Rheumatology Flashcards
1
Q
What are the characteristic features of osteoarthritis?
A
loss of cartilage, disordered remodelling of adjacent bone and associated inflammation.
2
Q
What type of joint does osteoarthritis most commonly affect?
A
Synovial joints
3
Q
What is the pathology of osteoarthritis?
A
It is the degradation of cartilage and remodelling of bone due to an active response of chondrocytes in the articular cartilage and the inflammatory cells surrounding tissues.
The process is mediated by cytokines.
The release of enzymes from these cells break down collagen and proteoglycans destroying the articular cartilage.
The exposure of the underlying subchondral bone results in sclerosis.
This is followed by reactive remodelling changes that lead to the formation of osteophytes and subchondral bone cysts.
Secondary inflammation.
4
Q
What cell has an active response in the osteoarthritis pathology?
A
Chondrocytes in the articular cartilage
5
Q
What type of aetiology does osteoarthritis have?
A
multifactorial aetiology
6
Q
What are the two types of osteoarthritis?
A
Can be primary (no obvious cause and generalised)
Can be secondary (to joint diseases or other conditions e.g obesity or occupational)
7
Q
Name 4 risk factors for developing osteoarthritis?
A
Ageing
Cumulative effect of traumatic insult
Female
Obesity
Being obese is a low grade proinflammatory state producing cytokines
Occupation
Manual labour is associated with OA of the hands
Farming associated with OA of the hips
Football associated with OA of the knees
8
Q
What are the most common joints affected by osteoarthritis?
A
Small joints of the hands
Small joints of the feet
Hip joint
Knee joint
9
Q
What are the symptoms of osteoarthritis?
A
Usually gradual on onset and progressively worse
Joint pain that is exacerbated by exercise and relieved by rest
Rest and night pain in advanced disease
Joint stiffness in the morning
Reduced function and participation restriction (walking and AODL)
10
Q
What exacerbates the pain in patients with osteoarthritis?
A
exercise
pain is relieved with rest
11
Q
What are the signs of osteoarthritis?
A
- Reduced range of movement
- Alteration in gait
- Pain on movement of the joint or at extremes of joint movement
- Joint swelling
- Bony enlargement
- Effusion
- Synovitis
- Periarticular tenderness
- Crepitus
- No systemic features (fever or rash)
- Muscle weakness or wasting around the affected joint
- Bony swelling and deformity due to osteophytes
- Distal interphalangeal joint : Heberden’s nodes
- Proximal interphalangeal joints: Bouchard’s nodes
12
Q
What is a bony swelling and deformity at the distal interphalangeal joint known as ?
A
Heberden’s nodes
13
Q
What is the bony swelling and deformity at the proximal interphalangeal joint known as?
A
Bouchard’s nodes
14
Q
What investigations do you do in osteoarthritis?
A
Bloods
- may be a raised CRP
Plain X-ray
15
Q
What are the diagnostic features you can see on an X-ray in a patient with osteoarthritis?
A
Joint space narrowing Osteophyte formation Subchondral sclerosis Subchondral cysts Abnormalities of bone contour
16
Q
What are the 3 core treatments for osteoarthritis?
A
Patient education
Activity and exercise (improves prognosis and muscle strength and general aerobic fitness)
Weight loss
17
Q
What are the non-pharmacological treatments for osteoarthritis?
A
Core treatments plus.. Physiotherapy Occupational therapy Footwear Orthoses Walking aids (stick, frame)
18
Q
What are the pharmacological treatment options for osteoarthritis?
A
Topical
- NSAIDs (voltarol gel)
- Capsaicin
Oral
- Paracetamol
- NSAIDs
- Opioids
Transdermal patches
- Buprenorphine
- Lignocaine
Intra-articular steroid injections
Only in patients that have no other options
19
Q
What are the surgical treatment options for osteoarthritis?
A
Arthroscopy to wash away loose debris
Osteotomy - bone is cut to shorten it to change its alignment
Arthroplasty
Fusion - used in complicated joints to stop pain
20
Q
When would a patient with osteoarthritis need an arthroplasty?
A
If the patient has uncontrolled pain, particularly at night or patient has a significant limitation of function
21
Q
How long does a joint replacement usually last for?
A
20-22 years
22
Q
When would you fuse joints together in a patient with osteoarthritis?
A
If it is a complicated joint and the pain is really unbearable
23
Q
Define rheumatoid arthritis?
A
A chronic systemic inflammatory autoimmune disease characterized by a symmetrical deforming peripheral polyarthritis affecting the synovial joints
24
Q
What is the pathology of rheumatoid arthritis?
A
- Chemoattractants produced in the joint recruit circulating inflammatory cells
- The inflammatory cells (macrophages, B lymphocytes and T lymphocytes and plasma cells) interact leading to the over production of TNF-alpha
- Generation of new synovial blood vessels force leukocytes into the synovium where they can trigger inflammation
- Synovium proliferates, thickens and grows out over the surface of the cartilage producing a tumour like mass (pannus)
- The pannus of inflamed synovium damages the underlying cartilage by blocking its route for nutrition and by direct effects of cytokines on the chondrocytes
- The cartilage becomes thin and the underlying bone is exposed
- The pannus destroys the articular cartilage and subchondral bone resulting in focal bony erosions
25
Aetiology of rheumatoid arthritis?
Autoimmune disease
Autoantibodies Rheumatoid Factor and anti-cyclic citrullinated peptide
RF is an antibody against the Fc portion of IgG that has a role in modulating the immune response
Cyclic citrullinated peptide is a marker of disease and is not pathogenic
26
What is the antigen that triggers the inflammatory response that causes rheumatoid arthritis?
Unknown!
27
Name 3 risk factors that can increase your likelihood of developing Rheumatoid Arthritis?
- Female (3x more likely to develop than males before menopause)
- Family history
- Genetics (HLA-DR4 and HLA-DRB1 are associated with development of a more severe erosive disease
- Smoking
28
What genes are associated with the development of a more severe rheumatoid arthritis disease?
HLA-DR4 and HLA-DRB1
29
What is the main symptom that suggests rheumatoid arthritis?
Symmetrical swollen, painful and stiff small joints of the hands and feet
30
What are the symptoms of rheumatoid arthritis?
- Symmetrical swollen, painful and stiff small joints of the hands and feet
- Pain is worse in the morning and in the cold
- Morning stiffness can last several hours
- Pain may improve with activity
- Loss of function
- General fatigue or malaise
- Shoulder and elbows may become swollen or stiff
- May be systemic illness (fever, weight loss, fatigue)
31
In a patient with rheumatoid arthritis when is their pain most likely to be worse?
In the morning and in the cold
32
What can relieve the pain experiences in rheumatoid arthritis?
activity
33
What are the early signs of rheumatoid arthritis?
Inflammation, no joint damage
Red, swollen, tender, warm joints
Swollen MCP, PIP or wrist or MTP joints (symmetrical) - usually the DIP is spared!
Tenosynovitis
34
What joint tends to be spared in the rheumatoid arthritis?
