rheumatology to work on COPY Flashcards
(133 cards)
1
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
2
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)
3
Q
Give 4 properties of bone that contribute to bone strength
A
- Bone mineral density
- Bone size
- Bone turnover
- Bone micro-architecture
- Mineralisation
- Geometry
4
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
5
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
6
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)
7
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
8
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
9
Q
What investigations might you do in someone you suspect to have Wegener’s Granulomatosis?
A
ANCA testing - c-ANCA
Tissue biopsy - (renal biopsy best) - shows granulomas
CT - assessment of organ involvement
FBC - high eosinophils
10
Q
What is the treatment for Wegener’s Granulomatosis?
A
- Glucocorticoids (prednisolone)
- Immunosuppresive drugs (cyclophosphamide OR rituximab)
- plasma exchange for specific complications
11
Q
Give 5 risk factors for developing OA
A
- Genetic predisposition - females, FHx
- Trauma
- Abnormal biomechanics (e.g. hypermobility)
- Occupation (e..g manual labor)
- Obesity = pro-inflammatory state
- Old age
12
Q
Describe the pathophysiology of osteoarthritis
A
Mechanical stress –> progressive destruction and loss of articular cartilage
exposed subchondral bone becomes sclerotic
cytokine mediated TNF/IL/NO involved
deficiency in growth factors
13
Q
Describe the pathogenesis of SLE
A
Type 3 hypersensitivity reaction = immune complex mediated
Autoantibodies to a variety of auto antigens result in formation and deposition of immune complexes
14
Q
What investigations might you do in someone who you suspect has SLE?
A
- Blood tests = anaemia, neutropenia, thrombocytopenia, RAISED ESR and NORMAL CRP
- Serum autoantibodies - ANA, anti-dsDNA
15
Q
Describe the pharmacological treatment for SLE
A
● Avoid excessive sunlight and reduce CVS risk factors ● NSAIDs - ibuprofen ● Chloroquine and hydroxychloroquine ● Corticosteroids - prednisolone ● cyclophosphamide ● methotrexate ● Topical steroids
first line = hydroxychloroquine
16
Q
Give 5 signs of limited scleroderma
A
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
17
Q
Give 4 signs of diffuse scleroderma
A
Skin changes develop more rapidly and are more widespread than inlimited cutaneous scleroderma/CREST
- Proximal scleroderma
- Pulmonary fibrosis
- Bowel involvement
- Myositis
- Renal crisis
18
Q
What is a diagnostic test for scleroderma?
A
Limited - ACAs
Diffuse - Anti-topoisomerase, Anti scl-70 ANAs ESR (normal)
If renal involvement, there may be anemia
19
Q
Describe the management of scleroderma
A
avoid smoking, handwarmers
GI - PPIs, Antibiotics
Renal - ACEi
Pulmonary fibrosis - cyclophosphamide
20
Q
Give 5 symptoms of sjögren’s syndrome
A
- Dry eyes and dry mouth
- dry skin and dry vagina
- Inflammatory arthritis
- Rash
- Neuropathies
- Vasculitis
- fatigue
- salivary and parotid gland enlargement
21
Q
What investigations might you do in someone who you suspect to have sjögren’s syndrome?
A
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
22
Q
What is the treatment for sjögren’s syndrome?
A
- Artificial tears, artificial saliva, vaginal lubricants
- Hydroxychloroquine
- NSAID
- M3 agonist - pilocarpine
23
Q
Give 3 symptoms of dermatomyositis
A
- Rash
- Muscle weakness
- Lungs are often affected too (e.g. interstitial lung disease)
24
Q
What investigations might you do in someone who you suspect has dermatomyositis?
A
- Muscle enzymes raised
- Electromyography (EMG)
- Muscle/skin biopsy
- Screen for malignancy
- CXR
25
What is the treatment for dermatomyositis?
Steroids - prednisolone
Immunosuppressants
26
which organisms can cause septic arthritis?
