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MSK Year 2 > Inflammatory arthritis disorders > Flashcards

Inflammatory arthritis disorders Flashcards

1
Q

Rheumatoid Arthritis

A

An autoimmune and inflammatory disease which mainly attacks the joints, usually many joints at once.

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2
Q

Epidemiology of Rheumatoid arthritis

A
  • Females affected more than men

* Peak incidence in the 50’s

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3
Q

Describe the clinical features of RA.

A
  • Pain worse in the morning (morning stiffness lasting greater than 1 hour)
  • Relieved by exercise
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4
Q

Describe the hand changes in Rheumatoid Arthritis

A
  1. Symmetrical joint tenderness, redness and swelling
  2. Sausage shaped fingers
  3. Loss of valleys around the knuckles
  4. Swan neck deformity
  5. Boutonniere deformity
  6. Carpal tunnel syndrome
  7. Ulnar deviation of MCPs
  8. Radial deviation of wrist
  9. Rheumatoid nodules
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5
Q

What is swan neck deformity?

A

Hyper-extension at the PIP joint and flexion of the DIP joint

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6
Q

Boutonniere deformity

A

Flexion of the PIP joint and hyper-extension of the DIP joint

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7
Q

X-ray changes in RA

A

Periarticular osteoporosis
Erosions
Increased joint space
Soft tissue swelling

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8
Q

Investigations in RA.

A
  1. FBC – anaemia of chronic disease
  2. ESR/CRP – raised
    3, Positive RF
  3. Positive anti-CCP
  4. CXR
  5. Pulmonary effusion
  6. Pulmonary fibrosis (caused by methotrexate)
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9
Q

Rheumatoid nodules

A

Firm lumps that appear under the skin in up to 20% of patients with RA. They usually occur overexposed joints that are subject to trauma, such as the finger joints and elbows.

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10
Q

What antibodies are present in RA

A

RF

AntiCCP

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11
Q

Management of RA

A

NSAIDs (+PPI)
Steroids
DMARDs
Anti-TNFs inhibitors (biological drugs)

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12
Q

First line DMARDs in RA

A

Methotrexate

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13
Q

Side effects of Methotrexate

A

Bone marrow suppression
Pulmonary fibrosis
Renal failure
Hepatotoxicity

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14
Q

Second line DMARDs in RA

A

Sulfasalazine

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15
Q

Side effects of Sulfasalazine

A

Oligospermia
Hepatotoxicity
Bone marrow suppression

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16
Q

How is the effectiveness of DMARDs measured?

A

CRP

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17
Q

Side effects of Azathioprine (DMARD)

A

Hepatotoxicity

Bone marrow suppression

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18
Q

Side effect of Penicillamine

A

Nephrotic syndrome

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19
Q

Side effects of Gold

A

Nephrotic syndrome

Skin reaction

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20
Q

Side effects of Hydroxychloroquine

A

Corneal micro deposits
Retinopathy
Tinnitus

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21
Q

Side effects of Anti-TNF inhibitors (etanercept, adalimumab, infliximab)

A

Blood dyscrasias
Reactivation of TB
Anaphylaxis

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22
Q

What investigation needs to be done before prescribing Anti-TNF inhibitors?

A

Chest Xray (reactivation of latent TB)

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23
Q

Examples of Anti-TNF inhibitors

A

Etanercept, adalimumab, infliximab

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24
Q

When can Anti-TNF inhibitors be prescribed in RA?

A

Only if 2 DMARDs have failed (with 1 of them being methotrexate).

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25
Q

Difference in symptoms between RA & OA.

A

Pain worse in the morning (morning stiffness lasting greater than 1 hour)
Relieved by exercise
–> In RA

Pain and stiffness less than 30 minutes in the morning, Pain worse with movement, and improves with rest.
–> OA

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26
Q

What is Gout?

A

Inflammatory arthritis

Results from uric acid deposition in synovium

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27
Q

What enzyme leads to the production of uric acid?

