MSK Flashcards
1
Q
Characteristics of pain in degenerative joint disease?
A
Pain increases with use, clinks and cluncks
2
Q
Characteristics of pain in inflammatory joint disease?
A
Pain eases with use
3
Q
When do you get stiffness in inflammatory joint disease?
A
Greater than 60 mins in the morning and when at rest
4
Q
When do you get stiffness in degenerative joint disease?
A
LEss than 30 mins, not prolonged in the morning
5
Q
What is the swelling like in inflammatory joint disease?
A
Synovial swelling can be bony, usually hot and red
6
Q
What is the swelling like in degenerative bone disease?
A
Swelling, not synovial, bony. clinically not inflammed
7
Q
What population is more typical of inflammatory bone disease?
A
Young, psoriasis, family history
8
Q
What population is more typical of degenerative bone disease?
A
Older, prior occupation/sport
9
Q
Where does inflammaotory joint disease affect?
A
Hands and feet
10
Q
Where does degenrative joint disease afffect?
A
1st CMCJ, DIPJ, knees
11
Q
How does degenerative joint disease respond to NSAID’s
A
Not convincingly
12
Q
How does inflammatory joint disease respond to NSAIDs?
A
Responds well
13
Q
What is the definition of osteoarthritis?
A
Long term chronic degenerative bone disease. Loss of cartilage in joints resulting in bones rubbing together. Creating stiffness pain and impaired movement
14
Q
What are the risk factors for OA?
A
High intensity labour, older age, high BMI
15
Q
How do patients with OA present?
A
Painful joints which are stiff for 30mins or less in the morning. pain worse throughout the day
16
Q
What are heberdens nodes?
A
A bony swelling in the distal interphalangeal joint
17
Q
What is a bouchard node?
A
A bony swelling in the proximal interphalangeal joint.
18
Q
What is the acronym for remebering signs on x-ray for OA?
A
LOSS
19
Q
What does LOSS stand for?
A
L - loss of joint space
O - Osteophytes
S - Sclerosis
S - Subchondral cycsts
20
Q
How do you manage OA?
A
Analgesia and joint replacaement
21
Q
What are the complications of OA?
A
Destruction of the joint and loss of function
22
Q
What is rheumatoid arthritis?
A
Autoimmune destruction of the synovium causing damage to bone cartilage, tendons and ligaments.
23
Q
Which joints are typically affected in RA?
A
Small symmetrical joints of the hands, wrists and feet.
24
Q
Risk factors for RA?
A
Young, female, family history, other autoimmune disease
25
Symptoms of RA?
Painful, swollen, stiff joints for more than an hour in the morning.
Better with movement
26
Signs of RA?
Swan neck thumb, ulnar deviation and boutonniere deformity.
27
What is a boutonniere deformity?
Where the middle joint of the finger will not straighten due to damage to the tendons in the finger.
28
What blood tests would you do for RA?
Anti CCP, rheumatoid factor, raised ESR/CRP
29
What is AntiCCP?
An antibody usually present in patients with RA
30
What is the acronym for X-ray signs in RA?
LESS
31
What does LESS stand for?
L - Lost joint space
E - Erosion
S - Soft tissue swelling
S - Soft bones
32
How would you treat RA?
NSAIDs, Steroids, Methotrexate, Rituximab
33
What are DMARDs?
They alter the disease process by stopping or slowing the inflammatory process, reducing pain.
34
What is rituximab?
Targets anti-TNF which causes inflammation, therefore reducing levels of inflam. Works quicker than DMARDs
35
What are the complications of RA?
Cervical spinal cord compression, weakness and loss of sensation.
Lung involvement, interstitial lung disease and fibrosis.
36
What is gout?
Overproduction and under excretion of uric acid causing build up in joints.
37
What are the risk factors for gout?
Middle age, overweight, male, high purine diet, increased cell turnover.
38
What type of crystals are formed in gout?
Mono-sodium urate crystals
39
What foods are rich in purines?
Red meat, liver and seafood
40
What foods can also cause gout?
High fructose (sweets), high saturated fat
41
What are the first-line investigations for gout?
Polarised light microscopy of the synovial fluid
42
What does microscopy show in gout?
Negatively birefringent urate crystals
43
What blood tests would you do for gout?
Serum urate, levels may be raised but could also be normal.
44
What are the differential diagnoses for gout?
Septic arthritis with any acute monoarthropathy
45
What pain releif can you give for gout?
High dose NSAIDS or colchicine if NSAIDs are CI.
46
What should you prescribe if greater than 1 attack of gout per year?
Allopurinol
47
How to prevent gout?
Lose weight, change diet, reduce alcohol consumption.
48
Which joints are most commonly affected in gout?
