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Pharmacology > Aspiring, NSAIDs, and Acetaminophen > Flashcards

Aspiring, NSAIDs, and Acetaminophen Flashcards

1
Q

function of NSAIDs

A

inhibit COX-1 and COX-2

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2
Q

how does aspirin inhibit function of COX-1 and COX-2

A

it covalently modifies the enzyme

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3
Q

how does NSAIDs inhibit COX-1 and COX-2

A

competes for the active site of cyclooxygenase (competitive inhibitor)

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4
Q

how does Acetaminophen inhibit COX-1 and COX-2

A
  • interfers with the oxidative state of cyclooxygenase site

- inhibition impaired by “peroxide tone”

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5
Q

acetaminophen metabolites can form a conjugation with arachidonate acid in the brain to yield

A

a neuroactive metabolite
-or inhibition of the nitric oxide pathway mediated by a variety of neurotransmitter receptors including N-methyl-D-aspartate and substance P

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6
Q

general properties of NSAIDs

A
  • anti-inflammatory
  • analgesia (inability to feel pain)
  • antipyresis
  • gastric erosion
  • cause renal dysfunction, impair renal function
  • variable effect on platelet aggregation; increase cardiovascular pathologic events due to COX-2 inhibition
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7
Q

side effects of NSAID therapy

A
  • gastric and intestinal ulceration
  • anemia from resultant blood loss
  • local irritation from drugs (organic acids) plus removal of PGE2 and PGI2 cytoprotective effects (less mucous covering GI)
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8
Q

how should patients at risk of GI toxicity be managed

A

-given celecoxib or other NSAID co-administered with a proton pump inhibitor or the PGE1 analong misoprostol

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9
Q

All NSAIDs have what effect on the cardiovascular system

A
  • prothrombotic effects that increase risk of stroke, TIA, symptomatic coronary artery disease
  • symptomatic peripheral vascular disease (COX-2 inhibition)
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10
Q

All NSAIDs can exacerbate

A

hypertension

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11
Q

what is the safest NSAIDs

A

naproxen bc it has the lowest cardiovascular toxicity effects

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12
Q

what are the adverse effects of NSAIDs on the renal system

A
  • decrease renal blood flow and GFR in patients with congestive heart failure, liver disease (ascites); chronic renal disease; or those who are hypovolemic or dehydrated
  • promote salt and water retention by producing PG-induced inhibition of both the reabsorption of chloride and the action of ADH
  • may cause increased intravascular volume/edema
  • analgesic nephropathy
  • idiosyncratic and dose-related hepatic injury
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13
Q

symptoms of aspirin “intolerance”

A

-vasomotor rhinitis, generalized urticaria (hives), and bronchospasm, laryngeal edema and bronchoconstriction, flushing, hypotension and shock

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14
Q

aspirin “intolerance” occurs in pts with

A
  • nasal polyps, asthma, and chronic urticaria

- asthma may be induced or exacerbated in such patients

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15
Q

what is the mechanism of aspirin intolerance

A
  • defect in mast cell histamine storage/shunting or arachidonic acid to lipoxygenase pathway
  • nonimmunologic mechanism
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16
Q

effects of aspirin in pregnancy

A
  • prolong labor

- promote premature closure of ductus arteriosus

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17
Q

common drug interactions of NSAIDs

A
  • prolong bleeding time (warfarin; heparin)
  • increase the ulcerogenic effects of glucocorticoids
  • reduce effects of diuretics and other antihypertensive agents
  • reduce lithium clearance; also methotrexate; cyclosporine; aminoglycosides
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18
Q

therapeutic uses of NSAID

A
  • relief pain and inflammation
  • reduce body temp in febrile states
  • closure of ductus arterioles
  • with antihistamines, in pts with systemic mastocytosis
  • adjunct in cancer-related hypercalcemia
  • Bartter’s syndrome
  • moderate cutaneous rxns in pts receiving niacin
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19
Q

aspirin in a — dependent pharmacokinetics

A

dose

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20
Q

MAO of aspirin

A

acetylates COX

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21
Q

what type of inhibitor is aspirin (salicylic acid)

A

competitive inhibitor

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22
Q

dose-dependent therapeutic effects of aspirin

A
  • anti-platelet effects
  • analgesia; reduction in febrile responses
  • anti-inflammatory
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23
Q

aspirin metabolism

A
  • aspirin is metabolized in plasam to yield salicylic acid

- salicylic acid is biotransformed in liver and mitochondria

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24
Q

therapeutic uses of aspirin

A

-antipyretic, analgesic, anti-inflammatory

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25
Q

aspirin can be used as a prophlaxis of disease assocaited with

A
  • platelet hyperaggreability (CAD; unstable angina; post_MI or stent; postoperative deep vein thrombosis; risk of stroke)
  • pre-eclampsia and hypertension indued by pregnancy
26
Q

adverse effects of aspirin

A
  • gastric irritation, ulceration, erosion, hemorrhage
  • increased bleeding time (2X for 4-7 days)
  • decreased renal function in patients at risk
  • hepatic injury (usually with larger doses associated with treatment of RA)
27
Q

low doses of aspirin inhibits

A

uric acid excretion

28
Q

large doses of aspirin promotes

A

uric acid excretion

29
Q

10 mg/dl of aspirin causes

A

analgesia, antipyretic, anti-platelet; gastric intolerance/bleeding, hypersensitivity

