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Pharm 3 > E2: NSAIDS > Flashcards

E2: NSAIDS Flashcards

1
Q

What are the 5 mediators of acute inflammation?

A

Histamine, serotonin, bradykinin, PGs, and leukotrienes

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2
Q

What role does histamine play in acute inflammation?

A

Vasodilation and increase vascular permeability

**strong vascular permeability

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3
Q

What role does serotonin play in acute inflammation?

A
  • some vasodilation

- increase vascular permeability

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4
Q

What role does bradykinin play in acute inflammation?

A

Vasodilation, increase vascular permeability, and pain

**most response for pain response

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5
Q

What role do prostaglandins play in acute inflammation?

A

Vasodilation, increase vascular permeability, chemotaxis, and pain

**strong vasodilation and chemotaxis

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6
Q

What role do leukotrienes play in acute inflammation?

A

Increase vascular permeability and chemotaxis, both strong

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7
Q

What are the 3 things that cyclooxygenase may produce?

A

PGs, thromboxane, and prostacyclin

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8
Q

What is the MOA of Aspirin?

A

No selective, irreversible inhibitor of COX1 and COX2

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9
Q

Which COX enzyme is inducible?

A

COX2: produces prostacyclin

** COX1 is not inducible and produces thromboxane

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10
Q

Does aspirin cross the placental and BBB?

A

Readily crosses the placental barrier and slowly crosses the BBB

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11
Q

What are the 4 main effects of aspirin?

A

Analgesia
Antipyretic
Anti inflammatory
Antiplatelet

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12
Q

What are the uses of aspirin?

A
  • Mild to moderate pain
  • antipyretic
  • anti inflammatory
  • MI and thrombosis prophylaxis
  • Long term use decreases colon cancer
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13
Q

What are the adverse effects of aspirin?

A

-Respiratory alkalosis, then metabolic and respiratory acidosis

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14
Q

Aspirin should be avoided in patients with what conditions?

A
  • Hypoprothrombinemia
  • vitamins K deficiency
  • hemophilia
  • severe hepatic damage
  • PUD
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15
Q

What effect does aspirin have on Uric acid?

A
  • Low doses of aspirin actually decreases uric acid excretion and elevates plasma urate concentration
  • at large doses aspirin enhances uric acid and lowers the plasma urate levels
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16
Q

Why should you avoid aspirin in asthmatics?

A

-it can cause aspirin asthma due to increased leukotriene synthesis (which causes bronchoconstriction)

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17
Q

What are the adverse effects of aspirin on the kidneys?

A

-Renal damage, acute renal failure, interstitial nephritis

18
Q

Why should aspirin be avoided in children?

A

-Risk of Reye’s syndrome (cerebral edema in children with viral infection, give Tylenol)

19
Q

What are the general effects of nonecetylated salicylates?

A
  • Effecitve anti-inflammatory
  • salicylic acid is the active drug
  • Less effective analgesics than aspirin and no irreversible COX inhibition
20
Q

What is the MOA of NSAIDs?

A
  • Specific reversible inhibitors of COX2 enzymes

- Nonspecific reversible inhibitors of COX1 and COX2 enzymes

21
Q

What kind of drug is Celecoxib?

A

An NSAID that is a selective and reversible COX2 inhibitor

-Has the potential to cause less gastropathy and risk of GI bleeding, since GI protective PGs are produced by COX1

22
Q

What are the adverse effects of Celecoxib?

A

GI disturbances including ulceration and bleeding, increased risk of CVD

23
Q

What are the contraindications of Celecoxib?

A

GI disease, asthma, breast feeding, pregnancy, renal failure

24
Q

What is the MOA of ibuprofen?

A

Nonspecific reversible inhibitors of COX1 and COX2

25
Q

What are the uses of Indomethacin?

A
  • Reduce PNM migration
  • Inhibit Phospholipase A
  • Very potent AI and AR agent, high incidence of side effects
  • used for patent ductus arteriosus
26
Q

What is the MOA of Diclofenac?

A
  • Potent COX inhibitor

- decreases arachidonic acid bioavailability

27
Q

What is Diclofenac often combined with and why?

A

Misoprostol to decrease GI side effects

28
Q

What is the main use of Ketorolac?

A

-Mostly as an analgesic in postsurgical pain

**Dont use for more than 5 days due to frequent GI side effects

29
Q

What is the peak and mean plasma concentrations of Naproxen?

A

Peak: 1-2 hours

Mean plasma: 13 hours

30
Q

What are the toxicites of Naproxen?

A

GI disturbances, heartburn, dyspepsia, abdominal pain, constipation, diarrhea, gastric bleeding is less severe than with aspirin

31
Q

What are the uses of Piroxicam and meloxicam?

A
  • Inhibits PMN migration, lymphocyte function

- Decreases oxygen radical production

32
Q

Why is acetaminophen often preferred to aspirin?

A
  • It is tolerated better
  • It lacks several undesirable side effects of aspirin, namely PUD, inhibition of blood clotting, acid base, imbalance, etc
33
Q

What does Tylenol OD cause?

A

Fatal Hepatic necrosis

34
Q

What specific actions of Tylenol?

A

-Antipyretic and analgesic action, no anti inflammatory action

35
Q

What are the adverse effects of Tylenol?

A
  • occasionally skin rash and allergic response
  • Occasional cross sensitivity with salicylate
  • neutropenia
36
Q

When does hepatotoxicity from Tylenol occur?

A
  • After ingestion of 10-15 grams. 25 grams may be fatal
  • Elevated serum transamination, Lactic acid dehydrogenase are signs of liver damage
  • Hepatotoxicity may progress into encephalopathy, coma, and death
37
Q

What is responsible for liver damage in Tylenol use?

A

-Hydroxylated intermediate metabolite, toxicity becomes serious when the circulating metabolites exceed the available reduced glutathione in the body

38
Q

What is the treatment of Tylenol intoxication?

A
  • Gastric emptying, forced diuresis, hemodialysis

- specific antidote is N-acetylcysteine

39
Q

What analgesics should be given to someone with a history of PUD, not not active?

A
  • Celecoxib with or without antacids

- Some NSAIDS with misoprostol or “prazols”

40
Q

What analgesics should be given to patients with active PUD?

A

Tylenol or opioids

Pharm 3 (20 decks)

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