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Pharmacology 4: psychoactive drugs, stimulants R190,26
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Pharmacology 4: psychoactive drugs, stimulants
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  • Course
  • Pharmacology
  • Institution
  • Imperial College London (ICL)

Lecture notes from Imperial College London, Medical Biosciences BSc, 2nd year, pharmacology module. Phar 4 on psychoactive drugs, stimulants (cocaine, nicotine): stimulate or increase the activity of nerves within the central nervous system - LO1: Administration: Predict how the route of admi...

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Document information

  • September 25, 2023
  • 5
  • 2022/2023
  • Class notes
  • Chris john
  • All classes

Subjects

  • psychoactive
  • stimulant
  • pharmacology
  • cocaine
  • nicotine
  • nervous system
  • administration
  • metabolism
  • addictive
  • pharmacodynamics
  • catecholamine
  • ph partition
  • henderson hasselbalch
  • anaesthetic
  • toxicity
  • target

Written for

  • Imperial College London (ICL)
  • Unknown
  • Pharmacology
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PD/PK theory: stimulant drugs
- stimulants: drugs that stimulate/ increase activity of nerves within central nervous system
=> ex: cocaine & nicotine

Pharmacokinetics: Cocaine & Nicotine
- plant-based (cocaine: erythroxylum coca plant - nicotine: nicotiana tabacum)
- induce an euphoric “high” in the brain
- routes of administration:



r
1) inhalational (smoking/ inhaling): max effets in 1.5 min in the brain
=> lungs (alveoli) - heart (LA) - systemic circulation
2) intravenous (injecting): max effets in 3 min in the brain
=> venous system - heart (RA) - lungs - heart (LA) - sys.
3) intranasal (snorting): max effets in 15 min in the brain
⑧ Hepatic portal
E
liver Small intestine
=> nasal sinus - diffuse into capillary system - venous system - heart - lungs - heart - sys.
4) oral (eating/ drinking): max effets in 60 min in the brain
=> gastrointestinal tract (stomach + small intestine) - hepatic portal venous system - liver - ...


- “crack” cocaine (mix of cocaine hydrochloride & alkaline solutions) => not degraded when heated
=> inhale cocaine


- cocaine metabolism: cholinesterase enzymes (or plasma cholinesterases) in liver
=> half-life = 20–90 min
deactivate the drugs
- nicotine metabolism: cytochrome P450 enzymes in liver
(metabolites are inactive)
=> half-life = 1-3h
- inhalation route + rapid metabolisation & clearance => addictive potential of the drugs
(re-administer the drug to maintain effects) => “crack” = most addictive (drug seeking behaviour)


Pharmacodynamics: targets
- nicotine: selective for nicotinic acetylcholine receptor
- cocaine: less selective for catecholamine reuptake proteins + sodium channels (only at high dose)

selectivity: linked to dose

, ex of catecholamines




- similarities (lipophilic ring structure - intermediate linking bond - amine group)


- dopamine (see noradrenaline after):
=> dopaminergic nerve terminal: enzymatic conversions tyrosine (precursor) - DOPA - dopamine
=> action potential promotes CA2+ influx => exocytosis => dopamine receptor complex
=> reuptake protein takes dopamine back into presynaptic terminal
=> dopamine metabolism (can recreate dopamine)




=> cocaine blocks dopamine reuptake proteins by using them BUT slowly (substrate)
=> dopamine can’t access => remain in synapse longer => larger response (0 affinity change)
(longer + more intense)
↑

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