Botten Flashcards
1
Q
Tendinitis
A
acute inflammation or irritation of a tendon
2
Q
Tendinosis
A
chronic tendon injury
characterized by swelling and pain of a tendon
3
Q
Tenosynovitis
A
problems involving tendon and overlying synovial covering
4
Q
Location tendon problems
A
Insertional – problems at the point of insertion at the bone
Non-insertional – problems with the tendon itself
5
Q
Tendinopathy
A
umbrella term for tendon disorders
6
Q
What is the function of tendons?
A
Transmit forces generated from the muscle to the bone to elicit movement.
Absorb external forces to prevent injury to the muscle.
7
Q
Pathophysiology of tendinopathy
A
Tendinopathy results from loss of balance between micro damage from overuse and reparative mechanisms
Tendon becomes damaged and the healing process cannot keep up = failed healing response
Chronic Tendon Injury or over use – repetitive loading- causes degeneration/disorganisation of collagen fibres
– May decrease in number
– May have an increase in surrounding matrix
– Invasion of blood vessels to try and stimulate healing
Increased cellularity, but little inflammation
8
Q
Risk factors for tendinopathy
A
Age – peak is middle age, because older population tend to be less active
Chronic Disease - Diabetes, RA - affect soft tissues and ability to heal
Adverse Biomechanics – e.g. a very tight calf always places the Achilles tendon under an increased load even during normal activities
Repetitive Exercise – recreational or occupational
Recent increase in activity
Quinolone Antibiotics – targets the tendons
• e.g. Ciprofloxacin
9
Q
Clinical Features of tendinopathy
A
- Pain
- Swelling
- Thickening
- Tenderness on palpation
Can be clarified with provocative tests – ask patient to contract muscle group against resistance -> pain
10
Q
diagnosis of tendinopathy
A
Ultrasound – can see the shape of tendon, determine vascularization using doppler
MRI – Tendinopathy best seen on T1.
• Helps exclude any other pathology
11
Q
Non-operative Treatment of tendinopathy
A
Most give a success rate of about 80% in two years
- NSAIDs
- Activity modification
- Physiotherapy – stretching, eccentric exercises
- GTN patches
- PRP (platelet rich plasma) injection
- Extracorporeal Shockwave Therapy
- Steroid injection (controversial)
12
Q
GTN patches for tendinopathy
A
Vasodilator
Increases local perfusion in an attempt to stimulate a healing response
Takes up to 12 weeks to see effects
Adherence may be poor
Side effects - headaches
13
Q
Extra Corporeal Shockwave Therapy for tendinopathy
A
Same mechanism as used to break up kidney stones
Breaks down calcification and causes local trauma to stimulate healing
14
Q
Operative treatment for tendinopathy
A
Considered if non-operative treatments fail
Debridement - excision of diseased tissue
(Tendon transfers) – in patients if the tendon is too diseased
15
Q
Compartment Syndrome
A
Elevated interstitial pressure within a closed fascial compartment resulting in microvascular compromise
Common sites
• Lower leg – most common site
• Forearm
• Thigh
These muscle groups are enclosed by fascial compartments -> no flexibility for swelling
Lack of perfusion causes tissue death within 4-6 hours
16
Q
Causes of Compartment Syndrome
A
1) Increased internal pressure
• Bleeding
• swelling
• iatrogenic infiltration – e.g. incorrect cannula insertion
2) Increased external compression
• Casts / bandages
• full thickness burns
3) Combination
17
Q
Pathophysiology of Compartment Syndrome
A
Pressure within the compartment exceeds pressure within the capillaries -> microcirculation collapses
Decreased perfusion causes muscle ischaemia. This results in
• muscle swelling
• Increased permeability – fluid leaks into interstitial space
These cause further increased pressure
Autoregulatory mechanisms are overwhelmed
Muscle necrosis/myoglobin release (due to damage)
• Myoglobin is toxic to the kidneys
• Loss of function of limb or loss of life due to renal failure
18
Q
Neurapraxia
A
temporary loss of motor and sensory function due to blockage of nerve conduction
Initially reversible if relieved early
permanent damage may result after as little as 4 hours
19
Q
End stage compartment syndrome
A
Stiff fibrotic muscle compartments
Impaired nerve function – if any muscle survives it will not be useable because the nerve supply is damaged
Clawing of limbs – contracture of the muscles
Loss of function
20
Q
Clinical Features of compartment syndrome
A
6 P’s
Pain – disproportionate to that expected from the injury
Pain on passive stretching of the compartment
• E.g. wiggling of toes, stretching of fingers
Pallor – compromised vascular supply
Parathesia – loss of nerve function
Paralysis
Pulselessness – very late sign
- Swelling
- Shiny Skin
- Autonomic Responses– sweating, tachycardia,
21
Q
Which body part (and nerve) will be impacted first with compartment syndrome of the lower leg?
