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Pharma 2- Semmelweis > B-18. NSAIDs, except ASA. Non-opioid analgesics. Drugs for gout. > Flashcards

B-18. NSAIDs, except ASA. Non-opioid analgesics. Drugs for gout. Flashcards

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1
Q

Acetic Acid Derivative Drugs (2)? COX effect?

A
  1. ) Indomethacin - COX1 > COX2

2. ) Diclofenac, ketorolac - COX1 = COX2

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2
Q

Indomethacin MOA

A

COX1 > COX2; also inhibits PLA2 + inhibits neutrophil migration

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3
Q

Indomethacin side effects

A

Side Effects: severe, drug rarely used
o Highly ulcerogenic - used experimentally to induce ulcers
o Aplastic anemia + agranulocytosis - high risk
o Severe headache

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4
Q

Indomethacin indications

A

Indications: normal NSAID indications, plus…
o Hodgkin lymphoma - for decreasing refractory fever
o Patent DA - especially useful for this
o Severe RA pain
o Gout

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5
Q

Diclofenac + ketorolac
MOA?
Kinetics?

A

MOA: COX1 = COX2
Kinetics: short DOA, longer effect in joints (↑ conc. in synovium)

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6
Q

Diclofenac + ketorolac sIDE EFFECTS

A
  1. ) Cardiotoxicity
  2. ) ↑ fluid retention (caution in hypertension patients)
  3. ) Gastric bleeding (even w/ 1 dose)
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7
Q

Aryl Propionic Acid Derivative Drugs (4)

A
  1. ) Ibuprofen - COX1 > COX2
  2. ) Tiaprofenic acid
  3. ) Naproxen
  4. ) Flurbiprofen
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8
Q

Ibuprofen

● MOA:?
● Kinetics:?
● Indications:?
● Side effects:?

A

Ibuprofen

● MOA: COX1 > COX2
● Kinetics: 1-2 h DOA, accumulates in joints
● Indications: normal NSAID indications + patent DA treatment
● Side effects: aseptic meningitis

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9
Q

Naproxen
● MOA:?
● Kinetics:?
● Proven to be?

A

Naproxen
● MOA: inhibits neutrophil migration
● Kinetics: 14 hr DOA, 1x/day
● Proven to be NOT cardiotoxic

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10
Q

Flurbiprofen
● MOA:?
● Indications:?

A

Flurbiprofen
● MOA: inhibits TNFα as well (good for RA)
● Indications: as an ophthalmological pre-op anti-miotic (solution); arthritis, incl. RA, and dental pain (oral)

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11
Q

Tiaprofenic Acid
● Indications:?
● Side effects:?

A

Tiaprofenic Acid
● Indications: mainly arthritis
● Side effects: less cartilage / kidney damage than others, but high risk of severe cystitis w/ long-term use

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12
Q

Oxicams drugs (2)

A
  1. ) Piroxicam - COX1 > 2

2. ) Meloxicam - COX2 > 1

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13
Q 
Piroxicam
● MOA:?
Meloxicam
● MOA:?
● Side Effects:?
A

Piroxicam
● MOA: COX1 > COX2
Meloxicam
● MOA: COX2 > COX1 → anti-inflammatory effect before ulcerogenic effect
● Side Effects: higher risk of edema (stronger kidney effects)

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14
Q

Fenamates drugs (3)

A
  1. ) Meclofenamic acid
  2. ) Flufenamic acid
  3. ) Mefenamic acid
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15
Q

Mefenamic acid
● Indications:?
● Side Effects:?

Flufenamic and Meclofenamic acid
● Are they still in use? Side effect?

A

Mefenamic acid
● Indications: menstrual pain and perimenstrual migraine prophylaxis
● Side Effects: can cause SJS

Flufenamic and Meclofenamic acid
● less used, high rate of GI sfx (diarrhea)

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16
Q

Pyrazolone Derivatives Drugs (3)

A

Pyrazolone Derivatives

  1. ) Phenylbutazone
  2. ) Phenazone
  3. ) Nor-/aminophenazone
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17
Q

Phenylbutazone
Still in use?

● MOA:?
● Side Effects:?
● Indication:?

A

Phenylbutazone - strong anti-inflammatory, less anti-fever/pain effects; withdrawn in US

● MOA: also increases urate elimination (helpful in gout)
● Side Effects: severe; use longer than 1 wk is CI (is used longer in ankylosing spondylitis)
1.) Fluid retention
2.) Myelosuppression - dose-dependent/reversible and irreversible/idiosyncratic forms
● Indication: Thrombophlebitis - as a local cream

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18
Q

Phenazone and amino-/noraminophenazone

● Anti-inflammatory effect? Anti-fever/pain indications?
● Aminophenazone side effect?
● Noraminophenazone extra benefit?

