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YEAR 3 & 5 CORE CONDITIONS > MSK > Flashcards

MSK Flashcards

1
Q

What joints are primarily affected by osteoarthritis?

A

Knee

Hip

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2
Q

What distinguishes between rheumatoid and osteoarthritis?

A

Rheumatoid - pain/stiffness relieved by exercise, exacerbated by lack of movement

Osteoarthritis - pain exacerbated by exercise, relieved by rest

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3
Q

What finger changes are seen in osteoarthritis?

A

Heberden’s nodes - DIP

Bouchard’s nodes - PIP

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4
Q

What changes are seen on an X-ray in osteoarthritis?

A

LOSS

Loss of joint space
Osteophytes
Subchondral cysts
Subarticular sclerosis

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5
Q

What would be noted on passive movement of the joint in osteoarthritis?

A

Decreased range of movement
Pain on movement
Crepitus

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6
Q

What is the treatment for osteoarthritis?

A

General
• Weight loss
• Physiotherapy
• Topical and heat therapy

Pharmacology
• NSAIDs + PPI
• Intraarticular steroid injections

Surgical - Joint replacement

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7
Q

Where does gout usually first present and why?

A

Big toe (1st MTP joint) - 70%

Presents in extremities as they are cooler so allows for precipitation of the crystals

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8
Q

Who is typically affected?

A

Obese, non-white males who drink a lot and eat a lot of meat

It almost never affects pre-menopausal women

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9
Q

Aside from metabolic syndrome, what are some other modifiable risk factors for gout?

A

Drugs

  • Thiazide diuretics
  • ACE inhibitors
  • Aspirin

Increased cell level/turnover

  • Malignancy
  • Psoriasis
  • Chemotherapy
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10
Q

What investigation do you do for gout?

A
  • Gout is usually a clinical diagnosis
  • Joint aspiration with polarised light microscopy - this would show negatively birefringent needle shaped crystals
  • If they are systemically unwell, you need to send the joint aspiration for MC&S to rule out septic arthritis
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11
Q

What is seen on an X-ray of chronic gout?

A

Punched out lesions (rat-bites)
Areas of sclerosis
Tophi

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12
Q

What is the onset of pain in gout? Compare this onset to that of septic arthritis

A

Quick onset - 3-12 hours

Septic arthritis is even more acute onset - 1-2 hours

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13
Q

What is the acute management for gout?

A

NSAIDs = 1st line
Colchicine = 2nd line
Intra-articular steroids = 3rd line
IM steroids - if it is widespread (e.g. midfoot, ankle, 1st MTP)

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14
Q

What is the main side effect of colchicine?

A

v v bad diarrhoea - stop if they get this

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15
Q

What drug is given for prophylaxis of gout? What class is it? When should it not be given?

A

Allopurinol = xanthine-oxidase inhibitor

Do not give in acute attack of gout

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16
Q

What is uric acid the end product of?

A

The breakdown of purines (adenine + guanine)

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17
Q

How is urate excreted by the body?

A

2/3rd by kidneys

1/3rd by GI tract

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18
Q

What joint is most commonly affected by septic arthritis?

A

Knee

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19
Q

What organisms can cause septic arthritis

A
  • Coagulase negative staphylococci - most common in prosthetic joints
  • Staph aureus - most common in children > 2 years
  • Streptococci
  • Neisseria gonorrhoea - most common in sexually active young people
  • Haemophilus influenzae - used to be the most common cause in children but less common now due to vaccination
  • E. Coli
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20
Q

What is the classic presentation of septic arthritis?

A

Classic triad of:

  • Fever
  • Joint pain
  • Reduced range of movement
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21
Q

What bloods would you need to do in suspected septic arthritis?

A

FBC - high WCC
CRP - monitors disease progression
Blood cultures

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22
Q

How do you treat septic arthritis?

A

Analgesia

Antibiotics

  • 2g IV flucloxacillin QDS for 2 weeks then 1g PO flucloxacillin QDS for 4 weeks
  • Clindamycin if penicillin allergic
  • If MRSA suspected - vancomycin
  • If gonococcal/E. Coli - cefotaxime

Surgical

  • Wash out the joint/surgical drainage if it is a deep joint e.g. hip
  • If contraindications to surgery, can do daily aspirations for symptom relief
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23
Q

What is rheumatoid arthritis?