A

Xanthine oxidase

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28
Q

Risk factors for Gout

A 
o	Male
o	Obesity
o	Alcohol
o	Purine rich diet
o	Thiazide diuretics
o	Renal insufficiency
o	Cyclosporine
o	Salicytates 
o	Hereditary
o	Occupational lead exposure
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29
Q

What drugs lead to gout?

A

Thiazide diuretics
Cyclosporine
Salicytates

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30
Q

Example of salicytates

A

Aspirin

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31
Q

What kind of diet leads to gout?

A

Purine rich diet

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32
Q

Symptoms of Gout

A 
Acute onset
Hot
Swollen
Red
Tender joint
Very painful
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33
Q

Where do the majority of gout attacks arise?

A

60-70% of attacks occur on big toe (known as podagra)

First metatarsalphalangeal joint

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34
Q

What joint does gout usually affect?

A

First metatarsalphalangeal joint

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35
Q

Gouty Tophi

A

Indicates chronic deposition of urate

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36
Q

Investigations in Gout

A 
Elevated serum uric acid
Xray
Soft tissue swelling
Polarised microscopy of synovial fluid
Negatively bifringent, needle shaped crystals
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37
Q

What does the polarised microscopy of synovial fluid in Gout show?

A

Negatively bifringent, needle shaped crystals

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38
Q

Management of gout

A

NSAIDs (1st line)
Colchicine (2nd line)
Corticosteroids (oral or intraarticular)

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39
Q

What is the preventative prophylaxis for gout?

A

Allopurinol - Do not start during flare-up as can potentiate further flare

Diet advice

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40
Q

Mechanism of action of Allopurinol

A

Xanthine oxidase inhibitor

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41
Q

Calcium pyrophosphate dehydrate disease (CPPD) aka Pseudogout

A

Calcium pyrophosphate dihydrate crystal deposition disease (CPPD) is a form of arthritis that causes pain, stiffness, tenderness, redness, warmth and swelling (inflammation) in some joints.

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42
Q

What is the main disease associated with CPPD?

A

Associated with OA

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43
Q

What disease/diseases is CPPD associated with in the elderly?

A 
Haemochromatosis 
Hyperparathyroidism
Hypothyroidism 
Renal osteodystrophy
Wilson’s disease
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44
Q

Calcium pyrophosphate dehydrate disease (CPPD) is divided into 2 syndromes - what are they?

A

Pseduogout – in joint space

(chondrocalcinosis) – in cartilage and soft tissue

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45
Q

What is Chondrocalcinosis?

A

A dorm of CPPD - Cartilage calcification is accumulation of calcium salts in hyaline cartilage and/or fibro-cartilage. It can be seen on radiography.

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46
Q

Investigations is CPPD

A

Increased CRP, PV, ESR

Ca2+/TSH to look for secondary causes of metabolic disease

Rhomboid shaped, positively bifringent crystals

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47
Q

What does the microscopy of the synovial fluid in CPPD/Pseudogout show?

A

Rhomboid shaped, positively bifringent crystals

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48
Q

Management of Pseudogout

A

NSAIDs
Corticosteroids – systemic & intra-articular
Colchicine

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49
Q

What is the difference in management of Pseudo-gout and gout?

A

Unlike gout (where you can use allopurinol) there is no prophylactic treatment for pseudogout

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50
Q

Osteoporosis

A

Brittle bones - Quantitative defect of bone characterized by reduced bone mineral density (BMD)

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51
Q

What are the typical fracture sites in osteoporosis?

A

distal radius, femoral neck, vertebral bodies

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52
Q

How is osteoporosis diagnosed?

A

Dexa scan to show BMD

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53
Q

What are the typical Dexa scan values in osteoporosis?

A

BMD >2.5 SD below normal = osteoporosis

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54
Q

What are the typical Dexa scan values in osteopenia?

A

BMD 1-2.5 standard deviations (SD) below normal = osteopenia

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55
Q

Osteopenia

A

Stage before osteoporosis is called osteopenia. This is when a bone density scan shows you have lower bone density than the average for your age, but not low enough to be classed as osteoporosis.

Osteopenia does not always lead to osteoporosis.

