Brainscape's Knowledge GenomeTM

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


See full index

NUR1142 > Module 4 - NSAID + Acetaminophen > Flashcards

Module 4 - NSAID + Acetaminophen Flashcards

1
Q

What is the concern regarding aspirin use in infants?

A

Aspirin should be avoided in infants due to the risk of Reye syndrome.

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

What are safe options for managing fever in infants?

A

Acetaminophen and ibuprofen can be used safely in small doses to manage fever in infants.

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

Why is aspirin usage discouraged in children and adolescents?

A

Aspirin should be avoided in children and adolescents due to the risk of Reye syndrome.

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

What can be safely used to treat fever in children and adolescents?

A

Acetaminophen and ibuprofen can be safely used in small doses to treat fever in children and adolescents.

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

Why is the use of NSAIDs contraindicated in the third trimester of pregnancy?

A

NSAID use is contraindicated in the third trimester of pregnancy due to the risk of premature closure of the ductus arteriosus.

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

Are NSAIDs safe for breastfeeding women?

A

Generally, NSAIDs and acetaminophen are safe for use in breastfeeding mothers.

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

What is the most common class of drugs used to treat chronic pain in older adults?

A

NSAIDs are the most common drugs used to treat chronic pain in older adults.

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

What potential risks are associated with NSAID use in older adults?

A

NSAID use in older adults may increase hospital admissions and contribute to elevated blood pressure, precipitate congestive heart failure decompensation, and provoke renal failure. Caution should be exercised when using NSAIDs in this population.

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

What is the family of cyclooxygenase inhibitors composed of?

A

The family of cyclooxygenase inhibitors consists of aspirin and related drugs.

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

What are the three common effects of cyclooxygenase inhibitors?

A

Cyclooxygenase inhibitors can suppress inflammation, relieve pain, and reduce fever.

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

What unique protective effect does aspirin have compared to other cyclooxygenase inhibitors?

A

Aspirin can protect against myocardial infarction (MI) and stroke, which is not a property of other cyclooxygenase inhibitors.

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

What is the central mechanism by which cyclooxygenase inhibitors exert their effects?

A

The central mechanism is the inhibition of cyclooxygenase, the enzyme responsible for the synthesis of prostanoids (prostaglandins and related compounds).

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

What are the principal adverse effects associated with cyclooxygenase inhibitors?

A

The principal adverse effects include gastric ulceration, bleeding, and renal impairment.

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

Which adverse events are linked to the inhibition of cyclooxygenase and can occur with most cyclooxygenase inhibitors?

A

Myocardial infarction (MI) and stroke can occur with most cyclooxygenase inhibitors, except aspirin, and these events are also associated with cyclooxygenase inhibition.

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

What is the common mechanism of action for the drugs discussed here?

A

These drugs work by inhibiting cyclooxygenase (COX), an enzyme that converts arachidonic acid into prostanoids.

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

What is the role of COX at sites of tissue injury?

A

At sites of tissue injury, COX catalyzes the synthesis of prostaglandin E2 (PGE2) and prostacyclin (PGI2), promoting inflammation and pain sensitization.

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

How does COX function in the stomach, and what is its protective role there?

A

In the stomach, COX promotes the synthesis of PGE2 and PGI2, which protect the gastric mucosa by reducing gastric acid secretion, increasing bicarbonate/mucus secretion, and maintaining submucosal blood flow.

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

What is the function of COX in platelets, and what is the product of COX activity in platelets?

A

COX in platelets promotes the synthesis of thromboxane A2 (TXA2), which stimulates platelet aggregation.

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

What effect does COX have on blood vessels, and what compound does it generate there?

A

In blood vessels, COX promotes the synthesis of prostacyclin, which causes vasodilation.

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

How does COX activity in the kidney contribute to renal function?

A

COX in the kidney catalyzes the synthesis of PGE2 and PGI2, promoting vasodilation and maintaining renal blood flow.

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

hat role do COX-derived prostaglandins play in the brain?

A

COX-derived prostaglandins in the brain mediate fever and contribute to the perception of pain.

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

What is the function of COX-derived prostaglandins in the uterus?

A

COX-derived prostaglandins in the uterus help promote contractions, particularly at term.

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

Do prostaglandins, prostacyclin, and TXA2 act locally or affect distant sites in the body?