1st metatarsal (big toe), distal interphalangeal joints.
49
What is pseudogout?
Deposition of calcium pyrophosphate crystals in the joint surface
50
Which joints does pseudogout affect?
KNEE, wrist, shoulder, elbows,
51
Presentation of pseudogout>?
Hot swollen tender joint, usually knees
52
Signs of pseudogout?
Recent injury to the joint in the history.
53
What investigations for pseudogout?
Joint aspirate and polarised light.
54
What crystals show under polarised light in pseudogout?
Rhomboid positive birefringent crystals
55
Management of pseudogout?
NSAIDS or colchicine
56
Complications of pseudogout>
Damage to the joint and loss of function over time
57
Risk factors for pseudogout?
Old age, Diabetes, osteoarthritis, joint trauma/injury, hyperparathyroidism and haemochromatosis, excess iron or calcium.
58
What is Ankylosing spondylitis?
An inflammatory condition that mainly affects the spine leading to stiffness and pain.
59
Which gene do most patients with AS have?
HLA-B27
60
Risk factors for AS?
Males:females 3:1, late teens/twenties
61
Which are the key joints affected in AS?
Sacroiliac joints, joints of the vertebral column
62
What is the pathophysiology of AS?
Inflammation caused pain and stiffness, fibrosis and scarring which progresses to bone formation and fusion of the spine.
63
What are the key presentations of AS?
Lower back pain and stiffness with sacroiliac pain that extends to the buttock.
Pain worse with rest, Improves with movement, worse at night and in the morning,
64
What X-ray changes might you see with AS?
Bamboo spine, very straight spine with fused vertebrae.
65
What investigations would you do for AS?
Inflammatory markers CRP and ESR, Genetic testing for B27, X-ray, MRI if X-ray doesn't show anything;.
66
What is Schober's test?
Tests the restriction in the lumbar spine
67
How do you perform schober's test?
Find L5 on patient, draw a mark 10cm above, draw a mark 5cm below.
Ask patient to bend, measure the distance between the 2 marks.
Less than 20cm shows lumbar spine restriction
68
What other conditions are assciated with AS?
Inflammatory bowel disease, such as crohns.
69
How would you manage AS?
NSAID's to control pain
| Steroids during flares, anti - TNF drugs, monoclonal antibody against IL17
70
What is osteoporosis?
Reabsorption of bone out competes the building of bone leading to reduced bone mass and brittle bones
71
What are the primary causes of OP?
Menopause and aging, oestrogen protects the bone.
72
What is an acronym for the secondary causes of OP?
SHATTERED
73
What does shattered stand for?
```
S - Steroid use
H - Hyperthyroidism
A - Alcohol/smoking
T - Thin/low BMI
T - Low testosterone
E - Early menopause
R - Renal or liver failure
E - Erosive/ inflammatory bone disease
D - Dietery calcium low, malabsorption.
```
74
What are the presentations of OP?
Usually asymptomatic until a fracture, usually a hip fracture.
75
What investigations can you do for osteoporosis?
DEXA - mineral bone density scan.
| Less than -2.5 is osteoporosis
76
What is the risk score used to predict fracture risk?
FRAX
77
What is the management of OP?
Lifestyle changes less alcohol, regular weight bearing exercise, vitD supplements and calcium rich diet.
Bisphosphates, alendronic acid
78
What advice should you give when taking bisphosphonates?
Take on an empty stomach first thing in the morning 30 mins before food. Stay upright for 30mins after taking it to prevent ulceration.
79
What is psoriatic arthritis?
T-cell mediated attack of the joints in people with psoriasis
80
What are the symptoms of psoriatic arthritis?
Joint pain, swelling and stiffness. Red and warm joints
81
What are the patterns of PA?
Oligoarthritis, asymmetrical., Affects distal interphalengeal joints
82
What investigations would you do in psoriatic arthritis?
Bloods - HLAB27, raised WBC and ESR/CRP. RF negative. X-ray
83
What x-ray changes would you see with psoriatic arthritis?
Pencil in cup erosive changes
84
What is the treatment for psoriatic arthritis?
Physio, NSAIDS and DMARDs
85
What is reactive arthritis?
Joint inflammation following a GI/GU infection.
86
When might you develop reactive arthritis?
If you've had an STI such as chlamydia or gonorrhea
| If you've had glandular fever or food poisoning.
87
Joint symptoms of reactive arthritis?
Inflammatory monoarthritis, most commonly affecting knees, hips, feet, toes and ankles
88
What other symptoms of reactive arthritis?
Can't see - conjuctivitis/uveitis
Can't pee - Urethritis
Can't climb a tree - oligoarthritis/polyarthritis
89
What investigations would you do in reactive arthritis?
