pain radiating to elbow - bilateral pelvic girdle pain - worse with movement and interferes with sleep - morning stiffness >45 mins
129
How is PMR diagnosed?
- ESR and CRP raised - Bloods: FBC, U&Es, LFTs - symptoms lasting 2+ weeks
130
How is PMR treated?
- 15mg prednisolone per day - assess after 1 week and 3-4 weeks - if symptoms improve start a reducing regime
131
What are the differential diagnoses for PMR?
- myeloma - myositis - RA/osteoarthritis - SLE - osteomalacia - fibromyalgia
132
What is septic arthritis and what is a common cause?
- infection in native or joint replacement - destroys joint and causes systemic illness - common complication of hip and knee replacements
133
How does septic arthritis present?
- affects single joint, often knee - hot, red, swollen, painful joint - stiffness and reduced range of motion - systemic: fever, lethargy
134
Which bacteria commonly cause septic arthritis?
- Staph aureus - Neisseria gonorrhoea - Strep pyogenes - Haemophilus influenza - E. coli
135
How is septic arthritis investigated?
- joint aspiration - gram staining, crystal microscope, culture - antibiotic sensitivities
136
How is septic arthritis managed?
- empirical IV antibiotics for 3-6 weeks - flucloxacillin + rifampicin - vancomycin if allergic to penicillin
137
What is osteomyelitis?
- inflammation in a bone and bone marrow - haematogenous: pathogen carried through blood to the bone - acute or chronic - most commonly caused by Staph aureus
138
What are the risk factors for osteomyelitis?
- open fractures - orthopaedic operations - diabetes - peripheral arterial disease - IV drug use
139
How does osteomyelitis present?
- fever - pain and tenderness - erythema - swelling - systemic symptoms
140
How is osteomyelitis investigated?
- MRI - Bloods: cultures, raised inflammatory - bone cultures
141
How is osteomyelitis treated?
- surgical debridement of infected bone and tissue - antibiotic therapy: 6 weeks of flucloxacillin ± rifampicin
142
What are potential signs of osteomyelitis on X-ray?
- periosteal reaction (changes to bone surface) - localised osteopenia (bone thinning) - destruction of areas of bone
143
What is the difference in age and speed of onset between inflammatory and degenerative joint disease?
- Inflammatory: can happen at any age, rapid (weeks-months) - Degenerative: usually in later life, slow - years
144
What is the mechanism of action of anti-TNF drugs?
- blocks tumour necrosis factor which is a cytokine that stimulates inflammation - infliximab is a monoclonal antibody to TNF
145
What is Paget's?
- excessive bone turnover due to excess activity of osteoblasts and osteoclasts - leads to areas of sclerosis and lysis - leads to enlarged and misshapen bones which increase risk of pathological fractures - affects axial bones
146
How does Paget's present?
- bone pain and deformity - fractures - hearing loss if ear bones affected
147
What does X-ray of someone with Paget's show?
- bone enlargement and deformity - osteoporosis circumscripta: well defined dense lesions - cotton wool appearance - V-shaped defects in long bones
148
What do bloods for Paget's show?
- raised ALP - normal calcium and phosphate
149
How is Paget's treated?
- bisphosphonates interfere with osteoclast activity - NSAIDs - calcium and vit D supplementation
150
What are key complications of Paget's?
- osteosarcoma - spinal stenosis
151
What is the pathology behind mechanical lower back pain?
- damage to the muscles and soft tissues of the back due to posture, physical activity, lifting - disorders of the facet joints of the spine - muscle spasm > pain > spasm > pain
152
What are the risk factors for chronic lower back pain?
- smoking - poor working conditions - psychological disorders - low socioeconomic status
153
How does mechanical back pain present?
- lower back pain - worse on movement (twisting/bending) - relieved by rest and at night - history of specific injury
154
How is mechanical back pain managed?
- mostly self resolving - heat - analgesia - physiotherapy - preventative: weight loss, muscle conditioning
155
From where do tumours most commonly metastasise to bone?
- Breast (Sclerotic/Mixed) - Lung (Lytic / Mixed) - Prostate (Sclerotic/Mixed) - Kidney (Lytic) - Thyroid (Lytic)
156
What is osteomalacia?
- defective bone mineralisation causes soft bones - results from insufficient vitamin D
157
What is the pathophysiology behind osteomalacia?
- vit D is created from cholesterol by the skin in response to UV radiation - it is essential in absorbing calcium and phosphate from the intestines and kidneys - low levels lead to defective bone mineralisation
158
How is low vitamin D related to PTH?
- low vit D > low serum calcium - this causes 2º hyperparathyroidism - parathyroid gland tries to raise calcium level by secreting PTH - PTH stimulates increased reabsorption from the bone
159
What is the presentation of osteomalacia?
- fatigue - bone pain - muscle weakness and aches - pathological/abnormal fractures - looser zones (partial fragility fractures)
160
What is the investigation of osteomalacia?
- serum 25-hydroxyvitamin D - <25 nmol/L: vit D deficiency - 25-50nmol/L: vit D insufficiency - X-ray shows osteopenia and DEXA shows low density

Osha 2a (15 decks)

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