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56
Q

Management of osteoporosis

A

Calcium supplements
Vitamin D supplements
Bisphosphonates

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57
Q

Mechanism of action of biphosphonates

A

Acts to reduce osteoclastic resorption

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58
Q

Osteomalacia

A

Marked softening of your bones, most often caused by inadequate amounts of Vitamin D, calcium and phosphorus

Qualitative defect of bone with abnormal softening of the bone due to deficient mineralisation of osteoid

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59
Q

What is the name for osteomalacia disease in children?

A

Rickets

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60
Q

Investigations for osteomalacia

A

Serum alkaline phosphatase levels are usually raised in osteomalacia

Low serum calcium

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61
Q

Treatment for osteomalacia

A

Vitamin D supplements
Calcium supplements
Phosphate supplements

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62
Q

Paget’s disease

A

The pelvis, skull, spine and legs are most commonly affected.

Bone making process becomes faster and out of control.

Newly formed bone is thicker, abnormally shaped and weaker

Prone to fractures

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63
Q

Most commonly affected bones in Paget’s disease

A

The pelvis, skull, spine and legs

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64
Q

What do the Radionuclide bone scans show in Paget’s disease?

A

Show areas of increased uptake, caused by increased vascularity.

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65
Q

Most common site for Paget’s sarcoma

A

Humerus

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66
Q

Features of Paget’s disease affecting the SKULL.

A

May cause hearing loss if it affects the bones of the skull

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67
Q

What are the Xray findings of Paget’s disease?

A

Thickening of cortex
Areas of osteolysis
Trabecular thickening and sclerosis

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68
Q

Investigations for Paget’s disease

A

Normal calcium and phosphate, raised alkaline phosphate

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69
Q

Treatment for Paget’s disease

A

Bisphosphonate therapy (risedronate)

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70
Q

Osteogenesis imperfecta

A

Autosomal dominant bone disorder that is present at birth. It is also known as brittle bone disease. A child born with OI may have soft bones that break (fracture) easily, bones that are not formed normally,

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71
Q

What is the mode of inheritance of Osteogenesis imperfecta

A

Autosomal dominant

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72
Q

Symptoms of Osteogenesis imperfecta

A 
Multiple fragility fractures of childhood
Short stature with multiple deformities 
Blue sclerae 
Loss of hearing
History of low energy fractures 
Malformation of the teeth
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73
Q

Marfan’s syndrome

A

A disorder of the body’s connective tissues, a group of tissues that maintain the structure of the body and support internal organs and other tissues.

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74
Q

Pectus excavatum

A

Hollowed chest

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75
Q

Marfan’s syndrome symptoms

A

Tall stature with disproportionately long limbs, fingers and loose ligaments, scoliosis, joint instability, high srched palate

Pectus excavatum (hollowed chest)

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76
Q

What is Gower’s sign?

A

A sign of proximal weakness, uses hands to get up from squatting position - usually muscular dystrophy

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77
Q

Ankylosing spondylitis (AS)

A

Type of arthritis that causes pain and stiffness in your spine, usually starts in your lower back.

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78
Q

What is the name given to the spine in Ankylosing spondylitis (AS)?

A

Bamboo spine

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79
Q

Symtoms of Ankylosing spondylitis (AS)

A

Primarily affects the spine - “Bamboo spine”
Usually males <30
Enthesopathy
Question mark posture
Hyperextension of the neck
Severe kyphosis of the thoracic spine
Earliest changes at the sacro-iliac joints

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80
Q

What condition is associated with Ankylosing spondylitis (AS)?

A

Associated with UC

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81
Q

Enthesopathy/enthesitis

A

Inflammation of the site of insertion of tendons into bones

82
Q

Clinical features of Ankylosing spondylitis (AS)

A 
Worse in the morning 
Relieved by exercise 
Enthesitis 
Anterior uveitis 
Aortic valve incompetence 
Pulmonary fibrosis (upper lobes)
Amyloidosis
83
Q

What X-ray change is shown in Ankylosing spondylitis (AS)

A

Sacroilitis
Bamboo spine
Syndesmophytes

84
Q

Investigations in Ankylosing spondylitis (AS)

A

Reduced chest expansion
ESR, CRP high
HLA-B27 positive
Xray changes

85
Q

Treatment for Ankylosing spondylitis (AS)

A 
NSAIDs
DMARDs
Anti-TNF
Steroids
Avoid bed rest
86
Q

Psoriatic arthritis

A

A type of arthritis that affects some people with the skin condition psoriasis.It typically causes affected joints to become swollen, stiff and painful

87
Q

What nail changes are seen in Psoriatic arthritis?

