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Y1 - Pharm > 5 - NSAIDs > Flashcards

5 - NSAIDs Flashcards

1
Q

NSAIDS:

  • define, fxns,*
  • prototype*
A
  • def: nonsteroidal anti-inflammatory drugs
  • fxn
    • anti-inflammatory
    • analgesic (reduce pain)
    • anti-pyretic (reduce fever)
  • prototype: aspirin
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2
Q

types of inflammation

A

acute

(immune response)

chronic

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3
Q

mediators of acute inflammation, and the effects on:

vasodilation, vascular perm, chemotaxis, pain

A
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4
Q

mediatros of CHRONIC inflammation:

& primary effects

A
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5
Q

where in the process do NSAIDs act? and what do they do?

A

Prevent arachidonic acid from being converted into PG, thromboxane, prostacyclin

*INHIBIT COX enzymes

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6
Q

where in the body is the NSAID working?

A

occurs locally at the site of action in the periphery

blocks competitively or non-competitively

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7
Q

what are autacoids, and how are they involved in inflammation?

A
  • biological factors (molecules) which act like local hormones, have a brief duration, and act near their site of synthesis after binding to nerve fiber receptors in the periphery
  • function to block pain and inflammation response in the periphery at the site of action (blocking the production of prostaglandins)
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8
Q

which have more adverse side effects and why?

corticosteroids, or NSAIDs?

A

*corticosteroids, because these act higher up in the process –> more downstream side effects

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9
Q

what are the therapeutic strategies of drugs?

A
  1. relief of pain
  2. slowing or arresting of the tissue damaging process
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10
Q

NSAIDs:

chief clinical use?

A
  • anti-inflammatory agent in tx of musculoskeletal disorders (OA and RA)
  • these DO NOT arrest the progression of pathological injury to tissue
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11
Q
  1. what is the current gold standard to which anti-inflammatory drugs are compared?
  2. which drug was historically the gold standard (prior to 1960s)
A
  1. current gold standard: IBUPROFEN
  2. previously/historically: aspirin
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12
Q

REVIEW: pharmacokinetics categories?

A

ADME

  • absorption
  • distribution
  • metabolism
  • excretion
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13
Q

Aspirin:

pharmacokinetics (ADME)

A
  • A - rapidly absorbed
  • D - found in synovial fluid
  • M - metabolized by cytochrome p450
  • E - renally excreted
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14
Q

Aspirin:

pharmacodynamics

A
  • IRREVERSIBLY inhibits COX activity
  • esp affects platelets
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15
Q

Aspirin:

clinical uses

A
  • analgesia: pain of mild-mod intensity
  • antipyretic: little effects on normal Tb
  • anti-inflammatory: inflammatory joint conditions

Other uses: prevention of ischemic attacks, unstable angina, thrombotic conditions

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16
Q

Aspirin:

adverse effects

A
  • GI upset; (intolerance) –> upper GI bleeding from erosive gastritis
  • Salicylism –> vomiting, tinnitus, dec. hearing, vertigo
  • Inc. serum uric acid levels
  • Inhibition of platelet function –> blocks (noncompetitively) COX-1 platelets –> change conformation and inactivate platelet (7-11 days) –> won’t function in coagulation response (bad for pt with bleeding disorder)
  • Renal BF alterations
  • Reye’s syndrome –> causes brain and liver damage
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17
Q

how common are the side effects of Aspirin?

A

very common!

  • Dyspepsia: 15-40%
  • Duodenal ulcers: 5-8%
  • Gastric ulcers: 15-20%
  • GI bleed: more rare, 1-2%

For every $1 spent on NSAIDs –> $0.66 spent on side effects

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18
Q

Can we prevent NSAID- induced adverse events?

A

Yes! There are some drugs that prevent these:

  1. **Proton pump inhibitor:
    • reduces chances of damaging gastric mucosa
    • cheapest and most effective
    • e.g. omeprazole, prilosec, nexium –> dec. liklihood of damaging mucosa
  2. Misoprostol: prostoglandin E1 analogue –> protects gastric mucosa from chemical irritation
    • PG is important for protection of the GI tract
    • replaces the PG that you’re blocking w/ the NSAID
    • but can cause diarrhea/ due to contraction of smooth muscles
  3. Cox-2 inhibitor
    • allows COX 1 to function
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19
Q

these are in which family of drugs?

