the patient Flashcards
(120 cards)
Rheumatoid Arthritis and
Osteoarthritis
what is RA
Most common autoimmune disease
Chronic, progressive, systemic inflammatory
disorder
Affects synovial joints
Many non‐articular manifestations, some of
which ↓ life expectancy
Causes significant disability
RA: Who is affected?
Affects 1% of UK population
↓ in past few decades
2‐3 times more common in women
more prevalence with age
Peak incidence 30‐50 years
Disease activity varies over time, but about
50% develop serious progressive disease
What causes RA?
Not clear
Genetic
Hormonal
Cigarette smoking
Infection?
RA: Pathophysiology ‐ much simplified
Widespread inflammation of synovium
‐ thickens
Infiltration by inflammatory cells
Synovium spreads onto the articular cartilage
surface (‘pannus’) isolating it from synovial fluid
Pannus erodes the articular cartilage; underlying
bone exposed → damage (osteoclasts sƟmulated)
Key inflammatory cells include T‐cells, B‐cells,
macrophages and plasma cells.
cytokines: IL‐6, IL‐1 and TNF‐α
Key inflammatory mediators are the cytokines
IL‐6, IL‐1 and TNF‐α
Autoantibodies such as rheumatoid factor and citrullainated peptides
acƟvate the complement system → sƟmulates macrophages
Characteristic bone loss is juxtra‐articular – immediately adjacent to both
sides of the joint. Eventually the joint is destroyed and undergoes fusion.
RA: How does it present?
Typically: slowly progressive, symmetrical
peripheral polyarthritis, evolving over few
weeks or months
Pain and stiffness of the small joints of the
hands and feet; patients feels tired and unwell
Also, wrists, elbows, shoulders, knees and ankles
Joints are warm and tender, with swelling; stiffness
esp. mornings; limited movement and muscle
wasting
Occasionally monoarthritis
Occasionally very sudden
RA of hands
Early disease – swelling and early joint damage
Late disease – deformity &
contractures
RA: Non‐ articular manifestations
symptoms and complications
Haematological
Anaemia
Neutrophilia
Thrombocytosis
Felty’s syndrome
Neurological
Nerve entrapment
Cervical myelopathy
Mononeuritis complex
Peripheral neuropathies
Pulmonary
Pulmonary nodules
Pleural effusions
Interstitial lung disease
Bronchiolitus oblitrans
Cardiac
Pericarditis
Pericardial effusion
Conduction defects
Valvular heart disease
Vasculitis
Nail fold
Systemic
Ocular
Keratoconjunctivitis sicca
Episcleritis
Scleritis
Cutaneous
Palmar erythema
Pyoderma gangrenosum
Vasculitic rashes
Leg ulceration
Alopecia
Amyloidosis
Nodules
The
manifestations are listed to
ensure you understand that
RA is a systemic disease,
that affects a lot more than
joints. dont need to memorise
RA: Co‐morbidities
MI, HF, CVA, CVD, HTN
E.g. Patients with RA have a 3‐6 fold ↑risk of
MI
Lymphoma and lymphoproliferative diseases
Lung cancer, skin cancer
Infections (disease & treatment)
Depression, GI disease, osteoporosis,
psoriasis, renal disease (disease & treatment)
How is RA diagnosed?
Patient history
Presenting symptoms / clinical examination
American College of Rheumatology classification criteria
(1987) – poor sensitivity for early disease
Clinical tests
↑ ESR & CRP (not always)
↑ platelet count
Rheumatoid factor – IgM present in 75‐80% of patients
with RA (seropositive) and 5% of patient without RA
Anti‐cyclic citrullinated peptide (anti‐CCP) antibodies is a more
specific test (90‐96% specificity)
Anaemia of chronic disease (normochromic, normocytic)
Radiology – X‐rays, MRI, ultrasound
RA: Monitoring of disease
Symptoms and clinical markers (CRP)
NICE refers to DAS28 – Disease Activity Score
which has 4 parameters:
1. Number of swollen joints out of a total of 28 specified joints
2. Number of tender joints out of a total of 28 specified joints
3. Erythrocyte sedimentation rate
4. Patient’s interpretation of wellbeing, 0 – best, 100 – worst
Disease Activity DAS28
High > 5.1
Moderate > 3.2 – 5.1
Low 2.6 ‐ 3.2
Remission < 2.6
RA: Management
Multidisciplinary Team
Medical – shared care (1° and 2° care)
Specialist RA nurses
Pharmacists
Psychology
Occupational therapy
Physiotherapy
Podiatry
Patient education is very important
RA management
Early diagnosis is important
Analgesics and NSAIDs only useful for:
Symptom relief including pain control
Corticosteroids, DMARDs and biologicals:
Slowing or prevention of joint damage
Preserving and improving functional ability
Achieving and maintaining disease remission
RA: Analgesics and NSAIDs
