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NSAIDs and Related Drugs Flashcards

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1
Q

What is the mechanism of action of aspirin?

A

Acetylation of cyclooxygenase.

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2
Q

What is the ceiling dose for aspirin?

A

650mg

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3
Q

What is overdose of aspirin called and what are its effects?

A

Salicyism. Effects are tinnitus, decreased hearing, headache, and vertigo.

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4
Q

What is the therapy for overdose of aspirin?

A

Sodium bicarbonate infusion and gastric lavage.

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5
Q

What are the side effects of aspirin?

A

Irritates gastric mucosa; inhibits platelet aggregation; hypersensitive reactions.

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6
Q

What is a contraindication of aspirin?

A

Allergy; Hemophilia; Children with Influenza (Reye’s Syndrome)

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7
Q

Why does aspirin irritate gastric mucosa?

A

It inhibits PG synthesis and removes protective PGs.

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8
Q

How can aspirin reduce gastric intolerance?

A

By buffering to increase stomach pH.

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9
Q

What is the use of enteric coated aspirin (Ecotrin)?

A

Used in patients in whom buffering fails to control gastritis.

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10
Q

What are examples of non-acetylacted salicylates?

A

Methyl salicylate (Oil of Wintergreen); Diflunisal; Magnesium Choline Salicylate; Sodium Salicylate; Salicylsalicylate.

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11
Q

When are non-acetyl salicylates preferred?

A

When cyclooxygenase inhibition is undesirable. As in patients with asthma, bleeding tendencies, and renal dysfunction.

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12
Q

What is the preferred drug for patients allergic to aspirin?

A

Acetaminophen.

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13
Q

True or false: Acetaminophen is a strong prostaglandin inhibitor in peripheral tissues.

A

False. It is a WEAK PG inhibitor.

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14
Q

What is the mechanism of action of acetominophen?

A

Unknown!

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15
Q

What are the therapeutic actions of acetaminophen?

A

It is an analgesic and antipyretic.

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16
Q

Is acetaminophen an anti-inflammatory?

A

No. It also does not have anti platelet activity.

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17
Q

What is the ceiling dose of acetaminophen?

A

650 to 1000mg.

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18
Q

What can 6 grams of acetaminophen do to the liver?

A

Damage the liver due to formation of N-acetyl-p-benzoquinone metabolite.

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19
Q

What is the antidote to acetaminophen toxicity?

A

Gastric lavage and N-acetylcysteine.

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20
Q

What are the side effects of acetaminophen?

A

Increase in hepatic enzymes; skin rash/ allergic reaction.

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21
Q

Ingestion of 15g of acetaminophen will case what?

A

Can be fatal. Severe hepatoxicity with centrilobular necrosis; acute renal tubular necrosis.

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22
Q

Why are NSAIDs inflammatory?

A

The decrease concentration PG (PGE2, PGI2). PGs are vasodilators, thus their absence causes decreased edema.

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23
Q

Is the accumulation of inflammatory cells significantly reduced by NSAIDs?

A

No.

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24
Q

Why are NSAIDs analgesic?

A

Decreased PG results in less sensitization of nociceptive nerve endings to mediators, such as bradykinin and 5-HT.

