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Pharm III > E2: NSAIDs and Acetaminophen > Flashcards

E2: NSAIDs and Acetaminophen Flashcards

1
Q

What are the 4 signs of inflammation?

A

Erythema (rubor)
Edema (calor)
Tenderness (tumor)
Pain (dolor)

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2
Q

Which 2 inflammatory mediators have opposite effects? Describe them.

A

Thromboxane: Vasoconstrictor, promotes platelet aggregation

Prostacyclin: most effective vasodilating agent and inhibitor of platelet aggregation

Must obtain a balance between the two!

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3
Q

Leukotrienes are responsible for what effect in the lungs?

A

Bronchospasm

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4
Q

MOA for Aspirin (ASA, Acetylsalicylic acid)

A

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

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5
Q

After being orally ingested, where does the distribution of aspirin occur? How does ASA cross the placental barrier? BBB?

A

Throughout the entire body (includes tissues and extracellular compartments)

READILY crosses placental barrier
Slowly crosses blood brain barrier

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6
Q

Why is plasma concentration of ASA low?

A

Rapidly hydrolyzed in the plasma, liver, and erythrocytes

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7
Q

What kinetics does ASA follow at low doses? High doeses?

A

Low doses: First order kinetics

High doses (above 600mg): Zero order kinetics

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8
Q

How is ASA excreted? What can increase excretion?

A

Renal excretion

-Alkalization of the urine promotes excretion

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9
Q

What are 6 primary effects/uses of ASA?

A
  • Anti-inflammatory effect
  • Analgesic effect
  • Antipyretic effect
  • Decreases incidence of MI (thrombosis prophylaxis)
  • Long term use decreases incidence of Colon CA
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10
Q

What is an adverse effect of ASA use? (Describe the process)

A

Respiratory alkalosis -> metabolic and respiratory acidosis

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11
Q

What effect does aspirin (NOT salicylic acid) have on platelets and how does this affect bleeding time? How long does this effect last?

A

ASA inhibits the platelet aggregation, therefore increasing the bleeding time.

Effect can last as long as 8-10 days

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12
Q

Aspirin should be avoided in patients with any of the following conditions (4):

A

Hypoprothembinemia
Vit K deficiency
Hemophilia
Severe hepatic damage

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13
Q

Aspirin should be discontinued how long in advance prior to elective surgery?

A

At least one week prior

Should also be avoided in last 3 months of pregnancy to avoid post-partum bleeding

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14
Q

Uricosuric effects of aspirin are _____ and ____ dependent.

A

Biphasic and dose dependent

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15
Q

How does aspirin affect uric acid excretion and plasma urate concentration at low doses? How about high doeses?

A

Low (1-2 g/day): DECREASES UA excretion, ELEVATES plasma urate conc.

High (5+ g/day): ENHANCES UA excretion, LOWERS plasma urate conc.

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16
Q

What adverse affect can aspirin have on the lungs?

A

Aspirin asthma (increased leukotriene synthesis)

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17
Q

What are 4 adverse effects of aspirin on the GI system?

A

GI upset
Gastritis
Ulcer (increased gastric acid production)
Bleeding

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18
Q

What are 4 severe effects of aspirin on the kidneys?

A

Renal damage
Acute renal failure
Interstitial nephritis
Nephrotic syndrome

Know this one!

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19
Q

What effect does salicylic acid (NOT aspirin) have on the skin? How can this be used therapeutically?

A
  • Irritant to skin and mucosa (destroys epithelial cells)

- Keratolytic effect is used to remove warts, corns, fungal infection, etc.

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20
Q

How much salicylic acid is required for a fatal dose (acute poisoning)?

A

10-30 g of aspirin

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21
Q

What is Reye’s syndrome? What is the DOC for children w/ fever?

A

Reye’s: Cerebral edema in children with viral infections

Give them acetaminophen for fevers instead

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22
Q

How is ASA different from all the other NSAIDs?

A

ASA is IRREVERSIBLE, all other NSAIDs are reversible!

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23
Q

How do nonacetylated salicylates differ from ASA?

A
  • Salicylic acid is active drug
  • Effective anti-inflammatory, but less effective analgesic than aspirin
  • No irreversible COX inhibition
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24
Q

MOA of Celecoxib (Celebrex)

A

Selective COX-2 inhibitor (REVERSIBLE)

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25
Q

Celebrex has less potential to cause this condition, but increased risk of developing another:

A

Less gastropathy and risk of GI bleeding (although still on FDA label)

Increased risk of cardiovascular dz!

26
Q

What are 4 adverse reaction of Celebrex?

A

Ulceration
Bleeding
Hypersensitivity
Increased risk of CVD

27
Q

Celebrex is C/I in the following populations: (5)

A 
GI disease
Asthma
Breast feeding
Pregnancy
Renal failure
28
Q

List the 3 effects of the COX-1 enzyme.

A

-Protects against gastric irritation

  • Promotes platelet aggregation (TXA2)
  • Vasoconstriction (TXA2)
29
Q

List the 3 effects of the COX-2 enzyme.

A
  • Vasodilation (PGI2)
  • Inhibits platelet aggregation (PGI2)

-Promotes inflammation

30
Q

MOA of Nonspecific COX inhibitors.

