Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a Medicine > Orthopaedics and Rheumatology > Flashcards

Orthopaedics and Rheumatology Flashcards

1
Q

What are the most commonly used treatments for osteoporosis?

A

Bisphosphonates, HRT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is osteoporosis?

A

A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue, with a consequent increase in bone fragility.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What condition can result from progressive vertebral fractures not being treated?

A

Kyphosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When does a person reach peak bone mass?

A

Around 30-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the biggest risk factor for fracture?

A

Age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does the risk of developing osteoporosis increase significantly following menopause?

A

The restraining effects of oestrogen on bone turnover are lost, which can result in bone resorption > formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does osteoporotic bone compared with non-osteoporotic bone on HR-pQCT imaging?

A

The trabeculae are larger and more numerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is osteoporosis diagnosed?

A

DEXA scan used to calculate bone density. T-score of 2.5 or lower is diagnostic of osteoporosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is classified as severe osteoporosis?

A

A T-score of -2.5 or lower + a fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do inflammatory diseases such as rheumatoid arthritis and inflammatory bowel disease increase the risk of osteoporosis?

A

Due to an increase in inflammatory cytokines, which increase bone resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why does Cushing’s disease increase the risk of osteoporosis?

A

Cushing’s disease results in increased cortisol, which increases bone resorption and induces osteoblast apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why do hyperthyroidism and primary hyperparathyroidism increase the risk of osteoporosis?

A

Thyroid hormone and PTH increase bone turnover.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why do low body weight and immobility increase the risk of osteoporosis?

A

Reduced skeletal loading increases resorption.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which medications increase the risk of osteoporosis?

A 
Glucocorticoids
Depo-provera
Aromatase inhibitors
GnRH analogues
Androgen deprivation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name 4 risk factors for osteoporosis aside from medications/other conditions.

A
  1. Smoking
  2. Alcohol
  3. Family history of osteoporosis or fracture
  4. Previous fracture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two types of osteoporosis treatment?

A
  1. Anti-resorptive, i.e. decreasing osteoclast activity and bone turnover
  2. Anabolic, i.e. increasing osteoblast activity and bone formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Bisphosphonates are the first line of treatment for osteoporosis. Name some.

A

Alendronate, risedronate, ibandronate, etidronate (oral)
Ibandronate can also be given intravenously
Zoledronate - once yearly intravenous infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do bisphosphonates work?

A

They block the cholesterol synthesis pathway by inhibiting FPP synthase enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Denosumab is a monoclonal antibody that can be used to treat osteoporosis. What is its mechanism of action?

A

It is a monoclonal antibody to RANKL, acts as a decoy receptor and therefore disrupts the RANK pathway by preventing osteoclast activation, thereby reducing bone resoprtion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the main problem with denosumab?

A

There is a rebound increase in bone turnover when the drug is stopped.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which drug is used as a second line treatment for osteoporosis?

A

Teriparatide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does teriparatide work?

A

It is a PTH analogue, which increases bone density and improves trabecular structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does inflammatory arthritis present?

A

Sudden onset of soft and squishy joint swelling, which is often red and warm to touch with stiffness in the morning and following periods of inactivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Name 4 types of inflammatory arthritis

A
  1. Rheumatoid arthritis
  2. Seronegative spondyloarthritis
  3. Crystal arthritis
  4. Septic arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the main risk factors for rheumatoid arthritis?

A

Family history

Smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which joints tend to be affected by rheumatoid arthritis?

A

Symmetrical small joints of the hands, wrists and feet with sparing of the DIP joints

Large joints may be involved later on in the disease process.

No spinal involvement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Which joints tend to be affected by seronegative arthritis?

A

Asymmetrical large joints

Spinal involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What non-joint symptoms are associated with seronegative arthritis?

A

Inflammatory bowel, GI infection, eye inflammation and psoriasis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the main clinical features of psoriatic arthritis?

A

Pitting of the nails, nails lifting off, sausage toe (whole digit swells up as opposed to just the joint).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What may be different about a blood result for psoriatic arthritis when compared to other forms of inflammatory arthritis?

A

CRP may not be significantly raised

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the main differences between inflammatory arthritis and osteoarthritis?

