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Phase 2a medicine > MSK > Flashcards

MSK Flashcards

1
Q

Characteristics of pain in degenerative joint disease?

A

Pain increases with use, clinks and cluncks

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2
Q

Characteristics of pain in inflammatory joint disease?

A

Pain eases with use

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3
Q

When do you get stiffness in inflammatory joint disease?

A

Greater than 60 mins in the morning and when at rest

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4
Q

When do you get stiffness in degenerative joint disease?

A

LEss than 30 mins, not prolonged in the morning

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5
Q

What is the swelling like in inflammatory joint disease?

A

Synovial swelling can be bony, usually hot and red

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6
Q

What is the swelling like in degenerative bone disease?

A

Swelling, not synovial, bony. clinically not inflammed

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7
Q

What population is more typical of inflammatory bone disease?

A

Young, psoriasis, family history

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8
Q

What population is more typical of degenerative bone disease?

A

Older, prior occupation/sport

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9
Q

Where does inflammaotory joint disease affect?

A

Hands and feet

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10
Q

Where does degenrative joint disease afffect?

A

1st CMCJ, DIPJ, knees

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11
Q

How does degenerative joint disease respond to NSAID’s

A

Not convincingly

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12
Q

How does inflammatory joint disease respond to NSAIDs?

A

Responds well

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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

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14
Q

What are the risk factors for OA?

A

High intensity labour, older age, high BMI

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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

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16
Q

What are heberdens nodes?

A

A bony swelling in the distal interphalangeal joint

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17
Q

What is a bouchard node?

A

A bony swelling in the proximal interphalangeal joint.

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18
Q

What is the acronym for remebering signs on x-ray for OA?

A

LOSS

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19
Q

What does LOSS stand for?

A

L - loss of joint space
O - Osteophytes
S - Sclerosis
S - Subchondral cycsts

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20
Q

How do you manage OA?

A

Analgesia and joint replacaement

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21
Q

What are the complications of OA?

A

Destruction of the joint and loss of function

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22
Q

What is rheumatoid arthritis?

A

Autoimmune destruction of the synovium causing damage to bone cartilage, tendons and ligaments.

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23
Q

Which joints are typically affected in RA?

A

Small symmetrical joints of the hands, wrists and feet.

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24
Q

Risk factors for RA?

A

Young, female, family history, other autoimmune disease

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25
Q

Symptoms of RA?

A

Painful, swollen, stiff joints for more than an hour in the morning.
Better with movement

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26
Q

Signs of RA?

A

Swan neck thumb, ulnar deviation and boutonniere deformity.

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27
Q

What is a boutonniere deformity?

A

Where the middle joint of the finger will not straighten due to damage to the tendons in the finger.

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28
Q

What blood tests would you do for RA?

A

Anti CCP, rheumatoid factor, raised ESR/CRP

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29
Q

What is AntiCCP?

A

An antibody usually present in patients with RA

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30
Q

What is the acronym for X-ray signs in RA?

A

LESS

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31
Q

What does LESS stand for?

A

L - Lost joint space
E - Erosion
S - Soft tissue swelling
S - Soft bones

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32
Q

How would you treat RA?

A

NSAIDs, Steroids, Methotrexate, Rituximab

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33
Q

What are DMARDs?

A

They alter the disease process by stopping or slowing the inflammatory process, reducing pain.

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34
Q

What is rituximab?

A

Targets anti-TNF which causes inflammation, therefore reducing levels of inflam. Works quicker than DMARDs

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35
Q

What are the complications of RA?

A

Cervical spinal cord compression, weakness and loss of sensation.
Lung involvement, interstitial lung disease and fibrosis.

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36
Q

What is gout?

A

Overproduction and under excretion of uric acid causing build up in joints.

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37
Q

What are the risk factors for gout?

A

Middle age, overweight, male, high purine diet, increased cell turnover.

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38
Q

What type of crystals are formed in gout?

A

Mono-sodium urate crystals

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39
Q

What foods are rich in purines?

