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Pharm III Unit II > 4 NSAIDs and Acetaminophen > Flashcards

4 NSAIDs and Acetaminophen Flashcards

1
Q

What are the clinical signs of inflammation?

A

Erythema
Edema
Tenderness
Pain

(Census in 100 AD said “Rubor, Calor, Tumor, Dolor” or “Redness, Heat, Swelling, and Pain”)

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2
Q

What are the body’s different mediators of acute inflammation?

A 
Histamine
Serotonin
Bradykinin
Prostaglandins
Leukotrienes
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3
Q

Which mediator(s) of inflammation causes the most vasodilation?

A

Bradykinin and Prostaglandins

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4
Q

Which mediator(s) of inflammation causes the most increase in vascular permeability?

A

Histamine and Leukotrienes

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5
Q

Which mediator(s) of inflammation causes the most Chemotaxis?

A

Prostaglandins and Leukotrienes

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6
Q

Which mediator(s) of inflammation causes the most pain?

A

Bradykinin

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7
Q

If you really want to stop inflammation, which mediator is it most important to inhibit?

A

PROSTAGLANDINS

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8
Q

What is the rate limiting step in the body’s production of prostaglandins?

A

Conversion of phospholipids into arachidonic acid (by Phospholipase)

This is why phospholipase inhibitors and corticosteroids are so good at shutting inflammation down (no prostaglandins = no inflammation)

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9
Q

Why does aspirin sometimes cause asthma?

A

Inhibition of the COX enzyme (and decreased prostaglandins/thromboxane) means more of the arachidonic acid gets shunted into the production of Leukotrienes —> alteration of vascular permeability, bronchial constriction, increased secretions —> bronchospasm, congestion, and mucus plugging

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10
Q

MOA for aspirin

A

Nonselective, irreversible inhibitor of COX-1 and COX-2

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11
Q

How is aspirin absorbed?

A

It’s a simple organic acid (pKa = 3.5), so it has good and fast oral absorption

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12
Q

How does distribution of aspirin to different parts of the body look?

A

Readily crosses the placental barrier

Slowly crosses the BBB

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13
Q

How is aspirin metabolized?

A

Rapidly hydrolyzed isn’t eh plasma, liver and erythrocytes

At low doses, eliminated by FIRST ORDER kinetics

At high doses, by ZERO ORDER (above 600mg body burden)

Renally excreted

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14
Q

How can you promote renal excretion of aspirin?

A

Alkalinization of the urine

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15
Q

Salicylate (aspirin) compete with these drugs for protein plasma binding sites, thereby causing drug interactions

A 
Thyroxin T3
Penicillin-G
Thiopental
Bilirubin
Phenytoin
Sulfinpyrazone
Naproxen
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16
Q

What are the four effects of aspirin?

A

Analgesic
Antipyretic
Anti-inflammatory
Antiplatelet

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17
Q

Why is aspirin the only “pain med” that has platelet effects?

A

It irreversibly inhibits the platelet COX enzymes

Platelets can not synthesize new enzymes

—> Inhibition of platelet aggregation —> increased bleeding time (single 650mg dose —> doubled bleeding time)

Effect lasts 8-10 days

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18
Q

Uses for aspirin

A

Mild and moderate pain relief

Antipyretic

Anti-inflammatory agent

MI, thrombosis prophylaxis

Long term use decreases colon cancer

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19
Q

What are the adverse effects of aspirin?

A

At lower doses —> Respiratory ALKALOSIS

At higher doses —> Metabolic AND Respiratory ACIDOSIS

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20
Q

Aspirin should be avoided in patients with these conditions

A 
Hypoprothrombinemia
Vitamin K deficiency
Hemophilia
Severe hepatic damage
Gastric ulcer
Hypersensitivity to aspirin or salicylates
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21
Q

Aspirin should be d/c prior to what procedures?

A

Stop at least one week before elective surgery

Avoid prior to labor

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22
Q

The uricosuric effects of aspirin are _____ and ______.

A

Biphasic

Dose dependent

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23
Q

What happens to uric acid when taking low doses (1-2g/day) of aspirin?

A

Aspirin actually decreases uric acid excretion and elevates plasma urate concentration

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24
Q

What happens to uric acid when taking high doses (>5g/day) of aspirin?

A

Aspirin enhances uric acid excretion (uricosuria) and lowers plasma urate levels

Too bad such large doses are poorly tolerated (stomach irritation and gastric bleeding)

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25
Q

What are the CV effects of aspirin?

