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General concepts
Pharmacology
| Question | Answer |
|---|---|
| pharmacodynamics | the study of molecular interactions bw drugs and body constituents. Biochemical, phisiologic effects and mechanisms of action of drugs. |
| First step in initiating a drug-induced effect | formation of a complex bw the drug and a receptor |
| Receptor site | the area where a drug acts to initiate a series of biochemical and physiological effects; site of action |
| Mechanism of action | events leading to an effect |
| Antacids | neutralize gastric acid (no receptor effect) |
| Receptor | Cellular macromoleecule. Metabolic regulatory enzymes/co-enzymes/proteins-glycoproteins |
| Drugs receptor interactions | Ionic, hydrogen, hydrophobic, Van der Waals, least desireable covalent |
| Affinity | Related to drug's chemical structure |
| Expression of affinity | dissociation constant Kd |
| Kd | concentration of a drug required to achieve 50 percent occupancy of its receptors |
| Governs drug-receptor interactions | Law of mass action- for a given concentration reactant and a given product is equal at a constant pressure |
| Agonist | Drug with stimulatory effect on a receptor |
| Weak agonist | must be bound to many receptors to produce the same effect as a strong agonist. |
| Antagonist | Drugs which interfere with activities of an agonist |
| Competitive antagonist | binds the agonist binding domain, but increasing the concentration of the agonist over the antagonist can produce a physiologic response.Thus the it forms a reversible drug-receptor complex and is consequently surmountable. |
| irreversible antagonist | antagonist, which competes with an agonist for the agonist-binding domain, and then forms a permanent drug-receptor complex, which cannot be overcome by high concentrations of the agonist;insurmountable |
| noncompetitive antagonist | antagonist, which binds a site on the receptor other than the agonist-binding domain, produces a conformational change, and irreversibly prevents an agonist-receptor interaction. increase in agonist will not produce expected response;insurmountable |
| Classification of receptors | type of drug that they interact with or according to the specific physiologic response a drug produces. Number of receptors can be up-down regulated depending. |
| Activate acetylcholine receptors | muscarine, nicotine, (aka ach binds two types of different receptors) |
| Antagonist of muscarine | atropine |
| Antagonist of nicotine | curare |
| Efficacy | magnitude of response obtained from optimal receptor site occupancy by a drug. related to its chemical structure (structural activity relationship (SAR) |
| dose-response curve | visual and mathematical representation of the response of a specific drug in relationship to the amount of the drug administered |
| plateau of dose- response curve | efficacy or the maximal effect of the drug |
| Potency | relates two or more drugs by comparing the doses required to produce a given effect |
| Drug A is more potent than drug B | If for any given effect, the dose of drug A is always smaller than that required for drug B. The maximal effect of drug A (A1) is reached at a lower dose than the same maximal effect of drug B (B1). Drug A is considered more potent than drug B yet they ha |
| Toxicity | those effects, which are not desired for the given therapeutic use of a drug. exaggerations of direct effects seen at higher available dosages or multiple concurrent "side" effects occurring at therapeutic dosage levels |
| Effectvie dose 50- (ED50) | The dose of a drug required to produce a response of specific intensity in 50 percent of the individuals within the same population |
| Lethal dose 50 | The dose of a drug required to cause death in 50 percent of the individuals within the same population |
| margin of safety | ratio of LD50/ED50. farther apart these two curves are the wider. |
| Most drugs ( in terms of getting into cells) | are weak acids or weak bases too large to pass through aqueous channels. passage of these drug molecules across cell membranes is achieved by passive diffusion along a concentration gradient based on molecular weight, lipid solubility,pka, structure |
| PHARMACOKINETICS | drug movement accross membranes. |
| Passive diffusion | The way most drugs pass throug membranes ( fairly large weak acids or weak bases) |
| Aqueous channels | Small water soluble drugs use this as a result of hydrostatic or osmotic differences across biologic membranes, by a process known as filtration |
| facilitated diffusion | drug to be carried forms a complex with a component of the cell membrane on one side, the complex is carried through the membrane, the drug is released, and the carrier returns to repeat the process. Does not require energy/not against conc. gradient. |
| active transport | transport system characterized by selectivity, competitive inhibition, requirement for energy, saturability, and movement against an electrochemical gradient |
| pinocytosis | Water-insoluble substances such as vitamins A, D, E, and K are engulfed by cell membranes and are released unchanged in the cytoplasm |
| More readily diffuse accross membrane: nonpolar vs polar | Nonpolar, unionized molecules are usually lipid soluble and will more readily diffuse across biological membranes. Ionized, polar fractions, on the other hand, are less lipid soluble |
| More absorbable in ECM? aqueous or oily | Aqueous solutions of drugs are more readily absorbed into the extracellular fluid than oily suspensions |
| More absorbable? High concentration of drug or low concentration | Solutions of high concentration are more readily absorbed than low concentrations of the same drug |
| Enteral administration of drug | oral route is the most common, convenient, and economical method of drug administration. It is also the most unpredictable |
