Revision List Rheum Flashcards
1
Q
What is a crystal?
A
Homogenous solid, stable high density, hard
2
Q
When are crystals pathological?
A
- Deposition causes inflammatory response and tissue damage
2. Deposition at abnormal sites
3
Q
Give 3 examples of pathological crystals?
A
- Joints: Crystal arthropathies, urate, calcium pyrophosphate, hydoxypatite
- Kidney: stones - calcium oxalate (nephrolithiases)
- Gallbladder: cholesterol
4
Q
What is crystal arthropathy?
A
Arthritis caused by deposition of crystals in joint lining
5
Q
What is gout?
A
Monosodium urate crystal deposition in the joints causing inflammation
6
Q
Epidemiology of gout?
A
M
>40
7
Q
Risk factors of gout?
A
- Purine rich foods e.g. red meat
- High saturated fat diet
- High alcohol intake
- High fructose intake
- Drugs - low dose aspirin
- IHD
8
Q
Renal causes of gout?
A
URAT1 transporter defect
Diuretics
High insulin levels
All impair uric acid excretion
9
Q
What can cause increased production of urate?
A
- Metabolic syndromes: hyperlipidaemia
- Proliferative: myelo/lymphoproliferative disorders, cytotoxic drugs
- Psoriasis
- Diet: alcohol, XS meat, shellfish, meat extract, yeast extract, fructose sweetened drinks
10
Q
What is the pathophysiology of gout?
A
Xanthine oxidase controls hypoxanthine –> xanthine –> uric acid and excreted by kidney - not very efficient –> hyperuricaemia
11
Q
Normal serum uric acid levels?
A
0.3micromol/l
12
Q
Hyperuricaemia plasma levels?
A
> 0.36umol/l
13
Q
Causes of underexcretion of urate?
A
- Alcohol
- Renal impairment
- Hypertension
- Hyperthyroid/PTH
- Obesity, diabetes
14
Q
Clinical presentation of acute gout?
A
Hot swollen red joint
Painful
Crescendo over 6-12 joint
Usually 1st MTP
15
Q
Clinical presentation of chronic polyarticular gout?
A
Rare only in elderly on diuretics+renal failure
16
Q
Clinical presentation of chronic trophaceous gout?
A
Persistently high levels of uric acid crystals –> large crystal depositis –> irregular nodules on fingers, forearms, achilles tendon
Asymmetrical tophi - chalky appearance under skin
17
Q
What are tophi?
A
0nion like aggregates of MSU with inflammatory cells
18
Q
How do tophi cause damage?
A
Cause deformity, crepitus, and decreased movement
May secrete proteolytic enzymes causing punched out lesions
19
Q
Precipitators of acute gout attack
A
- Sudden cessation/aggressive introduction to hypouricaemic therapy
- Alcohol, shellfish binges
- Sepsis/MI/Acute severe illness
- Trauma, surgery, dehydration
20
Q
Diagnosing gout?
A
- Clinical exam
- Joint aspiration fluid - microscopy and polarised light, gram stain exclude septic arthritis as cannot co-exist
- Serum UA raised
- Imaging - x-rays chronic gout - areas of sclerosis, punched out lesions, areas of sclerosis
21
Q
Non pharmacological management of gout?
A
Weight loss, decrease alcohol, avoid shellfish, avoid purine rich food
22
Q
Treatment of Acute Gout?
A
- NSAIDs - naproxen, ibuprofen
- Colchicine Se: diarrhoea, abdominal pain
- IM/oral/intra-articular corticosteroid e.g. prednisolone
23
Q
Prevention of Gout?
A
- Stop diuretics e.g. thiazides, switch to ARB
- Allopurinol act on Xanthine oxidase - start 3 weeks after acture episode SE: rash, fever, decreased WCC
- Febuxostat: non purine xanthine oxidase inhibitor
24
Q
What crystals in pseudogout?
A
Calcium pyrophosphate
25
Risk factors for pseudogout?
1. Diabetes
2. HyperPTH
3. Haemochromatosis
4. Hypothyroidism
4. Old age
26
Clinical presentation of pseudogout?
1. Knee>Wrist
2. Typical inflammed joint
3. Fever
4. Marked synovitis
27
Triggers of acute pseudogout attack?
1. Direct trauma to joint
2. Most are spontaneous
3. Blood transfusion/IV fluid
28
Diagnose pseudogout?
1. Joint fluid aspiration and microscopy - positively birefringent rhomboids on polarised light, joint fluid is pus like, culture to exclude septic arthritis
2. X ray - chondrocalcinosis
29
Management of acute pseudogout?
1. NSAIDs
2. Analgesia
3. Aspiration, injection
4. Physiotherapy
30
Management of long term pseudogout?
Continued inflammatory changes e.g. methotrexate, hydroxychloroquine
Synovectomy
Surgery
31
Systemic Lupus Erythematous
Inflammatory, multisystem autoimmune disorder with athralgia and rashes
32
Epidemiology of SLE?
More common in women
| Afrocarribeans
33
Risk factors for SLE?
1. Genetic predisposition
2. Fhx
3. Drugs - hydralazine, isoniazid,
4. UV light
5. EBV
34
Pathophysiology of SLE?
1. Failure of immune system to inactivate T and B cells that recognise self antigens and availability of self antigens.
2. Development of autoantibodies that are either circulating complexes or deposited by directly binding tissue.
3. Complement activation and neutrophil influx leads to inflammation of tissues and abnormal cytokine production --> increase IL10, and interferon alpha
35
Clinical presentation of SLE?