A

Phenazone and amino-/noraminophenazone

● Anti-inflammatory effect is weak, better for anti-fever/pain indications
● Aminophenazone has higher marrow toxicity risk
● Noraminophenazone (aka Metamizol, trade name Algopyrin) is less ulcerogenic

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19
Q

Alkanone Derivative Drug?

Others Drug?

A

Alkanone Derivative is Nabumetone - COX2&raquo_space; 1

Other - Nimesulide - COX2&raquo_space; 1

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20
Q

Nabumetone
● MOA:?
● Kinetics:?
● Side Effects:?

A

Nabumetone
● MOA: prodrug w/ COX2&raquo_space; COX1 effect → anti-inflamm. w/out ulcerogenic effects (is also non-acidic)
● Kinetics: long DOA (24 hrs); 1x/day
● Side Effects: ↑ stroke / MI risk - similar to selective NSAIDs

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21
Q

Nimesulide
● MOA:?
● Side Effect:?

A

Nimesulide
● MOA: COX2&raquo_space; COX1 and PLA2 inhibition (strong anti-inflammatory, no ulcers)
● Side Effect: Hepatotoxicity

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22
Q

Selective NSAID drugs (4)

A

Selective NSAIDs - COX2 only

Celecoxib, parecoxib, valdecoxib (rofecoxib - withdrawn)

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23
Q

Selective NSAID differences

Study These Flashcards
A
  1. ) only inhibit COX2 → no platelet aggregation inhibition via COX-1 synth’d TXA
  2. ) Less ulcerogenic (COX1 makes gastroprotective PGs), but ↑ TXA2 / ↓ PGI2 → ↑ thromboembolism
  3. ) Can ↓ Alzheimer progression and have anti-cancer effects (COX2 ↑ is oncogenic)
24
Q

Which of the selective NSAIDs are in use?