Distal interphalangeal joint
35
What are the later signs of rheumatoid arthritis?
Ulnar deviation
Boutonniere and swan-neck deformities of the fingers
Z-deformity of the thumb
36
What is the difference between boutonniere and swan neck deformities of the finger in rheumatoid arthritis?
Boutonniere: PIP in flexion, DIP in hyperextension
Swan neck: PIP in hyperextension, DIP in flexion
37
Name 5 extra-articular manifestations of rheumatoid arthritis?
Eyes
- Dry eyes
- Episcleritis (non-severe mild redness of the eye)
- Scleritis (corneal ulceration - severe pain)
Neurological
- Mild primary sensory peripheral neuropathy
- Entrapment neuropathies (soft tissue swelling due to inflammation at the site where rigid structures contain nerves)
- Cervical instability (usually seen in advanced disease. Erosive process that effects C1-C2 region. Can compress nerve roots)
Haematological
- Lymph nodes may be palable
- Spleen may be enlarged
- Anaemia (normochromic normocytic)
Lungs
- Pleural effusion
- Rheumatoid nodules
Kidneys
- Amyloidosis in advanced RA. Deposits of amyloid protein cause proteinuria and renal impairment
Skin
- Vasculitis
- Small digital infarcts along the nail bed
38
What is needed to diagnose Rheumatoid Arthritis?
Clinical history
- number of joints involved - small vs large
Serology
- Positive Rheumatoid Factor in 80%
- Positive anti-ccp
Bloods
- Raised CRP or ESR
Duration of symptoms
- more than 6 weeks = more likely
39
What does late diagnosis of rheumatoid arthritis increase the risk of?
erosive joint damage
40
What are the non-pharmacological treatment options for rheumatoid arthritis?
Physiotherapy (improve general fitness and encourage regular exercise. Learn exercises for enhancing joint flexibility, muscle strength and managing other functional impairments)
Occupational therapy (it patients have difficulty with any of their everyday activities)
Hand exercise programmes
Consider a tailored strengthening and stretching hand exercise programme for adults with RA with pain and dysfunction of the hands
Podiatry
- May need functional insoles
Psychological interventions
- Relaxation
- Stress Management
41
What are the pharmacological monotherapy treatments used in Rheumatoid Arthritis?
Disease modifying antirheumatic drugs
ORAL METHOTREXATE or leflunomide or sulfasalazine
Alternative: hydroxychloroquine as an alternative for mild disease
42
When should you start a patient who has rheumatoid arthritis on DMARDs ?
Within 3 months of onset of persistent symptoms
43
What is the dual therapy used in a patient with Rheumatoid arthritis?
DMARD + hydroxychloroquine
44
What biological agents are there that you can use in the treatment of rheumatoid arthritis?
TNF-alpha inhibitors
- Infliximab
- Used if methotrexate is contraindicated it can be used as a monotherapy
B-cell depletion
- Rituximab
- Used in combination with methotrexate
- severe RA where TNF-alpha inhibitor has failed
IL-1 and IL-6 inhibition
- Tocilizumab
- In combination methotrexate where TNF-alpha blocker has failed
Inhibition of T cell co-stimulation
- Abatacept
- Patients have not responded to DMARDs or TNF-alpha blocker
45
What are the side effects of DMARDs?
Immunosuppression
- increased susceptibility to infection and neutropenic sepsis
Oral ulcers
Pneumonitis
46
What is the difference in pain between rheumatoid and osteoarthritis?
RA : pain eases with use
| OA: Pain increases with use
47
What is the difference in stiffness between OA and RA?
RA: significant (Over 60 mins), early morning/rest
OA: not prolonged
48
What is the difference in speed of onset of RA and OA?
RA: relatively rapid, over weeks-months
OA: slow progression
49
What is the difference in pattern of joints affected between RA and OA?
RA: small and large joints on BOTH sides of the body
OA: Symptoms often begin on one side of the body and may spread to the other side. Often limited to one set of joints
50
What form of arthritis responds to NSAIDs and what does that suggest?
RA - it is inflammatory
51
what is a crystal?
homogeneous solid in an organised pattern. They consist of ions bonded closely in an ordered, repeating, symmetric arrangement
52
what are the two crystal arthropathies in joints?
Urate (gotut)
Calcium pyrophosphate (pseudogout)
53
What is the pathology of gout?
Uric acid is produced from nucleic acid/purine metabolism
If there is excess uric acid in the blood it combines with sodium to form monosodium urate
These crystals can get deposited in joints and cause inflammation and pain
54
What serum levels can suggest that crystal deposition is likely?
If serum levels rise above 0.36mmol/L there is a risk of crystal deposition
If plasma concentration rises above 0.42mmol/L this is supersaturation and crystal deposition is very likely.
55
What is the key enzyme in the purine metabolism pathway?
xanthine oxidase
56
What are the two different presentations of gout?
Acute attack/ inflammation
| Chronic, long term deposition
57
What are the causes of gout (under excretion of uric acid)
```
Alcohol
Renal impairment
Hypertension
Hypothyroid, hyperparathyroidism
Obesity
Diabetes (insulin resistance)
Drugs
- Low dose aspirin decreases renal excretion
- Diuretics (esp thiazides)
- Cyclosporin
- Ethambutol
```
58
What are the causes of gout (overproduction of uric acid)
```
Hyperlipidemia (metabolic)
Myeloproliferative disease
Psoriasis
Diet
- Alcohol
- Excess meat, shellfish, offal
- Gravy, meat extract
- Yeast extract
- Fructose sweetened drink
```
59
What are the risk factors for developing gout? Including diet.
```
High purine diet
- Shellfish
- Beer
- Red meat
- Liver
- Sugary/fizzy drinks
Kidney disease
Hyperuricaemia
- Affects up to 10% of the population
```
60
Name 3 scenarios that can precipitate an acute attack of gout?
Aggressive introduction of hypouricemic therapy
Alcohol or shellfish binge
Sepsis
MI
Acute severe illness
Sudden cessation of hypouricemic therapy
Trauma
61
What is the clinical presentation of acute gout?
Development of acute pain in a joint which becomes swollen, tender and erythematous and which reaches its crescendo over a 6-12 hour period is highly suggestive of crystal arthropathy
Florid synovitis and swelling and extreme tenderness with overlying erythema. Untreated the attack resolves spontaneously over 5-15 days usually with itching over the skin.
62
What joint is most commonly affected by gout? Name 2 other joints where gout can be?
BIG TOE
ankle/foot
knee/finger
Elbow
Wrist
63
What investigations do you do in gout?
Polarized light microscopy of the crystals in the joint
Bloods: serum urate is normally raised
X-ray
64
What type of crystals are gout crystals?
negatively birefringent urate crystals
65
What do radiographs show in a patient with gout?
Early : soft tissue swelling
| Late : rat bite erosions in the juxta-articular bone (these are irreversible!)
66
Name 3 preventative measures to reduce the likelihood of developing gout?
Lose weight
Avoid prolonged fasts
Avoid drinking excess alcohol
Avoid purine rich meats
67
What is the acute treatment for gout?
