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anti inflammatory drugs Flashcards

1
Q

signs of inflammation

A

redness, swelling, heat, discomfort, pain

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2
Q

inflammation process

A

damage to part of body, chemical release, chemicals act on pain nerve endings and dilate blood vessels and work on immune cells
- chemicals start process of nociception and signs of inflammation (vasodilation, vascular permeability, pain, chemotaxis leading to swelling, redness)

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3
Q

chemicals released during inflammation process (tissue injury)

A
  • prostaglandins (NSAIDs inhibit)
  • bradykinin
  • histamine
  • leukotrienes
  • serotonin
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4
Q

prostaglandin production

A

damaged cells release arachidonic acid which can be metabolized into prostaglandins by COX1 and COX2 enzymes

COX 1 prostaglandins: GI tract, renal, platelet function, blood vessels
COX 2 prostaglandins: signs of inflammation (swelling, redness, pain)

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5
Q

NSAIDs

A

non steroidal anti inflammatory drugs
- aka: cyclooxygenase inhibitors

large and chemically diverse group of drugs which are analgesic, antipyretic, anti inflammatory

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6
Q

NSAID mechanism of action

A

inhibit COX enzymes so prostaglandins not made and response stopped
- competitive inhibitor

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7
Q

NSAID indications

A
  • mild to moderate pain relief
  • osteoarthritis, rheumatoid arthritis
  • acute gout
  • bone, joint, muscle pain
  • dysmenorrhea (period cramps)
  • fever
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8
Q

non selective NSAIDS

A

inhibit COX 1 and COX 2
- alleviate pain
- used for inflammatory disorders

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9
Q

non selective NSAID examples

A
  • acetylsalicylic acid (ASA - aspirin)
  • ketorolac (toradol)
  • sodium salicylate
  • ibuprofen (advil, motrin)
  • naproxen
  • diclofenac sodium (voltaren)
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10
Q

acetylsalicylic acid (ASA, aspirin)

A

standard NSAID against which all others are compared
- from natural source with added acetyl group (acetylation spiraea)
- local anti inflammatory effect
- local analgesic effect (makes peripheral nociceptors less receptive)
- antipyretic (inhibit prostaglandin E2 production within hypothalamus)
- antiplatelet

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11
Q

antiplatelet action of ASA

A
  • lasts around 8 days (until COX enzyme metabolizes)
  • the release of chemicals activate platelet stickiness (thromboxane a2 which is made by COX enzymes)
  • used for clotting problems and atherosclerosis (daily low dose aspirin)
  • irreversible drug action: leaves a peice of drug on COX enzyme so it is inhibited until metabolized
  • prevention of MI, stroke, and other thromboembolic events (reduce risk of heart attack)
  • prophylactic 60-80mg
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12
Q

ASA contraindications and cautions

A
  • pregnancy: in late trimesters connected with low birthweight, intracranial bleed, death
  • bleeding disorders: extensive bleeding
  • discontinue 1 week before operation: all affected platelets and enzymes can be removed
  • caution in renal dysfunction: people with kidney problems rely on prostaglandins for blood flow and kidnye function
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13
Q

NSAID adverse effects

A

GI:
- ulcers
- bleeding and pain
- perforation (hole) in stomach
happens from high dose, long term use because some type of prostaglandins protect GI (mucus, bicarbonate, blood flow)

renal:
- inhibit prostaglandin mediated renal function
- reduce creatinine clearance (possible obstruction)
- acute tubular necrosis

  • hypersensitivity reactions
  • bleeding problems (blockage of platelet aggregation)
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14
Q

ASA adverse effects

A

kids and teens with viral infections (chickenpox, flu) can lead to: Reye’s syndrome
- vomiting
- liver damage
- CNS problems (encephalopathy)
- can be fatal

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15
Q

salicylate toxicity

A

ASA, Na salicylate, Mg salicylate
- adults: tinnitus and hearing loss
- children: hyperventilation (CNS stimulation), can lead to respiratory alkalosis bc breathing out more CO2 can make blood more basic

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16
Q

ASA interactions

A
  • increased bleeding with anticoagulants
  • glucocorticoids: gastic ulcers
  • non ASA NSAIDs: reduce antiplatelet effects of ASA (don’t mix if taking for antiplatelet effect)
17
Q

non ASA NSAIDs

A
  • fewer GI, renal, and hemorrhagic effects than ASA
  • inhibit COX 1 and COX 2
  • inhibition is reversible
  • do not protect against MI and stroke
18
Q

NSAID contraindications

A
  • conditions with bleeding as a risk (vitamin K deficiency, peptic ulcer disease, GI lesions)
  • severe renal or hepatic disease
  • breastfeeding
19
Q

selective COX2 inhibitors

A

COX 2 produce prostaglandins responsible for inflammatory mediators

  • celecoxib (allergies - sulfa drugs)
  • rofecoxib (withdrawn bc increased with of MI and stroke)

just as effective as non selective, lower risk for GI adverse effects, can impair renal function and cause hypertension and edema

still some GI effects bc some prostaglandins protect GI and are inhibited

20
Q

drug for reducing GI ulceration

A

misoprostol
- synthetic prostaglandin
- used in combination with NSAIDs to reduce ulceration

21
Q

NSAID nursing implications

A

enteric coated tablets should not be crushed or chewed (has barrier to prevent disintegration in gastric environment)

22
Q

acetaminophen (tylenol) generic info

A
  • non opioid analgesic
  • antipyretic
  • not anti inflammatory
  • not antiplatelet
  • alternative when NSAIDs cannot be taken
  • inhibits COX in the CNS
  • no peripheral therapeutic sites of action (& absence of adverse effects associated with NSAIDS - ulcers and bleeding)
  • maximum 400mg/day adult
  • sliding scale for children
  • extreme caution in alcohol abusers (impaired liver function)
  • single ingredient (325, 500, 650mg) or combination (codeine - 300mg acetaminophen/tab)
23
Q

acetaminophen contraindications

A
  • severe hepatic disease (viral infections, alcohol intake - cirrhosis)
  • severe renal disease (impairs excretion)
  • alcoholism
  • drug allergy
24
Q

acetaminophen toxicity

A

overdose can be unintentional
- chronic misuse (not knowing acetaminophen is active ingredient)
- dangerous interactions if taken with alcohol

  • hepatic necrosis (drug induced hepatitis)
  • long term ingestion of large doses may cause nephropathy
25
Q

alcohol and acetaminophen toxicity pathway

A

alcohol increased P450 enzyme to turn acetaminophen into toxic metabolite

alcohol and acetaminophen overdose depletes body of glutathione which turns toxic metabolite from acetaminophen into nontoxic form

26
Q

acetaminophen overdose antidote

A

acetylcysteine
- protects liver from acetaminophen-induced damage
- max protection within 8-10 hrs
- restores hepatic glutathione to make nontoxic metabolite

is also a mucolytic used to decrease viscosity of bronchial secretion

pharm (15 decks)

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