Analgesic drugs

NSAIDs

Paracetemol -> analgesic, antipyretic, antithrombotic, but lacks anti-inflammatory effects (brain COX-headaches)

Ulceration, GI bleeds (less so but cardiac for COX-2), renal toxicity

COX converts arachadonic acid to prostanoids -> prostaglandins + thromboxanes

Opiate action

Some opioids can act as agonists or partial agonists at one receptor and antagonists at another

Some have tissue selective agonism/antagonism

Receptors form homomeric and heteromeric complexes - even with non-opiod receptors

Morphine

euphoria, sedation, sleep

Free hydroxl on benzene ring (sub. hydroxyls)

Acute + chronic pain (slow-release tabs), less useful for neuopathic

3-4h half life, metabolized in liver

μ partial agonist (less afinity for others)

GI upset + lowered activity, antitussive, hormonal (red. LH, incr. prolactin + ADH)

Morphine-related antagonists

Morphine-analogue agonists

More potent antitussent, mild pain

Prodrug -> codeine-6-glucuronide + 10% morphine (7% caucasians dont have)

Codeine: weak μ agonist

Diarrhoea, IBS, narcolepsy

Diamorphine/heroin: Inactive, metabolised to μ agonist 6-monoacetylmorhpine then morphine (3x morphine)

Subcutaneous pallitative care

Naloxone: affinity for all 3 (μ > κ ≥ δ)

Blocks endogenous opiods (hyperalgesia in inflam. cond.) + morphine-like, reverse OD

2-4h half life, withdrawal symp. in addicts

Naltrexone: similar MoA, 10h half life

Addiction treatment, S/E's GI cramping + diahrroea

Nalorphine: μ antagonist, δ, κ agonist (reverse OD) Discontinued due to psychomimetic effects (+anx.)

(Syn.) Methadone series

Propoxyphene: discontinued dt OD's + arrhythmias

Tramadol: codeine analogue, short half life -> post-op

S/E's: nausea, sleepy, dizzy, sweaty

Meptamizol: High efficacy partial μ, shorter onset + duration., lacks euphoria

Oral, no tolerance, extensively metabolized

Methadone: 20-24h, μ agonist

Thebaine series

Benzamorphin series

Pentazocine: weak μ, strong κ (supraspinal agonism -> dysphoria + psychotic eff.), combined with naloxone

Buprenorphine: partial μ agonist, μ, κ antagonist, highly lipophillic 25-50x morphine, combined with naloxone

(Syn.) Pethidine series

Pethidine: fully syn. opiod, structurally diff to morphine, metabolic toxicity convulsions. Fentanyl 100x, Sufentanyl 500-100x

Neuropathic pain

Anaesthetics: Ketamine: NDMA antagonist reduce central sensitization, inhibits NO production

Local anaesthetic Lidocaine blocks VGNaC, increases depolariation threshold -> reduced spontaneous discharge from damaged neurons (fibromyalgia)

Gabapentin (designed as mimetic) binds to alpa2-delta subunit to modulate VGCCs, 30% metab + rest excreted - OD

Anticonvulsants Carbamazepine, lamotrigine, phenytoin stabilize inactive Na channels

Antidepressants block NA and 5-HT uptake, enhances inhibition

TRPV1

Phophorylation by PKC + PLC (PIP2) sensitize -> hyperalgesia, allodynia

Capsaicin

4 subunits, 6-membrane spanning domains

Competitve antagonists capsazepine

Non-competitive antagonists block aqueous pore (more active against over-activated), S/E hyperthermia

TRP fam respond to physical, protons, natural (capsaicin) + endovanillods, change in membrane potential, IC sig. cascades