A

Pitting
Onycholysis
Subungal hyperkeratosis

88
Q

Symptoms of Psoriatic arthritis

A 
•	Sacroilitis (asymmetrical)
•	Nails
•	Dactylitis (sausage fingers)
•	Enthesitis 
            - Achilles tendonitis
            - Plantar fasciitis 
•	Anterior uveitis
89
Q

Investigations in Psoriatic arthritis

A 
Synovial biopsy 
X-ray changes 
- Osteolysis (“Pencil-in-cup” deformity)
- Whiskering
- Enthesis
90
Q

X-ray changes seen in Psoriatic arthritis

A
  • Osteolysis (“Pencil-in-cup” deformity)
  • Whiskering
  • Enthesis
91
Q

Management in Psoriatic arthritis

A 
Physiotherapy 
NSAIDs
Steroid injections
DMARDs (methotrexate, sulfasalazine)
Anti-TNF (etanercept)
92
Q

Reactive arthritis/reiter’s syndrome

A

“Can’t see, can’t pee, can’t climb a tree” (conjunctivitis, urethritis, arthritis)

Infection induced systemic illness (follows a UTI or GI infection)

Symptoms appear 1-4 weeks post infection

93
Q

Commonest microorganisms in Reactive arthritis/reiter’s syndrome

A

Chlamydia
Salmonella
Shigella
Yersina

94
Q

Symptoms of Reactive arthritis/reiter’s syndrome

A 
o	Fever 
o	Malaise
o	Asymmetrical mono/oligo-arthritis 
o	Enthesis 
o	Mucocutaneous lesions
	Conjunctivitis/iritis 
o	Mild renal disease
o	Keratoderma blennorrhagica
95
Q

What is Keratoderma blennorrhagica?

A

Skin lesions commonly found on the palms and soles which may spread to the scrotum scalp and trunk. The lesions may resemble psoriasis

96
Q

Investigations in Reactive arthritis/reiter’s syndrome

A

Increased ESR, CRP, PV
HLA-B27
Joint fluid analysis (to rule out septic arthritis)

97
Q

Management of Reactive arthritis/reiter’s syndrome

A

Treat the original infection
o Rest/splint affected joints
o Self-limiting over months
o NSAIDs and steroid injections

98
Q

Enteropathic arthritis

A

Refers to acute or subacute arthritis in association with, or as a reaction to, an enteric inflammatory condition - IBD

99
Q

Septic arthritis

A

Infection of joint - Commonly causes by staphylococcus
Caused by haemophilus influenzae in those under 2.

Any joint with the following characteristics is septic arthritis until proven otherwise
o Hot
o Red
o Tender

100
Q

What are the common organisms that cause septic arthritis?

A

Commonly causes by staphylococcus

Caused by haemophilus influenzae in those under 2.

101
Q

What is the joint most commonly affected in septic arthritis?

A

Knee

Can rapidly cause irreversible joint damage

102
Q

Investigations for Septic arthritis

A

Raised inflammatory markers (ESV, CRP)

Joint Fluid analysis

103
Q

Treatment for septic arthritis

A

IV flucloxacillin

Don’t give intra-articular antibiotics are they cause chemical synovitis and may worsen the infection

104
Q

Why are intra-articular antibiotics not given in septic arthritis?

A

They cause chemical synovitis and may worsen the infection

105
Q

Epidemiology of SLE

A
  • Afro-Caribbean
  • Women
  • Peak age 25-35
106
Q

What is SLE?

A

Autoimmune disease in which the immune system attacks its own tissues, causing widespread inflammation and tissue damage in the affected organs.