1. Staphylococcus aureus
2. Streptococci
3. Neisseria Gonorrhoea
4. Gram negative = E. coli, pseudomonas aeruginosa
27
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
```
28
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
```
29
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
30
Name 2 predisposing conditions for osteomyelitis
1. Diabetes
| 2. PVD
31
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
32
Acute osteomyelitis: what changes to bone might you see histologically?
1. Inflammatory cells
2. Oedema
3. Vascular congestion
4. Small vessel thrombosis
33
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
34
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
35
What is acute osteomyelitis associated with?
Associated with inflammatory bone changes caused by pathogenic bacteria
36
What is chronic osteomyelitis associated with?
Involves bone necrosis
37
what are the signs of acute osteomyelitis?
1. Tender
2. Warm
3. Red swollen area around OM
38
what are the signs of chronic osteomyelitis?
1. Acute OM signs
2. Draining sinus tract
3. Non-healing ulcers/fracture
39
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
40
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
41
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
42
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
43
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
44
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
45
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
46
RA extra-articular involvement: describe the effect on soft tissues
Nodules
Bursitis
Muscle wasting
47
RA extra-articular involvement: describe the effect on the eyes
Dry eyes
Scleritis
Episcleritis
48
RA extra-articular involvement: describe the pulmonary effects
Pleural effusion
| Fibrosing alveolitis
49
RA extra-articular involvement: describe the effects on the heart
Pericardial rub
| Pericardial effusion
50
RA extra-articular involvement: describe the effects on the skin
Vasculitis - infarcts in nail bed
51
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
52
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
53
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
54
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
55
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
56
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
57
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
58
Name 6 factors that can cause an acute attack of gout
1. Sudden overload
2. Cold
3. Trauma
4. Sepsis
5. Dehydration
6. Drugs
59
What can cause pseudogout?
1. Hypo/hyperthyroidism
2. Haemochromatosis
3. Diabetes
4. Magnesium levels
60
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
61
What is the most likely differential diagnosis for pseudogout?
Infection
62
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
63
Name 4 diseases that fibromyalgia is commonly associated with
1. Depression
2. Choric fatigue
3. IBS
4. Chronic headache
64
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
65
Give 3 disease that might be included in the differential diagnosis for fibromyalgia
1. Hypothyroidism
2. SLE
3. Low vitamin D
66
Define sarcoma
A rare tumour of mesenchymal origin
| A malignant connective tissue neoplasm
67
where do secondary bone tumours come from?
Metastases from:
1. Lungs
2. Breast
3. Prostate
4. Thyroid
5. Kidney
68
How are malignant bone cancers staged using Enneking grading?
```
G1 = Histologically benign
G2 = Low grade
G3 = High grade
```
```
A = intracompartmental
B = extracompartmental
```
69
How are benign bone cancers staged using Enneking grading?
```
G1 = Latent
G2 = Active
G3 = Aggressive
```
70
Where do osteosarcomas usually present?
Knee - distal femur, proximal humerus
71
Where does Ewings sarcoma arise from?
mesenchymal stem cells
72
Give 3 side effects of NSAIDs
1. Peptic ulcer disease
2. Renal failure
3. Increased risk of MI and CV disease
73
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
74
How do DMARDs work?
Non-specific inhibition of inflammatory cytokines cascade = reduces joint pain, stiffness and swelling
75
Give 3 potential side effects of methotrexate
1. Bone marrow suppression
2. Abnormal liver enzymes
3. Nausea
4. Diarrhoea
5. Teratogenic
76
Describe the mechanism of action of infliximab
Inhibits T cell activation
77
How does alendronate work?
Reduces bone turnover by inhibiting osteoclast mediated bone resorption
78
what are the complications of rheumatoid arthritis?
Cervical spinal cord compression- weakness and loss of sensation
Lung involvement- interstitial lung disease, fibrosis.
79
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
80
what are the risk factors for gout?
Middle age overweight males.
high purine diet,
increased cell turnover
81
what are the complications of gout?
Infection in the tophi
| Destruction of the joint
82
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
```
83
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
84
what treatment should be used if reactive arthritis relapses?
methotrexate or sulfasalazine
85
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
86
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
87
what is antiphospholipid syndrome?