A

Osteoarthritis comes on much more gradually, typically in weight bearing joints (e.g. DIPJs, PIPJs, base of thumb, big toes), no early morning stiffness, normal CRP. Inflammatory arthritis usually symmetrical pattern and can be accompanied by fatigue, fever and night sweats.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is crystal arthritis?

A

Gout/pseudogout. Acute intermittent episodes of joint inflammation due to crystal deposits (uric acid in the case of gout, calcium pyrophosphate in the case of pseudogout)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the main risk factors for gout?

A

Beer, renal impairment, diuretics, aspirin, family history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What blood tests would you carry out for suspected rheumatoid arthritis?

A

Rheumatoid factor (RF)
CCP+
CRP +/- ESR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What blood test would you carry out for gout and when?

A

Uric acid to be checked between attacks of gout as the level drops during an actual attack.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Why should inflammatory arthritis be treated as soon as possible?

A

Inflammation is reversible but damage is not, therefore inflammation should be treated before damage occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How does rheumatoid arthritis present?

A

Pain and swelling of joints (typically small joints of hands, wrists and forefeet)
Early morning stiffness
Sudden change in function
Decreased grip strength/fist formation
DIPJs are spared
Usually symmetrical
No deformity (unless presenting at advanced stage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What changes may be seen on x-ray in rheumatoid arthritis?

A

Soft tissue swelling
Periarticular osteopenia
Joint space narrowing
Bone erosion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What cheap and effective drugs are often used to treat rheumatoid arthritis?

A

Methotrexate
Sulphasalazine
Leflunomide
Hydroxychloroquine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What biological treatments can be used to treat rheumatoid arthritis?

A

Anti-TNF medications (e.g. infliximab, etanercept, adalimumab)
Rituximab (anti CD20)
Abatacept (anti T cell)
Tocilizumab (anti IL-6)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What inflammatory conditions does the term ‘spondyloarthritis’ cover?

A

Ankylosing spondylitis
Enteropathic arthritis
Reactive arthritis
Psoriatic arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What antigen, which is more prevalent in Scandinavians and some native American tribes, is linked with spondyloarthritis?

A

HLA B27 - human leukocyte antigen, class I surface antigen present on all cells except RBCs and encoded by MHC on chromosome 6.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the clinical features of spondyloarthritis?

A

Inflammation of the spine with possible fusion of vertebrae leading to kyphosis and stiff neck
Swelling of Achilles tendon
Patella tendon swelling
Medial/lateral epicondyl swelling
Acute anterior uveitis (photophobic, blurred vision)
Skin psoriasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the features of spondyloarthritis denoted by the SPINEACHE acronym?

A 
Sausage digit
Psoriasis
Inflammatory back pain
NSAID good response
Enthesitis
Arthritis
Crohn's/Colitis/CRP elevation
HLA-27
Eye (uveitis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What features can be seen on x-ray of a person with ankylosing spondylitis?

A

‘Bamboo spine’ due to continuous line of calcification, which results in fusion of the vertebrae

  • Before this stage is reached, syndesmophytes can be seen in between the vertebrae, growing vertically along the anterior longitudinal ligament
  • Joint fusion of the sacroiliac joints
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Why is ankylosing spondylitis sometimes misdiagnosed as sciatica?

A

Because as the sacroiliac joints are fusing, this causes a constant ache at the top of the buttock going into the buttock, which can sometimes go right down to the knee.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Which investigation is considered the ‘gold standard’ for diagnosis of ankylosing spondylitis?

A

MRI, which can be used to visualise acute sacroilitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the features of inflammatory back pain?

A

Patients often under the age of 40

Stiffness in the morning and evening, which often builds up over years and usually gets better with movement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is a symptom of sacroilitis?

A

Alternating buttock pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

How is psoriatic arthritis treated?

A

Early intervention with DMARDs
Possible introduction of anti-TNF drugs (etanercept, infliximab etc)
IL-12/23 blockers (ustekinumab)
IL-17 blockers (secukinumab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are DMARDs?

