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MBBS - Year 1 > Clinical Skills - Connective Tissue > Flashcards

Clinical Skills - Connective Tissue Flashcards

1
Q

What is the reconstructive ladder

A

Systematic approach to close a wound, restore function and restore form
Starting with the simplest methods and culminating in the most complex methods

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2
Q

Steps on reconstructive ladder

A 
Dressings - simplest 
Suture 
Split thickness skin graft 
Full thickness 
Local random pattern flap 
Predicted flap 
Free flap - most complex
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3
Q

Skin graft

A

A piece of skin moved from one part of the body where it is reliant upon the recipient site fir its nutrition

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4
Q

What is harvested in a full thickness graft

A

The epidermis and whole of the dermis is harvested

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5
Q

Contraction of full thickness skin graft

A

Less

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6
Q

Healing of full thickness skin grafts

A

Quicker healing of donor site- great for face and hands

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7
Q

Which areas are full thickness skin grafts used for

A

Relatively small areas and donor site usually closed primarily

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8
Q

What is harvest in split thickness skin grafts

A

The epidermis and only upper parts of dermis

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9
Q

What kind of area is cropped for split thickness skin grafts

A

Large areas

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10
Q

Healing of split thickness skin grafts

A

Helps by re-epithelialization

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11
Q

Contraction of split thickness skin grafts

A

More

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12
Q

Skin graft takes

A 
Fibrin adherence 
Plasma imbibition 
Inosculation 
Revascularisation
Remodelling
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13
Q

Flap definition

A

Block of tissue moved from one part of a body to another part of the body where it incorporates its own blood supply for its own nutrition

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14
Q

Anatomy of tendons

A

Attach muscle to bone
Composed of fibres
Fibres made of fibrils
Surrounded by paratenon

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15
Q

Microstructure of tendons

A

Fibroblasts arranged in parallel rows (fibrils)
Secrete Type 1 collagen
Sharpey’s fibres
Bone

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16
Q

Sharpey’s fibres

A

Mineralised fibrocartilage

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17
Q

Effects of age and ageing on tendons

A

Degeneration
Trauma
Vascular reaction

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18
Q

Degeneration of tendons

A

Minute tears
Fibrocartiliginous metaplasia
Calcification
‘Critical zones’

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19
Q

Mesenchymal syndrome

A

Genetic predisposition to tendon degeneration

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20
Q

Trauma of tendons

A

Often insidious
Can be caused by lifting heavy weights, falls
At autopsy 60% have tears of rotator cuff or Long Head of Biceps tendon

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21
Q

Vascular reaction of tendons

A

Attempts at repair
Angiogenesis
Causes congestion and pain

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22
Q

Biomechanics of tendons

A

Strong in tension only
Can sustain tensile strain before failure
Viscoeleastic structures

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23
Q

Viscoelastic structures

A

Young’s modulus increases with increased rate of force application

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24
Q

Tendon rupture vs avulsion

A

Depends on speed of injury (rare of strain) - viscoelastic
Fast - tendon ruptures
Slow - bone avulses

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25
Q

Common sites of tendon injuries

A

Shoulder - rotator cuff
Elbow - Golfer’s and Tennis
Achilles tendon

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26
Q

Muscles making up rotator cuff

A

Supraspinatus
Infraspinatus
Subscapularis
Teres minor

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27
Q

Supraspinatus tendon

A

Inserts onto greater tuber tuberosity
Allows abduction of the shoulder
Rupture mainly occurs in aged tendons - degenerate tears

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28
Q

Critical zones

A

Areas of poor blood supply
Under surface of tendon as it inserts
Tears usually occur here

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29
Q

Clinical presentation of ruptured supraspinatus

A

Weak shoulder abduction
Unable to keep arm elevated
Drop arm sign

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30
Q

Tennis elbow syndrome

A

Common extensor origin on anterior aspect lateral epicondyle
Pain of resisted extension - wrist and fingers

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31
Q

Golfer’s elbow

A

Common flexor origin
Less common than tennis elbow
Pain on resisted flexion, wrist and fingers

