MSK Flashcards
(317 cards)
1
Q
What does arthropathy mean?
A
Something wrong with a joint
2
Q
What does arthralgia mean?
A
Joint pain
3
Q
What is arthritis?
A
Joint inflammation
4
Q
What are the common features of inflammatory conditions?
A
Joint pain with diurnal variation
Morning stiffness
Synovitis (soft tissue swelling)
5
Q
What are the common features of mechanical conditions?
A
Worse with activity
Generally localised
Normal blood tests
6
Q
Give an example of an inflammatory joint condition
A
RA
7
Q
Give an example of a non-inflammatory joint condition
A
OA
8
Q
Give an example of an inflammatory condition not related to the joint
A
Giant cell arteritis
9
Q
Give an example of an non-inflammatory condition not related to the joint
A
Fibromyalgia
10
Q
What are the 3 types of inflammatory joint conditions?
A
Connective tissue diseases and vasculitides (group of diseases that destroy blood vessels by inflammation)
Sero-negative arthritides
Crystal arthropathies
11
Q
Give examples of the Connective tissue diseases and vasculitides.
A
RA
SLE
Scleroderma
Wegener’s granulomatosis
12
Q
Give examples of Sero-negative arthritides
A
Ankylosing spondylitis
Psoriatic arthritis
Reiters syndrome
Gut associated arthropathy
13
Q
Give examples of crystal arthropathies
A
Gout
Pseudogout
14
Q
What is enthesitis?
A
Inflammation of the area where tendons and ligaments insert into bone
15
Q
What are some of the extra-articular symptoms of RA?
A
Raynauds Sicca (mucosal dryness) ILD Neuropathy Vasculitis
16
Q
What are some of the extra-articular symptoms of sero-negative arthritides?
A
Psoriasis
Uveitis/iritis
Tendonitis
IBD
17
Q
What does LOSS describe with relation to OA?
A
Loss of cartilage
Osteophyte formation
Subchondral cysts
Subchondral sclerosis (hardening of tissue)
18
Q
How can connective tissue diseases as a group be defined as?
A
They have spontaneous over-activity of the immune system and are often associated with specific auto-antibodies
19
Q
What is SLE?
A
A systemic AI disease that can affect any part of the body resulting in inflammation and tissue damage.
20
Q
Is SLE commoner in males or females?
A
Females
21
Q
Per 100,000 people, how many will have SLE?
A
20-150 depending on the ethnic group
22
Q
There are 4 factors which can influence SLE development, what are these?
A
Genetic
Environmental
Hormonal (higher oestrogen exposure)
Immunological
23
Q
What environmental factors can influence SLE development?
A
Viruses e.g. EBV
UV light
Silica dust is cigarette smoke and cleaning powders
24
Q
Name some of the general symptoms of SLE
A
Fever Malaise Poor apetite Weight loss Fatigue
25
What are the mucocutaneous features of SLE?
Photosensitivity
Malar rash
Discoid lupus erythematosus
Subacute cutaneous lupus
26
What are the MSK features of SLE?
Non-deforming polyarhritis
Jaccoud's arthritis = deforming arthropathy
Myopathy - weakness, myalgia (muscle pain) and myositis (muscle inflammation)
27
What are the pulmonary features of SLE?
```
Pleuricy
Infection
Diffuse lung infiltration and fibrosis
Pulmonary hypertension
Pulmonary infarct
```
28
What are the cardiac features of SLE?
Pericarditis
Cardiomyopathy
Pulmonary hypertension
Libmen Sacks endocarditis (sterile)
29
Golemulonephritis can occur in SLE, what does this present with?
Proteinuria
Hypertension
Acute or chronic renal failure
30
What are the neurological features of SLE?
```
Depression
Migranous headache
TIA/stroke
Cranial/peripheral neuropathy
Cerebellar ataxia (condition affecting balance)
```
31
What are the haematological features of SLE?
Lymphadenopathy (v.common)
Leucopenia (low WBC)
Anaemia
Thrombocytopenia (low platelets)
32
SLE can also increase an individuals susceptibility to infection. Why is this?
Individual has a compromised immune system and drugs used to treat lupus can compromise immune system more.
33
What screening tests would be done for an individual with suspected SLE?
```
FBC
Renal function tests
Anti-nuclear antibody
Anti-double stranded DNA antibodies
ENA
Complement levels
```
34
ANA is present in what % of SLE patients?
| What is the downside of ANA?
95%
| 20% of the healthy population have positive ANA. Also found in a variety of other conditions
35
A positive ANA test should be taken seriously if they have CTD symptoms or if other antinuclear antibodies are positive; what are these other autoantibodies?
Anti-dsDNA
Anti-Sm
Anti-Ro
Anti-RNP
36
How often does anti-dsDNA occur in SLE patients?
60% of patients
| Highly specific for SLE
37
What is Anti-Ro associated with?
Anti-La and cutaneous manifestations
| Also neonatal LE
38
How do you monitor SLE activity?
```
BP
Anti-dsDNA levels - +ve correlation
C3/C4 levels - -ve correlation
Urine
FBC and blood biochem
```
39
What is the 1st thing tried to treat mild SLE?
