Download Free Medical Pharmacology Basics PowerPoint Presentation

Pharmacology Basics PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Drug Interactions, which is titled "Pharmacology Basics", to know about the basics of Pharmacology.

Tags : Drug Interactions, Pharmacology Basics

Published on : Jul 20, 2021 | Views : 2317 | Downloads : 15

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ppt slide no 1 content not found
Slide 2-

Pharmacology Basics
Slide 3-

Definitions Pharmacokinetics The process by which a drug is absorbed, distributed, metabolized and eliminated by the body Pharmacodynamics The interactions of a drug and the receptors responsible for its action in the body
Slide 4-

The Life Cycle of a Drug(pharmacokinetics) Absorption Distribution Degradation Excretion
Slide 5-

Slow Absorption Orally (swallowed) through Mucus Membranes Oral Mucosa (e.g. sublingual) Nasal Mucosa (e.g. insufflated) Topical/Transdermal (through skin) Rectally (suppository)
Slide 6-

Faster Absorption Parenterally (injection) Intravenous (IV) Intramuscular (IM) Subcutaneous (SC) Intraperitoneal (IP) Inhaled (through lungs)
Slide 7-

Fastest Absorption Directly into brain Intracerebral (into brain tissue) Intracerebroventricular (into brain ventricles) General Principle: The faster the absorption, the quicker the onset, the higher the addictiveness, but the shorter the duration
Slide 8-

Absorption: Solubility Water-soluble Ionized (have electrical charge) Crosses through pores in capillaries, but not cell membranes Lipid(fat)-soluble Non-ionized (no electrical charge) Crosses pores, cell membranes, blood-brain-barrier Dissociation constant or pKa  indicates the pH where 50% of the drug is ionized (water soluble) and 50% non-ionized (lipid soluble); pKeq = pH + log [X]ionized/[X]non-ionized This affects a drug's solubility, permeability, binding, and other characteristics.
Slide 9-

(hydroxyl group) (amine group)
Slide 10-

Distribution: Depends on Blood Flow and Blood Brain Barrier
Slide 11-

Excludes ionized substances; Active transport mechanisms; Not uniform – leaky (circumventricular areas)
Slide 12-

Bioavailability The fraction of an administered dose of drug that reaches the blood stream. What determines bioavailability? Physical properties of the drug (hydrophobicity, pKa, solubility) The drug formulation (immediate release, delayed release, etc.) If the drug is administered in a fed or fasted state Gastric emptying rate Circadian differences Interactions with other drugs Age Diet Gender Disease state
Slide 13-

Depot Binding(accumulation in fatty tissue) Drugs bind to “depot sites” or “silent receptors” (fat, muscle, organs, bones, etc) Depot binding reduces bioavailability, slows elimination, can increase drug detection window Depot-bound drugs can be released during sudden weight loss – may account for flashback experiences?
Slide 14-

Degradation & Excretion Kidneys Traps water-soluble (ionized) compounds for elimination via urine (primarily), feces, air, sweat Liver Enzymes(cytochrome P-450) transform drugs into more water-soluble metabolites Repeated drug exposure increases efficiency  tolerance
Slide 15-

Excretion: Other routes Lungs alcohol breath Breast milk acidic ---> ion traps alkaloids alcohol: same concentration as blood antibiotics Also bile, skin, saliva ~~
Slide 16-

Metabolism and Elimination (cont.) Half-lives and Kinetics Half-life: Plasma half-life: Time it takes for plasma concentration of a drug to drop to 50% of initial level. Whole body half-life: Time it takes to eliminate half of the body content of a drug. Factors affecting half-life age renal excretion liver metabolism protein binding
Slide 17-

First order kinetics A constant fraction of drug is eliminated per unit of time. When drug concentration is high, rate of disappearance is high.
Slide 18-

Zero order kinetics Rate of elimination is constant. Rate of elimination is independent of drug concentration. Constant amount eliminated per unit of time. Example: Alcohol
Slide 19-

Comparison First Order Elimination [drug] decreases exponentially w/ time Rate of elimination is proportional to [drug] Plot of log [drug] or ln[drug] vs. time are linear t 1/2 is constant regardless of [drug] Zero Order Elimination [drug] decreases linearly with time Rate of elimination is constant Rate of elimination is independent of [drug] No true t 1/2
Slide 20-

Drug Effectiveness Dose-response (DR) curve Depicts the relation between drug dose and magnitude of drug effect Drugs can have more than one effect Drugs vary in effectiveness Different sites of action Different affinities for receptors The effectiveness of a drug is considered relative to its safety (therapeutic index)
Slide 21-

ED50 = effective dose in 50% of population 100 50 0 DRUG DOSE 0 X ED50 % subjects
Slide 22-

Therapeutic Index Effective dose (ED50) = dose at which 50% population shows response Lethal dose (LD50) =dose at which 50% population dies TI = LD50/ED50, an indication of safety of a drug (higher is better) ED50 LD50
Slide 23-

Potency Relative strength of response for a given dose Effective concentration (EC50) is the concentration of an agonist needed to elicit half of the maximum biological response of the agonist The potency of an agonist is inversely related to its EC50 value D-R curve shifts left with greater potency
Slide 24-

Efficacy Maximum possible effect relative to other agents Indicated by peak of D-R curve Full agonist = 100% efficacy Partial agonist = 50% efficacy Antagonist = 0% efficacy Inverse agonist = -100% efficacy
Slide 25-

Average Response Magnitude LO DRUG DOSE 0 X HI A B C Comparisons
Slide 26-

Tolerance(desensitization) Decreased response to same dose with repeated (constant) exposure or more drug needed to achieve same effect Right-ward shift of D-R curve Sometimes occurs in an acute dose (e.g. alcohol) Can develop across drugs (cross-tolerance) Caused by compensatory mechanisms that oppose the effects of the drug
Slide 27-

Sensitization Increased response to same dose with repeated (binge-like) exposure or less drug needed to achieve same effect Left-ward shift in D-R curve Sometimes occurs in an acute dose (e.g. amphetamine) Can develop across drugs (cross-sensitization) It is possible to develop tolerance to some side effects AND sensitization to other side effects of the same drug
Slide 28-

Mechanisms of Tolerance and Sensitization Pharmacokinetic changes in drug availability at site of action (decreased bioavailability) Decreased absorption Increased binding to depot sites Pharmacodynamic changes in drug-receptor interaction G-protein uncoupling Down regulation of receptors
Slide 29-

Other Mechanisms of Tolerance and Sensitization Psychological As the user becomes familiar with the drug’s effects, s/he learns tricks to hide or counteract the effects. Set (expectations) and setting (environment) Motivational Habituation Classical and instrumental conditioning (automatic physiological change in response to cues) Metabolic The user is able to break down and/or excrete the drug more quickly due to repeated exposure. Increased excretion
Slide 30-

Pharmacokinetic and pharmacodynamic With pharmacokinetic drug interactions, one drug affects the absorption, distribution, metabolism, or excretion of another. With pharmacodynamic drug interactions, two drugs have interactive effects in the brain. Either type of drug interaction can result in adverse effects in some individuals. In terms of efficacy, there can be several types of interactions between medications: cumulative, additive, synergistic, and antagonistic. Drug-drug Interactions
Slide 31-

Response Hi Lo Time Cumulative Effects Drug A Drug B The condition in which repeated administration of a drug may produce effects that are more pronounced than those produced by the first dose.
Slide 32-

Response Hi Lo Time A B Additive Effects A + B The effect of two chemicals is equal to the sum of the effect of the two chemicals taken separately, eg., aspirin and motrin.
Slide 33-

Response Hi Lo Time A B A + B Synergistic Effects The effect of two chemicals taken together is greater than the sum of their separate effect at the same doses, e.g., alcohol and other drugs
Slide 34-

Response Hi Lo Time A B A + B Antagonistic Effects The effect of two chemicals taken together is less than the sum of their separate effect at the same doses
Slide 35-

Pharmacodynamics Receptor target/site of drug action (e.g. genetically-coded proteins embedded in neural membrane) Lock and key or induced-fit models drug acts as key, receptor as lock, combination yields response dynamic and flexible interaction
Slide 36-

Pharmacodynamics (cont.) Affinity propensity of a drug to bind with a receptor Selectivity specific affinity for certain receptors (vs. others)
Slide 37-

Agonism and Antagonism Agonists facilitate receptor response Antagonists inhibit receptor response (direct ant/agonists)
Slide 38-

Modes of Action Agonism A compound that does the job of a natural substance. Does not effect the rate of an enzyme catalyzed reaction. Up/down regulation Tolerance/sensitivity at the cellular level may be due to a change in # of receptors (without the appropriate subunit) due to changes in stimulation Antagonism A compound inhibits an enzyme from doing its job. Slows down an enzymatically catalyzed reaction.
Slide 39-

Agonists/Antagonists Full Partial Direct/Competitive Indirect/Noncompetitive Inverse A single drug can bind to a single receptor and cause a mix of effects (agonist, partial agonist, inverse agonist, antagonist) Functional Selectivity Hypothesis: Conformational change induced by a ligand-receptor interaction may cause differential functional activation depending on the G-protein and other proteins associated with the target receptor
Slide 40-

Important implications ofdrug-receptor interaction drugs can potentially alter rate of any bodily/brain function drugs cannot impart entirely new functions to cells drugs do not create effects, only modify ongoing ones drugs can allow for effects outside of normal physiological range
Slide 41-

Law of Mass Action(a model to explain ligand-receptor binding) When a drug combines with a receptor, it does so at a rate which is dependent on the concentration of the drug and of the receptor Assumes it’s a reversible reaction Equilibrium dissociation (Kd) and association/affinity (Ka) constants Kd = Kon/Koff = [D][R]/[DR] Ka = 1/Kd = Koff/Kon = [DR]/[D][R]