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32
Q

Histology tennis elbow

A 
Ground glass appearance 
Not infl
Oedema 
Gelatinous material 
Angi-fibroblastic tendons
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33
Q

Jumper’s knee - patella tendinopathy

A

Overuse syndrome
Pain at inferior pole of patella
Can also occur at insertion of quadriceps

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34
Q

Distinguishing Jumper’s knee from Osgood-Schlatter’s disease

A

Tibial apophysiitis at attachment of patellar tendon in adolescent

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35
Q

Achilles Tendonitis

A

Pain over insertion onto Os-Calcis

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36
Q

Force transmitted from Achilles Tenon

A

Up to 10x body weight

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37
Q

Prognosis of most tendon insertion syndromes

A

Usually heal

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38
Q

What can chronic rotator cuff tears result in

A

OA

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39
Q

What is tendon insertion syndrome treatment aimed at

A

Modifying or speeding up the healing process

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40
Q

Types of treatment for tendon insertion syndrome

A

Conservative
Surgical
Medical

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41
Q

Conservative treatment for tendon insertion syndromes

A 
Reassurance 
Explanation 
Activity modification 
Resting splints 
Physiotherapy
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42
Q

Surgical treatment for tendon insertion syndromes

A

in general after failure of other methods

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43
Q

Medical treatment for tendon insertion syndrome

A

Analgesia e.g paracetamol
Anti-infl e.g. NSAIDs. Beware use of steroid infiltration. No evidence for benefit in many enthesopathy condns and risk of tendon rupture

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44
Q

Conservative rotator cuff tear treatment

A

Activity adaptation

Physiotherapy

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45
Q

Surgical rotator cuff tear treatment

A

Decompression

Repair

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46
Q

Treatment of Golfer’s and Tennis elbow

A

Physio can help
Splint
Steroid infiltration of no benefit
Surgery

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47
Q

Surgery for Golfer’s and Tennis elbow

A

Debridement of tendon origins
Elevation of tendon origin from anterior lateral epicondyle
Not curative - may help improve symptoms allowing return to work
Thought to modifying normal healing process

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48
Q

Treatment of Jumper’s knee

A 
Activity modification 
Physiotherapy 
Pain relief 
Orthotics 
Avoid steroid infiltration 
Surgery in exceptional cases
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49
Q

Surgery for Jumper’s knee

A

Tendon split

Gelatinous material scooped out

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50
Q

Treatment for Achilles Tendonitis

A

Physiotherapy
Activity avoidance
Shoe raise
Surgery reserved as a last resort

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51
Q

Why do we not give injections for Achilles Tendonitis

A

Risk of tendon rupture

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52
Q

Shoe raise

A

Sorbithane insert

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53
Q

Surgery for Achilles Tendonitis

A

Tendon sheath split

Gelatinous material scooped out

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54
Q

Types of connective tissue disease

A

Connective tissue diseases due to single-gene defects

Those characterised by infl of tissues (autoimmune diseases)

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55
Q

Examples of connective tissue disease due to single-gene defects

A

Ehler’s Danlos syndrome (EDS)
Epidermolysisbullosa (EB)
Marfan syndrome
OI

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56
Q

Connective tissue disease characterised by infl of tissues (autoimmune diseases )

A 
SLE 
Sjögren's syndrome 
Scleroderma 
Vasculitis 
Polymyositis
Dermatomyositis 
Polymyalgia rheumatica
RhA
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57
Q

SLE

A

Systemic Lupus Erythmatosus
An infl multisystem disease of unknown aetiology w diverse clinical and lab manifestation and a variable course and prognosis
Requires +ve ANA

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58
Q

Epidemiology of SLE

A

90% of affected patients are female
Peak age of onset is between 20 and 30 years
Fivefold increase in mortality compared to age and gender matched controls

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59
Q

Pathophysiology of SLE

A

Genetic factors

Autoantibdoy production

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60
Q

Systemic features of SLE

A 
Fever 
Wt loss 
Mild lymphadenopathy 
Fatigue 
Arthralgia
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61
Q