A

MOA: REVERSIBLY inhibit both COX enzymes (some may show slight specificity towards COX-2)

31
Q

What is the drug of first choice for nonspecific COX inhibitors? What is the worst (but potent) drug?

A

Best: ibuprofen
Worst: Indomethacin

32
Q

List the 7 areas of typical toxicities for the nonspecific COX inhibitors.

A
  1. GI - pain, bleeding, ulcer, diarrhea, pancreatitis
  2. CNS - depression, HA, dizziness
  3. Lung - bronoconstrction
  4. Bone marrow - Agranulocytosis, aplastic anemia
  5. Nephrotoxic
  6. Hepatotoxic
  7. Hypersensitivity rxns
33
Q

Aside from inhibition of COX enzymes, what are the 2 other MOAs for Indomethacin?

A
  • Reduce polymorphic nucleotide migration (immune system activation)
  • Inhibit phospholipase A (which reduces release of Pge)

*Very potent = lots of SE

34
Q

What is the primary use of indomethacin?

A

Tx of patent ductus arteriosus

35
Q

Aside from being a potent COX inhibitor, what is another MOA of Diclofenac (Voltaren)?

A

Decreases arachidonic acid bioavailability

36
Q

What are the primary side effects associated with Diclofenac and how can this be avoided?

A

GI side effects

Combine with misoprostol

37
Q

What is the primary use of Ketorolac (Toradol)? When should this med be discontinued?

A

Used as analgesic in post-surgical pain (can be combined with opioids)

Frequent GI effects after 5 days of use

38
Q

Which NSAID is the DOC and has the lowest incidence of side effects?

A

Ibuprofen

39
Q

Ibuprofen in combination with ASA will have what affect?

A

Decreases the effect on platelet aggregation

40
Q

How is ibuprofen excreted?

A

Renal excretion

41
Q

What are some adverse effects of ibuprofen?

A

Overall, toxicity is low!

  • N/V, diarrhea, constipation, heartburn
  • GI bleeding
  • Dizziness, light headedness, HA, etc.
42
Q

What is the mean plasma half-life of naproxen?

A

13 hours (take once a day)

43
Q

Where is naproxen primarily excreted?

A

Largely in the urine

44
Q

Naproxen is C/I in what pt population and why?

A

Pregnancy - crosses BBB

45
Q

Why does naproxen have drug interactions? Name 2 examples.

A

Naproxen extensively bound to plasma proteins so displacement causes adverse drug rxns

Ex: oral anticoagulants, hypoglycemic agnets

46
Q

List 5 adverse effects of naproxen.

A 
GI upset
Heartburn/dyspepsia
Abd pain
Constipation/diarrhea
Gastric bleeding (but less than ASA!)
47
Q

What 2 medications have a long half-life and high incidence of GI effcts?

A

Piroxicam and Meloxicam

48
Q

MOA for Piroxicam and Meloxicam (3)

A

Inhibits PMN migration and lymphocyte function

Decreases oxygen radical production

49
Q

Which NSAID is very potent but with serious side effects? (No longer prescribed in US)

A

Phenylbutazone

50
Q

Why is acetaminophen preferred over ASA?

A
  • Better tolerated

- Lacks several SE of ASA (ex: PUD, inhibition of blood clotting, etc.)

51
Q

What is one potentially fatal side effect of acetaminophen?

A

Fatal hepatic necrosis (overdose)

52
Q

What is the half life of acetaminophen? Where is it metabolized and where is it excreted?

A

T1/2= 2-3 hours

Metabolzied by liver, excreted by kidney

53
Q

What are the 2 pharmacodynamic properties of acetaminophen? What 2 pharmacodynamic properties is it lacking?

A

Antipyretic action
Analgesic action

*NO anti-inflammatory action or platelet effects

54
Q

What are 4 uses of acetaminophen?

A

Mild-moderate pain
Fever (CHILDREN)
Adjunct to anti-inflammatory therapy
Combined w/ codeine, sedatives, cough suppressants, etc.

55
Q

List 4 adverse effects of acetaminophen.

A

Skin rash
Cross-sensitivity with salicylates
Neutropenia
Dose-dependent fatal hepatic necrosis

56
Q

In adults, hepatotoxicity from acetaminophen occurs after ingestion of _____ grams. Why does this hepatotoxicity occur?

A

10-15

Due to hydroxylated intermediate metabolite causing liver damage (metabolites&raquo_space;> available glutathione)

57
Q

What are 2 signs of hepatotoxicity? What 3 conditions can hepatotoxicity progress to?

A

Signs: serum transaminase, lactic acid dehydrogenase

Can progress to encephalopathy, coma, and death

58
Q

What can increase toxicity of liver associated with acetaminophen overdose?

A

Chronic alcohol consumption

59
Q

What is the tx for acetaminophen intoxication?

A

Specific antidote: N-acetylcysteine

60
Q

If a pt has no hx of PUD, you can prescribe:

A

Any NSAID

61
Q

If a pt has a hx of PUD but not its not active, you can prescribe:

A
  • Celecoxib w/ or w/out antacids

- Some NSAIDs w/ misopristol or “-prazols”

62
Q

If a pt has active PUD, you can prescribe:

A

Acetaminophen and/or opioids only

Pharm III (7 decks)

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