A

Minimal at regular doses

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26
Q

What are the respiratory effects of aspirin?

A

Aspirin asthma - due to increased leukotriene synthesis

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27
Q

What are the GI effects of aspirin?

A

GI upset, gastritis, ulcer, bleeding (all b/c of decreased GI-protective prostaglandins)

Treat with buffering, food, misoprostol

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28
Q

What are the kidney effects of aspirin?

A

Renal damage (2˚ to vasodilation)
Acute renal failure
Interstitial nephritis

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29
Q

Is aspirin safe in pregnancy?

A

No teratogenic effect in humans convincingly documented, but has been seen in animals

Advisable to withhold aspirin several days prior to delivery to prevent excessive and prolonged post-partum bleeding

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30
Q

Local irritant effects of salicylates

A

Salicylic acid (but not aspirin) is quite irritant to the skin and mucosa —> destroys epithelial cells

Utilized for removal of warts, corns, fungal infection, and certain types of eczematous dermatitis

Methyl salicylates (oil of Wintergreen) is irritating to the skin and mucosa

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31
Q

Aspirin dose should be decreased during a long-term therapy with…

A 
Oral anticoagulants (WARFARIN - increases its effect)
Hypoglycemic agents
32
Q

What is the fatal dose of aspirin?

A

Approximately 20 grams (10-30g)

For methyl salicylate (oil of wintergreen), 4-5 mL can be fatal in children

33
Q

What is Reyes Syndrome?

A

Cerebral edema in children with viral infections

DOC is acetaminophen

34
Q

Magnesium choline salicylate, sodium salicylate, and salicyl salicylate are all…

A

Non-acetylated salicylates

Effective anti-inflammatory drugs but less effective analgesics than aspirin and no irreversible COX inhibition (so no antiplatelet activity)

35
Q

What is Diflunisal?

A

Salicylic acid derivative but not metabolized to salicylic acid

Does not have significant antipyretic effects probably due to poor penetration into the CNS

36
Q

What are the two categories of NSAID?

A

Specific reversible inhibitors of COX-2

Nonspecific reversible inhibitors of COX-1 and COX-2

37
Q

What is the only specific reversible inhibitor of COX-2 currently on the market?

A

Celecoxib (Celebrex)

Has the potential to cause less gastroparesis and risk of GI bleeding

38
Q

What are the main adverse effects of Celecoxib?

A

GI disturbances including ulceration and bleeding

INCREASED RISK OF CVD (b/c of an imbalance of prostaglandins)

39
Q

Contraindications for Celecoxib

A 
GI disease
Asthma
Breast feeding
Pregnancy 
Renal failure
40
Q

Which nonspecific reversible inhibitor of COX-1/2 is the first choice drug due to it having the best side effect profile?

A

Ibuprofen

41
Q

Which nonspecific reversible inhibitor(s) of COX-1/2 are potent but have the worst side effect profile?

A

Indomethacin and Phenylbutazone (not available in US)

42
Q

What are the different toxicities to nonspecific reversible inhibitors of COX-1/2?

A

GI - pain, bleeding, ulcer, pancreatitis, diarrhea

CNS - HA, dizziness, confusion, depression

Resp - bronchoconstriction

Bone marrow - agranulocytosis, aplastic anemia

Nephro - acute renal failure, interstitial nephritis, nephrotic syndrome

Hep - enzyme elevation, hepatitis

Hypersensitivity reactions

43
Q

Which NSAID works by reducing PMN migration and inhibiting phospholipase A?

A

Indomethacin (Indocin)

Very potent anti-inflammatory agent but with a high incidence of side effects

44
Q

How is Indomethacin (Indocin) used?

A

To close a patent ductus arteriosus

Works because you need to get rid of the prostaglandins and Indo works by inhibiting phospholipase A, which is the rate limiting step in the synthesis of prostaglandins

45
Q

Which NSAID works by decreasing arachidonic acid bioavailability?

A

Diclofenac (Voltaren)

46
Q

How is Diclofenac used?

A

Combined with misoprostol (Arthrotec) to decrease GI side effects

47
Q

Which NSAID is the DOC for post-surgical pain?

A

Ketorolac (Toradol)

Oral and IV/IM admin

May be combined with opiates

48
Q

What is the caution with using Ketorolac?

A

After 5 days of use, you will get frequent GI side effects

So only use it for a few days you dummy

49
Q

What happens when you combine ibuprofen and ASA?

A

Decreased effect on platelet aggregation b/c it reduces the irreversible binding of ASA

Warn your patient not to use ibuprofen when on ASA therapy

50
Q

How is ibuprofen metabolized?