A

Prostaglandins, prostacyclin, and TXA2 act locally and do not affect sites distant from where they were made.

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

What are the two forms of cyclooxygenase, and what are their names?

A

The two forms of cyclooxygenase are cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2).

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

Where is COX-1 predominantly found, and what essential functions does it mediate?

A

COX-1 is found in almost all tissues and mediates important functions such as protecting the gastric mucosa, supporting renal function, and promoting platelet aggregation.

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

What is the primary role of COX-2, and where is it mainly produced?

A

COX-2 is primarily produced at sites of tissue injury and mediates inflammation while increasing sensitivity to painful stimuli.

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

Besides injury sites, where else is COX-2 present in the body?

A

: COX-2 is also found in the brain (mediating fever and pain perception), kidneys (supporting renal function), blood vessels (promoting vasodilation), and the colon (potentially contributing to colon cancer).

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

Why is COX-1 referred to as the “good COX” and COX-2 as the “bad COX”?

A

COX-1 is called the “good COX” because it primarily mediates beneficial processes, whereas COX-2 is the “bad COX” because it mainly mediates harmful processes.

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

Can you name some of the important functions associated with COX-1 and COX-2?

A

Can you name some of the important functions associated with COX-1 and COX-2?

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

What are the two major categories of cyclooxygenase inhibitors based on their properties?

A

Cyclooxygenase inhibitors are categorized into drugs with anti-inflammatory properties and drugs without anti-inflammatory properties.

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

What are some representative members of the first category (anti-inflammatory) of cyclooxygenase inhibitors?

A

Representative members of the anti-inflammatory category (NSAIDs) include aspirin, ibuprofen, naproxen, and celecoxib.

32
Q

Which drug belongs to the non-anti-inflammatory category of cyclooxygenase inhibitors?

A

Acetaminophen (Tylenol) is the drug in the non-anti-inflammatory category. It can reduce pain and fever but does not have anti-inflammatory properties.

33
Q

How are NSAIDs further subdivided, and what is the difference between first-generation and second-generation NSAIDs?

A

NSAIDs are subdivided into first-generation (conventional) and second-generation (selective COX-2 inhibitors) groups. The key difference is that first-generation NSAIDs inhibit both COX-1 and COX-2, while second-generation NSAIDs selectively inhibit COX-2.

34
Q

What potential serious side effects are associated with first-generation NSAIDs (conventional NSAIDs)?

A

First-generation NSAIDs can lead to serious side effects, including gastric ulceration, bleeding, and renal impairment.

35
Q

Why might second-generation NSAIDs (COX-2 inhibitors) be considered as having a potential advantage over first-generation NSAIDs in terms of safety?

A

Second-generation NSAIDs (COX-2 inhibitors) theoretically have an advantage because they selectively inhibit COX-2, which might allow them to suppress pain and inflammation with fewer adverse effects compared to first-generation NSAIDs.

36
Q

What is the safety concern associated with COX-2 inhibitors despite their selectivity for COX-2?

A

COX-2 inhibitors are associated with an increased risk of myocardial infarction (MI) and stroke, raising safety concerns despite their selectivity for COX-2.

37
Q

What do first-generation NSAIDs primarily inhibit in the body?

A

First-generation NSAIDs inhibit both COX-1 and COX-2 enzymes in the body.

38
Q

What are some common medical conditions that traditional NSAIDs are used to treat?

A

traditional NSAIDs are used to treat inflammatory conditions like rheumatoid arthritis, osteoarthritis, bursitis, manage mild to moderate pain, reduce fever, and alleviate dysmenorrhea (menstrual pain).

39
Q

Why is it challenging to use first-generation NSAIDs for inflammation control without posing risks?

A

First-generation NSAIDs cannot selectively inhibit COX-2 without also inhibiting COX-1, making it difficult to suppress inflammation without risking serious harm.

40
Q

What is a significant health concern associated with the use of first-generation NSAIDs?

A

The use of first-generation NSAIDs can lead to NSAID-induced ulcers, resulting in over 100,000 hospitalizations and 7,000 to 10,000 deaths annually.

41
Q

Which drug is considered the oldest member and prototype for the first-generation NSAIDs?

A

Aspirin is the oldest member and serves as the prototype for the first-generation NSAIDs.

