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PLE_PHARMA > NSAIDS/DMARDS/GOUT > Flashcards

NSAIDS/DMARDS/GOUT Flashcards

1
Q

MOA PARACETAMOL

A

Selectively inhibits COX-3. Weak COX-1 and COX-2
inhibitor. Inhibits prostaglandin synthesis

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2
Q

Preferred antipyretic in children

A

Paracetamol

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3
Q

Mechanism of Paracetamol Overdose

A

Oxidation to a cytotoxic intermediate called N-acetyl-p-benzoquinoneimine
(NAPQI) by phase I CYP450 enzymes (CYP2E1)

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4
Q

Antidote of Paracetamol toxicity?

A

antidote is N-acetylcysteine (NAC), a sulfhydryl donor necessary
for detoxification of paracetamol.

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5
Q

Development of Paracetamol Overdose 24-48 hrs, what manifestation?

A

Hepatic injury

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6
Q

Development of Paracetamol Overdose 3-5 days, what manifestation?

A

Extremely high liver enzymes (>10,000 IU/L)

Maximal abnormalities and hepatic failure
Jaundice, hepatic encephalopathy, renal failure,
myocardial injury

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7
Q

MOA ASPIRIN (Acetylsalicylic acid, ASA), Salsalate,
Sodium salicylate, Choline salicylate, Magnesium salicylate

A

Nonselective, IRREVERSIBLE COX 1&2 inhibitor.
Reduces platelet production of thromboxane A2, a
potent stimulator of platelet aggregation.

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8
Q

Associated with Reye’s syndrome in children

Prevents uric acid excretion (don’t use in gout)

A

SALICYLATES

ASPIRIN (Acetylsalicylic acid, ASA), Salsalate,
Sodium salicylate, Choline salicylate, Magnesium salicylate

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9
Q

Dose range of aspirin
* low range (<300 mg/d)

for?

A

o effective in reducing platelet aggregation
o follows first-order elimination kinetics

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10
Q

Dose range of aspirin
* intermediate doses (300–2400 mg/d)

for?

A

o antipyretic and analgesic effects

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11
Q

Dose range of aspirin

  • high doses (2400–4000 mg/d)
    for?
A

o anti-inflammatory effects
o follows zero-order elimination kinetics

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12
Q

MOA?

IBUPROFEN, Diclofenac, Diflunisal, Etodolac, Fenoprofen,
Flurbiprofen, KETOPROFEN, Nabumetone, Naproxen,
Oxaprozin, PIROXICAM, Sulindac, Tolmetin, MEFENAMIC ACID,
Bromfenac, Meclofenamate, Suprofen, Aceclofenac

A

NON SELECTIVE NSAIDS

  • Reversible COX 1 and 2 Inhibition.
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13
Q

prevents NSAIDinduced
gastritis

A

MISOPROSTOL

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14
Q

NSAIDs (in general) may cause premature closure of

A

DUCTUS ARTERIOSUS

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15
Q

used to close PDA

A

Ibuprofen and Indomethacin

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16
Q

Post-surgical analgesic control (moderate to severe,
short-term), mainly used for analgesia not for antiinflammatory
effect

A

Ketorolac, Dexketoprofen

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17
Q

MOA?

CELECOXIB, Etoricoxib,
Rofecoxib, Valdecoxib, Parecoxib [X],

A

Selective COX-2 inhibitor.

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18
Q

which cox2 selective inhibitors are withdrawn from the
market due to increased incidence of thrombosis

A

Rofecoxib and Valdecoxib

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19
Q

Parecoxib is pregnancy category

A

Category X

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20
Q

MOA: Inhibits AICAR (5-Aminoimidazole-4-Carboxamide
Ribonucleotide) transformylase and thymidylate
synthetase, with secondary effects on
polymorphonuclear chemotaxis

A

METHOTREXATE

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21
Q

DMARD of first choice to treat rheumatoid arthritis

A

Methotrexate

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22
Q

MOA? Forms phosphoramide mustard, which cross-links
DNA to prevent cell replication. Suppresses T-cell and Bcell
function

A

Cyclophosphamide [D]

23
Q

RESCUE AGENT FOR CYCLOPHOSPHAMIDE?

A

MESNA

24
Q

MOA: Forms 6-Thioguanine, suppressing inosinic acid
synthesis, B-cell and T-cell function, immunoglobulin
production, and interleukin-2 secretion

A

AZATHIOPRINE

25
Q

MOA: Suppression of T-lymphocyte responses to mitogens,
decreased leukocyte chemotaxis, Stabilization of
lysosomal enzymes, Inhibition of DNA and RNA
synthesis, Trapping of free radicals

A

CINCHONA ALKALOIDS: CHLOROQUINE, HYDROXYCHLOROQUINE

26
Q

Cinchonism: Headache Tinnitus, Vertigo , irreversible
retinal damage, Dyspepsia, Nausea, Vomiting,
Abdominal pain, Rashes, Nightmares

side effects of?