```
High dose NSAIDs
Colchicine if NSAIDs are contraindicated
Steroids
Rest and elevate the joint
Ice packs
```
68
What is the long term treatment for gout? Name two examples of these drugs?
Xanthine oxidase inhibitors
Allopurinol
Febuxostat
69
When would a patient need long term treatment for chronic gout?
Used if have had more than 1 attack in the past year, have tophi or have renal stones
70
What is the pathology of pseudogout?
Deposition of calcium pyrophosphate crystals on joint surface causing an acute inflammatory response
71
What may precipitate a pseudogout attack?
```
May be precipitated by
Dehydration
Intercurrent illness
Hyperparathyroidism
Surgery
Direct trauma to the joint
Joint lavage
Blood transfusion
```
However most acute attacks are spontaneous
72
What joints are typically involved in pseudogout?
Typical distribution : Knee > wrist > shoulder > ankle > elbow
73
What is the usual symptom of pseudogout?
Often asymptomatic and is found incidentally on radiology
74
What are the symptoms of acute pseudogout?
Acute monoarticular arthritis - affecting the above joints
Acute joint pain and swelling (milder than gout)
Affected joints are acutely inflamed with swelling, effusion, warmth, tenderness and pain on movement (stiffness)
Resolution in 1-3 weeks
75
What are the symptoms of chronic psuedogout?
Can show destructive changes that resemble osteoarthritis
76
What are the differing features that distinguish pseudogout from osteoarthritis?
The pattern of involvement
Marked inflammatory component
Superimposition of acute attacks
77
What investigations do you do in pseudogout?
Joint X-ray
| Aspiration of the joint fluid
78
What would a joint X-ray show in a joint that had pseudogout?
Shows chondrocalcinosis (deposition of CPPD crystals into fibrous or hyaline cartilage)
79
What would the joint fluid show in a patient with pseudogout
```
Raised WCC (mainly neutrophils)
Intracellular and extracellular weakly positive birefringent rhomboids
```
80
What type of crystals are pseudogout
weakly positive birefringent rhomboids
81
What is the type of treatment for pseudogout?
Symptomatic treatment
82
What is the acute treatment for pseudogout?
Ice packs and temporary rest
Aspiration of the joint
NSAIDs (maybe not in elderly patients)
Physiotherapy
83
What is a potential long term treatment for patients with chronic pseudogout?
Trial of anti-rheumatic treatment e.g methotrexate if continued inflammatory changes
84
What is osteoporosis?
Systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue with consequent increase in bone fragility.
85
What is bone strength determined by?
Bone density
Bone size
Bone quality
86
What is happens to the bone density in osteoporosis?
Bone density declines as we age (faster in post-menopausal women). As ageing continues the bone mass density gets low enough so that bone strength is impaired.
87
What do we measure and use to clinically diagnose osteoporosis?
Bone mineral density
88
What is bone mineral density?
Combination of how much bone you have built while the skeleton is growing and developing and how much bone you have lost over time or due to injury
89
What is the age of peak bone mass?
25-30
90
Why at age 50 to women have a more rapid bone loss than compared to men?
Oestrogen declines during the menopause
91
What happens to bone quality in osteoporosis?
Bone quality decreases. In post-menopausal osteoporosis, the restraining effects of bone turnover by oestrogen are lost so bone turnover increases resulting in a net less of bone.
Additionally in the microarchitecture the horizontal trabeculae connections decrease in number which decreases the strength of the structure the bone is supporting. This leads to less stable bone architecture
92
What happens to the bone size in osteoporosis?
Decreases
93
What are the causes of osteoporosis?
Increasing age + pneumonic :
SHATTERED
```
Steroid use
Hyperthyroidism
Alcohol
Thin (low BMI)
Testosterone decreased
Early menopause
Renal or liver failure
Erosive or inflammatory bone disease (RA)
Dietary (decreased calcium, malabsorption)
```
94
What is the clinical presentation of osteoporosis?
The process that leads to established osteoporosis is asymptomatic and the condition usually presents only after a bone fracture
Be suspicious to low trauma fragility fractures
95
What investigations do you do in osteoporosis?
X-ray
Bone densitometry
DEXA scan
FRAX assessment to assess a fracture risk
96
What does DEXA stand for?
Dual energy X-ray absorptiometry
97
How do we use DEXA scanning to diagnose osteoporosis?
Bone mineral density is compared with that of a young healthy adult
T score is the number of standard deviations the bone mineral density is from the youthful average
98
What is the normal T score on a DEXA Scan
Greater than -1
99
What does a DEXA scan T score of -1 to -2.5 show?
What is the risk?
What advice do you give?
Osteopenia
Risk of later osteoporotic fracture
Offer lifestyle advice
100
What does a DEXA scan T score of -2.5 or worse show?
| What is the management?
Osteoporosis
Offer lifestyle advice and treatment
Repeat DEXA in 2 years
101
What does a T score of -2.5 + a fracture show?
Severe osteoporosis
102
What is the non-pharmacological treatment of osteoporosis?
```
Quit smoking
Reduce alcohol intake
Weight bearing exercise (may increase bone mineral density)
Balance exercises
Calcium and vitamin D rich diet
```
103
What are the pharmacological treatment options for osteoporosis?
Which is first line?
Are they anti-resorptive or anabolic?
FIRST LINE: Bisphosphonates
Hormone replacement therapy
Denosumab
Teriparatide (only one that is anabolic)
104
Name three examples of bisphosphonates?
alendronate, risedronate, ibandronate
105
What is the mechanism of action of bisphosphonates?
Inhibit the enzyme Farnesyl Pyrophosphate Synthase in the HMG-CoA pathway.
Stick to the hydroxyapatite on the bone surface and osteoclast resorbs the bone with the bisphosphonates on it, internalizes and disables itself slowing down bone resorption
106
Pros and cons of using HRT in treatment of osteoporosis?
Pros
- reduces risk of fractures
- stops bone loss
- prevents hot flushes and other menopausal symptoms
Cons
- Increase risk of breast cancer
- stroke
- CVD
107
What is the mechanism of action of Denosumab?
Monoclonal antibody to RANK ligand - slowing down osteoclast activity
108
What is the mechanism of action of teriparatide? What patients would you use this as a treatment?
Anabolic. Works as a PTH analogue and increases bone formation, restoring mechanical strength to the bone
It is expensive and so is reserved for patients with severe disease
109
Name three diseases that fall into the category 'Spondyloarthritises'
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
110
What tissue type is associated with spondyloarthritis?
HLA-B27
111
What is HLA-B27 and where is it expressed in the body?
Does everyone have it?
It is a tissue type with a role in antigen presentation within the immune system.
It is a class I surface antigen on all cells (except RBC)
You are either HLA-B27 positive or negative
112
Does everyone who is HLA-B27 positive develop spondyloarthropathies?
No, the vast majority of people who are B27 positive do not develop these diseases
113
What are the three theories as to why B27 is linked with spondyloarthropathies?
