Rheumatoid arthritis and osteoarthritis Flashcards

1
Q

How is the rheumatoid arthritis (RA) diagnose established?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DAS28

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Investigations

A

Inflammatory markers:
C-reactive protine
Erythrocyte sedimentation rate (ERS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Goals in treatment?

A

Symptom relief - pain control
Slowing or prevention of joint damage
Preserving and improving functional ability
Achieving and maintaining disease remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The four main categories of drugs

A

NSAIDs
Glucorticoids
DMARDS
Biologisk behandling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

NSAIDs

A

Reduce jount pain and swelling

SYMPTOMAIC RELIEF

Lowest effective dosis for the shortest possible period of time.

Use of PPI!

Avoid if possible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DMARDs

Hvilke bruges oftest, og har clear evidens of benefit?

A

Methotrexate (MTX)
Sulphasalazine
Leflunomide
Intramuscular Gold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

DMARDs som kombinationsterapi

A

First-line therapy: MTX + mindst en anden DMARD såsom sulphasalazine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hvordan virker de forskellige DMARDs?

A

Methotrexate: Folic acid antagonist
Salazopyrin: Sulfapyrin + Pentasa
Hydroxy-chloroquine: TLR-inhibition
Leflunomid: DHODH inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Glucocorticoider

A

Anvendes i starten af behandling af arthritis, da DMARDs har slow onset.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Biological treatment for rhematoid arthritis

A

Biologics are used after a patient has failed DMARDs.

  • anti-TNF-alpha. (First line agent)
  • Interleukines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Interlekukins, mechanism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Risk factors in gout

A

Increasing age
Gender (male)
Obesity
Hypertension

Lifestyle: Meat and red wine.
Uric acid is the end product of Purine (aminoacid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Treatment of gout?

A

During attacs: NSAIDs, steorids, colchicine

Prophylaxis: Allopurin, colchicine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is osteoarthritis (OA)?

Risk factors?

A

”degenerative” loss of cartilage

Risk factors: Obestiy, increasing age, genetic predisposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of osteoarthritis (OA)?

Medical treatment and non-medical treatment?

A
  • change of life-style -Weight loss & exercise!
  • analgetics
  • cirgury

Medical treatment: First line: Paracetamol

The exercise: If pain by running, alternatives: Swimming, bicycling.

17
Q

Symptoms and diagnosis of OA?

A

Clinical manifestations

Imaging

18
Q

Mechanism of action of colchicine

GOUT

A

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

19
Q

Interactions in treatment of GOUT?

A

NSAIDs counteract the effect of ACE-inhibitors. The effect of ACE-inhibitors is lowered.

–> Udskift ACE-hæmmer med evt. ANG II inhibitor.

20
Q

Diagnosis of OA?

A

Take a picture of the bone.

21
Q

Hvorfor kan en patient med gigt få anemia?

A

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.