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C. Year 3: Core Drugs > Analgesics - Non Selective NSAIDs and COX-2 Inhibitor > Flashcards

Analgesics - Non Selective NSAIDs and COX-2 Inhibitor Flashcards

1
Q

Which 2 of the following drugs are part of stage 1 of the analgesic ladder?

1 - codeine
2 - tramadol
3 - paracetamol
4 - NSAIDs

A

3 - paracetamol
4 - NSAIDs

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2
Q

Which 2 of the following drugs are part of stage 2 of the analgesic ladder?

1 - codeine
2 - tramadol
3 - paracetamol
4 - NSAIDs

A

1 - codeine
2 - tramadol

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3
Q

Which of the following is on stage 3 of the analgesic ladder?

1 - codeine
2 - morphine
3 - paracetamol
4 - NSAIDs

A

2 - morphine

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4
Q

NSAIDS have 3 properties: analgesic (pain-killing), anti-inflammatory and antipyretic (fever-reducing) properties. Which of the following is NOT classed as a NSAIDs?

1 - aspirin
2 - paracetamol
3 - ibuprofen
4 - diclofenac

A

2 - paracetamol

  • analgesic and antipyretic only
  • NOT anti-inflammatory
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5
Q

A 22-year-old man presents with complaints of ankle pain and swelling from a sports injury oneday prior. X-rays are negative for a fracture and he is directed to rest the joint and allow it to heal. Which drug will provide LESS benefit in alleviating pain and inflammation of the swollen joint?

A. Celecoxib
B. Naproxen
C. Diclofenac
D. Acetaminophen

A

D. Acetaminophen
- more commonly known as paracetamol

  • other 3 drugs are NSAIDS
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6
Q

A patient with which of the following conditions is the most appropriate candidate for use of acetaminophen to manage chronic pain associated with osteoarthritis?

A. Chronic malnutrition
B. Obesity
C. Alcoholism
D. Viral hepatitis

A

B. Obesity
- other conditions increase risk of acetaminophen (paracetamol) related hepatotoxicity.

  • acetaminophen depletes glutathione concentrations in the liver and NAPQI builds up.
  • low levels of glutathione are common in malnutrition, again increasing levels of NAPQI
  • alcoholism depletes endogenous glutathione
  • viral hepatitis damages the liver, and could reduce levels of glutathione
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7
Q

Among NSAIDs, aspirin is unique because it:

(A) Irreversibly inhibits its target enzyme
(B) Prevents episodes of gouty arthritis with long-term use
(C) Reduces fever
(D) Reduces the risk of colon cancer
(E) Selectively inhibits the COX-2 enzyme

A

(A) Irreversibly inhibits its target enzyme

  • non-selective irreversibly inhibition of cyclooxygenase 1 and 2
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8
Q

Which of the following is an analgesic and antipyretic drug that lacks an anti-inflammatory action?

(A) Acetaminophen
(B) Celecoxib
(C) Colchicine
(D) Indomethacin
(E) Probenecid

A

(A) Acetaminophen

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9
Q

An 18-month-old boy dies from an accidental overdose of acetaminophen. Which of the following is the most likely cause of this patient’s death?

(A) Arrhythmia
(B) Haemorrhagic stroke
(C) Liver failure
(D) Noncardiogenic pulmonary edema
(E) Ventilatory failure

A

(C) Liver failure

  • liver failure as a result of its conversion by hepatic cytochrome P450 enzymes to a highly reactive metabolite NAPQI
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10
Q

A 54-year-old woman presented with signs and symptoms consistent with an early stage of rheumatoid arthritis. The decision was made to initiate NSAID therapy. Which of the following patient characteristics is the most compelling reason for avoiding celecoxib in the treatment of her arthritis?

(A) History of alcohol abuse
(B) History of gout
(C) History of myocardial infarction
(D) History of osteoporosis
(E) History of peptic ulcer disease

A

(C) History of myocardial infarction

  • COX-2-selective inhibitor
  • increased risk of arterial thrombotic events.
  • history of MI would be a compelling reason to avoid a COX-2 inhibitor
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11
Q

Which of the following statements is correct regarding morphine?

1 - Morphine is the most lipophilic opioid.
2 - Morphine is metabolised through CYP2D6 and ­CYP3A4 and has numerous drug interactions.
3 - Morphine has active metabolites that can accumulate in renal impairment, leading to clinically relevant effects.
4 - Morphine can cause opioid-induced constipation upon initiation of opioid therapy, but tolerance occurs after 1 to 2weeks of opioid exposure.

A

3 - Morphine has active metabolites that can accumulate in renal impairment, leading to clinically relevant effects.

  • Morphine has two active metabolites M3G and M6G, which are renally eliminated.
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12
Q

Immune cells are able to use phospholipase A2 to take membrane phospholipids and make what?

1 - cyclooxygenase
2 - arachidonic acid
3 - linoleic acid
4 - adrenic acid

A

2 - arachidonic acid

  • this is the substrate for cyclooxygenase 1 and 2
  • COX-1 = constitutive enzyme (always active)
  • COX-2 = inducible enzyme (needs to be turned on to function)
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13
Q

COX-1 and COX-2 are able to create what 2 molecules that induce inflammation?

