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
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
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
4
Q
What is harvested in a full thickness graft
A
The epidermis and whole of the dermis is harvested
5
Q
Contraction of full thickness skin graft
A
Less
6
Q
Healing of full thickness skin grafts
A
Quicker healing of donor site- great for face and hands
7
Q
Which areas are full thickness skin grafts used for
A
Relatively small areas and donor site usually closed primarily
8
Q
What is harvest in split thickness skin grafts
A
The epidermis and only upper parts of dermis
9
Q
What kind of area is cropped for split thickness skin grafts
A
Large areas
10
Q
Healing of split thickness skin grafts
A
Helps by re-epithelialization
11
Q
Contraction of split thickness skin grafts
A
More
12
Q
Skin graft takes
A
Fibrin adherence Plasma imbibition Inosculation Revascularisation Remodelling
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
14
Q
Anatomy of tendons
A
Attach muscle to bone
Composed of fibres
Fibres made of fibrils
Surrounded by paratenon
15
Q
Microstructure of tendons
A
Fibroblasts arranged in parallel rows (fibrils)
Secrete Type 1 collagen
Sharpey’s fibres
Bone
16
Q
Sharpey’s fibres
A
Mineralised fibrocartilage
17
Q
Effects of age and ageing on tendons
A
Degeneration
Trauma
Vascular reaction
18
Q
Degeneration of tendons
A
Minute tears
Fibrocartiliginous metaplasia
Calcification
‘Critical zones’
19
Q
Mesenchymal syndrome
A
Genetic predisposition to tendon degeneration
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
21
Q
Vascular reaction of tendons
A
Attempts at repair
Angiogenesis
Causes congestion and pain
22
Q
Biomechanics of tendons
A
Strong in tension only
Can sustain tensile strain before failure
Viscoeleastic structures
23
Q
Viscoelastic structures
A
Young’s modulus increases with increased rate of force application
24
Q
Tendon rupture vs avulsion
A
Depends on speed of injury (rare of strain) - viscoelastic
Fast - tendon ruptures
Slow - bone avulses
25
Common sites of tendon injuries
Shoulder - rotator cuff
Elbow - Golfer's and Tennis
Achilles tendon
26
Muscles making up rotator cuff
Supraspinatus
Infraspinatus
Subscapularis
Teres minor
27
Supraspinatus tendon
Inserts onto greater tuber tuberosity
Allows abduction of the shoulder
Rupture mainly occurs in aged tendons - degenerate tears
28
Critical zones
Areas of poor blood supply
Under surface of tendon as it inserts
Tears usually occur here
29
Clinical presentation of ruptured supraspinatus
Weak shoulder abduction
Unable to keep arm elevated
Drop arm sign
30
Tennis elbow syndrome
Common extensor origin on anterior aspect lateral epicondyle
Pain of resisted extension - wrist and fingers
31
Golfer's elbow
Common flexor origin
Less common than tennis elbow
Pain on resisted flexion, wrist and fingers
32
Histology tennis elbow
```
Ground glass appearance
Not infl
Oedema
Gelatinous material
Angi-fibroblastic tendons
```
33
Jumper's knee - patella tendinopathy
Overuse syndrome
Pain at inferior pole of patella
Can also occur at insertion of quadriceps
34
Distinguishing Jumper's knee from Osgood-Schlatter's disease
Tibial apophysiitis at attachment of patellar tendon in adolescent
35
Achilles Tendonitis
Pain over insertion onto Os-Calcis
36
Force transmitted from Achilles Tenon
Up to 10x body weight
37
Prognosis of most tendon insertion syndromes
Usually heal
38
What can chronic rotator cuff tears result in
OA
39
What is tendon insertion syndrome treatment aimed at
Modifying or speeding up the healing process
40
Types of treatment for tendon insertion syndrome
Conservative
Surgical
Medical
41
Conservative treatment for tendon insertion syndromes
```
Reassurance
Explanation
Activity modification
Resting splints
Physiotherapy
```
42
Surgical treatment for tendon insertion syndromes
in general after failure of other methods
43
Medical treatment for tendon insertion syndrome
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
44
Conservative rotator cuff tear treatment
Activity adaptation
| Physiotherapy
45
Surgical rotator cuff tear treatment
