Arthritis Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Which kind of arthritis is more relevant in AAI

A

Rheumatoid arthritis

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

What causes arthritis?

A

Antibodies against “self”
Leads to tissue damage
Genetic factors
Can be potentially precipitated by pregnancy, infection, diet, environment

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

How does an autoimmune disease develop?

A

Auto antigens are present in everyone but not everyone develops auto antibodies to these (and of those that do, not everyone that has auto antibodies develops auto immune disease)

Self tolerance normally prevents auto antigens activating the immune system but in auto immune disease tolerance is lost and leads to self attack of the immune system

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

What is osteoarthritis?

A

Primarily a non inflammatory disorder (synovial joints)
Characterised by cartilage loss
Most commonly affects knees, hips and small hand joints
Link to overweight patients and obesity

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

What can we expect on diagram of a joint with osteoarthritis?

A

Bone spur (osteophyte)
Thinned cartilage
Cartilage fragments

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

Describe the pain in OA and which joints in commonly affects

A
Worsened by movement 
Eased by rest 
Worse at the end of the day 
Commonly affects; hands knees spine hips 
Usually unilateral (multiple joints)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pain management in OA

A

Steroid injections
NSAID / cox 2 inhibitors
Surgery

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

When are corticosteroid injections used to treat OA
What drugs can be used
What can these injections cause

A

Intra-articulated (into the joint)
Moderate to severe pain
Drugs used - triamcinolone, methylprednisolone
Can cause cartilage injury and loss

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

What is rheumatoid arthritis? Symptoms? Lab test results?

A

Chronic inflammatory disorder
Signs = joint damage, muscle wastage, deformity
Symptoms are pain stiffness joint swelling joint deformity

Lab tests are increased Wbc and erythrocyte (RBC - stick together and become heavier due to inflammatory response) sedimentation rate
Anaemia, rheumatoid factor (antibodies to IgG in some people)

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

Epidemiology risk factors in RA

A
Age 
Gender
Post partum 
Stress 
Genetic 
Smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pain in RA

A

Improves movement
Worse on waking
Affects small joints
Affects bilateral joints ( systemic inflammation therefore if affects one hand it is likely to develop in the other )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How is rheumatoid arthritis a systemic disease?

A

Emphasis on joints

Skin eyes vasculitis lungs salivary glands (reduced) pericarditis (inflammation of pericardium)

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

Aims of treatment of RA

Treatment options

A

Relieve pain
Modify disease process and prevent joint destruction
Preserve / improve functional ability

Symptomatic relief e.g pain (NSAIDs and PPI)
Slow progression of the disease 
-DMARD 
-steroids 
-biologicals

Monitor effectiveness

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

What is DMARD?

A

Disease Modifying Anti Rheumatic Drugs

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

Why must DMARDs be monitored closely?

How are they used in order to avoid adverse effect or poor efficacy?

A

Can be cytotoxic so must be monitored and counselled closely, reduce cautiously when symptoms are controls and if flare return to previous established dose

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

What is the main role of DMARDs ?

A

Directly inhibit cell proliferation

Inhibition of wide variety of cytokines including interleukins, interferons and TNF alpha

17
Q

What are the draw backs of DMARDs?

A

No analgesic activity

May take months for benefits to become apparent because turnover of cells

18
Q

When is DMARDs useful?

A

When cox inhibitors have not caused response in inflammation
To slow progression of disease

19
Q

What is the first line treatment of RA

A

DMARDs place in therapy - Methotrexate
Combination therapy of MTX and one other
Slow onset of action
Used with glucocorticoids until effective

20
Q

What are he general counselling points for first line treatment of RA (methotrexate and one other DMARD)?

A
Dose increased gradually 
Improvement may take some months 
Monitoring is necessary 
Nausea 
Report signs of blood dyscrasias, liver or lung toxicity
21
Q

List DMARDs

A
Methotrexate 1st line 
Sulfasalazine 
Leflunomide 
IM gold 
Less evidence for others
22
Q

How does methotrexate work?

A

Inhibits dihydrofolate reductase inhibitor (prevents pyrimidine synthesis)
Immunosuppressant
Weekly dosing
Once a week every week on the same day

23
Q

How does methotrexate inhibit DHF reductase?

A

Competes with DHF for enzyme that converts DHF to tetrahydrofolate ( DHF vital for pyrimidine synthesis)

24
Q

How does methotrexate reducing DHF reductase / tetrahydrofolate / methylene THF, treat RA?

A

Less DNA synthesis, reduces the proliferation of immune response cells in RA

25
Q

Describe possible methotrexate toxicity

A
Nausea 
Post dose flu 
Bone marrow
Hepatoxicity
Lung 
GIT effects 
Renal toxicity
Blood disorders
FOLIC ACID REDUCES SIDE EFFECTS
26
Q

How can the side effects of methotrexate treatment of RA be minimised?

A

Folic acid (not taken on the same day as methotrexate)

27
Q

What are the ADME considerations with methotrexate?

A

Absorption a unaffected with age
Deceased metabolism and clearance with age so just be clearly monitored as more risk of toxic effects

Interactions with NSAIDs so should avoid OTC Medicines

  • renal toxicity
  • reduced excretion of MTX
28
Q

What is the mode of actions of Sulphasalazine? Which arthritis does it treat?

A

Rheumatoid
Immune suppressant
Metabolised to 5 ASA which inhibits leukotriene and prostanoid synthesis, scavenge free radicals and decrease neutrophil chemotaxis

29
Q

How can we monitor and look out for ADRs to Sulfasalazine?

A

GI intolerance - nausea
Blood disorders - bruising, unexplained bleeding

Discolouration of urine and contact lenses

30
Q

What is Leflunomide’s mode of action and which arthritis does it treat?

A

Rheumatoid
Immunosuppressant
Metabolised to teriflunomide
Ultimately the same effect on cell proliferation as methotrexate

31
Q

How does Azathioprine differ from methotrexate

A

Inhibits purine synthesis and therefore cell proliferation (not pyrimidine)

32
Q

How and why are steroids used in treatment of rheumatoid arthritis?

A

Bridge therapy between starting or switching DMARDs

Rapid symptom control

33
Q

Prednisolone - the risks of the oral steroid

A

Side effects - PPI must be taken alongside

Bone protection needed as increases risk of osteoporosis

34
Q

Examples of biologicals ( TNF Alpha blocking) monoclonal antibodies
- the antibodies bind to TNF alpha

A

Adalimumab
Infliximab
Certilzumab
Golimumab

35
Q

What is Rituximab?

A

Monoclonal antibody that removes B cells
Used for treatment of RA
Licensed for use with MTX where treatment of combo DMARDs is not adequate

36
Q

What is Abatacept?

A

Biological agent - treatment of RA
B7 protein and CD28 protein must bind at the same time for the antigen presenting cell to communicate with the T cell
Abatacept blocks e B7 binding to CD28

37
Q

Drugs in development for RA

A

TNF alpha converting enzyme (TACE INHIBITORS)

Inhibitors of releasing TNF alpha

38
Q

How organ specific is rheumatoid arthritis?

A
  • not very