Rheumatology Flashcards
(436 cards)
1
Q
Define rheumatology
A
Medical management of musculoskeletal disease
2
Q
Define inflammation
A
Reaction of the micro-circulation that results in the movement of fluid and WBC’s into the extra-vascular tissue which causes the release of pro-inflammatory cytokines
3
Q
What are the 4 pillars of inflammation
A
Red (rubor)
Pain (Dolor)
Hot (Calor)
Swollen (Tumor)
4
Q
How might inflammation present in the joints
A
Hot, painful red and swollen joint
Stiffness
Poor mobility and function
Deformity
5
Q
What are the characteristics of an inflammatory rheumatological disease
A
Pain eases with use
Stiffness (Significant >60mins and early morning and at rest)
Swelling
Hot and red
Young, people with psoriasis and family history commonly affected
Joint distribution is commonly in hands and feet
Responds to NSAIDs
6
Q
What are the characteristics of a degenerative rheumatological disease
A
Pain increases with use
Stiffness that is not prolonged <30 mins and occurs in morning and evening
Swelling
Not clinically inflamed
Older patients with prior occupation or sport affected
less convincing response to NSAIDs
7
Q
Where does rheumatoid arthritis most commonly affect
A
Synovial joints
8
Q
What are the some of the characteristic signs of rheumatoid arthritis
A
Ulnar drift
Polyarthritis
Swan neck deformity
Erosion on X-ray
9
Q
Where does nodal oestoarthritis commonly affect
A
begins at the base of the tumblebug and affects the distal interphalangeal joints
Proximal interphalangeal joints = Bouchards nodes
Distal interphalangeal joints = Hebedens nodes
10
Q
What is Raynaud’s
A
White areas in the fingers due to a change in temperature, particularly cold which causes the clamping down of capillaries and subsequent hypoxia
11
Q
What are the enthesitis
A
where the muscle joins the bone
12
Q
What is dactylitis
A
Inflammation of all joints and tendon sheaths of toe or finger = sausage digits
13
Q
What investigations might you do insomene with a suspected rheumatological condition
A
Erythrocyte sedimentation rate CRP Autoantibodies - Rheumatoid factor - Anti-cycluc citrullinated peptide
14
Q
What antibody might you see in someone with lupus
A
ANA
15
Q
Give 3 causes of inflammatory joint pain.
A
- Autoimmune disease e.g. RA, vasculitis, connective tissue disease.
- Crystal arthritis.
- Infection.
16
Q
Give 2 causes of non-inflammatory joint pain.
A
- Degenerative e.g. osteoarthritis.
2. Non-degenerative e.g. fibromyalgia.
17
Q
How does inflammatory pain differ from degenerative non-inflammatory pain?
A
Inflammatory pain tends to ease with use whereas degenerative pain increased with use.
18
Q
Are you more likely to see swelling in inflammatory or degenerative pain?
A
In inflammatory pain you are likely to see synovial swelling. There is often no swelling in degenerative pain.
19
Q
Explain why ESR levels are raised in someone with inflammatory joint pain.
A
Inflammation leads to increased fibrinogen which means the RBC’s clump together. The RBC’s therefore fall faster and so you have an increased ESR.
20
Q
Explain why CRP levels are raised in someone with inflammatory joint pain.
A
Inflammation leads to increased levels of IL-6. CRP is produced by the liver in response to IL-6 and therefore is raised.
21
Q
What are seronegative spondyloarthropathies
A
Group of inflammatory arthritides affecting the spine and peripheral joints without the production of rheumatoid factor and associated with HLA-B27
22
Q
What is HLA-B27
A
Class 1 surface antigen involved with MHC and function as an APC
23
Q
What conditions are involved in seronegative spondyloarthopathies
A
Ankylosing Spondylitis Psoriatic Arthritis Reactive arthritis Enteropathic arthritis Juvenile Idiopathic arthritis
24
Q
What are the common features of seronegative spondyloarthropathies
A
Axial arthritis and sacroilitis Asymmetrical large joint oligoarthritis/monoarthritis Enthesitis Dactylitis Iritis Psoriaform rashes Oral ulcers Aortic regurgitation
25
Why is B27 linked with disease
Molecular mimicry
Misfolding theory
HLA-B27 heavy chain homodimer hypothesis
26
Describe the molecular mimicry theory
Infection leads to an immunee response - infectious agent has similar peptides to HLA-B27 molecule leading to an autoimmune response against HLA-B27
27
Describe the misfolding theory
Unfolded HLA-B27 proteins accumulate in the endoplasmic reticulum and trigger the ER unfolded protein response which causes IL-23 release and triggers proinfllamtoy response via interleukin 17+ T-lymphocytes
28
Describe the HLA-B27 heavy chain homodimer hypothesis
B27 chains form stable dimers and dimerise and accumulate in the ER which stimulates the ER unfolded protein response
Heavy chains bind immune regulators such as NK receptors causing expression and survival of leukocytes
29
What is the pneumonic for clinical features of seronegative spondyloarthropathies
SPINEACHE
```
Sausage digit = dactylics
Psoriasis
Inflammaotory back pain
NSAID good response
Enthesitis (Heel)
Arthritis
Crohns/Ulcerative colitis
HLA-B27
Eye - uveitis
```
30
What is ankylosing spondylitis
Chronic disease of unknown aetiology characterised by stiffening and inflammation of the spine and the sacroiliac joints leading to joint fusion
31
Describe the epidemiology of ankylosing spondylitis
It is more common in men that women and presents in men earlier around their late teens and early 20's
32
Describe the genetic basis of ankylosing spondylitis
95% of people who have the condition re HLA-B27+ve
33
Describe the presentation ankylosing spondylitis
Gradual onset back pain that radiates from the sacro-iliac joints (Sacrolitis) to the hips and the buttocks - pain is often worse @ night with morning stiffness and is relieved by exercise
Progressive loss of all spinal movements
Development of kyphosis and neck hyperextension
Enthesitis
Costochondritis
34
What are the extra-articular manifestations of ankylosing spondylitis
Osteoporosis
Acute iritis/anterior uveitis
Aortic valve incompetence
Apical pulmonary fibrosis
35
What are the investigations for someone with suspected ankylosing spondylitis
Radiological Changes (X-ray and MRI)
- Sacroilitis = irregularities, sclerosis and erosions
- Vertebra = Corner erosions, syndesmophwytes
- Bamboo spone
DEXA scan and CXR
HLA-B27 Test
FBC (Anaemia, Increased ESR, CRP and HLA-B27 +ve)
36
What is the management of ankylosing spondylitis
```
Exercise
Physio
Medical
- NSAIDs
- Anti-TNF = Infiliximab
- Local steroid injections
- Bisphosphonates
- IL-17 blockers
Surgical = hip replacement to decrease pain and increase mobility
```
37
Describe some of the clinical features of psoriatic arthritis
```
Asymmetrical oligoarthritis
Distal arthritis of the DIP joints
Symmetrical polyarthritis
Arthritis mutilans
Dactylitis
Psoriatic plaques
Nail changes
- Pitting
- Subungual hyperkeratosis
- onchyolysis
Enthesitis (Achilles Tendon and plantar fasciitis)
```
38
What changes of X-ray might you see in psoriatic arthritis
Erosion leading to pencil in cup deformity of the nails
39
What is the treatment of psoriatic arthritis
NSAIDs - ibuprofen
DMARD = Sulfasalazine, methotrexate and cyclosporin
Anti-TNF - Infiliximab
IL-12/23 blockers - ustekinumab
40
With what tissue type are all spondyloarthritis conditions associated?
They are all associated with tissue type HLAB27
41
What is the general treatment for all spondyloarthritis?
Initially DMARDs and then biological agents if DMARDs fail e.g. TNF blockers.
42
Describe the pathophysiology of ankylosing spondylitis.
Inflammation of spine -> erosive damage -> repair/new bone formation -> irreversible fusion of spine.
43
What is the diagnostic criteria for ankylosing spondylitis?
1. >3 months back pain.
2. Aged <45 at onset.
3. Plus one of the SPINEACHE symptoms.
44
Give 3 locations that psoriasis commonly occurs at.
1. Elbows.
2. Knees.
3. Fingers.
45
Define reactive arthritis
Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually GI or genital.
46
What gut infections are associated with reactive arthritis?
