rheumatology to work on Flashcards
1
Q
Give 6 signs of spondyloarthritis
A
SPINE ACHE
- Sausage digits = dactylics
- Psoriasis
- Inflammatory back pain
- NSAID responsive
- Enthesitis
- Arthritis
- Crohn’s/UC
- HLAB27
- Eye - uveitis
2
Q
what is the clinical presentation of ankylosing spondylitis
A
- Lower back pain + stiffness → worse with rest + improves with movement
- Sacroiliac pain - radiates to hips
- Flares of worsening symptoms
- loss of lumbar lordosis and increased kyphosis
- progressive loss of spinal movement
- anterior uveitis
3
Q
What is the treatment for ankylosing spondylitis?
A
NSAIDs
corticosteroids
anti-TNF drugs infliximab
Physio, lifestyle advice
Surgery for deformities
4
Q
what are the clinical features of psoriatic arthritis
A
- Asymmetrical oligoarthritis (60%)
- Large joint arthritis (15%)
- Enthesitis - inflammation of entheses
- Dactylitis - inflammation of full finger
- Nail changes (pitting, onycholysis)
- inflammatory joint pain
- plaques of psoriasis
5
Q
What investigations might you do in someone you suspect to have psoriatic arthritis?
A
X-ray
- Erosion in DIPJ + periarticular new-bone formation - Osteolysis - Pencil-in-cup deformity
Bloods
- ESR + CRP - normal or raised
- Rheumatoid factor -ve
- anti-CCP - negative
Joint aspiration - no bacteria or crystals
6
Q
What is reactive arthritis?
A
● A sterile synovitis which occurs following GI infection or STI
● Typically affects lower limb
7
Q
What GI infections are associated with causing reactive arthritis?
A
Salmonella Shigella Yersinia enterocolitica campylobacter
8
Q
What GU infections are associated with causing reactive arthritis?
A
Chlamydia
Ureaplasma
urealyticum
9
Q
What investigations might you do in someone you suspect to have reactive arthritis?
A
ESR + CRP - raised ANA - negative RF - negative X-ray - sacroiliitis or enthesopathy Joint aspirate - negative (exclude septic arthritis + gout)
10
Q
What type of spondyloarthritis occurs in 20% of patients with IBD?
A
Enteropathic arthritis
11
Q
Psoriatic arthritis commonly involved swelling of what joint?
A
DIP joint
12
Q
Give 4 properties of bone that contribute to bone strength
A
- Bone mineral density
- Bone size
- Bone turnover
- Bone micro-architecture
- Mineralisation
- Geometry
13
Q
Give 5 risk factors for osteoporosis
A
- old age, women, FHx, previous fracture, smoking, alcohol, Asian/Caucasian
‘SHATTERED’
- Steroid use
- Hyperthyroidism, hyperparathyroidism, hypercalciuria
- Alcohol + tobacco use
- Thin (BMI < 18.5)
- Testosterone (low)
- Early menopause
- Renal or liver failure
- Erosive/inflammatory bone disease (e.g. myeloma or RA)
- Dietary low calcium /malabsorption or Diabetes type 1
14
Q
Name 3 endocrine disease that can be responsible for causing osteoporosis
A
- Hyperthyroidism and primary hyperparathyroidism - TH and PTH increase bone turnover
- Cushing’s syndrome - cortisol leads to increase bone resorption and osteoblast apoptosis
- Early menopause, male hypogonadism - less oestrogen/testosterone to control bone turnover
15
Q
What cells might you see on a histological slide taken form someone with vasculitis?
A
Neutrophils
Giant cells
16
Q
What is Giant cell arteritis?
A
Granulomatous inflammation of large cerebral arteries as well as other large vessels (aorta) which occurs in association with Polymyalgia rheumatica
17
Q
Describe the pathophysiology of giant cell arteritis
A
Arteries become inflamed, thicken and can obstruct blood flow
18
Q
what are is the clinical presentation of giant cell arteritis?
A
- Headache, typically unilateral over temporal area
- Temporal artery/scalp tenderness
- Jaw claudication
- Visual symptoms - vision loss (painless)
- Systemic symptoms - fever, malaise, lethargy
19
Q
What are the investigations for giant cell arteritis?
A
- ↑ESR and/or CRP (=highly sensitive) ESR >50 mm/hr
- Halo sign on US of temporal and axillary artery
- Temporal artery biopsy = gold standard for Dx (show giant cells, granulomatous inflammation)
20
Q
What is the diagnostic criteria for giant cell arteritis?