A

Disease-Modifying Anti-rheumatic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Give four examples of DMARDs

A
  1. Methotrexate
  2. Leflunomide
  3. Ciclosporin
  4. Sulfasalazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How does methotrexate reduce inflammation?

A

Methotrexate inhibits several enzymes that are required for nucleotide synthesis, which reduces inflammation and also cell division (methotrexate is also used in cancer treatment).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is reactive arthritis?

A

Inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What kinds of infections are usually responsible for reactive arthritis?

A

GI infections such as salmonella, shigella and yersinia, STIs such as chlamydia and ureaplasma urealyticum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What other features may occur in reactive arthritis?

A

Mucopurulent discharge around the eye, keratoderma blenorrhagica, circinate balanitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is enteropathic arthritis?

A

An episodic asymmetric lower limb arthritis associated with inflammatory bowel disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which 5 things should make you think about spondyloarthritis?

A
  1. Inflammatory back pain
  2. Asymmetrical (large joint) arthritis
  3. Skin psoriasis
  4. Inflammatory bowel disease
  5. Inflammatory eye disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Name 2 inherited connective tissue diseases

A

Marfan’s syndrome

Elher Danlos syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Marfan’s syndrome results in faulty collagen. What are the features of Marfan’s syndrome?

A

Pectus excavatum
Arachnodactyly
Dilation of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the features of Ehler Danlos syndrome?

A

Hypermobile joints
Stretchy skin
Some types also cause vascular problems, which can lead to aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Name 4 autoimmune connective tissue diseases

A
  1. Systemic lupus erythematosus
  2. Systemic sclerosis
  3. Primary Sjogren’s syndrome
  4. Dermatomyositis/polymositis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

SLE sufferers can present with various rashes, but what type of rash is particularly common with this condition?

A

A ‘butterfly’ rash over the cheeks and nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How does systemic lupus erythematosus present?

A

Symptoms can present in many systems, so the patient can show up in any department!
Skin rashes, mucosa ulcers, alopecia, arthritis, neuro-psychiatric features (aseptic meningitis, strokes, headaches, seizures, anxiety), lupus nephritis, anaemia, thrombocytopenia, neutropenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How is SLE diagnosed?

A

Antibody testing
ANA (antinuclear antibody) should be positive, but not specific for lupus
Specific test: double-stranded DNA antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

How is SLE treated?

A

Can’t be cured, but symptoms can be managed:
Topical treatments: sunscreen, steroids
Short term NSAIDs
Hydroxychloroquine - safe option for arthritis and rashes
Cytotoxic drugs e.g. azathioprine, mycophenolate, ciclosporin, methotrexate, cyclophosphamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Raynaud’s phenomenon is often seen in patients with connective tissue disorders. How is it diagnosed?

A

From skin colour change on exposure to cold. From white, to blue, to red.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are the main features of systemic sclerosis?

A

Vasculopathy
Excessive collagen deposition
Auto-antibody production
Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the 3 clinical subsets of systemic sclerosis?

A
  1. Limited cutaneous
  2. Diffuse cutaneous
  3. SS without scleroderma (involves organs but not skin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the features of limited cutaneous systemic sclerosis?

A
  • Sclerodactyly
  • Long history of Raynaud’s phenomenon
  • Late-stage complications
  • Pulmonary arterial hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the features of diffuse cutaneous systemic sclerosis?

A
  • Proximal scleroderma and trunk involvement
  • Short history of Raynaud’s
  • Increased risk of renal crisis
  • Increased risk of cardiac involvement
  • Increased risk of interstitial lung disease (fibrosis due to excessive collagen)
  • Ulcers (esp. digital)
  • Calcinosis
  • Telangiectasia
  • GI symptoms ‘watermelon stomach’ with chronic anaemia due to bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How is Raynaud’s phenomenon managed?

A

Gloves

Vasodilators e.g. nifedipine, iloprost, sildenafil, bosentan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How is renal crisis prevented in patients with systemic sclerosis?

A

ACE inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How is the risk of pulmonary arterial hypertension managed in systemic sclerosis?

A

Early detection with annual echo and pulmonary function tests

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are the options for treating skin oedema in systemic sclerosis?

A

No treatment
Mycophenolate
Autologous stem cell transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How is pulmonary fibrosis treated in systemic sclerosis?