NSAIDs and simple analgesia
40
What other drug treatment can be used in SLE?
Anti-malarials: Chloroquine and hydroxychloroquine
Steroids: dose and type depends on symptoms
Immunosuppressives:
azathioprine, cyclophosphamide, methotrexate, mycophenolate mofetil
Biologics:
Rituximab and Belimumab
41
What is sjogrens syndrome?
AI condition - lymphocyte infiltration of exocrine glands causing xerostomia and keratoconjunctivitis sicca (dry mouth and dry eyes)
42
What are the classification criteria for Sjogrens?
```
Ocular symptoms (daily for >3 months)
Oral symptoms (daily for >3 months)
Evidence of ocular dryness
Evidence of salivary gland involvement
Immunology - Ro, La, or both
Biopsy evidence of lymphocytic infiltrate
```
Must have 4 of 6 inc. Immunology or biopsy
43
What test can be done to prove Sjogrens clinically?
Schirmers test
44
What classifies secondary Sjogrens syndrome?
Caused by or alongside other AI conditions
45
What other manifestations of Sjogren's disease are there?
Fatigue, arthralgia, raynauds, ILD, neuropathy, skin and vaginal dryness, Lymphoma (x40 risk), Neonate complete heart block (anti-Ro)
46
What is the prevalence of Sjogrens?
1-3%
47
Who is most likely to be affected by Sjogrens syndrome?
40-60 year old Females
48
How do you treat Sjogrens syndrome?
Eye drops, saliva replacement
Pilocarpine - for dry mouth (stimulates saliva production)
Hydroxychloroquine - anti-malarial and antinflammatory
Steroids and immunosupression
49
What are the 2 types of Systemic sclerosis?
Limited and Diffuse
50
What are the common symptoms of limited systemic sclerosis?
Calconosis - calcium deposits in the tissue
Raynaud's
Eosophageal dysmotility
Sclerodactyly -localized tightening and thickening of skin on fingers and toes
Telangiectasia - small widened blood vessels of the skin
Pulmonary hypertension (in 30%)
51
What autoantibodies are associated with limited systemic sclerosis?
anti-centromere
52
What are the common symptoms of diffuse systemic sclerosis?
Truncal and acral skin involvement
Early organ involvement
Quicker and more severe than the limited disease in general
53
What is systemic sclerosis?
A multisystem autoimmune disease in which there is increased fibroblast activity resulting in abnormal growth of connective tissue, causing vascular damage and fibrosis.
54
What autoantibody is associated with Diffuse systemic sclerosis?
Anti-Scl-70
55
What are the GI manifestations of Systemic sclerosis?
Small bowel, oesophageal and rectal hypomobility
| Pancreatic insufficiency
56
What are the Respiratory manifestations of Systemic sclerosis?
ILD
Pulmonary hypertension
Chest wall restriction
57
What are the Renal manifestations of Systemic sclerosis?
Hypertensive renal crisis
| Ischaemic
58
What are the Cardio manifestations of Systemic sclerosis?
Raynaud's with digital ulceration
Atherosclerotic disease
Hypertensive cardiomyopathy
59
Who is most likely to develop systemic sclerosis?
25-55 year old females
60
What can be used to treat systemic sclerosis?
```
CCbs
Prostacyclin (Iloprost)
ACEIs
Prednisolone
Immunosuppression
Bosentan, Sildenafil
```
61
What are some of the major criteria for Mixed Connective tissue Disease (MCTD)?
```
Severe myositis
Pulmonary involvement
Raynauds
Swollen hands
Sclerodactyly
Anti-U1-RNP
```
62
What are some of the minor criteria for MCTD?
```
Alopecia
Leukopenia - low WBCs
Anaemia
Pleuritis
Pericarditis
Arthritis
Malar rash
Thrombocytopenia
Mild myositis
Histroy of swollen hands
```
63
What is Anti-phospholipid syndrome?
An AI disorder characterised by arterial and venous thrombosis, adverse pregnancy outcomes (for mother and fetus), and raised levels of antiphospholipid (aPL) antibodies
64
What are the Diagnostic criteria for Anti-phospholipid syndrome?
+ anti-cardiolipin antibodies/
lupus anticoagulant activity/
Anti-beta2-glycoprotein; on 2 occasions 12 weeks apart
Arterial/Venous thrombosis
Pregnancy loss with no other explanation (10-34/40)/
3 pregnancy losses with no other explanation (<34/40) due to eclampsia, severe pre-eclampsia or placental insufficiency
1 lab and 1 clinical to make diagnosis
65
What are the features of anti-phospholipid syndrome?
Superficial thrombophlebitis and livedo reticularis ( mottled reticulated vascular pattern)
Mild/Mod thrombocytopenia
Migraine
Libman-Sacks endocarditis
66
How is anti-phospholipid syndrome treated?
Thrombosis - lifelong anticoagulation
| Pregnancy loss - aspirin + heparin during pregnancy
67
What are the 3 types of joint?
