Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHARM > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

What does NSAIDS stand for?

A

Non-steroidal anti-inflammatory drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Major mediators of inflammation, fever, and pain:

A

prostaglandins (PGs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PGs (prostaglandins) act on multiple types and subtypes of:

A

GPCRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

There are no good receptor antagonists to inhibit GPCRs, so what kind of drugs do we use?

A

We use drugs that inhibit their SYNTHESIS instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PGs are synthesized from arachidonic acid (AA) by:

A

cyclo-oxygenase enzymes (COXs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T/F. NSAIDs mediate their therapeutic effects by inhibiting the COX enzymes that generate PGs.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Because they decrease PG synthesis by COX enzymes, NSAIDs are:

A

anti-inflammatory, anti-pyretic, analgesic (inflammation, fever, pain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T/F. NSAIDs are steroidal anti-inflammatory drugs.

A

FALSE, NSAIDs are NON-steroidal, as opposed to anti-inflammatory steroids (GCs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do Gas inhibit COXs and PGs?

A

by regulating COX expression, not activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Another name for NSAIDs:

A

non-opioid analgesics (to contrast them with morphine and related opioid analgesics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Opioids are required for what?

A

Relieving strong sharp pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Are NSAIDs more or less powerful than opioids?

A

Less powerful, but adequate for mild pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What side effects do opioids have?

A

Sedation, respiratory depression, and tolerance and dependence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F. PGs are made by many/most cell types and many/most cell types respond to PGs.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In some of these cells, what is the desired therapeutic targets for NSAIDs?

A

COXs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why do side effects occur?

A

Due to NSAID inhibition of COXs and PG synthesis and/or actions in various other call types

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where/how are PGs synthesized?

A

DE NOVO and immediately released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is COX a good drug target to block PG synthesis?

A

COX activity is a rate-limiting step in PG synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name for inflammation mediators:

A

thromboxanes (TXs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are precursors to all PGs and TXs?

A

convert arachidonic acid (AA) to PG-G2 and PG-H2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why are there multiple COX isozymes?

A

critical for PG functions and for NSAID actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T/F. COX-1 and COX-2 are constitutively expressed.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

COX-1 roles in CNS, stomach, and platelets:

A

CNS: mediated fever and pain
Stomach: protects mucosal lining
Platelets: increases platelet aggregation and blood clotting (by altering thromboxanes, TXs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

COX-2 roles in CNS, stomach, and endothelial cells:

A

CNS: mediate SOME pain
Stomach: protects mucosal lining with COX-1
Endothelial cells: decreases platelet aggregation (by altering prostacyclin, PGIs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

COX-2 is an inducible isozyme that is critical for _____.

A

Inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the key target for NSAID anti-inflammatory effects?

A

COX-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Most NSAIDs inhibit both COX-1 and COX-2, but usually stronger on ________ making them useful for treating ________.

A

COX-1; pain (COX-1 and constitutive COX-2) and fever (COX-1).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What type of NSAIDs are selective for COX-2 compared to COX-1 and what are they used for?

A

celecoxib; used to treat inflammation and sometimes pain, with fewer unwanted COX-1 related adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What drug is the critical prototype of all of the NSAIDS and non-opioid analgesics?

A

Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Aspirin is ASA. What does ASA stand for?

A

Acetyl-salicylic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Aspirin starts as ASA but then what:

A

rapidly hydrolyzed (de-acetylated) and becomes salicylic acid (or salicylate ion).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

T/F. Salicylates, including the salicylate from aspirin, are irreversible and competitive COX inhibitors.

A

FALSE. salicylates ARE REVERSIBLE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which effects of aspirin are mediated by its salicylate metabolite?

A

the anti-inflammatory and analgesic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the standard oral dose of aspirin?

A

325 mg.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Aspiring has drug interactions due to displacing with which drugs?

A

warfarin, methotrexate, sulfonamides, others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

In regards to pharmacokinetics, what is the mechanism by which aspirin works?

A

salicylate metabolism and elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

At low to moderate doses, salicylate is what?

A

metabolized in the liver by conjugation; first-order kinetics and saturable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

At higher doses, salicylate is what?

A

excreted unmetabolized by kidneys; zero-order kinetics, half life increases with increasing dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

T/F. Higher doses that saturate the liver metabolism and exceed renal elimination are required for sufficient accumulation to achieve therapeutic levels for COX-2 inhibition and anti-inflammatory effect.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

T/F. Lower doses suffice for COX-1 mediated analogies and anti-pyretic effects.

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Would you use a low or high dose for analgesic and antipyretic?

A

low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Would you use a low or high dose for anti-inflammatory doses

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Low or high doses are associated with conjugation n live, first order kinetics, and saturable?

A

low

44
Q

Low or high doses are associated with excretion in the kidney, half life increases, and zero order kinetics?