A

A chronic inflammatory autoimmune disease affecting synovial joints, leading to joint and periarticular destruction

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24
Q

What joints are typically affected by RA? Is it symmetrical?

A

Symmetrical polyarthritis

Mostly affects small joints of the hands

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25
Q

What hand signs are seen in RA?

A

• Z thumb
• Swan neck deformity = fixed flexion of MCP and DIP, hyperextension of PIP
• Boutonniere’s = extension of MCP and DIP joint, flexion of PIP
• Ulnar deviation
- Hand muscle wasting

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26
Q

What are the key rheumatoid complaints across the body?

A

PRISMS

Pain - polyarthritis
Rashes + skin lesions - ulcers, rashes, nail fold infarcts
Immune - Sjorgen’s = dry eyes, dry mouth, chronic cough
Stiffness - worse in morning
Malignancy
Swelling + sweats - especially in the morning

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27
Q

What extra-articular manifestations of rheumatoid arthritis might you see?

A

Rheumatoid nodules on forearms, in eyes, in heart and lungs

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28
Q

What cardiac diseases can be caused by rheumatoid arthritis?

A
  • Ischaemic heart disease
  • Pericarditis
  • Pericardial effusion
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29
Q

What specific blood tests can you do for rheumatoid arthritis?

Explain which is more specific/sensitive for RA and which you would do first/second.

A

Rheumatoid factor (RF) - found in 70% of rheumatoid patients and 1% of general population

  • More sensitive for RA
  • High levels are associated with RA but it is a poor marker for monitoring disease (instead use inflammatory markers for disease monitoring)

Anti-CCP antibodies - found in 98%

  • More specific than RF
  • It is sent off second-line if RF comes back negative in a patient in whom you suspect disease
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30
Q

Name some DMARDs used in Rheumatoid Arthritis.

Which are used for mild or severe disease?

A
  • Methotrexate - used in more severe disease
  • Sulfasalazine - used in milder disease
  • Azathioprine
  • Hydroxychloroquine

It is important to commence DMARDs as early as possible after symptoms occur (ideally within 3 months)

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31
Q

What is a contra-indication of sulfasalazine?

A

Aspirin hypersensitivity because it is an aminosalicylate

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32
Q

What are some side effects of methotrexate?

A
  • Pneumonitis
  • Anaemia (inhibits folate production)
  • Mouth ulcers
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33
Q

What is reactive arthritis?

A

An autoimmune response to infection elsewhere in the body causing arthritis

Usually it is a male, who is HLA-B27 positive and had an STI or GI infection

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34
Q

What is the classic triad of reactive arthritis and when do the symptoms usually start?

A

Urethritis
Conjunctivitis
Arthritis

Can’t see, can’t pee, can’t climb a tree!

Symptoms occur 4 weeks post-infection

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35
Q

What skin changes might you see in reactive arthritis?

A
  • Erythema nodosum

- Keratoderma blenorrhagica = psoriasis-like lesions on soles of feet/palms of hands

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36
Q

What tests are done in reactive arthritis?

A

ESR/CRP - raised
Stool MC&S - GI infection
Urethral/cervical swabs - screen for STIs

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37
Q

What allele is associated with ankylosing spondylitis?

A

HLA B27

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38
Q

What are the outer and inner parts of vertebrae called?

A

Annulus fibrosus = peripheral fibrocartilaginous part

Nucleus pulposus = central gelatinous part

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39
Q

What part of the spine is most prone to disc lesions?

A

Lumbar spine
L5 to S1 is most common site for disc herniation
L4 to L5 is second most common site

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40
Q

What commonly causes cervical disc lesions?

A

Whiplash injury

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41
Q

How can herniation of a lumbrosacral disc present?

A

Sciatica - the leg pain is more severe than the back pain
Greater pain on raising the leg

Cauda equina syndrome = neurosurgical emergency

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42
Q

What are the symptoms of cauda equina syndrome?

A 
Back pain
Radicular pain down legs
Asymmetrical weakness and loss of sensation in the legs 
Saddle anaesthesia
Urinary retention
Faecal incontinence
Erectile dysfunction
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43
Q

What drugs can be given for nerve pains?

A

Tricyclic antidepressants e.g. amitriptyline

Gabapentin

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44
Q

What surgical procedure is done in acute cord compression?