1 - prostaglandin E2
2 - arachidonic acid
3 - prostacyclin (PGI2)
4 - nitric oxide

A

1 - prostaglandin E2
3 - prostacyclin (PGI2)

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14
Q

Prostaglandin (PGE2) and prostacyclin (PGI2) are created by COX-1 and COX-2. Which of the following do PGE2 and PGI2 NOT do?

1 - induce vasodilation
2 - chemotaxis attracting immune cells
3 - increase sensitivity of neurons to pain
4 - induce apoptosis at site of injury
5 - stimulate hypothalamus, increasing temperature and causing fever

A

4 - induce apoptosis at site of injury

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15
Q

In addition to the effects of inflammation, what other effects does Prostaglandin (PGE2) also have?

1 - induces uterine contractions
2 - reduces HCL secretion in stomach
3 - increases mucous production in stomach
4 - all of the above

A

4 - all of the above

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16
Q
  • COX-1 is constitutive enzyme (always active) and COX-2 = inducible enzyme (needs to be turned on to function). Typically, is COX-1 or COX-2 bad?
17
Q

The prostaglandins that are produced by COX-1 have good properties as well, such as inducing uterine contractions, reducing HCL secretion and increasing mucous production in stomach. What affect do prostaglandin have on the renal function?

1 - dilates the efferent arteries
2 - dilates the afferent arteries
3 - constricts the efferent arteries
4 - constricts the afferent arteries

A

2 - dilates the afferent arteries

  • this increases eGFR
  • inhibition of COX can therefore affect eGFR
18
Q

Which of the following is NOT a core non-selective-NSAID?

1 - Naproxen
2 - Ibuprofen
3 - Etoricoxib
4 - Diclofenac
5 - Aspirin

A

3 - Etoricoxib

  • this is the selective COX-2 inhibitor
19
Q

What is the mechanism of action of all NSAIDS?

1 - non-selective inhibition of COX-1 and COX-2
2 - elective inhibition of COX-2
3 - selective inhibition of COX-1
4 - nonselective inhibition of arachidonic acid

A

1 - non-selective inhibition of COX-1 and COX-2

  • COX-2 inhibitor Etoricoxib is specific to just COX-2
20
Q

NSAIDS are level 1 of the analgesic ladder. Which of the following are NSAIDS indicated in?

1 - mild to moderate pain (1-3)
2 - RA (chronic)
3 - gout
4 - osteoarthritis (chronic)
5 - all of the above

A

5 - all of the above

21
Q

All of the following are adverse events of NSAIDS, but which of these is the rarest?

1 - GI toxicity
2 - peptic ulcers
3 - renal impairment
4 - major adverse cardiovascular event (MACE)
5 - hypersensitivity
6 - fluid retention

A

4 - major adverse cardiovascular event (MACE)

  • MI and/or strokes
22
Q

Do non-selective NSAIDS or COX-2 inhibitors cause more GIT toxicity?

A
  • non-selective NSAIDS
23
Q

Do non-selective NSAIDS or COX-2 inhibitors increase the risk of cardiovascular events more?

A
  • COX-2 inhibitors
  • increase the risk of thromboembolism
24
Q

NSAIDS are contraindicated in all of the following EXCEPT which one?

1 - severe renal impairment
2 - heart failure
3 - liver failure
4 - peptic ulcer disease
5 - NSAID hypersensitivity

A

4 - peptic ulcer disease

  • not contraindicated, but should be used with caution
25
Q

NSAIDS should be used with caution in all of the following EXCEPT which one?

1 - cardiovascular disease
2 - gout
3 - renal impairment
4 - peptic ulcer disease

26
Q

The use of NSAIDs impairs the effectiveness of which class of drug?

1 - loop diuretics
2 - ACE-I or ARB-II
3 - nitrates
4 - vasodilators

A

2 - ACE-I or ARB-II

  • induce renal impairment
27
Q

Glucocorticoids combined with NSAIDS increases the risk of what?

1 - GI bleeds
2 - peptic ulceration
3 - renal impairment
4 - cardiogenic shock

A

2 - peptic ulceration

28
Q

Anticoagulants (DOACs and Warfarin) and SSRIs combined with NSAIDS increases the risk of what?

1 - GI bleeds
2 - peptic ulceration
3 - renal impairment
4 - cardiogenic shock

A

1 - GI bleeds

29
Q

ACE-I and ARB-II combined with NSAIDS increases the risk of what?

1 - GI bleeds
2 - peptic ulceration
3 - renal impairment
4 - cardiogenic shock

A

3 - renal impairment

30
Q

The dosage and type of NSAID administered depends on the patients symptoms and medical history. How can NSAIDS be administered?

1 - oral
2 - gel suppository
3 - injectable preparations
4 - all of the above

A

4 - all of the above

  • when taken orally, it should be with food
31
Q

In acute pain, typically how long should patients be taking NSAIDS?

1 - 3 days
2 - 10 days
3 - 2 weeks
4 - 4 weeks

A

2 - 10 days

32
Q

To reduce the GI effects, what is often prescribed alongside an NSAID?

1 - laxative
2 - PPI
3 - anti-emetic
4 - antipropulsives

A

2 - PPI

  • this is commonly Lansoprazole
33
Q

Do non-selective NSAIDS or COX-2 inhibitors cause more GIT toxicity?

A
  • non-selective NSAIDS

C. Year 3: Core Drugs (125 decks)

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