A
1st Dorsal webspace affected first
deep peroneal nerve
indicates a problem in the deeper compartments
22
Q
Treatment of compartment syndrome
A
Urgent
Open any constricting dressings / bandages
Reassess
Surgical Release
• Full length decompression of all compartments
• Excise any dead muscle
• Leave wounds open
• Repeat debridement until pressure decreases and all dead muscle is excised
Amputate if there is already irreversible damage
23
Q
Acute hot joint Differential diagnosis
A
- Septic arthritis
- Crystal arthropathy
- Trauma/haemarthrosis
- Early presentation of polyarthorpathy e.g. RA
24
Q
Investigation of an acute hot joint
A
Short history of acute, hot, swollen and tender joint(s) should be regarded as having septic arthritis until proven otherwise
Aspirate synovial fluid
o Gram stain and culture before antibiotics
o NB: may be negative!
o Microscopy
Blood culture should always be taken
FBC
X-ray of no value in this context
25
Septic arthritis - clinical presentation
* Pain
* Fever
* red, hot, swollen and agonisingly painful joint
* loss of function
* Effusion
26
most common Causative organisms or septic arthritis
Staphylococcus aureus – most common
Gram negative organisms in 5-20% - commonly children, elderly, immunocompromised/ IVDU
o Neisseria gonorrhoea
o Haemophilus influenzae (children)
NB: culture is negative in over 20%
27
risk factors for septic arthritis
* RA/OA/other inflammatory arthitides
* Biologic DMARD therapy
* Joint prosthesis/surgery
* Low SE status
* IVDU
* Alcoholic liver disease
* Diabetes
* Cutaneous infection/ulcers
28
Routes by which bacteria can reach a joint
1) Haematogenous route
2) Dissemination from osteomyelitis (bone infection)
3) Spread from an adjacent soft tissue infection
4) Diagnostic or therapeutic measures
5) Penetrating damage by puncture or trauma
29
Which conditions may cause septic arthritis?
* Lyme disease – borrelia burgdoferi
* Brucellosis
* Syphilitic arthritis – congenital and acquired
30
What are the types of Crystal arthropathy?
gout
| pseudogout
31
Gout
Most common inflammatory arthritis
characterised by recurrent attacks of a red, hot, tender and swollen joint
Caused by excess levels of uric acid
Leads to deposition of urate crystals in/near joints or soft tissue (tophi)
32
Causes of gout
Primary – hyperuricaemia due to genetic predisposition
```
Secondary – high uric acid due to:
o myeloproliferative disorder (PRV)
o leukaemia treated by chemo
o thiazides
o chronic renal disease
```
33
which factors can cause higher levels of uric acid?
```
o older ages
o Obesity
o high alcohol consumption
o high protein diet
o diabetes mellitus
```
34
Diagnosis of gout
Can be clinical diagnosis alone if obvious factors (hyperuricaemia and recurrent podagra)
Definitive diagnosis = MSU crystals
Diagnosed by aspirate
negatively birefringent needle shaped crystals seen on polarized microscopy
Serum urate levels and U&Es
35
Presentation of gout
typically presents with an acute monoarthropathy
• mainly (> 50%) occurs in the joint of the big toe (metatarsophalangeal joint)
• However it can be polyarticular.
* Hyperacute - Maximum intensity within 6-12 hours
* Rapid onset swelling and tenderness
36
Pathophysiology of gout
Chronic elevation of uric acid levels above the saturation point
Deposited preferentially in peripheral joints and subcutaneously as tophi
Asymptomatic period - crystal levels build
```
Acute attack can be precipitated by:
o Trauma
o Surgery
o Starvation
o Infection
o diuretics
```
If untreated -> further attacks/irreversible joint damage
37
Management of gout
Acute
o NSAIDs – high doses reduce pain and swelling
o Alternatives – colchicine, corticosteroids
o NB: stop statins as co-prescrition with colchinine increased the risk of myopathy
If attacks are repeated - urate lowering therapy
o Allopurinol – xanthine oxidase inhibitor
ULT should be offered to all patients who have a diagnosis of gout
38
Gout differential diagnosis
* Septic arthritis (in acute monoarthropathy)
* Reactive arthritis
* Haemarthosis
* Pseudogout
39
Pseudogout
Calcium pyrophosphate crystal deposition
crystals form in the synovial fluid, cartilage and extra-articular tissues (chondrocalcinosis)
acute monoathropathy typically of larger joints
usually spontaneous and self-limiting, but can be provoked by:
o Surgery
o Illness
o trauma
Can be secondary to hyperparathyroidism or haemochromatosis
40
Pseudogout diagnosis
Positively birefringent rhomboid shaped crystals on aspiration
41
Management of pseudogout
* Aspiration helps reduce the pain and swelling
* NSAIDs
* colchicine
42
Reactive arthritis
Sterile synovitis which occurs following a distant mucosal infection (classically GU or GI)
Occurs as an autoimmune response to infection elsewhere in the body
Triad (unusual) of:
o Post infectious arthritis
o Non-gonoccoccal urethritis
o Conjunctivitis
Preceding illness usually a urethritis or diarrhoeal
43
Trigger organisms for reactive arthritis
o Salmonella
o Shigella
o Yersinia
o chlamydia trachomatis
44