A

Laminectomy = removes the back of a vertebra to relieve pressure on nerves (surgical decomperssion)

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45
Q

What are the risk factors for osteoporosis?

A

SHATTERED

Steroid use/Cushing's syndrome
Hyperthyroidism/hyperparathyroidism
Alcohol
Thin
low Testosterone
Early menopause - oestrogen stimulates osteoblasts and inhibits osteoclasts 
Renal/liver failure
Erosive or inflammatory bone disease
Dietary low calcium/malabsorption
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46
Q

Describe the pathogenesis of osteoporosis

A

It is the end result of an imbalance between osteoclasts and osteoblasts

During ageing, bone breakdown by osteoclasts overtakes bone formation by osteoblasts

This results in reduced bone mineral density and changes in bone composition/architecture

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47
Q

How does osteoporosis usually present?

A

A fragility fracture

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48
Q

Where do fragility fractures most commonly occur?

A

Vertebrae
Proximal femur
Distal radius (Colles fracture)

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49
Q

What is the main investigation for osteoporosis and what values indicate what?

A

DEXA scan - calculates bone mineral density in g/cm2

Normal: > -1
Osteopenia: -2.5 < T < -1
Osteoporosis: < -2.5

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50
Q

What is the main drug treatment for osteoporosis?What is its mechanism?

A

Bisphosphonates e.g. alendronic acid

They inhibit resorption of bone by osteoclasts. This happens because they have similar structure to pyrophosphate (natural product of bone breakdown) so they are readily incorporated into the bone. The bisphosphonates accumulate in osteoclasts and promote apoptosis.

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51
Q

What are some other indications for bisphosphonates?

A

Bone metastases
Paget’s disease
Severe hypercalcaemia of malignancy

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52
Q

What are some side effects of bisphosphonates?

A

Oesophagitis - prevent by taking the tablet with water and sitting upright for 30 mins after

Jaw osteonecrosis - prevent with good dental hygiene and no smoking

Femoral fracture

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53
Q

What supplements should be given in osteoporosis?

A

Calcium and vitamin D = AdCal

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54
Q

What causes a hemiplegic gait and what does it look like?

A

Stroke
Unilateral weakness
Circumduction of leg = dragging of affected leg in semicircle
Foot drop

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55
Q

What is a Trendelenburg gait?

A

Drop of pelvis when lifting the leg opposite to the weak gluteus medius.

Usually due to muscular dystrophy.

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56
Q

What characterises a Parkisonian gait?

A

Shuffling - reduced stride length
Hesitant - difficulty initiating + turning
Festinating - walks faster and faster to not fall over
Lack of arm swing - increased tone
Stooped posture

57
Q

What causes a scissor gait?

A

Cerebral palsy

58
Q

What provides the definitive diagnosis of septic arthritis?

A

Ultrasound-guided arthrocentesis (aspiration of joint space under US) and culture

The fluid would appear yellowish-green and turbid
Increased WCC > 50,000 (mostly neutrophils) in the fluid

59
Q

What is the presentation of Felty’s syndrome?

A

Rheumatoid arthritis
Splenomegaly
Neutropenia
Lower limb pigmentation

60
Q

What genes are associated with rheumatoid arthritis?

A

HLA-DR1

HLA-DR4

61
Q

What drug is used in patients who have osteoporosis but also impaired renal function or no success with bisphosphonates?

A

Denusomab - a monoclonal antibody

62
Q

What investigation is required if a DEXA scan diagnoses osteopororsis?

A

X-Ray of the whole skeletal system - looking for any fractures and increased radiolucency

63
Q

What does the incidental finding of vertebral compression fractures on an X-Ray instantly diagnose?

A

Osteoporosis

64
Q

What is the typical presentation of polymyalgia rheumatica?

A

• Shoulder and neck pain
• Pelvic girdle pain
• Worse at night
- Morning stiffness > 45 mins

65
Q

What is the main investigation finding for polymyalgia rheumatica?

A

Raised ESR

66
Q

Who does Giant Cell Arteritis typically affect?

A

Elderly women > 50 years old

67
Q

What condition is GCA associated with?

A

Polymyalgia rheumatica

68
Q

What is the presentation of giant cell arteritis?

A
  • New-onset headache
  • Jaw claudication
  • Visual impairment leading to blindness
69
Q

What is the treatment for giant cell arteritis?