Synovial
Fibrous
Cartilaginous
68
Give an example of a fibrous joint
Bones in the skull
69
Give an example of a cartilaginous joint
Intervertebral discs
70
Give an example of a synovial joint
Knee
71
What is a simple synovial joint?
One pair of articular surfaces e.g. phalanges
72
What is a compound synovial joint?
More than one pair of articular surfaces e.g. elbow
73
What helps stabilise the joints during purposeful motion?
Shape of the bone
Ligaments
Synovial fluid
74
What helps lubricates the joints?
Cartilage interstitial fluid
| Synovium-derived hyaluronic acid and lubrcin
75
What is synovial fluid absorbed and replenished by?
Synovial membrane
76
The synovial fluid has few cells, but what cells usually do exist in it?
Mononuclear leucocytes
77
What is needed for rapid movement of a joint to occur?
Decreased viscosity and increased elasticity of the synovial fluid
78
What are the main roles of articular cartilage?
Helps prevent joint wear and tear by allowing a low-friction surface
Distributes contact pressure to sunchondral bone
79
What is the ECM of articular cartilage made of?
Water (70%) - lubrication
Collagen (mainly type II) (20%) - strength
Proteoglycans (10%) - compression
80
What are the proteoglycans in cartilage made mainly of?
Glycosaminoglycan
81
Cartilage is 98% ECM, what is the other 2%, and what is its role?
Chondrocytes - synthesise, organise, degrade and maintain the ECM
82
Articular cartilage is avascular, so how does it receive its nutrients and oxygen?
Via the synovial fluid
83
With regards to the structure of cartilage, what can cause joint disease?
Changes in relative amounts of water, collagen and proteoglycans
ECM degredation exceeding rate of synthesis
84
What do catabolic factors do to cartilage matrix turnover?
Stimulate proteolytic enzymes and inhibit proteoglycan synthesis (TNF + IL-1)
85
What do anabolic factors do to cartilage matrix turnover?
Stimulate proteoglycan synthesis and counteracts the effects of IL-1 (TGF + IGF-1)
86
How can you tell if cartilage degradation is occuring?
Increased serum and synovial keratin sulphate levels
| Type II collagen in the synovial fluid
87
What structural changes occur in an osteoarthritic knee?
```
Thickened joint capsule
Cyst formation
Subchondral sclerosis
Fibrillated cartilage (softer with gaps)
Synovial hypertrophy
Osteophyte formation
```
88
What is seen microscopically in gout?
Deposition of needle shaped uric acid crystals
89
What is seen microscopically in psuedo-gout?
Deposition of rhomboid shaped calcium pyrophosphate crystals
90
What is the prevalence of RA?
1%
91
What genes are thought to be associated with RA?
HLA DR4 and DR1
92
What happens to the synovium in RA?
Macrophage, fibroblast and multi-nucleated giant cell infiltration
Membrane expands and erodes bone and cartilage
93
What are some symptoms of RA?
Morning stiffness
Malaise
Fatigue
Joint pain and swelling
94
How is RA classified?
Number and site of involved joints
Serological abnormality
Elevated acute phase response
Symptom duration
95
How can RA be investigated for?
Anti-CCP
RF
Inflammatory markers
96
What are the principles of RA treatment?
Early initiation of DMARDs with steroids to cover the lag phase
97
What biologic approaches have proved important in RA treatment?
Anti-TNF
B cell depletion
Disruption of T cell costimulation
IL-1 inhibition
98
What drugs target TNF inhibition in RA?
Inflximab
Adalimumab
Etanercept
99
What drugs target B cell depletion in RA?
Rituximab
100
What drugs target disruption of T cell costimulation if RA?
Abatacept
101
What drugs target IL-1 inhibition in RA?
Anankira
102
What is a motor unit?
A single alpha motor neuron and all the skeletal muscle fibres it innervates
103
When is calcium released from skeletal muscle fibres?
Surface AP spreads down transverse T tubules
104
What does the A band in a sarcomere contain?
Thick filaments, with the overlapping parts of the thin filaments
105
What does the H-zone in the sarcomere contain?
Middle of A bands where thin filaments dont reach
106
What is the M-line of a sarcomere?
It extends vertically down the middles of the A-band and the H-zone
107
What does the I-band of a sarocomere consist of?
Remaining portion of thin filaments that the A-band does not cover.
108
What are Z-lines?
Connect 2 sarcomeres
109
When is ATP required in the muscles?
Contraction and relaxation
110
When is caqlcium required in muscle movement?
Calcium binds the thin to thick filaments, allowing the process of contraction to begin
111
How does calcium switch on cross bridge formation?
It binds to troponin on actin, and the troponin-tropomyocin complex moves to uncover the cross bridge binding sites
112
Where is calcium released from in skeletal muscle movement?
Sarcoplasmic Reticulum
113
If AP duration is shorter than the muscle "twitch" associated with it, what does this mean in terms of muscle work?
Possible to summate twitches to bring about stronger contraction
114
How does tetanus in skeletal muscle occur?
If the fibres are stimulated so rapidly, that they do not have a chance to relax between stimuli.
