Anti Inflammatory Drugs Flashcards

1
Q

What is the action of acetomenophen?

A

(Tylenol)

Reversibly inhibits Cox in the CNS- analgesic and anti-pyretic (inactive peripherally- not anti-inflammatory)

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2
Q

What is the clinical use of acetomenophen?

A

anti-pyretic, anagesic
NOT anti-inflammatory
Used instead of aspirin for children with viral infection bc of Reyes syndrome

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3
Q

What are the toxicities of acetomenophen?

A

hepatic necrosis (NAPQ1 metabolite depleates glutathione and forms toxic metabolites in the liver; treat with N-acetyl cysteine)

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4
Q

What is the method of action of aspirin?

A

Irreversibly inhibits COX1/2 via acetylation

Decrease synthesis of TxA2 to increase bleeding time

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5
Q

What is the clinical uses of aspirin?

A
Low dose (300 mg/day): anti-platelet
Medium dose (300-2400 mg/day): analgesic, anti-pyretic
High dose (2400-4000 mg/day): anti-inflamatory
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6
Q

Toxicity of aspirin?

A

Gastric ulceration
Tinnitis
Chronic use –> acute renal failure, interstilial nephritis, GI bleeding
Reyes in kids
Respiratory alkalosis early followed by a metabolic acidosis for a mixed picture
Can treat with alkalization

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7
Q

What is the mechanism of action of celecoxib?

A

reversible inhibition of COX2
Inflammatory cells and vasc endothelium to mediate inflammation and pain
(sparring of COX1 spares gastric mucosa and TxA2 function in platelets)

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8
Q

When is celecoxib used?

A

osteoarthritis, rheumatoid arthritis

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9
Q

What is the toxicity of celecoxib?

A

increased risk of thrombosis

sulfa allergy

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10
Q

What is the mechanism of action for NSAIDS?

A

ibuprofen, naproxen, indomethicin

Reversible COX1/2 inhibition

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11
Q

What are the clinical uses of NSAIDS?

A

anti-pyretic, anagesic, anti-inflammatory

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12
Q

What are toxicities of NSAIDS?

A

Interstitial nephritis, gastric ulcers (prostaglandins protect gastric mucosa/COX1), and renal ischemia (prostaglandins dilate afferent arteriole)

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13
Q

What are the mechanisms of bisphosphonates?

A

pyrophasphate analogs, bind to hydroxyappetite in bones and inhibit osteoclast action

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14
Q

When are bisphosphonates used?

A

Osteoporosis, hypercalcemia, Pagets disease of the bone

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15
Q

What are toxicities of bisphosphonates?

A
Corrosive esophagitis (take with water and stay upright for 30 mins)
osteonecrosis of the jaw
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16
Q

What is the mechanism of action of teriparatide

A

recombinant PTH
increase osteoblast activity
given subcutaenously

17
Q

When is teriparatide used?

A

osteoporosis

Can increase bone growth as opposed to anti-absorptive therapies like bisphophanates

18
Q

What is the toxicity of teriparatide?

A

transient hyerpcalcemia

May increase risk of osteosarcoma

19
Q

What is a toxicity of TNF-a inhibitors?

A

reactivation of infection, esp TB

TNF-a is important for granuloma formation and stabilization

20
Q

What is the mechanisms of etanercept?

A

Fusion protein (receptor for Ig Fc + TNF-a) produced by recombinant DNA that acts as a decoy receptor for TNF-a

21
Q

When do you use etanercept?

A

Rhematoid arthritis, psoriasis, ankalosing spondylitis

22
Q

What is the mechanisms of action of infliximab or adalimumab?

A

Monoclonal antibody to TNF-a

23
Q

When would you use infliximab /adalimumab?

A

IBS, RA, psoriasis, ankalosing spondylitis