A

Cyclophosphamide, nintedanib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What are the two types of Sjogren’s syndrome?

A

Primary

Secondary - from other autoimmune diseases e.g. SLE, rheumatoid arthritis, scleroderma, primary biliary cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What are the clinical features of primary Sjogren’s syndrome?

A 
Dry eyes and mouth
Arthritis
Rash
Neurological features
Vasculitis
Interstitial lung disease
Renal tubular acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Patients with primary Sjogren’s syndrome are more likely to be sensitive to what?

A

Gluten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Patients with primary Sjogren’s syndrome have an increased risk of developing which type of cancer?

A

Lymphoma

81
Q

What would you expect to see on lab tests for primary Sjogren’s syndrome?

A 
Positive ANA
Positive RF
Positive Ro and La antibodies
Negative double-stranded DNA
Raised immunoglobulins
Abnormal salivary gland biopsy
82
Q

How is primary Sjogren’s syndrome treated?

A

Tear and saliva replacement
Hydroxychloroquine for fatigue/myalgia/arthralgia/rash
Corticosteroids/immunosuppressants for organ-threatening extra-glandular disease

83
Q

What is the difference between dermatomyositis and polymyositis?

A

Polymyositis affects tendons and ligaments, dermatomyositis also affects the skin

84
Q

How do dermatomyositis and polymyositis present?

A

Muscle weakness
Dermatomyositis also presents with rash
Can also affect lungs (interstitial lung disease)

85
Q

What investigations are required for dermatomyositis and polymyositis?

A

Muscle enzymes, antibody screen, EMG, muscle/skin biopsy, PET-CT to check for malignancy (can also present as paraneoplastic syndrome), chest x-ray, pulmonary function tests, high resolution CT lungs.

86
Q

What types of drugs are used to manage dermatomyositis and polymyositis?

A

Steroids

Immunosuppressive drugs

87
Q

What is osteomyelitis?

A

Infection localised to the bone - literally means “bone marrow inflammation”

88
Q

Which age groups are most at risk of osteomyelitis?

A

Bimodal age distribution - younger patients and older patients?

89
Q

What possible cause of osteomyelitis is mostly seen in children and why?

A

Haematogenous seeding due to high blood flow in developing bones

90
Q

What normally causes osteomyelitis in adolescents and adults?

A

Contiguous spread from direct trauma

91
Q

What are the three routes via which a pathogen can find its way into the bone?

A
  1. Direct inoculation of infection into the bone ‘smashed window’ e.g. trauma, surgery
  2. Contiguous spread from soft tissues and joints
  3. Haematogenous seeding
92
Q

What three conditions affecting vasculature increase the risk of developing osteomyelitis?

A
  1. Arterial disease
  2. Sickle cell disease
  3. Diabetes mellitus
93
Q

What two conditions affecting the bones/joints increase the risk of developing osteomyelitis?

A
  1. Inflammatory arthritis

2. Prosthetic material

94
Q

Where is osteomyelitis more likely to develop in children?

A

In the long bones

95
Q

Where is osteomyelitis more likely to develop in adults over 50 years and why?

A

Vertebrae as vasculature increases with age, making bacterial seeding of the vertebral endplate more likely

96
Q

Where is osteomyelitis more likely to develop in IV drug users?

A

Clavicle and pelvis

97
Q

Which 3 pathogens are the usual causes of osteomyelitis?

A

Staph aureus
Coagulase-negative staph
Aerobic gram-negative bacilli

98
Q

What are the symptoms of osteomyelitis?

A

Onset over several days

Dull pain at the site of OM, which may be aggravated by movement

99
Q

What are the signs of osteomyelitis?

A

Systemic signs e.g. fever, rigors, sweats, malaise
Local: tenderness, warmth, erythema, swelling

In chronic OM may have non-healing ulcers and fractures

100
Q

What might blood tests for osteomyelitis show?

A

WCC will be raised in acute OM but may be normal in chronic OM
CRP may be normal or raised

101
Q

What might a plain x-ray show in cases of chronic osteomyelitis?

