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- AAI; Pharmacology & Cell Biology > Arthritis > Flashcards

Arthritis Flashcards

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1
Q

Is rheumatoid arthritis an organ-specific or non-organ specific autoimmune disease and where does it affect?

A

Non-organ specific; systemic disease affecting:

  • joints (emphasis)
  • eyes (50% of the time; inflammation)
  • skin (nodules)
  • vasculitis
  • lungs
  • salivary glands (reduced secretion)
  • pericardium (inflammation of lining of the heart)
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2
Q

What causes RA?

A
  • Antibodies against “self”; own proteins targeted
  • Genetic factors

Can be precipitated by:

  • Pregnancy
  • Infection
  • Diet(?)
  • Environment(?)

Leads to tissue damage.

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3
Q

How does autoimmune disease develop?

A
  • Autoantigens present in everyone
  • But self-tolerance prevents autoantigens activating the immune system (immune system recognises own antigens being targeted so allows it)
  • Thus not everyone develops autoantibodies to autoantigens; and of those that do, not everyone develops autoimmune disease from autoantibody production
  • In autoimmune disease, self-tolerance is lost leading to attack of “self”
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4
Q

What is osteoarthritis and how is it characterised?

A
  • Primarily non-inflammatory disorder (synovial joints being worn)
  • Characterised by cartilage loss
  • Thus grinding of bone; prostaglandin release as a result resulting in pain (can bring about inflammation)
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5
Q

Where does OA most commonly affect and what is it linked to?

A
  • The knees/hips/small hand joints/spine

- Linked to being overweight/obese (more weight = more risk)

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6
Q

What aggravates/eases pain in OA?

A
  • Worsened by movement
  • Eased by rest
  • Worse at the end of the day (with use of joints throughout)
  • Usually unilateral
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7
Q

What are the treatment options for OA?

A
  • Pain (treat)
  • Steroid injections (reduces PGA)
  • NSAIDs/COX-2 inhibitors (reduces PGA)
  • Surgery
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8
Q

Which COX pathway(s) do NSAIDs block and what are the consequences?

A
  • NSAID for inflammation
  • COX-1 involved in PG production in GIT
  • COX-2 involved in inflammation

BUT NSAIDs block both COX-1 and COX-2 pathways (selective COX-2 would treat pain w/less GI disturbances but alas less protective effective of PGAs seen with NSAIDs)

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9
Q

When are corticosteroids injections used for SA and how do they work?

A
  • When pain is moderate to severe

- Inhibits PLA-2 (phospholipase A2) thus reducing PGA production

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10
Q

Where are corticosteroid injections administered and why?

What are their possible side effects?

A
  • Injected directly to book the as blood flow to joints is poor
  • Possibly caused further cartilage injury and loss though
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11
Q

What is rheumatoid arthritis and how is it characterised?

A
  • Chronic inflammatory disorder
  • Autoimmune disease
  • Characterised by joint damage, muscle wastage, deformity (stiffness from not using joints as much)
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12
Q

What are the symptoms of RA?

A
  • Pain
  • Stiffness
  • Joint swelling
  • Joint deformity
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13
Q

How would WBC count, ESR (erythrocyte sedimentation rate) or rheumatoid factor be affected in RA?

A
  • WBC; increased
  • ESR; increased (in chronic inflammation erythrocytes stick together more thus becoming heavier and sinking; high ESR indicates inflammation)
  • Rheumatoid factor present (an autoantibody against the tail portion of the antibody IgG)
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14
Q

What aggravates/eases pain in RA?

A
  • Pain improves with movement (opposite of OA)

- Worse on waking (opposite of OA)

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15
Q

What type of joints does RA affect?

A
  • Small joints

- Bilateral joints (affecting both sides of the body thus both wrists etc)

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16
Q

What are the aims of RA treatment?

A
  • Relieve pain
  • Modify/slow down the disease process
    (Prevent joint destruction)
    (Preserve/improve functional ability)
  • Multidisciplinary approach
  • Treat promptly and introduce DMARDs early
17
Q

What treatment options are available for RA?

A
  • Symptomatic relief
    (analgesia to decrease need for NSAIDs; use PPI w/NSAIDs if needs be)
  • Slow progression of disease
    (DMARD/steroids/biologicals)
18
Q

What are DMARDs?

When would they be started?

A

Disease Modifying Anti Rheumatic Drugs

  • Ideally start within 3 months (start slowing disease progression ASAP)
  • Reduce dose (CYTOTOXIC) cautiously when symptom control achieved (if flare-up return to previous established dose)
  • Monitoring
  • Counselling
19
Q

How do DMARDs work and how long does it take?

A
  • Directly inhibits cell proliferation; inhibiting immune cell production (and thus fewer inflammatory mediators)
  • Inhibitions of a wide variety of cytokines (signalling/mediators) including: interleukins, interferons and TNF-alpha.
  • Slow-acting; may take up to 3/12 (a few months) for benefits to become apparent
  • No analgesic activity
20
Q

When are DMARDs used?

A
  • Primarily for rheumatic disorders and where inflammation does not respond to COX-inhibition
  • Slows course of disease
21
Q

What are DMARDs role in RA therapy?

A
  • First line treatment
    (combination therapy; methotrexate + 1 other DMARD)
    (monotherapy with rapid dose titration; if combination therapy not possible start with MTX and increase dose quickly)
  • Use with glucocorticoids until effective (type of corticosteroid; start off w/steroid treatment to reduce inflammation and then titrate down dose to zero when DMARD starts working)
22
Q

What are the counselling points for DMARDs?