  • diclofenac
  • flurbiprofen
  • ibuprofen
  • indomethacin
  • ketoralac
  • naproxen
  • piroxicam
A

NSAIDs

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20
Q

diclofenac:

characteristics, use

A
  • developed as a “super-aspirin” to be gentler on the stomach;
  • formulations:
    • diclofenac alone
    • diclofenac + PG analogue
  • Tx: dysmenorrhea and gout
  • Type of NSAID
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21
Q

flurbiprofen:

characteristics, tx for what

A
  • developed as ocular eye drop
  • pre-analgesic prior to eye surgery; or after to tx pain
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22
Q

Ibuprofen:

characteristics, fxn

A
  • **gold standard NSAID; works as antipyretic, anti-inflammatory, analgesic
    • thought to be safer than aspirin
  • ibuprofen is a COMPETITIVE inhibitor, so it doesn’t have the same effect on bleeding or platelets
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23
Q

Indomethacin:

characteristics, fxn, tx

A
  • works as antipyretic, anti-inflammatory, analgesic
    • 5-7 hour half-life
  • fxn: works as antipyretic, anti-inflammatory, analgesic
  • tx: HA, migraine, gout (more so than diclofenac)
  • (NSAID)
24
Q

Ketorolac:

characteristics, fxn, tx

A
  • only NSAID that is indicated for moderate to severe pain (all others are mild-moderate pain)
  • more potent –> more side effects
  • Administration –
    • developed as an injectible; used for parenteral use
    • IV drug or intramuscular injection
  • •ONLY INDICATED FOR ACUTE SETTING (up to 5 days)
25
Q

naproxen:

characteristics, fxn

A
  • available OTC; half-life is longer like 13 hours (BID) whereas ibuprofen is 4-6 hour half life
  • patients respond differently to the drugs
  • looks like Ibuprofen (but half-life is different)
26
Q

Piroxicam:

characteristics

A
  • drug has half-life of 45-55 hours; so it would last longer in the patients’ system
  • higher adverse event rate --> so blood levels are higher –> higher incidence of side effects, esp GI
  • NSAID
27
Q

NSAIDs in general:

mechanism and duration

A
  • Acts as reversible, competitive inhibitors of COX activity (in contrast to aspirin)
  • Duration of action is primarily related to the pharmacokinetic clearance of the drug from the body
28
Q

what are the COX types, and what are the key differences?

A
29
Q

which type of COX inhibitors do we want to block during acute injury?

A

Want to block COX-2, NOT COX-1

(because COX-2 is thought to be the one that produces the prostanoid mediators of inflammation)

30
Q

COX-2 inhibitors target what, and prevent which symptoms?

A
  • targets: COX-2, an inducible enzyme
  • Prevents conversion of Arachidonic acid –>
    • preventing pain and inflammation response
31
Q

when considering the COX-2 inhibitors, how does the affinity for COX-1 and COX-2 relate?

A
  • Diclofenac, for example – high affinity for COX-2 and low affinity for COX-1 (desirable)
  • Ibuprofen and Naproxen have comparatively high affinity for COX-1 –> can cause GI ulceration at a higher rate
32
Q

COX-2 inhibitors:

key characteristics

A
  • Efficacy is EQUAL to that of NSAIDs
  • Rapid onset (<30min)
  • Adverse events: variable
  • Mechanism: COX-1 and COX-2 selectivity
33
Q

Celecoxib:

family, characteristics, tx

A
  • COX-2 inhibitor
  • No known higher rates of adverse CV events
  • Tx: used in patients that you want to avoid GI side effects
34
Q

Acetominophen:

family, characteristics, tx, hx

A
  • COX-2 inhibitor
  • **ONE OF THE MOST IMPORTANT DRUGS for tx when anti-inflammatory is NOT needed
  • Tx for mild-mod pain w/o anti-inflammatory effect
  • Hx:
    • active metabolite of phenacetin (prodrug, but no longer used due to toxicities)
35
Q

Acetaminophen:

pharmacoKINETICS (adme)

A
  • A - rapidly & completely absorbed
  • D - most body fluids (uniformly distributed)
  • M - by hepatic microsomal enzymes
  • E - 90-100% excreted
36
Q

What is the major difference b/w Acetaminophen and NSAIDs?

A

Their METABOLISM!

  • Acetaminophen uses hepatic microsomal enzymes
  • NSAIDs uses cytochrome p450
37
Q

Acetaminophen:

pharmacoDYNAMICs

A
  • a weak inhibitor of COX activity
  • antipyretic effects of CNS-mediated COX inhibition?
  • UKNOWN MECHANISMS OF ACTION
38
Q

Acetaminophen:

therapeutic use, and adverse effects

A
  • Therapeutic use: for pts whome aspirin is contraindicated
    • bc there’s no effect on peptic ulcers
    • no platelet-inhibiting properties
    • can be used in pregnancy
  • Adverse effects:
    • Skin rash/ allergic rxn
    • Hepatic necrosis due ot overdose
      • minor metabolite –> can cause oxidative stress injury to hepatocytes
      • therefore, contraindicated in patients w/ compromised liver fxn
39
Q

Why would a patient use Acetaminophen over Aspirin?

A
  • If pregnant
  • If has GI issues like peptic ulcer
  • or Bleeding concern (bc there’s no platelet inhibiting properties)
40
Q

Tx for Acetaminophen overdose?

A
  • Needs vigorous supportive therapy
    • Gastric lavage –> to flush out of bloodstream
    • Administer N-acetylcysteine –> replenish hepatic stores of glutathione
      • Protects against further liver damage by mopping up electrophiles
41
Q

What are DMARDs and SAARDs?