A 
Cortical erosion
Periosteal reaction
Mixed lucency
Sclerosis
Sequestra
Soft tissue swelling
102
Q

Why would an MRI scan be preferable to a plain x-ray for detecting early osteomyelitis?

A

It takes 1-2 weeks before any bone changes are seen on plain x-ray
Marrow oedema can be seen from 3-5 days on MRI and can distinguish cortical, bone marrow and soft tissue inflammation.

103
Q

What investigation would be used to make a definitive diagnosis of osteomyelitis?

A

Bone biopsy with culture and 16s RNA PCR

104
Q

What are the differential diagnoses for osteomyelitis?

A 
Soft tissue infection (e.g. cellulitis)
Charcot joint
Avascular necrosis of bone
Gout
Fracture
Bursitis
Malignancy
105
Q

How is osteomyelitis treated?

A

Surgery with debridement/hardware replacement or removal
Antimicrobial therapy with initial empirical treatment with broad spectrum antibiotics, then tailor to culture and sensitivity findings, administer for prolonged duration (weeks).

106
Q

Which type of osteomyelitis requires treatment for at least six months?

A

TB osteomyelitis

107
Q

What is the usual method of infection of joints?

A

Haematogenous spread

108
Q

What investigations would be carried out for suspected joint infection?

A

Blood cultures

Aspiration of joint

109
Q

What joint aspirate appearances would suggest infection?

A

Thick, opaque, sticky, turgid fluid

110
Q

What would you expect to see on blood tests for a patient with joint infection?

A

Possibly raised WCC
Raised CRP
ESR rises and falls more slowly - depends on history

111
Q

How is joint infection managed?

A
  • Aspiration (always)
  • Antibiotics depending on aspiration - long course (minimum 6 weeks)
  • Joint washout/repeated aspiration until no recurrent effusion
  • Rest/splint/physio for rehab
  • Analgesia
  • Stop immunosuppression temporarily if possible
112
Q

What is the next step if you suspect infection in a joint and the joint aspirate doesn’t tell you?

A

Synovial biopsy (usually done by interventional radiologists)

113
Q

How does gonococcal arthritis present?

A

Occurs alongside gonococcal infection

Fever, arthritis, tenosynovitis, maculopapular - pustular rash

114
Q

What investigation should you carry out if you suspect gonococcal arthritis?

A

Mucous membrane swabs

115
Q

What are the three most common organisms that infect prosthetic joints?

A
  1. Coagulase negative staphylococcus
  2. Staph aureus
  3. Enterococcus
116
Q

What is the most common route of infection in prosthetic joints?

A

Infection introduced when the joint is fitted (not haematogenous spread)

117
Q

What precautions can be taken in theatre to help prevent infection of prostheses?

A

Sterility
Prophylactic antibiotics
Use of laminar flow

118
Q

How do prosthetic joint infections present?

A

Sometimes with evidence of acute infection (hot, red, swollen, pus etc) but sometimes only low grade symptoms, e.g. patient has not been quite right since it was put in.

119
Q

How should suspected prosthetic joint infection be investigated?

A

X-rays, FBC, ESR, CRP, aspirate and culture (preferably over extended period i.e. 14 days - patient must be off antibiotics)

120
Q

What would you expect to see on blood tests for prosthetic joint infection?

A

WCC may or may not be raised

CRP may only be slightly raised

121
Q

What are the treatment options for infected prosthesis?

A
  • Antibiotic suppression (not preferred)
  • Debridement and retention of prosthesis
  • Excision arthroplasty
  • One or two-stage exchange arthroplasty
  • Amputation
122
Q

What are the indications for antibiotic suppression?

A
  • Patient unfit for surgery
  • Multiple prosthetic joint infections
  • Poor distal skin/soft tissues
  • Low virulence infecting organisms
  • Available oral antibiotics
  • Patient tolerates antibiotics
  • Prosthesis not loose
  • If not possible to eradicate infection through surgery
123
Q

When would debridement and implant retention be used to treat prosthesis infection?

A
  • Early post-op infections
  • Acute haematogenous infections

i.e. not chronic infections

124
Q

When might excision arthroplasty be indicated?