115
Can cardiac muscle be tetanised?
No, the long refractory period prevents this occurring.
116
What is isotonic muscle contraction?
Body movements and moving objects.
| Muscle tension is constant as length increases.
117
What is isometric muscle contraction?
Supporting objects in fixed positions and maintaining body posture.
Muscle tension changes whilst muscle remains the same length
118
What is the stretch reflex?
Negative feedback system that resists passive change in muscle length to maintain optimal resting length of muscle
119
What are muscle spindles?
A collection of specialised muscle fibres.
120
Where are muscle spindles found?
Within the belly of muscles, running parallel to the ordinary muscle fibres.
121
What are muscle spindles also known as?
Intrafusal fibres
122
What are ordinary muscle fibres also known as?
Extrafusal fibres
123
What are the sensory nerve endings of muscle spindles called?
Annulospiral fibres
124
What neurons will increase firing rate when a muscle is stretched?
Afferent neurons
125
What are the efferent neurons called that supply the muscle spindles?
Gamma motor neurons
126
What do gamma motor neurons do?
Adjust the level of tension in muscle spindles to maintain their sensitivity when the muscle shortens in contraction
127
What are the main differences between types of muscle fibre?
Enzymatic pathways for ATP-synthesis
The resistance to fatigue
Activity of myosin ATP-ase
128
What is the immediate source of ATP for muscle fibres?
Transfer of high energy phosphate from creatine phosphate to ADP
129
What is the main source of ATP for muscle fibres in aerobic conditions?
Oxydative phosphorylation
130
What is the main source of ATp for muscle fibres in anaerobic conditions?
Glycolysis
131
What are slow oxidative type I muscle fibres?
Slow-twitch fibres
| Used mainly for prolonged, low-work, aerobic activities
132
What are fast oxidative Type IIa fibres?
Intermediate-twitch fibres
| Used in aerobic and anaerobic conditions when doing prolonged, relatively moderate work.
133
What are fast glycotic Type IIx fibres?
Fast-twitch fibres
| Used in anaerobic conditions for short-term, high intensity activities
134
What are the 4 main features of OA?
Loss of joint space
Osteophyte formation (articular cartilage failure)
Subchondral sclerosis
Subchondral cysts
135
What does cartilage mainly consist of?
Collagen type II
136
What is the matrix of the cartilage formed by?
Chondrocytes embedded within it
137
In disease the matrix is lost, but what else occurs?
Release of cytokines (TNF, IL1)
Release of mixed metalloproteinases
Prostaglandin release by chondrocytes
138
How does cartilage attempt to repair itself?
Osteophyte formation
139
Which joints are most commonly affected in OA?
```
Hands
Feet
Knee
Hip
Spine
```
140
What can cause secondary OA?
```
Previous injuries
RA
Genetic elements
Acromegaly
Calcium crystal deposition disease
```
141
What are the main risk factors for OA?
```
Increasing age
Female
Obesity
Occupation (physical)
Sports
Previous injury
Muscle weakness (body more reliant on bone
```
142
How would a person with OA present to a clinic?
Pain which worsens on activity and is relieved by rest
| Morning stiffness usually lasting <30mins
143
What would be seen/felt on examination of this patient?
```
Joint tenderness
Joint effusion
Crepitus
Bony enlargements (osteophytes)
```
144
Which joints in the hands are most commonly affected in OA?
DIP
PIP
1st CMC
145
What are the hand features of OA?
Bony enlargements at:
DIPs = Heberdens nodes
PIPs = Bouchards nodes
Squaring of the thumb
146
What are the knee features of OA?
Genu varus (wide knees) and valgus (knock-knees) deformities
Baker's cyst - swelling in the popliteal fossa
Restricted movements
147
What are the Hip features of OA?
Pain may be in groin or radiate to knee, or felt in lower back
Movements are restricted
148
What are the Spinal features of OA?
Cervical - pain and movement restriction. Osteophytes may impinge on nerve roots
Lumbar - osteophytes may cause spinal stenosis if they encroach on the spinal canal
149
What is the non-pharmalogical management of RA?
```
Physio - muscle strengthening
Walking aids (if necessary)
```
150
What is the pharmalogical management of OA?
Analgesia - paracetamol, topical treatments
NSAIDs
Pain modulators e.g. amitriptyline/gabapentin etc.
151
What can be done intra-articularly for OA?
Steroid injections
| Hyaluronic acid
152
What can be done surgically for OA?
Arthroscopic washout
Loose body/soft tissue trimming
Joint replacement
153
What is gout?
An acute inflammatory response to the deposition of urate crystals (needle shaped) as well as the phagocytosis of the crystals
154
Gout is caused by hyperuricaemia, but what can cause this? (generally)
Increased urate production OR Reduced urate excretion
155
What causes increased urate production?
Inherited enzyme defects
Psoriasis
Alcohol
High dietary purine intake
156
What causes reduced urate excretion?
```
CKD
Hypothyroidism
Diuretics
HF
Cytotoxins
```
157
Gout usually only affects 1 joint; which are the most commonly affected joint?