A

High-dose steroids (60mg OD prednisolone) to prevent blindness and stroke
Once symptoms resolve, pred is tapered over 1-2 years to reduce risk of relapse
Use PPI + bisphosphonates to prevent GI ulcers and osteoporosis

Low dose aspirin thereafter

70
Q

What investigations can be done for suspected GCA?

A

Bloods
• Raised ESR
• Autoantibodies absent

Duplex sonography - halo sign around the vessel

Temporal artery biopsy (definitive diagnosis)- granulomatous inflammation - must biopsy 3-5cm of artery due to skip lesions

71
Q

Who does Takayasu’s Arteritis typically affect?

A

Asian women between 10-40 years old

72
Q

What is Takayasu’s Arteritis and what does it primarily affect?

A

Chronic granulomatous vasculitis affecting the aorta and its main branches

73
Q

What cardiovascular findings are there on examination in Takayasu’s arteritis?

A

Absent upper extremity pulse

Discrepancy in BP between arms > 10mmHg

74
Q

What are the key diseases in the spondyloarthropathies group (4) ?

A

Ankylosing spondylitis
Reactive arthritis
Enteropathic arthritis
Psoriatic arthritis

75
Q

What are the predominant features of spondyloarthropathies?

A
  • Axial involvement (i.e. spine)
  • Peripheral joint involvement - predominantly asymmetrical and in lower extremities
  • Enthesitis - inflammation at site where tendons and ligaments insert to bone
  • High incidence of HLA-B27 (but negative for RF)
76
Q

What biologic agents can be used in rheumatoid arthritis?

A

Anti-TNF agents e.g. infliximab

Only used when disease is severe despite DMARD therapy

77
Q

What is recommended for patients on DMARDs?

A

Annual influenza vaccine
Pneumococcal vaccine every 5 years
(both vaccines are not live)

78
Q

What clinical sign is pathological of ankylosing spondylitis?

A

Chest expansion measurement < 2cm

79
Q

What is the diagnostic procedure for ankylosing spondylitits?

A
  1. Examination, history and pelvic X-ray - if results are conclusive, no additional tests required
  2. HLA-B27 testing
  3. Pelvic MRI
80
Q

What is typically seen on an X-Ray Spine in ankylosing spondylitis?

A

Bamboo spine (complete fusion of vertebral column)

First the vertebral bodies may become ‘squared’
In later stages, bony bridges called syndesmophytes form between adjacent vertebrae, and there is ossification of spinal ligaments
In late disease, there may be complete fusion of the vertebral column

81
Q

What is the most important treatment for ankylosing spondylitis?

A

Physiotherapy

82
Q

What pharmacological treatments can be offered for ankylosing spondylitis?

A

NSAIDs

Biologics - TNF-a inhibitors

83
Q

What is Sjogren’s syndrome characterised by?

A

Dry eyes - decreased lacrimal gland secretion

Dry mouth - decreased salivary gland secretion

84
Q

What is are complications of Sjogren’s syndrome?

A

Bacterial conjunctivitis in eyes
Dental caries and oral candidiasis in mouth
Gastritis in stomach

Increased risk of lymphoma in the affected glands/organs

85
Q

What are some extra-glandular features of Sjogren’s?

A
  • Systemic upset such as fever, myalgia, malaise or fatigue.
  • Arthritis which is usually episodic, non-erosive polyarthritis.
  • Raynaud’s phenomenon
  • Cutaneous vasculitis which manifests as purpura and skin ulcers.
  • Rarely other organ involvement in the form of interstitial lung disease, renal disease and neurological disease including seizures
86
Q

What autoimmune diseases may feature with secondary Sjogren’s syndrome?

A

SLE
Rheumatoid arthritis
Polymyositis/dermatomyositis
Systemic sclerosis

87
Q

What bloods should be requested for ?Sjogren’s?

A
  • Inflammatory markers - raised
  • ANA - most patients are positive but it is not specific for Sjogren’s
  • Anti-Ro and Anti-La antibodies - specific for Sjogren’s
88
Q

How can Sjogren’s be managed?

A
  • Dry eyes - artificial tears such as hypromellose
  • Dry mouth - artificial saliva, good dental hygiene, frequent drinks.
  • Vaginal dryness - topical lubrication.
  • Arthritis - hydroxychloroquine ± NSAIDs.
89
Q

What is Reiter’s syndrome also known as?

