Modify signaling.
Drugs can activate, block or modulate receptor responses.
Side 65
Pharmacology
A study of how chemical agents alter biological systems. Pharmacology connects molecular targets to drug exposure, physiological response, therapeutic effect and toxicity.
drug→target→exposure→response→safety
06pharmacology lenses
04PK stages
05response concepts
65Side
Drugs act by changing biological processes.
Targets can be receptors, enzymes, ion channels, transporters, nucleic acids or other molecular structures.
Change reaction rate.
Inhibitors or activators alter biochemical pathways.
Change membrane conductance.
Channel modulation alters electrical excitability and signaling.
Change movement across membranes.
Transport inhibition can alter neurotransmitter, nutrient or ion concentrations.
Disrupt physical cellular machinery.
Some drugs alter cytoskeletal, membrane or microbial structural processes.
Alter information flow.
Some agents interfere with DNA, RNA or protein synthesis.
Pharmacodynamics asks what the drug does to the body.
It links concentration at a target to biological effect.
How strongly does the drug bind?
Target interaction.
Binding strength affects occupancy but does not alone determine effect.
What response follows binding?
Maximum effect.
Two drugs can bind the same receptor yet produce different levels of activation.
How much concentration produces a given effect?
Position of dose-response curve.
Potency describes amount required, not maximum therapeutic usefulness.
How does effect change with exposure?
Shape + plateau.
Many responses rise with concentration before reaching a maximum.
How preferential is the intended target?
Target versus off-target effects.
Selectivity is usually concentration-dependent rather than absolute.
Pharmacokinetics asks what the body does to the drug.
Absorption, distribution, metabolism and excretion determine the concentration-time profile reaching tissues.
| Stage | Question | Key variables | Why it matters |
|---|---|---|---|
| Absorption | How does drug enter circulation? | Route, permeability, formulation | Controls onset and bioavailability |
| Distribution | Where does drug go? | Blood flow, protein binding, tissue affinity | Controls target exposure |
| Metabolism | How is drug chemically transformed? | Enzymes, liver function, genetics | Can inactivate or activate compounds |
| Excretion | How does drug leave? | Renal, biliary and other routes | Controls persistence and accumulation |
Clearance determines how quickly exposure falls.
Drug concentration depends on both distribution volume and the efficiency of elimination.
Clearance
Volume cleared per unit time.
Represents the body’s overall capacity to eliminate drug from plasma.
Half-life
Time for concentration to fall by half.
Half-life links clearance and distribution and influences accumulation and persistence.
First pass
Metabolism before systemic circulation.
Orally absorbed drugs may be metabolized in gut wall or liver before reaching the systemic circulation.
Prodrug
Inactive or less active precursor.
Metabolism can create the active compound rather than only destroy drugs.
Steady state
Input balances elimination.
Repeated exposure can approach a stable average concentration pattern over time.
Therapeutic benefit and harm occupy the same biological system.
Safety depends on target selectivity, exposure, susceptibility and the distance between effective and toxic effects.
Range between useful and harmful exposure.
Narrow windows make concentration variation more consequential.
Intended mechanism causes harm elsewhere.
The same target can serve useful and harmful functions in different tissues.
Drug binds unintended target.
Effects become more likely as concentrations rise or selectivity narrows.
Rare response not predicted by usual dose-response.
Genetic or immune factors can produce unusual susceptibility.
Response diminishes with repeated exposure.
Receptor, signaling or physiological adaptation can reduce effect.
Adaptation becomes visible when exposure stops.
Physiological compensation can create rebound effects after discontinuation.
The same dose does not create the same exposure in every person.
Genetics, age, organ function, concurrent compounds and physiology can alter pharmacokinetics or pharmacodynamics.
Genetic variation
Enzyme or target variants can alter metabolism, transport or response.
Age
Body composition, metabolism and elimination change across the lifespan.
Organ function
Renal and hepatic function can alter clearance and exposure.
Drug interaction
One compound can change another’s metabolism, transport or physiological effect.
Food / environment
Diet, smoking and other exposures can alter absorption or enzyme activity.
Disease state
Physiology and target expression can change the relationship between concentration and response.
Mechanism is not prescribing.
This Side studies how drugs behave and why responses vary; clinical drug choice and dosing require patient-specific medical judgment.
Goodman & Gilman’s The Pharmacological Basis of Therapeuticsmechanisms and therapeutic pharmacology
Basic & Clinical PharmacologyKatzung · broad pharmacology foundation
Rang & Dale’s Pharmacologyreceptors, systems and drug action
Pharmacokinetics Made Easyexposure and elimination concepts