1st MTP > ankle > knee
158
Gout will settle within 10 days without any treatment, but how long does it take to settle with treatment?
3 days
159
Does gout gradually or acutely present?
Acutely (often overnight)
160
A patient presenting with a red swollen 1st MTP with a 12 hour history has a normal uric acid measurement. Does this exclude gout?
No, uric acid is sometimes normal during an acute attack
161
What is chronic tophaceous gout?
A recurrent form of arthritis that is caused by a build up of uric acid crystals in the fluid around the joints
162
What drug type can be associated with tophaceous gout?
Diuretics
163
What investigations can be done to confirm a diagnosis of gout?
Serum uric acid - may be raised or normal
Inflammatory markers - raised
Polarised microscopy of synovial fluid
X-ray
Renal impairment - can be both a cause and an effect
164
What treatments are used in the acute gout attack?
NSAIDs
Colchicine
Steroids
165
What treatments are used for prophylaxis after a gout attack?
Allopurinol
Febuxostat
Started 2-4 weeks after the acute attack
166
What is Calcium Pyrophosphate Deposition Disease? (CPPD)
A metabolic arthropathy caused by the deposition of calcium pyrophosphate dihydrate in and around joints, esp. in articular cartilage and fibrocartilage
167
Is CPPd more common in older or younger patients?
Older
168
Where does CPPD affect the fibrocartilage?
Knees
Wrists
Ankles
169
An acute attack of CPPD is also known as what? What happens?
Pseudogout
| Shedding of envelope-shaped calcium pyrophosphate crystals into the joint
170
How is CPPD treated?
NSAIDs
Colchicine
Steroids
Rehydration
171
What is "Milwaukee shoulder"?
Hydroxyapatite crystal deposition in or around the joint - release of collagenases, serine proteinases + IL-1
172
What is the treatment for Milwaukee shoulder?
NSAIDs
Intra-articular steroid injection
Physio
Partial/total arthroplasty
173
What is soft tissue rheumatism?
Pain caused by inflammation/damage to ligaments, tendons, muscles or a nerve near a joint
174
Soft tissue rheumatism is usually well localised, if there is more generalised soft tissue pain, what diagnosis should be considered?
Fibromyalgia
175
Where is the commonest area for soft tissue injury?
Shoulder
176
Soft tissue rheumatism does not normally require investigation, but what ones can be done in some cases?
X-ray
MRI
Identification of precipitating factors
177
What can be used to treat soft tissue rheumatism?
```
Pain control
Rest + ice compressions
PT
Steroid injections
Surgery
```
178
Joint hypermobility syndrome is diagnosed using the modified Beighton score - what are the criteria in this list? How many must a patient have to be diagnosed?
>10 degree hyperextension of the elbows (R+L)
Passively touching forearm with the thumb whilst flexing the wrist (R+L)
Passive extension of the fingers or a 90 degree or more extension of the 5th finger (R+L)
Knees hyperextension >10 degrees (R+L)
Touching the floor with the palms of the hands, without bending the knees
Hypermobility = >= 4/9
179
What can be used to treat someone presenting with arthralgia due to joint hypermobility syndrome?
Physio
Explanation
Analgesia
180
What are sero-negative arthropathies?
Family of inflammatory arthritides characterised by involvement of both the spine and joints
181
There are a number of sero-negative arthropathies, but they all share some common features, what are these?
Sacroilliac and spinal involvement
Enthesitis
Inflammatory arthritis
Dactylitis ("sausage" digits)
182
What other extra-articular features can sero-negative arthropathies have in common?
Occular inflammation
Muco-cutaneous lesions
(Rare) Aortic incompetence or heart block
183
When does ankylosing spondylitis most commonly present?
Late adolescent/ early adult men
184
What HLA type is ankylosing spondylitis associated with?
HLA B27
185
What are the clinical features of ankylosing spondylitis?
Inflammatory low back pain
Enthesitis
Peripheral arthritis
Amylodosis
186
What are the extra-articular features of ankylosing spondylitis? (The "A" disease(
```
Anterior uveitis
Cardio involvement - aortic regurg
Pulmonary invovement - atypical fibrosis
Asymptommatic enteric mucosal inflammation
Neurological involvement
```
187
What investigations should be done to help diagnose ankylosing spondylitis?
```
FBC
U&E
Inflammatory markers
HLA-B27
X-ray
MRI
```
188
What are the New York criteria used in diagnosing Ankylosing spondylitis (AS)?
1. Lower back pain for 3 months (improved by exercise but not relieved by rest )
2. Limited lumbar motion - Schober's test (tape measure)
3. Reduced chest expansion
4. Bilateral, Grade 2-4, sacroiliitis on xray
5. Unilateral, grade 3-4, sacroiliitis on xray
189
What is sacroiliitis?
An inflammation of one or both of your sacroiliac joints
190
When can definite AS be diagnosed based on the New York criteria?
If criteria 4 or 5 present
PLUS
1, 2, or 3
191
How is AS treated?
```
Home exercise
Physio
OT
NSAID
Corticosteroids
Anti-TNF - Infliximab/Adalimumab
```
192
What is psoriatic arthritis?
