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Pharmacy stage 3 - pain > 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 (PG) made by cox-1 and 2 increase and decrease Na+ retention in response to changes in Cl- 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
18
Q

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

A

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

19
Q

what is the effect of aspirin on the GI system?

A

-inhibits COX-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 causes Reyes syndrome and dose dependent hepatitis

20
Q

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

A

it inhibits PG production hence prolonging gestation.

21
Q

why is paracetamol used?

A

no anti-inflammatory effect but has mild analgesic effects

22
Q

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

A

hepatotoxicity

23
Q

how does paracetamol cause analgesia?

A
  • works centrally and peripherally

- inhibits PG synthesis in inflamed tissues

24
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 prevent it from rising by preventing the increase in brain PGs.
25
Q

what role do brain PGs play in body temp?

A

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

26
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
27
Q

what is the disadvantage of COX-2 selective inhibitors?

A
  • associated with MI and stroke as they don’t inhibit platelet aggregation
  • potential toxicities in kidney therefore increased risk of thrombotic events
28
Q

what is the process of cell death called during inflammation?

A

apoptosis

29
Q

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

A

-signal macrophages to ‘clean up’ the dead cells from inflammation

30
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
31
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
32
Q

how do tricyclic antidepressants work in pain treatment?

A
  • e.g. amitryptiline
  • 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 - pain (6 decks)

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