A
  • DMARD: disease-modifying anti-rheumatic drug
  • SAARD: slow-acting anti-rheumatic drug
42
Q

Methotrexate:

family, fxn, structure, adverse effects

A
  • immunosuppressive
  • potent immunosuppressive drug at anti-cancer doses; works non-specifically
  • structure:
    • related to folic acid
    • dihydrofolase reductase inhibitor
  • adverse effects: (opportunistic infections)
    • N/V/rash urticaria
    • Renal damage, dec hepatic function
43
Q

Leflunomide (Arava):

family, fxn, adverse effects

A
  • immunosppressive
  • pyrimidine synthesis inhibitor; used as a 3rd line therapy as non-specific immunosuppresive drug
  • AE:
    • liver damage
    • lung dissease
    • immunosuppression
44
Q

Sulfasalazine (Azulfidine):

family, fxn, adverse effects

A
  • immunosuppressive
  • Second-line therapy for non-specific immune modulator drugs; metabolized by bacteria in the colon (into sulfapyridine and mesalazine)
  • AEs: hemolytic anemia, orange skin, and urine
45
Q

List the Anti-TNFalpha drugs;

what’s a short-cut for identifying them based on their name?

A
  • Most end in -mab (monoclonal antibody)
    • Etanercept (Enbrel)
  • Anti-Tumor Necrosis Factor Alpha –> Blocks cytokine (TNF-alpha) to prevent inflammation
46
Q

other agents for RA;

A
  • binds to diff’t immune cells; antibody (soluble receptor)
  • drugs
    • Tocilizumab (Actemra) - anti-IL-6
    • Abatacept (Orencia) - T cell co-stim modulator
    • Rituximab (Rituxan) - anti-CD20
    • Tofacitinib (Xeljanz) - JAK inhibitor
47
Q

TNFalpha mechanism:

A
  • can bind to surface receptors –> causing damage to joints
  • So the soluble TNF receptor “mops up the TNF”, preventing inflammation
48
Q

Etanercept (Embrel):

  • define/structure,
  • pharmacoKINETICS (A,D),
  • pharmacodynamics
A
  • A recombinant fusion protein that consists of 2 soluble TNF p75 receptor moieties linked to the Fc portion of human IgG1
    • Binds two TNF-alpha molecules
  • PK
    • A - slowly absorbed after subQ injection
    • D - serum peak conc in 72 hrs
  • PD
    • captures and inactivates some TNF molecules –> prevent triggering inflammation
49
Q

Etanercept (Embrel):

adverse effects

A
  • injection site rxns & headache
  • etanercept dosing should be discontinued in pts w/ serious infxn
  • possible reports of CNS disorders such as MS, seizures, inflammation of nerves of eyes
50
Q

Infliximab (Remicade):

structure/mech, admin, tx

A
  • struc: chimeric (25% mouse/75% human) monoclonal Antibody –> binds w/ high affinity and specificity to human TNF-a
  • admin by IV dosing intervals of 4-8 wks
  • Tx: for reducing signs/sxs of moderately to severely active rheumatoid arthritis in pt’s who have had an inadequate reponse to methotrexate
    • used in combination w/ methotrexate
51
Q

Infliximab (Remicade):

adverse effects

A
  • sxs
    • upper respiratory infection
    • nausea, headaches, sinusitus, rash
      • incidences of this is the same as methotrexate
    • some opportunistic infections
  • a chimeric biologic therapy –> can lead to formation of human antichimeric antibodies in up to 50% of patients
    • concurrent therapy w/ methotrexate greatly reduces the prevalence of HACAs and in the basis for the recommendation of the combined administration
52
Q

what are the other agents to treat rheumatoid arthritis?

(in addition to methotrexate, infliximab)

A
  • These are 4th adn 5th line treatments for RA
    • gold salts
    • antimalarials
    • penicillamine
53
Q

Gold Salts:

tx, mech, types, adverse effects

A
  • tx for rheumatoid arthritis
  • mech: unknown mechanism; slows the progression of bone and articular destruction
  • types
    • aurothio-malate; and aurothio-glucose: parenterally admin; water-soluble gold salts
    • auranofin: orally administered, gold-thioglucose derivative
  • adverse effects:
    • GI disturbances (diarrhea)
    • dermatitis
    • hematological abnormalities, stomatitis (metal taste in mouth), peripheral neuropathy
54
Q

Antimalarials:

example, mech, tx

A
  • Ex: Hydroxychloroquine
  • Mech: mech of anti-inflammatory action is unclear; –> suppresses responsiveness of T-lymphocytes
    • inhibits DNA and RNA synthesis
    • Trap free radicals
  • Tx: used in tx of Rheumatoid Arthritis
55
Q

Penicillamine:

tx, structure, mech

A
  • Tx: reserved for patients w/ progressive, erosive rheumatoid arthritis not controlled by conservative therapy
  • Struc: metabolite of penicillin w/ some anti-infective properties
  • Mech: unclear, but may interfere w/ synthesis of DNA, collagen, and mucopolysaccharides

Y1 - Pharm (12 decks)

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