A
- Age >50
- New headache
- Temporal artery tenderness
- Abnormal artery biopsies
21
Q
Describe the treatment for giant cell arteritis
A
- High dose corticosteroids - prednisolone ASAP
- DMARDs - methotrexate (sometimes)
- Osteoporosis prophylaxis is important - lansoprazole, alendronate, Ca2+, vit D
22
Q
What is the pathophysiology of Wegener’s granulomatosis?
A
Necrotising granulomatous vasculitis affecting arterioles and venules
ANCAs can activate primed circulating neutrophils which leads to fibrin deposition in vessel walls and deposition of destructive inflammatory mediators
23
Q
What organ systems can be affected Wegener’s granulomatosis?
A
- URT
- Lungs
- Kidneys
- Skin
- Eyes
24
Q
What is the affect of Wegener’s granulomatosis on the Upper respiratory tract?
A
- Sinusitis
- Otitis
- Cough
- Haemoptysis
- Saddle nose deformity
25
What is the affect of Wegener's granulomatosis on the lungs?
1. Pulmonary haemorrhage/nodules
| 2. Inflammatory infiltrates are seen on X-ray
26
What is the affect of Wegener's granulomatosis on the Kidney?
Glomerulonephritis --> haem/proteinuria
27
What is the affect of Wegener's granulomatosis on the skin?
Ulcers Pulpura
28
What is the affect of Wegener's granulomatosis on the eyes?
Uveitits
Scleritis
Episcleritis
29
What investigations might you do in someone you suspect to have Wegener's Granulomatosis?
ANCA testing - c-ANCA
Tissue biopsy - (renal biopsy best) - shows granulomas
CT - assessment of organ involvement
FBC - high eosinophils
30
What is the treatment for Wegener's Granulomatosis?
- Glucocorticoids (prednisolone)
- Immunosuppresive drugs (cyclophosphamide OR rituximab)
- plasma exchange for specific complications
31
Give 5 risk factors for developing OA
1. Genetic predisposition - females, FHx
2. Trauma
3. Abnormal biomechanics (e.g. hypermobility)
4. Occupation (e..g manual labor)
5. Obesity = pro-inflammatory state
6. Old age
32
What are the most important cells responsible for OA?
Chondrocytes
33
Describe the pathophysiology of osteoarthritis
Mechanical stress --> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors
34
Name the 2 main pathological features of osteoarthritis
1. Cartilage loss
| 2. Disordered bone repair
35
Give 5 radiological features associated with OA
LOSS
1. Loss of joint space - articular cartilage destruction
2. Osteophyte formation - calcified cartilaginous destruction
3. Subchondral sclerosis - exposed
4. Subchondral cysts
5. Abnormalities of bone contour
36
Nodal osteoarthritis can affect the DIP and PIP joints. What are the 2 terms sued for nodes on these joints?
1. PIP = Bouchard's nodes
| 2. DIP = Heberden's nodes
37
Give an example of an autoimmune connective tissue disease
1. SLE
2. Systemic sclerosis (scleroderma)
3. Sjogren's syndrome
4. Dermatomyositis/Polymyositis
38
Describe the pathogenesis of SLE
Type 3 hypersensitivity reaction = immune complex mediated
| Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes
39
what are the clinical features of SLE?
Symptoms:
butterfly rash, wt loss, fever, fatigue, joint pain, mouth ulcers
Signs: correctable ulnar deviation
1. Rash - photosensitive vs diced vs malar (butterfly rash)
2. Mouth ulcers
3. Raynaud's phenomenon
4. General - fever, malaise, fatigue
5. Depression
6. Lupus nephritis --> proteinuria, renal failure and renal hypertension
7. Arthritis - symmetrical
8. Serositis - pleurisy/pleural effusion
40
What investigations might you do in someone who you suspect has SLE?
1. Blood tests = anaemia, neutropenia, thrombocytopenia, RAISED ESR and NORMAL CRP
2. Serum autoantibodies - ANA, anti-dsDNA
41
Describe the non medical treatment for SLE
Patient education and support
UV protection
Screening for end organ damage
Reduce CV risk factors - smoking cessation
42
Describe the pharmacological treatment for SLE
```
● Avoid excessive sunlight and reduce CVS risk factors
● NSAIDs - ibuprofen
● Chloroquine and hydroxychloroquine
● Corticosteroids - prednisolone
● cyclophosphamide
● methotrexate
● Topical steroids
```
43
What is systemic sclerosis (scleroderma)?
