Pharmacodynamics Overview

Study Notes

Pharmacodynamics examines how drugs affect the body, encompassing the pharmacological actions and mechanisms of both therapeutic and toxic effects.
Explores dose-response phenomena that illustrate the relationship between drug dosage and biological response.

Enzyme Inhibition: Certain drugs inhibit enzyme activity, affecting metabolic processes. Examples include:
- ACE inhibitors and NSAIDs in patients
- Penicillins and sulfonamides in microbes
- 5-Fluorouracil (5-FU) and Mercaptopurine (6-MP) in cancer cells
Ion Channel Modulation: Local anesthetics block sodium (Na+) channels, while calcium channel blockers (e.g., Verapamil) inhibit L-type calcium channels in the heart and blood vessels.
Interference with Metabolic Pathways: Drugs like 6-MP compete with endogenous purine bases, disrupting DNA synthesis and cell division. Sulfonamides inhibit folic acid synthesis in bacteria by competing with PABA.

Receptors are specific cellular macromolecules that interact with ligands (e.g., drugs, hormones) to evoke biological responses, often described by the "Key and Lock Theory".
Types of Ligands:
- Agonists: Stimulate receptors mimicking endogenous ligands (e.g., adrenaline on adrenergic receptors).
- Antagonists: Block receptor activation, possessing affinity but no intrinsic activity (e.g., Prazosin, Propranolol).

Pharmacological Antagonism: Can be competitive (reversible binding) or non-competitive (irreversible or allosteric).
Chemical Antagonism: Involves rendering another drug inactive (e.g., Protamine with Heparin).
Physiological Antagonism: Different receptors initiating opposite physiological effects (e.g., epinephrine countering histamine).

Drug effect magnitude correlates with drug concentration at receptor sites, depicted as graded response curves.
EC50: Concentration causing 50% of maximum response, used to assess drug potency; lower EC50 indicates higher potency.
Efficacy: Reflects a drug's ability to produce a desired physiological response, reliant on the number of drug-receptor complexes formed.

Tolerance: Decreased response to a drug after repeated use, often requiring higher doses for the same effect.
Dependence: Refers to the body's reliance on a drug, leading to withdrawal symptoms upon cessation; can be psychological (e.g., tobacco) or physical (e.g., morphine).

Additive Effect: Combined effect of drugs equals the sum of each drug's effect (1 + 1 = 2).
Synergism: Combined use leads to a greater effect than the sum of individual effects (1 + 1 > 2).
Potentiation: An inactive drug enhances the effect of an active drug (0 + 1 > 1).