42
Q

What are some of the valuable therapeutic properties of aspirin?

A

Aspirin provides excellent relief for mild to moderate pain, reduces fever, and offers protection against thrombotic disorders. It’s also a preferred choice for treating rheumatoid arthritis and other inflammatory conditions.

43
Q

What chemical family does aspirin belong to, and what is its chemical structure?

A

Aspirin belongs to the salicylates chemical family, with its chemical structure derived from salicylic acid. An acetyl group substitution on salicylic acid gives rise to aspirin, also known as acetylsalicylic acid (ASA).

44
Q

What is the mechanism of action of aspirin in inhibiting cyclooxygenase (COX)?

A

Aspirin is a nonselective inhibitor of cyclooxygenase. It primarily reduces inflammation, pain, and fever by inhibiting COX-2.

45
Q

What beneficial effect of aspirin results from inhibiting COX-1?

A

Protection against myocardial infarction (MI) and ischemic stroke results from inhibiting COX-1.

46
Q

What are the major adverse effects associated with aspirin use, and what is their cause?

A

The major adverse effects of aspirin include gastric ulceration, bleeding, and renal impairment, which result from inhibiting COX-1.

47
Q

How does aspirin’s irreversibility as a COX inhibitor differ from other NSAIDs?

A

Aspirin is an irreversible inhibitor of cyclooxygenase, while all other NSAIDs are reversible (competitive) inhibitors.

48
Q

What determines the duration of action of aspirin, and how does it compare to other NSAIDs?

A

The duration of action of aspirin depends on how quickly specific tissues can synthesize new COX-1 and COX-2 molecules. In contrast, the effects of other NSAIDs decline as drug levels decrease.

49
Q

Where is aspirin primarily absorbed when taken orally, and how does its absorption compare to rectal suppository administration?

A

Aspirin is rapidly and completely absorbed in the small intestine after oral dosing. Rectal suppository administration leads to slower absorption and lower blood levels compared to oral dosing.

50
Q

What is the reason behind aspirin’s short half-life, and what does it convert into rapidly?

A

Aspirin has a short half-life due to its rapid conversion to salicylic acid, an active metabolite.

51
Q

How does the inactivation rate of salicylic acid vary with its concentration in the body?

A

The rate of inactivation of salicylic acid depends on its concentration. At low therapeutic levels, it has a half-life of approximately 2 hours, but at high therapeutic levels, it may exceed 20 hours.

52
Q

What is the primary binding protein for salicylic acid in the blood, and what is the typical degree of binding at therapeutic levels?

A

Salicylic acid extensively binds to plasma albumin, typically between 80% and 90% at therapeutic levels.

53
Q

Which organs and fluids in the body does aspirin distribute to?

A

Aspirin is distributed to all body tissues and fluids, including breast milk, fetal tissues, and the central nervous system (CNS).

54
Q

What is the primary route of excretion for salicylic acid and its metabolites, and how does urinary pH affect excretion?

A

Salicylic acid and its metabolites are primarily excreted by the kidneys. Excretion is highly dependent on urinary pH, with an increase in pH from 6 to 8 leading to a fourfold increase in the rate of excretion.

55
Q

At what plasma salicylate levels do signs of salicylism (toxicity) begin to appear, and when does severe toxicity occur?

A

Signs of salicylism begin when plasma salicylate levels exceed 200 µg/mL, with severe toxicity occurring at levels above 400 µg/mL.

56
Q

In what situations does aspirin rarely cause serious adverse effects when administered in short-term doses?

A

Aspirin rarely causes serious adverse effects when administered in short-term analgesic or antipyretic (fever-reducing) doses.

57
Q

When is toxicity commonly observed with aspirin use?

A

Toxicity is common with aspirin use in cases of inflammatory disorders that require long-term high-dose treatment.

58
Q

What are some of the common gastrointestinal side effects associated with aspirin use, and how can they be reduced?

A

Common gastrointestinal side effects include gastric distress, heartburn, and nausea. These can be reduced by taking aspirin with food or a full glass of water.

59
Q

What is occult GI bleeding, and how does it relate to aspirin use?

A

Occult GI bleeding is the hidden or not easily detectable bleeding in the gastrointestinal tract. It occurs often with aspirin use but typically involves insignificant daily blood loss.

60
Q

What severe GI complications can long-term aspirin use, even at low doses, lead to?

