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Finals > MSK > Flashcards

MSK Flashcards

1
Q

Define osteoarthritis

A
  • Cartilage destruction and loss with accompanying periarticular and articular inflammation and alteration of bone and cartilage structure
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2
Q

What is the epidemiology of non-inflammatory degenerative (NID) arthritis (4)

A
  • Usually seen in older people
  • more common in women
  • Most common type of arthritis
  • Mostly affects articular cartilage
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3
Q

What are the risk factors for NID arthritis (6)

A
  • Obesity
  • Inc. age
  • Female
  • Occupation (eg. manual labour)
  • Trauma
  • Diabetes
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4
Q

Describe the pathophysiology of NID arthritis

A
  • Progressive loss and destruction of articular cartilage leads to imbalance of articular cartilage destruction/production
  • This leads to the new cartilage produced being fissured
  • This causes the articular bones to undergo increased stress and leads to their damage
  • This causes the formation of jagged abnormal sclerotic bone (osteophytes)
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5
Q

How might NID arthritis present (6)

A
  • Gradual onset, progressive joint pain
  • Worse on exercise
  • Morning stiffness <30 mins
  • Heberdens/bouchards nodes
  • Muscle wasting around joints
  • Limited movement of joints
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6
Q

How do you diagnose NID arthritis (3)

A
  • X-ray (LOSS)
  • MRI
  • Joint aspiration (if possible)
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7
Q

How do you treat NID arthritis (5)

A
  • Paracetamol/ibuprofen/weak opioid
  • Ice/heat pack
  • Physio./exercise/weight loss
  • Surgery
  • Joint steroid injections
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8
Q

What is rheumatoid arthritis

A
  • A chronic inflammatory autoimmune disorder causing symmetrical polyarthritis
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9
Q

What is the epidemiology of rheumatoid arthritis (3)

A
  • More common in women
  • More common 30-50 less common in elderly than OA
  • Associated with smoking
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10
Q

What are the risk factors for rheumatoid arthritis (3)

A
  • Smoking
  • Female
  • Family history/genetic
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11
Q

Describe the pathophysiology of rheumatoid arthritis

A
  • Overproduction of TNF alpha in synovial joints
  • Causes inflammation (synovitis) and joint destruction
  • Synovium proliferates and forms a pannus
  • The pannus then destroys the joint cartilage leading to bone exposure, erosion and damage
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12
Q

How might rheumatoid arthritis present (5)

A
  • Progressive, symmetrical joint pain and inflammation
  • Joints are hot and tender
  • Morning stiffness >30 mins
  • Relived by exercise
  • Muscle wasting and hand deformities
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13
Q

How do you diagnose rheumatoid arthritis (3)

A
  • Bloods (raised CRP/ESR, anaemia RF positive)
  • X-ray/MRI (bone erosion)
  • Joint aspiration (high white cells)
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14
Q

How do you treat rheumatoid arthritis (5)

A
  • Weight loss/exercise/smoking cessation
  • Paracetamol/NSAID/codeine
  • Oral prednisolone
  • Disease modifying anti-rheumatic drugs (DMARDs)
    • Methotrexate (inhibit inflammatory cytokines)
  • TNF alpha blockers
    • Infliximab
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15
Q

What is osteoporosis (2)

A
  • Systemic skeletal disease with low bone mass and micro-architectural deterioration of bone leading to increased susceptibility to fracture
  • Bone mineral density >2.5 s.d from the mean young adult value on a DEXA scan
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16
Q

What is the epidemiology of osteoporosis (3)

A
  • Increases with age
  • More common in females
  • More common in caucasians and asians
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17
Q

What are the risk factors for osteoporosis (4)

A
  • Female
  • Increasing age
  • Caucasian/asian
  • SHATTERED
  • Steroid
  • Hyperthyroid/parathyroidism (PH/PTH inc. bone resorption)
  • Alcohol/tobacco
  • Thin
  • Testosterone low
  • Erosive/inflammatory bone disorder
  • Renal/liver failure
  • Early menopause (low oestrogen)
  • Diet (dec. calcium)
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18
Q