Clinical features of reactive arthritis
* Acute, asymmetrical lower limb arthritis
* Larger joints of lower limbs
* More common in men
* Days – weeks post infection
45
Enteropathic arthritis
reactive synovitis seen with UC and Crohn’s disease
An asymmetrical lower limb arthritis
Treatment of the bowel disease and NSAIDs
46
X-ray findings in osteoarthritis
```
LOSS:
• Loss of joint space
• Osteophytes
• Subarticular sclerosis
• Subchondral cysts
```
47
Osteoarthritis
* Degenerative joint disease
* disorder of articular cartilage
* Commonest form of arthritis
* Middle aged/elderly
* Affects weightbearing joints – hip, knee
* Pain and crepitus on movement
* Worse with prolonged activity
* Joint instability
* Stiffness after rest
48
functions of bone
Structural
o Support
o Protection
o Movement
Mineral Storage
o Calcium
o Phosphate
49
Indirect healing
Secondary healing via callus formation
‘Formation of bone via a process of differential tissue formation until skeletal continuity is restored’
INFLAMMATION, REPAIR AND REMODELLING
50
Steps of indirect healing
1. Fracture haematoma and inflammation
2. Fibrocartilage (SOFT) callus - lasts 3 weeks
3. Bony (HARD) callus - lasts 3 months
4. Bone Remodeling
51
Direct Fracture Healing
Unique ‘artificial’ surgical situation
‘Direct formation of bone, without the process of callus formation, to restore skeletal continuity’
Relies upon compression of the bone ends
52
Pattern of blood supply to bones
* Endosteal: Inner 2/3rds
| * Periosteal: Outer 1/3rd
53
Compromise of blood supply to bones
1) Anatomical factors:
Certain fractures are prone to problems with union or necrosis (bone death) because of potential problems with blood supply
Blood supply with an end artery (no collateral blood supply)
2) Surgical factors (iatrogenic) - e.g. stripping of periosteum
54
What type of fractures require surgical intervention because they compromise blood supply with an end artery?
* Proximal pole of scaphoid fractures
* Talar neck fractures
* Intracapsular hip fractures
* Surgical neck of humerus fractures
55
Which factors impair Fracture healing?
```
Patient factors
• Increasing age
• Diabetes
• Anaemia
• Malnutrition
• Peripheral vascular disease
• Hypothyroidism
• Smoking
• Alcohol
```
Medication
– NSAIDs - inhibit osteoblasts and osteoclasts, reduce vascularity
– Steroids - decrease bone metabolism
– Bisphosphonates - inhibit osteoclasts and induce apoptosis in osteoblasts
56
Osteonecrosis
also called AVascular Necrosis (“AVN”)
refers to bone infarction (tissue death caused by an interruption of the blood supply) near a joint
most common in the hip and shoulder
bilateral in majority
57
AVN Clinical Presentation
Osteonecrosis can be asymptomatic and found incidentally on imaging
Most patients present because of pain, either from the infarction itself or from secondary arthritis due to subchondral collapse
Rest pain occurs in about 2/3 of patients
o unlike OA patients – because it is an infarction process, not just related to movement
night pain occurs in about 1/3 of patients
58
Which movements of the hip are most limited with AVN of the femoral head?
osteonecrosis causes particular limitation in internal rotation and abduction
59
Pathophysiology of AVN
Always involves the medullary bone first
Blood flow disruption causes a period of ischaemia, followed by infarction. Areas of bone necrosis develop. Osteoclasts resorb the necrotic bone and try to replace it with new bone (creeping substitution).
If this is too slow, the necrotic cancellous bone collapses. Results in secondary damage --> subchondral collapse leads to end stage arthritis
60
Causes of AVN
may be unclear
o sickle cell anaemia
o Vascular damage - trauma
o Increased intraosseous pressure (oedema)
o mechanical stresses
61
Bone remodeling
process by which osteoclasts secrete acid and proteolytic enzymes to digest the bone matrix and osteoblasts synthesize new organic matrix leading to the deposition of newer, better bone
62
How does AVN cause arthritis?
If bone dies, it does not remodel
micro-damage does not get repaired
If enough damage accumulates, sub-chondral bone can be weakened to the point of collapse
sub-chondral bone collapse causes the joint surface to become irregular
If one side of the joint surface is not smooth, it will damage the other surface
63
What is the classical sign of AVN of x-ray?
crescent sign (subchondral radiolucency)
seen just before collapse
other:
o Subchondral collapse
o Bone remodelling
64
Risk factors for AVN
* History of trauma, especially a joint dislocation
* Corticosteroid use or Cushing's disease
* Alcohol abuse
* Sickle cell disease/haemoglobinopathies
65
How can you prevent AVN?
minimum effective dose of systemic corticosteroids should be used. If possible, steroid-sparing agents should be used
Patients at high risk of AVN should be educated about AVN and advised to report symptoms as soon as possible
66
What effect does the position of a femoral neck fracture have on the blood supply to the femoral head?
