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Access fundamental Pharmacology Theory Notes PDF. These notes provide a comprehensive introduction to the core principles of pharmacology, the science of drugs and their effects on living systems. The PDF covers essential topics including pharmacokinetics (what the body does to the drug: Absorption, Distribution, Metabolism, Excretion - ADME) and pharmacodynamics (what the drug does to the body: mechanisms of action, drug-receptor interactions, dose-response relationships). This resource is indispensable for students beginning their studies in medicine, pharmacy, nursing, veterinary medicine, and other health or biological sciences. You can download these "Pharmacology Theory Notes PDF" for free for offline study or view them directly online. Slides By DuloMix is dedicated to providing foundational educational materials for complex subjects.

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• Foundation of Drug Science: Covers the essential concepts that underpin all aspects of drug therapy and research.
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Fundamental Principles of Pharmacology Theory

Pharmacology is the branch of biomedical science concerned with the study of drug action, where a drug can be broadly defined as any man-made, natural, or endogenous molecule which exerts a biochemical or physiological effect on the cell, tissue, organ, or organism. More specifically, it is the study of the interactions that occur between a living organism and chemicals that affect normal or abnormal biochemical function. These "Pharmacology Theory Notes" aim to cover the foundational principles that govern these interactions, primarily focusing on pharmacokinetics and pharmacodynamics.

I. Introduction to Pharmacology

• Definition of Pharmacology: Study of drugs, their sources, properties, physiological and biochemical effects, mechanisms of action, absorption, distribution, metabolism, excretion, and therapeutic uses.
• Key Terms:
  • Drug: A substance used in the diagnosis, treatment, or prevention of disease, or for otherwise modifying physiological functions.
  • Pharmacotherapeutics: The use of drugs to treat diseases.
  • Toxicology: The study of adverse effects of chemicals (including drugs) on living organisms.
  • Pharmacy: The science and practice of preparing, compounding, and dispensing drugs.
• Sources of Drugs: Plants (e.g., digoxin, morphine), animals (e.g., insulin, heparin), minerals (e.g., lithium), microorganisms (e.g., penicillin), synthetic chemicals, and biotechnology (e.g., monoclonal antibodies).
• Drug Nomenclature: Chemical name, generic (non-proprietary) name, brand (proprietary/trade) name.

II. Pharmacokinetics: "What the Body Does to the Drug"

Pharmacokinetics (PK) describes the time course of drug absorption, distribution, metabolism, and excretion (ADME). These processes determine the concentration of a drug at its site(s) of action and, thus, the intensity and duration of its effects.

A. Absorption

• The process by which a drug moves from its site of administration into the systemic circulation.
• Factors Affecting Absorption:
  • Drug properties: Lipid solubility, molecular size, pKa (degree of ionization).
  • Route of administration: Oral, intravenous (IV), intramuscular (IM), subcutaneous (SC), transdermal, inhalation, topical, etc. IV administration bypasses absorption (100% bioavailability).
  • Physiological factors: Gastric pH, GI motility, blood flow to absorption site, presence of food.
• Mechanisms of Drug Transport Across Membranes: Passive diffusion, facilitated diffusion, active transport, endocytosis.
• Bioavailability (F): The fraction of an administered dose of unchanged drug that reaches the systemic circulation.
• First-Pass Metabolism (Presystemic Metabolism): Metabolism of a drug (usually orally administered) in the liver or gut wall before it reaches systemic circulation, reducing its bioavailability.

B. Distribution

• The reversible transfer of a drug from the systemic circulation to various tissues and organs of the body.
• Factors Affecting Distribution:
  • Blood flow to tissues: Highly perfused organs (brain, liver, kidneys) receive drug rapidly.
  • Plasma protein binding: Drugs can bind to plasma proteins (e.g., albumin, α₁-acid glycoprotein). Only unbound (free) drug is pharmacologically active and can distribute to tissues.
  • Lipid solubility and tissue permeability: Lipid-soluble drugs cross cell membranes more easily and distribute more widely, including into the CNS (if they can cross the blood-brain barrier).
  • Volume of Distribution (Vd): An apparent volume that relates the amount of drug in the body to its concentration in plasma. A large Vd suggests extensive tissue distribution. Vd = Amount of drug in body / Plasma drug concentration.

C. Metabolism (Biotransformation)

• The chemical alteration of a drug in the body, primarily in the liver, to make it more water-soluble and easier to excrete.
• Metabolites are usually less active or inactive, but some drugs are administered as inactive prodrugs that are converted to active metabolites. Some drugs have active metabolites.
• Phases of Drug Metabolism:
  • Phase I Reactions (Functionalization): Introduce or unmask a polar functional group (e.g., -OH, -NH₂, -SH) via oxidation, reduction, or hydrolysis. Primarily mediated by Cytochrome P450 (CYP450) enzyme system in the liver.
  • Phase II Reactions (Conjugation): Covalent attachment of an endogenous molecule (e.g., glucuronic acid, sulfate, glutathione, acetate) to the drug or its Phase I metabolite, forming a highly polar conjugate that is readily excreted.
• Factors Affecting Metabolism: Genetic polymorphisms (e.g., in CYP enzymes), age, liver disease, drug interactions (enzyme induction or inhibition).