A
  • Dose increased gradually
  • Improvement may take some months (patient needs to be aware effect is not immediate)
  • Monitoring necessary
  • Nausea
  • Report signs of blood dyscrasias, liver or lung toxicity.
23
Q

What DMARDs are available for treatment?

A
  1. ) Methotrexate
  2. ) Sulfasalazine (Crohn’s)
  3. ) Leflunomide
  4. ) IM gold (intramuscular)
24
Q

What is methotrexate and how does it work?

A
  • Dihydrofolate reductase inhibitor
  • Inhibits pyrimidine synthesis (and thus DNA/RNA)
  • Immunosuppressant
  • Dose individual to patient; made up each time, titrate to lower dose when effects shown
  • Weekly dosing (same day each week, once a week)
25
Q

How does MTX inhibit dihydrofolate reductase (DHFR) and what are the consequences?

A
  • MTX competitively inhibits DHFR (which essential for thymine synthesis)
  • MTX 1000x affinity to DHFR than folate
  • DHFR catalyses the conversion of dihydrofolate to the active tetrahydrofolate; thus MTX prevents this conversion leading to less Methylene THF for DNA synthesis
  • Affects cells with lots of proliferation; particularly where inflamed thus less inflammation
26
Q

What are the issues with methotrexate toxicity?

A
  • Nausea
  • Post dose ‘flu’
  • Bone marrow toxicity (uncommon)
  • Hepatotoxicity
  • Teratogenic (affects cell turnover in foetus; contra-indicated in pregnancy)
  • GIT effects
  • Renal toxicity
  • Blood disorders (bruising/unexplained bleeding)
27
Q

Why is taking folic acid with MTX beneficial?

A
  • Folic acid is the synthetic version of folate; what MTX is side-manning
  • Rather than being counter-productive taking folic acid when not taking MTX (avoid competitiveness) can reduce other systemic side effects w/o inhibiting the therapeutic effect of MTX
28
Q

What are the counselling points of MTX?

A
  • Weekly dose
  • Take folic acid as directed (once weekly or daily but not the same day as MTX)
  • Regular blood tests (monitor hepatotoxicity etc)
  • Recognise and report signs of serious side effects
  • Contraception (teratogenic effects)
  • Patient information book for MTX given
  • Sharps bin (purple lid for cytotoxicity) and its disposal
29
Q

What are the concerns of MTX and ADME?

A
  • Absorption unaffected with age
  • Decreased metabolism and excretion with age
    > Thus increased risk of toxic effects
  • Interaction with NSAIDs; avoid OTC (do not self-prescribe)
    > Renal toxicity
    > Reduced excretion of MTX; potentially toxic plasma levels of MTX
30
Q

How does the pro-drug sulfasalazine (SFZ) work in RA and how long does it take?

A
  • Immune suppressant
  • Metabolised to 5-ASA inhibiting leukotriene & prostanoid synthesis, scavenges free radicals and decreases neutrophil chemotaxis
  • Initially 500mg/day (increased weekly/max 2-3g a day in divided doses)
  • Onset of action; 6 weeks
31
Q

How should sulfasalazine be monitored/ADRs to look out for?

A
  • GI intolerance (nausea)
  • Blood disorders (bruising/unexplained bleeding - similar to MTX)
  • Discolouration of urine & contact lenses (counselling point; advise to wear glasses instead for duration of treatment)
32
Q

How does the immunosuppressant leflunomide work?

A
  • Inhibits dihydroorotate dehydrogenase
  • Is itself metabolised to teriflunomide
  • Impairs cell proliferation akin to MTX, dampening down immune response
33
Q

What adverse effects are associated with leflunomide?

A
  • Diarrhoea (20%)
  • Nausea/rash/alopecia (10%)
  • Abnormal LFT (liver function test; 5%)
  • Teratogenic
    > Contraception, INC. male treatment
    > +2 years post-stopping (can’t have child for)
    > Present in breast milk (use bottled)
34
Q

How does gold work for RA treatment and what adminstration methods are available?

A
  • Immune suppressant
  • Sodium aurothiomalate deep IM
  • Auranofin (oral); less toxic but less efficacy
  • 2nd or 3rd line treatment
  • Weekly regimen until response (then extend interval at which it is given)
  • Possible rashes/blood disorders
35
Q

When is hydroxychloroquine given and how does it work?

A
  • Used in mild/moderate cases
  • Add-on to MTX etc
  • Inhibits lymphocyte function
  • Long half-life
36
Q

What other DMARDs are available and how do they work?

Why are they not used as much?

A
  • Penicillamine; metabolite of penicillin (only used by experimental clinicians; toxicity)
  • Ciclosporin; severe RA (T-cells affected; usually used in tissue transplantation)
  • Azathioprine; inhibits purine synthesis (as seen in Crohn’s) thus DNA synthesis

Relieves symptoms but does not modify disease progression so less used.

37
Q

How are steroids used in RA and when/how are they administered?

A
  • Bridge therapy between starting new DMARD/switching to reduce inflammation by blunting immune response
  • Rapid symptom control
  • IM/IA/IV (better than oral; GI side effects, PGA reduction - PPI would be required)
  • IV possibly more toxic
38
Q

What oral steroid can be used/what precautions should be made?

A
  • Prednisolone
  • Conflicting evidence; long term use is discourages
  • Side effects present:
    > Increases risk of osteoporosis (calcium supplements to prevent bone degradation)
    > PPI needs to be given to protect stomach as PGA is reduced

- AAI; Pharmacology & Cell Biology (4 decks)

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