Vessels reflect along retinaculae
a subcapital (intracapsular) fracture will risk damaging vessels to femoral head
This can lead to avascular necrosis
different treatment:
• Hemiarthroplasty for displaced subcapital fracture to replace head with loss of blood supply
• Sliding hip screw for intertrochanteric fracture as blood supply is intact and therefore fracture will heal
67
PAGET’S DISEASE OF BONE
* increased bone turnover
* osteoclastic and osteoblastic activity
* raised alkaline phosphatase
complications include fracture deformity and rarely sarcoma
68
CHARACTERISTIC X-RAY FINDING OF PAGET’S DISEASE OF BONE
blade of grass sign
lucent leading edge in a long bone seen during the lytic phase
69
Chondrosarcoma
malignant cartilaginous tumour
70
What are the three main classes of bone disorders and their characteristic findings?
Degenerative - Bone production (sclerosis, osteophytes)
Inflammatory - Periarticular erosions
Depositional - Periarticular soft tissue masses
71
What would you see on imaging of an inflammatory bone disorder?
erosions
soft tissue swelling
symmetrical joint space narrowing
monoarthopathy = infection; polyarthropathy = RA/spondyloarthropathy
72
What would you see on imaging of a degenerative bone disorder?
asymmetrical joint space narrowing
osteophytes
sclerosis
73
How do Subchondral Cysts form?
Synovial fluid is forced into the subchondral bone, causing a cystic collection of joint fluid
74
How can you recognise Secondary Degenerative Arthritis?
– Atypical locations
– Atypical appearance
– Atypical age
75
Name 4 seronegative arthropathies. Which gene are they associated with?
(tend to have HLA-B27 association)
– Psoriatic arthritis
– Reactive arthritis
– Ankylosing spondylitis
– Inflammatory bowel disease
76
Discitis
inflammation that develops between the intervertebral discs of the spine
77
Ankylosis
abnormal stiffening and immobility of a joint due to fusion of the bones
78
What is the classical x-ray finding of ankylosing spondylitis?
bamboo spine
79
Name 3 Non-steroid Immunosuppressant Drugs
Inhibitors of DNA Synthesis
• Methotrexate
• Azathioprine
Lymphocyte Signalling Inhibitor
• Cyclosporin
80
Methotrexate Mechanism of Action
inhibits the action of the enzyme dihydrofolate reductase needed for production of DNA
causes S-phase arrest in cells
High Dose - Cytotoxic Chemotherapeutic Agent
Low Dose - Immunosuppressant
81
How can you minimise the toxic effects of methotrexate?
folate supplementation
Folic acid usually given 4 days after MTX
• Methotrexate on Mondays
• Folic acid on Fridays
82
Azathioprine - Mechanism of action
Converted within cells into a nucleoside analog
Incorporated into DNA and RNA chains, leading to termination of nucleic acid strands
Cell growth and metabolism halts
Preferential action on lymphocytes
83
Azathioprine - indications
Ulcerative colitis
Crohn’s disease
also:
Myaesthenia gravis
Eczema
84
Cyclosporin - Mechanism of action
inhibits signal transduction from the activated TCR complex
This causes profound inhibition of T-cell activation
85
Biologics
Synthesised biologicaly
target specific components of the immune system
minimal off-target effects
Usually delivered by parenteral route
86
Infections with Anti-TNF therapy
* Increased risk of TB, particularly disseminated TB.
* screen for latent TB before prescribing.
* increased risk of salmonella and listeria
87
Infections with Rituximab (anti-CD20)
Generalised increased risk of serious infection.
High risk of hepatitis B reactivation.
Screen and prophylax if necessary
88
Infections with Anti-IL-1 therapy
Increased risk of RTI and pneumonia
89
Infections with Abatacept (anti-CD86)
Increased risk of pneumonia & RTI
Increased risk of TB but less than TNF blockade.
90
What are the three main groups of Bone Tumours ?
1) secondary bone tumours (most common - metastatic)
2) primary bone tumours (rare)
3) myeloma
91
Name the 5 main metastatic carcinomas to bone
```
lung
prostate
thyroid
kidney
breast
```
Remember: LP Thomas Knows Best
92
which childhood cancers metastasise to bone?
* neuroblastoma
| * rhabdomyosarcoma
93
Which bones do tumours metastasise to?
Those with good blood supply
• long bones – femur, humerus
• vertebrae
94
Presentation of bone metastases
* often asymptomatic
* bone pain
* bone destruction - features of hypercalcaemia
* long bones - pathological fracture
```
spinal metastases:
• vertebral collapse
• spinal cord compression
• nerve root compression
• back pain
```
95
Types of bone metastases
* Lytic bone metastases (most common)
| * sclerotic bone metastases
96
Mechanism of bone destruction in lytic metastases
Osteoclast-mediated, not directly caused by the tumour cells
osteoclasts are stimulated by cytokines from tumour cells
treated with bisphosphonates to prevent osteoclast-mediated bone lysis
97
Mechanism of bone destruction in sclerotic metastases
Metastases, e.g. prostate cancer and breast cancer, stimulate osteoblasts to form new woven bone
reactive new bone formation, induced by tumour cells
98
Which types of cancer cause sclerotic metastases in bone?
