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Pharmacy Stage 3 > Pharmacology of Pain: Non-opioids > Flashcards

Pharmacology of Pain: Non-opioids Flashcards

1
Q

what is the classification of anti-inflammatory drugs?

A
  1. NSAIDS (antipyretic and anti-inflammatory drugs)
  2. steroid anti-inflammatory drugs
  3. 5-LOX inhibitors and Leukotriene receptor antagonist
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2
Q

what are prostaglandins synthesised from?

A

arachidonic acid

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3
Q

what do prostaglandins cause?

A
  1. smooth muscle contraction
  2. inhibition of platelet aggregation
  3. bronchoconstriction
  4. vasodilation
  5. Fever
  6. diuresis
  7. immunomodulation
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4
Q

what does thromboxane cause?

A
  1. vasoconstriction

2. platelet activation

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5
Q

what are common pharmacological effects of NSAIDS?

A
  1. Analgesic (CNS and peripheral effect) may involve non-PG related effects.
  2. Antipyretic (CNS effect).
  3. Anti-inflammatory (except acetaminophen) due mainly to PG inhibition.
  4. Inhibit activation, aggregation, adhesion
    of neutrophils & release of lysosomal enzymes.
  5. Uricosuric - uric acid in urine
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6
Q

what are common Adverse Effects of NSAIDS?

A
  1. platelet dysfunction
  2. Gastritis and peptic ulceration
  3. renal failure
  4. Na+ and H20 retention and edema
  5. analgesic nephropathy
  6. prolonged gestation and inhibition of labor
  7. hypersensitivity
  8. GI bleed and perforation
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7
Q

what effect do NSAIDs have when they inhibit cox-1 ?

A

-cause GI toxicity

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8
Q

what effect do NSAIDs have when they inhibit cox-2?

A

anti-inflammatory actions

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9
Q

give 3 examples of cox 2 selective inhibitors

A

celecoxib
etoricoxib
valdecoxib

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10
Q

what is the issue with cox 2 selective drugs?

A

-no cardio protection and increased MI

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11
Q

what is the effect of the uncoupling phosphorylation of aspirin on respiration?

A
  • increases CO2

- stimulates respiration

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12
Q

what effect does aspirin have on the direct stimulation of the respiratory centre?

A
  • can cause hyperventilation
  • respiratory alkalosis
  • renal compensation
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13
Q

what happens when aspirin depresses the respiratory and cardiovascular centres?

A
  • lower BP
  • respiratory acidosis
  • no compensation
  • metabolic acidosis
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14
Q

what is the metabolic effect of aspirin?

A
  1. uncoupling of oxidative phosphorylation due to increased CO2 production - resulting in hyperventilation.
  2. hyperglycemia and depletion of muscle and hepatic glycogen
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15
Q

why can’t you give children under 12 years old aspirin?

A

as their kidneys may not be well developed enough to metabolise and clear the aspirin which can cause toxicity.

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16
Q

what is the effect of aspirin on platelets?

A
  • irreversibly inhibits platelet cox-1 derived TxA2 hence increasing bleeding time by inhibiting platelet aggregation.
  • COX-2 derived PGI2 inhibit platelet aggregation
  • so basically aspirin only works on the thromboxane part to inhibit platelet aggregation as prostaglandins already inhibit platelet aggregation themselves.
17
Q

Explain how aspirin affects renal activity?

A
  1. prostaglandins made by COX-1 and 2 increase and decrease Na+ retention in response to changes in CI- extracellular tonicity or low BP
  2. aspirin (NSAIDs) promote Na+ retention whcih increases BP, this counteracts the effect of anti-hypertensives
  3. PGs are important when the kidney is comprised- making one at risk of renal ischemia
18
Q

what is the role of PGs, generated by COX-1 in the GI system

A

1) inhibit secretion acid secretion
2) stimulate mucus and HCO3- secretion, vasodilation and therefore
3) are cytoprotective for gastric mucosa

19
Q

what is the effect of aspirin on the GI system

A
  • inhibits COZ-1 hence producing opposite effects to COX-1:
  • gastric distress
  • gastric bleeding
  • acute haemorrhage all due to increased acid secretion, and reduced mucus production to protect the gastric lining.
  • this cuases Reyes syndrome and dose dependent hepattis
20
Q

Explain how aspirin affects renal activity?

A
  1. prostaglandins made by cox-1 and 2 increase and decrease Na+ retention in response to changes in CI- extracellular tonicity or low BP
  2. aspirin (NSAIDs) promote Na+ retention which can increase BP, this counteracts the effect of anti-hypertensives
  3. PGs are important when the kidney is compromised- making one at risk of renal ischemia
21
Q

what is the role of PGs, generated by COX-1, in the GI system?

A

1) inhbiit stomach acid secretion
2) stimulate mucus and HCO3- secretion; vasodilation and therefore
3) are cytoprotective for the gastric mucosa

22
Q

what is the effect of aspirin on the GI system?

A
  • inhibits COX-1 hence producing opposite effects to COX-1:
    1. gastric distress
    2. gastric bleeding
  • acute haemorrhage all due to increased acid secretion and reduced mucus production to protect the gastric lining
  • this cuases reyes syndrome and dose dependent hepatitis
23
Q

what is the effect of NSAID inhbiition of PGs generated by COX-2 on labor and delivery

A

it inhbiits PG production hence prolonging gestation

24
Q

why is paracetamol used?

A

no anti-inflammatory effect but has mild analgesic effects

25
Q

what is the result of high paracetamol doses in the body?

A

hepatotoxicity

26
Q

how does paracetamol cause analgesia?

A

works centrally and peripherally

inhibits PG synthesis in inflamed tissues

27
Q

what effect do NSAIDs have on decreasing body temperature?

A

none as temperature change is more to do with hypothalamic problems so NSAIDs don’t decrease body temp
but they do prevent it from rising preventing increase in brain PGs

28
Q

what role do brain PGs play in body temp?

A

as IL-1 release increases from the leukocytes they act on hypothalamus which increases body temp. this is associated wirh brain PGs

29
Q

what is the advantage of COX-2 selective inhibitors?

A

anti-inflammatory response with less adverse effects especially those associated with the GI system
can have a role in cancer prevention and Alzheimers disease

30
Q

what is the disadvantage of COX-2 selective inhbitors

A

associated with MI and stroke as they don’t inhbit platelet aggregation
potential toxicities in kidney therefore increased risk of thrombotic events

31
Q

what is the process of cell death called during inflammation?

A

apoptosis

32
Q

what is the role of Lipoxins as anti-inflammatory mediators?

A

signal macrophages to clean up dead cells from inflammation

33
Q

give an example of an anticonvulsant and its role in pain?

A

carbamazepine
used for trigeminal neuralgia more specifically but not good for neuropathic pain
na+ channel blocker
others anticonvulsants are used for migraines

34
Q

give an example of an anti-epileptic and its role in pain?

A

gabapentin and pregabalin
used for diabetic neuropathy, fibromyalgia and postherpetic neuralgia
act on alpha-beta subunit of the voltage gated Ca2+ channel

35
Q

how do tricyclic antidepressants work in pain treatment?

A

e.g. amitryptilline
work to increase serotonin levels hence engaging the descending pain inhibitory circuit
may also inhibit voltage-gated Na+ channels and NMDA receptors
used for neuropathic pain, diabetic neuropathy, facial pain and sometimes migraines

Pharmacy Stage 3 (51 decks)

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