Organs affected by clinical features of SLE

A 
Systemic features 
Infl in skin and mucous membranes 
Joint - most likely 
Kidneys 
Brain 
Skin 
Lung 
GI tract 
Cardiovascular disease 
Haemotological abnormalities
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62
Q

Prevalence of SLE

A

12/100,000

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63
Q

How are joints affected by SLE

A

Arthralgia seen in 90% w/ early morning stiffness

Tenosynovitis may result in tendon damage

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64
Q

What is rarely seen in joints affected by SLE

A

Synovitis

Jaccoud’s arthropathy

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65
Q

What is Jaccoud’s arthropathy related to

A

Chronic tenosynovitis/ damage as opposed to erosive disease

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66
Q

Clinical features of SLE in kidneys

A

Hallmark of severe disease
Proliferative glomerulonephritis
Presents w/ heavy haematuria, proteinuria and casts in microscopy

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67
Q

Common clinical features of SLE in brain

A

Headache

Poor concentration

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68
Q

Uncommon clinical features of SLE in brain

A 
Visual hallucinations
Chorea
Organic psychosis
Transverse myelitis
Lymphocytic meningitis
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69
Q

Clinical features of SLE in skin

A 
Classic facial rash 
Discoid rash 
Diffuse, non-scarring alopecia
Urticaria
Livedo reticularis 
Vasculitis
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70
Q

Classic facial rash in SLE

A

Up to 20% of patients

Erythematous, raised and painful or itchy over the cheeks with sparing of the nasolabial folds (malar butterfly rash)

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71
Q

Discoid rash in SLE

A

Hyperkeratosis and follicular plugging which can cause scarring alopecia if involves the scalp

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72
Q

Clinical features of SLE in lung

A

Pleuritic pain (serositis) or pleural effusion
Increased risk of thromboembolism
(DVT,PE), especially if antiphospholipid antibodies present

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73
Q

Cardiovascular disease seen in SLE - Heart

A

Pericarditis
Myocarditis
Libman–Sacks endocarditis (sterile vegetations – infls seen on valves of heart)

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74
Q

Cardiovascular disease seen in SLE - arteries

A

Atherosclerosis is greatly increased causing a higher risk of stroke and myocardial infarction

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75
Q

Why is the risk of atherosclerosis increased in SLE

A

Effects of inflammatory disease on the endothelium
Long term steroid therapy
Antiphospholipid antibodies

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76
Q

Clinical features of SLE in GI tract

A

Mouth ulcers - common
Peritoneal serositis can cause acute pain
Mesenteric vasculitis - v serious

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77
Q

Rare clinical features of SLE in GI tract

A

Hepatitis

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78
Q

Mesenteric vasculitis

A

Abdominal pain, bowel infarction or perforation

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79
Q

Haematological abnormalities seen in SLE

A

Neutropenia
Lymphopenia – the degree is an indicator of disease activity
Thrombocytopenia
Haemolytic anaemia

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80
Q

Spectrum of SLE

A

Late stage lupus, drug-induced lupus, latent lupus and anti-phospholipid syndrome all have overlap with classic lupus
APLS and latent lupus also overlap with each other

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81
Q

Secondary Raynaud’s - SLE

A

Age of onset of over 25 yrs.
Absence of a family hx of Raynaud’s phenomenon
Male pt

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82
Q

Examination for secondary Raynaud’s - SLE

A

Capillary nail-fold loops (and oil placed on the skin) can show loss of the normal loop pattern
Chronic ischaemia may lead to colour change

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83
Q

Drug induced lupus

A

Less severe, resolved on stopping the drug

Implicated drugs incl 
Carbamazepine (epilepsy)
Chlorpromazine (psychosis)
Hydralazine (BP)
Isoniazid (TB)
Methyldopa (BP)
Sulphazalazine (RhA)
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84
Q