Raised ESR/CRP, stool culture, STI screen, X-ray evidence of enthesitis.
90
How to treat reactive arthritis?
Treat cause of infection with antibiotics, NSAIDS +/- steroid joint injections.
91
What is septic arthritis?
A hot, swollen, acutely painful joint. It can destroy a joint in 24 hours
92
Which joint is most commonly affected in septic arthritis?
The knee joint
93
What are the risk factors for septic arthritis?
Pre-existing joint disease, DM, immunosuppression, chronic renal failure, recent joint surgery, prosthetic joints, IV drug abuse, over 80
94
How is the infection spread to the joint in septic arthritis?
Pathogenic inoculation of microbes. it either occurs by direct inoculation or haematogenous spread.
95
Which organisms commonly cause septic arthritis?
Staph aureus, streptococci and neisseria gonococcus.
96
What are the symptoms of septic arthritis?
Fever, large joint, single joint, Symptoms out of proportion with the underlying disease.
97
What are the differential diagnoses for septic arthritis?
Gout and pseudo gout.
98
What investigations should be done in septic arthritis?
Urgent joint aspiration for synovial fluid microscopy and culture.
99
What is osteomyelitis?
An inflammatory condition caused by an infection of bone typically only involving 1 bone.
100
What is the most common organism causing osteomyelitis?
Staph aureus
101
What are the risk factors for osteomyelitis>
Penetrating injury, IV drug use, diabetes, HIV infection, recent surgery, distant or local infection, sickle cell, RA.
102
What are the symptoms of osteomyelitis?
Limp or reluctance to weight bear, non specific pain at site of infection, malaise and fatigue, fever
103
What investigations for osteomyelitis?
FBC: WBC may be raised in acute, ESR/CRP usually raised. Blood cultures may be positive indicating infective organism.
104
Management of osteomyelitis
If patient is unwell give flucloxacillin upon reaching hospital.
Blood cultures to give right antibiotic.
105
What is SLE?
Antibodies attack soft tissue causing inflammation and damage
106
What are the risk factors for SLE?
Young, black, women
107
What is the presentation of SLE?
Butterfly rash, weight loss, fever, fatigue, joint pain, mouth ulcers.
108
What investigations would you do in SLE?
ESR raised, CRP normal
| ANA and aDsDNA antibodies present
109
How to manage SLE?
Ibuprofen, Cyclophosphamide (DMARD) hydroxychloroquine, prednisolone and methotrexate
110
What are the complications of SLE?
Cardiac, lung, and kidney involvement. Widespread inflammation causing damage.
111
What are the names of 3 primary bone tumours?
Osteosarcomas, fibromas and sarcomas
112
What are the 5 commonest cancers to metastasise to the bone?
Bronchus, Breast, Brostate, Byroid and Bidney (the 5 B's)
113
What are the symptoms of a secondary bone tumour>
Pain at tumour location, malaise, pyrexia, aches, pains, hypercalaemia
114
What is fibromyalgia?
Non-specific muscular disorder with unknown cause, can cause pain all over the body.
115
What are the risk factors for fibromyalgia?
Women, poor socioeconomic status, 20-50 years old.
116
What are the symptoms of fibromyalgia?
Fatigue, brain fog, pain, morning stiffness, chronic pain that is widespread.
117
What are the investigations for fibromyalgia?
Do FBC, X-ray to rule out any other causes
118
How to diagnose fibromyalgia?
Patient must have had pain/ tenderness lasting longer than 3 months on both right and left sides of the body above and below the diaphragm and at 11 out of 18 tender points.
119
Non-pharmacological treatments for fibromyalgia?
Keep patient active, i.e. going back to work. Graded exercise programmes such as strength and aerobic training.
Relaxation, physio and CBT
120
Pharmacological treatments for fibromyalgia?
10-20mg amitriptyline, 150-300mg of pregabalin if this doesn't work.
121
Complications of fibromyalgia
Affect quality of life, anxiety, depression, insomnia, opiate addiction.
122
What is osteomalacia?
Poor mineralisation of bone
123
Deficiency of which vitamin causes osteomalacia/rickets?
Vitamin D
124
How do rickets and osteomalacia differ?
Rickets occurs if this happens during bone growth and osteomalacia is after the epiphyses
125
What are the signs/symptoms of rickets?
Growth retardation, hypotonia, apathy in infants, knock knees and bowed legs.
126
What are the symptoms of osteomalacia?
Bone pain and tenderness, fractures, waddling gait, low phosphate, and vit D deficiency.
127
What would plasma tests show for osteomalacia>
Low calcium, low phosphate (not enough to mineralised the bone)high ALP, high pth, low 25 hydroxy vitamin D
128
Gold standard tests for osteomalacia?
