Rheumatology Flashcards
Give 3 causes of inflammatory joint pain.
- Autoimmune disease e.g. RA, vasculitis, connective tissue disease.
- Crystal arthritis.
- Infection.
Give 2 causes of non-inflammatory joint pain.
- Degenerative e.g. osteoarthritis.
- Non-degenerative e.g. fibromyalgia.
What are the 5 cardinal signs of inflammation?
- Rubor (redness).
- Calor (heat).
- Dolor (pain).
- Tumor (swelling).
- Loss of function.
How does inflammatory pain differ from degenerative non-inflammatory pain?
Inflammatory pain tends to ease with use whereas degenerative pain increased with use.
Are you more likely to see swelling in inflammatory or degenerative pain?
In inflammatory pain you are likely to see synovial swelling. There is often no swelling in degenerative pain.
Name 2 inflammatory markers that can be detected in blood tests.
- ESR (erythrocyte sedimentation rate).
- CRP.
Explain why ESR levels are raised in someone with inflammatory joint pain.
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.
Explain why CRP levels are raised in someone with inflammatory joint pain.
Inflammation leads to increased levels of IL-6. CRP is produced by the liver in response to IL-6 and therefore is raised.
Describe the ESR and CRP levels in someone with lupus.
ESR is raised and CRP is low.
With what tissue type are all spondyloarthritis conditions associated?
They are all associated with tissue type HLAB27.
Give 5 conditions that fall under the umbrella term spondyloarthritis.
- Ankylosing spondylitis.
- Reactive arthritis.
- Psoriatic arthritis.
- Enteropathic arthritis.
- Juvenile idiopathic arthritis.
What is the function of HLAB27?
It is an antigen presenting cell.
Describe the ‘molecular mimicry’ theory for explaining why HLAB27 is associated with spondyloarthritis.
Infectious agents have peptides very similar to HLAB27. An auto-immune response is triggered against HLAB27.
Name 3 theories that can explain why HLAB27 is associated with spondyloarthritis.
- Molecular mimicry.
- Mis-folding theory.
- HLAB27 heavy chain hypothesis.
Give 6 signs of spondyloarthritis.
- Psoriasis.
- Inflammatory spine and buttock pain.
- Good response to NSAIDS.
- Enthesitis.
- Arthritis.
- Crohn’s/colitis associated.
- Uveitis.
What is the general treatment for all spondyloarthritis?
Initially DMARDs and then biological agents if DMARDs fail e.g. TNF blockers.
Describe the pathophysiology of ankylosing spondylitis.
Inflammation of spine -> erosive damage -> repair/new bone formation -> irreversible fusion of spine.
Give 5 symptoms of ankylosing spondylitis.
- BACK PAIN!
- Morning stiffness.
- Waking in the second half of the night.
- Buttock pain.
- Insidious onset.
- Usually <40y/o at onset.
What investigations might you do in someone who you suspect to have ankylosing spondylitis?
- X-ray.
- MRI.
- HLAB27 test.
What is the diagnostic criteria for ankylosing spondylitis?
- > 3 months back pain.
- Aged <45 at onset.
- Plus one of the SPINEACHE symptoms.
Give 3 locations that psoriasis commonly occurs at.
- Elbows.
- Knees.
- Fingers.
What is reactive arthritis?
Sterile inflammation of the synovial membrane, tendons and fascia triggered by an infection at a distant site, usually GI or genital.
What gut infections are associated with reactive arthritis?
Salmonella, shigella.
What sexually transmitted infections are associated with reactive arthritis?
Chlamydia.
What is the triad of symptoms for reactive arthritis?
- Arthritis.
- Conjunctivitis.
- Urethritis.
What type of spondyloarthritis occurs in 20% of patients with IBD?
Enteropathic arthritis.
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.
What is the aetiology of JIA?
Unknown - idiopathic!
However, it is autoimmune so there are genetic factors associated.
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!
What type of JIA affects <4 joints and is usually ANA positive?