Neuropsychiatric manifestation of SLE

A

Neurological - Seizures, stroke, movement disorder, headache, transverse myelitis, cranial neuropathy, peripheral
Psychiatric - psychosis

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85
Q

Late complication of SLE

A

Glomerulonephritis – end stage renal disease, dialysis and transplantation
Vasculitis – atherosclerosis, PE
Arthritis – osteonecrosis
Cerebritis – neuropsychiatric dysfunction
Pneumonitis – shrinking lung syndrome

86
Q

Presentation of anti-phospholipid syndrome (APLS)

A

Vascular thrombosis

Pregnancy - early (<13 weeks) or late

87
Q

Lab criteria for APLS

A

Lupus anticoagulant
Anticardiolipin antibodies
On 2 occasions 3 months apart

88
Q

Infants - APLS

A

Pericardial effusion and conduction defects

Skin rash

89
Q

Management of lupus (+ APLS)

A

Educate the pt - control symptoms to prevent organ damage and maintain normal function
Avoid sun exposure and use sun block (factor 50)
Medicines

90
Q

Drug therapies for skin and joints - lupus

A

Analgesics, NSAIDs and hydroxychloroquine (also protective against heart).
Prednisolone, MMF, MTX, azathioprine
Belimumab

91
Q

Drug therapies for end organ disease - lupus

A 
High-dose glucocorticoids and immunosuppressants 
Iv methylprednisolone (10 mg/kg IV) plus iv cyclophosphamide for six cycles 
Rituximab may be of benefit in some
92
Q

S/E of methylprednisolone

A

Infection
Haemorrhagic cystitis
Infertility

93
Q

Maintenance therapy for lupus

A

Taper prednisolone - long term low dose
Immunosuppressant’s:
Address cardiovascular risk factors (hypertension and hyperlipidaemia) +HCQ
Pts should be advised to stop smoking.
Anticoagulation with warfarin if thrombosis and APLS
Assess risk of osteoporosis and hypovitaminosis D

94
Q

Immunosuppressants given for lupus

A

Azathioprine
Methotrexate
MMF

95
Q

Sjorgens syndrome

A

A slowly progressive infl autoimmune disease affecting primarily the exocrine glands
Lymphocytic infiltrates and fibrosis of salivary and lacrimal replace functional epithelium and reduce secretions
May occur w/ other autoimmune diseases (2’)

96
Q

Characteristic antibodies for sjorgen’s

A

Ro

La

97
Q

Epidemiology of Sjorgens

A

Typical ages of onset for Sjorgen’s is 40-50

9:1 female to male ratio

98
Q

Clinical spectrum of Sjorgen’s

A

Glandular
Extra glandular
Lymphoma

99
Q

Clinical features of Sjorgen’s

A

Mucosal dryness
Non-erosive polyarthritis/ small joint pain
Mouth - (dry xerostomia) w/ dental caries
Skin – Raynaud’s, digital ulcers
Fatigue

100
Q

Mucosal dryness in Sjorgen’s

A

Eyes, mouth, trachea, vagina

Major salivary gland enlargement and atrophic gastritis

101
Q

Investigations for Sjorgen’s

A 
Bloods 
Schirmer’s test 
U&E 
Major salivary gland biopsy 
ANA 
Rhf is usually quite high
102
Q

Bloods in Sjorgen’s

A

Anaemia, high ESR, normal CRP, hypergammaglobulinanaemia, ANA, Ro, La

103
Q

ANA in Sjorgen’s

A

SSA (Anti-Ro) and SS-B (anti-La)

104
Q

Schirmers test

A

Placing paper under eyes to test tear production

6mm and after 5 mins

105
Q

Management for Sjorgen’s

A

Follow for disease progression
Lubrication – eyes, mouth, vagina
DMARDs
Extra glandular disease e.g. interstitial nephritis – steroids, further immunosuppression
Treat lymphoma accordingly to histological type