A

Long-term aspirin use, even in low doses, can cause life-threatening gastric ulceration, perforation, and bleeding.

61
Q

What are the four causes of ulcers resulting from chronic aspirin use?

A

Ulcers from chronic aspirin use result from increased secretion of acid and pepsin, decreased production of cytoprotective mucus and bicarbonate, reduced submucosal blood flow, and the direct irritant action of aspirin on the gastric mucosa.

62
Q

What are the primary causes of aspirin-induced ulcers, and which enzyme inhibition is primarily responsible for them?

A

Aspirin-induced ulcers primarily occur due to the inhibition of COX-1 by aspirin.

63
Q

Why is direct injury to the stomach most likely with slow-dissolving aspirin preparations, and what happens as a result of this slow dissolution?

A

Slow-dissolving aspirin leads to particulate aspirin becoming entrapped in the folds of the stomach wall, causing prolonged exposure to high concentrations of the drug, which increases the risk of direct stomach injury.

64
Q

What complications can arise from asymptomatic aspirin-induced ulcers, and how does suppression of platelet aggregation contribute to these complications?

A

Asymptomatic aspirin-induced ulcers can lead to perforation and upper GI hemorrhage. Hemorrhage occurs partly due to erosion of the stomach wall and partly because aspirin suppresses platelet aggregation.

65
Q

What are some factors that increase the risk of developing aspirin-induced ulcers?

A

Factors that increase the risk of ulceration due to aspirin use include advanced age, a history of peptic ulcer disease, previous intolerance to aspirin or other NSAIDs, cigarette smoking, and a history of alcohol abuse (alcohol intensifies aspirin’s irritant effects and should be avoided).

66
Q

What is recommended for ulcer prophylaxis in patients at risk, according to expert panels from medical organizations?

A

Expert panels recommend prophylaxis with a proton pump inhibitor (PPI) for patients at risk of ulcers, including those with a history of peptic ulcers, glucocorticoid users, and older adults.

67
Q

How do PPIs like omeprazole and lansoprazole contribute to ulcer prevention?

A

PPIs reduce ulcer formation by suppressing the production of gastric acid.

68
Q

Besides PPIs, what are some other drugs that may be considered for ulcer prophylaxis?

A

Other drugs that may be considered include histamine-2 receptor antagonists (H2RAs) and misoprostol.

69
Q

Why might COX-2 inhibitors be considered as an alternative to traditional NSAIDs for some patients?

A

COX-2 inhibitors may be considered because they are thought to produce fewer gastrointestinal (GI) side effects compared to traditional NSAIDs.

70
Q

Why do expert panels recommend testing and treatment for Helicobacter pylori (H. pylori) infection in patients with ulcer histories before starting long-term aspirin use?

A

Many ulcers are caused by H. pylori infection, so testing and treatment for this bacterium are recommended to address the underlying cause of ulcers before initiating long-term aspirin use.

71
Q

How does aspirin promote bleeding, and how long can the effect of aspirin on bleeding time last?

A

Aspirin promotes bleeding by inhibiting platelet aggregation. The effect on bleeding time can last for about 1 week because platelets cannot replace aspirin-inactivated cyclooxygenase.

72
Q

Who should avoid taking aspirin due to its effects on bleeding, and what are some examples of bleeding disorders?

A

Patients with bleeding disorders, such as hemophilia, vitamin K deficiency, and hypoprothrombinemia, should avoid taking aspirin.

73
Q

What is the recommended action regarding high-dose aspirin before childbirth and elective surgery, and when should it be discontinued?

A

High-dose aspirin should be discontinued at least 1 week before childbirth and elective surgery to minimize blood loss.

74
Q

Is it necessary to stop aspirin before procedures with a low risk for bleeding, and can you provide examples of such procedures?

A

Aspirin does not need to be stopped before procedures with a low risk for bleeding, such as dental, dermatologic, or cataract surgery.

75
Q

What caution should be exercised when aspirin is used alongside anticoagulants?

A

Caution is needed when aspirin is used in conjunction with anticoagulants.

76
Q

How does high blood pressure affect the risk of hemorrhagic stroke in patients taking daily aspirin, and what blood pressure level is ideal before starting daily aspirin to reduce this risk?

A

NUR1142 (112 decks)

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