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Semester 1 (YEAR 3) - Lecture Notes > Week 9 - Osteoarthritis, Rheumatoid Arthritis and Gout > Flashcards

Week 9 - Osteoarthritis, Rheumatoid Arthritis and Gout Flashcards

1
Q

What is osteoarthiritis

A

A joint disease, which commonly affects the hand, knees and hip
- results in fractures + functional failure of synovial joints
- NO cure

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2
Q

What is the cause (ateiology) of osteoarthiritis

A

Remodelling of the joints:
- cartillage breakdown
- meniscal damage
- remodelling results in joint space narrowing = bone on bone grinding

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3
Q

What is the risk factors and symptoms of osteoarthiritis

A

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

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4
Q

How is osteoarthiritis treated: Non-pharmacological

A
  • 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)
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5
Q

How is osteoarthiritis treated: Pharmacological

A

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

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6
Q

What is gout

A

Painful joint disease, affects big toe / feet (commonly) but can affect any joint

  • Onset 40-50 in men (and later for women)
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7
Q

What is the cause (ateiology) of gout

A

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

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8
Q

What symtpoms and complications of gout

A

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)

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9
Q

How is gout treated: Non-pharmacological

i.e. lifestyle modifications

A
  • ↓ alcohol intake
  • ↑ fluid intake
  • Avoid foods ↑ in purine (= produce less urate)
  • Stop drugs which precipitate gout
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10
Q

How is gout treated: Parmacological

A

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

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11
Q

What is rheumatoid arthiritis

A

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.

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12
Q

What is the cause (ateiology) of rheumatoid arthiritis

A

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

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13
Q

How is rheumatoid arthiritis diagnosed

A
  • 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
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14
Q

How is rheumatoid arthiritis treated: Pharmacological

A
  1. 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

  1. 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
  2. Analgesics
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15
Q

List the 3 types of DMARDs

DMARDs - Disease Modifying Anti-Rheumatic Drugs

A
  1. Conventional synthetic DMARDs (csDMARDs)
    - always started 1st in the UK
  2. Biologic DMARDs (bDMARDs)
  3. Targeted synthetic DMARDs (tsDMARDs)
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16
Q

What is the MoA for DMARDs

A

ALL DMARDs reduce the amount of recruitment of white cells to joints
- by targeting receptors + cells associated with immune system

17
Q

List csDMARDs examples

csDMARDs = 1st line DMARDS | inc. dose, onset, side effects

A
  1. 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
  2. Sulfasalzine
    - Side effects: rashes, liver disorders
  3. Hydroxychloroquine
    - optical side effects
18
Q

List bDMARD and tsDMARD examples

A

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
19
Q

What monitoring is required with DMARDs

A

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

Semester 1 (YEAR 3) - Lecture Notes (25 decks)

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