106
Q

DMARDs for Sjorgens

A

Hydroxychloroquine 200mg BDS also helps w/ skin and msk features and fatigue

107
Q

Systemic sclerosis

A

A generalised disorder of connective tissue affecting skin and internal organs
Variable degrees of collagen accumulation in skin and viscera

108
Q

What is systemic sclerosis associated w/

A

Anti-centromere

Anti-Scl-70 autoantibodies

109
Q

Clinical features of systemic sclerosis

A

Raynaud’s phenomenon
Progressive fibrosis of skin, lung, heart, GI tract and kidney
May be diffuse cutaneous or limited scleroderma
Involvement of internal organs leads to morbidity and mortality
Risk of internal organ involvement is strongly linked to extent and progression of skin thickening

110
Q

Types of systemic sclerosis

A

Limited cutaneous systemic sclerosis (lcSScl: 70% of cases)
Diffuse cutaneous systemic sclerosis (dcSSc: 30% of cases)
CREST

111
Q

Presentation of diffuse systemic sclerosis

A

Skin thickening over proximal site to elbow and knee and/ or trunk (more aggressive form and more likely to develop organ involvement)

112
Q

Presentation of limited systemic sclerosis

A

Skin thickening over distal sites w hands and feet (sclerodactyly - fingers), face and neck

113
Q

CREST - systemic sclerosis

A

Calcinosis, Raynaud’s, o(E)sophageal involvement (dysmotility), sclerodactyly, telangiectasia

114
Q

Epidemiology of Raynaud’s phenomenon

A

4-15% of general population
Typically begins in teenage years
More common in women (4:1)

115
Q

Primary vs secondary Raynaud’s

A

Primary (non-ulcerating), cased by physiological response
Secondary – begins later and often with other CTD features (may cause ischaemia and ulceration, gangrene —> amputation)

116
Q

Features of Raynaud’s phenomenon

A

Usually triggered by cold temperatures, anxiety or stress
Temporary spasm of capillaries which blocks the flow of blood
Triphasic colour change – white, blue, red (paler if dark skin)

117
Q

Symptoms of Raynaud’s

A

Pain
Numbness
Pins and needles

118
Q

Management for Raynaud’s

A

Keep warm
Stop smoking
Calcium channel blockers
Iloprost – only given for severe Raynaud’s, must come into hosp for 5 days Sildenafil

119
Q

What do see in pts w/ scleroderma

A

Digital pitting, ulceration, gangrene and amputation

Usually elevated ESR and ANA +ve

120
Q

Systemic manifestation of scleroderma - MSK

A

Arthralgia and myalgia & later muscle atrophy and weakness from myositis
Flexor tenosynovitis is common
Restricted hand function is due to skin rather than joint disease

121
Q

Systemic manifestation of scleroderma - GI tract

A

Malabsorption - bacterial overgrowth
Dilation of bowel
Dysphagia
Erosive oesophagitis

122
Q

Systemic manifestation of scleroderma - pulmonary involvement

A

Interstitial fibrosis
Pulmonary arterial vascular disease
Pulmonary hypertension*
Honeycomb lung

123
Q

Systemic manifestation of scleroderma - Cardiac involvement

A 
Pericarditis
CCF
Pulmonary hypertension
Arrythmias
Myocardial disease
124
Q

Systemic manifestation of scleroderma - renal involvement

A

Kidney tissue replaced by fibrosis - hypertension

Scleroderma renal crisis

125
Q

Management of scleroderma

A

Treat appropriately
Drug therapies are aimed at vascular ischaemia, immune modulation and fibrosis
No steroids
ACE inhibitors in scleroderma renal crisis

126
Q

What does systemic sclerosis (SScl) cause

A

Fibrosis affecting skin, internal organs, vasculatures

127
Q

What is SScl characterised by

A

Raynaud’s phenomenon (+/- digital ischaemia), sclerodactyly and cardiac, lung, GI and renal disease.