A

In the liver (half life = 2-4 hours)

Renally excreted (both metabolite and parent compound)

51
Q

What are the signs of ibuprofen toxicity?

A

Overall toxicity is low

N/V/D/C, heartburn

GI bleeding

Dizziness, lightheaded ness, HA, hyperuricemia, fluid retention, edema

52
Q

Which NSAID has effects similar to aspirin and ibuprofen but can be given QD due to its 13 hour half-life

A

Naproxen (Naprosyn)

53
Q

How is Naproxen excreted?

A

Largely in the urine, small % in the feces

54
Q

Is Naproxen safe in pregnancy?

A

No - it crosses the placenta readily so it should not be given to pregnant women

55
Q

What drug interactions are possible with Naproxen?

A

It’s extensively bound to plasma proteins - displacement causes adverse drug reactions with oral anticoagulants (WARFARIN), hypoglycemic agents, etc

56
Q

Naproxen toxicity

A

GI disturbances, heartburn, dyspepsia, abdominal pain, constipation, diarrhea, gastric bleeding (less severe than with ASA)

57
Q

Which NSAIDs work by inhibiting PMN migration and lymphocyte function —> decrease oxygen radical production

A

PirOXicam (Feldene) and MelOXicam (Mobic)

58
Q

Very potent NSAID that is not available in the US but you can get in Canada/Mexico

A

Phenylbutazone

Serious side effects (GI, bone marrow)

59
Q

Why is Acetaminophen sometimes preferred to Aspirin?

A

It is tolerated better - no PUD, inhibition of blood clotting, acid-base imbalance, or auditory toxicity

Doesn’t have the GI side effects b/c no COX inhibition (therefore no reduction in prostaglandins)

60
Q

Overdose of acetaminophen causes…

A

Fatal hepatic necrosis

Use with caution, esp in kids

61
Q

What are the actions of acetaminophen?

A

Antipyretic
Analgesic

NOT an anti-inflammatory

62
Q

How is acetaminophen metabolized?

A

Conjugated in the liver and renally excreted

Dose dependent free radical production - eliminated by GSH (reduced glutathione)

63
Q

What are the indications for acetaminophen?

A

Mild, moderate pain

Fever (ESP IN KIDS)

Adjunct to anti-inflammatory therapy

Can be combined with codeine and derivatives, sedatives, cough suppressants, tramadol, diphenhydramine, caffeine, etc

64
Q

What is the current daily limit of acetaminophen?

A

2g (4 extra-strength tablets)

65
Q

Does acetaminophen influence urate excretion

A

Nope

66
Q

Adverse effects of acetaminophen

A

Occasional skin rash/allergy and cross-sensitivity with salicylates

Few cases of neutropenia, pancytopenia, and leukopenia

DOSE-DEPENDENT FATAL HEPATIC NECROSIS

67
Q

In adults, hepatotoxicity occurs after ingestion of ______ of acetaminophen at once, and ____ may be fatal.

A

10-15g (20-30 pills)

25g (50 pills)

68
Q

Lab findings indicative of liver damage as a result of acetaminophen

A

Elevated serum transaminase

Lactic acid dehydrogenase

69
Q

What is responsible for the liver damage in acetaminophen induced hepatic necrosis?

A

A hydroxylated intermediate metabolite

70
Q

The toxicity of acetaminophen becomes serious when the circulating metabolites exceed ____________ in the body

A

The available reduced glutathione

Normally, the available glutathione would be sufficient to neutralize the toxic metabolite of acetaminophen if the dose is below the toxic level

CHRONIC ALCOHOL CONSUMPTION increases toxicity

71
Q

When is gastric lavage indicated for acetaminophen overdose?

A

Within the first 4 hours of ingestion

72
Q

Treatment of acetaminophen intoxication

A

Gastric emptying (if within 4 hours of ingestion)
Forced diuresis
Hemodialysis
Specific antidote - N-acetylcysteine**** Must be administered parenterally as soon as possible, and within 10-12 hours of ingestion

73
Q

What analgesic should you pick for a patient with no history of PUD

A

Whatever one you want

74
Q

What analgesic should you pick for a patient with a history of PUD but no active disease?

A

Celecoxib w/ or w/o antacids

Some NSAIDs w/ misoprostol or “-Prazols”

75
Q

What analgesic should you pick for a patient with active PUD?

A

Acetaminophen and/or opioids (ie codeine) only

NO NSAID

Pharm III Unit II (8 decks)

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