A
  • High risk, frail patients with multiple comorbidities
  • Low functional demand
  • Uncontrolled with antibiotic suppression
  • High risk of re-infection (i.e. poor skin/soft tissues)
125
Q

What antibiotics should be given to empirically treat a prosthetic joint infection?

A

Trick question - prosthetic joint infections should not be treated empirically with antibiotics. Always aspirate first!

126
Q

What are the 4 Rs for treating fractures?

A
  1. Resuscitate - you can’t fix the fracture if the patient is dead
  2. Reduce - realign the fracture, restore anatomy (vessels, muscles, nerves etc need to be in the right place)
  3. Retain - keep in position e.g. fixation, plaster cast, skin traction
  4. Rehabilitation
127
Q

What 6 things need to be considered when looking at an x-ray of a fracture?

A
  1. Which bone is it?
  2. Is it intra- or extra-articular?
  3. Position
  4. Pattern
  5. Condition
  6. Displacement
128
Q

What are the different patterns of fractures?

A

Transverse
Oblique
Spiral

129
Q

What are the different ‘conditions’ of fractures?

A
  1. Comminuted (lots of bits)
  2. Segmental (two fractures with a segment in the middle with poor blood supply)
  3. Impacted (hasn’t moved far, blood supply likely intact)
130
Q

What things need to be considered regarding displacement?

A

Length
Alignment
Rotation

131
Q

What are the two forms of bone healing?

A
  1. Bone remodelling cycle - direct, primary bone healing

2. Callous formation - inflammatory reaction, indirect, secondary bone healing

132
Q

What are the 4 stages of the bone remodelling cycle?

A
  1. Resting
  2. Resorption
  3. Formation
  4. Mineralisation
133
Q

What conditions have to be met for primary healing of a fracture?

A

Absolute stability
Gap of <1mm
Compression

134
Q

What are the 4 stages of callous formation?

A
  1. Bleeding
  2. Soft callous
  3. Bony callous
  4. Remodelling
135
Q

What conditions have to be met for secondary healing of a fracture?

A

Relative but not absolute stability - if there is no movement at all, the cells are not stimulated and the callous doesn’t form.

136
Q

What can a patient do to improve bone healing?

A

Stop smoking
Stop NSAIDs
Improve nutrition

137
Q

What is the most common condition affecting synovial joints?

A

Osteoarthritis

138
Q

What mediates the pathogenesis of osteoarthritis?

A

Cytokines IL-1, TNF-a, NO

139
Q

What are the main pathological features of osteoarthritis?

A

Loss of cartilage

Disordered bone repair

140
Q

What causes synovial hypertrophy in osteoarthritis?

A

Wear and tear (as opposed to inflammatory response)

141
Q

What are the five main risk factors for osteoarthritis?

A
  1. Age
  2. Gender (female preponderance)
  3. Genetic predisposition
  4. Obesity
  5. Occupation
142
Q

What are the main symptoms of osteoarthritis?

A

Pain

Functional impairment

143
Q

What are the main signs of osteoarthritis?

A

Alteration in gait
Joint swelling
Other joint abnormalities (limited ROM, crepitus, tenderness, deformities)

144
Q

What radiological features are often seen in osteoarthritis?

A
  1. Loss of joint space
  2. Osteophytes
  3. Subchondral sclerosis
  4. Subchondral cysts
  5. Abnormalities of bone contour
145
Q

Involvement of which joint is commonly seen osteoarthritis, but not in rheumatoid arthritis?

A

Distal interphalangeal joint (DIPJ)

146
Q

Osteoarthritis can affect which joints in the hands?

A

DIP, PIP and CMC joints

147
Q

Which nodes are seen at which joints of the hands in osteoarthritis?

A

Heberden’s nodes seen at the DIP joints

Bouchard’s nodes seen at the PIP joints

148
Q

Which compartment of the knee is most likely to be affected by osteoarthritis?

A

Medial

149
Q

What is used to treat erosive/inflammatory osteoarthritis in addition to standard management?

A

DMARDs - usually milder agents e.g. hydroxychloroquine as opposed to methotrexate

150
Q

What is associated with ‘locking’ of the knee in osteoarthritis?