128
Q

Epidemiology of SScl

A

Peak age of onset is 4th and 5th decades
Overall prevalence is 10-20/ 100,000
4:1 f to m ratio

129
Q

Prognosis of dcSScl

A

Poor

5 yrs survival is 70%

130
Q

Dysphagia

A

Difficulty swallowing

131
Q

Clinical features of skin in SScl

A

Non-pitting oedema of fingers and flexor tendon sheaths then becomes shiny and taut
Possible capillary loss
The face and neck are often involved, with thinning of the lips and radial furrowing
Tight mouth - perioral puckering

132
Q

Investigation in SScl

A

Bloods

Imaging

133
Q

Bloods in SScl

A 
FBC 
U&E
LFTs
Bone group 
Urinalysis is essential 
ANA is +ve in 70%
Scl70 +ve in 30% of pts w/ dsSScl 
Anti-centromere antibodies in 60% of pts w/ lcSScl syndrome
134
Q

Imaging in SScl

A

Chest x-ray/ CT chest
ECG
Lung function test
Barium swallow can assess oesophageal involvement

135
Q

Management of SScl - general

A

Nil to stop or reverse fibrosis

Try to slow the effects of the disease on target organs

136
Q

Management for Raynaud’s and digital ulcers in SScl

A 
Avoid cold
Thermal gloves/ socks
High core temp
Calcium channel blockers
Losartan
Fluoxetine
Sildenafil
137
Q

Management for GI complication in SScl

A

Protein pump inhibitors

138
Q

Management for hypertension in SScl

A

ACE inhibitors

139
Q

Management for joint involvement in SScl

A

NSAIDs

Analgesia

140
Q

Management for pulmonary involvement in SScl

A

Bosentan or heart-lung transplant

141
Q

Management for interstitial lung disease in SScl

A

Glucocorticosteroids and (pulse intravenous) cyclophosphamide

142
Q

Mixed connective tissue disease

A

A condn in which some clinical features of SScl, myositis and SLE all occur in the same pt
Most pts have anti-RNP antibodies

143
Q

Management of connective tissue disease

A

Focuses on treating the components of the disease

144
Q

Polymyositis and dermatomyositis

A

Proximal skeletal, cardiac, and GI smooth muscle infl
In DM, skin changes also occur
Can occur with autoimmune diseases
Both associated with underlying malignancy

145
Q

Incidence of PM and DM

A

2-10 cases per million/ year

146
Q

Clinical features of PM and DM

A

Weakness: insidious onset of symmetrical proximal muscle weakness
Lung involvement
Skin involvements

147
Q

Systemic features of DM and PM

A

Pyrexia
Wt loss
Fatigue

148
Q

Lung involvement in PM and DM

A

Respiratory or pharyngeal muscle involvement

Interstitial lung disease occurs in up to 30% of pts associated with antisynthetase (Jo-1) antibodies

149
Q

Skin involvement in DM and PM

A

Gottron’s papules over PIP and DIP

Heliotrope rash

150
Q

Gottron’s papules

A

Scaly, violaceous, psoriaform plaques

151
Q

Macules vs papules

A

Can palpate macules but not see them and can see but not palpate papules

152
Q

Heliotrope rash

A

Violaceous discoloration of the eyelid

153
Q

Investigations for PM and DM

A 
Serum levels of creatinine kinase – sign of muscle infl 
MRI 
Muscle biopsy
Electromyography
Screening for underlying malignancy
154
Q

Muscle biopsy for DM and PM

A

Fibre, necrosis, regeneration and infl cell infiltrate

155
Q

Electromyography for DM and PM

A

Very useful for highlighting non-autoimmune/ non-infl myopathies

156
Q

Screening for malignancy in PM and DM

A 
History
Examination
CXR
CT of chest/abdomen/pelvis
PSA mammography
157
Q

Mangement for DM and PM

A

Oral glucocorticoids (IV if severe)
Immunosuppressive therapy
Rituximab probably efficacious
IV immunoglobulin (IVIg) may be effective in refractory cases