It can affect the joints, skin, brain, lungs, kidneys, and blood vessels.

107
Q

Triggers for SLE

A 
o	Infection (typically EBV)
o	UVA/UVB treatment
o	Drugs (procainamide, hydralazine)
108
Q

What drugs can trigger SLE?

A

procainamide, hydralazine

109
Q

Key features in SLE

A

LOTS!

Photosensitivity 
Malar --> butterfly rash --> purple scaly rash over eyes 
Discoid lupus erythematosus 
Raynaud’s 
Polyarthritis
110
Q

What are the renal features in SLE?

A

Proteinuria (0.5g/day)
Red cell casts in urine
Glomerulonephritis
• IgG deposition

111
Q

Investigations for SLE

A 
Urine dipstick – proteinuria 
Blood – anaemia, thrombocytopenia, leukopenia, raised ESR/CRP
ANA – 90%+
dsDNA – highly specific to SLE
Antiphospholipid
Anticardiolipid
112
Q

What antibodies are found in SLE?

A

ANA

dsDNA – highly specific to SLE

113
Q

What antibody is highly specific to SLE?

A

dsDNA Antibodies

114
Q

Management of SLE

A 
Mild disease
 - No specific treatment needed
 - NSAIDs
- Lifestyle (avoid sun)
Anti-malarials
- Chloroquine 
- Hydroxychloroquine 
Steroid 
 - Injections 
 - Oral
Immunosuppression 
Protection from photosensitivity (sun block creams)
115
Q

Complications of SLE

A

Increased incidence of atherosclerotic disease
Increased risk of thrombosis
Increased risk of infection

116
Q

Systemic sclerosis (CREST)

A

Connective tissue disorder

C – calcinosis –
R – raynaud’s phenomenom
E – oesophageal dysmotility
S – sclerodactyly (thickening of the skin)
T – telangiectasia (red spots on the skin)

117
Q

Epidemiology of Systemic sclerosis (CREST)

A

Women
30-50s
Smoking is a risk factor

118
Q

Clinical signs of systemic sclerosis

A 
Calcinosis of the fingertips 
Raynaud’s phenomenon
Eosophogeal reflux
Sclerodactyl
Telangiectasia
Arthritis 
Progressive fibrotic lung disease
Pulmonary hypertension
“Pinched face” with beaked nose
Skin pigmentation changes
119
Q

Sclerodactyly

A

Thickening of the digits of the hands and feet (sausage fingers)

120
Q

Investigations for Systemic sclerosis

A

Raised ESR and CRP

Diagnosis based on have 1 major and 2 minor cutaneous features

Major - Centrally located skin sclerosis that affects arms, face and/or neck

Minor
• Sclerodactyly & atrophy of fingertips
• Bilateral lung fibrosis

LFTs - primary biliary cirrhosis
CXR - pulmonary infiltrates

121
Q

There are 2 types of systemic sclerosis, what are they?

A

Limited VS Diffuse

122
Q

What is diffuse systemic sclerosis?

A

Rapid cutaneous involvement – can affect trunk as well. Organ involvement in early disease

Anti-Scl-70 (antinucleur)

123
Q

What is limited systemic sclerosis?

A

Limited – cutaneous involvement confiened to face, hands, forearms and feet. Organ involvement later

Anti-centromere antibodies

124
Q

Antibodies in limited systemic sclerosis?

A

Anti-centromere antibodies

125
Q

Antibodies in diffuse systemic sclerosis?

A

Anti-Scl-70 (antinucleur)

126
Q

Epidemiology of Sjogren’s syndrome

A
  • Women
  • 40-50s

Can be primary or can occur secondary to other autoimmune conditions

127
Q

Sjogren’s syndrome

A

Caused by the immune system mistakenly attacking the body. It mainly affects areas that produce fluids like tears or saliva.

