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Pharmacology > Analgesia > Flashcards

Analgesia Flashcards

1
Q

NSAIDs mechanism of action

A

Prevent breakdown of arachadonic acid and synthesis of prostaglandins by inhibiting COX enzymes.

COX-1 in found in all tissue and COX-2 is induced in inflammation. NSAIDs inhibit both. Produces analgesia, anti-inflammatory action and antipyretic action.

Can be irreversible: aspirin

Competitive: ibuprofen

Reversible: paracetamol

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2
Q

Describe the analgesic effect of NSAIDs

A

Analgesic effect produced by inhibition of prostaglandins at the site of pain and inflammation. Largely a peripheral effect.

Prostaglandins sensitise nocicepors to bradykinin, histamine and 5HT (inflammatory mediators) which amplify the pain signal.

Prostaglandins in the CNS act on prostanoid receptors to increase activity of VG-Na+ channels increasing sensitivity to pain signals.

Inhibting prostaglandin production reduces the effect.

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3
Q

Why can NSAIDs be used as an anti-inflammatory?

A

Prostaglandins produce increased vasodilation, vascualar permeability and oedema in an inflammatory reaction.

Inhibiton of prostaglandin synthesis therefore reduces this.

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4
Q

Name 3 classes of NSAIDS

A

Salicylic acid: aspirin

Propionic acid: ibuprofen

Acetic acid: indometacin

Fenemates: Mefenamic acid

para-aminophenols: paracetamol

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5
Q

Adverse effects of NSAIDs

A

GI: nausea, dyspepsia, vomiting, ulcer formation. PGs normally inhibit acid secretion and promote gastric mucus production.

CV incidents: causes thrombosis

Tinnitus

Renal: damage and nephrotoxicity. PGs cause vasodilation in the renal medulla and glomeruli to control renal blood flow and excretion of salt and water. Reduced renal blood flow may result in renal failure.

Hypersensitivity: Bronchospasm, rash,

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6
Q

Name 3 endogenous opiods

A

enkephalin

endorphin

endomorphin

dynorphin

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7
Q

Downstream effects of opiod receptor activation

A

Activation of receptors by opiods results in:

inhibiton of adenylate cyclase, therefore reduced CAMP

Inhibiton of VG-Ca2+ channel opening

K+ channel activation, causing hyperpolarisation

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8
Q

Clinical effects of NSAIDs

A

Anit-inflammation

Anti-pyretic

Analgesic (Ibuprofen)

Anti-coagulant (Aspirin)

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9
Q

Drug interactions of NSAIDs

A

Increased risk of bleeding with SSRIs

Increased risk of nephrotoxicity with ACEi and diuretics

Enhances effects of other anti-coagulant drugs

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10
Q

Describe the effects of PLA2

A

Activation of PLA2 converts phospholipids in the cell membrane to Arachadonic acid.

Arachadonic acid is converted to endoperoxides (PGH2) by COX enzymes.

PGH2 is the precursor for prostaglandins which result in hyperalgesia, thromoxane A2 which causes platelet activation and vasoconstriction and prostacyclins which cause vasodilation

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11
Q

Analgesic action of NSAIDs

A

When tissue is damaged, chemical mediators e.g. bradykinin, 5-HT and H+ depolarise C fibres. Prostaglandins sensitise nociceptors to these mediators which lower the threshold for firing.

Inhibiting PG synthesis produces analgesia

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12
Q

Give 3 examples of clinical uses of NSAIDs

A

Analgesia:
Short term - ibuprofen, naproxen (stronger)
Non-inflammatory - paracetamol
Chronic - piroxicam

Anti-inflammatory:
ibuprofen/naproxen to start, then piroxicam
COX-2 inhibitors used in patients with risk of GI effects (etoricoxib, celecoxib)

Fever: paracetamol

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13
Q

Anti-pyretic action of NSAIDs

A

During fever, endogenous pyrogens (IL-1) are is produced in the hypothalamus to increase temperature. This is associated with an incrase in prostaglandins in the brain.

NSAIDS prevent the effects of IL-1 by preventing an increase in prostaglandins.

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14
Q

Side effects of opiods

A

Respiratory Depression
Conscious Depression/Mood Alterations
Miosis
Reduced Gastric Motility
Nausea and Vomiting
Smooth muscle spasm
Anaphylaxis
Psychiatric changes

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15
Q

Clinical uses of opiods

A

Analgesia

Anaesthesia (fentanil, alfentanil)

Antitussive (relieves or suppresses cough)

Antidiarrhoeal (codeine, loperamide)

Coronary care

Cancer care (diamorphine, morphine)

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16
Q

Mechanism of action of opiods

A

Opiods inhibit transmission of pain in the dorsal horn mainly by presynaptic inhibition of afferent impulses.

Opiods receptors are GPCRs that inhibit adenylate cyclase, decreasing cAMP.

Activation causes K+ channels to open, hyperpolarising the cell and closes Ca2+ channels which inhibits transmitter release. This reduces post-synaptic activity, action potentials in nociceptive fibres are inhibited.

Opiods also activate descending inhibition of pain by inhibiting GABA-ergic interneurones in the PAG (disinhibition)

17
Q

What are endorphins

A

Endogenous compounds released in the CNS in response to pain.

µ-receprots cause analgeia at a supraspinal level and are responsible for drug-induced euphoria, respiratory depression and drug dependence

K-receptors cause analgesia at the spinal level. Produce miosis and sedation.

18
Q

Treatment of neurogenic pain

A

Neurogenic pain normally results from damage to the CNS, and is felt in the periphery e.g. neuralgia

Does not respond to analgesics.

Treated with Tri-cyclic antidepressants and anti-epileptic drugs

19
Q

How does morphine produce analgesia?

A

Morphine relieves both sensory and emotional components of pain.

It produces analgesia by:

  • inhibiting the transmission of pain in the dorsal horn
  • activating the descending pathways in the PAG that inhibit pain transmission in the dorsal horn
  • inhibiting activation of nociceptive afferents in the tissues

Feeling of euphoria mediated by µ-receptors.

20
Q

Side effects of opiods

A

Respiratory depression: activation of µ-receptors reduces teh sensitivity of the respiratory centre to CO2.

Nausea and vomiting: stimulation of the chemoreceptor zone in the medulla

Miosis: stimulates the oculomotor nucleus which mediates parasympathetic constriction of the pupil

Constipation: Opiods inhibit enteric nerves, reducing gut motility. Useful in treatment of diarrhoea

Biliary spasm: causes spincter of Oddi to contract

21
Q

Opiate antagonists

A

Naloxone.

Used in opiate overdose and to reverse the effects of opiates e.g. respiratory depression and coma.

22
Q

Symptoms of aspirin overdose

A

Tinnitus

Hypoventilation

Dyskinesia

Hallucinations

Tachycardia/bradycardia

Pharmacology (16 decks)

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