Study These Flashcards
A

Celecoxib and parecoxib mostly in use; valdecoxib less so + rofecoxib withdrawn

25
Celecoxib and parecoxib indications
○ Arthritis - osteoarthritis, RA and juvenile RA ○ Ankylosing spondylitis ○ Pain - acute pain and menstrual pain (Has also been used to reduce polyps in FAP)
26
Celecoxib and parecoxib contraindications
○ Acute MI / unstable angina / prior MI - due to thromboembolic side effects ○ Sulfa allergy - celecoxib is a sulfa drug
27
Non-Opioid Analgesics
Paracetamol / Acetaminophen
28
Paracetamol / Acetaminophen effects?
● Was classified as an NSAID; now is known to NOT be anti-inflammatory; only painkiller / anti-fever effects ● Inhibits COX only in CNS (“COX3”, sketchy says some COX2 as well); not ulcerogenic ● May modulate the endogenous cannabinoid system + activate TRPV1 receptors → analgesic effects
29
Paracetamol / Acetaminophen indication
○ Pain / fever - mild-moderate pain, as in osteoarthritis
30
Paracetamol / Acetaminophen side effects? What is the formula side effect?
Hepatotoxic at high dose - Toxic metabolite NAPQI needs sulfhydryl groups of glutathione for inactivation - At >4 g dose, glutathione can not fully neutralize NAPQI; can give NAC to restore glutathione and/or oral activated charcoal within 4 hours of ingestion
31
What is gout?
● A metabolic disease with recurrent episodes of acute arthritis due to elevated serum uric acid → urate deposition in skin + joints → crystal precipitation and tophi formation ● Renal calculi and interstitial nephritis may also result from hyperuricemia
32
Uric acid is a byproduct of?
purine metabolism
33
How are nucleic acids and purines metabolized to form uric acid?
○ In the liver, nucleic acids are broken down into nucleotide monomers and individual purine nucleosides ○ Purine intermediate hypoxanthine is converted to xanthine by xanthine oxidase; xanthine oxidase further catalyzes conversion of xanthine to uric acid
34
Pathogenesis of uric acid
Can be due to overproduction or underexcretion (more common) of uric acid
35
Causes of uric acid production
○ Lifestyle - purine-rich foods such as seafood, organ meat, beer yeast ↑ urate levels ○ Genetics - variations in genes encoding for urate transport proteins in kidney ↑ gout risk ○ Other Diseases - metabolic syndrome, kidney failure, hemolytic anemia, obesity, enzyme deficiencies (such as the HGPRT deficiency in Lesch-Nyhan syndrome) ○ Medications - many drugs decrease urate excretion: ASA, ACE-Is, ARBs, BBs, ritonavir, pyrazinamide, thiazide diuretics, niacin, etc.
36
How is tophi formation cyclical?
↑ urate level in joints → precipitation of Na-Urate crystals → phagocytosis of crystals by synoviocytes → chemokines released + pH ↓ → neutrophils attracted to joint + further precipitation occurs
37
Gout drugs for acute attacks (3)
Gout drugs for acute attacks: a) NSAIDs - indomethacin b) Corticosteroids - prednisolone c) Tubulin inhibitor - colchicine
38
When can acute gout drugs be used?
● These drugs can also be used to treat calcium pyrophosphate dihydrate crystal deposition disease (“pseudogout”) ● Diff dx is performed by synovial fluid microscopy → gout = non-birefringent needle crystals; CPPD = birifringent, rhomboid crystals)
39
Acute gout NSAIDs MOA
NSAIDs - especially indomethacin; high dose ASA ↑ urate excretion but is not used due to sfx
40
Acute gout corticosteroid drug, dose, kinetics
Glucocorticoids - oral prednisolone (40 mg); can also be intra-articular or s.c.
41
Colchicine is? | MOA?
Colchicine - toxic plant alkaloid ● MOA: binds intracellular tubulin → inhibits polymerization to microtubules → inhibits neutrophil migration, phagocytosis + degranulation
42
Cochicine side effects?
● GI effects - diarrhea / nausea / vomiting due to tubulin disruption in enteric epithelial cells ● Liver/kidney damage - including hepatic necrosis and ARF ● Myelosuppression - via ↓ mitosis due to microtubule effects ● Peripheral neuritis
43
For chronic gout prophylaxis | drug classes?
a) XO inhibitors b) Uricases c) Uricosurics
44
For chronic gout Uricases
1. ) Rasburicase | 2. ) Pegloticase
45
For chronic gout Uricosurics
1. ) Probenecid | 2. ) Sulfinpyrazone
46
For chronic gout XO inhibitors
1. ) Allopurinol | 2. ) Febuxostat
47
Allopurinol ● MOA:? ● Kinetics:?
Allopurinol ● MOA: competitive xanthine oxidase inhibition via an active metabolite ● Kinetics: oral absorption, 1x/day
48
Allopurinol | ● Indications:?
Allopurinol ● Indications: 1.) Gout prophylaxis - taken life-long in patients with recurrent episodes 2.) Chemotherapy - as in tumor lysis syndrome (↑ K+, Pi, urate + BUN; ↓ Ca++) 3.) Lesch-Nyhan syndrome - X-linked defic. of HGPRT; children pick at skin / bite lips where urate deposits
49
Allopurinol | ● Side Effects:?
Allopurinol ● Side Effects: 1.) Hypersensitivity - most common side effect, “allopurinol rashes”; common cause of SJS 2.) DRESS syndrome - fever, general LAP, facial edema, morbilliform rash 3.) Rarely, myelosuppression
50
Allopurinol | ● Interaction:?
Allopurinol ● Interaction: If given with azathioprine + 6-mercaptopurine (purine analogs), allopurinol inhibits their metabolism via xanthine oxidase → ↑ toxicity of cytotoxic agents
51
Febuxostat ● MOA:? ●Side Effects:?
Febuxostat ● MOA: XO inhibitor ● Side Effects: Hepatic effects and nausea
52
Rasburicase and pegloticase ● MOA:? ● Indication:?
Rasburicase and pegloticase ● MOA: recombinant uric oxidase (uricase) → transforms urate to allantoin (more water-soluble) ● Indication: used if allopurinol causes HS rxn
53
Rasburicase and pegloticase | ● Side Effects:?
Rasburicase and pegloticase ● Side Effects: 1.) Hemolytic anemia - can precipitate anemia in G6PD deficiency patients 2.) Anaphylaxis - in ~10% pts → must be given in-patient i.v. by rheumatologist
54
Uricosurics are?
Uricosurics - urate excretion enhancers; 2nd line for underexcretion
55
Probenecid and Sulfinpyrazone | ● MOA:?
Probenecid and Sulfinpyrazone | ● MOA: competitively inhibits reabsorption of urate by OAT (organic anion transporter) in PCT
56
Probenecid and Sulfinpyrazone | ●Side Effects:?
Probenecid and Sulfinpyrazone ●Side Effects: 1.) Kidney stones - ↑ urate in urine; prevent with hydration and adequate urination 2.) Also inhibits penicillin elimination → ↑ toxicity 3.)Sulfa allergy - rare, but is a sulfa drug 4.) Can worsen / precipitate an acute attack; start drug 2-3 weeks after last attack

Pharma 2- Semmelweis (43 decks)

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