30
Q

10-49 mg/dl of aspirin causes

A

anti-inflammatory, uricosuric

31
Q

50-80 mg/dl of aspirin causes

A

mild intoxication; tinnitus, central hyperventilation

32
Q

80-100 mg/dl causes

A

moderate intoxication; fever, dehydration, metabolic acidosis

33
Q

110-160 mg/dl of aspirin causes

A

severe intoxication; hypoprothrombinemia, vasomotor instability; coma

34
Q

> 160 mg/dl of aspirin causes

A

lethal blood levels; renal and respiratory failure

35
Q

what is salicylism

A

aspirin overdose

36
Q

effects of salicylism

A

-confusion; tinnitus, dizziness

37
Q

how does salicylism affect respiration

A
  • contributes to acid-base disturbances
  • stimulation via uncoupling of oxidative phosphorylation
  • direct stimulation of respiratory centre
  • toxic doses suppress respiration
38
Q

what metabolic effects does salicylism have

A
  • increases uncoupling
  • inhibit aerobic respiration
  • release epinephrine
  • reduces lipogenesis
  • large doses stimulate glucocorticoid secretion
39
Q

uncoupling of oxidative phosphorylation causes

A

increase of O2 consumption and CO2 production

40
Q

toxic doses of aspirin inhibit aerobic respiration leading to

A

accumulation of pyretic, lactic and acetoacetic acids

41
Q

aspirin promotes epinephrine release which promotes

A

hyperglycemia and depletes muscle and hepatic glycogen

42
Q

aspirin reduces lipogenesis which causes

A

increase in oxidation of F/A

43
Q

full therapeutic dose of aspirin produces respiratory alkalosis, how does compensation occur

A

-increase renal excretion of bicarbonate, accompanied by increased Na+ and K+ excretion

44
Q

extreme metabolic acidosis is caused by

A
  • salicylate accumulation
  • renal dysfunction with accumulation of organic acids
  • derangement of carbohydrate metabolism
45
Q

what is Acetaminophen (Tylenol)

A

an effective antipyretic and analgesic

46
Q

does Acetaminophen have anti-inflammatory effects

A

very little

47
Q

Acetaminophen does not effect the — and —

A

GI tract

platelets

48
Q

main toxicity of Acetaminophen is directed toward

A

liver

49
Q

mechanism of action of Acetaminophen

A

-inhibits cyclooxygenase, by altering oxidate state of active site

50
Q

ability of Acetaminophen to inhibit cylooxygengase is impaired in the presence of

A

peroxides (ie. inflammation)

51
Q

ability of Acetaminophen to inhibit cylooxygenase is enhanced in the presence of

A

high [ ] of antioxidants (ie. brain)

52
Q

experimental demonstration of novel metabolite of acetaminophen in

A

CNS which inhibits COX and stimulates TRPV1 receptor or possible interference with nitric oxide pathway and interface with central neurotransmitters

53
Q

Large dose of Acetaminophen (>7.5 g) may cause

A

hepatotoxicity

54
Q

hepatotoxicity of acetaminophen is mediated by

A

a metabolite formed by P450, which is normally inactived by glutathione

55
Q

hepatotoxic dose may be substantially smaller in individuals with

A

preexisting liver disease or who consume alcohol regularly

56
Q

acetaminophen over dose is the most common cause of

A

-acute liver failure
50% of adults
13% of pediatric cases

57
Q

treatment of acetaminophen toxicity

A

N-Acetylcysteine

58
Q

administration of N-Acetylcysteine is based on

A

a nonogram derived from time-dependent acetaminophen [ ] data generated in adults with a single, acute ingestions of drug who presented to medical centres with 24 h of the overdose

59
Q

FDA issued manufactuers of TC pain delivers and fever reducers to revise their labelling to include warnings about potential safety risks. Products covered by the FDA action included

A 
-acetaminophen (in a class by itself)
NSAIDs
-aspirin
-ibuprofen
-naproxen
-ketoprofen
60
Q

acetaminophen prescription products limited to

A

325 mg per dose

61
Q

what were the changes in Aceaminophen dosing regulations and warnings

A
  • require boxed warning highlighting the potential for liver injury, as well as allergic runs
  • used in many combination products; label abbreviations are currently not standardized

Pharmacology (23 decks)

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