Rheumatoid arthritis and osteoarthritis Flashcards
How is the rheumatoid arthritis (RA) diagnose established?
- Morning stiffness > 1 time*
- Arthritis in 3 or more joints areas*
- Arthritis involving the jount of the hands*
- Symmetrical arthritis*
- Rheumatic nodules
- Rheumatoic factor
- Erosions
4 ud af 7 skal være tilstede. *Present for more than 6 weeks
DAS28
Disease activity score using 28 joints.
High disease activity DAS28 of > 5.1
Moderate: DAS28 of > 3.2 to 5.1
Low activity: 2.6-3.2
Remission: < 2.6
Investigations
Inflammatory markers:
C-reactive protine
Erythrocyte sedimentation rate (ERS)
Goals in treatment?
Symptom relief - pain control
Slowing or prevention of joint damage
Preserving and improving functional ability
Achieving and maintaining disease remission
The four main categories of drugs
NSAIDs
Glucorticoids
DMARDS
Biologisk behandling
NSAIDs
Reduce jount pain and swelling
SYMPTOMAIC RELIEF
Lowest effective dosis for the shortest possible period of time.
Use of PPI!
Avoid if possible.
DMARDs
Hvilke bruges oftest, og har clear evidens of benefit?
Methotrexate (MTX)
Sulphasalazine
Leflunomide
Intramuscular Gold
DMARDs som kombinationsterapi
First-line therapy: MTX + mindst en anden DMARD såsom sulphasalazine
Hvordan virker de forskellige DMARDs?
Methotrexate: Folic acid antagonist
Salazopyrin: Sulfapyrin + Pentasa
Hydroxy-chloroquine: TLR-inhibition
Leflunomid: DHODH inhibitor
Glucocorticoider
Anvendes i starten af behandling af arthritis, da DMARDs har slow onset.
Biological treatment for rhematoid arthritis
Biologics are used after a patient has failed DMARDs.
- anti-TNF-alpha. (First line agent)
- Interleukines
Interlekukins, mechanism
Anakinra which bloks the binding of interleukin-1 to its receptor. (weak evidens)
Rituximab: Human-murine monoclonal antibody.
Abtacept: Bloking the activation of T-cells
Tocilizumab: Binding to interleukin-6 receptors
Risk factors in gout
Increasing age
Gender (male)
Obesity
Hypertension
Lifestyle: Meat and red wine.
Uric acid is the end product of Purine (aminoacid)
Treatment of gout?
During attacs: NSAIDs, steorids, colchicine
Prophylaxis: Allopurin, colchicine
What is osteoarthritis (OA)?
Risk factors?
”degenerative” loss of cartilage
Risk factors: Obestiy, increasing age, genetic predisposition
Treatment of osteoarthritis (OA)?
Medical treatment and non-medical treatment?
- change of life-style -Weight loss & exercise!
- analgetics
- cirgury
Medical treatment: First line: Paracetamol
The exercise: If pain by running, alternatives: Swimming, bicycling.
Symptoms and diagnosis of OA?
Clinical manifestations
Imaging
Mechanism of action of colchicine
GOUT
Modulation of chemokine and prostanoid
production and inhibition of neutrophil and endothelial cell
adhesion molecules by which it interferes with the initiation
and amplification of the joint inflammation
Interactions in treatment of GOUT?
NSAIDs counteract the effect of ACE-inhibitors. The effect of ACE-inhibitors is lowered.
–> Udskift ACE-hæmmer med evt. ANG II inhibitor.
Diagnosis of OA?
Take a picture of the bone.
Hvorfor kan en patient med gigt få anemia?
Ved gigt kan der dannes autoantistoffer mod kroppens med de røde blodlegemer, som herefter nedbrydes. Dette medfører at blodlegemerne nedbrydes hurtigere end normalt, hvorfor der opstår en normochromisk normocytisk anæmi, altså hvor blodlegemerne har normalt udseende og funktion, men blot nedbrydes hurtigere end den normale halveringstid på 120 dage.