Campylobacter
Salmonella
Shigella
Yersinia
47
What STIs are associated with reactive arthritis
Chlamydia
Ureaplasma
HIV
48
Describe the clinical presentation of reactive arthritis
```
Asymmetrical lower limb oligoarthritis - esp knee
Iritis and conjunctivitis
Keratoderma blenorrhagica
Circinate balanitis
Enthesitis
Mouth ulcers
Sterile urethritis
```
49
What are the investigations for someone with reactive arthritis
Increased CRP and ESR
| Stool culture if diarrhoea
50
What is the management of reactive arthritis
NSAIDs and steroids
Relapse may require sulfsalazine and methotrexate
Antibiotics to treat infection
51
Enteropathic arthritis is associated with patients of what other disease
IBD - Crohns or UC
52
What is the presentation of enteropathic arthritis
Asymmetrical Large joint oligoarthritis mainly affecting lower limbs
Sacroilitis may occur
53
What is the treatment of enteropathic arthritis
Treat the IBD
NSAIDs and articular steroids for arthritis
Colectomy for remission in UC
54
What is the criteria for making a clinical diagnosis of juvenile idiopathic arthritis?
Joint swelling/stiffness >6 weeks in children <16 and no other cause is identified.
55
What is the aetiology of JIA?
Unknown - idiopathic!
| However, it is autoimmune so there are genetic factors associated.
56
Why is it important to check the eyes in JIA?
The lining of the eyes and the joints is very similar. Children with JIA are at a high risk of developing uveitis!
57
What type of JIA affects <4 joints and is usually ANA positive?
Oligoarthritis.
| High risk of developing uveitis!
58
What JIA is similar to adult ankylosing spondylitis?
Enthesitis related JIA - inflammation of where the tendon joins a bone. HLAB27 positive.
59
Describe the non-medical treatment for JIA.
1. Information.
2. Education.
3. Support.
4. Liaison with school.
5. Physiotherapy.
60
Describe the medical treatment for JIA.
1. Steroid joint injections.
2. NSAIDS.
3. Methotrexate.
4. Systemic steroids.
61
Give 5 potential consequences that can occur if you fail to treat JIA.
1. Damage.
2. Deformity.
3. Disability.
4. Pain.
5. Bony overgrowth.
6. Uveitis.
62
What is vasculitis?
Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.
63
What are the consequences of vasculitis
Vessel wall destruction = haemorrhage
Endothelial injury = thrombosis and infarction
64
What cells might you see on a histological slide taken from someone with vasculitis?
Neutrophils and giant cells.
65
What are the two different systems used for classifying vasculitis
Chapel Hill
| By vessel size
66
Chapel Hill classification: give an example of a large artery primary disorder.
Giant cell arteritis
| Takayasu's Arteritis
67
Chapel Hill classification: Give an example of a medium vessel disorder
Polyarteritis nodosa
| Kawasakis Disease
68
Chapel hill classification: Give an example of a small vessel disorder
Churg-strauss
Wegners granulomatosis
Goodpasture's disease
69
How are the small vessel vasculitis's categorised
By the presence of certain anti-neutrophil cytoplasmic antibodies (ANCA)
70
Define giant cell arteritis
Granulomatous inflammation of aorta, external carotid branches
71
What are the two types of giant cell arteritis
Cranial GCA
| Large vessel GCA
72
Describe the epidemiology of giant cell arteritis
Affects those over 50 more commonly
Incidence increases with age
Twice as common in women
73
What are the features of Giant cell arteritis
```
Systemic signs (Fever, malaise, fatigue)
Visual loss - diplopia
Headache (Abrupt, temporal, unilateral)
Temporal artery and scalp tenderness
Jaw and tongue claudication
Amaurosis fugax
Prominent temporal artery pulsation
Polymyalgia
Limb claudication
```
74
What might you find on clinical investigation in someone with giant cell arteritis?
1. Palpable and tender temporal arteries with reduced pulsation.
2. Sudden monocular visual loss, the optic disc is pale and swollen.
75
What is the diagnostic criteria for giant cell arteritis?
1. Age >50.
2. New headache.
3. Temporal artery tenderness.
4. Abnormal artery biopsies.
76
What investigations might you do in someone who you suspect has giant cell arteritis?
1. Bloods for inflammatory markers e.g. CRP, ESR.
| 2. Temporal artery biopsy.
77
What is the management for giant cell arteritis
Prompt corticosteroids - prednisolone.
- Methotrexate is sometimes adeed.
- Osteoporosis prophylaxis is important e.g. lifestyle advice and vitamin D.
78
What is the pathophysiology of Giant cell arteritis
1. Activation of dendritic cells in adventitia
2. Recruitment and activation of T cells
3. Recruitment of CD8+ and monocytes
4. Vascular damage and remodelling
79
Define Wegner's Granulomatosis
Rare, life threatening multi system necrotising granulomatous disease causing damage to predominantly small arteries
80
Is Wegener's granulomatosis associated with c-ANCA or p-ANCA?
c-ANCA.
81
What organ systems can be affected by Wegener's granulomatosis?
1. URT.
2. Lungs.
3. Kidneys.
4. Skin.
5. Eyes.
82
What is the affect of Wegener's granulomatosis on the URT?
- Sinusitis.
- Otitis.
- Epistaxis
- Saddle nose deformity
- Nasal crusting.
83
What is the affect of Wegener's granulomatosis on the lungs?
```
Cough
Haemoptysis
PLeuritis
- Pulmonary haemorrhage/nodules.
- Inflammatory infiltrates are seen on X-ray.
```
84
What is the affect of Wegener's granulomatosis on the kidney?
Glomerulonephritis.
Haematuria
Proteinuria
85
What is the affect of Wegener's granulomatosis on the skin?
Palpable purpura
| Vasculitic rash
86
What is the affect of Wegener's granulomatosis on the eyes?
- Uveitis.
- Scleritis.
- Episcleritis.
- ocular keratitis
- Conjunctivitis
87
What is the investigations for Wagner's granulomatosis
cANCA
Dipstick for haematuria and proteinuria
CXR = Bilateral nodular and cavity infiltrates
88
What is the management of Wagner's granulomatosis
Steroids, methotrexate and cyclophosphamide
Induction of remission = cyclophosphamide/rituximab/ glucocorticoids and plasma exchange
Maintenance of remission = DMARDS, Rituximab, glucocorticoid taper
89
What is the pathophysiology of the ANCA positive Vasculidities (Wegners and Churg strauss
Necrotising granulomatous vasculitis affecting the arterioles and venules
- ANCA's can activate primed circulating neutrophils which lead to fibrin deposition in vessel wall and deposition of destructive inflammatory mediators
90
Define osteoarthritis
Non-inflammatory degenerative joint disorder characterised by progressive loss of hyaline articular cartilage and formation of new bone
91
What are the risk factors for the development of osteoarthritis
1. Old age
2. Obesity - pro inflammatory state
3. Predisposing joint abnormality
4. Family history
5. Trauma
6. Occupation
7. Abnormal biomechanics (Hypermobility)
92
Where is osteoarthritis most common
In the synovial joints
93
What are the two classifications of osteoarthritis
Primary - no underlying causes
Secondary - known underlying cause suc as obesity
94
Name a few locations where osteoarthritis is common
```
Knees
Hips
DIPs
PIPs
Thumb carpometacarpal joint
```
95
What are the most important cells responsible for OA?
Chrondrocytes.
96
Name 5 symptoms of osteoarthritis
1. Morning stiffness (<30 minutes).
2. Pain - aggravated by activity and worse at night and with rest
3. Tenderness.
4. Walking and ADLs affected.
5. Joint swelling and bony enlargement.
6. Deformities.
7. Crepitus.
8. Decreased range of movement and functional impairment
9. Asymmetrical
97
What are the signs of osteoarthritis
Bouchards nodes at PIPJ
Heberdens nodes at DIPJ
Thumb CMC squaring
Fixed flexion deformity
98
What is the diagnostic investigation for OA
X-ray
99
Give 5 radiological features associated with OA.
1. Joint space narrowing.
2. Osteophyte formation.
3. Sub-chondral sclerosis.
4. Sub-chondral cysts.
5. Abnormalities of bone contour.
100
What is the non-medical management for OA
```
Education
Decrease Exercise, increase rest
Weight loss
Physio
Walking aids, supportive footwear
```
101
What is the pharmacological management of OA
- NSAIDS (topical better than PO).
- Paracetamol.
- Intra-articular steroid injections.
- DMARDs if there is an inflammatory component.
102
Describe the surgical management of OA
- Arthroscopy for loose bodies.
- Osteotomy (changing bone length).
- Arthroplasty (joint replacement).
- Fusion (usually ankle and foot).
103
Give 3 indications for surgery in OA
1. Significant limitation of function.
2. Uncontrolled pain.
3. Waking at night from pain.
104
A patient complains of 'locking', what is the most likely cause of this?