| What influences the absorption of a enterally administered drug? | drug’s formulation, the pH of the gastrointestinal tract, the presence of food in the stomach, gastric motility, splanchnic blood flow, first pass .metabolism in the liver, and importantly, patient compliance |
| Parenteral | Intravenous (IV) administration provides for accurate and immediate deposition of drugs, at the desired concentration, into the blood stream. No recall. |
| subcutaneous (SC) injections | rate of absorption into the blood stream is slow and sufficiently constant to provide a sustained effect |
| incorporation of a vasoconstrictor | retard the rate of absorption |
| Intramuscular (IM) injections | rapid absorption of aqueous solutions into the blood stream. Oily or other nonaqueous vehicles may provide slow, constant absorption |
| Topical | passive diffusion is proportional to their concentration and lipid solubility. direct absorption has advantages over enteric administration, since it circumvents the metabolic first-pass breakdown in the liver |
| Inhalation of drug | must cross the alveoli, travel the systemic blood flow and then act at the appropriate effector site. Concentration is controlled at the alveolar level, since most of these drugs are exhaled immediately |
| Rectal administration of drug | may be useful in young children and for unconscious or vomiting patients, however, absorption is unpredictable |
| Organs that recieve most of drugs upon minutes of absorption | heart, liver, kidney, and brain will receive most of the drug within minutes of absorption. Muscle, most viscera, skin, and fat may require much longer time before equilibrium is achieved |
| Drugs to the CNS | restricted by the blood-brain barrier. However, the only limiting factor associated with highly lipid-soluble drugs is cerebral blood flow |
| Following absorption | drugs are distributed both into the extracellular and intracellular environment. Diffusion into the extracellular space occurs rapidly. However, many drugs are bound to plasma proteins, which limit their concentration in tissues and at their site of actio |
| Protein binding | non-selective process and many drugs compete with each other and endogenous substances for these binding sites. Drugs may also accumulate in tissues in higher than expected concentration as a result of the pKa of the drug and the pH of the environment |
| Elimination of lipid-soluble weak acids and bases | not readily eliminated from the body. Metabolism fosters drug excretion by biotransforming them into more polar, water-soluble fractions although many drug metabolites maintain a degree of pharmacological activity |
| biotransformation | termination of drug action if drug metabolites are active (or by excretion) |
| chemical reactions associated with biotransformation | nonsynthetic (Phase I) or synthetic (Phase II) |
| Phase I chemical reaction assoc with biotransformation | a drug is oxidized or reduced to a more polar compound |
| Phase II chemical reaction associated with biotransformation | endogenous macromolecule is conjugated to the drug. Drugs undergoing conjugation reactions (Phase II) may have already undergone Phase I biotransformation |
| biotransformation of most drugs | hepatic microsomal enzyme (cytochrome P450) system; inducible |
| secondary contrbutors to p450 system in biotransformation | plasma, kidney, lung, and the gastrointestinal tract also make notable contributions (also, noninducible nonmicrosomal enzymes) |
| Eliminated more readily? polar or high lipid soluble drugs | Polar |
| Before lipid soluble drugs are secreted | have to be metabolized to more polar fractions |
| Most important organ for elimination of drugs | kindney |
| Renal excretion may involve three processes | glomerular filtration which depends on fractional plasma protein binding and filtration rate; active tubular excretion, a non-selective carrier system for organic ions; and passive tubular reabsorption of unionized drugs, which result in net passive reabs |
| metabolites formed in the liver | excreted via the bile into the intestinal tract. If these metabolites are subsequently hydrolyzed and reabsorbed from the gut (enterohepatic recirculation), drug action is prolonged |
| Pulmonary excretion | important mainly for the elimination of anesthetic gases and vapors. Other routes, such as saliva, sweat, and tears, are quantitatively unimportant |
| elimination of most drugs from the body follows | follows exponential or first-order kinetics. Assuming a relatively uniform distribution of a drug within the body (considered to be a single compartment), first-order kinetics implies that a constant fraction of the drug is eliminated per unit time |
| exponential kinetics may be expressed | by its constant (k), the fractional change per unit time, or its half-life (t1/2), the time required for the plasma concentration of a drug to decrease by 50 percent. |
| distribution half-life (t 1/2) | represents the rapid decline in plasma drug concentration as 50 percent of the drug is distributed throughout the body |
| elimination half-life (t 1/2) | reflects the time required to metabolize and excrete 50 percent of the drug from the system |
| plateau level of accumulation of the drug over four half-lives | plateau, known as the steady-state concentration, represents a rate of administration that is equal to the rate of elimination |
| Half lives to eliminate drug from the body | half-lives to eliminate a drug from the body |
| zero-order kinetics | implying that a constant amount of the drug is eliminated per unit time;alcohol |
| Pharmacotherapeutic principles | relate to the use of drugs in the diagnosis, prevention, and treatment of disease |
| influences the onset and duration of drug action | The dosing regimen (route, amount, and frequency of drug administration) |
| desired full effect of a drug must be achieved promptly | a loading dose, larger than the maintenance dose, must be employed |
| individual effective dose | dose of a drug required to produce a specific response in an individual. If takes unexpectedly high dose, the patient is said to be hyporeactive,may also be described as tolerance |