A

Loose body in the knee, i.e. a bone/cartilage fragment

151
Q

What topical treatments can be used in the management of osteoarthritis?

A

NSAIDs

Capsaicin

152
Q

What oral medications can be used in the management of osteoarthritis?

A

Paracetamol
NSAIDs (with caution)
Opioids

153
Q

What transdermal patches can be used in the management of osteoarthritis?

A

Buprenorphine, lignocaine

154
Q

What surgical procedures can be performed to help manage osteoarthritis?

A

Arthroscopy (for loose bodies)
Osteotomy
Arthroplasty
Fusion (usually ankle and foot)

155
Q

What type of crystals are formed in gout?

A

Urate crystals

156
Q

What type of crystals are formed in pseudogout?

A

Pyrophosphate crystals

157
Q

How does gout normally present?

A

Sudden onset of a hot, swollen joint with excruciating pain that normally resolves in a few weeks

158
Q

Which joint is affected in 70% of gout cases?

A

1st MTPJ (big toe)

159
Q

What is the target for gout treatment?

A

Xanthine, which is the precursor to uric acid formed from purines

160
Q

At what level of urate in plasma does the risk of crystal deposition start to increase?

A

> 0.36mmol/l

161
Q

What things in a person’s diet can increase the risk of gout?

A

Alcohol (especially beer)
Fructose sweetened drinks
Excess meat/shellfish/offal
Yeast extract

162
Q

What diseases can increase the risk of gout?

A 
Myeloproliferative disease
Psoriasis
Tumour lysis syndrome
Lesch-Nyhan syndrome
Renal impairment
163
Q

What medications can increase the risk of gout?

A 
Thiazide diuretics
Low dose aspirin
Tacrolimus
Ciclosporin
Ethambutol
Pyrazinamide
164
Q

Most attacks of gout are spontaneous, but what things can possibly trigger an attack?

A 
Direct trauma to the joint
Intercurrent illness
Alcohol/shellfish binge
Surgery
Dehydration
165
Q

What investigations can be performed for gout?

A
  • Fluid aspiration from the joints (needle-shaped crystals may be seen on sediment)
  • Routine bloods to exclude other diagnoses
  • Inflammatory markers (CRP often >100)
  • Uric acid (may not necessarily be raised but needed to inform treatment dose)
  • X-ray
166
Q

What drugs are used to treat acute attacks of gout?

A

NSAIDs (use with caution as renal impairment is a risk factor for gout)
Colchicine 500mg bd
Prednisolone (oral or inject into joint)

167
Q

What drug can be prescribed for chronic gout, but should not be started during an attack?

A

Allopurinol (or Febuxostat) - xanthine oxidase inhibitors

168
Q

How does pseudogout present?

A

Sudden onset of hot, swollen joint similar to gout. However, affects different joints.
Knees > wrist > shoulder > ankle > elbow

169
Q

What conditions increase the risk of developing pseudogout?

A 
Haemochromatosis
Hyperparathyroidism
Hypophosphatasia
Hypomagnesaemia
Diabetes
Hyper/hypothyroidism
170
Q

What investigations should be performed for pseudogout?

A

Routine bloods (including iron, PTH, PO4, Mg and TSH)
Inflammatory markers
Uric acid (should be normal)
Joint aspiration (rhomboid-shaped crystals)
X-ray

171
Q

How are acute attacks of pseudogout treated?

A

NSAIDs if safe
Colchicine
Prednisolone (oral/injection)

172
Q

How is chronic pseudogout treated?

A

Long term low dose prednisolone (if frequent attacks) - monitoring required
Long term low dose colchicine
Trial of hydroxychloroquine/methotrexate (~6 months only)

173
Q

What is vasculitis?

A

Inflammation and necrosis of blood vessels with subsequent impaired blood flow

174
Q

What are the local consequences of vasculitis?

A

Vessel wall destruction

Endothelial injury

175
Q

What is seen on histology of vasculitis?

A

Vessel wall infiltration with the presence of neutrophils, mononuclear cells +/- giant cells
Fibrinoid necrosis
Leukocytoclasis (dissolution of leukocytes)

176
Q

How is vasculitis classified?

