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Year 2 MIS > Management of Musculoskeletal Pain and Inflammation > Flashcards

Management of Musculoskeletal Pain and Inflammation Flashcards

1
Q

What is the main mode of action of NSAIDs therapeutic effect?

1 - inhibition of COX-1
2 - inhibition of COX-2
3 - inhibition of COX-3
4 - inhibition of miu-opioid receptor
5 - Inhibition of transcriptions of inflammatory genes
A

2 - inhibition of COX-2

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2
Q

What is the main cause of NSAIDs gastric adverse reactions?

1 - Inhibition of COX-1
2 - Inhibition of COX-2
3 - Inhibition of COX-3
4 - Inhibition of miu-opioid receptor
5 - Inhibition of transcriptions of inflammatory genes
A

1 - Inhibition of COX-1

- COX-1 is helpful in producing gastric juice

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3
Q

What effect do prostaglandins have on the afferent arteriole (kidney/glomerulus)?

1 - No effect
2 - Occlusion
3 - Vasoconstriction
4 - Vasodilation
5 - Vasospasm
A

4 - Vasodilation

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4
Q

What are the 3 key core drugs we need to know that come under NSAID category?

1 - aspirin, atorvastatin, naproxen
2 - aspirin, paracetamol, naproxen
3 - aspirin, ibuprofen, naproxen
4 - paracetamol, ibuprofen, aspirin

A

3 - aspirin, ibuprofen, naproxen

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5
Q

Are paracetamols classed as an NSAIDs?

A
  • no
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6
Q

Which pathway are NSAIDs ultimately trying to inhibit?

A
  • cyclooxygenase pathway
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7
Q

Do NSAIDs mainly work centrally or peripherally?

A
  • peripherally reducing prostaglandins
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8
Q

In a direct response to prostaglandins there is an increased pain sensation at the nocioceptors. An influx of what 2 cations is the cause of this increased pain sensation?

1 - Mg+ and Ca2+
2 - Na+ and Cl-
3 - Na+ and K+
4 - Na+ and Ca2+

A

4 - Na+ and Ca2+

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9
Q

Aspirin has its affect through an irreversible binding. What is the mechanism of action or aspirin?

A
  • inhibits cyclooxygenase
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10
Q

What are the most common side effects of aspirins?

A
  • tinnitus
  • reyes syndrome (swelling in the liver and brain)
  • asthma
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11
Q

Out of COX-1 and COX-2, which is pro-inflammatory and which is protective and function and maintenance of tissues?

A
  • COX-I = protective and function and maintenance of tissues

- COX-II = pro-inflammatory

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12
Q

COX-I and COX-II has a number of adverse effects. What are the 3 key adverse effects of inhibiting COX-I and II?

A

1 - peptic ulcers
2 - renal failure
3 - fluid retention and heart failure

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13
Q

Prostaglandins can cause problems if there is too much as we seen in inflammatory conditions. What 2 positive effects to prostaglandin, specifically E2 and I2 have on the stomach?

A

1 - increased gastric acid secretion
2 - increased mucus production
- TOO MUCH NSAIDS WILL STOP BOTH OF THE ABOVE AND CAUSE PEPTIC ULCERS

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14
Q

What can be taken alongside chronic NSAIDs to reduce stomach symptoms?

A
  • proton pump inhibitors
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15
Q

How do NSAIDs lead to renal problems?

A
  • prostaglandins are vasodilators and increase afferent blood flow to kidneys
  • NSAIDs inhibit prostaglandins and reduce blood flow causing acute kidney disease
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16
Q

How can NSAIDs lead to water and Na+ retention?

A
  • reduced blood flow means reduced filtration of water and Na+
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17
Q

Selective COX-2 inhibitors all have what letters at the end of their names?

A
  • all end in coxib

- core drug is etoricoxib (binds and inhibits COX-II)

18
Q

What are the 3 main effects of NSAIDs?

A

1 - analgesic
2 - anti-inflammatory
3 - antipyretic

19
Q

What are the 3 key adverse events of selective COX-2 inhibitors?

A
  • fertility issues
  • CVD
  • prothrombin (inhibits clotting, whilst increasing blood flow)
20
Q

What is the main organ/system affected paracetamol toxicity?

1 - Brain
2 - Heart
3 - Kidney
4 - Liver
5 -Lungs
A

4 - Liver

21
Q

Paracetamol is directly toxic to the liver, and can lead to liver failure (hepatic necrosis) in overdose.

1 - True
2 - False

A
  • false

- paracetamol creates a compound and this is toxic, not paracetamol

22
Q

Does paracetamol perform the same 3 functions as NSAIDs?

A
  • no
  • only analgesic and antipyretic
  • NOT ANTI-INFLAMMATORY
23
Q

Does paracetamol work mainly on the central or peripheral nervous system?

A
  • centrally
24
Q

What organ metabolises paracetamol?

1 - heart
2 - liver
3 - kidney
4 - pancreas

A

2 - liver

25
Q

Paracetamol is metabolised in the liver and generally is excreted by the kidneys. However, there is a small portion of paracetamol that is metabolised by the enzyme cytochrome P450. This metabolism then leads to a very toxic compound called what?