128
Q

Symptoms of Sjogren’s syndrome

A 
o	Keratoconjunctivitis sicca (dry eyes)
o	Xerostomia (dry mouth)
o	Xerotrachea (dry throat) 
o	Vaginal dryness 
o	Dry eyes, mouth, vagina
o	Enlargement of major salivary glands
o	Sicca symptoms
o	Non-specific symptoms - Arthralgia, fatigue
129
Q

Investigations in Sjogren’s syndrome

A 
Schirmer test – Ocular dryness
Rose-bengal’s staining 
Sialometry and sialography 
Anti-Ro
Anti-La
130
Q

Auto antibodies in Sjogren’s syndrome

A

Anti-Ro

Anti-La

131
Q

Schirmer test in Sjogren’s syndrome

A

Ocular dryness - determines whether the eye produces enough tears to keep it moist.

132
Q

Management of Sjogren’s syndrome

A

Lubricants
Artificial saliva and tears
Regular dental care
Pilocarpine to stimulate saliva production
Hydroxycholoroquine for anthralgia & fatigue

133
Q

Side effect of pilocarpine

A

side effects include flushing
Chest pain.
diarrhea (continuing or severe)
fast, slow, or irregular heartbeat (continuing or severe)
headache (continuing or severe)
nausea or vomiting (continuing or severe)
shortness of breath

134
Q

Antiphospholipid syndrome

A

Autoimmune disorder that causes an increased incidence of venous or arterial thrombosis and/or foetal loss.

Usually presents as DVT, but can be any venous or arterial thrombosis

135
Q

Symptoms of Antiphospholipid syndrome

A

Increased frequency of stroke or MI in young people
Recurrently pulmonary emboli
Livedo reticularis
Pregnancy loss/misscariage

136
Q

Investigations in Antiphospholipid syndrome

A

Thrombocytopenia
Prolongation of activated partial thromboplatin time (APTT)

Auto antibodies

  1. Lupus anticoagulant
  2. Anti-cardiolipin antibodies
  3. Anti-beta 2 glycoprotein
137
Q

Thrombocytopenia

A

Low blood platelet count.

138
Q

Livedo reticularis

A

Is a skin symptom. Refers to a netlike pattern of reddish-blue skin discoloration. Legs often affected. The condition is linked to swollen blood vessels.

139
Q

Management of Antiphospholipid syndrome in non pregnant woman and men.

A

Anticoagulation – Warfarin

In pregnancy LMWH used as warfarin is teratogenic

140
Q

Management of Antiphospholipid syndrome in pregnant woman

A

In pregnancy LMWH used as warfarin is teratogenic

141
Q

Giant cell arteritis

A

Granulomatous arteritis of aorta and major branches

Transmural inflammation of intima, media and adventitia.

142
Q

Granuloma

A

Small area of inflammation - InInfiltration of lymphocytes, macrophages and multinucleated giant cells

143
Q

Epidemiology of Giant cell arteritis

A
  • Women

* Elderly (65+), rare before 50

144
Q

Clinical signs of Giant cell arteritis

A

Headache
Tender, non-pulsatile, thickened temporal artery
Fever
Scalp tenderness
Pain on chewing
Jaw claudication (ischaemia of maxillary artery)
Amaurosis fugax (and other visual disturbances)

145
Q

What causes jaw claudication in Giant cell arteritis

A

Ischemia of maxillary artery

146
Q

Amaurosis fugax

A

A transient loss of vision in one or both eyes

147
Q

Investigations in Giant cell arteritis

A

Increased ESR/PV & CRP
US (color duplex)
Biopsy –> definitive diagnosis - Mononuclear infiltration or granulomatous inflammation

148
Q

What is the definitive diagnostic approach for Giant cell arteritis

A

Biopsy - shows mononuclear infiltration or granulomatous inflammation

149
Q

Treatment of Giant cell arteritis

A

Corticosteroids – Prednisolone 40mg if no visual impairment, 60mg if.

