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Pharm III Unit II > 4 NSAIDs and Acetaminophen > Flashcards

4 NSAIDs and Acetaminophen Flashcards

(75 cards)

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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
What are the CV effects of aspirin?
Minimal at regular doses
26
What are the respiratory effects of aspirin?
Aspirin asthma - due to increased leukotriene synthesis
27
What are the GI effects of aspirin?
GI upset, gastritis, ulcer, bleeding (all b/c of decreased GI-protective prostaglandins) Treat with buffering, food, misoprostol
28
What are the kidney effects of aspirin?
Renal damage (2˚ to vasodilation) Acute renal failure Interstitial nephritis
29
Is aspirin safe in pregnancy?
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
30
Local irritant effects of salicylates
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
31
Aspirin dose should be decreased during a long-term therapy with...
``` Oral anticoagulants (WARFARIN - increases its effect) Hypoglycemic agents ```
32
What is the fatal dose of aspirin?
Approximately 20 grams (10-30g) For methyl salicylate (oil of wintergreen), 4-5 mL can be fatal in children
33
What is Reyes Syndrome?
Cerebral edema in children with viral infections DOC is acetaminophen
34
Magnesium choline salicylate, sodium salicylate, and salicyl salicylate are all...
Non-acetylated salicylates Effective anti-inflammatory drugs but less effective analgesics than aspirin and no irreversible COX inhibition (so no antiplatelet activity)
35
What is Diflunisal?
Salicylic acid derivative but not metabolized to salicylic acid Does not have significant antipyretic effects probably due to poor penetration into the CNS
36
What are the two categories of NSAID?
Specific reversible inhibitors of COX-2 Nonspecific reversible inhibitors of COX-1 and COX-2
37
What is the only specific reversible inhibitor of COX-2 currently on the market?
Celecoxib (Celebrex) Has the potential to cause less gastroparesis and risk of GI bleeding
38
What are the main adverse effects of Celecoxib?
GI disturbances including ulceration and bleeding INCREASED RISK OF CVD (b/c of an imbalance of prostaglandins)
39
Contraindications for Celecoxib
``` GI disease Asthma Breast feeding Pregnancy Renal failure ```
40
Which nonspecific reversible inhibitor of COX-1/2 is the first choice drug due to it having the best side effect profile?
Ibuprofen
41
Which nonspecific reversible inhibitor(s) of COX-1/2 are potent but have the worst side effect profile?
Indomethacin and Phenylbutazone (not available in US)
42
What are the different toxicities to nonspecific reversible inhibitors of COX-1/2?
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
Which NSAID works by reducing PMN migration and inhibiting phospholipase A?
Indomethacin (Indocin) Very potent anti-inflammatory agent but with a high incidence of side effects
44
How is Indomethacin (Indocin) used?
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
Which NSAID works by decreasing arachidonic acid bioavailability?
Diclofenac (Voltaren)
46
How is Diclofenac used?
Combined with misoprostol (Arthrotec) to decrease GI side effects
47
Which NSAID is the DOC for post-surgical pain?
Ketorolac (Toradol) Oral and IV/IM admin May be combined with opiates
48
What is the caution with using Ketorolac?
After 5 days of use, you will get frequent GI side effects So only use it for a few days you dummy
49
What happens when you combine ibuprofen and ASA?
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
How is ibuprofen metabolized?
In the liver (half life = 2-4 hours) Renally excreted (both metabolite and parent compound)
51
What are the signs of ibuprofen toxicity?
Overall toxicity is low N/V/D/C, heartburn GI bleeding Dizziness, lightheaded ness, HA, hyperuricemia, fluid retention, edema
52
Which NSAID has effects similar to aspirin and ibuprofen but can be given QD due to its 13 hour half-life
Naproxen (Naprosyn)
53
How is Naproxen excreted?
Largely in the urine, small % in the feces
54
Is Naproxen safe in pregnancy?
No - it crosses the placenta readily so it should not be given to pregnant women
55
What drug interactions are possible with Naproxen?
It’s extensively bound to plasma proteins - displacement causes adverse drug reactions with oral anticoagulants (WARFARIN), hypoglycemic agents, etc
56
Naproxen toxicity
GI disturbances, heartburn, dyspepsia, abdominal pain, constipation, diarrhea, gastric bleeding (less severe than with ASA)
57
Which NSAIDs work by inhibiting PMN migration and lymphocyte function —> decrease oxygen radical production
PirOXicam (Feldene) and MelOXicam (Mobic)
58
Very potent NSAID that is not available in the US but you can get in Canada/Mexico
Phenylbutazone Serious side effects (GI, bone marrow)
59
Why is Acetaminophen sometimes preferred to Aspirin?
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
Overdose of acetaminophen causes...
Fatal hepatic necrosis Use with caution, esp in kids
61
What are the actions of acetaminophen?
Antipyretic Analgesic NOT an anti-inflammatory
62
How is acetaminophen metabolized?
Conjugated in the liver and renally excreted Dose dependent free radical production - eliminated by GSH (reduced glutathione)
63
What are the indications for acetaminophen?
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
What is the current daily limit of acetaminophen?
2g (4 extra-strength tablets)
65
Does acetaminophen influence urate excretion
Nope
66
Adverse effects of acetaminophen
Occasional skin rash/allergy and cross-sensitivity with salicylates Few cases of neutropenia, pancytopenia, and leukopenia DOSE-DEPENDENT FATAL HEPATIC NECROSIS
67
In adults, hepatotoxicity occurs after ingestion of ______ of acetaminophen at once, and ____ may be fatal.
10-15g (20-30 pills) 25g (50 pills)
68
Lab findings indicative of liver damage as a result of acetaminophen
Elevated serum transaminase Lactic acid dehydrogenase
69
What is responsible for the liver damage in acetaminophen induced hepatic necrosis?
A hydroxylated intermediate metabolite
70
The toxicity of acetaminophen becomes serious when the circulating metabolites exceed ____________ in the body
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
When is gastric lavage indicated for acetaminophen overdose?
Within the first 4 hours of ingestion
72
Treatment of acetaminophen intoxication
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
What analgesic should you pick for a patient with no history of PUD
Whatever one you want
74
What analgesic should you pick for a patient with a history of PUD but no active disease?
Celecoxib w/ or w/o antacids | Some NSAIDs w/ misoprostol or “-Prazols”
75
What analgesic should you pick for a patient with active PUD?
Acetaminophen and/or opioids (ie codeine) only NO NSAID

Pharm III Unit II (8 decks)

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