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Owenpharm Block 2 > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What are the three general properties of NSAIDs?

A
  1. Anti-inflammatory
  2. Anti-pyretic
  3. Analgesic
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2
Q

What differentiates ASAs mechanism from other NSAIDs?

A

It is irreversible inhibition due to acetylation of serine 230

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3
Q

How is salicylate alone different from acetylsalicylic acid?

A

It is a competitive inhibitor but reversible.

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4
Q

What is the main point of absorption pharmacokinetics of ASA? (2 points)

A

Limited by dissolution rate

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5
Q

What factors are considerations in distribution of ASA? (2 points)

A
  1. Significant plasma protein binding

2. Crosses blood-brain barrier and placental barrier

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6
Q

What factors are to be considered in the metabolism of ASA? (2 points)

A
  1. It is hydrolyzed into salicylic acid

2. Salicylic acid is then metabolized to multiple less polar metabolites.

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7
Q

How is ASA eliminated?

A

Renal elimination

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8
Q

How does ASA create its anti-platelet effect?

A

Inhibition of COX1 on platelets prevents thromboxane formation

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9
Q

How long does a dose of aspirin have an anti-platelet effect?
Why?

A

Approx. 7 days
Platelets don’t have the ability to create new COX1 enzyme as they cannot synthesize proteins. So new platelets must be made.

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10
Q

What effect does ASA have on vascular endothelial cells?

A

Reduces the amount of vascular prostacyclin synthesis that create contribute to platelet adherence.

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11
Q

Why is the plasma half-life of ASA dose dependent?

A

Elimination of salicylate is based on zero order kinetics

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12
Q

What effect does ASA have on Uric acid levels?

A

ASA promotes uric acid excretion at high doses

ASA increases serum levels at low doses and decreases excretion.

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13
Q

What effects can ASA have on the CNS? (2 points)

A

Delirium and psychoses

nausea/vomiting

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14
Q

What effects does increased ASA levels have on respiration?

A

Direct stimulation of respiratory center to increase rate

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15
Q

What is the mechanism for gastric irritation in the use of NSAIDs?

A

Inhibition of COX-1 prevents production of cytoprotective prostaglandins in stomach and duodenum.

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16
Q

What is the mechanism for bronchoconstriction and edema in patients with NSAID hypersensitivity?

A

May be due to action of leukotrienes because of shunting of arachidonate from COX to lipoxygenase.

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17
Q

What effects do NSAIDs have on the Kidneys and why?

A

Decreased renal blood flow and glomerular filtration rate
salt and water retention
This is due to inhibition of COX1 and possibly COX2 derived vasodilatory PGs.

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18
Q

What type of patients are renal effects of NSAIDs more prominent in? (3 ponts)

A

CHF
Chronic renal failure
Liver disease
(COX 2 may be upregulated in these diseases.)

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19
Q

What is the significance of NSAID use in late stage pregnancy?

A

Reduction in uterine contraction which may prolong labor.

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20
Q

What is the mechanism for NSAID associate prolongation of labor?

A

Inhibition of uterine stimulating PGs

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21
Q

Do NSAIDs affect the fetus? If so how?

A

Yes, they could. Prostaglandins maintain a patent ductus arteriosus. Inhibition of this could close the PDA.

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22
Q

What are the effects of salicylate overdose? (8 points)

A 
slight respiratory stimulation
nausea/vomiting
tinnitius
deafness
confusion
fever
dehydration
metabolic acidosis
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23
Q

What is the mechanism for ASA overdose?

A

ASA is metabolized to salicylate. Enzymes that convert Salicylate to an inactive metabolite are then saturated and a build-up of salicylate develops

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24
Q

Why isn’t aspirin given to children?

A

Concern for Reye’s syndrome where a viral illness can result in liver failure and death.

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25
Q

What is the only COX2 selective inhibitor?

A

Celecoxib

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26
Q

What are the major therapeutic uses for NSAIDs? (5 points)

A 
Fever
Low intensity pain
Inflammatory disorders (High dose)
Cancer
ASA for anti-platelet in CV disease.
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27
Q

What are the two propionic derivative NSAIDs?

A

Ibuprofen

Naproxen

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28
Q

What is the only COX2 selective inhibitor?

A

Celecoxib

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29
Q

What are the major therapeutic uses for NSAIDs? (5 points)

A 
Fever
Low intensity pain
Inflammatory disorders (High dose)
Cancer
ASA for anti-platelet in CV disease.
30
Q

What are the two propionic derivative NSAIDs?

A

Ibuprofen

Naproxen

31
Q

What is the half life for ibuprofen?

A

2 hours

32
Q

What are the therapeutic applications for Naproxen? (9 points)

A 
Ankylosing spondylitis
Osteoarthritis
Rheumatoid disorders
Acute gout
Mil-to-moderate pain
Tendonitis
Bursitis
Dysmenorrhea
Fever
33
Q

What are the acetic acid derivative NSAIDs?

A

Indomethacin, Ketorolac, and Nabumetone

34
Q

What is the IV preparation for ibuprofen and what is it used for?

A

Ibuprofen lysine injection (NeoProfen)

Induces closure of a clinically significant PDA in premature infants <32weeks.

35
Q

What are the therapeutic applications for Naproxen? (9 points)

A 
Ankylosing spondylitis
Osteoarthritis
Rheumatoid disorders
Acute gout
Mil-to-moderate pain
Tendonitis
Bursitis
Dysmenorrhea
Fever
36
Q

What percent of Indomethacin is plasma protein bound?