How might osteoporosis present

A
  • Fracture (wrist, femur, vertebrae)
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19
Q

How do you diagnose osteoporosis

A
  • Dual energy X-ray absorpimetry (DEXA)
    • > 2.5 sd from mean = osteoporosis
    • 1.5-2.5 sd from mean = osteopenia
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20
Q

How do you treat osteoporosis (3)

A
  • Smoking cessation/exercise/calcium in diet
  • Biphosphonates (decrease bone resorption)
    - Aldendronate
  • HRT (oestrogen/testosterone)
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21
Q

What is systemic lupus erythromatosus (SLE)

A
  • An inflammatory systemic autoimmune disorder characterised by rash and arthralgia as most common and renal/cerebral as most serious symptoms
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22
Q

What is the epidemiology of SLE (3)

A
  • More common in women
  • Onset typically 20-40
  • Most common in Afro-Caribbeans and Asians
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23
Q

What are the risk factors for SLE (4)

A
  • Family history/genetics
  • EBV
  • Female
  • Afro-Caribbean/Asian
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24
Q

Describe the pathophysiology of SLE

A
  • Cellular remnants that are usually hidden from immune system during apoptosis are inefficiently destroyed
  • Hence they get into the lymphoid system and antibodies are produced against them
  • This causes inflammatory autoimmune attack with neutrophillic invasion and abnormal cytokine production
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25
Q

How might SLE present (6)

A
  • Fever and malaise/arthralgia
  • Skin (85%)
    • Butterfly erythema
    • Photosensitive rash
  • Joint (90%)
    • Symptoms similar to RA
  • Mouth ulcers very common
  • Renal (30%)
    • Glomerulonephritis
  • CNS (60%)
    • Seizure
    • Psychosis
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26
Q

How do you diagnose SLE

A
  • Bloods
    • Raised ESR but not CRP
    • Anaemia
    • Serum anti nuclear antibodies (ANA) positive
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27
Q

How do you treat SLE (5)

A
  • Acute attack
    • High does prednisolone and iv cyclophosphamide
  • Prednisolone
  • Immunosupression (Azathioprine)
  • NSAIDs for arthritis/fever
  • Reduce CVS risk (B.P and statins)
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28
Q

What is antiphospholipid syndrome

A
  • A syndrome characterised by thrombosis and/or recurrent miscarriage with positive serum antiphospholipid antibodies
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29
Q

What is the epidemiology of antiphospholipid syndrome (2)

A
  • Associated with SLE

- More common in females

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30
Q

Describe the pathophysiology of antiphospholipid syndrome

A
  • Antiphospholipids bind to phospholipid on the surface of platelets causing thrombus formation
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31
Q

How might antiphospholipid syndrome present (3)

A
  • Thrombosis (PE, stroke, DVT, MI)
  • Miscarriage
  • Thrombocytopenia (bleeding, bruising, purpura)
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32
Q

How do you diagnose antiphospholipid syndrome

A
  • Anticardiolipin test
    • Tests for antibodies that bind to phospholipid
  • At least 2 positive tests 12 weeks apart
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33
Q

How do you treat antiphospholipid syndrome (3)

A
  • Warfarin
  • Aspirin
  • LMW heparin (clopidogrel)
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34
Q

What is Sjorgens syndrome

A
  • Chronic autoimmune destruction of epithelial exocrine glands especially the lacrimal and salivary glands
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35
Q

Describe the pathophysiology of Sjorgens

A
  • Lymphocytic infiltration, inflammation and hence fibrosis of exocrin glands, especially lacrimal and salivary
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36
Q

How might Sjorgens present (4)

A
  • Dry eyes
  • Dry mouth
  • Dry vagina
  • Dry skin
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37
Q

How do you diagnose Sjorgens

A
  • Schirmer tear test

- Filter paper on eyelid, <5mm tears = Sjorgens

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38
Q

What is the treatment for Sjorgens

A
  • Artificial tears and Saliva replacement therapy
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39
Q

What is the epidemiology of systemic sclerosis (scleroderma) (2)