158
Q

Maintenance dose of oral glucocorticoids for DM and PM

A

5 - 7.5 mg

159
Q

Immunosuppressive therapy for DM and PM

A

MTX, MMF, azathioprine

160
Q

Vasculitis

A

Infl and necrosis of blood vessel walls, w/ associated damage to skin, kidney, lung, heart, brain and GI tract
Wide spectrum of symptoms and severity (from mild and transient disease to life-threatening disease)

161
Q

What do clinical features of vasculitis result from

A

A combination of local tissue ischemia (due to vessel infl and narrowing) and the systemic effects of widespread infl

162
Q

Who should we consider vasculitis in

A

Anyone w/ fever, wt loss, fatigue, multisystem involvement, rashes, raised infl markers and/ or abnormal urinalysis

163
Q

Giant cell arteritis (GCA)

A

Granulomatous arteritis that affects any larger (incl) aorta and medium sized arteries
Often w/ PMR – symmetrical, neck and shoulder/ hip girdle pain and stiffness
As often coexists, probably same disease

164
Q

Epidemiology of GCA

A

Rare under 60yrs
Avg age of onset is 70 yrs w/ f:m ration of 3:1
Prevalence is about 20/100,000 in those 50+

165
Q

PMR

A

Polymyalgia Rheumatica

166
Q

Clinical features of GCA and PMR

A

GCA usually presents with headache
May be accompanied by scalp tenderness
Jaw pain develops in some pt, brought on by chewing or talking
Visual disturbance can occur (transient = amaurosis) or with blindness in one eye

167
Q

Symptoms in PMR that are not present in GCA

A

Stiffness and painful restriction of active shoulder movements on waking but no muscle weakness or tenderness

168
Q

Systemic symptoms in PMR and GCA

A

Wt loss, fatigue, malaise and night

169
Q

Headaches in GCA

A

Often localised to temporal or occipital region

Temporal arteries may be prominent

170
Q

Visual disturbance in GCA and PMR

A

Occlusion of the posterior ciliary artery

171
Q

Rare symptoms in GCA and PMR

A

Neurological symptoms, w/ TIA’s, brainstem infarcts and hemiparesis

172
Q

Condns that can mimic PMR

A 
Calcium pyrophosphate disease 
Spondylarthritis 
Hyper/ hypothyroidism 
Psoriatic arthritis (entheseopathic)
Systemic vasculitis 
Multiple myeloma 
Infl myopathy 
Lambert-Eaton syndrome 
Multiple separate lesions (cervical spondylosis, cervical radiculopathy, bilateral, subacromial, impingement, facet joint arthritis, OA of the acromioclavicular joint)
173
Q

Investigation results for GCA and PMR

A

High ESR/CRP - rarely present w/ normal levels

Anaemia

174
Q

Which investigations should be considered for GCA and PMR

A

Temporal artery biopsy
Ultrasound of temporal arteries
PET scan

175
Q

Ultrasound for GCA and PMR

A

Affected temporal arteries show a ‘halo’ sign

176
Q

Management of GCA and PMR

A

Medical emergency so prednisolone if suspect because of the risk of vision
Bisphosphonates for bone

177
Q

Dosage of prednisolone in GCA and PMR

A

Higher doses in GCA (60-80 mg prednisolone) than in PMR (15-20mg)
Dose should be progressively reduced

178
Q

How long do GCA and PMR pts need glucocorticoids for

A

An avg of 12-24 months

179
Q

Ages affected in polymyositis vs in PMR

A

Any age vs 50+

180
Q

Muscles involved in polymyositis vs in PMR

A

Proximal muscle involvement i.e. shoulder and hip vs none

181
Q

CPK in polymyositis

A

Elevated due to muscle damage

182
Q

CPK in PMR

A

No muscle involvement so normal CPK. EMS and high infl markers

183
Q

What does the spectrum of PM incl

A

Skin involvement

184
Q

What does the spectrum of PMR incl

A

GCA (vasculitis)

185
Q

Occurrence of polymyositis vs PMR

A

Rare and need referral vs common and often managed by GP’s

186
Q

Reducing dosage of prednisolone in GCA and PMR

A

Guided by symptoms and ESR, with the aim of reaching a dose of 1-15mg by about 8 weeks
The rate of reduction should then be slowed by 1mg/month