Decompression
| Repair
46
Treatment of Golfer's and Tennis elbow
Physio can help
Splint
Steroid infiltration of no benefit
Surgery
47
Surgery for Golfer's and Tennis elbow
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
48
Treatment of Jumper's knee
```
Activity modification
Physiotherapy
Pain relief
Orthotics
Avoid steroid infiltration
Surgery in exceptional cases
```
49
Surgery for Jumper's knee
Tendon split
| Gelatinous material scooped out
50
Treatment for Achilles Tendonitis
Physiotherapy
Activity avoidance
Shoe raise
Surgery reserved as a last resort
51
Why do we not give injections for Achilles Tendonitis
Risk of tendon rupture
52
Shoe raise
Sorbithane insert
53
Surgery for Achilles Tendonitis
Tendon sheath split
| Gelatinous material scooped out
54
Types of connective tissue disease
Connective tissue diseases due to single-gene defects
| Those characterised by infl of tissues (autoimmune diseases)
55
Examples of connective tissue disease due to single-gene defects
Ehler’s Danlos syndrome (EDS)
Epidermolysisbullosa (EB)
Marfan syndrome
OI
56
Connective tissue disease characterised by infl of tissues (autoimmune diseases )
```
SLE
Sjögren's syndrome
Scleroderma
Vasculitis
Polymyositis
Dermatomyositis
Polymyalgia rheumatica
RhA
```
57
SLE
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
58
Epidemiology of SLE
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
59
Pathophysiology of SLE
Genetic factors
| Autoantibdoy production
60
Systemic features of SLE
```
Fever
Wt loss
Mild lymphadenopathy
Fatigue
Arthralgia
```
61
Organs affected by clinical features of SLE
```
Systemic features
Infl in skin and mucous membranes
Joint - most likely
Kidneys
Brain
Skin
Lung
GI tract
Cardiovascular disease
Haemotological abnormalities
```
62
Prevalence of SLE
12/100,000
63
How are joints affected by SLE
Arthralgia seen in 90% w/ early morning stiffness
| Tenosynovitis may result in tendon damage
64
What is rarely seen in joints affected by SLE
Synovitis
| Jaccoud's arthropathy
65
What is Jaccoud's arthropathy related to
Chronic tenosynovitis/ damage as opposed to erosive disease
66
Clinical features of SLE in kidneys
Hallmark of severe disease
Proliferative glomerulonephritis
Presents w/ heavy haematuria, proteinuria and casts in microscopy
67
Common clinical features of SLE in brain
Headache
| Poor concentration
68
Uncommon clinical features of SLE in brain
```
Visual hallucinations
Chorea
Organic psychosis
Transverse myelitis
Lymphocytic meningitis
```
69
Clinical features of SLE in skin
```
Classic facial rash
Discoid rash
Diffuse, non-scarring alopecia
Urticaria
Livedo reticularis
Vasculitis
```
70
Classic facial rash in SLE
Up to 20% of patients
| Erythematous, raised and painful or itchy over the cheeks with sparing of the nasolabial folds (malar butterfly rash)
71
Discoid rash in SLE
Hyperkeratosis and follicular plugging which can cause scarring alopecia if involves the scalp
72
Clinical features of SLE in lung
Pleuritic pain (serositis) or pleural effusion
Increased risk of thromboembolism
(DVT,PE), especially if antiphospholipid antibodies present
73
Cardiovascular disease seen in SLE - Heart
Pericarditis
Myocarditis
Libman–Sacks endocarditis (sterile vegetations – infls seen on valves of heart)
74
Cardiovascular disease seen in SLE - arteries
Atherosclerosis is greatly increased causing a higher risk of stroke and myocardial infarction
75
Why is the risk of atherosclerosis increased in SLE
Effects of inflammatory disease on the endothelium
Long term steroid therapy
Antiphospholipid antibodies
76
Clinical features of SLE in GI tract
Mouth ulcers - common
Peritoneal serositis can cause acute pain
Mesenteric vasculitis - v serious
77
Rare clinical features of SLE in GI tract
Hepatitis
78
Mesenteric vasculitis
Abdominal pain, bowel infarction or perforation
79
Haematological abnormalities seen in SLE
Neutropenia
Lymphopenia – the degree is an indicator of disease activity
Thrombocytopenia
Haemolytic anaemia
80
Spectrum of SLE
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
81
Secondary Raynaud's - SLE
Age of onset of over 25 yrs.