A
  • More common in females

- Usually presents 30-50

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40
Q

Describe the pathophysiology of systemic sclerosis

A
  • Vascular endothelial damage leads to vasoconstriction
  • Continuous vascular damage leads to uncontrolled and irreversible proliferation of fibroblasts and other connective tissue
  • This leads to vascular wall thickening and fibrosis hence lumen narrowing
  • This causes widespread ischaemia
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41
Q

How might limited cutaneous scleroderma present (5)

A
  • CREST
  • Calcium deposits
  • Raynauds
  • Eosphageal stricture/dysmotility
  • Sclerodatyly (tight skin/ulcers on digits)
  • Telenagiectasia (spider veins)
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42
Q

How might diffuse cutaneous scleroderma present (5)

A
  • Raynauds
  • GI (oesophageal, SI, LI dysmotility)
  • Renal (AKI/CKD)
  • Pulmonary fibrosis/hypertension (pulmonary vessel fibrosis)
  • Myocardial fibrosis (arrythmia)
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43
Q

How do you diagnose systemic sclerosis (3)

A
  • Positive anti nuclear antibodies
  • Limited - positive anti centromere antibodies
  • Diffuse - positive anti RNA polymerase antibodies
44
Q

How do you treat systemic sclerosis (4)

A
  • Raynauds
    • Hand warmers
    • CCB (vasodilators) (verapamil)
  • PPI (lansoprazole) for GI
  • Renal (B.P control)
  • Pulmonary fibrosis (prednisolone/azathioprine)
45
Q

What is polymyositis/dermatomyositis

A
  • Inflammation and necrosis of skeletal muscle fibres of unknown aetiology, skin involvement is dermatomyositis
46
Q

How might Polymyositis/dermatomysositis present (4)

A
  • Progressive shoulder/pelvic muscle weakness
  • May also affect respiratory and swallowing muscles
  • Raynauds (demato)
  • Purple discolouration of eyelids and knuckle plaques
47
Q

How do you diagnose Polymyositis/dermatomysositis

A
  • Muscle biopsy

- Shows necrosis/inflammation of muscle fibres

48
Q

How do you treat Polymyositis/dermatomysositis (2)

A
  • Oral prednisolone

- Azathioprine

49
Q

What do seronegative spondyloarthropathies have in common (4)

A
  • Axial inflammation
  • Peripheral arthritis
  • Rheumatoid factor negative (seronegative)
  • HLA-B27 association
50
Q

What is HLA-B27 (4)

A
  • Human leucocytic antigen B27
  • Surface antigen present in all cells
  • Plays a role in immunity
  • You are either HLA-B27 positive or negative
51
Q

What might indicate you to think seronegative spondyloarthropathy

A
  • SPINEACHE
  • Sausage digits
  • Psoriasis
  • Inflammatory back pain
  • NSAID response
  • Enthesitis
  • Arthritis
  • CRP raised
  • HLA-B27
  • Eye (uveitis)
52
Q

What is ankylosing spondylitis

A
  • A chronic inflammatory disorder of the spine, ribs and sacro-iliac joints
  • Ankylosing means stiffness due to new bone formation
53
Q

What is the epidemiology of ankylosing spondylitis (3)

A
  • More common in males
  • Usually presents <30
  • 88% HLA-B27 positive
54
Q

Describe the pathophysiology of ankylosing spondylitis

A
  • Lymphocytic infiltration and erosion of ligament insertions at rib, spine and sacro-iliac joints
  • Leads to new bone formation which causes pain and stiffness and eventually bamboo spine
55
Q

How might ankylosing spondylitis present (5)

A
  • Gradual onset back pain/stiffness
  • Episodic sacro-iliac inflammation
  • Peripheral arthritis
  • Worse in morning/at night
  • releived by exercise
56
Q

How do you diagnose ankylosing spondylitis (2)

A
  • Bloods
    • Raised ESR/CRP
    • HLA-B27 positive
  • X-ray
    • Joint erosion/new bone formation
57
Q

How do you treat ankylosing spondylitis (5)

A
  • Exercise/posture for back
  • NSAIDs for pain
  • DMARDs (methotrexate) for peripheral arthritis
  • TNF alpha blockers (infliximab)
  • Joint steroid injections
58
Q

