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Flashcards:SPLE Pharma

SPLE Pharma

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ADME

ADME is a pharmacokinetic acronym representing absorption, distribution, metabolism, and excretion, which collectively dictate the concentration-time profile of a drug in the body.

Absorption describes how a drug enters systemic circulation from its site of administration.
Distribution involves reversible transfer of drug between the systemic circulation and extravascular tissues.
Metabolism and excretion constitute drug clearance, transforming parent compounds into polar metabolites and eliminating them via renal or biliary pathways.
Students often confuse apparent volume of distribution with true anatomical compartments.

Pharmacophore

A pharmacophore is the ensemble of steric and electronic features necessary to ensure the optimal supramolecular interaction with a specific biological target and trigger its biological response.

It defines essential functional groups like hydrogen bond donors, acceptors, hydrophobic domains, and charges.
Mnemonic: Remember 'Shape and Charge' (SaC) to recall core pharmacophoric requirements.
Essential in rational drug design to modify lead compounds for improved affinity and selectivity.
Students often mistake the entire molecular skeleton for the pharmacophore rather than just the specific interacting atomic features.

Structure-Activity Relationship (SAR)

SAR is the relationship between the chemical or 3D structure of a molecule and its biological activity, guiding optimization of drug potency and selectivity.

Systematically alters functional groups to observe changes in pharmacological potency and toxicity.
Helps identify toxicophores responsible for adverse drug reactions and organ toxicity.
Crucial during the lead optimization stage of drug discovery to improve pharmacokinetic profiles.
Students sometimes assume linear correlation between lipophilicity changes and biological activity across all drug classes.

First-Pass Metabolism

First-pass metabolism is the phenomenon whereby the concentration of a drug is greatly reduced before it reaches systemic circulation, typically due to hepatic and intestinal enzyme activity.

Primarily occurs in the liver via CYP450 enzymes and enterocytes in the gastrointestinal tract following oral administration.
Substantially lowers the systemic bioavailability of high extraction ratio drugs.
Bypassed entirely by administering drugs via intravenous, sublingual, or transdermal routes.
Students frequently confuse first-pass metabolism with simple chemical degradation in gastric acid.

Bioavailability

Bioavailability is the rate and extent to which the active moiety or active ingredient is absorbed from a drug product and becomes systematically available at the site of action.

Denoted as fraction F, where intravenous administration has a defined bioavailability of 100% (F = 1).
Calculated using the area under the plasma concentration-time curve (AUC) comparing extravascular routes to intravenous dosing.
Critical parameter for determining equivalent therapeutic dosing when switching between routes of administration.
Students often confuse absolute bioavailability with relative bioavailability between two different oral formulations.

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Volume of Distribution (Vd)

Volume of distribution is the theoretical proportionality factor relating the total amount of drug in the body to the measured concentration of drug in the blood or plasma.

A high Vd indicates extensive tissue binding and high lipid solubility, resulting in low plasma concentrations.
Calculated as dose divided by initial plasma concentration (Vd = Dose / C0).
Helps determine the loading dose required to achieve target therapeutic plasma concentrations rapidly.
Students commonly mistake Vd for a real physiological fluid volume rather than an apparent pharmacokinetic parameter.

Zero-Order Kinetics

Zero-order elimination kinetics occurs when a constant amount of drug is eliminated per unit of time, independent of the drug concentration in the body.

Occurs when drug elimination pathways or metabolizing enzymes become saturated at high concentrations.
Notable examples include ethanol, high-dose aspirin, and phenytoin elimination.
Half-life is not constant; it increases as the plasma concentration of the drug rises.
Students often confuse zero-order saturation kinetics with standard linear first-order elimination.

First-Order Kinetics

First-order elimination kinetics describes a process where a constant fraction of the drug present in the body is eliminated per unit of time.

Elimination rate is directly proportional to the plasma concentration of the drug.
The elimination half-life remains constant regardless of the drug's concentration or dose.
Most therapeutic drugs follow first-order kinetics at normal clinical therapeutic doses.
Students frequently mix up the constant elimination rate of zero-order with the constant elimination half-life of first-order kinetics.

Phase I Drug Metabolism

Phase I metabolism involves functionalization reactions—such as oxidation, reduction, or hydrolysis—that introduce or unmask a polar functional group on the drug molecule.

Predominantly mediated by the cytochrome P450 (CYP450) enzyme superfamily located in the smooth endoplasmic reticulum of hepatocytes.
Often converts lipophilic drugs into more polar intermediate metabolites, preparing them for Phase II conjugation or excretion.
Can result in active, inactive, or toxic metabolites depending on the parent compound.
Students often incorrectly assume Phase I always results in complete detoxification and loss of pharmacological activity.

Phase II Drug Metabolism

Phase II metabolism consists of synthetic conjugation reactions where endogenous polar molecules are attached to drug molecules to facilitate rapid elimination.

Common conjugation pathways include glucuronidation, sulfation, acetylation, and glutathione conjugation.
Substantially increases water solubility of xenobiotics to promote renal or biliary excretion.
Generally results in pharmacologically inactive and nontoxic metabolites ready for clearance.
Students often confuse conjugation additions with Phase I functional group modifications.

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Competitive Antagonist

A competitive antagonist is a pharmacological agent that binds reversibly to the same receptor active site as the agonist, preventing agonist binding without activating the receptor.

Shifts the agonist dose-response curve to the right without changing the maximum achievable efficacy.
Overcome by increasing the concentration of the agonist at the receptor site.
Maintains parallel rightward displacement on logarithmic concentration-response plots.
Students frequently confuse competitive antagonism with noncompetitive antagonism regarding maximal efficacy depression.

Bioequivalence

Bioequivalence is the absence of a significant difference in the rate and extent to which the active ingredient or active moiety becomes available at the site of drug action.

Evaluated using pharmacokinetic parameters including area under the curve (AUC) and peak concentration (Cmax).
Typically requires a 90% confidence interval for the ratio of test to reference parameters to fall within 80.00% to 125.00%.
Ensures pharmaceutical alternatives or generic substitutes produce identical clinical safety and efficacy profiles.
Students often confuse pharmaceutical equivalence with therapeutic and bioequivalence.