Absence of a family hx of Raynaud’s phenomenon
Male pt
82
Examination for secondary Raynaud's - SLE
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
83
Drug induced lupus
Less severe, resolved on stopping the drug
```
Implicated drugs incl
Carbamazepine (epilepsy)
Chlorpromazine (psychosis)
Hydralazine (BP)
Isoniazid (TB)
Methyldopa (BP)
Sulphazalazine (RhA)
```
84
Neuropsychiatric manifestation of SLE
Neurological - Seizures, stroke, movement disorder, headache, transverse myelitis, cranial neuropathy, peripheral
Psychiatric - psychosis
85
Late complication of SLE
Glomerulonephritis – end stage renal disease, dialysis and transplantation
Vasculitis – atherosclerosis, PE
Arthritis – osteonecrosis
Cerebritis – neuropsychiatric dysfunction
Pneumonitis – shrinking lung syndrome
86
Presentation of anti-phospholipid syndrome (APLS)
Vascular thrombosis
| Pregnancy - early (<13 weeks) or late
87
Lab criteria for APLS
Lupus anticoagulant
Anticardiolipin antibodies
On 2 occasions 3 months apart
88
Infants - APLS
Pericardial effusion and conduction defects
| Skin rash
89
Management of lupus (+ APLS)
Educate the pt - control symptoms to prevent organ damage and maintain normal function
Avoid sun exposure and use sun block (factor 50)
Medicines
90
Drug therapies for skin and joints - lupus
Analgesics, NSAIDs and hydroxychloroquine (also protective against heart).
Prednisolone, MMF, MTX, azathioprine
Belimumab
91
Drug therapies for end organ disease - lupus
```
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
S/E of methylprednisolone
Infection
Haemorrhagic cystitis
Infertility
93
Maintenance therapy for lupus
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
Immunosuppressants given for lupus
Azathioprine
Methotrexate
MMF
95
Sjorgens syndrome
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
Characteristic antibodies for sjorgen's
Ro
| La
97
Epidemiology of Sjorgens
Typical ages of onset for Sjorgen's is 40-50
| 9:1 female to male ratio
98
Clinical spectrum of Sjorgen’s
Glandular
Extra glandular
Lymphoma
99
Clinical features of Sjorgen's
Mucosal dryness
Non-erosive polyarthritis/ small joint pain
Mouth - (dry xerostomia) w/ dental caries
Skin – Raynaud’s, digital ulcers
Fatigue
100
Mucosal dryness in Sjorgen's
Eyes, mouth, trachea, vagina
| Major salivary gland enlargement and atrophic gastritis
101
Investigations for Sjorgen's
```
Bloods
Schirmer’s test
U&E
Major salivary gland biopsy
ANA
Rhf is usually quite high
```
102
Bloods in Sjorgen's
Anaemia, high ESR, normal CRP, hypergammaglobulinanaemia, ANA, Ro, La
103
ANA in Sjorgen's
SSA (Anti-Ro) and SS-B (anti-La)
104
Schirmers test
Placing paper under eyes to test tear production
| 6mm and after 5 mins
105
Management for Sjorgen's
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
DMARDs for Sjorgens
Hydroxychloroquine 200mg BDS also helps w/ skin and msk features and fatigue
107
Systemic sclerosis
A generalised disorder of connective tissue affecting skin and internal organs
Variable degrees of collagen accumulation in skin and viscera
108
What is systemic sclerosis associated w/
Anti-centromere
| Anti-Scl-70 autoantibodies
109
Clinical features of systemic sclerosis
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
Types of systemic sclerosis
Limited cutaneous systemic sclerosis (lcSScl: 70% of cases)
Diffuse cutaneous systemic sclerosis (dcSSc: 30% of cases)
CREST
111
Presentation of diffuse systemic sclerosis
Skin thickening over proximal site to elbow and knee and/ or trunk (more aggressive form and more likely to develop organ involvement)
112
Presentation of limited systemic sclerosis
Skin thickening over distal sites w hands and feet (sclerodactyly - fingers), face and neck
113
CREST - systemic sclerosis
Calcinosis, Raynaud’s, o(E)sophageal involvement (dysmotility), sclerodactyly, telangiectasia
114
Epidemiology of Raynaud's phenomenon
4-15% of general population
Typically begins in teenage years
More common in women (4:1)
115
Primary vs secondary Raynaud's
Primary (non-ulcerating), cased by physiological response
Secondary – begins later and often with other CTD features (may cause ischaemia and ulceration, gangrene ---> amputation)
116
Features of Raynaud's phenomenon
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
Symptoms of Raynaud’s
Pain
Numbness
Pins and needles
118
Management for Raynaud's
Keep warm
Stop smoking
Calcium channel blockers
Iloprost – only given for severe Raynaud’s, must come into hosp for 5 days Sildenafil
119
What do see in pts w/ scleroderma
Digital pitting, ulceration, gangrene and amputation
| Usually elevated ESR and ANA +ve
120
Systemic manifestation of scleroderma - MSK
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
Systemic manifestation of scleroderma - GI tract
Malabsorption - bacterial overgrowth
Dilation of bowel
Dysphagia
Erosive oesophagitis
122
Systemic manifestation of scleroderma - pulmonary involvement
Interstitial fibrosis
Pulmonary arterial vascular disease
Pulmonary hypertension*
Honeycomb lung
123
Systemic manifestation of scleroderma - Cardiac involvement
```
Pericarditis
CCF
Pulmonary hypertension
Arrythmias
Myocardial disease
```
124
Systemic manifestation of scleroderma - renal involvement
Kidney tissue replaced by fibrosis - hypertension
| Scleroderma renal crisis
125
Management of scleroderma
Treat appropriately
Drug therapies are aimed at vascular ischaemia, immune modulation and fibrosis
No steroids
ACE inhibitors in scleroderma renal crisis
126
What does systemic sclerosis (SScl) cause
Fibrosis affecting skin, internal organs, vasculatures
127
What is SScl characterised by
Raynaud’s phenomenon (+/- digital ischaemia), sclerodactyly and cardiac, lung, GI and renal disease.