A

high

45
Q

What are the beneficial effects and uses for aspirin?

A

Analgesia (pain of inflammation) (650-1000 mg/4) hr, antipyresis (decrease fever) (works on hypothalamus)(650-1000 mg/4 hr), anti-inflammatory effects (COX2 effect that requires high dose)(1200 mg or more/ 4 hr)

46
Q

What are miscellaneous effects and uses aspirin is used for?

A

reducing GI cancer risk: many cancers ahem elevated COX2

Alzheimer’s disease: possible benefit

47
Q

Adverse effects of salicylate:

A

GI irration: gastric irritation, GI bleeding, gastric ulceration and hemorrhage
GI Hemmorrhage is responsible for 16,000 aspirin related deaths in US each year! (most significant limitation in use of these drugs)

48
Q

How is GI irritation lessened?

A

using enteric coasted tablets: prevent tablet from dissolving in stomach and damaging GI mucosa, absorption from intestine instead

49
Q

T/F. There is some dilution of peripheral vessels by large doses of salicylate.

A

TRUE

50
Q

How can you avoid Reye’s syndrome?

A

aspiring should not be used in children <16, stopping aspiring use in children has nearly eliminated occurrence of Reye’s syndrome, we give Tylenol to babies rather than aspirin

51
Q

What effects can salicylate have on baby maturation?

A

can cause premature closure of duct arterioles, all NSAIDs can potentially cause premature closure, some NSAIDs are used to promote closure

52
Q

Term used for MILD toxicity of salicylate:

A

salicylism

53
Q

Salicyism usually occurs in what population and what are side effects?

A

Typically excess chronic use in older adults; ringing in ears (tinnitus), dizziness, headache, confusion, deafness, drowsiness, thirst, nausea, vomiting

54
Q

Overdose toxicity od salicylate usually occurs when how much is taken?

A

5-30 grams

55
Q

How does overdose usually occur?

A

typically children ingesting large doses acutely (15-100 tablets; >150 tablets is lethal)

56
Q

Symptoms of overdose:

A

decrease blood flow, respiratory depression, GI disturbances, CNS disturbances, respiratory failure is eventual cause of death

57
Q

Treatment of salicylate overdose:

A

activated charcoal, sodium bicarbonate (salicylic acid pka=3, ion trapping of salicylate in urine by alkalinizing), monitor blood levels of salicylate, monitor urine pH, provide supplemental glucose and potassium; hemodialysis may be required

58
Q

Equation to known for treating salicylate overdose (regards pka and ph):

A

pKa-pH = protonated/unprotanated; OR: Ka = [H+][A-]/[AH]

59
Q

One unique us of aspirin only:

A

to prevent thrombus formation (blood clotting) and prolong bleeding time

60
Q

How is aspiring different from other salicylate and NSAIDS:

A

irreversibly inactivate COXs in some tissues
by covalently acetylating the enzyme: reversible binding of salicylate to COXs can inhibit them reversibly
covalent acetylation of COXs can inhibit them also, but irreversibly

61
Q

Why are platelets an important target for aspirin?

A

Platelets near site of GI absorption are the main cells exposed to acetyl-salicylic acid and covalent acetylation of COXs

62
Q

Besides pain, fever, and antiinflmmation, what can aspirin also be used for?

A

prevent/reduce risk of MI and stroke; other salicylates do not share this action, this is an acetyl effect

63
Q

T/F. Platelets are the main cells with acetylated COX.

A

TRUE

64
Q

T/F. Anti-inflammatory actions of aspirin are mediated by its salicylate metabolite, after it has lost its acetyl group.

A

TRUE

65
Q

Platelets use COX-1 to make:

A

Thromboxanes (TXs); that increase clotting and thrombosis risk

66
Q

Endothelial cells use COX-2 to make:

A

prostacyclin (PGIs); that decrease clotting and thrombosis risk

67
Q

Low aspiring doses only inhibit COX-1, shifting balance to more anti-thrombotic PGIs formation from endothelial cells.

A

TRUE

68
Q

Prolonged inhibition of platelet COX-1 causes sustained reduction in TXs.

A

TRUE

69
Q

Aspirin dose for thrombosis prevention:

A

75-81 mg/day

70
Q

Aspiring contraindicated in those with:

A

clotting deficiency

71
Q

Examples of PROpionic acid derivates:

A

Ibuprofen and Naproxen

72
Q

Difference of ibuprofen and naproxen from aspirin:

A

less toxic, fewer side effects, ONLY reversible and competitive; prolong bleeding time

73
Q

Ibuprofen and naproxen have specific approval for:

A

dysmenorrhea (menstrual cramps); pain and cramps mediated by PGs

74
Q

Ibuprofen 98% binds:

A

very heavily to albumin, can displace warfarin

75
Q

All propionic acid derivates show cross-sensitivity with salicylate; because of this what should you not do?