Oligoarthritis.
High risk of developing uveitis!
What JIA is similar to adult ankylosing spondylitis?
Enthesitis related JIA - inflammation of where the tendon joins a bone. HLAB27 positive.
Describe the non-medical treatment for JIA.
- Information.
- Education.
- Support.
- Liaison with school.
- Physiotherapy.
Describe the medical treatment for JIA.
- Steroid joint injections.
- NSAIDS.
- Methotrexate.
- Systemic steroids.
Give 5 potential consequences that can occur if you fail to treat JIA.
- Damage.
- Deformity.
- Disability.
- Pain.
- Bony overgrowth.
- Uveitis.
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.
Give 3 factors that increase the volume of pain.
- Substance P.
- Glutamate.
- Serotonin.
Give 3 factors that decrease the volume of pain.
- Opioids.
- GABA.
- Cannabanoids.
Name 4 diseases that fibromyalgia is commonly associated with.
- Depression.
- Chronic fatigue.
- Chronic headache.
- IBS.
Give 5 symptoms of fibromyalgia.
- Neck and back pain.
- Pain is aggravated by stress, cold and activity.
- Generalised morning stiffness.
- Subjective swelling of extremities.
- Frequent waking during the night.
- Waking unrefreshed.
- Low mood, irritable, weepy.
- Headache and IBS common.
Give 5 triggers of fibromyalgia.
- Physical trauma.
- Distress.
- Hormonal alterations e.g. hypothyroid.
- Infections.
- Certain catastrophic events e.g. wars.
Give 3 diseases might be included in the differential diagnosis for fibromyalgia?
- Hypothyroidism.
- SLE.
- Low vitamin D.
Describe the management for fibromyalgia.
- Educate the patient and family.
- ‘Resent the pain thermostat’.
- Low does amitriptyline can help with sleep.
- Graded aerobic exercise.
- Acupuncture.
What 2 things are essential in the management of fibromyalgia?
- Explaining that sleep disturbance is central to what they’re feeling.
- Emphasising the importance of exercise and fitness.
What is vasculitis?
Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow.
What cells might you see on a histological slide taken from someone with vasculitis?
Neutrophils and giant cells.
Chapel Hill classification: give an example of a large artery primary disorder.
Giant cell arteritis.
Chapel Hill classification: give an example of a large artery secondary disorder.
Aortitis in RA.
Chapel Hill classification: give an example of a medium/small artery primary disorder.
Wegener’s granulomatosis (GPA).
Chapel Hill classification: give an example of a medium/small artery secondary disorder.
Vasculitis secondary to autoimmune disease, malignancy, drugs.
What does ANCA stand for?
Anti-neutrophil cytoplasmic antibodies.
Describe the epidemiology of giant cell arteritis.
- Affects those >50y/o.
- Incidence increases with age.
- Twice as common in women.
Give 5 symptoms of giant cell arteritis.
- Headache.
- Scalp tenderness.
- Jaw claudication.
- Acute blindness.
- Malaise.
What might you find on clinical investigation in someone with giant cell arteritis?
- Palpable and tender temporal arteries with reduced pulsation.
- Sudden monocular visual loss, the optic disc is pale and swollen.
What is the diagnostic criteria for giant cell arteritis?
- Age >50.
- New headache.
- Temporal artery tenderness.
- Abnormal artery biopsies.
What investigations might you do in someone who you suspect has giant cell arteritis?
- Bloods for inflammatory markers e.g. CRP, ESR.
- Temporal artery biopsy.
Describe the treatment for giant cell arteritis.
- Prompt corticosteroids - prednisolone.
- Methotrexate is sometimes adeed.
- Osteoporosis prophylaxis is important e.g. lifestyle advice and vitamin D.
Is Wegener’s granulomatosis associated with c-ANCA or p-ANCA?
c-ANCA.
What organ systems can be affected by Wegener’s granulomatosis?
- URT.
- Lungs.
- Kidneys.
- Skin.
- Eyes.
What is the affect of Wegener’s granulomatosis on the URT?
- Sinusitis.
- Otitis.
- Nasal crusting.
What is the affect of Wegener’s granulomatosis on the lungs?
- Pulmonary haemorrhage/nodules.
- Inflammatory infiltrates are seen on X-ray.
What is the affect of Wegener’s granulomatosis on the kidney?
Glomerulonephritis.
What is the affect of Wegener’s granulomatosis on the skin?
Ulcers.
What is the affect of Wegener’s granulomatosis on the eyes?
- Uveitis.
- Scleritis.
- Episcleritis.
What is the treatment for Wegener’s granulomatosis?
- If severe: high dose steroids.
- If non-end organ threatening: moderate steroids.
What is rheumatoid arthritis?
An auto-immune inflammatory synovial joint disease.
Describe the epidemiology of RA.
- 2 to 3 times more common in women.
- Approximately 1% of the population affected.
Describe the aetiology of RA.
Auto-antibodies e.g. RF and anti-CCP lead to a defective cell mediated immune response.
Describe the pathophysiology of RA.
- Chronic inflammation. B/T cells and neutrophils infiltrate.
- Proliferation -> pannus formation.
- Pro-inflammatory cytokines -> proteinases -> cartilage destruction.
Give 5 symptoms of RA.
- Early morning stiffness (>60 mins).
- Pain eases with use.
- Swelling.
- General fatigue, malaise.
- Extra-articular involvement.
Give 5 signs of RA.
- Symmetrical.
- Deforming.
- Polyarthropathy.
- Erosion on X-ray.
- 80% are RF positive.
RA extra-articular involvement: describe the effect on soft tissues.
- Nodules.
- Bursitis.
- Muscle wasting.
RA extra-articular involvement: describe the effect on the eyes.
- Dry eyes.
- Scleritis.
- Episcleritis.
RA extra-articular involvement: describe the neurological effects.
- Sensory peripheral neuropathy.
- Entrapment neuropathies e.g. carpal tunnel syndrome.
- Instability of cervical spine.
RA extra-articular involvement: describe the haematological effects.
- Palpable lymph nodes.
- Splenomegaly.
- Anaemia.
RA extra-articular involvement: describe the pulmonary effects.
- Pleural effusion.
RA extra-articular involvement: describe the effects on the heart.
- Pericardial rub.
- Pericardial effusion.
RA extra-articular involvement: describe the effect on the kidneys.
Amyloidosis.
What is rheumatoid factor?
An antibody against the Fc portion of IgG.
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.
Describe the treatment for rheumatoid arthritis.
- NSAIDS.
- Corticosteroids.
- DMARDs.
- Biological agents.
Define osteoarthritis.
A non-inflammatory degenerative disorder of moveable joints characterised by the deterioration of articular cartilage and the formation of new bone.
Why does the prevalence of OA increase with age?
Due to the cumulative effect of trauma and a decrease in neuromuscular function.
Give 5 risk factors for developing OA.
- Genetic predisposition.
- Trauma.
- Abnormal biomechanics e.g. hypermobility.
- Occupation e.g. manual labour.
- Obesity; pro-inflammatory state.
What are the most important cells responsible for OA?
Chrondrocytes.
Give 5 symptoms of OA.
- Morning stiffness (<30 minutes).
- Pain - aggravated by activity.
- Tenderness.
- Walking and ADLs affected.
- Joint swelling and bony enlargement.
- Deformities.
- Crepitus.
Give 5 radiological features associated with OA.
- Joint space narrowing.
- Osteophyte formation.
- Sub-chondral sclerosis.
- Sub-chondral cysts.
- Abnormalities of bone contour.
Name 3 joints of the hand that are commonly affected in osteoarthritis.
- Distal interphalangeal joint.
- Proximal interphalangeal joint.
- Carpal metacarpal joint.