How psoriatic arthritis present (3)

A
  • May be symmetrical or asymmetrical
  • Most commonly only affects DIPJs
  • Skin psoriasis
59
Q

How do you diagnose psoriatic arthritis

A
  • X-ray

- Central joint bone erosion

60
Q

How do you treat psoriatic arthritis (4)

A
  • NSAIDs
  • Joint steroid injection
  • DMARDs (methotrexate)
  • TNF alpha blockers (infliximab)
61
Q

What is reactive arthritis

A
  • Sterile inflammation of joint in response to distal infection
62
Q

What is the epidemiology of reactive arthritis (3)

A
  • HLA-B27 increases risk 30x
  • More common in males
  • Usually caused by GI/STI
63
Q

How might reactive arthritis present (3)

A
  • Acute asymmetrical lower limb arthritis
  • Days to weeks post infection
  • Cant see, cant wee, cant climb tree
    • Uveitis
    • Penis ulcers
    • Enthesitis
64
Q

How do you diagnose reactive arthritis (2)

A
  • ESR/CRP raised
  • Joint aspiration
    • Sterile with high neutrophils
65
Q

How do you treat reactive arthritis (3)

A
  • NSAIDs
  • Treat infection
  • Methotrexate/infliximab if persistent
66
Q

What is systemic vasculitis

A
  • Inflammation and necrosis of blood vessels leading to aneurysm/rupture and thrombosis/ischaemia/infarct
67
Q

What conditions are associated with vasculitis (6)

A
  • Infective endocarditis
  • SLE
  • Systemic sclerosis
  • Polymyositis/dermatomyositis
  • Rheumatoid arthritis
  • IBD
68
Q

What is the epidemiology of polymyalgia rheumatica (3)

A
  • Type of vasculitis
  • More common in females
  • Only in over 50s
69
Q

How might polymyalgia rheumatica present (4)

A
  • Sudden onset severe pain and stiffness in neck, shoulders, back and hips
  • Worse in mornings
  • Peripheral arthritis
  • May have fever/malaise
70
Q

How do you diagnose polymyalgia rheumatica (2)

A
  • ESR and CRP raised

- History and over 50

71
Q

How do you treat polymyalgia rheumatica

A
  • Oral prednisolone

- PPI, biphosphonates, calcium (long term steroids)

72
Q

What is giant cell arteritis

A
  • Granulatomous inflammation of the large cerebral arteries in association with polymyalgia rheumatica
73
Q

How might giant cell arteritis present (5)

A
  • Severe headache
  • Scalp tenderness
  • Jaw claudication
  • Sudden painless vision loss
  • Polymyalgia rheumatica
74
Q

How do you diagnose giant cell arteritis

A
  • Temporal artery biopsy
75
Q

What is the treatment for giant cell arteritis

A
  • High dose prednisolone, taper down
76
Q

What is the epidemiology of gout (3)

A
  • More common in males
  • Increases with age
  • Most common inflammatory arthritis in the UK
77
Q

What are the risk factors for gout (6)

A
  • Obesity
  • Diabetes
  • Renal disease
  • Diet (high purine food/high sugar)
  • Family history
  • IHD
78
Q

Describe the pathophysiology of gout

A
  • Purine (red meat/seafood, but mostly energy pproduction) is broken down into uric acid
  • If the amount produced exceeds amount excreted by kidneys leads to hyperuricamia
  • This leads to monosodium urate crystal formation in the joints causing pain and inflammation
79
Q

How might gout present (2)

A
  • Acute
    • Sudden onset pain, swelling and redness usually
      of big toe (MTP)
    • May be polyarthritic
  • Tophaceous
    • Formation of tophi (aggregates of m.s urate and
      inflammatory cells)
    • Lead to bone erosion, pain and stiffness
80
Q

How do you diagnose gout (2)

A
  • Joint aspiration
    • Long needle like crystals, negative to polarised
      light
  • Hyperuricaemia
81
Q

How do you treat gout (4)

A
  • Dietary change (inc. dairy, dec. red meat/seafood)
  • Weight loss
  • Acute
    • NSAIDs
    • Prednisolone
  • Prevention
    • Allopurinol (dec. uric acid production)
82
Q

