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hlsc final > rheumatoid arthritis > Flashcards

rheumatoid arthritis Flashcards

1
Q

rheumatoid arthritis

A

autoimmune disease
- appears 3rd or 4th decades
- older than 60
- mean and women equal
- progressive disease causing joint deformities and limitation

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2
Q

progression of RA

A

A) Healthy joint

B) Inflammation of synovial membrane
= membrane thickens

C) Synovial membrane begins to erode articular cartilage (overgrowth referred to as “pannus”)

D) Pannus enzymes destroy articular cartilage
= initiation of synovial space inflammation

E) Complete destruction of joint cavity and fusion of articulating bones

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3
Q

what is joint destruction caused by

A

autoimmune process

  • immune cells cytokines and cytotoxins attack synovial tissue
  • TNF: tumor necrosis factor
    -IL-1: interleukin-1
  • IL-6: interleukin- 6
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4
Q

antiarthritic drugs: 3 groups

A

1) NSAIDS

2) Glucocorticoids

3) Disease-modifying antirheumatic drugs (DMARDs)

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5
Q

NSAIDs for RA

A

rapid relief of symptoms

dont prevent joint damage

don’t slow disease

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6
Q

Glucocorticoids for RA

A

Rapid relief
- via inhibition of prostaglandins

Slow disease progression

Serious TOXICITY with longterm use

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7
Q

DMARs for RA

A

Reduce joint destruction

Slow disease progression

  • interferes with immune and anti-inflammatory responses
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8
Q

3 categories for DMARDs

A

1) Conventional
- synthesized molecule
- extensive effect on immune system

2) Biologic:
- large molecules produced through recombinant DNA technology
- work on cytokines

3: Targeted:
- latest drug
- synthetic molecules that block specific pathways inside cells of immune system

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9
Q

Recombinant DNA technology

A

altering genetic materials outside of organism to enhance characteristics

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10
Q

Synthetic peptides

A

made by chemical peptide synthesis

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11
Q

drug selection for RA

A

Starting DMARD within 3 months may prevent serious joint injury

NSAIDs given while DMARDs develop (takes months)

Glucocoticoid- used for short-term management of flare-ups

If injury continues another DMARD can be added

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12
Q

Glucocoricoid drug name

A

Prednisone

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13
Q

Prednisone

A

powerful anti-inflammatory drugs

POif RA systemic
- can be toxic long-term

One or two joints affected
- interarticular injections are employed

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14
Q

Conventional DMARDs drug name

A

Methotrexate (M)

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15
Q

Methotrexate

A
  • immunosuppression

First choice DMARD with RA

Works faster than other DMARDs
- 3-6 weeks

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16
Q

Methotrexate Mechanism of action

A

unclear

Is a folate antagnoist
- folate necessary for DNA synthesis and cellular replication

Process used to reduce B and T lymphocyte activity

17
Q

Conventional DMARs adverse effects

How to help some side effects

Contraindications

A

Various toxicities
- hepatic fibrosis
- GI ulceration
- bone marrow suppression

Reduce GI and hepatic effects use supplementation of folic acid

Contraindicated for patients with blood dyscrasias

18
Q

Methotrexate Interactions

A

any drug that causes any of adverse effects should not be used with M

19
Q

Biological DMARs drug

A

Tumor Necrosis Factor Antagonists (TNF-a)

Prototype: Etanercept

20
Q

Mechanism of Entanercept

A

Antagonizing actions of TNF-a during RA

  • TNF-a is a main mediator of joint inflammation
  • (1) increases osteoclast function
  • (2) blocks osteoblast action
    = bone mass loss
21
Q

Entanercept function

A

Designed etanercept receptors are identical to TFN-a’s

becomes a competitive inhibitor of TFN-a

22
Q

Adverse Reaction Etanercept (5)

A

Should not be given to pt with active infection

Black box Warning

Neutropenia: decreased

Skin Reactions: associated with Sub Q injection

Risk of Heart Failure

23
Q

Targeted DMARDs

A

Janus Kinase Inhibitors (JAKs)

prototype: Tofacitinib

24
Q

Tofacitinib

A

newest drug for RA

JAKs: Intracellular enzymes initiate cytokine signalling as part of a transcription pathway

Inhibiting JAK: inhabitation of immune and inflammatory response

25
Q

Mechanism of Tofacitnib

A

competitively bind to JAK binding site
- suppression of cytokine signalling and transcription

26
Q

Adverse reaction of Tofacitinib

A

increased risk of infection

hlsc final (12 decks)

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