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Pharmacology > NSAIDs, Acetaminophen, DMARDS and Drugs Used in Gout > Flashcards

NSAIDs, Acetaminophen, DMARDS and Drugs Used in Gout Flashcards

1
Q

Acetylation of COX-1 and COX-2 results in decreased prostaglandin synthesis

Nonselective IRREVERSIBLE COX1 and COX 2

USES:
prevention of arterial thrombosis (MI, TIA, CVD)

A

SALICYLATE

Aspirin

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2
Q

The ONLY IRREVERSIBLE INHIBITOR of COX

A

Aspirin

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3
Q

Non-Selective COX Inhibitors

A 
Aspirin
Ibuprofen
Ketoprofen
Furbiprofen
Naproxen
Nabumetone
Etodolac
Ketorolac
Piroxicam
Indomethacin
Sulindac
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4
Q

Side effects of Non-Selective COX Inhibitors

A

GI bleeding

nephrotoxicity

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5
Q

Propionic Acid Derivatives

A

Ibuprofen - less gastric irritation; NOT given w/ aspirin
Ketoprofen
Flurbiprofen - longest duration

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6
Q

Side effects of Flurbiprofen

A

severe gastric irritation

MI

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7
Q

Only NON-ACID derived Non-Selective COX Inhibitors

A

Nabumetone

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8
Q

Used as analgesia for post operational therapy

A

Etodolac

Ketorolac

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9
Q

Non-Selective COX Inhibitor that is related to Sulfonamides

A

Sulindac

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10
Q

Non-Selective COX Inhibitors that also (-) phospholipase A2

for closure of PDA

A

Indomethacin

Paracetamol IV - alternative

physiologic closure of DU - 14-15 hrs
anatomic closure of DU - 2-3 weeks

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11
Q

COX II Selective Inhibitors

A

Celecoxib
Parecoxib
Etoricoxib

Lumiracoxib
Valdecoxib
Rofecoxib

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12
Q

Not used COX II Selective Inhibitors d.t. THROMBOSIS, MI and HPN

A

Lumiracoxib
Valdecoxib
Rofecoxib

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13
Q

Selective inhibits COX-3

A

Paracetamol (Acetaminophen)

Phenacetin

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14
Q

Antidote for paracetamol toxicity

A

N-acetylcysteine - sulfhydryl donor

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15
Q

MOA of Methotrexate

A

INHIBITS FOLATE SYNTHESIS BY

(-) AICAR TRANSFORMYLASE
(-) THYMIDYLATE SYNTHETASE
(-) DIHYDROFOLATE REDUCTASE

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16
Q

Current DMARD of choice for the treatment of Rheumatoid Arthritis

A

Methotrexate

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17
Q

Side effects of Methotrexate

A

mucositis/mucosal ulcers

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18
Q

Rescue agent for Methotrexate

A

LEUCOVORIN (FOLINIC ACID)

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19
Q

Binds to TNF-a and prevents it from activating TNF-a receptor

A 
Infliximab
Adalimumab
Certolizumab
Golimumab
Etanercept
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20
Q

Side effects of TNF-a inhibitors

A

TB reactivation

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21
Q

MOA of Azathioprine

A

forms 6-THIOGUANINE –> suppresses INOSINIC ACID SYNTHESIS –> DNA synthesis

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22
Q

MOA of Chloroquine

A

suppression of T-lymphocyte responses to mitogens

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23
Q

Side effects of Chloroquine

A

ocular toxicity

prolonged QT interval

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24
Q

MOA of Cyclophosphamide

A

ALKYLATING AGENT

form PHOSPHORAMIDE MUSTARD –> cross links to prevent cell replication

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25
Q

Rescue agent for Cyclophosphamide

A

2-mercaptoethane sulfonate sodium (MESNA)

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26
Q

MOA of Cyclosporine

A

(-) IL-1 and IL-2 receptor production

targets CALCINEURIN

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27
Q

Side effects of Cyclosporine

A

hirsutism

gingival hyperplasia

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28
Q

MOA of Mycophenolate Mofetil

A

(-) cytosine monophosphate (CMP)

(-) T cell lymphocyte proliferation

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29
Q

Side effects of Mycophenolate Mofetil

A

aplastic anemia

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30
Q

MOA of Sulfasalazine

A

active metabolite (SULFAPYRIDINE) –> (-) release of inflammatory cytokines

31
Q

Side effects of Sulfasalazine

A

allergies

SJS

32
Q

MOA of Abatacept

A

(-) activation of T cells by binding to CD80 and CD86

33
Q

Side effects of Abatacept

A

increased risk of infections

URTI

34
Q

MOA of Leflunomide

A

active metabolites –> (-) DIHYDROOROTATE DEHYDROGENASE –> decreased synthesis of ribonucleotide and arrest of stimulated cells in the G1 phase of cell growth