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25
Why are NSAIDs antipyretic?
Centrally mediated; Partly the result of a decrease in PG response to cytokines (IL-1).
26
Why are NSAIDs anti platelet?
They induce reversible inhibition of thromboxane. Except for aspirin which is irreversible.
27
What are the side effects of NSAIDs?
GI ulceration and renal injury. GI ulceration possibly due to inhibition of CO.
28
Indomethacin (NSAID)
Used in gout. More toxic than aspirin.
29
Ibuprofen (NSAID)
Fewer side effects than aspirin.
30
Naproxen (NSAID)
Half life of 13 hours.
31
Piroxicam (NSAID)
Long acting; half life of 45 hours.
32
Diclofenac (NSAID)
Well tolerated; enteric coated.
33
Flurbiprofen (NSAID)
Ocular use.
34
Ketorolac (NSAID)
Not used in most cases. Reserved for patients, postoperatively, who cannot take opioids.
35
Which 2 NSAIDs are used in acute attacks of flare-ups?
Sulindac and Phenylbutaxone.
36
Sulindac
500x more potent than indomethacin. It is a prodrug sulfoxide. Enterohepatic cycling occur.
37
Phenylbutoxone
For RA. Side effects include agranulocytosis and aplastic anemia.
38
What are the two COX-2 inhibitors?
Celecoxib and Rofecoxib.
39
Celecoxib
Highly selective COX-2 inhibitor; Treatment of RA
40
True or false: Celecoxib has been shown to cause fewer endoscopic ulcers than most other NSAIDs.
True.
41
What are the effects of Celecoxib on platelet aggregation?
None.
42
Rofecoxib
Potent, highly selective COX-2 inhibitor.
43
What is Rofecoxib approved for?
Osteoarthritis and RA; Acute pain in adults; treatment of primary dysmenorrhea
44
What are the effects of Rofecoxib on platelet aggregation?
None
45
What are the effects of Rofecoxib on gastric mucosal prostaglandins?
Appears to have little affect on gastric mucosal prostaglandins.
46
What are DMARDs?
Disease Modifying Antirheumatic Drugs. Can alter the course of rheumatic disorders.
47
Aurothiomalate
A gold salt used in chrysotherapy; possibly suppresses the immune system; used for active RA.
48
How is aurothiomalate administered?
IM as a water soluble gold salt (50% gold).
49
Auranofin
A gold salt used in chrysotherapy; possibly suppresses the immune system; used for active RA.
50
How is auranofin administered?
As a substituted gold thioglucose derivative (29% gold). Administered P.O.
51
What are the contraindication of gold salts?
History of previous toxicity to gold, pregnancy, impaired living or renal function, blood dyscrasias.
52
What is hydroxychloroquine?
An antimalarial.
53
When should hydroxychloroquine be used and how long does it take to get maximal effects?
Used when other measures have failed. More popular than Chloroquine. Takes several weeks of treatment for maximal effects.
54
What are antimalarials usually taken alongside with?
NSAIDs
55
What is a major toxicity of Hydroxychloroquine?
Ocular toxicity. Deposition of the drug in the cornea causing blurring of vision. Can be irreversible.
56
In what case can Hydroxychloroquine make the rheumatoid state worse?
In the presence of psoriasis. Can cause Psoriatic Rheumatoid Syndrome and exacerbate the psoriasis.
57
What is used in the treatment of heave metal poisoning?
Penicillamine
58
What are the toxic effects of penicillamine?
Skin changes (mild); decrease in B6 after prolonged use; bone marrow depression; proteinuria; autoimmune syndromes.
59
How long must Penicillamine be used to obtain maximum effect?
14-16 weeks.
60
Which patients should penicillamine be reserved for?
Those not responding to gold.
61
What is the use of glucocorticoids?
Short term use to inhibit COX-2 induction? It is a relatively non-specific inhibitor of protein synthesis.
62
Methotrexate, Azathioprine, and cyclophosphamide are what kind of drugs?
Immunosuppressives.
63
How does methotrexate work?
It is an inhibitor of dehydrofolate reductase. It is a potent immunosuppressive drug.
64
What is the maximum weekly dose of methotrexate?
7.5 mg
65
What percentage of patients exhibitor hepatotoxicity from taking methotrexate?
40%
66
What is the use for azathioprine?
Used in renal transplants; some cases of RA; as a chemotherapeutic agent. Results in severe myelosuppression and GI intolerance. Acts to inhibit DNA synthesis.
67
Does allopurinol enhance or decrease the effects of azathioprine, and why?
Enhance, because azathioprine is metabolized by xanthine oxidase.
68
What type of agent is Cyclophosphamide?
An alkylating agent.
69
What is the use for Cyclophosphamide?
It destroys proliferating lymphoid cells. Used in severe, unresponsive RA.
70
What percentage of patients exhibit side effects from Cyclophosphamide, and what are they?
90%. GI and bone marrow toxicity.
71
What kind of drugs are Infliximab and Etanercept?
Anti-TNF alpha.
72
How does Infliximab work?
It is an antibody that binds with high affinity and specificity to human TNF alpha.
73
Infliximab has been approved for use only in conjunction with another drug. Which one?
Methotrexate.
74
What are the side effects of Infliximab?
Upper respiratory tract infection; Nausea, headaches, sinusitis, rash, cough.
75
How does Etanercept work?
It is a protein that binds to two TNF alpha molecules.
76
Can Etanercept be used alone/
Yes. It is the first TNF inhibitor that can be used alone.
77
What are the side effects of Etanercept?
Erythema, local pain, swelling, itching at the site of injection.

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