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HDID 1 > 17. Anti-Inflammatory Drugs > Flashcards

17. Anti-Inflammatory Drugs Flashcards

1
Q

RA is an indication for which types of anti-inflammatory drugs?

A

DMARDs, salicylates, NSAIDs, steroids

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2
Q

ankylosing spondylitis is an indication for which types of anti-inflammatory drugs?

A

NSAIDs, salicylates

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3
Q

osteoarthritis is an indication for which types of anti-inflammatory drugs?

A

acetaminophen, salicylates, NSAIDs

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4
Q

systemic lupus erythematosus (SLE) or crohn’s disease are indication for which types of anti-inflammatory rx?

A

salicylates, steroids, DMARDs

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5
Q

calling acetaminophen NOT an NSAID is due to the fact that it is not really anti-inflammatory. Why is this a problem?

A

it does reduce prostaglandins, which people assume it doesn’t as it is not an NSAID

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6
Q

acetaminophen/paracetamol (big facts)

A
  • not an NSAID
  • = tylenol
  • used to treat pain and fever (just the same as NSAIDs)
  • only weakly anti-inflammatory (so limited use for chronic conditions)
  • no GI irritation or effects on blood
  • frequently used in children
  • often combo with codeine to enhance analgesic effect and reduce opiate use
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7
Q

when to take acetaminophen?

A
  • most common OTC pain and fever reducer
  • good for indiv’s w/aspirin sensitivity or those who need to avoid aspirin
  • allergic reactions rare
  • not useful vs RA or stained/sprained muscles because only weakly anti-inflammatory
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8
Q

acetaminophen and personalized medicine?

A
  • lack of effect on bleeding, so given to pts on warfarin for blood thinning
  • interaction b/w acetaminophen and warfarin can increase hemorrhagic complications
  • involves CYP metabolism in the liver
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9
Q

acetaminophen mechanism?

A

controversy, but included theories:

  • brain specific COX-3 is inhibited (reduced pain and fever but no anti-inflammatory effects)
  • maybe a metabolite of acetaminophen activates TRPV1 channel involved in pain perception (but this doesn’t explain fever reduction)
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10
Q

acetaminophen side effects

A
  • foremost cause of liver damage in the western world
  • hepatotoxicity is exacerbated when combo w/alcohol (chronic, high use)
  • hidden sources in OTC meds can contribute to toxicity
  • alco causes SCAR in rare occasions, incl stevens-johnson syndrome
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11
Q

acetaminophen toxicity

A
  • mediated by metabolite created in the liver called NAPQI
  • conversion (to metabolite) via mult p450 enzymes
  • initial damage can either be repaired or accelerated depending on the balance of pro- vs anti-inflammatory cytokines
  • alcohol abuse can tip ^ balance, as can genetics
  • if not enough glutathione or if glutathione transferases are not available (thanks to excessive alcohol) then NAPQI doesn’t get transformed to safe metabolite
  • N-acetylcysteine can restore depleted glutatione stores and reduce cellular damage
  • good cytokines (IL-10) help hepatocytes recover
  • bad cytokines (TNF, IL-1) cause hepatocyte death
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12
Q

Glucocorticoids are naturally occuring compounds that serve the body many functions, esp being ________. The purpose is for ______ protection.

A

anti-inflammatory; acute protection (in an emergency like an injury)
…long term exposure to both natural and synthetic steroids can be costly

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13
Q

Glucocorticoids generally do what to the immune response? What particular cytokines do they effect?

A

generally shut down the immune response

  • inhibit DCs from releasing IFN-gamma, TNF-alha, IL-6, and IL-12 (the bad pro-inflammatory cytokines)
  • increase Treg production of IL-10 (the good anti-inflammatory cytokine)
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14
Q

glucocorticoids mechanisms of action? Genomic and non-genomic

A

genomic:

  • direct binding of GR to DNA at GRE to induce txn (of anti-inflamm cytokines like IL-10)
  • direct binding of GR to DNA at non-GRE to repress txn
  • indirect via sequestering of other TFs
  • indirect via modification of histone acetylating and deacetylating enzymes (binds CBP = HAT to open DNA)

non-genomic effects

  • interaction w/the lipid bilayer of the cell or mitochondria
  • binding to a membrane GR

selective responses of different cell types is in part a function of the number and nature of the GR population

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15
Q

clinical utility of glucocorticoids for systemic use?

A

for achievement of adequate control - never the sole treatment, never the drug of choice, but used when conservative measures fail, or on the short term while waiting for other drugs to become effective

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16
Q

dexamethasone

A
  • synthetic cortisol analog
  • anti-inflammatory and immunosuppressant
  • 27X more potent than cortisol and &X more potent than prednisone
  • use for RA or other forms of arthritis
  • given to pts w/bacterial meningitis prior to antibiotics to suppress the immune response to dead bacteria (because dead bacteria dump contents and you get sepsis thanks to massive immune response - you don’t want that)
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17
Q

prednisone

A
  • glucocorticoid pro-drug that is converted into active form, prednisolone, in the liver by 3B-HSD
  • used for many anti-inflammatory responses (allergy, asthma) and putative autoimmune diseases, most commonly Crohn’s
  • side effects may be more tolerable than the disease it treats
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18
Q

systemic lupus erythematosus?

A
  • autoimmune disease
  • attacks joints, organs and skin, but highly variable b/w indivs
  • 4x more common in women
  • butterfly rash

tx w/…

  • NSAIDs in milder cases and during remission
  • steroids are most common tx re: flares
19
Q

cost to using prednisone (re: side effects)?