- Syndrome characterised by thrombosis (arterial or venous) and/or recurrentmiscarriages with positive blood tests for antiphospholipid antibodies (aPL) - hypercoagulable state
88
what are the risk factors for antiphospholipid syndrome?
- diabetes
- hypertension
- obesity
- female
- underlying autoimmune condition
- smoking
- oestrogen therapy
89
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
90
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)
91
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
92
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
93
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
94
what condition is osteosarcoma associated with?
Paget's disease
95
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
96
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
97
where does chrondosarcoma commonly present?
Common sites are pelvis, femur, humerus, scapula and ribs
98
what is the clinical presentation of chrondrosarcoma?
Associated with dull, deep pain and affected area is swollen and tender
99
what are the risk factors for scleroderma?
- exposure to vinyl chloride, silica dust, rapeseed oil, trichloroethylene
- bleomycin
- genetic
100
what is the clinical presentation of dermatomyositis?
- heliotrope (purple) discolouration of eyelids
- scaly erythematous plaques over knuckles (Gotton's papules)
- arthralgia, dysphagia and raynauds
101
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
102
what is the treatment for polymyositis/dermatomyositis?
- bed rest + exercise plan
- oral prednisolone
- steroid sparing immunosuppressive - azathioprine, methotrexate, ciclosporin
- hydroxychloroquine for skin disease
103
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
104
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
105
what is limited scleroderma?
- skin involvement limited to hands, face, feet and forearms
- characteristic ‘beak’-like nose and small mouth
- Microstomia - small mouth
106
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)
107
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)
108
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
109
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
110
what is the management for paget's disease?
Bisphosphonates,
| NSAIDS
111
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)
112
what are the causes of osteomalacia?
malnutrition (most common)
drug induced
defective 1-alpha hydroxylation
Liver disease
113
what is the clincial presentation of osteomalacia?
```
Osteomalacia
widespread bone pain and tenderness
gradual onset and persistent fatigue
muscle weakness, parasthesia, waddling gait
fractures
```
114
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’)
115
what are the investigations for Osteomalacia / rickets?
Bloods - U&Es, Serum ALP, Vit D
| X-rays - defective mineralisation, rachitic rosary
116
what is the management for osteomalacia/rickets?
Lifestyle - nutrition, sunlight
Medications - Vit D replacement
Malabsorption/Renal disease - IM calcitriol
117
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
118
what are the common sites for bone changes in paget's disease?
pelvis
vertebrae - thoracic + lumbar
femur
skull tibia
119
what are the complications of Paget's?
nerve compression - deafness and paraparesis
hydrocephalus
oestosarcoma
high output cardiac failure and myocardial hypertrophy
120
what enzyme expressed by osteoclasts is responsible for bone resorption?
cathepsin K
121
what is the effect of unopposed RANK ligand?
leads to increased bone loss
| more osteoclasts stimulated due to less OPG
122
what is the function of OPG?
inhibits osteoclast formation, function and survival by binding to RANK ligand
prevents RANK ligand from binding to osteoclast
123
what protein inhibits RANK ligand?
OPG
124
what is the function of RANK ligand?
binds to osteoclasts and is essental for formation, functio nand survivl
125
what cells secrete RANK ligand?
osteoblasts
126
what is the classification system for fractures involving the physis
salter-harris fracture classification
127
what is the physiological pathway to monosodium urate formation
purine -> hypoxanthine -> xanthine -> uric acid -> monosodium urate
128
name a drug that can increase monosodium urate?
bendroflumethiazide
| impair urate excretion
129
give 3 factors that increase pain
substance P
glutamate
serotonin
130
give 3 factors that decrease pain volume
opioids
GABA
cannabanoids
131
what is a complication of RA?
felty's syndrome - anaemia and splenomegaly and neutropenia
132
what are the extra-articular manifestations of RA?
```
skin = nodules, vasculitis
sjogrens
glomerulonephritis
peripheral neruopathy
MI, pericarditis
pulmonary = pleuritis, effusions
```
133
what type of crystals are seen in gout?
needle-shaped, negatively birefringent monosodium urate crystals