A

Red meat, liver and seafood

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40
Q

What foods can also cause gout?

A

High fructose (sweets), high saturated fat

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41
Q

What are the first-line investigations for gout?

A

Polarised light microscopy of the synovial fluid

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42
Q

What does microscopy show in gout?

A

Negatively birefringent urate crystals

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43
Q

What blood tests would you do for gout?

A

Serum urate, levels may be raised but could also be normal.

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44
Q

What are the differential diagnoses for gout?

A

Septic arthritis with any acute monoarthropathy

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45
Q

What pain releif can you give for gout?

A

High dose NSAIDS or colchicine if NSAIDs are CI.

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46
Q

What should you prescribe if greater than 1 attack of gout per year?

A

Allopurinol

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47
Q

How to prevent gout?

A

Lose weight, change diet, reduce alcohol consumption.

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48
Q

Which joints are most commonly affected in gout?

A

1st metatarsal (big toe), distal interphalangeal joints.

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49
Q

What is pseudogout?

A

Deposition of calcium pyrophosphate crystals in the joint surface

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50
Q

Which joints does pseudogout affect?

A

KNEE, wrist, shoulder, elbows,

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51
Q

Presentation of pseudogout>?

A

Hot swollen tender joint, usually knees

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52
Q

Signs of pseudogout?

A

Recent injury to the joint in the history.

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53
Q

What investigations for pseudogout?

A

Joint aspirate and polarised light.

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54
Q

What crystals show under polarised light in pseudogout?

A

Rhomboid positive birefringent crystals

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55
Q

Management of pseudogout?

A

NSAIDS or colchicine

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56
Q

Complications of pseudogout>

A

Damage to the joint and loss of function over time

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57
Q

Risk factors for pseudogout?

A

Old age, Diabetes, osteoarthritis, joint trauma/injury, hyperparathyroidism and haemochromatosis, excess iron or calcium.

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58
Q

What is Ankylosing spondylitis?

A

An inflammatory condition that mainly affects the spine leading to stiffness and pain.

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59
Q

Which gene do most patients with AS have?

A

HLA-B27

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60
Q

Risk factors for AS?

A

Males:females 3:1, late teens/twenties

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61
Q

Which are the key joints affected in AS?

A

Sacroiliac joints, joints of the vertebral column

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62
Q

What is the pathophysiology of AS?

A

Inflammation caused pain and stiffness, fibrosis and scarring which progresses to bone formation and fusion of the spine.

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63
Q

What are the key presentations of AS?

A

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,

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64
Q

What X-ray changes might you see with AS?

A

Bamboo spine, very straight spine with fused vertebrae.

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65
Q

What investigations would you do for AS?

A

Inflammatory markers CRP and ESR, Genetic testing for B27, X-ray, MRI if X-ray doesn’t show anything;.

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66
Q

What is Schober’s test?

A

Tests the restriction in the lumbar spine

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67
Q

How do you perform schober’s test?

A

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

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68
Q

What other conditions are assciated with AS?

A

Inflammatory bowel disease, such as crohns.

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69
Q

How would you manage AS?

A

NSAID’s to control pain

Steroids during flares, anti - TNF drugs, monoclonal antibody against IL17

70
Q

What is osteoporosis?

A

Reabsorption of bone out competes the building of bone leading to reduced bone mass and brittle bones

71
Q

What are the primary causes of OP?

A

Menopause and aging, oestrogen protects the bone.

72
Q

What is an acronym for the secondary causes of OP?

A

SHATTERED

73
Q

What does shattered stand for?

A 
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
Q

What are the presentations of OP?

A

Usually asymptomatic until a fracture, usually a hip fracture.

75
Q

What investigations can you do for osteoporosis?

A

DEXA - mineral bone density scan.

Less than -2.5 is osteoporosis

76
Q

What is the risk score used to predict fracture risk?

A

FRAX

77
Q

What is the management of OP?

A

Lifestyle changes less alcohol, regular weight bearing exercise, vitD supplements and calcium rich diet.
Bisphosphates, alendronic acid

78
Q

What advice should you give when taking bisphosphonates?

A

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
Q

What is psoriatic arthritis?

A

T-cell mediated attack of the joints in people with psoriasis

80
Q

What are the symptoms of psoriatic arthritis?

A

Joint pain, swelling and stiffness. Red and warm joints

81
Q

What are the patterns of PA?

A

Oligoarthritis, asymmetrical., Affects distal interphalengeal joints

82
Q

What investigations would you do in psoriatic arthritis?

A

Bloods - HLAB27, raised WBC and ESR/CRP. RF negative. X-ray

83
Q

What x-ray changes would you see with psoriatic arthritis?

A

Pencil in cup erosive changes

84
Q

What is the treatment for psoriatic arthritis?

A

Physio, NSAIDS and DMARDs

85
Q

What is reactive arthritis?

A

Joint inflammation following a GI/GU infection.

86
Q

When might you develop reactive arthritis?

A

If you’ve had an STI such as chlamydia or gonorrhea

If you’ve had glandular fever or food poisoning.

87
Q

Joint symptoms of reactive arthritis?

A

Inflammatory monoarthritis, most commonly affecting knees, hips, feet, toes and ankles

88
Q

What other symptoms of reactive arthritis?

A

Can’t see - conjuctivitis/uveitis
Can’t pee - Urethritis
Can’t climb a tree - oligoarthritis/polyarthritis

89
Q

What investigations would you do in reactive arthritis?

A

Raised ESR/CRP, stool culture, STI screen, X-ray evidence of enthesitis.

90
Q

How to treat reactive arthritis?

A

Treat cause of infection with antibiotics, NSAIDS +/- steroid joint injections.

91
Q

What is septic arthritis?

A

A hot, swollen, acutely painful joint. It can destroy a joint in 24 hours

92
Q

Which joint is most commonly affected in septic arthritis?

A

The knee joint

93
Q

What are the risk factors for septic arthritis?

A

Pre-existing joint disease, DM, immunosuppression, chronic renal failure, recent joint surgery, prosthetic joints, IV drug abuse, over 80

94
Q

How is the infection spread to the joint in septic arthritis?

A

Pathogenic inoculation of microbes. it either occurs by direct inoculation or haematogenous spread.

95
Q

Which organisms commonly cause septic arthritis?

A

Staph aureus, streptococci and neisseria gonococcus.

96
Q

What are the symptoms of septic arthritis?

A

Fever, large joint, single joint, Symptoms out of proportion with the underlying disease.

97
Q

What are the differential diagnoses for septic arthritis?

A

Gout and pseudo gout.

98
Q

What investigations should be done in septic arthritis?

A

Urgent joint aspiration for synovial fluid microscopy and culture.

99
Q

What is osteomyelitis?

A

An inflammatory condition caused by an infection of bone typically only involving 1 bone.

100
Q

What is the most common organism causing osteomyelitis?

A

Staph aureus

101
Q

What are the risk factors for osteomyelitis>

A

Penetrating injury, IV drug use, diabetes, HIV infection, recent surgery, distant or local infection, sickle cell, RA.

102
Q

What are the symptoms of osteomyelitis?

A

Limp or reluctance to weight bear, non specific pain at site of infection, malaise and fatigue, fever

103
Q

What investigations for osteomyelitis?

A

FBC: WBC may be raised in acute, ESR/CRP usually raised. Blood cultures may be positive indicating infective organism.

104
Q

Management of osteomyelitis

A

If patient is unwell give flucloxacillin upon reaching hospital.
Blood cultures to give right antibiotic.

105
Q

What is SLE?

A

Antibodies attack soft tissue causing inflammation and damage

106
Q

What are the risk factors for SLE?

A

Young, black, women

107
Q

What is the presentation of SLE?

A

Butterfly rash, weight loss, fever, fatigue, joint pain, mouth ulcers.

108
Q

What investigations would you do in SLE?

A

ESR raised, CRP normal

ANA and aDsDNA antibodies present

109
Q

How to manage SLE?

A

Ibuprofen, Cyclophosphamide (DMARD) hydroxychloroquine, prednisolone and methotrexate

110
Q

What are the complications of SLE?

A

Cardiac, lung, and kidney involvement. Widespread inflammation causing damage.

111
Q

What are the names of 3 primary bone tumours?

A

Osteosarcomas, fibromas and sarcomas

112
Q

What are the 5 commonest cancers to metastasise to the bone?

A

Bronchus, Breast, Brostate, Byroid and Bidney (the 5 B’s)

113
Q

What are the symptoms of a secondary bone tumour>

A

Pain at tumour location, malaise, pyrexia, aches, pains, hypercalaemia

114
Q

What is fibromyalgia?

A

Non-specific muscular disorder with unknown cause, can cause pain all over the body.

115
Q

What are the risk factors for fibromyalgia?

A

Women, poor socioeconomic status, 20-50 years old.

116
Q

What are the symptoms of fibromyalgia?

A

Fatigue, brain fog, pain, morning stiffness, chronic pain that is widespread.

117
Q

What are the investigations for fibromyalgia?

A

Do FBC, X-ray to rule out any other causes

118
Q

How to diagnose fibromyalgia?

A

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
Q

Non-pharmacological treatments for fibromyalgia?

A

Keep patient active, i.e. going back to work. Graded exercise programmes such as strength and aerobic training.
Relaxation, physio and CBT

120
Q

Pharmacological treatments for fibromyalgia?

A

10-20mg amitriptyline, 150-300mg of pregabalin if this doesn’t work.

121
Q

Complications of fibromyalgia

A

Affect quality of life, anxiety, depression, insomnia, opiate addiction.

122
Q

What is osteomalacia?

A

Poor mineralisation of bone

123
Q

Deficiency of which vitamin causes osteomalacia/rickets?

A

Vitamin D

124
Q

How do rickets and osteomalacia differ?

A

Rickets occurs if this happens during bone growth and osteomalacia is after the epiphyses

125
Q

What are the signs/symptoms of rickets?

A

Growth retardation, hypotonia, apathy in infants, knock knees and bowed legs.

126
Q

What are the symptoms of osteomalacia?

A

Bone pain and tenderness, fractures, waddling gait, low phosphate, and vit D deficiency.

127
Q

What would plasma tests show for osteomalacia>

A

Low calcium, low phosphate (not enough to mineralised the bone)high ALP, high pth, low 25 hydroxy vitamin D

128
Q

Gold standard tests for osteomalacia?

A

Bone biopsy showing incomplete mineralisation

129
Q

How to treat osteomalacia/rickets?

A

Give vitamin D supplements, give calcium D3 forte if dietary insufficient, IM calcitriol if due to malabsorption.

130
Q

What is vasculitis?

A

Inflammation of the wall surrounding the blood vessels.

131
Q

How is vasculitis catorgarised?

A

By the size of the vessel

132
Q

Which blood vessels does GCA affect?

A

The aorta and its major branches (carotid and verteral arteries) temporal artery often involved

133
Q

What are the risk factors for GCA>

A

Over 50 years, northern european descent, females more common, history of polymyalgia rheumatica

134
Q

What are the presentations of GCA?

A

New onset headache particularly over temporal area, scalp tenderness (hurts to brush hair), jaw claudication, visual disturbances such as amaurosis fugax.

135
Q

What investigations for GCA?

A

Raised ESR and CRP, Halo sign on temporal and axillary artery, temporal artery biopsy/

136
Q

Whats the gold standard for GCA diagnosis?

A

Temporal artery biopsy showing giant cells.

137
Q

Whats the management of GCA?

A

High dose prednisalone ASAP

40-60mg

138
Q

What are the complications of GCA?