A
  • central obesity
  • moon face
  • buffalo hump
  • thin, wrinkled skin w/constant surface sores
  • straie on skin
  • purpura
  • cognitive effects (depression, insomnia, nervousness, psychosis)

the longer you take it, the worse it gets

20
Q

betamethasone

A
  • same immunosuppressive and anti-inflammatory actions as others but only used TOPICALLY
  • use for skin irritation
  • given as injection w/slight chemical modifications for MS flares or in premature babies to promote lung maturation or for acute asthma attack
21
Q

flonase

A
  • aerosol spray of micronised fluticasone proprionate
  • used for allergic rhinitis (to aboid sleepy-side effects of antihistamines)
  • lipid-soluble steroids delivered in aerosolized form for asthma and related uppre respiratory disorders to reduce vasodilation and decrease fluid exudation while agoiding systemic side effects
  • daily dose much reduced (25-35 fold reduction)
22
Q

what does DMARD stand for?

A

disease modifying anti-rheumatic drugs

23
Q

DMARDs are distinguished from NSAIDs how? What are their two general categories?

A

distinguished from NSAIDS by altering the disease (not a cure, but don’t just treat symptoms, instead block the progression of the disease and prevent deteriorating damage that will accum)

categories: small molecules and biologics

24
Q

what are the “bad” cytokines re: RA?

A

IL-6 and TNF

25
Q

what are the two small molecule DMARDs?

A

methotrexate and leflunimide

26
Q

methotrexate (MTX)

A
  • DMARD of 1st choice
  • originally and currently used in cancer therapy
  • now 1st line therapy for RA and crohns/lupus/other autoimmune disorders
  • mechanism vs cancer is different than immunosuppressive effect
  • —-use as chemotherapy based on disruption of folic acid metabolism which prevents purine synthesis and therefore DNA synthesis. Reuires high doses and induces side effects
  • —-immunosuppressive effect at lower doses is due to accumulation of adenosine (also due to disruption of folic acid metabolism) which suppresses T cell activation and B cell proliferation
27
Q

methotrexate contraindications?

A

pregnancy and breast feeding, major organ disease (except heart), excess alcohol ingestion, immunodeficiency, and blood dyscrasias

28
Q

methotrexate side effects

A

good response rate/durability of response, incidence of side effects is low

toxicity includes cytopenias, liver disease (fibrosis, cirrhosis), and rare pulmonary toxicity

adverse drug effects mild and treatable (generally GI) and most can be alleviated with folic acid supplementation

29
Q

leflunomide (ARAVA)

A
  • usually second line of defense if methotrexate isn’t working
  • tx for RA (not other diseases too like methotrexate)
  • distinct from others by inhibiting pyrimidine synthesis (and therefore DNA) but effect is the same in that it blocks proliferation of activated lymphocytes (similar mechanism as methotrexate)
  • serious side effects on liver and hematologically (diarrhea, GI disturbances, other) and TERATOGEN - so don’t use in pregnancy or in breast-feeding women (can stay in the body for 2 years)
  • long 1/2 life precludes using many other drugs to avoid potential drug interactions
30
Q

biologics or TNFs

A
  • fastest growing class of DMARDs
  • etanercept and infliximab are most frequently used but only because they’ve been around longer
  • relatively equal in efficacy, but frequency and route of admin vary
  • customer decides, and rxn at site of infusion since this is an immunosuppressive drug = problem
31
Q

DMARDs that inhibit TNF-alpha?

A

Adalimumab, etanercept, golimumab, infliximab

32
Q

DMARDs that inhibit IL-1?

A

anakinra

33
Q

DMARDs that inhibit IL-6/IL-6R?

A

tocilizumab

34
Q

DMARDs that inhibit JAK/STAT?

A

tofacitinib

35
Q

DMARDs that inhibit CD80/CD86 (immune cell receptors)?

A

abatacept

36
Q

infliximab (remicade)

A
  • mechanism: binds to both soluble and membrane-bound TNF-a
  • induces programmed cell death of T-activated lymphocytes
  • chimeric
  • used in RA, AS, and crohn’s
  • can have serious infusion reactions, so combine w/methotrexate
  • human IgG1, Fc Hc, and partial K Lc fused to murine hypervariable region
37
Q

etanercept (enbrel)

A
  • mechanism: binds soluble TNF
  • fusion protein made from recombinant DNA coding for the TNF receptor combined with human IgG1
  • used for tx of RA, AS, and crohn’s

side effects: erythema, pain, pruritis, headaches, abdominal pain

38
Q

adalimumab (humira)

A
  • mechanism: the mAb binds to solube TNFa, acting like a sponge
  • down regulates macrophages and T cell function
  • 1st fully human mAb
  • RA and crohn’s
  • used also for psoriasis and psoriatic arthritis

increased risk for infections if used long-term

39
Q

tocilizumab (actemra)

A

humanized mAb vs IL-6/IL-6R

  • use if TNFs dont work or are not tolerated

don’t use in combo w/DMARDs vs TNF-a

40
Q

anakinra (kineret)

A

mAb vs IL-1/IL-1R

  • use if TNFs don’t work or are not tolerated

(only FDA approved drug for NOMID)

41
Q

abatacept (orencia)

A

inhibit T-cells

  • inhibits the activation of T cells by selectively blocking the specific binding of CD80/CD86 to the CD28 (on T cells) receptor and thus inhibits T cell proliferaiton and immune responses of B cells
  • decreased inflammatory cytokines
    0 in combo w/methotrexate, prevents the progression of joint damage and improves physical function in RA patients

(extracellular domain of CTLA4 and genetically modified Fc region of IgG1, designed to interfere w/the regulation of costimulation of T lymphocytes)

42
Q

rituximab

A

inhibit B cells

43
Q

golimumab (simponi)

A

mAb vs TNF

- longer term efficacy and fewer injections

HDID 1 (24 decks)

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