Methotrexate

150
Q

First line treatment of Giant cell arteritis with no visual impairement

A

Corticosteroids – Prednisolone 40mg

151
Q

First line treatment of Giant cell arteritis with visual impairment present

A

Corticosteroids – Prednisolone 60mg

152
Q

Takayasu’s Arteritis

A

Large Vessel vasculitis of the aorta
Chronic granulomatous inflammation
Affexts <40 year olds

153
Q

Clinical signs of Takayasu’s Arteritis

A

Early Features - Low-grade fever, malaise, night sweats, weight loss, arthralgia and fatigue

Bruit
Claudication in upper and lower limbs
Reduced/absent peripheral pulses
Arthralgia

154
Q

Investigations for Takayasu’s Arteritis

A

Increased CRP/ESV

MR angiography – to detect thickened vessel walls and stenosis

155
Q

Treatment for Takayasu’s Arteritis

A

High dose steroids then gradually reducing

Immunosuppressants like methotrexate and azathioprine

156
Q

Polymyositis

A

Disease that causes muscles to become irritated and inflamed

May be automimmune but not know - Idiopathic inflammatory myopathy - T cell mediated cytotoxic process against muscle antigens

157
Q

Epidemiology of Polymyositis

A

30s-40s

More commonly women

158
Q

Clinical signs for Polymyositis

A 
o	Symmetrical Proximal muscle weakness - Upper and lower extremeties
o	Muscle pain
o	Fever
o	Pain on brushing hair
o	Pain on climbing stairs
o	Weight loss
o	Insidious onset
o	Worsening over months
o	Dysphagia secondary to oropharyngeal and oesophageal involvement
159
Q

Dermatomyositis

A

Variant of Polymyositis causing skin symptoms

160
Q

Clinical signs for Dermatomyositis

A

V-shaped rash over chest
Heliotrope rash
Gottron’s papules
Dilated capillary nail fold

161
Q

Heliotrope rash

A

Purple peri-orbital rash

162
Q

Gottron’s papules

A

Rough red papules on knuckles, elbows and knees

163
Q

Dermatomyositis is associated with malignancy, what kind of malignancy?

A

Breast, ovarian, lung, colon, oesophagus, bladder

164
Q

What disease is Dermatomyositis associated with?

A

Malignancy - Breast, ovarian, lung, colon, oesophagus, bladder

165
Q

Investigations for Dermatomyositis/polymyositis

A

o Greatly increased creatinine kinase
o Increased inflammatory markers
o Biopsy of muscle (this is the definitive diagnosis)
o ANA, anti-jo-1, anti-SRP antibodies
o MRI – Localise the extent of muscle involvement
o EMG

166
Q

Autoantibodies in Dermatomyositis/polymyositis

A

ANA, anti-jo-1, anti-SRP antibodies

167
Q

What is the definitive diagnosis for polymyositis/Dermatomyositis?

A

Biopsy of muscle

168
Q

Treatment for Dermatomyositis/polymyositis

A

Prednisolone

Immunosuppressants (azathioprine or methotrexate)

169
Q

Subungul hyperkeratosis

A

Refers to the accumulation of scales under the nail plate, which is detached and uplifted.

Results from excessive proliferation of keratinocytes and failure to shed off from the stratum corneum

170
Q

Septic arthritis

A

an infection in the joint (synovial) fluid and joint tissues. It occurs more often in children than in adults. The infection usually reaches the joints through the bloodstream.

171
Q

Sialometry

A

A measure of saliva flow

172
Q

Sialography

A

An x-ray test using contrast to look in detail at the larger salivary glands (the parotid or submandibular)

173
Q

Systemic sclerosis/scleroderma

A

A rare chronic autoimmune disease of unknown cause characterized by diffuse fibrosis and vascular abnormalities in the skin, joints, and internal organs

174
Q

Differnce between takayasu and giant cell arteritis

A

The key difference between Takayasu arteritis and giant cell arteritis is the age of the patients affected by the disorders.

Takayasu arteritis affects younger patients, generally less than 40 years of age, while giant cell arteritis affects older patients, generally over 50 years of age.

175
Q

Polymyalgia Rheumatica

A

Is an inflammatory disorder that causes muscle pain and stiffness, especially in the shoulders and hips.

176
Q

What condition is Polymyalgia Rheumatica associated with?