Inflammatory arthritis found in those with psoriasis. RF-ve and equally affects both men and women
193
What are the clinical features of psoriatic arthritis?
```
Inflammatory arthritis (5 subgroups)
Sacroiliitis
Nail invovement (pitting, onycholysis)
Dactylitis
Enthesitis
```
194
What are the clinical subgroups of psoriatic arthritis?
1. Confined to DIPs (hands/feet)
2. Symmetric polyarthritis
3. Spondylitis with or without peripheral joint involvement
4. Asymmetric oligoarthritis with dactylitis
5. Arthritis mutilans (severe derangement of any joint)
195
What is AS?
Inflammation of multiple articular and para-articular structures, frequently resulting in bony ankylosis. "stiffening of the vertebrae"
196
How is psoriatic arthritis diagnosed?
```
Inflammatory markers are raised
RF -ve
Marginal erosions on x-ray
"pencil in cup" deformity on xray
osteolysis
```
197
How is psoriatic arthritis treated medically?
NSAIDs
Corticosteroids/joint injections
Disease modifying drugs - methotrexate
Anti-TNF - etanercept
198
How is psoriatic arthritis treated non-pharmacologically?
Physio
OT
Orthotics
Chiropodist
199
What is reactive arthritis?
Infection-induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorganisms cannot be cultured.
200
How long is it before reactive arthritis occurs after an infection?
1-4 weeks
201
What are the most common infections causing reactive arthritis?
Chlamydia
Salmonella
Shigella
Yersinia
202
What are the clinical features of reactive arthritis?
```
Fever, fatigue, malaise
Asymmetric mono- or oligo-arthritis
Enthesitis
Mucocutaneous lesions
Occular lesions (conjuctivitis, iritis)
Visceral manifestations (mild renal disease and carditis)
```
203
What is Reiter's syndrome?
A form of reactive arthritis
204
What is the classical traid of symptoms in Reiter's syndrome?
Arthritis
Urethritis
Conjunctivitis
205
How do you diagnose reactive arthritis?
```
History
Examination
Bloods (Inflammatory markers, FBC, U&Es)
Cultures (blood, urine stool)
Joint fluid analysis
xray
```
206
How is reactive arthritis treated?
```
NSAIDs
Corticosteroids
Antibiotics
DMARDS - if resistant/chronic
Physio
OT
```
207
What is the prognosis of reactive arthritis?
Generally good
Recurrences not uncommon
Some develop a chronic form
208
What is vasculitis?
Inflammation of the blood vessel walls
209
What are the general types of vasculitis?
Large vessel
Medium vessel
Small vessel
210
Give 2 examples of a large vessel vasculitis.
```
Polymyalgia rheumatica (PMR)
Giant cell (temporal) arteritis
```
211
How does PMR present?
Sudden onset of severe pain and stiffness of the shoulders, neck, hips and lumbar spine
Symptoms are worse in the morning - lasting from 30 minutes to several hours
212
What age group is PMR most likely to affect
>50s
213
1/3 of patients with PMR develop systemic features, what are some of these?
```
Tiredness
Fever
Weigh loss
Depression
Occasionally night sweats
```
214
How is PMR investigated?
Raised ESR and/or CRP is almost always present
Serum ALP may also be raised
Anaemia is often present
Temporal artery biopsy - shows GCA in some cases but rarely done unless GCA is also suspected.
215
What is Giant cell arteritis (GCA)?
An inflammatory granulomatous arteritis of large cerebral arteries, occuring alongside PMR.
216
How does GCA present?
Severe headaches
Scalp tenderness
Jaw claudication
Tenderness and swelling of 1 or more temporal or occipital artery
Sudden painless temporary or permanent loss of vision in 1 eye
217
What are the systemic manifestations of GCA?
Severe malaise
Tiredness
Fever
218
What investigations are done for GCA?
Normochromic, normocytic anaemia
ESR (raised)
ALP (raised)
Temporal artery biopsy is the definitive test
219
What are the histological features seen on a temporal artery biopsy showing GCA?
Cellular infiltrates id CD4+ T lymphocytes, macrophages and giant cells in the vessel wall
Granulomatous infiltration of the intima and media
Breaking up of elastic lamina
Giant cells, lymphocytes and plasma cells in the interal elastic lamina
220
What is the main treatment used in PMR and GCA and why?
Corticosteroids - significantly reduces risks of irreversible visual loss and produces a dramatic reduction of symptoms
221
Give 2 examples of medium vessel vasculitis
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Polyarteritis nodosa (PAN)
Kawasaki's disease
```
222
What is PAN?
A rare condition accompanied by severe systemic manifestations.
223
What is found pathologically in PAN?
Fibrinoid necrosis of vessel walls with microaneurysm formation, thrombosis and infarction.
224
What are the clinical features of PAN?
Fever, weight loss, malaise and myalgia
| This is followed by dramatic acute features due to organ infarction
225
What investigations should be done for PAN?
FBC - anaemia, leucocytosis and a raised ESR
Biopsy - of affected organs
Angiography - demonstration of microaneurysms
Others - depending on organs affected
226
What is the treatment of PAN?