128
Epidemiology of SScl
Peak age of onset is 4th and 5th decades
Overall prevalence is 10-20/ 100,000
4:1 f to m ratio
129
Prognosis of dcSScl
Poor
| 5 yrs survival is 70%
130
Dysphagia
Difficulty swallowing
131
Clinical features of skin in SScl
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
Investigation in SScl
Bloods
| Imaging
133
Bloods in SScl
```
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
Imaging in SScl
Chest x-ray/ CT chest
ECG
Lung function test
Barium swallow can assess oesophageal involvement
135
Management of SScl - general
Nil to stop or reverse fibrosis
| Try to slow the effects of the disease on target organs
136
Management for Raynaud's and digital ulcers in SScl
```
Avoid cold
Thermal gloves/ socks
High core temp
Calcium channel blockers
Losartan
Fluoxetine
Sildenafil
```
137
Management for GI complication in SScl
Protein pump inhibitors
138
Management for hypertension in SScl
ACE inhibitors
139
Management for joint involvement in SScl
NSAIDs
| Analgesia
140
Management for pulmonary involvement in SScl
Bosentan or heart-lung transplant
141
Management for interstitial lung disease in SScl
Glucocorticosteroids and (pulse intravenous) cyclophosphamide
142
Mixed connective tissue disease
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
Management of connective tissue disease
Focuses on treating the components of the disease
144
Polymyositis and dermatomyositis
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
Incidence of PM and DM
2-10 cases per million/ year
146
Clinical features of PM and DM
Weakness: insidious onset of symmetrical proximal muscle weakness
Lung involvement
Skin involvements
147
Systemic features of DM and PM
Pyrexia
Wt loss
Fatigue
148
Lung involvement in PM and DM
Respiratory or pharyngeal muscle involvement
| Interstitial lung disease occurs in up to 30% of pts associated with antisynthetase (Jo-1) antibodies
149
Skin involvement in DM and PM
Gottron's papules over PIP and DIP
| Heliotrope rash
150
Gottron's papules
Scaly, violaceous, psoriaform plaques
151
Macules vs papules
Can palpate macules but not see them and can see but not palpate papules
152
Heliotrope rash
Violaceous discoloration of the eyelid
153
Investigations for PM and DM
```
Serum levels of creatinine kinase – sign of muscle infl
MRI
Muscle biopsy
Electromyography
Screening for underlying malignancy
```
154
Muscle biopsy for DM and PM
Fibre, necrosis, regeneration and infl cell infiltrate
155
Electromyography for DM and PM
Very useful for highlighting non-autoimmune/ non-infl myopathies
156
Screening for malignancy in PM and DM
```
History
Examination
CXR
CT of chest/abdomen/pelvis
PSA mammography
```
157
Mangement for DM and PM
Oral glucocorticoids (IV if severe)
Immunosuppressive therapy
Rituximab probably efficacious
IV immunoglobulin (IVIg) may be effective in refractory cases
158
Maintenance dose of oral glucocorticoids for DM and PM
5 - 7.5 mg
159
Immunosuppressive therapy for DM and PM
MTX, MMF, azathioprine
160
Vasculitis
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
What do clinical features of vasculitis result from
A combination of local tissue ischemia (due to vessel infl and narrowing) and the systemic effects of widespread infl
162
Who should we consider vasculitis in
Anyone w/ fever, wt loss, fatigue, multisystem involvement, rashes, raised infl markers and/ or abnormal urinalysis
163
Giant cell arteritis (GCA)
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
Epidemiology of GCA
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
PMR
Polymyalgia Rheumatica
166
Clinical features of GCA and PMR
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
Symptoms in PMR that are not present in GCA
Stiffness and painful restriction of active shoulder movements on waking but no muscle weakness or tenderness
168
Systemic symptoms in PMR and GCA
Wt loss, fatigue, malaise and night
169
Headaches in GCA
Often localised to temporal or occipital region
| Temporal arteries may be prominent
170
Visual disturbance in GCA and PMR