This is probably due to a loose body e.g. a bone or cartilage fragment.
105
What is the treatment for loose bodies?
Arthroscopy.
106
Give an example of an inherited connective tissue disease.
1. Marfan's syndrome.
| 2. Ehler Danlos syndrome.
107
Give an example of an autoimmune connective tissue disease.
1. SLE.
2. Systemic sclerosis.
3. Sjögren's syndrome.
4. Dermatomyositis.
108
Describe the pathophysiology and common features of marfan's syndrome
Abnormal fibrillar production
- long limbs
- pectus excavatum
- aortic root enlargement
- arachnodactyly
109
Describe the pathophysiology and common features of Ehlers danlos syndrome
Abnormal collagen production
- stretchy skin
- joint hyper-mobility
110
Define SLE
Systemic lupus erythamatosus is an autoimmune multi system inflammatory disease in which auto-antibodies to a variety of auto-antigens result in the formation and desposition of immune complexes
111
What are the causes of lupus
Interplay between EBV and genetics
Drugs (Isoniazid, hydralazine and anti-TNF)
Genetic association with HLA DR2, DR3 and C4 A null gene
112
What is the epidemiology of SLE
More prevalent in females
most common around child bearing age
More common in afro-caribbeans and asians
113
What are the symptoms of lupus
1. Arthritis that is symmetrical, non-erosive and affects the peripheral joints
2. Renal - proteinuria and BP increase due to lupus nephritis
3. ANA +ve in 95%
4. Serositis
- Pericarditis
- Pleuritis
5. Haematological
- Neutro and lymphocytopaenia
- Thrombocytopenia
6. Reynauld's
7. Mouth ulcers
8. Malar Butterfly rash
9. Neurological
- Seizures
- Psychosis
10. Constitutional = Fatigue, weight loss, fever and myalgia
114
Describe the pathogenesis of SLE.
- Inefficient phagocytosis means cell fragments are transferred to lymphoid tissue where they are taken up by APC. T cells stimulate B cells to produce antibodies against self-antigens.
- Immune complex deposition -> neutrophil and cytokine influx -> inflammation and tissue damage.
115
What can cause thrombosis in patients with SLE?
The presence of antiphospholipid antibodies.
116
What autoantibody is specific to SLE?
Anti-dsDNA.
117
Describe the immunology of lupus
95% are ANA+ve
dsDNA is very specific
Anticardiolipin +ve
118
What investigations might you do in someone who you suspect has SLE?
What investigations might you do in someone who you suspect has SLE?
1. Blood count may show normocytic anaemia; neutropenia; thrombocytopaenia. Raised ESR, normal CRP.
2. Serum autoantibodies: ANA, anti-dsDNA.
119
Describe the non-medical treatment for SLE.
- Education and support.
- UV protection.
- Screening for organ involvement.
- Reduce CV risk factors e.g. smoking cessation
120
Describe the pharmacological treatment for SLE.
- Corticosteroids.
- NSAIDS.
- Anti-malarials (DMARDs).
- Anticoagulants (for those with antiphospholipid antibodies).
- Biological therapy targeting B cells e.g. rituximab.
Treat the proteinuria with ACEi
121
What is systemic sclerosis
Excess collagen production leading to inflammation, vasculopathy and autoantibody production
122
Describe the epidemiology of systemic sclerosis
Females affected more than males
| 30-50 years most common
123
What are the two types of systemic sclerosis
Limited (70%)
| Diffuse (30%)
124
What are the symptoms of limited systemic sclerosis (CREST)
Calcinosis
Raynaud's
Oesophageal and gut dysmotility
Sclerodactyly (Tightening and thick skin on fingers and toes
Telangiectasia - dilated facial spider veins
Skin involvement is limited to the face, hands and feet
125
What are the symptoms of diffuse systemic sclerosis
```
Diffuse skin involvement
Organ fibrosis
- GOR, aspiration, dysphagia
- lung fibrosis and pulmonary hypertension
Cardiac arrthymias
Renal = acute hypertensive crisis
Short reynaulds history
```
126
What are the ivestigations for someone with systemic sclerosis
FBC (anaemia) U+E (renal impairment
Urine = dipstick'
Imaging
- CXR (Cardiomegaly, bibasal fibrosis)
- Hands = calcinosis
- Ba swallow shows impaired oesophageal motility
ECG and Echo show evidence of pulmonary hypertension
127
What is the conservative management of systemic sclerosis
Exercise and skin lubricants
| Hand warmers
128
What is the medical management of systemic sclerosis
1. Immunosuppression
2. Reynauld's needs vasodilators = CCb's ACEis and IV prostacyclin
3. Renal = ACEi
4. Oesophageal = PPIs
5. Pulmonary fibrosis needs cyclophosphamide
129
What is dermatomyositis
A rare disorder of unknown aetiology. There is inflammation and necrosis of skeletal muscle fibres and skin.
130
Give 3 symptoms of dermatomyositis.
1. Rash.
2. Symmetrical proximal Muscle weakness.
3. Lungs are often affected too e.g. ILD.
131
What are the extra-muscular features of dermatomyositis
Fever
Arthritis
Pulmonary fibrosis
Reynauld's
132
What investigations might you do in someone who you suspect has dermatomyositis?
1. Muscle enzymes - raised.
2. EMG.
3. Muscle/skin biopsy.
4. Screen for malignancy.
5. CXR.
133
What is the treatment for dermatomyositis?
Immunosuppression
- steroids
- Cytotoxic (Azathioprine and methotrexate)
134
What is the pathophysiology of sjögren's syndrome?
Immunologically mediated destruction of epithelial exocrine glands, especially lacrimal and salivary glands.
135
What are the two types of sjorgens syndrome
Primary
- female more common and in 4th to 5th decade of life
Secondary
- second to RA, SLE, Systemic sclerosis and primary biliary cirrhosis
136
What are the features of Sjorgens
Decreased tear production = dry eyes
decreased salvation = xerostomia
Bilateral parotid swelling
Vaginal dryness = dyspareunia
137
What other autoimmune conditions of sjorgens associated with
Thyroid disease
PBC
MALT lymphoma
138
What is the investigations for sjorgens syndrome
Look for serum antibodies
- ANA and RF
Schimmer tear test - ability for eyes to self hydrate
Parotid biopsy
139
What is the treatment for sjorgens syndrome
- Tear and saliva replacement.
- Immunosuppression for systemic complications
- NSAIDs ans hydroxychloroquine for arthralgie, rashes and fever .
140
What is Reynaulds
Peripheral digital ischaemia precipitated by cold or emotion
141
What is the classification of Reynauld's
Primary = Idiopathic
Secondary = second to systemic sclerosis, SLE, RA, sjorgens, Thrombocytosis, B-blockers, Atherosclerosis, frost bite,
Vibrating tools cause vascular damage
142
What is the presentation of Reynauld's
Digit pain with triphasic colour change from white to blue to crimson
143
What is the treatment of Reynauld's
Wear gloves
CCb's (nifedipine)
ACEi
IV prostacyclin
144
Define osteoporosis.
A systemic skeletal disease characterised by low bone mass and micro-architectural deterioration. The patient is at increased risk of fracture and bone fragility
145
Describe the epidemiology of osteoporosis.
50% of women and 20% of men over 50 are affected. The incidence increases with age.
146
What 2 factors are important for determining the likelihood of osteoporotic fracture?
1. Propensity to fall -> trauma.
| 2. Bone strength.
147
What is post menopause osteoporosis
Loss of the restraining effects of oestrogen on bone turnover characterised by
1. high bone turnover
2. Predominantly cancellous bone formation
3. Microarchitectural disruption
148
What happens to bone micro-architecture as we get older that leads to a reduction in bone strength?
Trabecular thickness decreases; especially in the horizontal plane. There are fewer connections between trabecular and so an overall decrease in trabecular strength -> increased risk of fracture.
Remodelling due to increased osteoclast and decreased osteoblast activity
149
What are the causes of osteoporosis
1. AI conditions because inflammatory cytokines increase resorption
- RA and IBD
2. Cushing's disease (Induces osteoblast apoptosis)
3 Post menopause
4. Hyperthyroidism and primary hyperparathyroidism as TH and PTH increase bone turnover
5. Steroids (Testosterone and oestrogen control bone turnover
6. Reduced skeletal loading increases resorption
150
What medications can increase osteoporosis risk
```
Glucocorticoids
Depo-provera contraception
Aromatase inhibitors
GnRH analogues
Androgen deprivation
```
151
What are the other risk factors for osteoporosis
```
Previous fracture
Family history
Alcohol
Smoking
Medications
immobility
```
152
What are the signs and symptoms of osteoporosis
asymptomatic development with fragile bone and pathological fractures
153
Give 4 properties of bone that contribute to bone strength
1. Bone mineral density
2. Bone size
3. Bone micro-architecture
4. Mineralisation
5. Bone turnover
6. Geometry
154
Why can RA cause osteoporosis?