Corticosteroids usually in combination with immunosupressives (azothioprine)
227
What is Kawasaki's disease?
An acute systemic vasculitis mainly affecting children <5.
228
What are the clinical features of Kawasaki's disease?
```
(think avatar)
Fever lasting >5 days
Bilateral conjunctival congestion
Dry and red lips
Cervical lymphadenopathy
Polymorphic rash
Redness and oedema of palms and soles
```
229
What investigation findings can help diagnose Kawasaki's disease?
Leucocytosis, thrombocytosis and a raised CRP
230
What is the treatment of Kawasaki's disease?
Single dose IV immunoglobulin to prevent coronary artery disease
Aspirin after the acute phase
231
Small vessel vasculitis diseases are based on whether they are ANCA positive or ANCA negative. What is ANCA?
Anti-neutrophil cytoplasmic antibodies - IgG autoantibodies directed against the primary granules of neutrophil and macrophage lysosomes
232
What are some of the ANCA positive small cell vasculitis diseases?
Wegener's granulomatosis
Churg-Strauss granulomatosis
Microscopic polyangitis
233
What is Wegener's granulomatosis characterised by?
Lesions in the URT, lungs and kidneys
234
What are the symptoms of Wegener's granulomatosis?
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Rhinorrhoea
Nasal mucosal ulceration
Cough
Haemoptysis
Pleuritic pain
```
235
What can be seen on x-ray in Wegener's granulomatosis?
Single or multiple nodular masses which clear and appear spintaneously.
236
What treatment is used for Wegener's granulomatosis?
Cyclophosphamide
| Rituximab
237
How does Churg-Strauss syndrome present?
rhinitis
asthma
eosinophillia
systemic vascultis
238
Where does Churg-Strauss syndrome typically affect?
lungs
peripheral nerves
skin
239
What changes may be seen on x-ray in Churg-Strauss syndrome?
Pneumonia-like shadows
240
What skin changes may be associated with Churg-Strauss syndrome?
subcutaneous nodules and petechial or purpuric lesions
241
What is the recommended treatments for Churg-Strauss syndrome?
Corticosteroids
242
What organs are involved in microscopic vasculitis?
Kidneys
| Lungs (recurrent haemoptysis)
243
Give examples of ANCA negative small vessel vascultis diseases
Henoch-Schonlein purpura
Cryoglobulinaemic vasculitis
Cutaneous leucocytoclastic vasculitis
244
What is the treatment of small cell vascultis?
Depends on organ involvement
| May range from topical skin treatment to high dose corticosteroids
245
What name is given to the structure that completely surrounds a muscle?
epimysium
246
What name is given to the structure that completely surrounds bundles of muscle fibres?
Perimysium
247
What name is given to the structure that completely surrounds each individual muscle fibre?
Endomysium
248
What are the distinguishing features of a red muscle fibre (Type 1)
Slow twitch fibre
Large mitochondria
Increased myoglobulin
249
What are the distinguishing features of a white muscle fibre? (Type 2)
Fast twitch fibre
Small mitochondria
Large motor end-plates
250
What are the indications for a muscle biopsy?
Evidence of muscle disease
Presence of neuropathy
Presence of vascular disorder
251
What level of CK would be considered high, and what muscular disease(s) could this indicate?
200-300x normal
| Muscle dystrophies
252
What level of CK would be considered intermediate, and what muscular disease(s) could this indicate?
20-30x normal
| Inflammatory myopathy
253
What level of CK would be considered low, and what muscular disease(s) could this indicate?
2-5x normal
| Neurogenic disorder
254
What is the age of onset for DMD?
2-4 years
255
What is the life expectancy of an individual with DMD?
~20 years
256
What are the symptoms of DMD?
Proximal weakness
Pseudohypertrophy of calves
Raised CK
257
What causes DMD?
Mutations in the dystrophin gene on the long arm of the X-chromosome
258
What is the histopathological process behind DMD?
Mutation causes alterations in how the actin cytoskeleton anchors to the basement membrane
This means that muscle fibres are liable to tearing
And there is uncontrolled calcium influx into the muscle cells
259
What histological changes are seen in DMD?
Muscle fibre necrosis and phagocytosis
Regeneration
Chronic inflammation and fibrosis
Hypertrophy
260
What is Becker's muscular dystrophy? (BMD)
A varient of DMD with a later onset and a slower progress
261
What are the symptoms of myotonic dystrophy?
Muscle weakness
| Myotonia
262
What are the genes affected by myotonic dystrophy?
Ch19 and Ch3
263
What muscles are most commonly affected by myotonic dystrophy?
Face
Distal limbs
Late stage - respiratory muscles
264
What are the histological features of myotonic dystrophy?
```
atrophy of type 1 nerve fibres
central nuclei
ring fibres
fibre necrosis
fibrofatty replacement
```
265
What are the symptoms of polymyositis?
progressive muscular weakness, pain and tenderness
266
What is the mortality rate of polymyositis?
5-15%
267
What is the pathophysiology of polymyositis?