1. Molecular mimicry
- infection induces an immune response. Infectious agent looks like HLA-B27 peptides - generates an autoimmune response against HLA-B27.
2. Mis-folding theory
- unfolded HLA-B27 proteins accumulate in the ER. Proinflammatory stress response chain happens. IL-23 and IL-12 are released activating the pro inflammatory response
3. HLA-B27 heavy chains homodimer hypothesis
- B27 heavy chains dimerize and accumulate in the ER. Initiates a proinflammatory stress response chain
114
What are important therapeutic targets for spondyloarthropathies?
IL-23 and IL-12
115
Are spondyloarthropathies positive or negative for Rheumatoid Factor?
Negative
116
What are the features of spondyloarthritis?
```
SPINEACHE
Sausage digit
Psoriasis
Inflammatory back pain
NSAID (good response)
Enthesitis (inflammation of the site of insertion of tendon or ligament into bone)
Arthritis (spinal or peripheral)
Crohn's or colitis (may be subclinical)
HLA-B27
Eye (iritis)
```
117
What is enthesitis?
inflammation of site of insertion of tendon or ligament into bone
118
Define ankylosis?
abnormal stiffening and immobility of joint due to new bone formation
119
What is the pathology of ankylosing spondylitis?
There is chronic inflammation of the spine, ribs and sacroiliac joints.
Then there is erosive damage repair where fat is lay down in the corners of bone (irreversible)
Then there is new bone formation and bony proliferations due to enthesitis- which can fuse with the above vertebrae in the spine.
In later stages of the disease these can calcify causing bamboo spine
120
Aetiology of ankylosing spondylitis?
Unknown
121
Risk factor for ankylosing spondylitis?
HLA-B27
122
What is the clinical presentation of Ankylosing Spondylitis?
Inflammatory back pain
Progressive loss of spinal movement in all directions and thoracic expansion is decreased
Peripheral enthesitis
Peripheral arthritis
Characteristic spinal abnormalities
123
What are the features of the inflammatory back pain experienced in ankylosing spondylitis?
Gradual onset of lower back pain
Worse at night
Spinal morning stiffness that may be relieved by exercise
Pain may radiate to the hips/buttocks
124
What is usually the first manifestation of ankylosing spondylitis?
Episodic inflammation of the sacroiliac joints (where it starts) in the late teens / early twenties is usually the first manifestation of the disease.
125
What are the common peripheral enthesitis that can present as ankylosing spondylitis?
Achilles tendonitis
Plantar fasciitis
Tibial tuberosity
126
What is the joint involvement in peripheral arthritis that present in 1/3 of patients with ankylosing spondylitis?
Joint involvement is usually asymmetrical
| Involves hips, shoulder girdle, joints of the chest wall and symphysis pubis
127
What are the characteristic spinal abnormalities in patients with ankylosing spondylitis?
```
Loss of lumbar lordosis (normal inward curving of the spine)
Increased kyphosis (rounded back)
Reduced spinal flexion
Vertebral syndesmophytes are characteristic
```
128
Vertebral syndesmophytes are often characteristic of ankylosing spondylitis. What are they?
Bony proliferation due to enthesitis between ligaments and vertebrae. They fuse with the vertebrae above causing ankylosis
Later, in more advanced disease, calcification of ligaments with ankylosis lead to a bamboo spine appearance
129
What investigations do you do in ankylosing spondylitis?
| What do they show?
MRI
- Detection of active inflammation (bone marrow oedema)
- Shows destructive changes
- Sacroiliitis (one or both sacroiliac joints becomes inflamed)
- Erosions
- Sclerosis
- Ankylosis
X-ray
- Can show sacroiliac joint space narrowing or widening, sclerosis, erosions and fusion
130
What is the diagnostic criteria for ankylosing spondylitis in a patient who has had 3 or more months of back pain and age of onset is less than 45?
Sacroiliitis on imaging + 1 or more SpA feature
| HLA-B27 + 2 or more SpA features
131
What is the treatment for ankylosing spondylitis?
Exercise for backache
Intense exercise regimes
Specialist physiotherapist
Maintain posture and mobility
NSAIDs
Usually relieve symptoms within 48 hours and may slow radiographic progress
TNF-alpha blockers
Etanercept, adalimumab
Severe disease
Local steroid injections
Surgery
Hip replacement
Rarely : spinal osteotomy
132
Name 2 TNF-alpha blockers that can be used in the treatment of ankylosing spondylitis?
Etanercept, adalimumab
133
Ankylosing spondylitis is associated with an increased risk of what other disease? What could you give to minimise this risk
There is an increased risk of osteoporitic fractures so consider bisphosphonates
134
What is psoriatic arthritis? What patients can develop this condition?
Chronic inflammatory disease of the joints and the places where tendons and ligaments connect to bone. The immune system creates inflammation that can lead to swelling, pain, fatigue and stiffness in the joints.
Occurs in 10-40% of people with psoriasis but it can develop without having psoriasis!
135
Name 2 risk factors of psoriatic arthritis?
Associated with HLA-B27
Risk factors: history of psoriasis, have psoriasis
136
What are the symptoms of psoriatic arthritis?
Joint stiffness
Pain and swelling
Tenderness of the joints and surrounding ligaments and tendons
137
What are the 5 patterns of disease of psoriatic arthritis
Symmetrical polyarthritis of small joints
Distal interphalangeal joints only
Most typical. Often with adjacent nail dystrophy
Asymmetrical large joint oligoarthritis (2-4 joints)
Axial (spinal)
Psoriatic arthritis mutilans
138
What is the characteristic appearance does psoriatic arthritis mutilans?
Resorption of the terminal phalanx, giving a telescopic, shortened digit appearance
139
What is the most common pattern of psoriatic arthritis disease?
DIP joints involvement only
140
Where are hidden sites for psoriasis?
behind/inside the ear, scalp, pitting in nails or onycholysis (nail lifts off the nail bed and looks brittle and flaky), umbilicus, penile psoriasis
141
What sign may you see on radiology in a patient with psoriatic arthritis?
Erosive changes with pencil in a cup deformity in severe cases
142
What is the treatment options for psoriatic arthritis?
NSAIDs to relieve MSK symptoms
Early intervention with DMARDs
- Methotrexate
- Leflunomide
Anti-TNF drugs
- Etanercept
- Adalimumab
IL-12 and IL-23 blockers
- Ustekinumab
143
What is reactive arthritis?
Sterile inflammation of the synovial membrane, tendons, fascia triggered by an infection at a distant site
144
Aetiology of reactive arthritis?
Autoimmune response to infection elsewhere in the body
Gut associated infections
Salmonella
Shigella
Yersinia
STIs
Chlamydia
145
What is the characteristic triad of symptoms associated with reactive arthritis?
```
Arthritis
- Typically 2 - 14 days post infection
- Pain and inflammation in the joint
Conjunctivitis
Sterile urethritis
```
146
Aside from the triad, what other symptoms are present in reactive arthritis?