* prostatic carcinoma
* breast carcinoma
* carcinoid tumour
99
What types of cancer typically give rise to Solitary bone metastases?
renal and thyroid carcinomas
100
What is the commonest malignant primary bone tumour?
myeloma
101
Myeloma
monoclonal proliferation of plasma cells
• plasmacytoma (solitary)
• multiple myeloma (if multifocal in bone)
Causes punched out sclerotic lesions in bone
Marrow replacement causes pancytopaenia
Bence jones proteins in urine
102
Name 3 benign primary bone tumours
* Osteoid osteoma
* Chondroma
* Giant cell tumour
103
Name 3 malignant primary bone tumours
* Osteosarcoma
* Chondrosarcoma
* Ewing’s tumour
104
Osteoid Osteoma
benign osteoblastic proliferation
common in adolescents
Classical presentation:
• Pain that is worse at night
• relieved by aspirin
• scoliosis
105
Osteosarcoma
malignant bone-forming tumour
age peak = 10-25 years old
affects metaphysis
early lung metastases
usually presents late
106
Paget’s disease
chronic remodelling disorder of the bone
results in abnormal bone architecture
Asymmetrical involvement of individual bones
causes bone pain, deformity and pathological fracture
Can cause deafness if the skull is affected
Increases risk of osteosarcoma
107
Ewing’s sarcoma
Malignant primary bone tumour seen in children
Affects the long bones
Onion skin appearance
very aggressive
108
What is the most common benign bone lesion?
osteochondroma
109
Which genes is rheumatoid arthritis associated with?
HLA-DR4
HLA-DR1
110
Clinical features of RA
Symmetrical synovitis
Preference for small joints of hands and feet
o Pain
o Erythema
o Swelling
• Constitutional symptoms
111
RHEUMATOID FACTOR
Autoantibody against Fc portion of IgG
Usually IgM against IgG
Forms immune complexes with other RF, IgG and complement
These complexes are deposited in synovial fluid, and promote inflammation = type III hypersensitivity
112
ANTI-CCP/ACPA
antibodies to citrullinated peptides (Anti-CCP)
as sensitive & more specific than RF for RA diagnosis
Predictor of worse prognosis, more erosions, resistant disease
Linked with smoking (increases citrullination)
113
X-ray changes found in rheumatoid Arthritis
1) Soft Tissue Swelling
2) Peri-articular osteopenia
3) Joint erosions
4) Loss of joint space (symmetrical)
114
Pharmacological management of RA
Symptomatic
o NSAIDs
o Analgesia etc.
```
Disease Modifying (DMARDs)
o Glucocorticoids (oral, IA, IM)
o MTX/Sulphasalazine/Hydroxychloroquine
o Biologics (anti-TNF, anti-CD20, anti-IL6)
```
115
Which are the most commonly used DMARDs?
* Methotrexate
* Sulphasalazine
* Hydroxychloroquine
DMARDs can be used in monotherapy or combination.
Early and aggressive treatment is key to a better long-term outcome
116
Which DMARD is safe for use in pregnancy?
Sulphasalazine
117
Name 2 Anti-TNF therapies
etanercept
| infliximab
118
When is biologic therapy indicated in RA patients?
can be used in patients who still have high disease activity despite treatment with at least two standard DMARD therapies including methotrexate.
patients on biologic therapy should be warned about increased infection risk and advised to seek medical help promptly at the first sign of infection.
119
Spondylolisthesis
forward slippage of one vertebral body with respect to the one beneath it
pars interarticularis defect
asymptomatic in most
120
What are the three broad causes of back pain?
1) Mechanical - non-specific low back pain (NSLBP)
2) Systemic
o Infection
o Malignancy
o Inflammatory
3) Referred
121
non-specific low back pain
Onset at any age, variable rate
Generally worsens with movement or prolonged standing
Better with rest
Early morning stiffness <30 mins
122
Causes of mechanical back pain
1) Lumbar strain/sprain
2) Degenerative discs/facets joints – Disc prolapse, spinal stenosis
3) Compression fractures
123
What exacerbating factors do you expect with Degenerative disc disease?
worse pain with any increase in abdominal pressure, e.g. with flexion, sitting, sneezing
this is because the problem is anterior
124
What exacerbating factors do you expect with Degenerative facet joint disease?