Bone biopsy showing incomplete mineralisation
129
How to treat osteomalacia/rickets?
Give vitamin D supplements, give calcium D3 forte if dietary insufficient, IM calcitriol if due to malabsorption.
130
What is vasculitis?
Inflammation of the wall surrounding the blood vessels.
131
How is vasculitis catorgarised?
By the size of the vessel
132
Which blood vessels does GCA affect?
The aorta and its major branches (carotid and verteral arteries) temporal artery often involved
133
What are the risk factors for GCA>
Over 50 years, northern european descent, females more common, history of polymyalgia rheumatica
134
What are the presentations of GCA?
New onset headache particularly over temporal area, scalp tenderness (hurts to brush hair), jaw claudication, visual disturbances such as amaurosis fugax.
135
What investigations for GCA?
Raised ESR and CRP, Halo sign on temporal and axillary artery, temporal artery biopsy/
136
Whats the gold standard for GCA diagnosis?
Temporal artery biopsy showing giant cells.
137
Whats the management of GCA?
High dose prednisalone ASAP
| 40-60mg
138
What are the complications of GCA?
Blindness, irreversible neuropathy.
139
What is Takayasu's arteritis?
A large cell arteritis
140
Which vessels does Takayasus most commonly affect?
Aorta and its branches, also affect the pulmonary arteries.
141
What people are typically affected by takayasu's arteritis?
below 40, female and Asian populations
142
What is the presentation of takayasu's arteritis
Pulseless disease, arm claudication, syncope
143
What are the investigations for Takyasu's
Angiography, granulomatous inflammation on histology, elevated ESR and CRP
144
How to manage takayasu's?
Steroids
145
What is polyarteritis nodosa?
A medium artery vasculitis
146
Which parts of the body does polyarteritis nodosa most commonly affect?
Nerve/ skin involvement
147
Features of polyarteritis nodosa
Peripheral neuropathy, subcut nodules, abdo pain, unilateral orchitis.
148
What disease is commonly associated with polyarteritis nodosa?
Hep B
149
How to manage polyarteritis nodosa?
Corticosteroids and antivirals if associated with hep B.
150
What is Kawasaki disease ?
A medium cell arteritis associated with mucocutaneous lymph nodes
151
What ages does kawasaki disease most commoinly affesct?
Children under 5
152
What are the symptoms of Kawasaki disease?
Fever for greater than 5 days, nonpurulent bilateral conjunctivitis, strawberry tongue, erythema, and desquamation of palms and soles.
153
What is the treatment for kawasaki disease?
Aspirin and IV immunoglobulins
154
What is pagets disease of the bone?
Abnormal osteoclast activity causes excessive bone resorption followed by haphazard bone growth
155
What are the developing sy,ptoms of pagets?
Bone growth can impinge on nerves and cause pain, overgrowth of the cranial and facial bones, hearing loss and vision loss from impingement on those nerves.
156
What would blood tests for pagets disease show?
Elevated alkaline phosphatase, normal calcium, phosphate ad PTH.
157
What do X-rays for pagets show?
Lytic lesions, thickened bone cortices.
158
How to manage pagets?
analgesia and bisphosphonates
159
What is marfans syndrome?
A connective tissue disorder affecting the fibrillin gene resulting in connective tissue issues
160
What is the presentation of marfans?
Tall, long limbs and fingers, hypermobility, high arch palate
161
What is the ghent criteria for diagnosing marfans?
It takes into accoint, enlarged aorta, lens dislocation, and at least 4 skeletal problems in the diagnosis.
162
Management of marfans?
Avoid intense exercise and caffeine, beta blockers or ARBS
| yearly echo and review by opthamologists.
163
Complications of marfans?
Mitral/aortic valve prolapse
| aortic aneurysms, lens dislocation, pneumothorax, gord, scoliosis.
164
What is pectus excavatum?
An indented breast bone
165
What is pectus carniatum?
Protruding breast bone
166
What is ehlers danlos syndrome?
A group of connective tissue disorders caused by faulty collagen.
167
What is the presentation of ehlers danlos?
joint hypermobility, easily stretched skin, easy brising, chronic joint pain, re-occuring dislocations
168
Treatment for ehlers danlos
Physio, OT, psycological support
169
What is antiphospholipid syndrome?
An immune condition with antiphospholipid antibodies causing the blood to become prone to clotting and is in a hypercoaguable state.
170
What are the risk factors for antiphospholipid?
Diabtests, HTN, obesity, female, Autoimmune disease, smoking, oestrogen therapy for menopause
171
Presentation of antiphospholipid?
Thrombosis, recurrent miscarragees, thrombocytopaenia
172
Management of antiphospholipid
Long term warfairn, preganant women on LMWH.