Iritis
Keratoderma blennorrhagica (brown, raised plaques on the soles and palms)
Circinate balanitis (painless penile secretion due to chlamydia)
Mouth ulcers
Enthesitis
147
What investigations do you do in reactive arthritis?
```
Inflammatory markers
- Increased ESR and CRP
Stool culture if there is diarrhoea
Infectious serology
Aspirate joint to exclude infection or crystals
Contact tracing if necessary (chlamydia)
```
148
What is the treatment for reactive arthritis?
Splint the affected joints acutely
NSAIDs or local steroid injections
149
What is septic arthritis ?
The invasion of a joint by an infectious agent resulting in joint inflammation.
150
What is the most frequent pathogen responsible for septic arthritis?
Staph aureus
151
Name 3 organisms that can cause septic arthritis?
```
Staph aureus
Streptococci - Gp A (beta haemolytic)
Neisseria gonorrhoea
Gram negative bacilli
- E.coli
- pseudomonas aeruginosa
```
152
What are 3 risk factors that increase your likelihood for developing septic arthritis?
```
Increasing age
IVDU
Diabetes
Prior joint damage
- Rheumatoid arthritis
-Gout
-Systemic connective tissue disorder
Joint surgery
Hip or knee prosthesis
Immunodeficiency
Immunosuppression
Chronic renal failure
```
153
Clinical presentation of septic arthritis?
What are the majority of cases?
Painful, red, hot swollen joint
Pain on active or passive movement
Fever
90% of cases are monoarthritis
154
What joints does septic arthritis tend to affect?
Affects mainly Knee > hip > shoulder
155
What is the investigation in septic arthritis?
Urgent joint aspiration for synovial fluid microscopy and culture
Must be done with patient off antibiotics for 2 weeks at least
Blood cultures
156
What is the treatment for septic arthritis?
Antibiotics guided by the results of the aspiration
Can start empirical IV antibiotics until sensitivities are known
Long course antibiotics
At least 6 weeks
Flucloxicillin
Joint wash out / repeat aspiration until there is no recurrent effusion
Rest/splint/physiotherapy
Analgesia
Stop any immunosuppression temporarily if you can
157
Name three techniques used to prevent infection in joint prosthesis surgery?
- Barrier between surgical and anaesthetic team
- Aseptic techniques
- Cement used has antibiotics in
- Give patients systemic antibiotics as prophylaxis (usually gentamicin)
158
What is the presentation of an infected joint prosthesis?
- Scar can be red and hot and swollen
- Pus
- Most of time presentation is subtle and can be difficult to make a diagnosis
159
What features on an X-ray may suggest that the joint prosthesis is infected?
features suggestive of infection
- periosteum is fluffy around the joint replacement
- lytic areas
Irritable joint
160
What may the inflammatory markers be like in an infected prosthetic joint?
Increased ESR and CRP
161
What are the treatment options for an infected prosthetic joint?
1. Antibiotic suppression (patients that are unfit for surgery)
2. Debridement and retention of prosthesis (do when infection is acute)
3. Excision arthroplasty (take out the infected joint with no plan to put in a replacement)
4. One stage exchange arthroplasty (take out the old joint and replace with new one straight away)
5. Two stage exchange arthroplasy (take the joint out and leave it for a while and then put it back)
6. Amputation
162
What is osteomyelitis?
Infection localized to the bone
163
What is the difference between acute and chronic osteomyelitis?
Acute: associated with inflammatory bone changes caused by pathogenic bacteria
Chronic: involves bone necrosis
164
What is the routes of transmission that cause osteomyelitis. Who is most likely to develop which OM?
Children mainly have acute haematogenous osteomyelitis
Adults mainly have contiguous osteomyelitis
165
What is the pathology of haematogenous osteomyelitis in children?
In long bone (children) the metaphysis is very metabolically active so has a large flow of blood.
Vasculature penetrates the midshaft and then goes to either end of the long bone to form vascular loops in the metaphysis.
In the metaphysis the blood flow is slower and there are no endothelial basement membranes. Capillaries also lack phagocytic lining cells. These factors allow transmission of bacteria from the blood to this site allowing the growth of microorganisms.
166
Adults can get haematogenous osteomyelitis as well, where are they most likely to get this and why?
Can get this type of transmission in adults but it is in the vertebrae as they become more vascular with age
167
What is contiguous spread that causes osteomyelitis mainly in adults?
Spread of infection from adjacent soft tissues and joints to bone.
168
What are 3 risk factors that increase a persons risk for developing osteomyelitis?
```
Vascular supply
- Arterial disease
- Diabetes
- Sickle Cell
Pre-existing bone/joint problems
Immune deficiency / immunosuppression
Behavioural
Increasing the risk of trauma
```
169
What are the causative organisms of osteomyelitis?
```
Staphylococcus aureus
MRSA
Coagulase negative staphylococci
Aerobic Gram-negative bacilli
In the immunocompromised
- Fungi
- Mycobacterium tuberculosis
Sickle cell
- Salmonella
```
170
What are the symptoms of osteomyelitis?
Onset over several days
Dull pain at the site of infection
May be aggravated by movement
171
What are the signs of osteomyelitis?
Systemic
- Fever
- Rigors
- Sweats
- Malaise
Local
Acute : tenderness, warmth, erythema, swelling
Chronic : swelling, tenderness, deep/large ulcers that fail to heal despite several weeks treatment, non-healing fractures
172
What investigations do you do in osteomyelitis?
Labs
Acute : Increased WCC, Increased ESR and CRP
Chronic : Can all be normal
X-rays
MRI
Bone biopsy
Blood cultures
173
What is the benefit of using MRI compared to X-rays in diagnosing osteomyelitis?
X-rays have poor sensitivity and specificity in early osteomyelitis whereas MRI can show marrow oedema after 3-5 days
174
What may X-rays show in chronic osteomyelitis (name 2 things) ?
```
Cortical erosions
Periosteal reaction
Mixed lucency
Sclerosis
Sequestra (dead bone tissue formed within a diseases or injured bone)
Soft tissue swelling
```
175
What does a bone biopsy of a patient with osteomyelitis show?
Histology shows inflammatory exudate in the marrow
| Shows osteonecrosis
176
What is the treatment options for osteomyelitis?
Surgical
Debridement
Replacement or removal of bone
Antimicrobial
Start broad spectrum empirical therapy : FLUCLOXACILLIN
Then later tailor the antibiotics to the culture and sensitivities
Prolonged duration of antimicrobials
Need to consider the bone penetration of the drugs
177
What antibiotic do you start patients with osteomyelitis on?
Flucloxacillin
178
What is Systemic Lupus Erythematosus ?
Multisystemic autoimmune disease.
179
What is the pathology of SLE?
1. Cells die by apoptosis and cellular remnants (e.g DNA, histones that are normally hidden from the immune system) appear on the cell surface as small blebs.