A

90%

37
Q

What are the problems with Indomethacin? (3 points)

A

Frequent adverse reactions
GI toxicity
CNS effect-sever frontal headache

38
Q

What is the plasma half-life of Indomethacin?

A

3 hours

39
Q

What percent of Indomethacin is plasma protein bound?

A

90%

40
Q

What is unique about Nabumetone compared to Indomethacin or Ketorolac?

A

Active metabolite is greater inhibitor of COX2 than COX1

41
Q

Whic of the three NSAID effects does Ketorolac have less action? Analgesia, Anti-pyretic, or Anti-inflammatory

A

decreased anti-inflammatory activity

42
Q

What are the therapeutic applications for Ketorolac?

A

Short term (<5days) management of moderate-to-severe acute pain requiring analgesia at the opioid level.

43
Q

What is notable about the pharacokinetics of Nabumetone?

A

Metabolite is the active substance (6-methoxy-2-naphthylacetic acid)
it has a long half life

44
Q

What are the advantages of Nabumetone over Indomethacin?

A

It is more well tolerated
It has less GI effects
More “like” a COX2 inhibitor

45
Q

What are the two major therapeutic applications of Nabumetone?

A

Osteoarthritis

Rheumatoid arthritis

46
Q

What is the Oxicam derivate NSAID for this course?

A

Piroxicam

47
Q

What is the plasma-half life of Piroxicam?

A

50 hours

48
Q

What percentage of Piroxicam is bound to plasma protein?

A

99%

49
Q

What are the potential sites of action for Sulfasalazine? (4 points)

A

Inhibition of IL-1 and TNFalpha
Inhibition of lipoxygenase pathway
Scavenging of free radicals and oxidants
Inhibition of NF-kB.

50
Q

What is another salicylate that is used for ulcerative colitis, rheumatoid arthritis, and ankylosing spondylitis

A

Sulfasalazine

51
Q

What allows Sulfasalazine to be absorbed in the distal GI tract instead of upper GI tract?

A

Azo linkage between 5-ASA and Sulfapyridine prevents absorption. Colonic bacteria cleave this bond.

52
Q

What is the chemical profile of Sulfasalazine?

A

5-aminosalicylic acid (5-ASA) linked to Sulfapyridine by an azo bond.

53
Q

What is the active component of Sulfasalazine?

A

5-aminosalicylic acid

54
Q

What is the theoretical advantage of a selective COX2 inhibitor?

A

Anti-inflammatory effects without GI-side effects of other NSAIDS

55
Q

What seemingly unrelated allergy creates a contra-indication for Celecoxib?
Why?

A

Sulfa Allergy

Celecoxib contains a sulfonamide side chain

56
Q

What is the only approved COX 2 selective anti-inflammatory agent on the market?

A

Celecoxib (Celebrex)

57
Q
  1. What is the mechanism of action of Celecoxib?

2. What about the mechanism makes this COX-2 selective?

A
  1. Binds tightly to hydrophilic side pocket of COX-2
    This blocks the active site because of proximity.
  2. This particular binding site is not present on COX-1
58
Q

What is the time to peak concentration for oral Celecoxib?

A

3 hrs.

59
Q

What degree of plasma protein binding is present with Celecoxib?

A

High

60
Q

How is Celecoxib metabolized?

A

CYP2C9

61
Q

What are the contra-indications for use of Celecoxib? (6 items)

A
  1. Patients with sulfa allergy
  2. Prior NSAID hypersensitivity
  3. Pre-existing CV risk factors or disease
  4. Hx of GI bleeding
  5. Following CABG
  6. Deficiency of CYP2C9
62
Q

What are the therapeutic uses of Celecoxib? (4 items)

A
  1. Rheum. Arthritis and Osteoarthritis
  2. Primary dysmenorrhea
  3. Acute pain
  4. Colorectal polyps (COX-2 contributes to certain cancers)
63
Q

What non-NSAID is commonly associated with them but is actually a para-aminophenol derivative?

A

Acetaminophen

64
Q

Does Acetaminophen have any affinity for COX?

A

No

65
Q

What is the mechanism of action of Acetaminophen?

What ramification does this have on its usefulness?

A

Not fully understood but may prevent the reduction of COX to peroxidase form.
Cells or tissues with high levels of peroxide, life inflammatory sites, are resistant to the action of acetaminophen.

66
Q

What is the plasma half life of Acetaminophen?

A

2 hours

67
Q

How is Acetaminophen metabolized?

It undergoes mainly what metabolic process?

A

CYP2E1

Glucuronidation and Sulfation

68
Q

How is Acetaminophen excreted?

A

Renally

69
Q

What is the most serious adverse effect of Acetaminophen?

What is the mechanism for this?

A

Hepatic Toxicity

CYP2E1 converts APAP to NAPQI –> Glutathione gets depleted and cannot inactivate NAPQI–> build up is hepatotoxic

70
Q

When would one first see evidence of liver injury following APAP overdose?

A

24/36 hours

71
Q

What is the treatment for APAP overdose?

How does it work?

A

N-acetylcysteine

It replenishes glutathione stores.

72
Q

Why does alcohol use increase risk of liver damage by APAP? (2 items)

A
  1. ETOH induces CYP2E1

2. ETOH depletes glutathione

Owenpharm Block 2 (11 decks)

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