A

Blindness, irreversible neuropathy.

139
Q

What is Takayasu’s arteritis?

A

A large cell arteritis

140
Q

Which vessels does Takayasus most commonly affect?

A

Aorta and its branches, also affect the pulmonary arteries.

141
Q

What people are typically affected by takayasu’s arteritis?

A

below 40, female and Asian populations

142
Q

What is the presentation of takayasu’s arteritis

A

Pulseless disease, arm claudication, syncope

143
Q

What are the investigations for Takyasu’s

A

Angiography, granulomatous inflammation on histology, elevated ESR and CRP

144
Q

How to manage takayasu’s?

A

Steroids

145
Q

What is polyarteritis nodosa?

A

A medium artery vasculitis

146
Q

Which parts of the body does polyarteritis nodosa most commonly affect?

A

Nerve/ skin involvement

147
Q

Features of polyarteritis nodosa

A

Peripheral neuropathy, subcut nodules, abdo pain, unilateral orchitis.

148
Q

What disease is commonly associated with polyarteritis nodosa?

A

Hep B

149
Q

How to manage polyarteritis nodosa?

A

Corticosteroids and antivirals if associated with hep B.

150
Q

What is Kawasaki disease ?

A

A medium cell arteritis associated with mucocutaneous lymph nodes

151
Q

What ages does kawasaki disease most commoinly affesct?

A

Children under 5

152
Q

What are the symptoms of Kawasaki disease?

A

Fever for greater than 5 days, nonpurulent bilateral conjunctivitis, strawberry tongue, erythema, and desquamation of palms and soles.

153
Q

What is the treatment for kawasaki disease?

A

Aspirin and IV immunoglobulins

154
Q

What is pagets disease of the bone?

A

Abnormal osteoclast activity causes excessive bone resorption followed by haphazard bone growth

155
Q

What are the developing sy,ptoms of pagets?

A

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
Q

What would blood tests for pagets disease show?

A

Elevated alkaline phosphatase, normal calcium, phosphate ad PTH.

157
Q

What do X-rays for pagets show?

A

Lytic lesions, thickened bone cortices.

158
Q

How to manage pagets?

A

analgesia and bisphosphonates

159
Q

What is marfans syndrome?

A

A connective tissue disorder affecting the fibrillin gene resulting in connective tissue issues

160
Q

What is the presentation of marfans?

A

Tall, long limbs and fingers, hypermobility, high arch palate

161
Q

What is the ghent criteria for diagnosing marfans?

A

It takes into accoint, enlarged aorta, lens dislocation, and at least 4 skeletal problems in the diagnosis.

162
Q

Management of marfans?

A

Avoid intense exercise and caffeine, beta blockers or ARBS

yearly echo and review by opthamologists.

163
Q

Complications of marfans?

A

Mitral/aortic valve prolapse

aortic aneurysms, lens dislocation, pneumothorax, gord, scoliosis.

164
Q

What is pectus excavatum?

A

An indented breast bone

165
Q

What is pectus carniatum?

A

Protruding breast bone

166
Q

What is ehlers danlos syndrome?

A

A group of connective tissue disorders caused by faulty collagen.

167
Q

What is the presentation of ehlers danlos?

A

joint hypermobility, easily stretched skin, easy brising, chronic joint pain, re-occuring dislocations

168
Q

Treatment for ehlers danlos

A

Physio, OT, psycological support

169
Q

What is antiphospholipid syndrome?

A

An immune condition with antiphospholipid antibodies causing the blood to become prone to clotting and is in a hypercoaguable state.

170
Q

What are the risk factors for antiphospholipid?

A

Diabtests, HTN, obesity, female, Autoimmune disease, smoking, oestrogen therapy for menopause

171
Q

Presentation of antiphospholipid?

A

Thrombosis, recurrent miscarragees, thrombocytopaenia

172
Q

Management of antiphospholipid

A

Long term warfairn, preganant women on LMWH.

Phase 2a medicine (14 decks)

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