Increased pain with extension
problem is at the back of the spine, so pain is worse when bending backwards
125
Non-specific LBP management
* Reassurance
* Education, promote self-management ->stay active
* Targeted exercise programme and physiotherapy
* Analgesics as appropriate
126
Disc herniation
Posterior herniation – causes cauda equina/myelopathy (injury to the spinal cord due to severe compression)
Lateral herniation – causes radiculopathy (pinched nerve)
127
Disc prolapse: Herniated nucleus pulposus
May be acute, increased pain with cough
Typically, the pain in the leg is worse than the back pain
• “sciatica” “radiculopathy”
• Leg pain = dermatomal distribution
Straight-leg raising test positive
Reduced reflexes
128
spinal stenosis
Anatomical narrowing of spinal canal
o Congenital or degenerative (osteophytes)
Often presents with “claudication” in legs/calves
Worse walking, rest in flexed position (leaning forward)
Treat conservatively
129
Give 4 causes of referred back pain
AAA
Acute pancreatitis
Peptic ulcer disease
Acute pyelonephritis
130
What does damage to both sides of a joint suggest?
infection
131
Inflammatory back pain (IBP)
Onset <45 years (often teens)
Insidious onset
Early morning stiffness >30mins
Back stiff after rest & improves with movement
May wake in the second half of night with buttock pain
improves with exercise but not with rest
132
Axial Spondyloarthritis
a type of chronic inflammatory arthritis involving the spine and/or sacroiliac joints.
133
Back pain red flags
```
Symptoms:
• New onset age <16 or >50
• Following significant trauma
• Previous malignancy
• Systemic symptoms
• Previous steroid use
• IV drug abuse, HIV or immunosuppressed
• Recent significant infection
• Urinary retention
• Non-mechanical pain (worse at rest “night pain”)
• Thoracic spine pain
```
```
Signs:
• Saddle anaesthesia
• Reduced anal tone
• Hip or knee weakness – suggests cauda equina
• Generalised neurological deficit
• Progressive spinal deformity
```
134
Yellow flags back pain
Remember: ABCDE
Attitudes - towards the current problem.
Beliefs - misguided belief that they have something serious
Compensation - awaiting payment for an accident/ RTA? Less incentive to get better
Diagnosis - Inappropriate communication, patients misunderstanding what is meant
Emotions - depression/ anxiety
Family - either over bearing or under supportive.
135
Ankylosing Spondylitis
diagnosis requires radiographic evidence of sacroiliacitis
136
SLE
Systemic lupus erythematosus
multisystemic autoimmune disease in which autoantibodies are made against a variety of autoantigens
Causes B-cell secretion of pathogenic auto antibodies, causing tissue damage via:
• immune complex formation and deposition
• complement activation
137
When should you suspect SLE?
whenever someone has a multisystem disorder and raised ESR but normal CRP.
If raised CRP, think instead of infection, serositis or arthritis.
138
Presentation of SLE
remitting and relapsing illness of variable presentation
```
typically presents with non-specific constitutional sx:
• malaise
• fatigue
• myalgia
• fever
```
o Cutaneous manifestations
o Arthralgia and arthritis
```
Other features include:
• Lymphadenopathy
• weight loss
• alopecia
• nail-fold infarcts
• non-infective endocarditis
• Raynaud’s
• migraine
• stroke
• retinal exudates
```
139
What happens to complement in SLE?
SLE is a complement consuming disease
complement is consumed in the formation of immune complexes
this results in low C3 and C4
140
Diagnostic criteria for SLE
≥ 4 criteria (≥ 1 clinical and 1 immunological criteria)
OR biopsy proven lupus nephritis with positive ANA or Anti-DNA
Remember: I AM PORN HSDT
```
Immunologic Criteria (6)
I = Immunological disorder
A = ANA/Anti-dsDNA/Antiphospholipid antibodies
```
```
Clinical Criteria (11)
M = Malar Rash
```
```
P = photosensitivity
O = oral ulcers
R= renal disorder
N = Non-erosive Arthritis/Non scarring alopecia/Neurological disorder
```
```
H = Haemolytic anaemia
S = Serositis
D = Discoid rash
T = Thrombocytopenia
```
141
SLE treatment
hydroxychloroquine
belimumab
prednisolone
topical therapies for cutaneous symptoms
142
Why are antinuclear antibodies formed in SLE?
SLE causes activation of the innate/adaptive immune systems
This results in cell death. SLE patients are unable to properly clear the debris, resulting in exposure of nuclear antigens
the body forms antibodies to these.
ANA are not specific to SLE
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Name the autoimmune connective tissue diseases
1) Sjorgen's syndrome
2) SLE
3) Systemic sclerosis
4) Myositis
consider as a differential in unwell patients with multi-organ involvement, especially if there is no evidence of infection
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Myositis
characterised by insidious onset of progressive symmetrical proximal muscle weakness and autoimmune-mediated striated muscle inflammation (myositis), associated with myalgia ± arthralgia.
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Systemic sclerosis
autoimmune disease of the connective tissue.
characterised by thickening of the skin caused by accumulation of collagen, and vascular disease
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Sjogren’s syndrome
* chronic inflammatory autoimmune disorder
| * lymphocytic infiltration and fibrosis of exocrine glands, especially lacrimal and salivary glands
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Sjogren’s syndrome presentation
Decreased tear production (dry eyes, keratoconjunctivitis sicca)
Decreased salivation
Other glands are affected - e.g. vaginal dryness
Systemic signs, e.g. polyarthritis/arthralgia, vasculitis, fatigue.