35
Q

MOA of Rituximab

A

depletes B cells by cell mediated and complement dependent cytotoxicity and stimulation of cell apoptosis –> reduced inflammation by decreasing the presentation of antigens to T lymphocytes and (-) secretion of cytokine

36
Q

MOA of Tocilizumab

A

binds to IL-6 –> decreased T cell activation and inflammatory process

37
Q

(-) MICROTUBULE assembly and LTB4 production –> decrease macrophage migration

A

Colchicine

for ACUTE ATTACK of GOUT

38
Q

Side effects of Colchicine

A

diarrhea
GI disturbance
hepatotoxicity
nephrotoxicity

39
Q

The adverse which signals toxicity from colchicine

A

diarrhea

40
Q

active metabolite ALLOXANTHINE – irreversibly (-) XANTHINE OXIDASE

A

Allopurinol

for CHRONIC GOUT
tumor lysis syndrome

41
Q

NONPURINE reversible (-) of xanthine oxidase

A

Febuxostat

for CHRONIC GOUT
tumor lysis syndrome
allopurinol intolerance

42
Q

URICOSURIC AGENTS

A

Probenecid

Sulfapyrazone

43
Q

MOA of Uricosuric Agents

A

(-) reabsorption of uric acid in PCT

44
Q

Prolongs the action of PENICILLIN by (-) tubular secretion

A

Probenecid

45
Q

Novel urate lowering recombinant mammalian urate oxidase enzyme

A

Pegloticase

46
Q

IL-1 pathway (-)

A

Anakinra
Canakinumab
Rilonacept

47
Q

Among NSAIDs, aspirin is unique because it

(A) Irreversibly inhibits its target enzyme
(B) Prevents episodes of gouty arthritis with long-term use
(C) Reduces fever
(D) Increases the risk of colon cancer
(E) Selectively inhibits the COX-2 enzyme

A

(A) Irreversibly inhibits its target enzyme

48
Q

Which of the following is an analgesic and antipyretic drug that lacks an anti-inflammatory action?

(A) Acetaminophen
(B) Celecoxib
(C) Colchicine
(D) Indomethacin
(E) Probenecid
A

(A) Acetaminophen

49
Q

Clinical Presentation of ASPIRIN OVERDOSE

A 
HAGMA
dehydration
hyperthermia
collapse
coma
50
Q

A 16-year-old girl comes to the emergency department suffering from the effects of an aspirin overdose.

Which of the following syndromes is this patient most likely to exhibit as a result of this drug overdose?

(A) Bone marrow suppression and possibly aplastic anemia
(B) Fever, hepatic dysfunction, and encephalopathy
(C) Hyperthermia, metabolic acidosis, and coma
(D) Rapid, fulminant hepatic failure
(E) Rash, interstitial nephritis, and acute renal failure

A

(C) Hyperthermia, metabolic acidosis, and coma

51
Q

Which of the following drugs is most likely to increase serum concentrations of conventional doses of methotrexate, a weak acid that is primarily cleared in the urine?

(A) Acetaminophen
(B) Allopurinol
(C) Colchicine
(D) Hydroxychloroquine
(E) Probenecid
A

(E) Probenecid

52
Q

The main advantage of ketorolac over aspirin is that ketorolac

(A) Can be combined more safely with an opioid such as codeine
(B) Can be obtained as an over-the-counter agent
(C) Does not prolong the bleeding time
(D) Is available in a parenteral formulation that can be
injected intramuscularly or intravenously
(E) Is less likely to cause acute renal failure in patients with some preexisting degree of renal impairment

A

(D) Is available in a parenteral formulation that can be

injected intramuscularly or intravenously

53
Q

An 18-month-old boy dies from an accidental overdose of acetaminophen.

Which of the following is the most likely cause of this patient’s death?

(A) Arrhythmia
(B) Hemorrhagic stroke
(C) Liver failure
(D) Noncardiogenic pulmonary edema
(E) Ventilatory failure
A

(C) Liver failure

In overdose, acetaminophen causes fulminant liver failure as a result of its conversion by hepatic cytochrome P450 enzymes to a highly reactive metabolite

54
Q

A 52-year-old woman presented with intense
pain, warmth, and redness in the first toe on her left foot. Examination of fluid withdrawn from the inflamed joint revealed crystals of uric acid.

In the treatment of this woman’s acute attack of gout, a high dose of colchicine will reduce the pain and inflammation. However, many physicians prefer to treat acute gout with a corticosteroid or indomethacin because high doses of colchicine are likely to cause

(A) Behavioral changes that include psychosis
(B) High blood pressure
(C) Rash
(D) Severe diarrhea
(E) Sudden gastrointestinal bleeding
A

(D) Severe diarrhea

55
Q

Over the next 7 mo, the patient had 2 more attacks of acute gout. Her serum concentration of uric acid was elevated. The decision was made to put her on chronic drug therapy to try to prevent subsequent attacks.

Which of the following drugs could be used to decrease this woman’s rate of production of uric acid?

