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The gateway drug effect (alternatively, stepping-stone theory, escalation hypothesis, or progression hypothesis) is a comprehensive catchphrase for the often observed effect that the use of a psychoactive substance is coupled to an increased probability of the use of further substances.
The mechanism of action is a crucial factor in determining effect and toxicity of the drug, taking in consideration the pharmacokinetic (PK) factors. [12] The sort and extent of altered cellular physiology will depend on the combination of the drug's presence (as established by pharmacokinetic (PK) studies) and/or its mechanism and duration of ...
[4] [3] Responses to a drug cue can be physiological (e.g., sweating, salivation, brain activity), behavioral (e.g., drug seeking), or symbolic expressive (e.g., craving). [3] The clinical utility of cue reactivity is based on the conceptualization that drug cues elicit craving which is a critical factor in the maintenance and relapse to drug use.
The specific interaction between drugs and their receptors is referred to as "drug action", and the widespread changes in physiological or psychological function is referred to as "drug effect". [2] These drugs may originate from natural sources such as plants and animals, or from artificial sources such as chemical synthesis in the laboratory.
NIDA-supported research has also shown that this compulsion results from specific drug effects in the brain. This definition opens the way for broad strategies and common approaches to all drug addiction. The physical/psychological addiction dichotomy is reflected in the Controlled Substances Act's criteria for drug scheduling. Placement in ...
Type A: augmented pharmacological effects, which are dose-dependent and predictable [5]; Type A reactions, which constitute approximately 80% of adverse drug reactions, are usually a consequence of the drug's primary pharmacological effect (e.g., bleeding when using the anticoagulant warfarin) or a low therapeutic index of the drug (e.g., nausea from digoxin), and they are therefore predictable.
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The occupancy model was the first model put forward by Clark to explain the activity of drugs at receptors and quantified the relationship between drug concentration and observed effect. It is based on mass-action kinetics and attempts to link the action of a drug to the proportion of receptors occupied by that drug at equilibrium.