A multi system disease characterised by excess production and accumulation of collagen --> inflammation and vasculopathy
44
Describe the pathophysiology of scleroderma
Various factors cause endothelial lesion and vasculopathy
| Excessive collagen deposition --> inflammation and auto-antibody production
45
Give 5 signs of limited scleroderma
CREST
1. Calcinosis - skin calcium deposits
2. Raynauds
3. Esophageal reflux/stricture
4. Sclerodactyly - thick tight skin on fingers/toes
5. Telangiectasia - dilated facial spider veins
Pulmonary arterial hypertension
46
Give 4 signs of diffuse scleroderma
Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST
1. Proximal scleroderma
2. Pulmonary fibrosis
3. Bowel involvement
4. Myositis
5. Renal crisis
47
What is a diagnostic test for scleroderma?
Limited - ACAs
```
Diffuse -
Anti-topoisomerase,
Anti scl-70
ANAs
ESR (normal)
```
If renal involvement, there may be anemia
48
Describe the management of scleroderma
avoid smoking, handwarmers
GI - PPIs, Antibiotics
Renal - ACEi
Pulmonary fibrosis - cyclophosphamide
49
Give 5 symptoms of sjögren's syndrome
1. Dry eyes and dry mouth
2. dry skin and dry vagina
3. Inflammatory arthritis
4. Rash
5. Neuropathies
6. Vasculitis
7. fatigue
8. salivary and parotid gland enlargement
50
What investigations might you do in someone who you suspect to have sjögren's syndrome?
Serum auto-antibodies --> anti-RO, anti-La, RF, ANA
Raised immunoglobulins and ESR
Schirmer's test
- ability for eyes to self-hydrate - <10mm in 5 minutes
Rose bengal staining and slit lamp exam
51
What is the treatment for sjögren's syndrome?
- Artificial tears, artificial saliva, vaginal lubricants
- Hydroxychloroquine
- NSAID
- M3 agonist - pilocarpine
52
What is dermatomyositis?
A rare disorder of unknown aetiology
| Inflammation and necrosis of skeletal muscle fibres and skin
53
Give 3 symptoms of dermatomyositis
1. Rash
2. Muscle weakness
3. Lungs are often affected too (e.g. interstitial lung disease)
54
What investigations might you do in someone who you suspect has dermatomyositis?
1. Muscle enzymes raised
2. Electromyography (EMG)
3. Muscle/skin biopsy
4. Screen for malignancy
5. CXR
55
What is the treatment for dermatomyositis?
Steroids - prednisolone
Immunosuppressants
56
What are the 3 phases of Raynaud's?
White (vasoconstriction) --> Blue (tissue hypoxia) --> red (vasodilation)
57
which organisms can cause septic arthritis?
1. Staphylococcus aureus
2. Streptococci
3. Neisseria Gonorrhoea
4. Gram negative = E. coli, pseudomonas aeruginosa
58
what are the risk factors for septic arthritis?
```
Pre-existing joint disease (OA or RA)
Joint prostheses
IVDU
Immunosuppression
Alcohol misuse
Diabetes
Intra-articular corticosteroid injection
Recent joint surgery
```
59
What investigation would you do to someone you suspect has septic arthritis?
Aspirate joint → MC+S
Blood culture
WCC → may be raised
ESR + CRP → raised
60
Describe the treatment for septic arthritis
```
Aspirate joint
Empirical Abx - flucloxacillin
- if allergic to penicilin = clindamycin
- if MRSA = vancomycin
- if gram negative = cefotaxime
Analgesia - NSAIDS
```
61
What organisms can cause osteomyelitis?
1. Staph. aureus
2. Coagulase negative staph (s. epidermidis)
3. Aerobic gram negate bacilli (salmonella)
4. haemophilus influenza
5. Mycobacterium TB
62
Name 2 predisposing conditions for osteomyelitis
1. Diabetes
| 2. PVD
63
Osteomyelitis: Who is most likely to be effected by contagious spread of infection?
Affects older adults, those with DM, chronic ulcers, vascular disease, arthroplasties
64
Give 4 host factors that affect the pathogenesis of osteomyelitis
1. Behavioural (risk of trauma)
2. Vascular supply (arterial disease, DM)
3. Pre-existing bone/joint problems (RA)
4. Immune deficiency
65
Acute osteomyelitis: what changes to bone might you see histologically?
1. Inflammatory cells
2. Oedema
3. Vascular congestion
4. Small vessel thrombosis
66
Chronic osteomyelitis: what changes to bone might you see histologically?
1. Necrotic bone - 'squestra'
2. New bone formation 'involucrum'
3. Neutrophil exudates
4. Lymphocytes and histiocytes
67
Why does chronic osteomyelitis lead to sequestra and new bone formation?