1 - glucuronidation
2 - N-acetyl-p-benzoquinone imine (NAPQI)
3 - sulfation
4 - CYP450

A

2 - N-acetyl-p-benzoquinone imine (NAPQI)

26
Q

Paracetamol is metabolised in the liver and generally is excreted by the kidneys. However, there is a small portion of paracetamol that is metabolised by the enzyme cytochrome P450. This metabolism then leads to a very toxic compound called N-acetyl-p-benzoquinone imine or NAPQI. At normal levels of paracetamol there is an enzyme in the liver that is able to neutralise NAPQI. What is this enzyme called?

1 - glutathione
2 - phenyotoin
3 - sulfation
4 - CYP450

A

1 - glutathione

27
Q

Paracetamol is metabolised in the liver and generally is excreted by the kidneys. However, there is a small portion of paracetamol that is metabolised by the enzyme cytochrome P450. This metabolism then leads to a very toxic compound called N-acetyl-p-benzoquinone imine or NAPQI. At normal levels of paracetamol there is an enzyme in the liver that is able to neutralise NAPQI, called glutathione. What can happen if a patient takes too much paracetamol and how can this become toxic?

A
  • lots of paracetamol needs metabolising, meaning more NAPQI will be produced
  • hepatocytes are unable to produce sufficient glutathione to neutralise NAPQI
  • NAPQI then damages the liver and can cause liver failure
28
Q

Overdose of paracetamol leads to excessive levels of NAPQI in the liver, which is very toxic and can cause liver failure. What can patients be give to treat this?

1 - metformin
2 - atorvastatin
3 - antibiotic
4 - N-acetylcysteine (intravenously)

A
  • N-acetylcysteine (intravenously)

- precursor of glutathione, so will neutralise NAPQI

29
Q

What is the treatment for paracetamol overdose?

A
  • N-acetylcysteine (IV)

- glutathione precursor that neutralises NAPQI

30
Q

The therapeutic actions of corticosteroids are achieved in majority by which type of receptor?

1 - Cytoplasmic / Nuclear 
2 - Enzyme-linked receptor 
3 - G-protein coupled receptor
4 - Ionotropic 
5 - Tyrosine-kinase receptor
A

1 - Cytoplasmic / Nuclear

  • steroids can cross plasma membrane and enter cells
  • then bind with glucocorticoid receptor inside cell creating a complex
  • this complex can then enter nucleus and bind with DNA and change DNA transcription
31
Q

The main corticosteroids adverse reactions are predictable.

1 -True
2 - False

A

1 -True

- we know the effects and adverse effects of too much glucocorticoids so we can predict the drugs effects

32
Q

When prescribing corticosteroids for longer than a few days, is important to discuss with the patient a slow withdrawal of the drug.

1 - True
2 - False

A

1 - True

  • body could stop producing cortisol
  • can take a long time for the body to begin producing them again
33
Q

Corticosteroids given as medication mimic what in the body?

A
  • glucocorticoids
34
Q

What are the 4 core drugs corticosteroids?

A

1 - Methylprednisolone
2 - Prednisolone
3 - Hydrocortisone
4 - Beclometasone

35
Q

Mechanism of action of corticosteroids?

A
  • same effect that glucocorticoids have
  • down-regulate pro-inflammatory genes
  • able to inhibit phospholipase A2 and inhibit arachidonic acid, so also COX-I and II
36
Q

Why is abrupt removal of corticosteroids dangerous?

A
  • can take time for body to produce corticosteroids again so van be dangerous
37
Q

Immune cells are able to utilise an enzyme called phospholipase A2 and get it to act on membrane phospholipids in order to create a 20 carbon poly-unsaturated fatty acid called what?

1 - cyclooxygenase
2 - arachidonic acid
3 - C reactive protein
4 - lactate dehydrogenase

A

2 - arachidonic acid

38
Q

Immune cells are able to utilise an enzyme called phospholipase A2 and get it to act on membrane phospholipids in order to create a 20 carbon poly-unsaturated fatty acid called arachidonic acid (AA). The AA provides a substrate for cyclooxygenase. What 2 things can this then go on to create?

A
  • COX-I

- COX-II

39
Q

Immune cells are able to utilise an enzyme called phospholipase A2 and get it to act on membrane phospholipids in order to create a 20 carbon poly-unsaturated fatty acid called arachidonic acid (AA). The AA provides a substrate for cyclooxygenase. creating COX-I and II. COX-II and I can the produce 3 things, what are they?

1 - prostaglandins, TNF-a, prostacyclin
2 - prostaglandins, prostacyclin, thromboxane
3 - prostaglandins, IL-6, prostacyclin
4 - prostaglandins, thromboxane, IL-1

A

2 - prostaglandins, prostacyclin, thromboxane

40
Q

What do the terms inducible and constitutive refer to?

A
  • inducible = molecule needs to be activates (COX-II)

- constitutive = molecule is always switched on (COX-I)

Year 2 MIS (48 decks)

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