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Anti-dsDNA
one of several antinuclear antibodies (ANA), a group of antibodies directed against substances found in the nucleus of cells.
primarily associated with SLE
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entheses
sites where the ligaments and tendons attach to the bones
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What can cause back pain to radiate in a “belt” around chest/abdomen?
compression fracture
sudden onset severe pain due tosudden vertebral body collapse
belt around chest is caused by dermatomal radiation of pain
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systemic causes of back pain
1) infection - discitis, osteomyelitis, epidural abscess
2) malignancy
3) inflammatory causes
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Infective discitis: presentation
fever
weightloss
Constant back pain – at rest, night pain
patient may be immunosuppressed
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Most common cause of infective discitis
Staph aureus
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Which gene is associated with spondyloarthritis?
HLA-B27
NB: associated with extra-articular inflammation (uveitis, psoriasis, IBD)
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Vasculitis
Group of conditions characterised by inflammation of the blood vessels
May be a primary disorder (autoimmune) or secondary to other diseases
can involve vessels of any size and can affect any organ system
Presentation depends on the organ involved
We classify and define the vasculitides according to the size of blood vessels involved
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Which is the most common large vessel vasculitis?
giant cell arteritis
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Giant Cell Arteritis
= temporal arteritis
large vessel vasculitis affecting the ageing population
Systemic vasculitis affecting aorta + its major branches.
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Clinical presentation of Giant Cell Arteritis
Temporal headache with tenderness
– Subacute onset
– Constant
– Little relief with analgesics
Visual symptoms
Jaw claudication
Constitutional upset
Symptoms of polymyalgia rheumatica
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Complications of Giant Cell Arteritis
1) irreversible visual loss -> acute ischaemic optic neuropathy. Sudden painless loss of vision
2) CVA -> Obstruction/occlusion of internal carotid §or vertebral arteries
3) large vessel vasculitis -> stenosis/aneurysm
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Clinical examination findings of Giant Cell Arteritis
* Temporal artery asymmetry
* Thickening
* loss of pulsatility
* tenderness
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What is the gold standard investigation for Giant Cell Arteritis?
temporal artery biopsy
considered to be positive if there is interruption of the internal elastic lamina with infiltration of mononuclear cells into the vessel wall.
Multinucleated giant cells are typical
NB: causes skip lesions -> biopsy is negative in many patients with GCA. Length of biopsy is important
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Giant Cell Arteritis: treatment
prednisolone
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Diagnosis of Giant Cell Arteritis
Diagnosis relies upon a typical history (tender headache with associated symptoms) coupled with an elevated acute phase response
temporal artery biopsy to confirm diagnosis
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Henoch-Schönlein Purpura (HSP)
* Small vessel vasculitis
* More common in children
* Male > Females
* Frequently self-limiting illness
present as cutaneous vasculitis in classical distribution
Occasionally triggered by streptococcal sore throat.
* Classic purpuric rash (nonblanching purple papules due to intradermal bleeding)
* Arthralgia/ Arthritis (lower limb) in 75%
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HSP treatment
Often no treatment required
Corticosteroids for certain complications:
• testicular torsion
• GI disease
• occasionally arthritis.
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Causes of cutaneous vasculitis
* Idiopathic
* Drugs
* Infection: HCV, HBV, gonococcus, meningococcus
* Secondary to RA/ CTD/ PBC/ UC
* Malignancy: haematological > solid organ
* Manifestation of ANCA associated vasculitis
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ANCA associated vasculitis
Remember: MEG
group of conditions that share a lot of manifestations:
1) M = Microscopic polyangiitis (MPA)
2) E = EGPA - eosinophilic granulomatosis with polyangiitis (Churg Strauss vasculitis)
3) G = GPA - granulomatosis with polyangiitis (Wegener’s)
associated with significant end organ damage and mortality if untreated
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Granulomatosis with polyangiitis (GPA)
Characterised by granulomatous necrotising inflammatory lesions of the upper and lower respiratory tract and glomerulonephritis
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Antineutrophil cytoplasmic antibodies (ANCA)
Autoantibodies directed against the cytoplasmic constituents of neutrophils and monocytes
should always be tested by 2 methods
1) Indirect immunofluorescence of peripheral blood neutrophils
- cytoplasmic pattern (cANCA) = PR3 antibodies
- perinuclear pattern (pANCA) = MPO antibodies.
2) followed up with specific ELISA tests for specific ANCAs against the most commonly observed antigens = proteinase 3 and myeloperoxidase
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Interpreting ANCA results
cANCA with PR3 very suggestive of GPA
pANCA with strong MPO suggestive of MPA (or EGPA)
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Treatment of ANCA associated vasculitis
Immunosuppression. potency of immunosuppressant agent dictated by severity of presenting illness
Remission Induction - Switch off vasculitis activity
Remission maintenance - Prevent relapse
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Achondroplasia
autosomal dominant
Affected gene is for fibroblast growth factor receptor
Limbs short but trunk normal
Failure of endochondral ossification
In contrast bones that develop from connective tissue (intramembranous ossification) such as the vault of the skull are normal.
Normal intelligence and life span.