- Inflammation in BM increase intramedullary pressure exudate into bone cortex which rupture through periosteum
- this causes interruption of periosteum blood supply which results in necrosis and sequestra
- therefore new bone forms
68
What is acute osteomyelitis associated with?
Associated with inflammatory bone changes caused by pathogenic bacteria
69
What is chronic osteomyelitis associated with?
Involves bone necrosis
70
what is the clinical presentation of osteomyelitis?
1. Slow onset
2. Dull pain at OM site, aggravated by movement
3. Systemic = fever, rigors, sweating, malaise
71
what are the signs of acute osteomyelitis?
1. Tender
2. Warm
3. Red swollen area around OM
72
what are the signs of chronic osteomyelitis?
1. Acute OM signs
2. Draining sinus tract
3. Non-healing ulcers/fracture
73
What is the differential diagnosis of osteomyelitis?
1. Cellulitis
2. Charcot's joints (sensation loss --> degeneration)
3. Gout
4. Fracture
5. Malignancy
6. Avascular bone necrosis
74
What investigations might you do on someone who you suspect may have osteomyelitis?
1. Bloods - raised inflammatory markers (CRP, ESR) and WCC
2. X-rays (cortical erosion, sequestra, sclerosis) and MRI (delineates inflammatory layers, marrow oedema)
3. Bone biopsy - gold standard
4. Blood cultures
75
Describe the usual treatment for osteomyelitis
Large dose IV antibiotics tailored to culture findings (S. aureus = flucloxacillin)
immobilisation
Surgical treatment = debridement +/- arthroplasty of joint involved
76
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 = 12 months
77
Why is osteomyelitis difficult to treat?
Antibiotics struggle to penetrate bone and bone has a poor blood supply
78
Name 3 risk factors of RA
1. Smoking
2. Women
3. family history
4. Other AI conditions
5. genetic factors - HLA-DR4 and HLA-DRB1
79
Describe the pathophysiology of RA
1. Chronic inflammation - B/T cells and neutrophils infiltrate
2. Proliferation --> pannus formation (synovium grows out and over cartilage)
3. Pro-inflammatory cytokines --> proteinases --> cartilage destruction
80
what are the symptoms of RA?
1. Early morning stiffness (>60 mins)
2. Pain eases with use
3. Swelling
4. General fatigue, malaise
5. Extra-articular involvment
81
what are the signs of RA?
1. Symmetrical polyarthorpathy
2. Deforming --> ulnar deviation, swan neck deformity, boutonniere deformity
3. Erosion on X-ray
4. 80% = RF positive
82
RA extra-articular involvement: describe the effect on soft tissues
Nodules
Bursitis
Muscle wasting
83
RA extra-articular involvement: describe the effect on the eyes
Dry eyes
Scleritis
Episcleritis
84
RA extra-articular involvement: describe the neurological effects
Sensory peripheral neuropathy
Entrapment neuropathies (carpal tunnel syndrome)
Instability of cervical spine
85
RA extra-articular involvement: describe the haematological effects
Felty's syndrome (RA + splenomegaly + neutropenia) Anaemia
86
RA extra-articular involvement: describe the pulmonary effects
Pleural effusion
| Fibrosing alveolitis
87
RA extra-articular involvement: describe the effects on the heart
Pericardial rub
| Pericardial effusion
88
RA extra-articular involvement: describe the effects on the kidney
Amyloidosis
89
RA extra-articular involvement: describe the effects on the skin
Vasculitis - infarcts in nail bed
90
What investigations might you do in someone you suspect has rheumatoid arthritis?
- Blood for inflammatory markers
- ESR and CRP raised
- RF and Anti-CCP
X-ray- Synovial fluid is sterile with high neutrophil count
91
What is rheumatoid factor?
An antibody against the Fc portion of IgG
92
What is seen on an X-ray of someone with RA?
LESS:
- Loss of joint space (due to cartilage loss)
- Erosion
- Soft tissue swelling
- Soft bones = osteopenia
93
What joints tend to be affects in RA?
MCP
PIP
Wrist (DIP often spared)
94
Describe the pathophysiology of gout
Purine --> (by xanthine oxidase) xanthine --> uric acid --> monosodium rate crystals OR excreted by kidneys
Urate blood/tissue imbalance --> rate crystal formation --> inflammatory response through phagocytic activation
Overproduction/under excretions of uric acid causes build up and precipitated out in joints
95
Give 3 causes of gout
= Hyperuricaemia
1. Impaired excretion - CKD, diuretics, hypertension
2. Increased production - hyperlipidaemia
3. Increased intake - high purine diet = red meat, seafood, fructose, alcohol
96
Name 3 common precipitants of a gout attack
1. Aggressive introduction of hypouricaemic therapy
2. Alcohol or shellfish binges
3. Sepsis, MI, acute severe illness
4. Trauma
97
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
98
What investigations might you do in a patient you think has gout?
first line = bloods
- U&E and eGFR - renal failure
- Uric acid levels - 4-6 weeks after to confirm hyperuricaemia
- gold standard = joint aspiration
99
What is the aim of treatment for gout?