A

With some difficulty is there is a lot of overlap.
Generally classified by:
1. Size of vessel affected (small/medium/large)
2. Target organs
3. Presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA)

177
Q

Name 3 primary vasculitis disorders of large arteries

A
  1. Giant cell arteritis
  2. Takayasu’s arteritis
  3. Isolated CNS angiitis
178
Q

What disorders can cause secondary vasculitis in large arteries?

A

Aortitis

Infection e.g. syphilis

179
Q

Name 2 primary vasculitis disorders of medium arteries

A
  1. Classical polyarteritis nodosa

2. Kawasaki disease

180
Q

What disorders can cause secondary vasculitis in medium arteries?

A

Infection e.g. hep B

Hairy cell leukaemia

181
Q

Name 3 types of primary vasculitis that affect medium/small arteries

A
  1. Wegener’s granulomatosis
  2. Churg-Strauss syndrome
  3. Microscopic polyangiitis
182
Q

What disorders can cause secondary vasculitis in medium/small arteries?

A

Autoimmune diseases
Malignancy
Drugs
Infection e.g. HIV

183
Q

Name 3 types of primary vasculitis affecting small vessels

A
  1. Henoch Schonlein purpura
  2. Essential mixed cytoglobulinaemia
  3. Cutaneous leukocytoclastic angiitis
184
Q

What disorders can cause secondary vasculitis in small vessels?

A

Drugs
Malignancy
Infection e.g. hep B/C

185
Q

How does vasculitis present?

A

No single typical presentation, can be easily confused with other diseases
Systemic illness, fever, arthralgia/arthritis, rash, weight loss, headache, foot drop, major event (e.g. stroke/bowel infarction)

186
Q

Which type of vasculitis is ANCA positive?

A

Small/medium vessel vasculitis

187
Q

What is giant cell arteritis?

A

Granulomatous arteritis affecting the aorta and larger vessels + extracranial branches of the carotid arteries

188
Q

Which demographics are more at risk of developing giant cell arteritis?

A

Over 50s, twice as common in females

189
Q

How does giant cell arteritis present?

A 
Headache
Scalp tenderness
Jaw claudication
Acute blindness (medical emergency)
Non-specific malaise
Associated symptoms of polymyalgia rheumatica
190
Q

What are the diagnostic criteria for giant cell arteritis?

A 
3 or more of:
Age > 50
New headache
Temporal artery tenderness/decreased pulsation
ESR > 50
Abnormal temporal artery biopsy
191
Q

What is AION?

A

Arteritic anterior ischaemic optic neuropathy - causes sudden, painless monocular visual loss. The optic disc becomes pale and swollen, often with flame-shaped haemorrhages at the margin.

192
Q

What investigations should be performed if giant cell arteritis is suspected?

A
  • Suspect in >50 developing new type of headache with jaw claudication and unexplained fever
  • Check ESR/CRP
  • Temporal artery biopsy
193
Q

How is giant cell arteritis treated?

A

Prednisolone (prompt treatment) - 30-40mg per day if no visual disturbance, 80mg/day if visual disturbance
Should respond within 48 hours
Also:
- Steroid sparing agents e.g. azathioprine, methotrexate, biologics
Prophylaxis of osteoporosis (lifestyle advice, calcium/vitamin D, bisphosphonate)

194
Q

What is Wegener’s granulomatosis also known as?

A

Granulomatosis with polyangiitis

195
Q

What antibodies are associated with Wegener’s/GPA?

A

cANCA

196
Q

What are the symptoms of Wegener’s/GPA?

A 
Depends on system affected e.g.
URT - sinusitis/otitis/nasal crusting
Lungs - pulmonary nodules, haemorrhage
Kidneys - glomerulonephritis
Skin - purpura, ulcers
Nervous system - mononeuritis, multiplex/CNS, vasculitis
Eye - proptosis, scleritis, episcleritis, uveitis
etc. etc.
197
Q

What nasal deformity might be seen in Wegener’s/GPA?

A

Saddle nose deformity

198
Q

How is Wegener’s/GPA treated?

A

Steroids (dose depending on severity)
Cyclophosphamide
Biologics
Methotrexate, mycophenolate, azathioprine

Phase 2a Medicine (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions