Pharmacology Lecture Notes Review

Pharmacology flashcards for exam review, covering key terms, drug classes, mechanisms, and clinical applications from lectures.

Agonist

A molecule that binds to a receptor and activates it to produce a biological response.

Antagonist

Binds to a receptor but does not activate it; instead, it blocks the action of the agonists.

Affinity

A measure of how tightly a drug binds to its receptor.

Efficacy

The ability of a drug to produce maximal biological response once bound to the receptor.

Potency

The concentration of a drug needed to produce a specified effect; commonly expressed as EC50.

EC50

The concentration of a drug that gives 50% of its max effect.

IC50

The concentration of an inhibitor where the response or binding is reduced by half.

Pharmacodynamics

What the drug does to the body (receptor interaction, signal transduction, etc.).

Pharmacokinetics

What the body does to the drug (absorption, distribution, metabolism, excretion).

Desensitization/Tachyphylaxis

Decreased response to a drug after repeated administration; may involve receptor internalization or depletion of second messengers.

Full agonists

Produce max receptor activation and response.

Partial agonists

Bind and activate receptors but elicit a submax response even at full receptor occupancy.

Inverse agonists

Reduce the basal activity of receptors, producing effects opposite to those agonists.

Competitive antagonists

Binds reversibly to the same site as the agonist. Their effects can be overcome by increasing the agonist concentration.

Non-competitive antagonists

Binds to an allosteric site or irreversibly to the agonist site, making the receptor unavailable to agonists regardless of their concentrations.

Uncompetitive antagonists

Bind only after the receptor has been activated by an agonist.

Ligand-gated ion channels

Very fast response (milliseconds), opens ion channel upon ligand binding.

GPCR

Seconds to minutes, initiate second messenger cascades.

Enzyme linked tyrosine kinase linked receptors

Ligand binding activates intrinsic enzymatic activity, Speed: minutes to hours.

Nuclear receptors

Ligand diffuses into cell, binds to cytoplasm/nuclear receptor, alters gene transcription, speed: hours to days.

Absorption

Process of drug movement from administration site to bloodstream.

Distribution

Dispersion throughout body fluids/tissues.

Metabolism

Biotransformation into active/inactive forms (mostly in liver).

Excretion

Removal via kidney (urine), bile (faeces), lungs, sweat.

First-order kinetics

Drug eliminated at a rate proportional to its concentration (most drugs).

Zero-order kinetics

Elimination is constant regardless of concentration (e.g., ethanol, phenytoin at high doses).

Single-compartment model

Assumes uniform distribution instantly.

Two-compartment model

Central (plasma) and peripheral (tissues) compartments with drug movement between them.

Sympathetic Nervous System (SNS)

"Fight or flight" system; Increases heart rate, dilates bronchi, inhibits digestion, vasoconstriction; Uses noradrenaline (norepinephrine) at postganglionic synapses (adrenergic receptors).

Parasympathetic Nervous System (PaNS)

"Rest and digest" system; Slows heart rate, stimulates digestion, bronchoconstriction; Uses acetylcholine (ACh) at both ganglion and effector level (muscarinic receptors).

Atherosclerosis

Plaque buildup in arterial walls. Leads to angina, MI, stroke.

Clotting (thrombosis)

Platelet aggregation and fibrin. Risk of embolism, infarction.

Hypertension

Elevated systemic vascular resistance. Leads to LV hypertrophy, stroke.

Dysrhythmias

Abnormal cardiac rhythm. Includes AFib, VT, bradycardia.

Angina

Cardiac ischaemia w/o infarction. Exertional chest pain.

Cardiac hypertrophy

Myocyte enlargement due to pressure/volume overload. Leads to HF.

Heart Failure

Impaired cardiac output. Fluid overload, breathlessness.

ACE inhibitors, Angiotensin II receptor blockers, β- blockers, Ca2+ channel blockers, diuretics

Reduces BP by various mechanisms.

Nitrates, β-blockers, Ca2+ blockers

Improves O2 delivery or decreases O2 demand.

ACE inhibitors, β-blockers, diuretics, aldosterone antagonists

Improves cardiac function, reduce preload/afterload.

ACE inhibitors / ARBs

Reduce RAAS activity.

Beta-blockers

Reduce HR and contractility.

Calcium channel blockers

Vasodilation, reduced contractility.

Diuretics

Reduce fluid load.

Penicillins, cephalosporins, vancomycin

Inhibit peptidoglycan formation, leading to cell lysis.

Tetracyclines, aminoglycosides, macrolides

Bind bacterial ribosomes (30S or 50S).

Quinolones, rifampin

Inhibit replication or transcription enzymes.

Sulphonamides, trimethoprim

Block folate synthesis.

Polymyxins

Disrupt integrity, increase permeability.

Azoles

Inhibits lanosterol demethylase, decreasing ergosterol.

Polyenes

Binds ergosterol leading to membrane pores and leakage.

Echinocandins

Inhibits beta-glucan synthesis.

Asthma

Chronic inflammatory disorder, leading to hyperreactive airways, bronchoconstriction, mucus secretion, and airway remodelling.

Chronic Obstructive Pulmonary Disease (COPD)

Progressive airflow limitation; usually irreversible; Chronic bronchitis + emphysema.

Parietal cells

secretes HCl via H/K ATPase (“proton pump”).

G cells

secrete gastrin, stimulating parietal cells.

Enterochromaffin-like (ECL) cells

Release histamine, acting on H2 receptors to increase acid secretion.

Leptin

signals satiety from adipose tissue.

Orlistat

inhibits pancreatic lipase, decreasing fat absorption.

Liraglutide

GLP-1 agonist, increasing satiety and decreasing gastric emptying.

Phentermine/topiramate

appetite suppressant (CNS stimulant).

Combined oral contraceptive

Inhibits LH/FSH to prevent ovulation; thickens cervical mucus.

Progestin only pill (mini pill)

Thickens cervical mucus; may inhibit ovulation.

Emergency contraceptive

Delays/inhibits ovulation; Must be taken within 72-120 hours.

Sildenafil (Viagra), tadalafil

Inhibit PDE-5 to increase cGMP, leading to smooth muscle relaxation and erection.

SSRIs

Blocks 5-HT reuptake.

SNRIs

Blocks 5-HT and NA reuptake.

TCAs

Non-selective NA/5-HT reuptake block.

MAOIs

Inhibits breakdown of monoamines.

Atypical Antidepressants

Variable mechanisms.

Typical (First-Generation) Antipsychotics

D2 receptor antagonists.

Atypical (Second-Generation) Antipsychotics

D2 + 5-HT2A antagonism.

GABAA receptor

Ligand-gated chloride ion channel. Activation leads to Cl influx, hyperpolarizing the neuron.

Benzodiazepines

Enhance GABA binding to the receptor, increasing frequency of Cl channel opening.

Barbiturates

Increase duration of Cl channel opening.

General Anesthetics

Potentiate GABAA transmission at high doses.

Ketamine

NMDA receptor Antagonist, produces dissociative anaesthesia.

MDMA (Ecstasy)

Increases release and inhibits reuptake of 5-HT, dopamine, and noradrenaline.

Amphetamines

↑ release of dopamine and noradrenaline via transporter reversal (DAT/NET).

Cocaine

Blocks reuptake of dopamine, NA, 5-HT.