To get urate levels < 300 mol/L
100
How would you treat acute gout?
1st line = NSAID or colchicine
2nd line = intra-articular steroid injection
lifestyle advice - wt loss, exercise, diet, alcohol and fluid intake
101
what is the management for chronic gout?
1st line = allopurinol - inhibits xanthine oxidase
2nd line = febuxostat
consider co-prescribing colchicine with allopurinol for 6 months
102
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
103
Name 6 factors that can cause an acute attack of gout
1. Sudden overload
2. Cold
3. Trauma
4. Sepsis
5. Dehydration
6. Drugs
104
Describe the pathophysiology of pseudogout
Calcium pyrophosphate crystals are deposited on joint surfaces - produces the radiological appearance of chondrocalcinosis
Crystals elicit an acute inflammatory response
105
What can cause pseudogout?
1. Hypo/hyperthyroidism
2. Haemochromatosis
3. Diabetes
4. Magnesium levels
106
what is the clinical presentation of pseudogout?
SYMPTOM
hot, swollen, tender joint, usually knees
SIGNS
recent injury to the joint in the history
Typically the wrists and knees
107
What investigations might you do in someone you suspect might have pseudogout?
Aspiration --> fluid for crystals and blood cultures = positive birefringent rhomboid crystals
X-rays --> can show chondrocalcinosis
108
What is the most likely differential diagnosis for pseudogout?
Infection
109
Describe the treatment for pseudogout
- high dose NSAIDs - ibuprofen
- Colchicine - anti-gout
- IM prednisolone
- Aspiration, intra-articular steroid injections
110
How can you distinguish OA from pseudogout?
Pattern of involvement --> Pseudo = wrists, shoulders, ankle, elbows
Marked inflammatory component --> Elevated CRP and ESR Superimposition of acute attacks
111
What kind of crystals do you see in pseudogout?
Positive birefringent calcium pyrophosphate rhomboid crystals
112
What kind of crystals do you see in gout?
Monosodium urate crystals = negatively birefringent
113
What kind of crystals fo you see in pseudogout?
Calcium pyrophosphate crystals = positively birefringent
114
Name 4 diseases that fibromyalgia is commonly associated with
1. Depression
2. Choric fatigue
3. IBS
4. Chronic headache
115
Give 4 symptoms of fibromyalgia
1. Neck and back pain
2. Pain is aggravated by stress, cold and activity
3. Generalised morning stiffness
4. Paraesthesia of hands and feet
5. Profound fatigue
6. Unrefreshing sleep
7. poor concentration, brain fog
116
Give 3 disease that might be included in the differential diagnosis for fibromyalgia
1. Hypothyroidism
2. SLE
3. Low vitamin D
117
Define sarcoma
A rare tumour of mesenchymal origin
| A malignant connective tissue neoplasm
118
What are the red flag symptoms for bone malignancy?
```
Rest pain
Night pain
Loss of function
Neurological problems
Weight loss
Growing lump
Deformity
```
119
What are secondary bone tumours?
Metastases from:
1. Lungs
2. Breast
3. Prostate
4. Thyroid
5. Kidney
120
What investigations might you do in someone you suspect has bone cancer?
1st line → x-ray
Gold standard → biopsy
Bloods → FBC, ESR, ALP, lactate dehydrogenase, Ca, U+E
CT chest/abdo/pelvis
121
What might you seen on an X-ray of someone with bone cancer?
Onion skin/sunburst appearance = Ewings
Colman's triangle = osteosarcoma, Ewings, GCT, Osteomyelitis, metastasis
122
What staging is used for bone cancers?
Enneking grading
123
How are malignant bone cancers staged using Enneking grading?
```
G1 = Histologically benign
G2 = Low grade
G3 = High grade
```
```
A = intracompartmental
B = extracompartmental
```
124
How are benign bone cancers staged using Enneking grading?
```
G1 = Latent
G2 = Active
G3 = Aggressive
```
125
How are bone cancers treated?
```
MDT management
Benign
- NSAIDS
- Bisphosphonates (alendronate)
- symptomatic help
```
Malignancy = surgical excision --> limb sparing/amputation
radio/chemotherapy
126
Give 4 local complications with surgery for bone cancers
1. Haematoma
2. Loss of function
3. Infection
4. Local recurrence
127
Where do osteosarcomas usually present?
Knee - distal femur, proximal humerus
128
What is an osteosarcoma?
Malignant tumour of bone
Spindle cell neoplasm that produce osteoid
rapidly metastases to the lung
129
Give 3 features of osteosarcoma
1. Fast growing
2. Aggressive - Destroys bone and spreads into surrounding tissues, rapidly metastasises to lung
3. Typically affects 15-19 year olds
4. often relatively painless
130
Name a boney sarcoma that responds well to chemotherapy
Ewings sarcoma
131
Where does Ewings sarcoma arise from?
mesenchymal stem cells
132
Give 3 side effects of NSAIDs
1. Peptic ulcer disease
2. Renal failure
3. Increased risk of MI and CV disease
133
What can you do to reduce the risk of gastric ulcers and bleeding in someone taking NSAIDs?
1. Co-prescribe PPI
| 2. Prescribe low doses and short courses
134
Give 5 potential side effects of steroids
1. Diabetes
2. Muscle wasting
3. Osteoporosis
4. Fat redistribution
5. Skin atrophy
6. Hypertension
7. Acne
8. Infection risk
135
How do DMARDs work?
Non-specific inhibition of inflammatory cytokines cascade = reduces joint pain, stiffness and swelling
136
Give 3 potential side effects of methotrexate
1. Bone marrow suppression
2. Abnormal liver enzymes
3. Nausea
4. Diarrhoea
5. Teratogenic
137
What are cytokines?
Short acting hormones
138
Describe the mechanism of action of infliximab
Inhibits T cell activation
139
How does alendronate work?
Reduces bone turnover by inhibiting osteoclast mediated bone resorption
140
what are the signs of osteoarthritis?
● Deformity and bony enlargement of the joints
● Limited joint movement
● Muscle wasting of surrounding muscle groups
● Crepitus (grafting) due to disruption of normally smooth articulating surfaces of joints
● May be joint effusion
● Heberden’s nodes are bony swellings at DIPJs
● Bouchard’s nodes occur at proximal interphalangeal joints
141
what are the investigations for osteoarthritis?
● FBC and ESR normal
● Rheumatoid factor is negative but positive low titre tests may occur incidentally in elderly
● XRs abnormal in advanced disease
142
what are the complications of rheumatoid arthritis?
Cervical spinal cord compression- weakness and loss of sensation
Lung involvement- interstitial lung disease, fibrosis.
143
what is the difference between the presentation of early and late septic arthritis
● Early infection presents with inflammation, discharge, joint effusion, loss of function and pain
● Late disease presents with pain or mechanical dysfunction
144
what are the risk factors for gout?
Middle age overweight males.
high purine diet,
increased cell turnover
145
what are the complications of gout?
Infection in the tophi
| Destruction of the joint
146
what are the risk factors for osteomyelitis?
```
Previous osteomyelitis
Penetrating injury
IVDU
Diabetes
HIV
Recent surgery
Distant or local infection
Sickle cell disease
RACKD
Children → upper resp tract or varicella infection
```
147
what are the risk factors for ankylosing spondylitis?
HLA-B27
| environment - klebsiella, salmonella, shigella
148
what is arthritis mutilans?
Most severe form of psoriatic arthritis
Occurs in phalanxes
Osteolysis of bones around joints in digits → leads to progressive shortening
Skin then folds as digit shortens → telescopic finger
149
what are the different types of psoriatic arthritis?
● Distal interphalangeal arthritis – most typical pattern of joint involvement – dactylitis is characteristic
● Mono- or oligoarthiritis
● Symmetrical seronegative polyarthritis – resembling RA
● Arthritis mutilans – a severe form with destruction of the small bones in the hands and feet
● Sacroiliitis – uni- or bilateral
150
what treatment should be used if reactive arthritis relapses?
methotrexate or sulfasalazine
151
what is the pathophysiology of reactive arthritis?
● Bacterial antigens or DNA have been found in the inflamed synovium of affected joints – suggests persistent antigenic material is driving the inflammatory response
152
what are the complications for SLE?
Cardiac, lung, kidney involvement. Widespread inflammation causing damage.
153
what is the the pathophysiology of fibromyalgia?
Unknown, possibly pain perception/hyper excitability of pain fibres
154
what are the complications of fibromyalgia?
- can really affect quality of life
- anxiety, depression, insomnia
- opiate addiction
155
what is rickets?
Rickets: inadequate mineralization of the bone and epiphyseal cartilage in the growing skeleton of CHILDREN.
156
what are the complications of Sjogren's syndrome?
- eye infections- oral problems (dental cavities, candida infections)
- vaginal problems (candidiasis, sexual dysfunction)
RARE
- pneumonia and bronchiectasis
- non-hodgkin's
- vasculitis
- renal impairment
- peripheral neuropathy
157
which arteries are particularly affected by giant cell arteritis?
- aorta and vertebral arteries
- Cerebral arteries affected in particular e.g. temporal artery
- Opthalmic artery can also be affected potentially resulting in permanent ortemporary vision loss
158
what is found on physical examination of giant cell arteritis?
temporal arteries may be tender on palpation and thickened. Pulses may be diminished.
159
what is antiphospholipid syndrome?
- Syndrome characterised by thrombosis (arterial or venous) and/or recurrentmiscarriages with positive blood tests for antiphospholipid antibodies (aPL) - hypercoagulable state
160
what are the risk factors for antiphospholipid syndrome?
- diabetes
- hypertension
- obesity
- female
- underlying autoimmune condition
- smoking
- oestrogen therapy
161
what is the clinical presentation of antiphospholipid syndrome?
- thrombosis
- miscarriage
- livedo reticularis - purple lace rash
- ischaemic stroke, TIA, MI
- DVT, budd-chiari syndrome
- thrombocytopenia
- valvular heart disease, migraines, epilepsy
162
what is the pathophysiology of antiphospholipid syndrome?
- Antiphospholipid antibodies (aPL) play a role in thrombosis by binding tophospholipid on the surface of cells such as endothelial cells, platelets andmonocytes
- Once bound, this change alters the functioning of those cells leading tothrombosis and/or miscarriage
- Antiphospholipid antibodies (aPL) cause CLOTs:
• Coagulation defect
• Livedo reticularis - lace-like purplish discolouration of skin
• Obstetric issues i.e. miscarriage
• Thrombocytopenia (low platelets)
163
what are the investigations for antiphospholipid syndrome?
Hx of thrombosis/ pregnancy complications + Antibody screen with raised:
- anticardiolipin antibodies
- lupus anticoagulant
- anti-beta-2 glycoprotein I antibodies
164
what is the treatment for antiphospholipid syndrome?
- long term warfarin
- Pregnant women on low molecular weight heparin (e.g. enoxaparin) + aspirin
- lifestyle - smoking cessation, exercise, healthy diet
165
what are the complications of antiphospholipid syndrome?
- Venous thromboembolisms (e.g. DVT, pulmonary embolism)
- Arterial thrombosis (stroke, MI, renal thrombosis)
- Pregnancy complications (recurrent miscarriage, pre-eclampsia,…)
166
what is the clinical presentation of wegener's granulomatosis?
Classic sign on exams: saddle shaped nose
Epistaxis - nosebleed
Crusty nasal/ ear secretions 🡪 hearing loss
Sinusitis
Cough, wheeze, haemoptysis
167
what are the complications of wegener's granulomatosis?
Glomerulonephritis
168
what is the most common primary bone malignancy in children?
osteosarcoma
169
what condition is osteosarcoma associated with?
Paget's disease
170
what is the appearance of osteosarcoma on x-rays?
bone destruction and formation,
| soft tissue calcification produces a sunburst appearance
171
what is the clinical presentation of ewing's sarcoma?
● Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk
● Painful swelling, redness in surrounding area, malaise, anorexia, weight loss, fever, paralysis and/or incontinence if affecting the spine, numbness in affected limb
172
where is Ewing's sarcoma commonly found?
Presents with mass/swelling, most commonly in long bones of the
o Arms, legs, pelvis, chest
o Occasionally skull and flat bones of the trunk
173
where does chrondosarcoma commonly present?
Common sites are pelvis, femur, humerus, scapula and ribs
174
what is the clinical presentation of chrondrosarcoma?
Associated with dull, deep pain and affected area is swollen and tender
175
which is the most common sarcoma in adults?
chondrosarcoma
176
which types of malignancy cause bone pain?
- multiple myeloma
- lymphoma
- primary bone tumours
- metastases - secondary bone tumour
177
other than bone pain, what other symptoms can indicate bone tumours?
- Mobility issues → unexplained limp, joint stiffness, reduced ROM
- Inflammation + tenderness over bone
- Systemic symptoms
178
what is the prophylactic treatment for antiphospholipid syndrome?
aspirin or clopidogrel for people with aPL
179
what are the risk factors for scleroderma?
- exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
- bleomycin
- genetic
180
what is polymyositis?
a rare muscle disorder of unknown aetiology in which there is inflammation and necrosis of skeletal muscle fibres
181
what is dermatomyositis?
polymyositis with skin involvement
182
what is the clinical presentation of polymyositis?