```
Arthritis - non erosive - peripheral joints
Renal failure
ANA+ve
Serositis - pleuritis/pericarditis
Haematological - Leukopoenia, thombocytopoenia etc
Photosensitivity
Oral ulcers
Immunological - Anti- dsDNA,Anti-sm, Anti-Rho,
Neurological - seizures and psychosis
ts
Malar rash
Discoid rash
```
36
SLE differential diagnosis?
```
Acute pericarditis
Antiphospholipid syndrome
Fibromyalgia
Lymphoma
Scleroderma
Sjorgren Syndrome
```
37
SLE investigations?
1. Raised ESR, normal CRP
2. FBC - normochromic normocytic anaemia
3. Urinalysis - proteinuria/haematuria
4. Autoantibody test:
- ANA+ve highly sensitive
- anti-dsDNA - highly specific
5. Histologically:
- SLE of skin and kidneys: deposition of compliment and IgG antibodies and influx of neutrophils and leukocytes
- Vasculitis - affects arterioles, capillaries, venules
- Haemotoxylin bodies are seen in inflammatory infiltrates = result of ANA and inflammatory body
38
How to manage SLE?
1. Education and support
2. Reduce UV exposure
3. Assess lupus activity - clinical/immunological
4. Screen for major organ development
5. Identify patients with phospholipid Ab
4. Assess and mange atherosclerosis and CVD risk - identify patients at risk of blood clots
5. Planned pregnancy
39
How to treat SLE?
1. No treatment
2. Topical:
- sunscreen, steroids, toxic for rashes
3. NSAIDs
4. Antimalarial drugs - chloroquine
5. Steroids - high dose prednisolone
6. Cytotoxics: azathioprine, methotrexate, cyclophosphamide
7. Anticoagulants
8. Biological - target inflammatory cytokine, usually mAb, e.g. Rituximab
9. Stem cell transplant
40
What is giant cell arteritis?
Commonest large vessel vasculitis
| - inflammatory granulomatosis arteritis of cerebral arteries and other large vessels.
41
Epidemiology of GCA?
1. F>M
| 2. >50
42
Pathophysiology of GCA?
1. Activation of dendritic cells in the adventitia
2. Recruitment and activation of T cells
3. Recruitment of CD8+cells and monocytes
4. Vascular damage and remodelling
43
Clinical presentation of GCA?
1. Headache
2. Scalp tenderness
3. Jaw claudication
4. Acute vision loss
44
Medical emergencies associated with GCA?
Stroke
| Blindness
45
Signs of GCA?
Scalp tenderness leads to scalp ischaemia
Superficial temporal artery tenderness
Decreased or absent pulsation of artery
46
GCA differential diagnosis?
1. Migraine
2. Tension headache
3. Trigeminal neuralgia
4. Polyarteritis nodosa
5. Herpes zoster
47
GCA diagnostic criteria?
1. >50 with:
a. New onset localised headache
b. temporal artery abnormality - tenderness, thickening
c. Occasional overlying red skin and decreased pulsation
48
Investigations for GCA?
1. ESR/CRP raised
2. Normochromic normocytic anaemia
3. US/PET
4. Temporal artery biopsy = diagnostic
49
How to treat GCA?
1. High dose glucocorticoids
2. Uncomplicated: 40mg prednisolone
3. Complicated: 60mg prednisolone/ IV methylprednisolone
4. GI protective drugs - PPI
5. If fail to wean off glucorticoids -
- DMARDs: methotrexate
- Tocilizumab
50
Ankylosing Spondylitis what is it?
Chronic inflammatory disorder of spine, ribs, and sacroiliac joints
51
Epidemiology of ankylosing spondylitis?
M>F
| <30 years
52
Risk factors of AS?
1. HLA B27
| 2. Environment: shigella, salmonella, klebsiella
53
Pathophysiology of AS?
Lymphocyte and plasma infiltration occurs with local erosion of bone at attachments of ligament
- heal with new bone formation.
= SYNDESMOPHYTE
54
What is syndesmophyte?
New bone formation and vertical growth from anterior vertebral corners
55
Diagnostic criteria of clinical presentation of ankylosing spondylitis?
1. Morning stiffness > 30 minutes
2. Improve with exercise /not with rest
3. Waking in second half of night because of pain
4. Insidious onset
5. Duration of back pain >3months
6. <45 years
56
Two characteristic spinal abnormalities with AS?
1. Loss of lumbar lordosis (inward curve of spine) and increased kyphosis - top of spine becomes more rounded
2. Limitation of lumbar spine mobility in both the sagittal and frontal planes --> decrease spinal flexion
57
How to diagnose AS?
1. ESR/CRP raised
2. Normochromic normocytic anaemia
3. HLA B27 +ve
4. X ray - can be normal but erosion, sacrolitis, fusion of sacroiliac joint
6. MRI - with gadolinum - show sacrolitis before on X ray
58
How to treat AS?
QUICK -to prevent irreversible syndesmophytes formation and progressive calcification
- morning exercise to maintain posture and spinal mobility
- NSAIDs at night
- Methotrexate aids peripheral arthritis but not spinal disease
- TNF alpha blocker - improve spinal and peripheral joint inflammation - infliximab
- Local steroid injection - temporary relief
- Surgery - hip replacement to improve pain and function
