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Stage 2: Inflammation > Anti-Inflammatory Drugs > Flashcards

Anti-Inflammatory Drugs Flashcards

1
Q

How do NSAIDs work?

A
  • They inhibit COX enzyme, thus inhibiting prostaglandin production from arachidonic acid
  • Analgesic, anti-inflammatory and anti-pyretic
  • They don’t affect the course of the disease
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2
Q

What are 4 examples of non selective (inhibit all COX enzymes) NSAIDs?

A
  • Ibuprofen
  • Aspirin
  • Naproxen
  • Indomethacin
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3
Q

What do prostaglandins do?

A

They are pro-inflammatory, vasodilating and sensitise the pain pathway

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4
Q

What are side effects of non-selective NSAIDs?

A
  • Side effects in gut and kidney

- They stop blood flow and mucus secretion which can lead to ulcer formation and internal bleeding

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5
Q

What are two examples of COX-2 (enzyme found at inflammatory site) selective inhibitors?

A
  • Celecoxib

- Meloxicam

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6
Q

How do you use oral NSAIDs (COX inhibitors) in patients with a cardiovascular risk?

A

1) Associated use of PPIs e.g. omeprazole to inhibit GI reflux due to excess acid
2) OR use prostaglandin analogue/agonist e.g. misoprostol which helps with vasodilation and increased mucus production
3) Do a gradual increase in NSAID use via topical application e.g. diclofenac (Voltaren)

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7
Q

What are 3 examples of anti-inflammatory steroids (glucocorticoids /corticosteroids)?

A
  • Hydrocortisone
  • Dexamethasone
  • Prednisolone
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8
Q

How do anti-inflammatory steroids work (why are they beneficial)?

A

1) Multiple anti-inflammatory actions
- Inhibit arachidonic acid (and therefore prostaglandin) release
- Cytokine inhibition
- Down regulation of adhesion molecules
- Inhibition of enzyme induction (COS, NOS)
2) Effects on immune response
- Inhibition of lymphocyte proliferation
- Induces apoptosis of inflammatory cells

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9
Q

What are 5 side effects of anti-inflammatory steroids?

A
  • Osteoporosis
  • Diabetes
  • Glaucoma
  • Increased risk of infection
  • Adrenal atrophy
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10
Q

When are anti-inflammatory steroids given (short term)?

A
  • Local flare ups
  • When waiting for other DMARDs to work
  • ‘Steroid sparing’
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11
Q

Describe giving steroids locally (intra-articular)?

A
  • High effective first time
  • If given again/multiple times doesn’t have the same effective effect
  • Decreased side effects
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12
Q

How do disease modifying anti-rheumatic drugs (DMARDs) work?

A
  • They suppress the overactive immune and/or inflammatory systems, to inhibit the damaging process (all work via different mechanisms)
  • Combat the ongoing and destructive inflammation (via immunosuppression or cytotoxicity) - affects course of disease, doesn’t just treat symptoms
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13
Q

How long to most DMARDs take to work and therefore how are they often prescribed?

A
  • Weeks to months

- They are often prescribed together as combination therapies

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14
Q

What might you prescribe along with a DMARD until it takes its effect?

A

NSAID and/or steroid

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15
Q

What are the 3 subsets of DMARDs?

A

1) Traditional DMARDs
2) Biologics/biosimilars
3) ‘Targeted’ DMARDs

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16
Q

Describe traditional DMARDS

A
  • Taken orally
  • Broad immunosuppressants
  • Adverse effects common with most
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17
Q

Describe biologics/biosimilars

A
  • Taken by self-injection or infusion
  • Target specific mediators
  • Well tolerated (immunogenic)
  • Fewer side effects but still immunosuppressant e.g. more vulnerable to TB
18
Q

Describe ‘targeted’ DMARDs?

A
  • Taken orally
  • Target specific immune system signalling molecules
  • Small molecular weight inhibitors
19
Q

What are 5 examples of traditional DMARDs?

A
  • Methotrexate
  • Hydroxychloroquine
  • Sulfasalazine
  • Leflunomide
  • Azathioprine
20
Q

Which traditional DMARD is the gold standard for inflammatory arthritis and most widely used DMARD for RA?

A

Methotrexate

21
Q

Describe use of methotrexate

A
  • Substantial efficacy in RA (30% of patients)
  • Acceptable safety
  • Low cost
  • Steroid sparing
  • Can be mixed with other anti-inflammatories
  • Low doses are useful and high doses aren’t any better (low dose associated with good clinical outcome)
  • Used in young and old
22
Q

What is the recommended dosage of methotrexate?

A

7.5-15mg once weekly (low dose compared to its use in chemotherapy)

23
Q

What is the primary mechanism of action of methotrexate?

A

Folate antagonist - inhibits dihydrofolate reductase (DHFR)

  • Affects intracellular metabolic pathways dependant on folinic acid dependent
  • Decreases purine and pyrimidine (polyamine) production/metabolism and interferes with DNA synthesis (anti-proliferative effect in cancer)
24
Q

What are the anti-inflammatory effects of methotrexate (via folate antagonist and other mechanisms)?