187
Q

What happens if symptoms recur for GCA and PMR after raising dose

A

The dose should be increased to that which previously controlled the symptoms, and reduction attempted again in another few weeks

188
Q

ANAs associated with CTDs

A 
dsDNA/ smith - lupus
Jo1 - DM
Ro – Sjorgens 
La - Sjogens 
Scl-70 - dcSScl
Centromere - lcSScl
189
Q

Prognosis of GCA

A

Can be good as long as pt receives early and appropriate treatment
Treatment may last years and pt needs follow up appt

190
Q

Discoid lupus

A

Lupus only affecting the skin (not entire system)

191
Q

Mnemonic for SLE

A

SOAP BRAIN MD

Serositis
Oral or nasopharyngeal ulcers
Arthritis ≥ 2 peripheral joints
Photosensitivity

Blood disorder
Renal disorder
ANA positive titre
Immunological disorder
Neurological disorder

Malar ‘Butterfly’ rash
Discoid rash

192
Q

Epidemiology of PMR

A

F:M ratio of 3:1
Starts at 50+ but mainly affects those 70+
15% develop GCA

193
Q

EMS in PMR

A

45+

Symptoms improve w/ activity

194
Q

Blood tests for PMR

A 
Anti-CCP
Antinuclear Antibody (ANA)
Full Blood Count (FBC)
CRP
ESR
Rheumatoid Factor (RhF)
195
Q

EULAR criteria for diagnosing PMR

A 
Must have these:
Aged > 50 Years
Bilateral Shoulder Discomfort
Abnormal ESR or CRP
and an addn 4 points
196
Q

Points for diagnosing PMR

A 
Morning stiffness (2 points)
Hip pain (1 point)
Absence of RhF/ANA (2 points)
Absence of other joint pain (1 point).
197
Q

Prognosis for PMR

A

Pts typically respond well to treatment and most recover within 1-5 yrs
Some pts have a relapse

198
Q

Mnemonic for PMR clinical features

A

SECRET

Stiffness and pain 
Elderly individuals 
Constitutional symtoms 
Rheumatism (arthralgia/ arthritis)
Elevated ESR 
Temporal Arteritis
199
Q

Amaurosis fugax

A

Painless temporary loss of vision in one or both eyes due to lack of blood flow
Can be seen in GCA

200
Q

Diseases with +ve ANA

A

SLE and mixed connective tissue disease - 95%

RhA and autoimmune thyroid disease - 30-50%

201
Q

Is a high titre ANA indicative of more severe disease

A

No

202
Q

CLOT acronym for APLS

A

Coagulation defect
Livedo Reticularis
Obstetric - recurrent miscarriages
Thrombocytopenia

203
Q

When is APLS secondary

A

With hx of SLE

204
Q

Complement levels in SLE

A

Abnormal (low)

205
Q

When to suspect CTD

A 
Young female pt
Arthralgia & myalgia
Fatigue & malaise
Skin/ Lung/ Heart/ kidney involvement
Raynaud's phenomenon
206
Q

Is primary Raynaud’s bilateral or unilateral

A

Bilateral

207
Q

Indicators that it is secondary Raynaud’s

A

Digital ulceration —> scleroderma, check for indentation or depression in finger
Digital gangrene —> scleroderma, sepsis
Abnormal nail fold capillaries (periungal erythema) due to dilated capillaries
Onset early childhood or later

208
Q

Rashes for lupus

A

Malar butterfly rash
Discoid rash
Photosensitive rash - seen in exposed areas to sun
Vasculitic rash
Rashes can causes alopecia
Livedo reticularis → APLS, rbc’s become very sticky

209
Q

Neurological disorders in SLE

A

Headaches
Seizures
Psychosis

210
Q

Why might a biopsy be normal in GCA

A

Scalp ischemia

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MBBS - Year 1 (93 decks)

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