Anti-inflammatories Flashcards

1
Q

Four signs of inflammation

A

pain
redness
swelling
heat

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2
Q

Tissue injury causes the release of:

A

Prostaglandins

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3
Q

What do prostaglandins do?

A

cause sensitivity to pain by activating nerves, vasodilation (swelling), and redness

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4
Q

Arachidonic acid is converted to ______ by an enzyme called _________

A

prostaglandins

cyclooxygenase (COX-1 and COX-2)

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5
Q

Of the two COX drugs, we want our drugs to affect ____ but we do not want them to affect _____

A

COX-2 (inflammation)

do not want affect COX-1 (platelet function)

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6
Q

NSAIDs
what does it stand for?
another name for them?

A
Non-Steroidal Anti-inflammatory Drugs
cyclooxygenase inhibitors (binds directly to them)
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7
Q

NSAIDs have three properties:
Mechanism:
Indications:

A

analgesic
anti-inflammatory
antipyretic

Mechanism: reversibly binding to one of the COX enzymes

Indications: mild to moderate pain (esp chronic) and fever

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8
Q

Is acetylsalicylic acid a selective or non-selective NSAID?

A

non-selective
meaning it inhibits both COX-1 and COX-2
this poses a risk of harm

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9
Q

Acetylsalicylic acid (ASA)

Where and how:
analgesic
anti-inflammatory
antiplatelet (lasts for 8 days-why?)

A

“the standard” NSAID

Analgesia – local effect at the site of damage

Anti-inflammatory - binds to and irreversibly inhibits COX

Antiplatelet – thins the blood, prevents clotting by irreversibly inhibiting COX-1. Can be very good for preventing formation of thrombus.
8 days because that’s the lifespan of platelets. In 8 days, your body makes more platelets

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10
Q

Daily prophylactic dose of ASA for MI, stroke?

A

80 - 160 mg
Low dose compared to the dose required to achieve anti-inflammatory effect

(Prostaglandins cause platelets to become sticky and form clots, but ASA stops the action of COX and prevents the formation of prostaglandins, which means that platelets are made less often and that they are not as sticky )

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11
Q
ASA 
Contraindications:
Adverse effects:
Salicylate toxicity:
Interactions (3):
A

irreversible inhibition of COX

Contraindications: pregnancy, bleeding disorders, upcoming operation, renal dysfunction, any children under 12

Adverse effects: GI bleeding and ulcers (because prostaglandins protect the GI tract)
Reye’s syndrome - swelling in the liver and brain in children who had influenza or chickenpox

Salicylate toxicity: tinnitus, hearing loss, hyperventilation in children (CNS stimulation)

Interactions: anticoagulants (increased bleeding), glucocorticoids (ulcers), and other NSAIDs like ibuprofen (they decrease the antiplatelet activity of ASA - use acetaminophen instead)

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12
Q

NSAIDs
Adverse effects:
Contraindications:

A

fewer GI, renal, hemorrhagic effects than ASA

reversible inhibition of COX
- but no antiplatelet activity so do not protect against MI or stroke

Adverse effects: Renal /kidney problems - causes reductions in creatinine clearance
(measuring creatinine is a way to measure the kidneys’ ability to function normally)
- GI bleeding and ulceration (leads to black, tarry stool)

Contraindications: conditions with bleeding as a risk (vitamin K deficiency and peptic ulcer disease), severe renal or hepatic disease, any children under 12

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13
Q

Selective COX-2 Inhibitors
Name one:
Risk:

A

celecoxib (sulfa drug allergies)

increased risk of MI and stroke
can also cause hypertension and edema

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14
Q

What is used in combination with NSAIDs to reduce GI ulceration?

A

misoprostol, a synthetic prostaglandin

The cause of GI ulceration is reduced prostaglandin production (since PGs protect the stomach)

Don’t get it confused with metaprolol!

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15
Q

How are NSAIDs antipyretic?

A

They inhibit prostaglandin E2 production within the area of the brain that controls temperature (hypothalamus)

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16
Q

Enteric-coated tablets - crushed or no?

A

DO NOT CRUSH

crushing them may contribute to ulceration development