A

Reactive arthritis

90
Q

Who does SLE most commonly affect?

A

Females (90%)

African/Caribbean origin

91
Q

What is the classical presentation of SLE?

A 
Systemic upset - fever, myalgia, fatigue, weight loss
Peripheral joint arthritis
Malar rash (butterfly rash) - erythema of the malar eminences and across the bridge of the nose; classically the nasiolabial folds are spared - this is due to photosensitivity

It has a relapsing-remitting course and organs become involved in flares

92
Q

What can trigger a flare of SLE?

A
  • Oestrogen-containing contraception
  • Overexposure to sunlight
  • Infections
  • Stress
93
Q

What is the most common cause of lupus-related death?

A

Lupus nephritis
It can be asymptomatic for a time before it presents as either nephritic or nephrotic syndrome
Patients should be monitored- blood pressure (in case of sudden hypertension) and urinalysis (for proteinuria or haematuria)

94
Q

What is the most common cardiac feature of SLE?

A

Pericarditis

95
Q

How can the lungs be affected by SLE?

A

Pleuritis - sharp pain in the chest when inhaling

Pneumonitis

96
Q

What antibodies are used to test for SLE?

A

Antibodies

  • ANA - screening test
  • Anti-dsDNA - highly specific and high levels is a marker of worse outcome in lupus nephritis
  • Anti-Smith - highly specific
97
Q

What are the mainstay of SLE treatment?

A
  • NSAIDs
  • Hydroxychloroquine

+/- short courses of corticosteroids for flares

98
Q

What treatments are used if there is more prominent organ involvement in SLE?

A
  • Long-term corticosteroids
  • DMARDs
  • Cyclophosphamine (an immunosuppressant)
99
Q

What bones are most commonly affected by Paget’s?

A 
Pelvis
Vertebrae
Skull
Femur
Tibia
100
Q

How is Paget’s disease usually found in a patient?

A

Patients are usually asymptomatic
Diagnosis is often an incidental finding:
- Abnormally shaped/sized bone on X-Ray
- Raised ALP marker (due to bone resorption)

101
Q

What is the classic presentation of Paget’s disease?

A

Frontal bossing (enlargement of the skull) so their hat no longer fits

If symptomatic - deep, boring pain over affected bones

102
Q

What type of fracture is typical of Paget’s disease?

A

Transverse fractures - due to weakened bones from the chaotic remodelling process

103
Q

What condition after patients more likely to develop in Paget’s disease?

A

Congestive heart failure - especially if more than 40% of their skeleton is affected

104
Q

What is the management of Paget’s disease?

A

Analgesia

Bisphosphonates e.g. alendronic acid, pemidronic acid for 6 months (after which bone activity may return to normal)

105
Q

How is disease activity measured in Paget’s?

A

Monitoring ALP levels - levels correlate with how widespread the condition is

106
Q

What is the commonest primary bone malignancy? Who does it primarily present in?

A

Osteosarcoma

Adolescent males

107
Q

How does osteosarcoma present?

A

Warm, painful swelling most commonly at the knee

Pain is worse at night
Pain is not associated with movement

108
Q

What is seen on an X-Ray of osteosarcoma?

A

Periosteal reaction with codman’s triangle and a sunburst appearance

109
Q

What is a chondrosarcoma?

A

Cartilaginous malignancy

110
Q

What does an X-Ray of a chondrosarcoma show?

A

Lytic lesion with fluffy popcorn calcification

111
Q

What are bone marrow malignancy called?

A

Myeloma

Ewing’s sarcoma (a paediatric malignancy)

112
Q

Where do most bone metastases spread from?

A 
Kidneys
Thyroid
Lung
Prostate
Breast
113
Q

What is the most common site for a bony metastasis?

A

Spine

114
Q

How can you differentiate between a benign or malignant bone tumour on an X-Ray?

A

Benign - sharp, well-defined, lack soft tissue involvement and no cortical destruction

Malignant - poorly defined, rough borders, involve soft tissues and have cortical destruction

115
Q

What is the management of polymyalgia rheumatica?