| tachyphylaxis | When tolerance develops rapidly, subsequent to the administration of only a few doses of a drug |
| idiosyncrasy | unusual reaction of any intensity, irrespective of drug dosage, observed in a small percentage of the patients |
| Optimum therapeutic doses | amount of drug per kilogram of body weight of the patient |
| Fetal abnormalities | drugs are considered to be responsible for 1 to 5 percent Each drug has a threshold concentration above which fetal abnormalities can occur and below which no effects are discernible |
| Whether a drug reaches the threshold concentration in the fetus depends on | chemical nature of the agent (molecular weight, protein binding, lipid solubility, pKa) and maternal pharmacokinetic factors |
| Most drugs in the maternal bloodstream cross the placenta by | simple diffusion along the concentration gradient. During early pregnancy the placental membrane is relatively thick which tends to reduce permeability. The thickness decreases and the surface area of the placenta increases in the later trimesters. |
| Category A fetal risks | Controlled studies in both humans and animals have failed to show a risk to the fetus, the risk appears remote |
| Category B fetal risks | Animal studies have shown no risk, but there are no controlled human studies; or animal studies have shown a risk, but human studies have not |
| Category C fetal risks | Animal studies have shown a risk, but there are no controlled human studies; or there are no available animal or human studies |
| Category D fetal risks | Evidence of risk exists, but benefit may outweigh risk in certain situations |
| Category X fetal risks | Risk exists and outweighs any possible benefit of use |
| Human teratogenecity | not predictable |
| Most common trimester to see major defects | during the critical period of organogenesis (first trimester) Exposure during the second and third trimesters will primarily affects organ function) |
| Any drug in the fetal compartment at the time of birth | must rely on the infant’s own metabolic and excretory capabilities, which have not yet fully developed. Consequently, drugs given near term, especially those with long half-lives, may have a prolonged action on the newborn |
| rate of passage of a drug from plasma to milk depends on | characteristics of the drug such as the drug’s molecular weight, lipid solubility, pKa, and plasma protein binding |
| Small water-soluble nonelectrolytes pass into milk by | simple diffusion through aqueous channels in the mammary epithelial membrane that separates plasma from milk, equilibrium is reached rapidly and the drug’s concentration in milk approximates plasma levels |
| larger molecules and the mammary epithelial membrane | only the lipid soluble, nonionized form passes through the membrane |
| drug concentration in milk | pKa of weak electrolytes is an important because the pH of milk is generally lower (more acidic) than that of plasma and milk can act as an “ion trap” for weak bases |
| At equilibrium in milk | basic drugs may become more concentrated in milk. Conversely, acidic drugs are limited in their ability to enter milk because the concentration of nonionized free form in milk is higher than it is in plasma and a net transfer of the drug from milk to plas |
| milk-to-plasma drug-concentration ratio | The ratio of drug concentration in breast milk to drug concentration in maternal plasma |
| Most drugs for which data are available have a milk-to-plasma ratio of | 1 or less; about 25 percent have ratios of more than 1; and about 15 percent have ratios of more than 2 |
| For most drugs, the dose below which there is no clinical effect in infants is | unknown |
| Factors that determine the advisability of using a particular drug in a nursing mother | includes the potential for acute or long-term dose-related and non-dose related toxicity, dosage and duration of therapy, age of the infant, quantity of milk consumed by the infant, and the drug’s effect on lactation |
| Drug safety for infants | is determined primarily on the basis of the level of exposure of an infant (exposure index <10 percent) or the presence or absence of substantial short-term adverse effects |
| To minimize the infant’s exposure to medications in milk | withhold drug therapy, delay drug therapy temporarily, choose a drug that passes poorly into milk, use alternative routes of drug administration (i.e., topical, inhalation), advise the mother to avoid nursing at peak plasma concentrations of the drug |
| To minimize the infant’s exposure to medications in milk 2 | administer the drug to the mother before the infant’s longest sleep period, and/or withhold breastfeeding temporarily |
| Dosage forms are usually designed | with the adult population in mind, and the dosage cannot easily be individualized for children |
| Even when appropriate dosage forms for children are available | palatability, resistance to taking medications, and compliance issues may hinder optimal therapy. Finally, children often react differently than adults to certain medications (i.e., paradoxical hyperactivity, which may be observed in children taking chlor |
| inappropriate for pediatric patients | acetylsalicylic acid (Reye syndrome) |
| At birth, the gastric pH is | neutral but falls to values of 1-3 in the first day of life |
| Drugs, which require an acid environment for absorption, may have what in children | poor bioavailability |
| medications, which are acid-labile, may actually have what in children | increased bioavailability in young children |
| Absorption in children is sometimes | Absorption may also be reduced by the relatively high frequency of gastroesophageal reflux (which may cause an oral dose to be spit up or vomited) and diarrhea. The rectal route may be used in situations where the oral route is not practical |
Created by:
doctor red77
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