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CPT > NSAIDs & Opioids > Flashcards

NSAIDs & Opioids Flashcards

1
Q

How are prostaglandins, thromboxanes and leukotrienes produced?

A

From the eiconsaonid pathway.

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2
Q

Describe the eicosanoid pathway.

A

When tissues get damaged, inflammation produces phospholipase A2, which converts phospholipids in the membrane into arachidonic acid. COX enzymes (cyclooxygenase) then convert arachidonic acid into eiconsanoids.

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3
Q

What is the rate limiting enzyme in the eiconsanoid pathway?

A

Phospholipase A2

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4
Q

What is the difference between COX-1 and COX-2?

A

COX-1 is constantly expressed throughout the body and is responsible for normal gastric function, platelet aggregation and regulation of blood flow.
COX-2 is only expressed at sites of inflammation, mediates the inflammatory response.

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5
Q

What is the MOA of NSAIDs?

A

Inhibit COX enzymes by competing with arachidonic acid for the active site on COX enzymes - reduces production of prostanoids.

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6
Q

What are the 3 effects of NSAIDs?

A

Anti-inflammatory
Analgesic
Anti-pyretic

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7
Q

What are the 3 different types of NSAIDs?

A
  • selective COX-1 inhibitors
  • selective COX-2 inhibitors
  • non-selective COX inhibitors
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8
Q

How are NSAIDs metabolised?

A

Metabolised hepatically to inactive products (not prodrugs).

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9
Q

Name 3 selective COX-1 inhibitors.

A

Aspirin
Ibuprofen
Naproxen

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10
Q

Name a non-selective COX inhibitor.

A

Diclofenac

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11
Q

Name a selective COX-2 inhibitor.

A

Celecoxib

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12
Q

Which of the eicosanoids does COX-1 produce?

A

Thromboxane A2 (TXA2)

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13
Q

Which of the eicosanoids does COX-2 produce?

A

PGI-2

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14
Q

What is the MOA and effects of selective COX-1 inhibitors.

A

Inhibit COX-1 enzyme, decreasing production of TXA2 - causes vasodilation and reduced platelet aggregation.

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15
Q

What is the function of TXA2?

A

Platelet aggregation

Vasoconstriction

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16
Q

Name some side effects of COX-1 inhibitors.

A
  • prolonged bleeding due to reduced platelet aggregation

- high risk of GI ADRs e.g. GI bleeding, ulcers

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17
Q

What is the MOA and effects of selective COX-2 inhibitors?

A

Inhibit COX-2 enzyme, which reduces PGI-2 production, leads to increased vasoconstriction and platelet aggregation.

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18
Q

What are the effects of PGI2?

A

Vasodilation

Inhibits platelet aggregation

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19
Q

Name some side effects of COX-2 selective inhibitors.

A
  • GI ADRs (but less likely than COX-1 inhibitors)

- renal ADRs

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20
Q

Name some contraindications for NSAIDs.

A
  • decreased renal function - in someone who has decreased renal function, prostaglandins are a significant factor in maintaining blood flow. Use of NSAIDs could increase risk of kidney injury
  • cardiovascular disease
  • GI disease
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21
Q

What is the effect of NSAIDs on the kidney?

A

Inhibits prostaglandin-driven afferent arteriole vasodilation, leading to arterial wall thickening, narrowed lumen and reduced blood flow to kidney - risk of kidney injury.

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22
Q

Use of NSAIDs can decrease renin secretion if the kidney is damaged. What ECG changes may this cause?

A

Decreased renin means reduced aldosterone. Aldosterone causes Na+ reabsorption and K+ secretion, therefore there is less K+ secretion.

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23
Q

What is the effect of NSAIDs on the GI system?

A

Increased risk of GI bleeding, ulceration, dyspepsia, perforation and nausea because prostaglandins have an important role in mucous production and normal blood flow.

24
Q

What is the effect of NSAIDs on the cardiovascular system?

A
  • COX-1 inhibitors are protective as they reduce platelet aggregation
  • COX-2 inhibitors increase the risk of cardiovascular events due to increased vasoconstriction and platelet aggregation
25
Q

What is the effect of NSAIDs on ADH release?

A

Prostaglandins normally antagonise ADH release, therefore NSAIDs reduce ADH antagonism and lead to increased vasoconstriction.

26
Q

Aspirin has different effects depending on its dose, what are these effects?

A

Low dose - antiplatelet drug

Moderate and high doses - NSAID

27
Q

What is the effect of paracetamol?

A

Anti-pyretic

28
Q

How is a therapeutic dose of paracetamol metabolised?

A

Conjugated by glucoronide to a non-toxic metabolite that can be safely metabolised.

29
Q

What happens when a paracetamol overdose is taken?

A

Normal glucoronide pathway is saturated, so paracetomol is converted to NAPQI, which is toxic to hepatocytes. NAPQI is conjugated by glutathione and metabolised by the liver. Depletion of glutathione and excess NAPQI causes liver damage and necrosis.

30
Q

What is the antidote for paracetamol overdose?