2. In SLE the removal of blebs is inefficient
3. Blebs are transferred to the lymphoid tissue where are taken up to become an antigen presenting cell
4. Self-antigens from blebs are presented to T cells which stimulate B cells to produce autoantibodies directed against the antigens
5. These autoantibodies either form circulating complexes or deposit by binding directly to tissues
6. Activation of complement and influx of neutrophils → inflammation
7. Abnormal cytokine production → increased IL-10 and interferon alpha
8. High activity of inflammation
180
What is the cause of SLE?
unknown
181
What are the genetic associations in SLE?
HLA-DR2
| HLA-DR3
182
What are the symptoms of SLE? What organs are involved?
```
Fatigue
Malaise
Arthritis
- Symmetrical
- Less proliferative than rheumatoid arthritis
- Can be deforming
- Non-erosive
- 90% of cases
Mouth ulcers (v common)
```
```
SKIN
Butterfly rash - acute
Discoid rash - chronic
Can have photosensitive rashes
Alopecia
Raynaud’s phenomenon
```
LUNG
Recurrent pleural effusions
KIDNEY
Glomerulonephritis with persistent proteinuria
CNS
Depression
Epilepsy
Seizures (with no causative agent)
```
EYES
Retinal vasculitis
Episcleritis
Conjunctivitis
Sjogren’s
```
```
Other
Weight loss
Arterial thrombosis
Anaemia
Thrombocytopenia
Neutropenia
Lymphopenia
```
183
What tests do you do in SLE?
Immunology
Inflammatory markers
Screening for major organ involvement
Complement
184
What immunological markers are you looking for in a patient with SLE?
Positive antinuclear antibody
High anti-dsDNA is highly specific
Extractable nuclear antigen may be positive
Antiphospholipid antibodies may be positive
185
What is the treatment for SLE?
Patient education and support
UV protection
Hydroxychloroquine
Topical steroids for skin flares (rashes)
186
What is the treatment for severe SLE?
```
High dose prednisolone
Cytotoxic drugs
- Azathioprine
- Cyclophosphamide
- Ciclosporin
- Mycophenolate
```
Anticoagulants for antiphospholipid syndrome
Biological therapies
- Rituximab
- Belimumab
187
What is antiphospholipid syndrome?
Body’s immune system produces abnormal antiphospholipid antibodies.
Immune system produces these that mistakenly bind to the phospholipid surface on blood cells and endothelium.
Causes the blood to clot more easily.
188
Clinical presentation of antiphospholipid syndrome?
```
Thrombosis
Livedo reticularis - lace like purplish discolouration of the skin
Miscarriage (recurrent)
Ischaemic stroke
Thrombocytopenia
```
189
Treatment of antiphospholipid syndrome?
```
Anticoagulant (warfarin, low dose aspirin, heparin)
Don't smoke
Eat a healthy and balanced diet
Regular exercise
Maintain a healthy body weight
```
190
What can cause bone pain?
Myeloma
Lymphoma
Primary bone tumours
Secondary bony metastases
191
Name 4 malignant primary bone tumours?
Osteosarcoma
Ewing's sarcoma
Fibrosarcomas
Chondrosarcoma
192
What are the 5 most common tumours that form bony mets?
```
Breast
Lung
Prostate
Kidney
Thyroid
```
193
What are the red flag signs in bone tumours?
```
Rest pain
Night pain
Lump present
- Tender
- Enlarging
- Deep to fascia
- Above 5cm in diameter
Loss of function
Neurological symptoms
Unwell/weight loss
```
194
What are three special signs that you may be able to see on an X-ray in a patient with bone tumour?
Codman's triangle
Sunburst appearance
Onion skin appearance
195
What investigations can you do in a patient who presents with a bony mass?
```
Blood tests (FBC, U&Es, Ca2+, ALP (usually raised))
Plain X-rays
- looks for definition, bone density, periosteal reaction
Ultrasound
- Assessing soft tissue masses
CT Scan
- does 3D construction which can help plan plan resection
- also used for staging
MRI
- Soft tissue involvement of bony mass
- Skip lesions
Bone scan
Biopsy
```
196
What is Codman's triangle?
triangular area of new subperiosteal bone that is created when a lesion, often a tumour, raises the periosteum away from bone
197
What is a sunburst appearance on X-ray?
Occurs when the lesion grows too fast and the periosteum does not have enough time to lay down a new layer
198
What is an onion skin appearance on X-ray?
multiple concentric parallel layers of new bone adjacent to the cortex. Thought to be due to periods of variable growth
199
These are the prefixes, who would each tumour relate to?
1. Osteo
2. Chondro
3. Rhabdomyo
4. Lipo
1. bone
2. cartilage
3. skeletal muscle
4. fat
200
These are suffixes, what does each one mean?
1. ..oma
2. ...sarcoma
3. ..carcinoma
4. ..blastoma
1. benign
2. malignant connective tissue
3. malignant epithelial/endothelial tumour
4. malignant tumour of embryonic cells
201
What is the pathology of osteosarcoma?
Spindle cell neoplasms that produce osteoid (the unmineralized organic compound of bone)
202
What are osteosarcomas associated with?
Associated with p53 mutation
203
Name the three places most likely for osteosarcoma to present?
Knee
Proximal humerus
Distal femur
204
How may an osteosarcoma present?
Pulmonary metastases in 10-20%
High-grade is a relatively painless tumour.
Lump present
205
What would the X-ray show of an osteosarcoma?
Codman’s triangle
| Sunburst appearance
206
Treatment for osteosarcoma?
Multi-agent chemotherapy pre-operative 8-12 weeks
Limb salvage surgery
207
What cells does Ewing's sarcoma arise from?
Arises from neural crest cells
208
Where does Ewing's sarcoma commonly present?
Femur
| (pelvis, distal tibia, proximal humerus_
209
What is Ewing's sarcoma associated with?
Banded translocation t(11;22)
210
What is the average age of onset for Ewing's sarcoma>
15
211
What are the symptoms of Ewing's sarcoma?
```
Painful swelling
Redness in the area surrounding the tumour
Malaise
Anorexia
Weight loss
Fever
Paralysis
Numbness in the affected limb
```
212
What type of lesion is Ewing's sarcoma usually?
diaphyseal lesion and presents with a mass/swelling in the long bones
213
What would the X-ray show in a patient with Ewing's sarcoma?
Onion skin appearance
| Codman's triangle, sunburst appearance
214
What would the bone biopsy of a Ewing's sarcoma tumour show?
Monotonous blue cell tumour
Indistinct cell borders
No matrix production by the tumour cells
215
What is the treatment for Ewing's sarcoma?
Chemotherapy
Radiotherapy
Surgical excision / reconstruction
216
What is a chondrosarcoma?
Cancer of the cartilage
| Most common adult sarcoma
217
What is the presentation of a chondrosarcoma?
Dull deep pain
| Affected area is swollen and tender
218
Where do chondrosarcomas typically present?
Pelvis
219
What is the treatment for chondrosarcoma?
Surgery and adjuvant chemotherapy
220
What are the symptoms of bony metastases?
Bone pain
| Systemic symptoms such as malaise, pyrexia, anorexia, weight loss
221
What investigations do you do in bony metastases? What do they show?