D. Excretion

• The irreversible removal of drug and its metabolites from the body.
• Major Routes of Excretion:
  • Renal Excretion (Kidneys): Most common route. Involves glomerular filtration, active tubular secretion, and passive tubular reabsorption. Factors affecting renal excretion include GFR, urine pH (for ionizable drugs), and protein binding.
  • Biliary/Fecal Excretion: Drugs or metabolites excreted into bile, then into feces. Enterohepatic circulation can occur (reabsorption of drug from intestine after biliary excretion, prolonging its action).
  • Other Routes: Lungs (for volatile anesthetics, alcohol), sweat, saliva, breast milk.
• Clearance (CL): The volume of plasma cleared of drug per unit time. Total body clearance is the sum of clearances by all routes. CL = Rate of elimination / Plasma drug concentration.
• Half-life (t_1/2): The time required for the plasma drug concentration to decrease by 50%. t_1/2 = (0.693 × Vd) / CL. Determines dosing interval and time to reach steady state.

Pharmacokinetic Models: (e.g., one-compartment, two-compartment models) Mathematical descriptions of how drugs move through the body.

III. Pharmacodynamics: "What the Drug Does to the Body"

Pharmacodynamics (PD) describes the biochemical and physiological effects of drugs and their mechanisms of action.

A. Mechanisms of Drug Action

• Receptor-Mediated Action: Most drugs exert their effects by interacting with specific macromolecular components of the cell called receptors.
  • Receptors: Proteins (or glycoproteins) located on the cell surface or within the cytoplasm/nucleus that bind specific ligands (drugs, neurotransmitters, hormones) and initiate a cellular response.
  • Types of Receptors:
    • Ligand-gated ion channels (Ionotropic receptors): E.g., Nicotinic ACh receptor, GABA_A receptor.
    • G protein-coupled receptors (GPCRs - Metabotropic receptors): Largest family. E.g., Adrenergic receptors, Muscarinic ACh receptors, Opioid receptors. Involve second messengers (cAMP, IP₃, DAG).
    • Enzyme-linked receptors (Kinase-linked receptors): E.g., Insulin receptor, Growth factor receptors.
    • Intracellular (Nuclear) receptors: E.g., Steroid hormone receptors, Thyroid hormone receptors. Regulate gene transcription.
• Non-Receptor-Mediated Action: Some drugs act by mechanisms not involving specific receptors.
  • Enzyme Inhibition: E.g., NSAIDs inhibit cyclooxygenase, Statins inhibit HMG-CoA reductase.
  • Altering Ion Channels: E.g., Local anesthetics block voltage-gated Na⁺ channels.
  • Physical/Chemical Properties: E.g., Antacids neutralize stomach acid, Osmotic diuretics.
  • Incorporation into Macromolecules: E.g., Some antiviral/anticancer drugs are DNA/RNA analogues.

B. Drug-Receptor Interactions

• Affinity: The tendency of a drug to bind to its receptor. Measured by the dissociation constant (K_d) – lower K_d means higher affinity.
• Intrinsic Activity (Efficacy): The ability of a drug, once bound to its receptor, to activate the receptor and produce a biological effect.
  • Agonist: A drug that binds to a receptor and produces a biological response (has affinity and intrinsic activity).
    • Full Agonist: Produces maximal response.
    • Partial Agonist: Produces submaximal response even at full receptor occupancy; can act as an antagonist in the presence of a full agonist.
    • Inverse Agonist: Binds to the same receptor as an agonist but produces an opposite effect (reduces basal receptor activity).
  • Antagonist: A drug that binds to a receptor but does not activate it, preventing agonists from binding and producing an effect (has affinity but no intrinsic activity).
    • Competitive Antagonist: Binds reversibly to the same site as the agonist. Can be overcome by increasing agonist concentration. Shifts dose-response curve to the right.
    • Non-competitive Antagonist: Binds irreversibly to the agonist site or to an allosteric site, reducing the maximal response. Cannot be fully overcome by increasing agonist concentration.
    • Physiological (Functional) Antagonist: Two drugs acting at different receptors producing opposing physiological effects.
    • Chemical Antagonist: Drug directly interacts with and inactivates another drug.

C. Dose-Response Relationships

• Describe the relationship between the dose (or concentration) of a drug and the magnitude of its effect.
  • Graded Dose-Response Curve: Plots effect against log dose for an individual or tissue. Characterized by:
    • Potency (EC₅₀ or ED₅₀): Dose or concentration required to produce 50% of the maximal effect. A measure of how much drug is needed.
    • Maximal Efficacy (E_max): The maximum effect a drug can produce.
  • Quantal Dose-Response Curve: Plots the percentage of a population exhibiting a defined all-or-none effect (e.g., sleep, death) against log dose. Used to determine:
    • Median Effective Dose (ED₅₀): Dose at which 50% of individuals exhibit the specified effect.
    • Median Toxic Dose (TD₅₀): Dose at which 50% of individuals exhibit a specific toxic effect.
    • Median Lethal Dose (LD₅₀): Dose at which 50% of animals die.
• Therapeutic Index (TI): A measure of drug safety. TI = TD₅₀ / ED₅₀ (or LD₅₀ / ED₅₀ in animals). A larger TI indicates a wider margin of safety. For NTI drugs, TI is small.
• Therapeutic Window (Range): Range of plasma concentrations associated with therapeutic efficacy and minimal toxicity.

IV. Drug Development and Evaluation

A brief overview of the process by which new drugs are discovered, developed, and approved for clinical use, involving preclinical studies (in vitro, animal toxicology) and clinical trials (Phases I, II, III, IV).

V. Factors Modifying Drug Action

Age, sex, body weight, genetic factors (pharmacogenomics), disease states (e.g., renal/hepatic impairment), drug interactions, tolerance, tachyphylaxis, placebo effect.

These fundamental theories of pharmacology provide the scientific basis for understanding how drugs work and for using them safely and effectively in treating diseases. This PDF aims to serve as a foundational resource for students embarking on their journey into this fascinating field.

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