Which surface of the knee is most commonly affected by OA?
The medial surface.
What is the primary investigation used to make a diagnosis of OA?
X-ray.
Look for asymmetric loss of joint space; sclerosis; cysts and osteophytes.
Describe features of the non-medical management for OA.
- Education.
- Exercise.
- Weight loss.
- Physiotherapy.
- Occupational therapy.
- Walking aids.
Describe the pharmacological management for OA.
- NSAIDS (topical better than PO).
- Paracetamol.
- Intra-articular steroid injections.
- DMARDs if there is an inflammatory component.
Describe the surgical management for OA.
- Arthroscopy for loose bodies.
- Osteotomy (changing bone length).
- Arthroplasty (joint replacement).
- Fusion (usually ankle and foot).
Give 3 indications for surgery.
- Significant limitation of function.
- Uncontrolled pain.
- Waking at night from pain.
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.
What is the treatment for loose bodies?
Arthroscopy.
Give an example of an inherited connective tissue disease.
- Marfan’s syndrome.
- Ehler Danlos syndrome.
Give an example of an autoimmune connective tissue disease.
- SLE.
- Systemic sclerosis.
- Sjögren’s syndrome.
- Dermatomyositis.
What is SLE?
Systemic Lupus Erythematosus is an inflammatory multi-system disease characterised by the presence of serum anti-nuclear antibodies (ANA).
Describe the epidemiology of SLE.
- 90% of cases are in young women.
- More common in afro-Caribbeans.
- Genetic association.
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.
What can cause thrombosis in patients with SLE?
The presence of antiphospholipid antibodies.
What autoantibody is specific to SLE?
Anti-dsDNA.
Give 5 symptoms of SLE.
- Butterfly rash.
- Mouth ulcers.
- Raynaud’s phenomenon/’cold pale fingers’.
- Fatigue.
- Depression.
- Weight loss.
What investigations might you do in someone who you suspect has SLE?
- Blood count may show normocytic anaemia; neutropenia; thrombocytopaenia. Raised ESR, normal CRP.
- Serum autoantibodies: ANA, anti-dsDNA.
Describe the non-medical treatment for SLE.
- Education and support.
- UV protection.
- Screening for organ involvement.
- Reduce CV risk factors e.g. smoking cessation.
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.
What is scleroderma?
A multi-system disease characterised by skin hardening and Raynaud’s phenomenon.
Give 5 signs of limited scleroderma.
- Calcinosis.
- Raynaud’s phenomenon.
- Oesophageal reflux.
- Sclerodactyly (thickening and tightening of the skin).
- Telangectasia (visible small red blood vessels).
- Pulmonary arterial hypertension.
Give 4 signs of diffuse scleroderma.
- Proximal scleroderma.
- Pulmonary fibrosis.
- Bowel involvement.
- Myositis.
- Renal crisis.
Describe the pathophysiology of scleroderma.
- Various factors cause an endothelial lesion and vasculopathy.
- There is excessive collagen deposition (skin hardening), inflammation and auto-antibody production.
Describe the management of scleroderma.
- Raynaud’s: physical protection and vasodilators.
- GORD: PPI’s.
- Annual Echo and pulmonary function tests to monitor arterial pulmonary pressure.
- ACEi to prevent renal crisis.
What is the pathophysiology of sjögren’s syndrome?
Immunologically mediated destruction of epithelial exocrine glands, especially lacrimal and salivary glands.
What does sjögren’s syndrome often occur secondary to?
Other auto-immune disorders e.g. SLE, RA, scleroderma, primary biliary cirrhosis.
Give 5 symptoms of sjögren’s syndrome.
- Dry eyes and dry mouth.
- Inflammatory arthritis.
- Rash.
- Neuropathies.
- Vasculitis.
Why does someone with sjögren’s syndrome have dry eyes and a dry mouth?
There is immunologically mediated destruction of epithelial exocrine glands meaning the lacrimal and salivary glands produce fewer secretions.