RA is an Inflammatory disease. There are high levels of IL-6 and TNF; these are responsible for increased bone resorption.
155
What investigations might you do in someone who you suspect to have osteoporosis
DEXA scan to produce a T score
| FRAX (10yr fracture risk)
156
Name 2 areas of the skeleton commonly affected by osteoporosis that the DEXA scan focuses on.
1. Lumbar spine.
2. Hip.
3. Proximal femur
4. Distal radius
157
What is a T score?
A T score is a standard deviation that is compared to a gender-matched young adult mean.
158
What is a FRAX score
predicts 10 year fracture chance but cannot be used in people under 40
159
What T score signifies that a patient has osteoporosis?
T >-2.5
160
What T score signifies that a patient has osteopenia?
-2.5 < T < -1
161
What is a normal T score?
-1
162
Give 2 examples of anti-resorptive treatments used in the management of osteoporosis.
1. Bisphosphonates (Alendronate, risedronate)
- inhibit cholesterol formation leading to osteoclast apoptosis
2. HRT.
Anti-resorptive treatments decrease osteoclast activity.
163
Give an example of an anabolic treatment used in the management of osteoporosis.
Teriparatide.
- analogue of PTH
Anabolic treatments increase osteoblast activity.
164
What cells do anti-resorptive treatments target in people with osteoporosis?
They decrease osteoclast activity.
165
What cells do anabolic treatments target in people with osteoporosis?
They increase osteoblast activity.
166
Give 3 advantages of HRT.
1. Reduces fracture risk.
2. Stops bone loss.
3. Prevents menopausal symptoms.
167
Give 3 disadvantages of HRT.
1. Increased risk of breast cancer.
2. Increased risk of stroke and CV disease.
3. Increased risk of thrombo-embolism.
168
Give an example of a bisphosphonate.
Alendronate.
169
What pathway do bisphosphonates target?
HMGCoA pathway.
170
What is the diagnostic criteria for fibromyalgia?
Chronic widespread pain lasting for >3months with other causes excluded. Pain is at 11 of 18 tender point sites.
171
Give 3 factors that increase the volume of pain.
1. Substance P.
2. Glutamate.
3. Serotonin.
172
Give 3 factors that decrease the volume of pain.
1. Opioids.
2. GABA.
3. Cannabanoids.
173
Name 4 diseases that fibromyalgia is commonly associated with.
1. Depression.
2. Chronic fatigue.
3. Chronic headache.
4. IBS.
174
What are the risk factors for fibromyalgia
```
Neurosis
- Depression, anxiety and stress
Disatisfaction at work
Overprotective family or lack of support
Middle age
Low income
Divorced
Low educational status
```
175
Give 5 symptoms of fibromyalgia.
1. Neck and back pain.
2. Pain is aggravated by stress, cold and activity.
3. Generalised morning stiffness.
4. Subjective swelling of extremities.
5. Frequent waking during the night.
6. Waking unrefreshed.
7. Low mood, irritable, weepy.
8. Headache and IBS common.
176
Give 5 triggers of fibromyalgia.
1. Physical trauma.
2. Distress.
3. Hormonal alterations e.g. hypothyroid.
4. Infections.
5. Certain catastrophic events e.g. wars.
177
Describe the management for fibromyalgia.
1. Educate the patient and family.
2. 'Resent the pain thermostat'.
3. Low does amitriptyline can help with sleep.
4. Graded aerobic exercise.
5. Acupuncture.
178
What 2 things are essential in the management of fibromyalgia?
1. Explaining that sleep disturbance is central to what they're feeling.
2. Emphasising the importance of exercise and fitness.
179
Define rheumatoid arthritis
Chronic systemic auto-immune inflammatory disease of the joints characterised by a symmetrical, deforming, peripheral polyarthritis
180
Describe the epidemiology of RA
More common in females
| occurs in 5th to 6th decade of life
181
Which genes are associated with RA
HLA-DR4 and DR1
182
What are the risk factors for RA
HLA-DR4/DR1
Smoker
Female
Having other auto-immune conditions
183
Describe the aetiology of RA.
Auto-antibodies e.g. RF and anti-CCP lead to a defective cell mediated immune response.
184
Describe the pathophysiology of RA.
1. Chronic inflammation. B/T cells and neutrophils infiltrate.
2. Proliferation -> pannus formation.
3. Pro-inflammatory cytokines -> proteinases -> cartilage destruction.
185
Give 5 symptoms of RA
1. Early morning stiffness (>60 mins).
2. Pain eases with use.
3. Swelling/deformity
4. General fatigue, malaise.
5. Extra-articular involvement.
186
Which joints are commonly affected in RA
MCP's
| PIPs of the hand and feet
187
Which joint is sparred in rheumatoid arthritis
DIP
188
What are some of the characteristic features of arthritis in rheumatoid arthritis
Swan neck = hyperextended PIP and flexed DIP
Boutonniere = Hyperextended DIP and flexed PIP
Z-thumb
Ulnar deviation of the fingers
189
Give 5 signs of RA.
1. Symmetrical.
2. Deforming.
3. Polyarthropathy.
4. Erosion on X-ray.
5. 80% are RF positive.
190
RA extra-articular involvement: describe the effect on soft tissues
- Nodules on the elbows, fingers, feet, heal and lungs
- Bursitis.
- Muscle wasting.
Atlanto-axial sublimation
191
Describe the composition of RA nodule
Palisading ring of macrophages and fibroblasts with a central fibrinoid necrosis
192
What is Atlanta-axial sublimation
Axis and odontoid peg shift with the atlas due to synovitis and ligament damage around the peg leading to spinal cord compression
193
RA extra-articular involvement: describe the effect on the eyes.
- Dry eyes (Secondary sjogrens syndrome)
- Scleritis.
- Episcleritis.
- Sicca complex
194
RA extra-articular involvement: describe the neurological effects.
- Sensory peripheral neuropathy.
- Entrapment neuropathies e.g. carpal tunnel syndrome.
- Instability of cervical spine.
195
RA extra-articular involvement: describe the haematological effects.
- Palpable lymph nodes.
- Splenomegaly.
- Anaemia.
196
Felty's syndrome is a sign of RA, What is felty's syndrome
RA + Splenomegaly + neutropaenia
197
RA extra-articular involvement: describe the pulmonary effects.
- Pleural effusion.
- Fibrosing alveolitis
- Caplan's syndrome
- Interstitial lung disease
198
RA extra-articular involvement: describe the effects on the heart.
- Pericardial rub.
- Pericardial effusion
- Pericarditis .
199
RA extra-articular involvement: describe the effect on the kidneys.
Amyloidosis
| Analgesic nephropathy
200
Is reynauld's a common presentation of RA?
Yes
201
What is rheumatoid factor?
An antibody against the Fc portion of IgG.
202
What investigations might you do in someone who you suspect has rheumatoid arthritis?
Bloods for inflammatory markers; ESR and CRP will be raised.
- Test for anaemia.
- Test for RF and anti-CCP.
- US and MRI
203
What might you see in radiography of RA
Decreased joint space
Soft tissue swells
Erosion
Soft bones = osteopenia
204
What is the conservative treatment for RA
Refer to rheumatology
Regular exercise
PT
Aids and splints
205
What is the medical management of RA
NSAIDSs for flare ups
Steroids
Disease modifying anti-rheumatic drugs (DMARDs)
Biologics (Anti-TNF)
206
How do DMARDs work
Interferre with folate metabolism
207
Which antibiotic cannot be prescribed with DMARDs
Trimethoprim
208
Name the three main DMARDs
Methotrexate
Sulfsalazine
Hydroxychloroquine
209
What are the SE of methotrexate
Hepatotoxic
| Pulmonary fibrosis
210
What are the SE of hydroxychloroquine
Retinopathy and seizures
211
When would a patient be given biologics for RA
If their RA was severe and they were unresponsive to DMARDs
212
What are the main biologics (Anti-TNF) drugs
```
Infliximab = Anti-TNF ab
Etanercept = TNF-receptor
Adalimumab = Anti TNF ab
```
213
What are the side effects of anti-TNF
increased infection risk (Sepsis and Tb)
| Increased AI disease
214
Name some other classes and drug names of biologics for RA
Anti-IL1 = Anakira
Anti-IL6 = Toclizumab
JAK inhibitors = Taclifinib
215
What might you give to an RA patient who is unresponsive to DMARDs and anti-TNF therapy
Rituximab = anti-CD20 mab
216
When are crystals pathological
When they are deposited in abnormal sites leading to local inflammation and tissue damage
217
What is crystal arthropathy
Arthritis caused by calcium deposits in the joint lining
Urate = gout
Pyrophosphate = pseudo gout
218
How can you determine between gout and pseudo gout using light microscopy
Gout = -ve birefringent needles
Pseudogout = +ve birefringent needles
219
Define gout
deposition of monosodium rate crystals in and around the joints = erosive arthritis
220
Describe the pathological pathway that leads to gout
Purines -> hypoxanthine -> xanthine -> uric acid -> monosodium urate.
221
What enzyme converts hypoxanthine to xanthine?
Xanthine oxidase.
222
Describe the epidemiology of gout
More common in males mainly over 75
223
What is the cause of gout
Hyperuricaemia due to either impaired excretion, increased production or increased intake
224
What are the causes of impaired excretion of urate
```
CKD
Diuretics
Hypertension
Hypothyroid
Hyperparathyroid
Obesity
DM
Low dose aspirin
Cyclosporin
Lead poisoning
```
225
What are the causes of increased production of urate
```
Metabolic syndrome
Myeloproliferative disease
Cytotoxic drugs
Lesch-nyhan syndrome
Alcohol
Excess meat, shellfish, offal, gravy, yeast extract and fructose sweetened drinks
```
226
What things might contribute to increased purine intake
High purine diet = red meat, seafood and fructose
227
What can precipitate a gout attack
Anything that suddenly causes an alteration in uric acid concentration
- Aggressive introduction of hypouricaemic therapy
- Alcohol and shellfish
- Sepsis, MI and actue severe illness
- Sudden cessation of hypouricaemic therapy
- Trauma surgery and dehydration
228
What are the symptoms of gout
Hot and swollen joint
Acute mono arthritis
Tophi
229
What are tophi
Urate deposits in the pinna and tendons
230
Which joints are commonly affected by gout
Big toe MTP
| but also ankle, foot, hand joints, wrist, elbow and knee
231
Name 4 diseases that someone with gout might have an increased risk of developing.
1. Hypertension.
2. CV disease e.g. stroke.
3. Renal disease.
4. Type 2 diabetes.
232
What might investigations for someone with suspected gout show
Polarised light microscopy produces negatively birefringent needle-shaped crystals
Joint fluid aspirate and microscopy
X-ray changes produces punched out erosions in junta-articular bone (Rat bites)
233
What is the aim of treatment for gout?
To get urate levels < 300μmol/L.
234
What are the treatment options for gout
1. Conservative = Wt loss, avoid fasting and EtOH excess
2. Xanthine oxidase inhibitor (Allopurinol)
3. Colchicine and NSAIDs
4. Uricosuric drugs
235
Name 2 NSAIDs used in management of gout
Diclofenac and indomethacin
236
What are the SE of colchicine
Diarrhoea
237
In renal impaired gout patients where NSAIDs and colchicine are CI, what is given
Steroids
238
What are the side effects of allopurinol
Rash
Fever
Decreased WCC
239
When might the xanthine oxidase inhibitor febuxostat be used
If patient has hypersensitivity or renal impairment
240
You see a patient with gout who is taking bendroflumethiazide. What drug might you replace this with to help treat their gout?
You would switch bendroflumethiazide to cosartan as bendroflumethiazide is a diuretic and so impairs urate excretion.
241
Name a drug that can lead to increased monosodium urate.
Bendroflumethiazide.
| Diuretics impair urate excretion.
242
Pseudogout is otherwise known as
Pyrophosphate arthropathy
243
Describe the pathophysiology of pyrophosphate arthropathy (pseudogout).
Calcium pyrophosphate crystals are deposited on joint surfaces. The crystals elicit an acute inflammatory response.
244
What are the causes of pseudogout
```
Dehydration
Hypo/hyperthyroidism
Diabetes
Haemochromatosis
hypomagnesia
Hyperparathyroidism
```
245
Give a symptom of pyrophosphate arthropathy (pseudogout).
```
Can be asymptomatic
Acute mono arthritis
Pain, stiffness, swelling, hot
Marked synovitis
Fever
resolution within 1-3 weeks
```
246
Which joints does pseudo gout commonly effect
Knee>wrist>Shoulder>Ankle>elbow
247
What investigations might you do in someone who you suspect might have pyrophosphate arthropathy (pseudogout)?
Chondrocalcinosis on X-ray
Joint fluid aspirate and microscopy
+ve birefingent rhomboid crystals
248
What is the most likely differential diagnosis for pyrophosphate arthropathy (pseudogout)?
Infection
249
What might trigger an acute attack of pseudo gout
```
Direct trauma to the joint
Intercurrent illness
Surgery - esp parathyroidesctomy
Blood transfusion, IV fluid
T4 replacement
Joint lavage
```
250
What is the treatment of pseudo gout
Intra-articular steroid injections and colchicine and NSAIDs
If continued inflammatory changes then trial of anti-rheumatic treatment such as methotrexate and hydroxychloroquine
Surgery
251
Define fracture
A soft tissue injury with discontinuity of the bone
252
What is the management of a fracture
1. Reduce the fracture (Restore length, align, rotate)
2. Immobilise
3. Rehabilitate
253
Describe the physiology of fracture healing
Blood rushes to the site forming a haematoma and brings fibroblasts that begin granulation forming a soft callus
Osteoblasts come along and form woven bone which makes the bone stable
Woven bone gets remodelled into lamellae bone
254
Name the 7 different types of fractures
1. Transverse
2. Linear
3. Oblique-non displaced
4. Oblique-displaced
5. Spiral
6. Greenstick
7. Communicated
255
What are the potential complications of fractures
Damage to surrounding structures such as vascular, nerve and soft tissue and organs
Contamination --> infection
Compartment syndrome
256
What is compartment syndrome
Where there is damage to the blood supply and build up of pressure in the compartment as there is nowhere for the fluid to go leading to restrictions in blood flow to the limb
- Increase in intra-compartmental pressure due to fluid increase (Blood) puts pressure on the viens causing collapse then collapse the nerves and puts pressure on arteries (Pain, pallor, perishingly cold, paralysis and pulselessness and parathesia)
257
What are the early systemic complications of fractures
Fat embolus - fat droplets escape bone marrow and form emboli which hit the lungs causing rash and dyspnoea
Shock - vessel injury causing harm-dynamic instability and shock
Crush syndrome - crush causes muscle to die and release myohaemoglobin which blocks kidneys and causes renal failure
Pneumonia
258
What are the late complications of fractures
Delayed union, non-union and Mal union (Bone heals with deformity)
Avascular necrosis
Stiffness
Arthritis
Osteomyelitis
259
What are the different classifications of neck of femur fractures
Intracapsular
| Extracapsular
260
What are the different types of extracapsular neck of femur fracture
Interochanteric
| Extratrochanteric
261
What is the presentation of a neck of femur fracture
```
Fall
Shorter leg on side of fracture
Groin pain
Inability to weight bear
Externally rotated
Pain on axial loading
```
262
What is the management of intracapsular neck of femur fractures
Analgesia with morphine or nerve block
Need to replace
1. Total hip replacement
2. Hemiarthroplasty
263
What is the management of extra capsular neck of femur fractures
Cannulated hip screws
| DHS - compression screw
264
What is the classification method for ankle fractures
Weber classification
A = below the syndesmosis
B = at the level of the syndesmosis
C = Above the level of the syndesmosis
265
What are the Ottawa rules for who gets an x-ray
Bone tenderness at the posterior edge of the lateral malleolus, medial malleolus or inability to weight bear immediately or after 4 steps
266
What is the management of ankle sprains
Analgesia
Ice
Elevation
Early mobilisation
267
What is the treatment of open fractures
Get antibiotics and tetanus
Splint and align the foot
Stabilise
Debridement
268
What is the treatment for compartment syndrome
Fasciotomy after 24 hours so the dead tissue can be removed
269
What is the function of the ACL
Important stabiliser of the knee joint, limits anterior translation of the tibia and also contributes to knee rotation stability
270
What is the presentation of an ACL tear
Swelling, pain and the knee giving way
271
What are the investigations for ACL injuries
Postive lachmanns
Anterior draw test
MRI
272
What is the management of ACL injury
Physiotherapy
Surgery
Tendon repair
Artificial graft
273
What is cauda equina
Progressive bilateral neurological deficit of the legs leading to major motor weaknesses with knee extension, ankle eversion or foot dorsiflexion
274
What are the symptoms of cauda equina
Difficult in initiating micturition or impaired sensation of urinary flow - urinary retention with overflow urinary incontinence
Loss of sensation of rectal fullness - faecal incontinence
Perianal or genital sensory loss
Laxity of the anal sphincter
275
What is the management of cauda equina
Urgent decompression and discectomy
276
Shoulder dislocation can cause damage to what nerve
Axillary nerve damage which supplies the deltoid
277
What is the management of shoulder dislocation
Popping the joint back in and trying to get early mobilisation
278
What are the rotator cuff muscles
Supraspinatus
Infraspinatus
Subscapularis
Teres minor
279
What are the investigations for rotator cuff injuries
Jobes test for supraspinatus
Put hand behind back and ask to push away
Push hands outwards from forward position - theres minor
280
What is the management of rotator cuff injuries
```
analgesia
Physio
Activity modification
Corticosteroid injections
Surgery ie. arthroplasty
```
281
Define osteomyelitis
Infection localised to the bone
282
Describe the epidemiology of osteomyelitis.