A

1-2 year course of oral prednisolone

116
Q

Name some complications of corticosteroid therapy

A
  • Immunosuppression

Skin

  • Skin thinning
  • Acne
  • Stretch marks
  • Hair growth

CV
- Hypertension

Metabolism

  • Weight gain
  • Buffalo hump
  • Moon face
  • Hyperglycaemia leading to diabetes

CNS

  • Mood disorders
  • Psychosis

MSK

  • Osteoporosis
  • Avascular necrosis of the bone
  • Myopathy

GI
- Peptic ulcers

117
Q

What is the main risk factor for pseudogout?

A

Osteodegenerative joint - age, injury, previous joint surgery

118
Q

What is diagnostic of pseudogout?

A

Fluid aspiration from affected joint - positively birefringent rhomboid shaped crystals made of calcium pyrophosphate

119
Q

What is commonly seen on an X-ray of a joint affected by pseudogout?

A

Chondrocalcinosis

120
Q

What is the treatment of pseudogout?

A
  • NSAIDs - first line
  • Colchicine - second line
  • Intra-articular steroids - third line
121
Q

What is scleroderma otherwise known as?

A

Systemic sclerosis

122
Q

What is the most recognisable feature of scleroderma?

A

Skin fibrosis

123
Q

What are the 2 different types of scleroderma? What is the difference?

A

Limited cutaneous (AKA CREST) = skin fibrosis is limited to the hands and forearms, feet and legs and head and neck

Diffuse = lung + kidney involvement

124
Q

What are the core features of limited cutaneous scleroderma?

A
  • Calcinosis
  • Raynaud’s phenomenon
  • Esophageal dysmotility - dysphagia/GORD
  • Sclerodactyly - bright shiny skin of hands and feet; swollen, painful fingers with reduced mobility and function
  • Telangiectasia
125
Q

What can occur due to renal involvement in diffuse scleroderma? How can this be prevented?

A

Scleroderma crisis - renal arteries affected, leading to uncontrolled hypertension, causing headaches and seizures

Monitor BP regularly and treat with ACE inhibitors

126
Q

What antibodies should be tested for in scleroderma?

A

ANA positive - this is not specific

Anti-centromere antibodies (ACA) - specific to limited cutaneous

Anti-SCL70 - specific to diffuse

127
Q

What signs are typically found in psoriatic arthritis?

A

Dactylitis

Nail changes

128
Q

What are the ANCA positive small/medium vessel vasculitides?

A

Wegener’s aka granulomatosis polyangiitis - ANCA-PR3

Churg-Strauss aka eosinophilic granulomatosis with polyangiitis - ANCA-MPO

129
Q

What are the ANCA negative small/medium vessel vasculitides?

A

Polyarteritis nodosa

Goodpasture’s aka anti-GBM

130
Q

How does Wegener’s (granulomatosis polyangiitis) present?

A
  • Upper respiratory tract - chronic sinusitis, epistaxis, saddle-nose deformity
  • Lower respiratory tract - cough, haemoptysis, pleuritis
  • Glomerulonephritis - haematuria, proteinuria
131
Q

What is the most common sign in Churg-Strauss (eosinophilic granulomatosis with polyangiitis)?

A

Asthma

132
Q

How does Goodpasture’s (anti-GBM) present?

A

Haematuria

Haemoptysis - pulmonary haemorrhage due to cross-reactivity with basement membrane in lungs

133
Q

What test needs to be done at baseline as part of the monitoring protocol for hydroxychloroquine?

A

Baseline ophthalmology assessment including visual acuity

Will also require annual eye screenings

This is required for the rare complication of hydroxychloroquine-induced retinopathy

134
Q

What examinations and tests must be done in suspected cauda equina before referring to neurosurgery?

A

Neurological examination of lower limbs

DRE - decreased anal sphincter tone

Bladder scan (pre- and post-void) - post-void < 200ml has 97% negative predictive value

MRI spine

135
Q

Where is the conus medullaris located?

A

Located above cauda equina at T12-L2

136
Q

What are the main features of conus medullaris compression?

A

Urinary retention
Constipation
(nerve root pain is less prominent than in cauda equina)

137
Q

What is a disc herniation (aka prolapse)?

A

A tear in the annulus fibrosus results in extrusion of the nucleus pulposus and potential spinal nerve compression

138
Q

Where is the cauda equina?

A

Below L2 with nerve fibres of L3-S5

YEAR 3 & 5 CORE CONDITIONS (30 decks)

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