E2: NSAIDS Flashcards

(40 cards)

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
What are the uses of Indomethacin?
- Reduce PNM migration - Inhibit Phospholipase A - Very potent AI and AR agent, high incidence of side effects - used for patent ductus arteriosus
26
What is the MOA of Diclofenac?
- Potent COX inhibitor | - decreases arachidonic acid bioavailability
27
What is Diclofenac often combined with and why?
Misoprostol to decrease GI side effects
28
What is the main use of Ketorolac?
-Mostly as an analgesic in postsurgical pain **Dont use for more than 5 days due to frequent GI side effects
29
What is the peak and mean plasma concentrations of Naproxen?
Peak: 1-2 hours | Mean plasma: 13 hours
30
What are the toxicites of Naproxen?
GI disturbances, heartburn, dyspepsia, abdominal pain, constipation, diarrhea, gastric bleeding is less severe than with aspirin
31
What are the uses of Piroxicam and meloxicam?
- Inhibits PMN migration, lymphocyte function | - Decreases oxygen radical production
32
Why is acetaminophen often preferred to aspirin?
- It is tolerated better - It lacks several undesirable side effects of aspirin, namely PUD, inhibition of blood clotting, acid base, imbalance, etc
33
What does Tylenol OD cause?
Fatal Hepatic necrosis
34
What specific actions of Tylenol?
-Antipyretic and analgesic action, no anti inflammatory action
35
What are the adverse effects of Tylenol?
- occasionally skin rash and allergic response - Occasional cross sensitivity with salicylate - neutropenia
36
When does hepatotoxicity from Tylenol occur?
- 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
What is responsible for liver damage in Tylenol use?
-Hydroxylated intermediate metabolite, toxicity becomes serious when the circulating metabolites exceed the available reduced glutathione in the body
38
What is the treatment of Tylenol intoxication?
- Gastric emptying, forced diuresis, hemodialysis | - specific antidote is N-acetylcysteine
39
What analgesics should be given to someone with a history of PUD, not not active?
- Celecoxib with or without antacids | - Some NSAIDS with misoprostol or “prazols”
40
What analgesics should be given to patients with active PUD?
Tylenol or opioids