- Increasing incidence of chronic OM.
| - Bimodal age distribution.
283
What are the two predisposing factors for osteomyelitis
Diabetes
| Peripheral vascular disease
284
What are 2 methods of classifying osteomyelitis
1. Acute = inflammatory bone changes caused by pathogenic bacteria with symptom presentation within 2 weeks
2. Chronic = bone necrosis with symptom onset after 6 weeks
285
Describe three ways in which pathogens can get into bone
1. Direct inoculation of infection into bone via trauma/surgery
2. Contiguous spread of infection from adjacent soft tissues and joints to the bone
3. Haematogenous seeding
286
Contiguous spread of infection from soft tissue to joints is more common in what individuals
Older patients and those with DM, chronic ulcers, vascular disease and arthoplasties
287
Haematogenous seeding occurs in which individuals
IVDU
| Those with central lines, dialysis, sickle cell disease, self catheterisation, UTIs
288
What bones are likely to be affected by hematogenous seeding in adults?
Vertebrae.
289
What bones are likely to be affected by hematogenous seeding in children?
Long bones.
290
Why do vertebrae tend to be affected by hematogenous seeding in adults?
With age, the vertebrae become more vascular meaning bacterial seeding is more likely.
291
Why do long bones tend to be affected by hematogenous seeding in children?
In children the metaphysis of long bones has a high blood flow and BM are absent meaning bacteria can move from the blood to bone.
292
Give 4 host factors that affect the pathogenesis of osteomyelitis.
1. Behavioural e.g. risk of trauma.
2. Vascular supply e.g. arterial disease, DM, sickle cell disease
3. Pre-existing bone/joint problems e.g. RA, prosthetic material
4. Immune deficiency ie. immunosuppressive drugs
293
What is the histopathology of osteomyelitis
1. Inflammatory exudate in marrow
2. Increased intramedullary pressure
3. Extension of exudate into bone cortex
4. Rupture through periosteum
5. Interruption of periosteal blood supply causing necrosis
6. Leaves pieces of separated dead bone = Sequestra
7. New bone forms here = involcrum
294
Acute osteomyelitis: what changes to bone might you see histologically?
1. Inflammatory cells.
2. Oedema.
3. Vascular congestion.
4. Small vessel thromboses
295
Chronic osteomyelitis: what changes to bone might you see histologically?
1. Necrotic bone - 'sequestra'.
2. New bone formation = involcrum
3. Neutrophil exudates.
4. Lymphocytes and histiocytes
296
What can cause osteomyelitis.
1. Gram +ve = S.aureus, streptococcus, enterococci
2. Coagulase negative staphylococci e.g. s.epidermidis.
3. Aerobic gram negative bacilli.
4. Mycobacterium TB in immunocompromised
5. Salmonella in sickle cell disease
6. Pseudomonas auerginoase and serratia marcescens in IVDU
297
What is the presentation of osteomyelitis
Local slow onset dull pain @ osteomyelitis site aggregated by movement with systemic fever, riggers, sweats and malaise
298
What are the acute signs of osteomyelitis
Tender, warm and red and swollen at the osteomyelitis site
299
What are the chronic signs of osteomyelitis
Non healing ulcers
| Draining sinus tract if sequestra is draining to surface
300
What is the differential diagnosis for osteomyelitis
Cellulitis
Charcots joint
Gout
Avascular necrosis
301
What investigations might you do on someone who you suspect may have osteomyelitis?
1. Bloods: raised inflammatory markers and WCC.
2. Plain radiographs and MRI.
3. Bone biopsy.
4. Blood cultures.
302
What things might you see on X-ray for someone with osteomyelitis
Cortical erosion
Sequestra
Sclerosis
Periosteal reaction
303
Describe the usual treatment for osteomyelitis.
- Large dose IV antibiotics tailored to culture findings (often flucloxacillin).
- Surgical treatment: debridement +/- arthroplasty
304
What are the potential complications of osteomyelitis
Vertebral OM which can lead to abscess formation and meningitis
305
Give 4 ways in which TB osteomyelitis is different to other osteomyelitis.
1. Slower onset.
2. Epidemiology is different.
3. Biopsy is essential - caseating granuloma.
4. Longer treatment.
306
What is septic arthritis
Infection producing inflammation in the joints
307
What is the most common cause of septic arthritis?
Staphylococcus aureus.
308
Give 3 causes of septic arthritis.
1. Staphylococcus aureus (RA/DM)
2. Streptococci.
3. Neisseria.
4. Gonococcus (In sexually active)
5. Haemophilus influenza in children
6. Gram -ve bacilli (E.coli and pseudomonas)
309
Give 5 risk factors for septic arthritis.
1. Any cause of bacteraemia e.g. cannula, UTI.
2. Local skin breaks/ulcers.
3. Damaged/prosthetic joints.
4. RA (Joint disease)
5. Elderly.
6. IVDU
7. Immunosuppressed
8. Chronic renal failure
310
Give 4 symptoms of septic arthritis.
1. Painful.
2. Red.
3. Swollen.
4. Hot.
5. Fever.
6. Decreased range of movement
311
Which joints are more commonly affected by septic arthritis
Knee>hip>shoulder
312
What are the investigations for someone with septic arthritis
Joint aspiration but needs to occur before giving antibiotics
Increased WCC, ESR and CRP
X-ray
Blood culture and microbiology
313
What Is the management for septic arthritis
IV Abx: Vanc + cefotaxime
Consider joint washout
Splint joint
Physiotherapy after infection resolved
Prosthetic joint needs to be debridement and arthroplasty
Stop methotrexate and give prednisolone
Flucoxicillin for S.aureus and IV cefotaxime for gram -ve/gonococcal
314
What is the differential for septic arthritis
Crystal arthropathy
| Reactive arthritis
315
What is bacteraemia?
Bacteria in the blood.
316
What is debridement?
The removal of damaged tissue.
317
What is the most serious complication of arthroplasty surgery?
Prosthetic joint infection.
318
Why is the incidence of prosthetic joint infections increasing
Due to increasing incidence of old age, DM and obesity
319
What are the causative agents of prosthetic joint infections
```
S.aureus
MRSA
Anaerobes
Enterobacter
Pseudomonas
Diptheroides
Haem strep
Enterococcus
Coagulase -ve staph
```
320
What is the presentation of a prosthetic joint infection
Pus, redness, hot and swelling of scar
321
What is the history of someone with prosthetic joint infection likely to contain
History of UTIs
322
What investigations might you do on someone who you suspect might have a prosthetic
1. Aspirate (Must be done with patient off antibiotics for 2 weeks) -> microbiology.
2. Bloods for inflammatory markers and FBC.
3. X-rays.
4. Microbiology culture
323
What must you never do before aspirating a joint?
Never give antibiotics before aspiration!
324
What are the three aims of treatment for prosthetic joint infections?
1. Eradicate sepsis.
2. Relieve pain.
3. Restore function.
325
Prosthetic joint infections: what treatment might you choose for a patient that is unfit for surgery?
Antibiotic suppression.
326
Prosthetic joint infections: Which patients might you choose for debridements and retention of prosthesis
Early postoperative infections and acute haematogenous infections
NOT FOR CHRONIC
327
What is the gold standard treatment for prosthetic joint infections?