(A) Allopurinol
(B) Aspirin
(C) Colchicine
(D) Hydroxychloroquine
(E) Probenecid
A

(A) Allopurinol

Aspirin actually slows renal secretion of uric
acid and raises uric acid blood levels. It should not be used in gout

56
Q

A 54-year-old woman presented with signs
and symptoms consistent with an early stage of rheumatoid arthritis. The decision was made to initiate NSAID therapy.

Which of the following patient characteristics is the most compelling reason for avoiding celecoxib in the treatment of her arthritis?

(A) History of alcohol abuse
(B) History of gout
(C) History of myocardial infarction
(D) History of osteoporosis
(E) History of peptic ulcer disease
A

(C) History of myocardial infarction

Celecoxib is a COX-2-selective inhibitor. Although the
COX-2 inhibitors have the advantage over nonselective
NSAIDs of reduced gastrointestinal toxicity, clinical data
suggest that they are more likely to cause arterial thrombotic events. A history of myocardial infarction would be a compelling reason to avoid a COX-2 inhibitor

57
Q

Although the patient’s disease was adequately controlled with an NSAID and methotrexate for some time, her symptoms began to worsen and radiologic studies of her hands indicated progressive destruction in the joints of several fingers.

Treatment with another second-line agent for rheumatoid arthritis was considered.

Which of the following is a parenterally
administered DMARD whose mechanism of anti-inflammatory action is antagonism of tumor necrosis factor?

(A) Cyclosporine
(B) Etanercept
(C) Penicillamine
(D) Phenylbutazone
(E) Sulfasalazine
A

(B) Etanercept

58
Q

Common NSAIDs TOXICITIES

A 
GI Toxicity 
Nephrotoxicity
Hypersensitivity
Hematologic
Hepatic
Pulmonary
CNS
CVS
59
Q

NON-SELECTIVE NSAIDS

reversible COX 1 and 2 inhibition

USES:
analgesia
antipyretic
anti-inflammatory

A

ORAL

Ibuprofen
Diclofenac
Ketoprofen
Piroxicam
Mefenamic Acid
Sulindac
60
Q

NON-SELECTIVE NSAIDS

reversible COX 1 and 2 inhibition

USES:
post surgical analgesic control
for analgesia

A

INTRAVENOUS

Ketorolac
Dexketoprofen

61
Q

NON-SELECTIVE NSAIDS

reversible COX 1 and 2 inhibition

USES:
for PDA CLOSURE

A

Indomethacin (COX 1 > COX2)

62
Q

COX 2 SELECTIVE NSAIDS

Selective COX-2 Inhibitor

USES:
analgesia
antipyretic
anti-inflammatory

A 
Celecoxib
Etoricoxib
Rofecoxib
Valdecoxib
Parecoxib

SE:
MI
Stroke - Rofecoxib and Valdecoxib

63
Q

Selectively inhibits COX 3
Inhibits prostaglandin synthesis

USES:
analgesia (mild)
antipyretic

A

Paracetamol (Acetaminophen)

64
Q

DMARDS

Suppression of T lymphocyte responses to mitogens
Stabilization of lysosomal enzymes

USES:
RA
SLE
Sjogren syndrome
Malaria
A

ANTI-MALARIALS

Chloroquine
Hydroxychloroquine

SE:
CINCHONISM - headache, tinnitus, vertigo

65
Q

DMARDS

Binds to TNF-a and prevents it from activating TNF-a receptor

USES:
Crohn’s disease
RA

A

TNF-ALPHA INHIBITOR

Infliximab
Adalimumab
Etanercept
Certolizumab
Golimumab
66
Q

DMARDS

Forms 6- thioguanine – suppresses inosinic acid synthesis

A

Azathioprine

67
Q

DMARDS

Inhibits IL-1 and IL-2 receptor production

USES;
tissue transplantation

A

Cyclosporine

68
Q

DMARDS

Active product (mycophenolic acid) inhibits inosine monophosphate dehydrogenase and (-) T cell lymphocyte proliferation

A

Mycophenolate Mofetil

69
Q

DMARDS

Active metabolites (sulfapyridine) inhibits the release of inflammatory cytokines

A

Sulfasalazine

70
Q

DMARDS

Inhibits activation of T cells by binding to CD80 and CD86 on the APC

USES:
moderate - severe

A

Abetacept

71
Q

DMARDS

Its active metabolite (-) dihydroorotate dehydrogenase – decreased synthesis of ribonucleotide and arrest of stimulated cells in the G1 phase of cell growth

USES:
RA

A

Leflunomide

72
Q

DMARDS

CD20 Inhibitor

A

MONOCLONAL ANTIBODIES

Rituximab

73
Q

DMARDS

Binds to IL-6 – decreased T cell activation and inflammatory process

A

MONOCLONAL ANTIBODIES

Tocilizumab

SE:
TB
Fungal, Viral and other Opportunistic Infections

Pharmacology (72 decks)

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