Analgesics – adjunct for pain relief
NSAIDs ‐ analgesic and anti‐inflammatory effect,
but only provide symptomatic relief
Use lowest dose possible and withdraw if
possible once patient responses to DMARDs
Side effects:
Gastrointestinal – consider gastroprotection
Renal
Cardiac / thrombotic
RA: Corticosteroids
Inhibit cytokine release
Rapid relief of symptoms / ↓ inflammaƟon
Long‐term oral steroids associated with long‐
term side effects
Oral therapy – bridging therapy until respond
to DMARDs (withdraw slowly)
Intra‐articular injection into target joints
RA: Disease Modifying Anti‐Rheumatic Drugs
The sooner the better to prevent damage
Ideally within 3 months of start of persistent
symptoms
NICE – first line treatment is a
combination of DMARDs, unless inappropriate; if
so monotherapy
Oral methotrexate, leflunomide or
sulfasalazine
RA: Biologic Response Modifiers
Huge change in management of RA in past
decade
Currently only used if DMARDs fail ‐ NICE
Specialist supervision
Expensive
Balance cost of treatment vs cost of disability
Tumour necrosis factor‐α blocker
Adalimumab, Certolizumab, Etanercept, Infliximab
NICE: TNF‐α blockers are the first‐line biologicals
JAK inhibitor – Baracitinib, Tofacitinib
Interleukin‐6 antagonist – Tocilizumab, Sarilumab
T‐cell co‐stimulation modulator ‐ Abatacept
B‐cell depleting ‐ Rituximab
what are biologics RA
Biologic response modifiers (BRMs) are a class of medications used in the treatment of rheumatoid arthritis (RA). They work by targeting specific components of the immune system involved in the inflammatory process, helping to reduce inflammation and prevent joint damage. BRMs are typically prescribed when conventional disease-modifying antirheumatic drugs (DMARDs) have been ineffective or are not well tolerated.
how are biologics given RA
Given along with DMARD, e.g. methotrexate
Assessment using DAS28 at least every 6
months
Continue if improvement in DAS28 of 1.2
points or more
Often given by injection – mostly s/c, but some
by infusion (big proteins), except JAK inhibitors
Different regimens – daily, twice weekly, weekly,
every 2 weeks, every 4 weeks, every 8 weeks
Not just licensed for RA
RA: Biologic Response Modifiers ‐
Problems
↑ risk of infecƟon, parƟcularly with TNF‐α
inhibitors
Particularly reactivation of latent TB (screen
before commencing Tx)
Rituximab associated with 3 cases of
progressive multifocal leukoencephalopathy
Injection site and infusion reactions
TNF‐α inhibitors C/Id in advanced heart failure
Systemic lupus erythematosus – SLE
“lupus”
Autoimmune, multisystem
90% of patients are female
Rare – more common in black and Asian
women than white women
Peak age onset 20‐30 years
Strong genetic link; triggers
5 fold increase in mortality compared to
age and gender matched controls, mainly
due to increased risk of premature CVD
SLE – clinical features
Typically follows pattern of flares and remissions,
but some patients have active disease for
prolonged periods
Fever, weight loss and mild lymphadenopathy
during disease flares
Fatigue and low grade joint pain may be constant
– symmetrical joints typically knees, wrists and
small joint of hands
70‐90% of patients will have arthralgia and morning
stiffness, but joint swelling is rare
80‐90% of patients have skin manifestations,
e.g. malar rash
Renal disease – a major determinant of
prognosis
Vascular ‐ Raynaud’s syndrome is common
Also affects cardiovascular and pulmonary,
peripheral and central nervous system, GI
systems; ocular disease, haematological
abnormalities, recurrent miscarriages
SLE ‐ treatment
Analgesics and NSAIDs
* Hydroxychloroquine – first line maintenance
* Acute & chronic: combination of low and high dose
glucocorticosteroids and immunosuppressants such as
methotrexate, azathioprine, mycophenolate mofetil or
cyclophosphamide
* Biologicals – belimumab
* Management of co‐morbidities
* Non‐pharmacological – sun protection, vit D
supplementation, smoking cessation, exercise
Osteoarthritis: What is it?
Most common musculoskeletal condition in
older people
Chronic, degenerative disorder of the joints
Most commonly affects knee, hip, spine and
small joints of the hand
Causes significant pain and functional disability
Interfers with ADLs, esp hand OA
OA: Who is affected?
About 1/3rd of UK population ≥ 45 have
sought Tx for OA
More common in women
Steep prevalence with age
Knee > Hip > Hand
Overweight/obese