Cell-mediated immune response to muscle antigens
Endomysial lymphocytic infiltrate of muscle by CD8+ T lymphocytes
Segmental fibre necrosis
268
How does dermatomyositis differ from polymyositis?
Skin changes are present
269
How does dermatomyositis present?
Upper body erythema
| Eyelid swelling with purple discolouration
270
How likely is it that dermatomyositis is associated with malignancy?
10% chance
271
What is the histopathology of dermatomyositis?
Immune complex and complement deposition around capillaries within muscle
Perifascicular muscle fibre injury
272
What immune cells are involved in dermatomyositis?
B lymphocytes
| CD4+ T cells
273
Define a neurogenic disorder of muscle.
Stereotyped changes after nerve damage with subsequent re-innervation
274
What would be seen on biopsy in an individual with a neurogenic muscle disorder?
Small angulated nerve fibres
Target fibres
Fibre type grouping
Grouped atrophy
275
What is motor neuron disease?
Progressive degeneration of anterior horn cells
276
What symptoms would a person with motor neuron disease present with?
Denervation atrophy
Weakness
Fasciculation (muscle fibres twitch visibly under skin)
277
What is spinal muscular atrophy?
An inherited AR trait affecting Ch5 where degeneration of the anterior horn cells in the spinal cord occurs
278
What is myasthenia gravis?
An AI condition causing weakness, proptosis, fatigue and dysphagia
279
Who is most likely to get myasthenia gravis?
Women 20-40
280
What do 25% of those with myaethenia gravis have?
Thymoma (tumour of the thymus)
281
What is rhabdomyolysis?
A breakdown of skeletal muscle causing myoglobulinuria, hyperkalaemia, necrolysis and shock
282
What is the result of rhabdomyolysis?
AKI
Hypovolaemia and hyperkalaemia
Metabolic acidosis
Disseminated intravascular coagulation
283
What common features do CTD's share?
Multi-system features
Affect women more commonly than men
Immunological abnormalities are common
Usually respond to anti-inflammatories
284
What is SLE?
An AI multi-system disorder
285
What antibodies are usually present in individuals with SLE?
ANAs (antinuclear)
286
What drugs may induce SLE?
Hydralazine
| Pracainamide
287
How may SLE affect the skin?
"butterfly" rash, discoid lupus erythematosus
288
How may SLE affect the joints?
arthralgia
289
How may SLE affect the kidneys?
GN
290
How may SLE affect the CNS?
psychiatric symptoms
| Focal neurological symptoms
291
How may SLE affect the CVS?
Pericarditis
Myocarditis
Necrotising vasculitis
292
How may SLE affect the lymphatic system?
Lymphadenopathy and splenomegaly
293
How may SLE affect the lungs?
Pleuritis
| Pleural effusions
294
How may SLE affect the blood?
Anaemia
Leucopenia
Thrombophilia
295
What type of hypersensitivity are the visceral lesions in SLE mediated by?
Type 3
296
What type of hypersensitivity are the haematological effects in SLE mediated by?
Type 2
297
What is polyarteritis nodosa (PAN)?
Inflammation and fibrinoid necrosis of small/medium arteries
298
What are the main organs which PAN affects?
Kidneys, heart, liver, GI tract
299
What other organs does PAN affect other than the major ones?
```
Skin
Joints
Muscles
Nerves
Lungs
```
300
How does PAN present clinically?
Depends on organ(s) affected.
301
How is PAN diagnosed?
Biopsy for fibrinoid necrosis of vessels
| Serum samples for pANCA
302
What is pANCA?
Perinuclear antineutophil cytoplasmic autoantibody
303
How does PMR present?
Pain and stiffness in the shoulder and pelvic girdles esp in the elderly
304
What is used to treat PMR?
Corticosteroids
305
What is temporal arteritis?
Inflammation affecting the cranial vessels
306
What are the risks of temporal arteritis?
Blindness if the terminal branches of the opthalmic artery are affected
307
How does temporal arteritis present?
Headaches and scalp tederness
308
How is temporal arteritis diagnosed?
By raised ESR
| Temporal artery biopsy
309
What is scleroderma?
Excessive fibrosis of organs and tissues (excessive collagen production)
310
How can scleroderma affect the skin?
Tight, tethered skin causing decreased joint movement
311
How can scleroderma affect the GI tract?
Fibrous replacement of the muscularis
312
How can scleroderma affect the heart?
Pericarditis and myocardial fibrosis
313
How can scleroderma affect the lungs?
Interstitial fibrosis
314
How can scleroderma affect the kidneys?
Renal artery hypertension
315
How can scleroderma affect the MSK system?
Polyarteritis and myositis
316
What syndrome is scleroderma associated with?
```
CREST
C = calcinosis
R = Raynaud's
E = (O)esophageal dysfunction
S = Slerodactyly
T = Telangectasia (dilation of blood vessels close to the skin surface)
```
317
How can scleroderma eventually cause death?
Renal failure secondary to malignant hypertension
Severe respiratory compromise
Cor pulmonale
HF or arrhythmias secondary to myocardial fibrosis