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Child onset inflammatory arthritis
Pale, cachexic, red swollen knuckles
Z-shaped due to sitting in a chair for extended periods
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Marfans syndrome
Defect in FBN1 gene encoding for fibrillar a glycoprotein essential for formation and integrity of elastic fibres
unusually tall stature, long arm span, dislocation of lenses of the eye, aortic and mitral valve incompetence
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Osteogenesis imperfecta (brittle bone disease)
Error in type 1 collagen synthesis
Type 1 collagen is most abundant in bone so the principal manifestation is skeletal weakness resulting in deformities and a susceptibility to fracture
Sclerae are blue
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Fibrous dysplasia
Benign disorder of children and young adults - lesions composed of fibrous and bony tissue develop, usually in the ribs, femur, tibia and skull.
Histologically lesions are composed of irregular masses of immature woven bone
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Developmental hip dysplasia
Deformation or misalignment of the hip joint - dislocation or instability
The presence of the spherical femoral head within the acetabulum is critical for stimulating the normal development of the acetabulum
Have a leg drop on one side
Hip has risen up
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Slipped capital femoral epiphysis
ball at the upper end of the femur slips off in a backward direction.
due to weakness of the growth plate.
Most often, it develops during periods of accelerated growth, shortly after the onset of puberty
Deformity can look like fractured neck of femur
- shortened and externally rotated leg
Goal is to prevent avascular necrosis
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What is different between adult inflammatory arthropathy and juvenile idiopathic arthritis?
JIA is more common
Ddx for a single joint is broader
Treatment can be more complicated
Children normally seronegative
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Juvenile idiopathic arthritis
childhood onset
characterised by an inflammatory arthritis that persists for at least 6 weeks
different types of JIA
Commonest rheumatic disease of childhood
Uveitis is a common feature - can result in permanent blindness
should be screened using a slit lamp
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Which chidlhood disease causes a strawberry tongue?
Kawasaki disease = vasculitis
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What blood tests would you do in suspected OA?
FBC
ESR/CRP
RF/Anti-CCP
Calcium/phosphate/ALP
Rule out differentials. Should all be normal, although findings may be abnormal in secondary OA
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OA management
Pain relief – analgesics and anti inflammatory agents
Increasing mobilisation – joint movement and muscle tone may be improved by physiotherapy
Reducing load – weight loss, walking stick
Surgical options – osteotomy, arthrodesis (fusion), joint replacement, excision arthroplasty
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Microscopic/macroscopic changes in OA
fissuing and loss of articular cartilage with eburnation (polishing) of surface
subarticular cyst formation
osteophyte formation at the joint margins
sclerosis (thickening) of subchondral bone
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Histological appearance of cartilage in OA
normal articular cartilage is made up of chondrocytes which manufacture and lie in a matrix of collagens, proteoglycans, and non-collagenous proteins.
Osteoarthritic cartilage is characterised by
- increased water content
- alterations in proteoglycans
- collagen abnormalities
- binding of proteins to hyaluronic acid.
rate of synthesis of DNA, collagen and proteoglycans is increased.
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What changes would you see in the synovium with OA?
detritus synovitis
flakes of bone and cartilage from damaged joint embed in synovium, causing mild villous hyperplasia and chronic inflammation
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causes of Secondary osteoarthritis
```
AVN
Trauma
Paget's disease
intra articular fracture
previous joint sepsis
haemochromatosis
```
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What investigations would you carry out to confirm a diagnosis of RA?
1) FBC + ESR/CRP - low Hb, high ESR
2) Blood film - normochromic normocytic anaemia of chronic disease.
3) Haematinics - depends on anaemia
4) Liver function tests -Normal, except a mildly elevated ALP and possibly GGT. Commonly raised during acute flares of joint disease (acute phase reactants)
5) autoantibodies - ANA/RF/anti-CCP/complement studies.May have RF/anti-ccp
6) immunoglobulins – increased total globulins and IgG and IgA with normal IgM
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Felty’s syndrome
(RA + splenomegaly)
can develop haemolytic anaemia (microcytic)
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X –ray changes in RA
periarticular osteopaenia
periarticular erosions
soft tissue swelling around MCP joints
Late changes:
Ulnar deviation
Subluxation of the joints
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What abnormalities are seen in synovial tissue in RA?
Villous architecture
Synovial lining cell hyperplasia
Fibrin exudation
Marked chronic inflammation with lymphoid aggregates and plasma cells
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Which other organ systems can be affected in RA?
CVS – pericarditis, myocarditis, vasculitis
Resp – pleuritis, pulmonary fibrosis, rheum. nodules
Skin – rheumatoid nodules
Eyes - Sjogren’s
Haem – anaemia, splenomegaly (Felty’s syndrome)
Amyloidosis
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RA management
NSAIDs – reduce and inflammation
DMARDs (disease modifying anti rheumatic drugs)
o Salazopyrin
o Hydroxychloroquine
o Methotrexate
corticosteroids often used as bridging therapy until DMARDs have taken effect (2-3 months)
biologic therapies - infliximab, rituximab
Have to try at least 2 different DMARDs before biologics will be given
Surgical interventions: tendon repair, synovectomy, joint replacement, joint fusion
