Week 9 - Osteoarthritis, Rheumatoid Arthritis and Gout Flashcards
What is osteoarthiritis
A joint disease, which commonly affects the hand, knees and hip
- results in fractures + functional failure of synovial joints
- NO cure
What is the cause (ateiology) of osteoarthiritis
Remodelling of the joints:
- cartillage breakdown
- meniscal damage
- remodelling results in joint space narrowing = bone on bone grinding
What is the risk factors and symptoms of osteoarthiritis
RISK FACTORS:
- increasing age
- increasing weight
- female
- genetics
- previous joint injury
- diet, nutritional deficiency e.g. Calcium, Vitamin D3
SYMPTOMS:
- Joint pain (relieved by rest, exacerbated by excercise)
- Joint swelling
- Stiffness
- Reduced movement + function
- Noise in joint
How is osteoarthiritis treated: Non-pharmacological
- Weight management
= ↑ QoL, function and ↓ pain esp. in hands - Therapeutic excercise
= stregthen muscle = reduce burden on joint - Manual therapy (chiropractor)
- Walking aids
- Joint replacement (hip or knee)
- ONLY option which has most benefit (others benefit is limited)
How is osteoarthiritis treated: Pharmacological
Analgesics
1st line = Topical NSAIDs
- e.g. ibuprofen gel
2nd line = Oral NSAIDs with gastroprotection
- if topical is ineffective
- gastroprotection = omeprazole
3rd line = Paracetamol or Weak opioids
- only given if NSAIDs is unsuitable / ineffective
- weak opioid - codeine, tramadol
What is gout
Painful joint disease, affects big toe / feet (commonly) but can affect any joint
- Onset 40-50 in men (and later for women)
What is the cause (ateiology) of gout
Hyperuricaemia (high levels of uric acid in blood)
- ONLY occurs in patients that have genetic predispositon to gout + immune response to urate crystals has been triggered
Urate (= salt) crystalises in joint space when have too much present in blood
- urate is a by-product of purine
- urate is over-produced due to extreme excercise or disorders
- reduced urate excretion is due to renail failure or excess alcohol consumption
What symtpoms and complications of gout
SYMPTOMS:
- Joint pain
- Joint swelling, redness
- Another gout attack within 12 months
- Ocuurence after binge drinking (>14 units weekly)
COMPLICATIONS:
- Bone remodelling / damage to joints
- Can take 10 years from inital diagnosis to develop
- Tophi (hard growth from urate crystals)
How is gout treated: Non-pharmacological
i.e. lifestyle modifications
- ↓ alcohol intake
- ↑ fluid intake
- Avoid foods ↑ in purine (= produce less urate)
- Stop drugs which precipitate gout
How is gout treated: Parmacological
Acute Attacks:
- Analgesics; to relieve pain + inflammation
- NSAIDs e.g. Naproxen 500mg BD
- Cholchicine 500mcg 2-4 times
- Corticosteroids; releive inflammation
- e.g. prednisolone (low dose)
Chronic:
- Allopurinol 100mg OD
- ↓ chronically elevated urate levels (<300micromol/L)
- initiate 2-4 weeks after attack
- ↓ dose if have renal impairment
- titrate dose up
- Febuxostat 80mg OD
- Colchicine as prophylaxis for flares
What is rheumatoid arthiritis
Autoimmune inflammatory condition which can affect the whole body
- specifically, hands (knuckles)
Causes patient to have ↓ life expectancy + ↑ risk of osteoporosis, hear disease, infections etc.
What is the cause (ateiology) of rheumatoid arthiritis
Immune system attacks joints + produces auto antibodies against cells in synovial membrane
- antibodies can affect other cells in body
- WBC and osteoclasts recruit creating a group of cells which attack the joint
How is rheumatoid arthiritis diagnosed
- Use DAS 28 Score
- this inc. counting the amount of swollen and tender joints
- C-reactive protein (CRP) in blood
- ESR (erythrocyte sedimentation rate) blood
- scale of global health (ask patient how they feel from 1-10) - Blood tests
- presence of cytokines
- presence of Anti-CCP antibodies
- rheumatoid factors
How is rheumatoid arthiritis treated: Pharmacological
- DMARDs
- started within 12 weeks of onset
- DO NOT get immediate symtpomatic relief
- they slow down disease progression by inhibiting structural damage to cartilage and bone
- e.g. methotrexate
SYMPTOMATIC RELIEF:
1. NSAIDs + PPI (gastroprotection)
- ↓ inflammation
- try use for shortest possible time as it causes CV side effects, ↑ BP, nephrotoxic
- Corticosteroids
- ↓ inflammation = ↓ pain
- used as bridging therapy whilst waiting for DMARD to kick in
- e.g. prednisolone 40mg for 1 week, reduce by 5mg weekly till reach 0
- short term treatment, ↓ dose and ween patient off them slowly - Analgesics
List the 3 types of DMARDs
DMARDs - Disease Modifying Anti-Rheumatic Drugs
- Conventional synthetic DMARDs (csDMARDs)
- always started 1st in the UK - Biologic DMARDs (bDMARDs)
- Targeted synthetic DMARDs (tsDMARDs)
What is the MoA for DMARDs
ALL DMARDs reduce the amount of recruitment of white cells to joints
- by targeting receptors + cells associated with immune system
List csDMARDs examples
csDMARDs = 1st line DMARDS | inc. dose, onset, side effects
- Methotrexate = 1st line
- weekly dosing
- prescribed with folic acid 5mg to reduce gastric effects (BUT f.acid is taken on a diff. day to the day methotrexate took)
- onset 4-12 weeks
- can use SC injecetions if: patient is responding well to oral, ↓ side effects + ↑ bioavailability
- AVOID if have HEPATIC DISEASE, pregnant, have peptic ulcer, eGFR <10ml/min
- SIDE EFFECTS: pulmonary fibrosis
- Sulfasalzine
- Side effects: rashes, liver disorders - Hydroxychloroquine
- optical side effects
List bDMARD and tsDMARD examples
switching to bMARDs or tsDMARDs from csDMARDs if had inadequate respone to csDMARDs
- switch only if have tried 2 csDMARDs
- may try combination therapy (bDMARD and methotrexate)
bMARDS:
1. Infliximab (TNF inihibitor ~ partly human / mouse mAB = can be recognised as foreign by immune system)
2. Adalimumab (TNF inhibitor - fully human mAB = preffered less likeley to get ADA / immunogenecity responses = not recognised as foreign)
3. Golimumab
Above are Anti-TNF modulators, these are most commonly prescribed (have other mabs)
tSDMARDs:
Are janus kinase inhibitors
1. Barictinib
2. Tofacitinib
- Oral instead of injectable
- avoid in >65s, history of smoking
- regular skin checks for skin cancer
What monitoring is required with DMARDs
ALL DMRADs cause blood disorders due to reduce WBC response = need to monitor regularly
- FBC
- LFT + albumin
- eGFR
- CRP (C-reactive protein)
- ESR (erythrocyte sedimentation rate)
- DAS28
For bDMARDS:
- Screen for TB, HIV, Varicella, Hepatitis B and C