Exchange arthroplasty.
- Know the organisms and their sensitivities
- Radical debridement of all infected and dead tissue.
- Systemic and local antibiotic cover.
- Sufficient joint and soft tissue reconstruction.
328
What is excisions arthroplasty
Removal of the prosthetic -
| Effective in removing the infection but poor at restoring function
329
What is one stage exchange arthroplasty
'Take something out and put a replacement in'
- radical debridement
- Implantation of new prosthetic
- Systemic and local antibiotics
330
What is a two stage exchange arthroplasty
'Take something out, leave it a while and then replace
- radical debridement
- Local antibiotic spacer
- Interval stage
- Implantation of new prosthesis as per aseptic reconstruction
331
Define good musculoskeletal health
Healthy/disease free joints and bones
| Ability to carry out a wide range of physical activities both effectively and symptom free
332
What is the Wilson and Junger screening criteria for secondary prevention
1. Condition should be an important health problem
2. Should be an accepted treatment for patients with recognised disease
3. Facilities for diagnosis and treatment should be available
4. Should be a recognisable latent or early symptomatic stage
5. Should be a suitable test or examination
6. Test should be acceptable to the population
7. Natural history of the condition including development from latent to declared disease should be adequately understood
8. There should be an agreed policy on whom to treat as patients
9. Cost of case finding should be economically balanced in relation to possible expenditure on medical care as a whole
10. Case finding should be a continuing process and not a one and for all project
333
Is developmental dysplasia of the hip screened for
Yes as part of the 6-8 week baby check as early detection can reduce the need for surgery
334
Why is ultrasound not offered to all babies when screening for developmental dysplasia of the hip
can lead to over diagnosis and treatment of causes that would have otherwise resolved without treatment
335
When are individuals routinely tested for vitamin D deficiency
If they have deficiency symptoms
Are considered as high risk of deficiency
There is clinical reason to do so
336
What are the benefits of working
```
Lower mortality
Social relationships
Structure to life
Improved fitness + mental health
Reduced state benefits
```
337
What are the high risk activities for MSK problems
```
Heavy manual handling
Lifting above shoulder heights
Lifting below the knee
Incorrect manual handling techniques
Forceful repetitive work
Poor posture
```
338
When is an illness due to work
Symptoms improve away from work
Characteristic distribution of rash ie. contact dermatitis
Clusters of cases at workplace
Exposure to hazard linked to disease
339
What are the epidemiological principles of causality according to Bradford Hill
```
Strength of association
Consistency in association
Exposure-response relationship
Specificity
Temporal relationship
Coherence of evidence
Biological plausible
```
340
What are the work related conditions associated with the neck
Tension neck
thoracic outlet syndrome
Cervical spondylosis
341
What are the work related conditions associated with the shoulder
Rotator cuff tendonitis
Shoulder tendonitis
Bicipital tendonitis
Shoulder capsulitis
342
What are the work related conditions associated with the elbow
Lateral and medial epicondylitis
343
What are the work related conditions associated with the wrist and the forearm m
Carpal tunnel syndrome
Tensosynovitis of wrist
De quervain's disease of the wrist
344
What is tension neck
2nd most common condition after back pain
| May be due to whiplash
345
What is thoracic outlet syndrome
Pinching of the brachial plexus nerves leading to tingling and wasting of the hands
Associated with poor posture and loading of the shoulders by working at keyboard
346
What is the management of thoracic outlet syndrome
surgery
347
What is rotator cuff tendonitis
rotator cuff tears leading to swelling
348
What is the test for rotator cuff tears
Elevate extended arm against resistance
349
What is carpal tunnel syndrome
Pain/tingling and numbness due to compression of the median nerve by flexor tendons
350
Who is at risk of carpal tunnel syndrome
Pregnancy, obesity, occupation with repetitive wrist movement
351
What is tenosynovitis
Local tenderness and swelling of tendon sheaths and crepitus at the wrist
352
What is the treatment for tenosynovitis
NSAIDs and steroid injections and rest
353
When does mechanical back pain first present
between 20-55
354
What are the red flags for serious spinal pathology
```
Age of onset 20/55
violent trauma
Systemically unwell
Persisting severe restriction of lumbar flexion
Widespread neurology
```
355
What are the markers for chronic conditions
```
Reduced activity levels
Low mood patients
Expectation that passive treatment will help
Dissatisfaction at work
Lack of support
```
356
Causes of MSK injury
Single excessive force
Static loading
Repetitive wear and tear
357
What are important questions to ask during history taking for bone tumours
```
Presenting complaint (Mass, pain, loss of function)
social history (current level of function)
Past medical history
```
358
What are the red flag symptoms for bone tumours
Rest pain, LOF, Neuro problems, weight loss, growing lump deep to fascia, night pain, deformity, gross loss of movement
359
When examining the joint in bone tumours what should be done
Look feel and move the joint and assess function, range of movement and neuromuscular status
If any masses are present, size, shape, pain, smooth/irregular, skin or deep tissue
360
What is the zone of transition
Area between normal and abnormal bone
361
What does a wide zone of transition indicate
ill-defined border
Cardinal sign of malignancy
Can be mimicked by infection and eosinophilic granuloma
362
What does a narrow zone of transition indicate
Well defined border
In young almost certainly benign
In >40 consider plasacytoma, myeloma and metastases
363
If the patient is > 30 then what bone tumour are they likely to have
Metatasis or myeloma
364
If the patient is <30 then what bone tumours are they likely to have
primary bone tumour
365
What is a periosteal reaction
Reaction caused by any irritation to periosteum, trauma and infection
366
Sunburnt spicules are indicative of which bone tumours
Osteosarcoma and Ewing's
367
Onion skinning periosteal reaction is indicative of which bone tumour
Ewings
368
Codmanns triangle perisoteal reaction is indicative of what bone tumour
osteosarcoma, Ewing's, osteomyelitis an metastasis
369
What investigations would you carry out in someone with suspected primary bone tumour
XR - look for bone lesions interactions (Onion skin, sunburnt spicules)
CT scan for assessing bone quality and solid tumours
MRI reactive changes in soft tissue an bone marrow
Bone scan
370
Describe the Enneking grading system for malignant primary bone tumours
G1 (Benign history - well differentiated, resembles cell of origin with low mitotic count)
G2 (Low grade malignant - moderate differentiations with few mitosis and local spread)
G3 (high grade malignant, poorly differentiated with frequent mitoses)
371
What are the common primary bone tumours
Osteosarcoma of the knee
Chondrosarcoma of the pelvis
Giant cell tumours of the knee
Chondroma of the sacrum
372
Tumours from where metastases to the bone
Thyroid, prostate, breast, kidney and lung
373
What is the management of primary bone tumours
Benign - NSAIDs
| Malignant - Surgical excision with radio/chemotherapy
374
What is a chondroid bone tumour and what is its appearance
Cartilaginous tumour which is popcorn stippling, rings and arcs
375
What is an osteoid bone tumour and what is its appearance
Bone forming tumour with cloud like or trabecular appearance
376
Most common bone tumours are metastases from where
Bronchus
Breast
Prostate
377
X-ray shows metastases as what
Osteolytic areas with bony destruction
378
What must have happened for a lytic tumour to be visible on X-ray
Must have lost greater than 60% bone density
379
Where in the bone does osteosarcoma occur
Metaphyses of long bones
380
What is the most common primary bone malignancy in children
Osteosarcoma
381
Ewing's sarcoma arises from which cell type
Mesenchymal stem cells
382
Where does Ewings sarcoma present
In the long bones
383
What are the symptoms of Ewing's sarcoma
Painful, swelling, redness in the area surrounding the tumour
Malaise, anorexia, Wt loss, fever, paralysis
384
What is a chondrosarcoma
Cancer of the cartilage
385
What are the symptoms of a chondrosarcoma
Dull deep pain and affected area is swollen and tender
386
What are the common sites of chondrosarcoma
Pelvis, femur, humerus, scapula and ribs
387
What is an osteoid osteoma
Benign bone lesion in young patients that causes localised pain and is self limiting
388
Where is an osteoid osteoma found
In the proximal femur, tibial diaphysis and spine
389
What are the investigations for osteoid osteoma
CT and X-ray
390
What is the treatment for osteoid osteoma
NSAIDs
| Surgery --> Radiofrequency ablation
391
What is an osteoblastoma
Bone producing tumour that presents with non self limiting pain
392
Where are osteoblastomas found
Spine, proximal humerus and the sacrum
393
What is the treatment for osteoblastoma
excision
394
What is osteochondroma
Metaphyseal lesion covered by cartilage that grows away from the growth plate and stops growing after puberty
395
How does an osteochondroma present
Painless lump
396
What is the management of an osteochondroma
Surgical excision
397
Define osteosarcoma
Spindle cell neoplasm that produce osteoid
398
What is the most common osteosarcoma
Intramedullarly osteosarcoma found in the knee, proximal humerus and proximal femur
399
Osteosarcoma occurs secondary to
Paget's disease
Post radiation
Fibrous dysplasia
400
What is the treatment for osteosarcoma
Multi agent chemotherapy
401
What are endochondromas
Benign lesions in the small bones that produce metaphysical popcorn on X-ray
402
What is a chondroblastoma
Rare epiphyseal tumour arising from chondral precursor cells located at the distal femur and proximal humerus
403
What is fibrous dysplasia
A developmental abnormality of the bone leading to a failure to produce lamellar bone
404
What is the treatment for fibrous dysplasia
```
Bisphosphonates
Surgical (Curettage and cortical autograph)
```
405
What class of drug is alendronate?