Skeletal isotope scan
- Show bony mets before radiological changes occur
X-rays
- May show mets as osteolytic areas with bony destruction
- Osteosclerotic mets (increased bone density) are characteristic of prostate carcinoma
222
What are the treatment options for bony metastases?
Analgesics and anti-inflammatory drugs
Local radiotherapy to bone mets relieves pain and reduces risk of fracture
Some may respond to chemotherapy
Some tumours are hormone dependent and may respond to hormonal therapy
Bisphosphonates help symptomatically
223
What are 5 risk factors that may increase likelihood of developing fibromyalgia?
```
Depression
Anxiety
Stress
Dissatisfaction at work
Middle aged
Low income
Divorced
Low educational status
```
224
What are the symptoms of fibromyalgia?
Chronic widespread pain associated with unrefreshing sleep and tiredness
Chronic pain at multiple sites and widespread
- Lower back pain with/without radiation to the buttocks and legs and pain in the neck and across shoulders
```
Fatigue
Sleep disturbance
Morning stiffness
Problems with cognition
- Poor concentration
Fluctuations in weight
Anxiety and depression
```
225
What makes the symptoms of fibromyalgia worse?
cold weather
humid weather
stress
226
What investigations do you in fibromyalgia?
```
Bloods will all be normal
FBC
ESR
CRP
CK
TFTs
Ca2+
```
Pain at 11 out of 18 tender points on digital palpation (neck, back, elbows, hips, lower back, knees)
Full social, personal, family and psychological history should be taken.
227
how is fibromyalgia diagnose?
diagnosed after other diseases have been excluded
228
What is the non-pharmacological treatment for fibromyalgia?
Educate the patient and family
```
Exercise programmes
Aerobic exercise
Strength training
Tailored programmes to the individual
Cognitive behavioural therapy
```
Relaxation, rehabilitation, physio and psychological support
229
What is the pharmacological treatment for fibromyalgia?
Paracetamol, weak opioids, tramadol
Venlafaxine - antidepressants
Pregabalin - small benefit in reducing pain and sleep problems
230
What can is the pathology of mechanical back pain?
Spinal movement occurs at the disc and the posterior facet joints - stability is normally achieved by a complex mechanism of spinal ligaments and muscles.
Any of these structures may be a source of pain
231
Name 3 causes of mechanical lower back pain?
```
Lumbar disc prolapse
Osteoarthritis
Fractures
Spondylolisthesis
Heavy manual handling
Stooping and twisting whilst lifting
Exposure to whole body vibration
```
232
Name 3 risk factors for mechanical back pain?
Risk Factors
Psychosocial distress
Smoking and dissatisfaction with work
```
Risk factors for recurrent back pain
Female
Increasing age
Pre-existing widespread chronic pain
Psychosocial factors (high levels of distress, poor self-rated health)
```
233
What are the symptoms of mechanical back pain?
Back is stiff and scoliosis may be present when the patient is standing
Muscular spasm is visible and palpable and causes local pain and tenderness
Pain is often unilateral and helped by rest
Episodes are generally short lived and self-limiting
Sudden onset
Pain is worse in the evening
Morning stiffness is absent
Exercise aggravates pain
234
What are the red flag signs for serious spinal pathology?
```
Age of onset is less than 20 or over 55
Violent trauma (fall, RTC)
Constant-progressive, non-mechanical back pain
Thoracic pain
Systemic steroids, drug abuse, HIV
Systemically unwell, weight loss
Widespread neurology
Persisting severe restriction of lumbar flexion
Structural deformity
```
235
What investigations do you do in mechanical back pain?
Spinal X-rays are only used if a red flag sign occurs
MRI
Bone scans
236
What is the treatment for mechanical back pain?
Analgesic - paracetamol, NSAIDs
Physiotherapy, back muscle training regimens and manipulation
Acupuncture
AVOID excessive rest
Re-education in lifting and exercises to prevent further attacks of pain
Comfortable sleeping position
237
What is osteomalacia?
Poor bone mineralisation after the fusion of the epiphyses in an adult leading to soft bone due to the lack of Ca2+.
238
What is the aetiology of osteomalacia?
```
Hypophosphatemia
Vitamin D deficiency
Renal disease
Drug induced
Liver disease
Tumour induced
```
239
How can Hypophosphatemia lead to osteomalacia?
Due to hyperparathyroidism
Excess release of PTH results in decreased absorption of phosphate in the kidneys resulting in more excretion in the urine in response to a decreased Ca2+ absorption
240
How may someone be vitamin D deficient?
Malabsorption
Since vitamin D is fat soluble, may be due to GI disease
Poor diet
Lack of sunlight
241
How can renal disease cause osteomalacia?
Renal failure means that there is inadequate conversion of 25-hydroxyvitamin D to 1,24-hydroxyvitamin D
242
What are the symptoms of osteomalacia?
Muscle weakness
Waddling gait
Difficulting climbing stairs
Difficulting getting out of a chair
Bone pain and tenderness
Fractures
Particularly of the femoral neck
243
What tests do you do in osteomalacia?
Bloods
Biopsy
X-rays
244
What do the blood tests show in a patient with osteomalacia?
```
Low Ca2+
Low phosphate
Raised ALP
Elevated PTH
Low 25-hydroxyvitamin D
```
245
What does the bone biopsy show in a patient with osteomalacia?
incomplete mineralisation
246
What does the X-ray show in a patient with osteomalacia?
Shows defective mineralisation
Looser’s pseudofractures/zones
- Low density bands extending from the cortex inwards in the shafts of the long bones
247
What is the treatment for osteomalacia where the cause is...
1. lack of dietary vitamin D?
2. lack of vitamin D caused by malapsorption?
3. Renal disease
1. Calcium D3 forte
2. Oral ergocalciferol
3. Alfacidol
248
What are the vasculitides?
inflammatory disorders of the blood vessel.
Inflammation and necrosis of the blood vessel walls with subsequent impaired blood flow
- vessel wall destruction
- endothelial injury
249
How are vasculitide diseases classified?
Size of the blood vessel
| Presence or absence of anti-neutrophil cytoplasmic antibodies (ANCA)
250
What vessels are classified as large vessels in vasculitis?
Branches of the aorta
- common carotid
- subclavian
- pulmonary
- axillary
- brachial
- renal
- iliac
- femoral
251
What vessels are medium size in vasculitis?
Medium and small sized arteries and arterioles
252
What vessels are small in vasculitis?
```
small arteries
small arterioles
venules
capillaries
tend to be ANCA positive
```
253
What conditions are associated with secondary vasculitus?
```
Subacute infective endocarditis
Vasculitis with rheumatoid arthritis
SLE
Scleroderma
Polymyositis
Good pasture syndrome and IBC (crohn's and UC)
```
254
What is the pathology of giant cell arteritis?
Inflammatory granulomatous arteries of large cerebral arteries as well as other large vessels (e.g aorta) which occurs in association with polymyalgia rheumatica in 50% of cases
Arteries become inflamed, thickened and can obstruct blood flow.