A

Acetylcysteine - replenishes glutathione so that NAPQI can be safely metabolised. Needs to be given within 8 hours of overdose to be effective.

31
Q

What is nociception?

A

The body’s response to potentially harmful stimuli. Nociceptors are pain fibres that respond to potentially damaging stimuli e.g. Heat, cold, pressure, chemicals. When they become activated they send sensory impulses to the brain. The brain assesses the threat and if it perceives serious threat, it creates the sensation of pain and sends impulses to make you pull away. If it perceives low threat, it might make us reposition ourselves without paying attention, or we may not even notice anything.

32
Q

Out of nociception and pain, which can be modulated?

A

Pain can be modulated, nociception can’t.

33
Q

Describe the pain pathway.

A

Spinothalamic pathway is the ascending pathway - nociceptors are stimulated, substance P and glutamate released from 1st order neurone in the dorsal horn of grey matter, 2nd order neurone decussates, synapses with 3rd order neurone in thalamus and projects to post-central gyrus. Descending pathway inhibits/modulates ascending pathway.

34
Q

Name the 2 areas involved in pain modulation.

A

CNS - periaqueductal grey in the midbrain.

PNS - substantia gelatinosa in the dorsal horn of grey matter in the spinal cord.

35
Q

Explain the modulation of pain in the substantia gelatinosa.

A

Descending neurones inhibit the release of substance P from the 1st order neurone of spinothalamic pathway. Also stimulates an interneurone (opioid neurone) to release enkephalins, which also inhibit release of substance P.

36
Q

What are the 3 types of fibres in peripheral pain modulation?

A

A-delta fibres
C fibres
A-beta fibres

37
Q

What is the function of C fibres and A-delta fibres?

A

Inhibit substantia gelatinosa, inhibiting pain modulation.

38
Q

What is the function of A-beta fibres and when are they stimulated?

A

Stimulate the substantia gelatinosa, inhibiting pain - stimulated when rubbing skin - this is why rubbing something makes it feel better.

39
Q

How does the peri-aqueductal grey modulate pain?

A

Sends inhibitory signals down to the spinal cord which release serotonin and endogenous opioids such as enkephalins - this inhibits neurones of the spinothalamic pathway and prevents signals reaching the thalamus and cortex, reducing the pain.

40
Q

What is the MOA of opioids?

A

When an opioid binds to a receptor, it hyperpolarises the cell and decreases substance P release, decreasing the nociceptor response and decreasing pain.

41
Q

What are the 3 natural opioids in the body and what receptors do they bind to?

A

Enkephalins - bind to mu and delta receptors
Dynorphins - bind to kappa receptors
B-endorphins - bind to mu receptors

42
Q

Name some side effects of opioids.

A

-analgesia
-depression
-respiratory sedation
These effects occur because opioid receptors are found elsewhere throughout the body.

43
Q

Name the classes of opioids and give some examples.

A
  • strong agonists - morphine, fentanyl
  • moderate agonists - codeine
  • mixed agonist/antagonist - buprenorphine
  • partial agonist
  • antagonist - naloxone
44
Q

How can morphine affect a foetus?

A

It can cross the placenta, therefore baby can have respiratory sedation or withdrawal.

45
Q

How is morphine metabolised?

A

Renal - be cautious with patients with CKD or AKI.

46
Q

How can morphine be given?

A

PO, IV, IM, SC, PR - many routes.

47
Q

Name some side effects of morphine.

A
  • respiratory depression
  • emesis (stimulates CTZ)
  • constipation
  • histamine release due to mast cell degranulation
48
Q

What is the MOA of buprenorphine?

A

Has a very high affinity for mu receptors so will displace another opioid, but is a partial agonist so has lower efficacy. Also has antagonism at kappa receptors. Therefore can be used for opioid addiction treatment.

49
Q

How is buprenorphine metabolised?

A

Metabolised by the liver, therefore is safe in renal impairment.

50
Q

What is the MOA of naloxone?

A

Has a greater affinity for receptors than morphine, therefore displaces it. Is useful for overdose treatment. (Although affinity is less than buprenorphine so can’t displace it).

51
Q

Why do you get side effects with opioid withdrawal?

A

Addition of synthetic opioids increases the number of receptors. 50% receptors need to be bound to get a response, so the dose has to be increased to get the same response. With withdrawal, endogenous opioids cannot bind 50% of the receptors so there is no response - leads to side effects.

52
Q

What drug can be given to reduce opioid withdrawal side effects?

A

Methadone - reduce the dose slowly as the number of receptors decrease.

53
Q

Name some side effects of opioid overdose.

A
  • vomiting
  • constipation
  • hypotension
  • bradycardia
  • drowsiness
  • respiratory depression
54
Q

Name some contraindications for opioid use/considerations when dose needs to be altered?

A
  • renal impairment
  • pregnancy - babies can experience withdrawal effects as opioids can cross placenta
  • elderly
  • respiratory distress
55
Q

How are opioids used in palliative care?

A

Can be given to help ease pain and shortness of breath (as they also have slight respiratory depression).

CPT (24 decks)

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