Occlusion of the posterior ciliary artery
171
Rare symptoms in GCA and PMR
Neurological symptoms, w/ TIA’s, brainstem infarcts and hemiparesis
172
Condns that can mimic PMR
```
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
Investigation results for GCA and PMR
High ESR/CRP - rarely present w/ normal levels
| Anaemia
174
Which investigations should be considered for GCA and PMR
Temporal artery biopsy
Ultrasound of temporal arteries
PET scan
175
Ultrasound for GCA and PMR
Affected temporal arteries show a ‘halo’ sign
176
Management of GCA and PMR
Medical emergency so prednisolone if suspect because of the risk of vision
Bisphosphonates for bone
177
Dosage of prednisolone in GCA and PMR
Higher doses in GCA (60-80 mg prednisolone) than in PMR (15-20mg)
Dose should be progressively reduced
178
How long do GCA and PMR pts need glucocorticoids for
An avg of 12-24 months
179
Ages affected in polymyositis vs in PMR
Any age vs 50+
180
Muscles involved in polymyositis vs in PMR
Proximal muscle involvement i.e. shoulder and hip vs none
181
CPK in polymyositis
Elevated due to muscle damage
182
CPK in PMR
No muscle involvement so normal CPK. EMS and high infl markers
183
What does the spectrum of PM incl
Skin involvement
184
What does the spectrum of PMR incl
GCA (vasculitis)
185
Occurrence of polymyositis vs PMR
Rare and need referral vs common and often managed by GP’s
186
Reducing dosage of prednisolone in GCA and PMR
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
What happens if symptoms recur for GCA and PMR after raising dose
The dose should be increased to that which previously controlled the symptoms, and reduction attempted again in another few weeks
188
ANAs associated with CTDs
```
dsDNA/ smith - lupus
Jo1 - DM
Ro – Sjorgens
La - Sjogens
Scl-70 - dcSScl
Centromere - lcSScl
```
189
Prognosis of GCA
Can be good as long as pt receives early and appropriate treatment
Treatment may last years and pt needs follow up appt
190
Discoid lupus
Lupus only affecting the skin (not entire system)
191
Mnemonic for SLE
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
Epidemiology of PMR
F:M ratio of 3:1
Starts at 50+ but mainly affects those 70+
15% develop GCA
193
EMS in PMR
45+
| Symptoms improve w/ activity
194
Blood tests for PMR
```
Anti-CCP
Antinuclear Antibody (ANA)
Full Blood Count (FBC)
CRP
ESR
Rheumatoid Factor (RhF)
```
195
EULAR criteria for diagnosing PMR
```
Must have these:
Aged > 50 Years
Bilateral Shoulder Discomfort
Abnormal ESR or CRP
and an addn 4 points
```
196
Points for diagnosing PMR
```
Morning stiffness (2 points)
Hip pain (1 point)
Absence of RhF/ANA (2 points)
Absence of other joint pain (1 point).
```
197
Prognosis for PMR
Pts typically respond well to treatment and most recover within 1-5 yrs
Some pts have a relapse
198
Mnemonic for PMR clinical features
SECRET
```
Stiffness and pain
Elderly individuals
Constitutional symtoms
Rheumatism (arthralgia/ arthritis)
Elevated ESR
Temporal Arteritis
```
199
Amaurosis fugax
Painless temporary loss of vision in one or both eyes due to lack of blood flow
Can be seen in GCA
200
Diseases with +ve ANA
SLE and mixed connective tissue disease - 95%
| RhA and autoimmune thyroid disease - 30-50%
201
Is a high titre ANA indicative of more severe disease
No
202
CLOT acronym for APLS
Coagulation defect
Livedo Reticularis
Obstetric - recurrent miscarriages
Thrombocytopenia
203
When is APLS secondary
With hx of SLE
204
Complement levels in SLE
Abnormal (low)
205
When to suspect CTD
```
Young female pt
Arthralgia & myalgia
Fatigue & malaise
Skin/ Lung/ Heart/ kidney involvement
Raynaud's phenomenon
```
206
Is primary Raynaud’s bilateral or unilateral
Bilateral
207
Indicators that it is secondary Raynaud’s
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
Rashes for lupus
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
Neurological disorders in SLE
Headaches
Seizures
Psychosis
210
Why might a biopsy be normal in GCA
Scalp ischemia
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