Activation of dendritic cells in the adventitia
Recruitment and activation of T cells
Recruitment of CD8+ cells and monocytes
Vascular damage and remodelling
255
What arteries are affected in giant cell arteritis?
Cerebral
| Commonly temporal arteries
256
What are the symptoms of giant cell arteritis?
Symptoms
Headache that is : new, abrupt, unilateral and temporal pulsating
Temporal artery and scalp tenderness
Tongue/jaw claudication
Indicates a high risk of ischaemic complications
Visual disturbances
Amaurosis fugax
Diplopia
SUDDEN UNILATERAL BLINDNESS: medical emergency that needs to be treated ASAP. Optic disc is pale/swollen
```
Extracranial symptoms
Malaise
Myalgia
Dyspnea
Weight loss
Morning stiffness
Unequal or weak pulses
```
257
What are the signs of giant cell arteritis?
Temporal arteries may be prominent, beaded, tender and pulseless
Fever
258
What are the complications of giant cell arteritis?
Stroke
| Visual loss
259
What tests do you do in giant cell arteritis?
Blood tests
Temporal artery biopsy (take a large sample as skip lesions occur)
Ultrasound
PET-CT scan
260
What are the blood results in a patient with GCA?
```
ESR and CRP are high
High platelets
High ALP
Low Hb
ANCA negative
```
261
What are the histological features of the temporal artery biopsy ?
Cellular infiltrates of CD4+ T lymphocytes, macrophages and giant cells in the vessel wall
Granulomatous inflammation of the intima and media
Breaking up of the elastic lamina
262
What is the treatment for GCA?
Start prednisolone immediately
- Stops vision loss
- High dose
- Gradual reduction of steroids over 12-18 months. Reduce once symptoms have resolved and ESR has decreased.
Give GI and bone protection
- Lansoprazole
- Alendronate
- Calcium
- Vitamin D
263
If you cannot wean a patient with GCA off glucocorticoids what is the next treatment option?
If failure to wean of glucocorticoids
DMARDs
Tocilizumab
264
What are three key conditions of ANCA associated vasculitis?
Granulomatosis with polyangiitis (PR3 ANCA pattern)
Eosinophilic granulomatosis with polyangiitis
Microscopic polyangiitis (MPO-ANCA pattern)
265
What vessels do ANCA associated vasculitis affect?
Small
266
Pathology of ANCA associated vasculitis
Anti-neutrophil cytoplasmic antibodies can activate primed circulating neutrophils causing them to enter the vessel wall and cause fibrin deposition
267
Symptoms of ANCA associated vasculitis?
```
ENT symptoms
Epistaxis
Crusts
Stuffiness
Hearing loss
Hoarseness
Stridor
```
```
Iritis
Cough
Rash (red dots on fingers)
Numbness, tingling, foot/wrist drop
Joint pain, swelling
- Asymmetric polyarthritis
```
268
What investigations do you do in ANCA associated vasculitis?
```
ANCA testing
Tissue biopsy
Assessment of organ involved
CT thorax (abdo/pelvis - exclude malignancy, look for lung nodules)
Urine protein/creatinine ratio
CT head/sinuses/neurophysiology
Bony erosions
Mononeuritis multiplex
```
269
What is the treatment for ANCA associated vasculitis?
Induction into remission
Glucocorticoids
Cyclophosphamide OR Rituximab
Plasma exchange if the patient has pulmonary haemorrhage or severe renal disease
Maintenance of remission
DMARDs
Taper glucocorticoid
270
what is acute vertebral disc prolapse often caused by?
strenuous activity
271
Symptoms of acute vertebral disc prolapse
Sudden onset of back pain (usually lumbar region)
Pain is aggravated by movement
Muscle spasm leads to a sideways tilt when standing
Radiation of pain and clinical findings depend on the disc
272
What are the features of a root lesion at S1?
(buttock pain down back of thigh to ankle/foot. Loss of ankle jerk reflex)
273
What are the features of a root lesion at L4?
(pain across knee to medial malleolus. Lost knee jerk reflex)
274
What are the features of a root lesion at L5?
L5 (pain from buttock to lateral aspect of leg and top of foot)
275
Investigations in acute vertebral disc degeneration?
X-ray
| MRI in surgery is being considered
276
Treatment of acute vertebral disc degeneration?
Bed rest on a firm mattress
Analgesia
In severe cases - epidural corticosteroid injection
Surgery only if severe or increasing neurological symptoms
Physiotherapy in the recovery phase
277
What is chronic vertebral disc degeneration associated with?
Symptoms?
Treatment?
degenerative changes in the lower lumbar discs and facet joints
Mechanical pain
Sciatic radiation may occur
Pain is long-standing
NSAIDs, physiotherapy and weight loss can be helpful
278
What is the pathology of Paget's disease?
Increased bone turnover associated with increased numbers of osteoblasts and osteoclasts
Bone remodelling, bone enlargement, deformity and weakness
Increased bone mass but the bone is disordered and weak
279
Symptoms of Paget's disease?
Where does it typically present?
Asymptomatic in 70%
Dull, boring pain
Bony enlargement and deformity
```
Typically of
Pelvis
Lumbar spin
Skull
Femur
Tibia
```
280
Complications of Paget's disease?
```
Pathological fracture
Osteoarthritis
Increased Ca2+
Nerve compression due to bone overgrowth (deafness)
Osteosarcoma
```
281
investigations in Paget's disease?
X-ray
| Bloods
282
what does the X-ray of a patient with Paget's disease show?
Localized enlargement of bone
Patchy cortical thickness with sclerosis
Osteolysis
Deformity
283
Treatment for Paget's disease?
Analgesia
Alendronic acid may be tried to reduce pain and / or deformity
284
What complications can occur with a fracture?
```
Nerve injury
Damage to blood supply
Contamination
Compartment syndrome
Fat embolism
Shock
Crush syndrome
PE
Pneumonia
```
285
Why does crush syndrome cause kidney failure?
Myoglobin is released that blocks the kidneys
286
What are late complications of a fracture?
```
Delayed union
Non-union
Mal-union
Avascular necrosis
Arthritis
Osteomyelitis
```
287
What can increase a person's risk of delayed union/non-union of a fracture
Smoker
Diabetic
Steroids
288
What is the blood supply to the femur
comes from the medial femoral circumflex artery
| Supply comes distal and goes proximal
289
What 2 fractures are usually associated with avascular necrosis?
hip and scaphoid
290
what is the presentation of a femoral fracture?
Externally rotated and short leg
groin pain
inability to weight bare
pain on axial loading
291
Management of a femoral fracture
Morphine
Regional nerve block
If intracapsular - surgical may need a hemi or total hip replacement
292
What is compartment syndrome?
There is damage to the blood supply which causes veins to collapse to blood enters the compartment. The fascia means that blood continues to build up in the compartment and compresses the nerves
293
What are the features of compartment syndrome?
Pain that is disproportionate to injury - passive stretching of the muscle in the calf makes symptoms worse
```
Pain
Pallor
Perishingly cold
Paralysis
Pulselessness
```
294
Treatment of compartment syndrome?
Fasciotomy