A

1) Suppresses NF-kappaB activation - inhibits production of cytokines (+ other effects below)
2) Inhibits T cell and macrophage activation (apoptosis of activated lymphocytes)
3) Decreases pro-inflammatory cytokines
4) Inhibits endothelial adhesion molecule activation (which bring inflammatory cells towards joint) - helps CV protection
5) Increases adenosine release - anti-inflammatory, reduces cell activation

25
Q

What are the adverse effects of methotrexate and therefore what do you have to do?

A
  • Cytopenia (bone marrow suppression due to anti-proliferative effects)
  • Nausea
  • Infection
  • Intestinal
  • Hepatotoxicity - problems with liver function
  • Embryotoxic (not safe in pregnancy)
  • Acute pneumonitis (rarely, inflammation of lungs where pt presents with SoB + fever)
  • Need to monitor and administer folate
26
Q

What do biologics reduce?

A

The number of surgeries (still happens e.g. knees and hips)

27
Q

What are the two types of biologic used in RA?

A

1) Anti-TNF antibodies - infliximab, adalimumab (Humira)

2) Soluble TNF receptor - etanercept

28
Q

Describe use of biologics

A
  • Used when other DMARDs have failed
  • Effective for 30% of cases
  • Can be less successful in follow up treatments
  • Expensive
  • Can be given as co-treatments
29
Q

How do anti-TNF antibodies work?

A
  • Antibody (MAbs) to TNF (inflammatory cytokine released by inflammatory cells e.g. macrophages)
  • The antibodies bind to and get rid of TNF, stopping it getting to the receptor and causing its inflammatory effects
30
Q

What is the effect of preventing TNFalpha in RA (main mediator)?

A
  • Stop cartilage and bone degradation
  • Decrease inflammation
  • Quite soon after taking the biologic pts feel better and have less pain
31
Q

What are 3 types of cytokine biologics (block mediator systems)?

A

1) IL-1 antibodies/receptor antagonists e.g. canakinumab (effective in juvenile arthritis and atherosclerosis)
2) IL-6 blocker e.g. tocilizumab - used for non-responders to MTX/anti-TNF
3) IL-17 receptor antagonist - used in psoriatic arthritis

32
Q

What are 2 types of cell based biologics?

A

1) Rituximab - removes B cells

2) Abatacept - inhibits action of T cells and reduces damaging effects

33
Q

What are biosimilars?

A
  • A biologic medical product which is almost identical copy of an original product i.e. biologic
  • May be manufactured by a different company but has the same effect
  • Cheaper by ~ 40%
34
Q

What are two examples of the newer targeted DMARDs?

A

1) Janus kinase (JAK) inhibitors e.g. baricitinib

2) Apremilast

35
Q

Describe JAK inhibitors

A
  • Target intracellular pathways (different from biologics)
  • When the cytokine is circulating in the blood it binds to a cell via JAK-STAT receptors which cause intracellular effects
  • JAK inhibitors bind to these receptors that the cytokines work on so they can’t bind (don’t need to block cytokine)
  • Target the JAK-STAT inflammation pathway
  • Inhibits cell signalling e.g. T cells via blocking JAK kinases
  • Oral daily (small molecule, easier to make)
  • Cheaper than biologics
  • Used when other DMARDs are not tolerated in moderately to severely active RA
  • Effective
36
Q

Describe apremilast

A
  • Inhibits the activity of phosphodiesterase type 4 (PDE4)
  • Suppresses pro-inflammatory mediator synthesis and promotes anti-inflammatory mediators
  • Oral
  • Good for patients with psoriatic arthritis (w DMARDs or alone)
  • Good for patients intolerant to DMARDs e.g. MTX
37
Q

Why is there a problem with adherence to DMARDs?

A
  • Takes weeks to work
  • Needs monitoring and injections
  • Complex treatment
38
Q

How can the bioavailability of methotrexate be enhanced in ⅔ patients who have incomplete response?

A
  • S/C administration

- Introducing combination therapies with other DMARD which has synergistic effect

39
Q

When can methotrexate possibly cause pulmonary fibrosis?

A
  • In patients with severe disease who may have underlying lung damage
  • Can use it safely in almost all patients (link overinflated)
  • Only won’t use it in patients who already have lung disease
40
Q

What is an example of a cytotoxic drug?

A

Cyclosporin

41
Q

What are the 5 TNF inhibitors (anti-TNF therapy) which differ slightly in make up but all bind to TNF and stop the effects of TNF driving inflammation in the joints and body?

A

1) Infliximab
2) Adalimumab
3) Etanercept
4) Golimumab
5) Certolizumab pegol

42
Q

Risk of which infections can be increased when using biologics and what happens?

A

1) TB - common in patients on biologics so need to screen for previous exposure and if they have had it, would give medication to prevent TB coming back
2) Shingles

Stage 2: Inflammation (39 decks)

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