A

CINCHONA ALKALOIDS: CHLOROQUINE, HYDROXYCHLOROQUINE

27
Q

MOA?
Mabs: bind and neutralize TNF-a
Etanercept: a ‘decoy receptor’ that forms a complex with
TNF-a and promotes its phagocytosis

A

INFLIXIMAB, ADALIMUMAB, ETANERCEPT,
CERTOLIZUMAB, GOLIMUMAB

28
Q

MOA: Binds to cyclophilin to act as a calcineurin inhibitor.
Inhibits interleukin-1 and interleukin-2 receptor
transcription thereby blocking T-cell activation

A

Cyclosporine

29
Q

Most important and limiting side effect of Cyclophosphorine?

A

Nephrotoxicity (most important and limiting SE)
Gingival hyperplasia and hirsutism

30
Q

MOA: Active product (mycophenolic acid) inhibits inosine
monophosphate dehydrogenase (important enzyme in
the guanine nucleotide synthesis) and inhibits T-cell
lymphocyte proliferation

A

Mycophenolate Mofetil

31
Q

Least Toxic for SLE nephritis

A

Mycophenolate Mofetil [D]

32
Q

Associated with invasive CMV infection

A

Mycophenolate Mofetil [D]

33
Q

MOA: * Inhibits the activation of T Cells by binding to CD80 and
CD86 on the APC
* CTLA-4-IgFc fusion protein

A

ABATACEPT

34
Q

MOA: Its active metabolite inhibits Dihydroorotate
dehydrogenase → decreased synthesis of
ribonucleotide and arrest of stimulated cells in the G1
phase of cell growth. Inhibits T cell proliferation and
production of autoantibodies by B cells.

A

LEFLUNOMIDE [X]

35
Q

MOA: Binds to CD20 antigen on the surface of B lymphocytes
→ reduced inflammation by decreasing the presentation
of antigens to T lymphocytes and inhibits secretion of
cytokines

A

RITUXIMAB

36
Q

MOA : Binds to IL-6 → decreased T cell activation and
inflammatory process

A

Tocilizumab (To6lizumab)

37
Q

A monoclonal antibody against IL-17; used for
psoriasis and ankylosing spondylitis

A

SECUKINUMAB

38
Q

A monoclonal antibody against IL-2; used to
prevent rejection during organ transplantation

A

BASILIXIMAB

39
Q

A monoclonal antibody against IL-12 and IL-
23; used for Crohn’s disease and psoriasis
(Paskuhan sa UST on 12/23)

A

USTEKINUMAB

40
Q

The management of gout has 3 strategies:

A
  1. reducing inflammation during acute attacks
  2. accelerating renal excretion of uric acid with uricosuric drugs
  3. reducing the conversion of purines to uric acid by xanthine
    oxidase
41
Q

is commonly used in the initial treatment of
gout as the replacement for colchicine

A

INDOMETHACIN

42
Q

Aspirin is not used in GOUT due to

A

Aspirin is not used due to its renal retention of uric acid at low
doses

43
Q

MOA Inhibits microtubule assembly and LTB4 production
leading to decreased macrophage migration and
phagocytosis

A

COLCHICINE

44
Q

adverse effect which signals toxicity from
colchicine
* Not to be given to patients with eGFR of <30

A

DIARRHEA

45
Q

MOA: A urate oxidase that catalyzes oxidation of uric acid into
allantoin (more soluble and inactive metabolite)

A

PEGLOTICASE, RASBURICASE

46
Q

MOA: Compete with uric acid for reabsorption in the proximal
tubules via the URAT1 transporter. Increase uric acid
excretion.

A

PROBENECID, Lesinurad

47
Q

A required minimum 30 ml/min GFR is important before
starting what drug?

A

Probenecid

48
Q

MOA: Active metabolite
(alloxanthine) that
irreversibly inhibits
Xanthine Oxidase and
lowers production of uric
acid

A

ALLOPURINOL

49
Q

MOA: Nonpurine reversible that is
an inhibitor of xanthine
oxidase (more selective than
allopurinol). Lowers
production of uric acid.

A

FEBUXOSTAT

50
Q

1st line treatment for chronic
gout, Tumor lysis syndrome

A

ALLOPURINOL

51
Q

USED FOR Chronic gout, Tumor lysis
syndrome, Allopurinol
intolerance

A

FEBUXOSTAT

52
Q

Inhibits metabolism of
mercaptopurine and
azathioprine
* Withheld for 1–2 weeks
after an acute episode of
gouty arthritis

A

ALLOPURINOL

(coadministered
with
colchicine or
indomethacin to avoid an
acute attack)

53
Q

Withheld for 1–2 weeks
after an acute episode of
gouty arthritis

A

FEBUXOSTAT

(coadministered
with
colchicine or
indomethacin to avoid an
acute attack)
* Febuxostat is more
effective than
Allopurinol

PLE_PHARMA (16 decks)

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