A

Associated with giant cell arteritis

177
Q

Clinical features of Polymyalgia Rheumatica

A

Proximal myalgia of hip & shoulder girdles
Morning stiffness
Symmetrical
Reduction of movements of Shoulder, Hips and Neck
Normal muscle strength

178
Q

Investigations for Polymyalgia Rheumatica

A

No specific test for PMR - Exclude other diagnosis
High CK for polymyositis
Raised CRP, ESR
Temporal artery biopsy

179
Q

Management for Polymyalgia Rheumatica

A

Steroids – very good response - Low dose prednisolone and gradually reduced. Symptoms should subside in 18 months

180
Q

Fibromyalgia

A

A condition that causes widespread pain and extreme tiredness - not associated with inflammation
• Women
• 22-50
• Lower threshold of pain and other stimuli (heat, noise, strong odours)

181
Q

Secondary causes of Fibromyalgia

A

Rheumatoid arthritis, SLE

182
Q

What is the commonest cause of chronic MSK pain?

A

Fibromyalgia

183
Q

Features of Fibromyalgia

A 
>   Persisten (>3months widespread pain 
>   Fatigue; disrupted & unrefreshing sleep
>   Symptoms worse with exercise
>   Pins and needles
>   Abdominal pain/IBS
>   Poor concentration/memory
184
Q

Diagnosis of Fibromyalgia

A

o Excessive tenderness of soft tissues on palpation
o No other abnormality of MSK
o No investigations needed
o Rule out other conditions

185
Q

Management of Fibromyalgia

A

o Rest
o Ice compressions
o Atypical Analgesia
o Psychological input - CBT

186
Q

What atypical analgesics are available for Fibromyalgia?

A

> Tricyclics (amitriptyline),
Gabapentin
Pregabalin

187
Q

Elhers-danlos syndrome (EDS)

A

Inherited connective tissue disorder that cause very flexible joints and stretchy and fragile skin. Caused by defective collagen synthesis - Insufficient or ineffective

188
Q

Ehlers-danlos syndrome inheritance

A

Autosomal dominant

189
Q

Clinical features of Ehlers-danlos syndrome

A 
o	Hyperelasticity of the skin
o	Hypermobility of the joints
o	Vascular (easy bruising, aneurysms)
o	Kyphoscoliosis of the spine
o	Bilateral congenital dislocation of the hip
o	Flat feet
o	Poor healing/thin skin
o	GI bleeds/perforation
o	Aneurysm
o	Increased risk of pneumothorax
190
Q

Management of Ehlers-danlos syndrome

A

Physiotherapy

191
Q

Osteolysis

A

Osteolysis is defined as the process of progressive destruction of periprosthetic bony tissue

192
Q

Synovitis

A

Synovitis (or synovial inflammation) is when the synovium of a joint becomes inflamed (swollen).

193
Q

Tenosynovitis

A

Tenosynovitis is the inflammation of the fluid-filled sheath (called the synovium) that surrounds a tendon

194
Q

Tenosynovitis vs synovitis

A

Both inflammation of the synovium but tenosynovitis is the inflammation of the synovium SURROUNDING a tendon

195
Q

Polymyalgia VS Polymyositis

A

Polymyositis is an inflammatory, destructive, autoimmune muscle disease, usually with weakness but unusually with pain.

Polymyalgia rheumatica is an inflammatory disease of muscle that always causes symmetrically painful muscles. Polymyalgia rheumatica is not destructive to muscles.

196
Q

Osteochondritis

A

A joint condition in which bone underneath the cartilage of a joint dies due to lack of blood flow.

197
Q

Dorsiflexion vs palmarflexion of wrist

A

Dorsiflexion of the hand/wrist involves bending the hand upward towards the top of the forearm. This is compared to palmar flexion of the hand/wrist which is the downward bending or flexing of the hand/wrist.

198
Q

Annulus Fibrosus

A

The annulus fibrosus is the tough circular exterior (ligamentous) of the intervertebral disc that surrounds the soft inner core, the nucleus pulposus.

199
Q

What organism usually causes osteomyelitis in sickly cell patients?

A

Salmonella species

200
Q

Radiculopathy

A

Describes a range of symptoms produced by the pinching of a nerve root in the spinal column.

MSK Year 2 (3 decks)

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