Bisphosphonate.
406
How does alendronate work?
Alendronate reduces bone turnover by inhibiting osteoclast mediated bone resorption.
407
What is polymyalgia rheumatica (PMR)?
A condition that causes pain, stiffness and inflammation in the muscles around the shoulders, neck and hips
408
How can you differentiate between polymyalgia rheumatica (PMR) and fibromyalgia?
PMR will show raised inflammatory markers.
409
What disease is giant cell arteritis associated with?
Polymyalgia rheumatica.
410
Psoriatic arthritis commonly involves swelling of what joint?
DIP joint.
411
How would describe the swelling of fingers seen in psoriatic arthritis?
Dactylitis, sausage like swelling.
412
Describe a psoriatic plaque.
Pink, scaling lesions. Occur on extensor surfaces of the limbs.
413
Give 3 differences between RA and psoriatic arthritis.
- Psoriatic: psoriatic lesions; sausage like swelling around DIP joint; pencil in cup erosion on XR; HLAB27 associated.
- RA: hands and wrists typically affected; peri-articular erosion on XR; rheumatoid nodules.
414
What 2 features would be seen on an X-ray taken from someone with ankylosing spondylitis.
1. Sacroiliitis.
| 2. Syndesmophytes (bamboo spine).
415
1. Which of the following is a clinical feature of osteoarthritis?
a. 60 minutes of early morning stiffness
b. Painful swelling across MCP and PIP
c. Pain in the 1st carpo-metacarpal
d. Mobile subcutaneous nodules and points of pressure
e. Alternating buttock pain
c. Pain in the 1st carpo-metacarpal
OA is common in the carpo-metacarpal joint, DIP and Knee
416
2. Which of the following is an extra-articular feature of RA?
a. Subcutaneous nodules
b. Episcleritis
c. Peripheral sensory neuropathy
d. Pericardial effusion
e. All of the above
All of the above
417
Which of the following is a classical feature of RA on X-ray?
a. Peri-articular sclerosis
b. Sub-chondral cysts
c. Osteophytes
d. Peri-articular erosions
e. New bone formation
d. Peri-articular erosions
418
4. 53yr old patient presents with 3 day history of lower back pain. Pain started a work and has been unable to work for the past three days and is keen to have a sick note. Physical exam shows lightly overweight with BMI of 29 but no neurological deficit or spinal deformity and pain is not easily located. Which is best management
a. Given his age he should be referred to a specialist
b. He should be sent for X-ray to look for pathological changes in spine
c. He should not be given a sick note and advised to return to work straight away
d. He should be reassured and advised to take a simple analgesic and return to normal activity as soon as he can manage
e. He should advised to seek other employment
d. He should be reassured and advised to take a simple analgesic and return to normal activity as soon as he can manage
419
5. For a lytic tumour to be visible on X-ray, it must have lost
a. Greater than 6% bone density
b. Greater than 16% bone density
c. Greater than 60% bone density
d. Greater than 90% bone density
e. 100% bone density
c. Greater than 60% bone density
420
6. 57yr old man presents with 3-day history of painful first MTP joint. On examination there are is red and very warm. He has a BMI of 32 and hypertension and has had identical episodes before. Which of the following dietary changes would reduce his risk of future episodes?
a. A diet with high red meat content
b. A diet rich in dairy products
c. Drinking >5 cans of non-diet fizzy drink per day
d. A diet rich in sugary food stuffs
e. Switching from drinking beer to drinking lager
b. A diet rich in dairy products
421
7. Which of the following is not an autoimmune connective tissue disorder?
a. SLE
b. Ehler danlos
c. Primary Sjogren’s
d. Systemic sclerosis
e. Dermatomyositis
b. Ehler danlos
422
8. 23yr old woman presents with mouth ulcers, fever, painful white fingers and pleuritic chest pain. She is ANA positive, her ESR is 52 and her white cell count is low. Which of the following features would you not expect with her illness?
a. Deforming arthritis
b. Photosensitive rash
c. Seizures
d. PE
e. Thrombocytosis
e. Thrombocytosis
423
In lupus, what happens to the ESR and CRP
ESR is high but the CRP is NORMAL
424
9. Which of the following is used in the treatment of SLE?
a. Anti-TNF
b. Anti-malarials - Hydroxychloroquine
c. Ustekinuab
d. Sulfsalazine
e. Allopurinol
b. Anti-malarials - Hydroxychloroquine
425
10. Adult male presents with a 6 week right sided headache, general malaise, early morning stiffness and pain in his jaw when eating. His CRP is 63, ESR 78. Which of the following is true regarding his underlying disease?
a. It is associated with ANCA positivity
b. It typically affects those between 50 and 60
c. It can present with acute sight loss
d. It rarely responds to corticosteroids
e. It is vasculitis affecting the small blood vessels
c. It can present with acute sight loss
426
11. Which of the following is now a rare cause for joint infection in infants due to standard childhood immunisation schedule in the UK?
a. Staph.Aureus
b. Gp A strep
c. Varicella zoster
d. Rubella
e. Haemophilus Influenza
e. Haemophilus Influenza
427
12. 64 yr old woman with T2 DM has been struggling with cellulitis in her right forefoot for 4 weeks. After making no progress with oral antibiotic she has now had IV flucloxacillin and co-amoxiclavulanic acid but the pain and erythema persist and her CRP has only fallen to 47 from its peak of 91. What is the next appropriate investigation?
a. Blood cultures
b. MRI right forefoot
c. Plain X-ray right forefoot
d. Skin biopsy of right forefoot
e. Ultrasound scan of right forefoot
c. Plain X-ray right forefoot
428
1. Which of the following is a. non-inflammatory cause of joint pain?
a. Rheumatoid
b. Septic arthritis
c. Spondylarthritis
d. Fibromyalgia
e. Gout
d. Fibromyalgia
429
2. Which of these is not a feature of rheumatoid arthritis?
a. NSAIDs help
b. Pain eases with use
c. Effects the DIP
d. Pain lasts for an hour or so in the morning
e. Ulnar deviation
c. Effects the DIP
430
3. Alendronic acid is a bisphosphate used in osteoporosis. Which describes the method of action of bisphosphates?
a. Cause increase bone deposition
b. Cause reactivation of metaphysis and epiphysis
c. Inhibit osteoclast and cause osteoclast apoptosis
d. Reduce the signalling pathway between osteoblasts, clasts by increasing RANK ligand
e. Increased removal of calcium into the haversian canal within bone
c. Inhibit osteoclast and cause osteoclast apoptosis
431
4. Gout – What is the investigative result from microscopy
a. Tophi
b. Needle +ve birefringent
c. Needle -ve birefringent
d. Rhomboid shaped +ve birefringent
e. Rhomboid shaped -ve birefringent
c. Needle -ve birefringent
432
5. What is the most likely causative organism for urethritis, conjunctivitis, arthritis? – reactive arthritis
a. S. Aureus
b. E. coli
c. Strep pneumonia
d. Hemophilus Influenza
e. Chlamydia
e. Chlamydia
433
6. Pins and needles in thumb, index and middle fingers, Carpal tunnel syndrome is caused by what
a. Cervical spine fracture
b. Compression of median nerve
c. Compression of radial nerve
d. CC8-T1 lesion
e. Compression of ulnar nerve
b. Compression of median nerve
434
7. Ankylosing spondylitis is associated with what genetics
a. HLA B27
435
8. Which of the following is the most common cause of osteomyelitis?
a. Staph aureus
436
10. DXA score of -1.6 means what
a. Osteopenia