What are the risk factors for pseudogout (4)

A
  • Mostly affects old women !!!!!!!!!!
  • Diabetes
  • Osteoarthritis
  • Trauma
83
Q

How can pseudogout present (3)

A
  • Acute severe pain and swelling in knees/wrists
  • Red, warm swelling
  • Fever
84
Q

How do you diagnose pseudogout

A
  • Joint aspiration
    • Sodium pyrophosphate crystals
    • Small rhomboid and positive to polarised light
85
Q

How do you treat pseudogout (3)

A
  • NSAIDs
  • Prednisolone
  • Joint aspiration
86
Q

What is fibromyalgia

A
  • Widespread musculoskeletal pain for more than 3 months, with pain on 11/18 tender sites on palpitation and all other causes excluded
87
Q

What is the epidemiology of fibromyalgia (3)

A
  • More common in females
  • Usually seen in older people
  • Association with rheumatoid arthritis
88
Q

What are the risk factors for fibromyalgia (4)

A
  • Female
  • Chronic disease
  • Inc. age
  • Poor socio-economic status
89
Q

How might fibroyalgia present (6)

A
  • Widespread chronic pain
  • Usually centres around back and neck
  • Morning stiffness
  • Feet and hand paraesthesiae
  • Aggravated by exercise, cold and stress
  • Usually extreme fatigue and sleep problems
90
Q

How do you diagnose fibromyalgia (2)

A
  • 11/18 tender sites on digital palpitation, >3 months

- All other causes excluded

91
Q

How do you treat fibromyalgia (4)

A
  • Educate patients and family
  • Treat sleep problems
  • Try to increase their fitness
  • Low dose antidepressants/anticonvulsants
92
Q

What are the red flags for back pain (6)

A
  • Progressive
  • Neurology
  • Violent trauma
  • > 20, <55
  • Systemic unwell/weight loss
  • Drugs
93
Q

What is the epidemiology of mechanical back pain (3)

A
  • Usually 20-55
  • Associated with manual labour
  • Smoking and stress association
94
Q

What are the causes of mechanical back pain (3)

A
  • Disc prolapse
  • Osteoarthritis
  • Heavy manual handling
95
Q

How might mechanical back pain present (5)

A
  • Stiff painful back +/- scoliosis
  • Sudden onset
  • Relieved by rest, exacerbated by exercise
  • Worse in evening, better in morning
  • Palpable spasm
96
Q

How do you treat mechanical back pain (2)

A
  • Physiotherapy

- NSAIDs, paracetamol, codeine

97
Q

What is the epidemiology of septic arthritis (2)

A
  • Increases with age

- Most common cause is staph areus

98
Q

What are the risk factors for septic arthritis (6)

A
  • Immunosuppresion
  • Rheumatoid arthritis
  • Trauma
  • Joint surgery
  • Prosthetic joint
  • Diabetes
99
Q

How might septic arthritis present (3)

A
  • Acute severe pain, swelling and redness of joint
  • Fever
  • Usually mono, can be polyarthritis
100
Q

How do you diagnose septic arthritis

A
  • Joint aspiration + culture
101
Q

How do you treat septic arthritis (5)

A
  • If on steroids then double the dose
  • Immobilisation
  • Antibiotics
  • NSAIDs for pain
  • Joint aspiration
102
Q

What is the epidemiology of osteomyelitis (3)

A
  • Most common in children
  • In children usually secondary to direct trauma
  • in elderly usually due to risk factors
103
Q

What are the risk factors for osteomyelitis (5)

A
  • Immunosuppression
  • Trauma
  • Diabetes
  • Prosthetic implant
  • RA
104
Q

How might osteomyelitis present (3)

A
  • Dull ache in bone affected, may be aggravated by movement
  • Warm, tender erythema
  • Fever, sweats, rigors
105
Q

How do you diagnose osteomyelitis

A
  • Bone biopsy + culture
106
Q

How do you treat osteomyelitis (3)

A
  • Antibiotics
  • Immobilisation
  • Surgery to remove dead bone

Finals (11 decks)

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