Chapter 2.2 Flashcards

1
Q
  1. State the mechanism of prostaglandins in inflammation
A

Certain prostaglandins, such as PGE2, are thought to help mediate the local erythema and edema associated with inflammation in certain tissues by increasing local blood flow

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2
Q

pain

A

The compounds do not usually produce pain directly but are believed to increase the sensitivity of pain receptors to mechanical pressure and the effects of other pain producing substances such as bradykinin

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3
Q

fever

A

they play a role in promoting fever associated with systemic infection and other pyretogenic disorders

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4
Q

thrombus formation

A

The thromboxanes, especially TXA2, cause platelet aggregations that result in blood clot formation

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5
Q
  1. State the primary effects of nonsteroidal anti-inflammatory drugs (NSAIDs).
A

analgesic, anti-inflammatory, antipyretic and anticoagulant

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6
Q
  1. State the therapeutic, safety and cost differences between prescribed and over-the-counter NSAIDs.
A

No therapeutic difference if the dosage is the same. If a lower dose of OTC, some of the serious side effects are minimized. Patients need to not take high dosages of OTC drugs. OTC drugs are remarkably less expensive to prescription.

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7
Q
  1. State the mechanism of action of NSAIDs.
A

inhibit synthesis of prostaglandins by inhibiting cyclooxygenase. Prostaglandins are lipid compounds with various effects

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8
Q
  1. Differentiate the effects of the prostaglandins produced by the COX-1 and COX-2 subtypes of the cyclooxygenase (COX) enzyme
A

COx-1 PG to protect cells or maintain function

Cox-2: Synthesizes PGs that mediate pain or inflammation

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9
Q
  1. State the function of the prostaglandins produced by the COX-1 enzyme in the stomach, kidney, and platelets.
A

IE in stomach, the PG is to help protect from HCl.
COX-1 enzymes in the kidneys produce beneficial prostaglandins that help maintain renal function
COX-1 is also the enzyme responsible for synthesizing prostaglandins and thromboxanes regulating normal platelet activity

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10
Q
  1. State the reasons that COX-2 selective NSAIDs are associated with increased risk for myocardial infarction and stroke.
A

vasodilation and vasoconstriction are in balance normally. COX-2 drugs inhibit vasodilation leading to increase constriction and increased chance of cardiovascular disease.

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11
Q
  1. Identify the only currently available COX-2 selective NSAID.
A

Celecoxib

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12
Q
  1. State the advantage of using a COX-2 selective NSAID over an NSAID that non-selectively inhibits both COX-1 and COX-2 enzymes
A

Selective COX-2 inhibitors should decrease the production of prostaglandins that mediate pain and inflammation while sparing the synthesis of protective prostaglandins that are synthesized by COX-1

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13
Q
  1. Identify the adverse effects associated with NSAIDs
A

GI problems, cardiovascular problems, liver disease

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14
Q
  1. State the pharmacological actions of acetaminophen (APAP) and distinguish them from the pharmacological actions of NSAIDs.
A

Used in kids besides NSAIDs to avoid disease called Reye’s disease. It doesn’t produce gastric irritation and no anti-inflammatory or anticoagulant effects

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15
Q
  1. State the mechanism of action of APAP
A

inhibit cyclooxygenase enzyme

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16
Q
  1. State the most serious adverse effect of APAP us
A

liver toxicity

17
Q
  1. Classify the following NSAIDS as either non-specific COX inhibitors or COX-2 selective agents: aspirin, ibuprofen, meloxicam, celecoxib.
A

COX1: aspirin, ibuprofen, meloxicam
COX2: celecoxib

18
Q
  1. Identify the NSAIDs currently available over-the-counter
A

aspirin, ibuprofen and naproxen