- symmetrical progressive muscle weakness and wasting - affects proximal muscles of shoulder and pelvic girdle
- difficulty squatting, going upstairs, rising from chair and raising hands above head
- involvement of pharyngeal, laryngeal and respiratory muscles = dysphagia, dysphonia and respiratory failure
- pain and tenderness = uncommon
183
what is the clinical presentation of dermatomyositis?
- heliotrope (purple) discolouration of eyelids
- scaly erythematous plaques over knuckles (Gotton's papules)
- arthralgia, dysphagia and raynauds
184
what are the investigations for polymyositis/dermatomyositis?
Muscle Biopsy
Bloods
- serum creatine kinase, aminotransferases, lactate dehydrogenase (LDH) and aldolase all raised
Immunology
ANA, Anti jo1, anti mi2
185
what is the treatment for polymyositis/dermatomyositis?
- bed rest + exercise plan
- oral prednisolone
- steroid sparing immunosuppressive - azathioprine, methotrexate, ciclosporin
- hydroxychloroquine for skin disease
186
what factors are used in the FRAX score calculation?
- age
- sex
- height and weight
- previous fractures
- smoking
- parent fractured hip (FHx)
- steroid (glucocorticoid use)
- RA
- secondary osteoporosis
- alcohol consumption (>3 units)
- femoral neck bone mineral density
187
what is the diagnostic criteria for RA?
RF RISES - >6 weeks and >4 of following:
- RF positive
- Finger/hand/wrist involvement
- Rheumatoid nodules present
- Involvement of >3 joints
- Stiffness in morning >1 hr
- Erosions on x-ray
- Symmetrical involvement
188
what is the treatment for raynauds phenomenon?
Lifestyle - protect the hands, stop smoking
| Medications - CCB
189
what is limited scleroderma?
- skin involvement limited to hands, face, feet and forearms
- characteristic ‘beak’-like nose and small mouth
- Microstomia - small mouth
190
what is diffuse scleroderma?
skin changes develop more rapidly and are more widespread
Raynaud’s phenomenon coincident with skin involvement
GI, Renal, Lung involvement
191
what is paget's disease?
localized disorder of bone remodelling
↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)
192
what is the pathophysiology of paget's disease?
↑ osteoclastic bone resorption followed by ↑ formation of weaker bone
Leads to structurally disorganized mosaic of bone (woven bone)
193
what are the clinical features of paget's disease?
60-80% are asymptomatic
- bone pain
- joint pain
- deformities -> bowed tibia and skull enlargement
- neurological complications
- CN8 compression -> deafness
- blockage of aqueduct of sylvius causing hydrocephalus
194
what are the investigations for paget's disease?
Bloods - Increased ALP, normal calcium and phosphate
Urinary hydroxyproline increase
X-rays - Findings of osteoarthritis, sclerotic changes, bone loss and reduced density
isotope bone scan
195
what is the management for paget's disease?
Bisphosphonates,
| NSAIDS
196
what is osteomalacia?
Defective mineralization of newly formed bone matrix or osteoid in adults, due to inadequate phosphate or calcium, or due to ↑ bone resorption (hyperPTH)
197
what are the causes of osteomalacia?
malnutrition (most common)
drug induced
defective 1-alpha hydroxylation
Liver disease
198
what is the clincial presentation of osteomalacia?
```
Osteomalacia
widespread bone pain and tenderness
gradual onset and persistent fatigue
muscle weakness, parasthesia, waddling gait
fractures
```
199
what is the clincial presentation of rickets?
leg-bowing and knock knees
- tender swollen joints
- growth retardation
- bone and joint pain
dental deformities – delayed formation of teeth, enamel hypoplasia
- enlargement of end of ribs (‘rachitic rosary’)
200
what are the investigations for Osteomalacia / rickets?
Bloods - U&Es, Serum ALP, Vit D
| X-rays - defective mineralisation, rachitic rosary
201
what is the management for osteomalacia/rickets?
Lifestyle - nutrition, sunlight
Medications - Vit D replacement
Malabsorption/Renal disease - IM calcitriol
202
what is the sepsis 6?
1. administer O2
2. take blood cultures
3. give IV antibiotics
4. give IV fluids
5. check serial lactates
6. measure urine output
203
what are the common sites for bone changes in paget's disease?
pelvis
vertebrae - thoracic + lumbar
femur
skull tibia
204
what are the complications of Paget's?
nerve compression - deafness and paraparesis
hydrocephalus
oestosarcoma
high output cardiac failure and myocardial hypertrophy