A

don’t use in patients with aspirin allergy or with aspirin-sensitive asthma

76
Q

T/F. Only some NSAIDs can cause renal toxicity/failure.

A

FALSE, ALL NSAIDs can cause renal toxicity/failure

77
Q

How should toxicity be treated in propionic acid derivatives?

A

activated charcoal in first 2 hours

78
Q

When is urine alkalization effective vs. not effective?

A

NOT effective in ibuprofen, naproxen and other propionic acid derivates (because so much of drug is protein bound). IS effective for aspirin.

79
Q

Doses for Ibuprofen:

A

200 mg (analgesia and antipyresis), 400 mg (anti-inflammatory)

80
Q

What is ibuprofen specifically approved for?

A

patent ductus arteriosus

81
Q

Doses for naproxen:

A

200-250 mg twice a day; enteric-coated delayed-release.

82
Q

What is naproxen specifically approved for?

A

gout and for migraine specifically

83
Q

Acetic acid derivates:

A

IndomethACin, diclofenAC, ketorolAC

84
Q

Is Indomethacin more or less potent than aspirin? How much more or less?

A

10-20x MORE potent than aspiring (works in lower doses)

85
Q

What is the dose for indomethacin?

A

25 mg / 4-6 hours.

86
Q

When is indomethacin mainly used?

A

in severe inflammation: rheumatoid arthritis, gouty arthritis (use cautiously)

87
Q

CeleCOXib is an example of what?

A

selective COX-2 inhibitor

88
Q

Celecoxib is great for what?

A

inhibiting COX-2; treat inflammation without serious adverse effects

89
Q

Dose of Celecoxib:

A

100-200 mg two days a day, oral, rapidly absorbed, metabolized by liver

90
Q

Approved uses for Celecoxib:

A

(for all “itis”): osteoarthritis, rheumatoid arthritis, relief of acute pain, primary dysmenorrhea

91
Q

How does Celecoxib compare to naproxen?

A

Celecoxib is equal to naproxen for osteoarthritis and rheumatoid arthritis, but is is poorer than naproxen for acute pain

92
Q

T/F. Celecoxib has fewer problems for asthmatics than aspirin and other NSAIDs.

A

TRUE

93
Q

Drug interactions of Celecoxib:

A

metabolized by CYP 2C9, may inhibit CYP 2D6 in some patients, can slow metabolism of tricyclic and SSRI anti-depressants, anti-arrythmics

94
Q

What is the most adverse effects of celecoxib?

A

edema, GI problems (less than with ibuprofen and naproxen), increased risk of MI (COX2 inhibits platelet aggregation in endothelial cells)

95
Q

T/F. Celecoxib is an example of a more selective drug causing new problems, even as they solve older problems.

A

TRUE.

96
Q

T/F. Now black-box warnings for MI risk can be found on ALL NSAIDs, not just Celecoxib.

A

TRUE, because all can inhibit COX2

97
Q

A drug that is a non-opioid analgesia like NSAIDs, but NOT an NSAID:

A

acetaminophen

98
Q

Do we know how acetaminophen works?

A

NO! we do not know mechanism; we THINK inhibition of COXs and PG synthesis.

99
Q

T/F. Acetaminophen has anti-inflammatory effects.

A

FALSE, it does NOT have anti-inflammatory effects

100
Q

Dose for acetaminophen:

A

325 mg, oral tablet

101
Q

Reasons to pick acetaminophen over aspirin:

A

no GI effects of concern, no hematologic effects, no CV effects or concerns, no respiratory effects or concerns, no effects on acid-base balance, no association with Reye’s syndrome; but NO anti-inflammatory effects :(

102
Q

Major adverse effects and concerns:

A

hepatic damage/liver damage with long-term persistent use, don’t drink with alcohol, limit dose when taking with opioids and other analgesics, skin rash, drug fever, NEPHRO-toxicity

103
Q

Overdose toxicity dose of acetaminophen:

A

10-25 g

104
Q

overdose reactions to acetaminophen:

A

hepatotoxicity; jaundice, usually reversible, but hepatic coma and death can occur

105
Q

What causes the hepatic toxicity from acetaminophen overdose?

A

a reactive electrophile: NAPZQI (N-acetyl-p-benzo-quinone-amine)

106
Q

Treatment of overdose toxicity of acetaminophen:

A

after 4 hr, treat with reactive sulfhydryl reagents (N-acetyl-cysteine): Acetadote to reverse toxicity by restoring endogenous glutathione.

107
Q

What drug should you use to reverse overdose toxicity of acetaminophen?

A

n-acetyl-cysteine (acetadote)

PHARM (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions