Pharmacodynamics
From DrugPedia: A Wikipedia for Drug discovery
(New page: '''Pharmacodynamics''' is the study of the biochemical and physiological effects of drugs on the body or on microorganisms or parasites within or on the body and the mechanisms of drug act...) |
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where L=ligand (drug), R=receptor (attachment site), reaction dynamics that can be studied mathematically through tools such as free energy maps. Pharmacodynamics is often summarized as the study of what a drug does to the body, whereas pharmacokinetics is the study of what the body does to a drug. Pharmacodynamics is sometimes abbreviated as "PD", and when referred to in conjunction with pharmacokinetics can be referred to as "PKPD". | where L=ligand (drug), R=receptor (attachment site), reaction dynamics that can be studied mathematically through tools such as free energy maps. Pharmacodynamics is often summarized as the study of what a drug does to the body, whereas pharmacokinetics is the study of what the body does to a drug. Pharmacodynamics is sometimes abbreviated as "PD", and when referred to in conjunction with pharmacokinetics can be referred to as "PKPD". | ||
| + | '''Pharmacokinetics''' is the study of what the body does to a drug. | ||
| + | |||
| + | '''Pharmacodynamics''' is the study of what a drug does to the body. | ||
| + | A drug's pharmacodynamics can be affected by physiologic changes due to disorders, aging, or other drugs. Disorders that affect pharmacodynamic responses include genetic mutations, thyrotoxicosis, malnutrition, myasthenia gravis, Parkinson's disease, and some forms of insulin-resistant diabetes mellitus. These disorders can change receptor binding, alter the level of binding proteins, or decrease receptor sensitivity. | ||
| + | ==Effects on the body== | ||
| + | The majority of drugs either (a) mimic or inhibit normal physioloical/biochemical processes or inhibit pathological processes in animals or (b) inhibit vital processes of endo- or ectoparasites and microbial organisms. | ||
| + | |||
| + | There are 4 main drug actions: | ||
| + | *[[Depression (mood)|depressing]] | ||
| + | *[[Stimulation|stimulating]] | ||
| + | *destroying cells | ||
| + | *replacing substances | ||
| + | ===Desired activity=== | ||
| + | The desired activity of a drug is mainly due to one of the following: | ||
| + | *[[Cellular membrane]] disruption | ||
| + | *[[Chemical reaction]] | ||
| + | *Interaction with [[enzyme]] proteins | ||
| + | *Interaction with [[structural]] proteins | ||
| + | *Interaction with [[Carrier-protein|carrier]] proteins | ||
| + | *Interaction with [[ion channel]]s | ||
| + | *[[Ligand binding]] to [[Receptor (biochemistry)|receptors]]: | ||
| + | **[[Hormone]] receptors | ||
| + | **[[Neuromodulator]] receptors | ||
| + | **[[Neurotransmitter]] receptors | ||
| + | |||
| + | [[General anesthetic]]s were once thought to work by disordering the neural membranes, thereby altering the Na<sup>+</sup> influx. [[Antacid]]s and [[chelating agent]]s combine chemically in the body. Enzyme-substrate binding is a way to alter the production or metabolism of key [[endogenous]] chemicals, for example [[aspirin]] irreversibly inhibits the enzyme [[cyclooxygenase|prostaglandin synthetase (cyclooxygenase)]] thereby preventing [[Inflammation|inflammatory]] response. [[Colchicine]], a drug for gout, interferes with the function of the structural protein [[tubulin]], while [[Digitalis]], a drug still used in heart failure, inhibits the activity of the carrier molecule, [[Na-K-ATPase pump]]. The widest class of drugs act as ligands which bind to receptors which determine cellular effects. Upon drug binding, receptors can elicit their normal action (agonist), blocked action (antagonist), or even action opposite to normal (inverse agonist). | ||
| + | |||
| + | In principle, a pharmacologist would aim for a target [[blood plasma|plasma]] concentration of the drug for a desired level of response. In reality, there are many factors affecting this goal. Pharmacokinetic factors determine peak concentrations, and concentrations cannot be maintained with absolute consistency because of metabolic breakdown and excretory clearance. [[Genetics|Genetic]] factors may exist which would alter metabolism or drug action itself, and a patient's immediate status may also affect indicated dosage. | ||
| + | |||
| + | ===Undesirable effects=== | ||
| + | Undesirable effects of a drug include: | ||
| + | *Increased probability of cell [[Mutagen|mutation]] ([[carcinogen]]ic activity) | ||
| + | *A multitude of simultaneous assorted actions which may be deleterious | ||
| + | *Interaction (additive, multiplicative, or metabolic) | ||
| + | *Induced physiological damage, or abnormal chronic conditions | ||
| + | |||
| + | ===Therapeutic window=== | ||
| + | {{Main|Therapeutic window}} | ||
| + | The therapeutic window is the amount of a [[medication]] between the amount that gives an effect ([[effective dose]]) and the amount that gives more [[adverse effects]] than desired effects<ref>[http://www.freepatentsonline.com/20040197415.html freepatentsonline.com]</ref>. For instance, medication with a small pharmaceutical window must be administered with care and control, e.g. by frequently measuring blood concentration of the drug, since it easily loses effects or gives adverse effects. | ||
Revision as of 15:52, 29 August 2008
Pharmacodynamics is the study of the biochemical and physiological effects of drugs on the body or on microorganisms or parasites within or on the body and the mechanisms of drug action and the relationship between drug concentration and effect.[1] One dominant example being drug-receptor interactions as modeled by:
L + R \ \leftrightarrow \ L\! \cdot \!R
where L=ligand (drug), R=receptor (attachment site), reaction dynamics that can be studied mathematically through tools such as free energy maps. Pharmacodynamics is often summarized as the study of what a drug does to the body, whereas pharmacokinetics is the study of what the body does to a drug. Pharmacodynamics is sometimes abbreviated as "PD", and when referred to in conjunction with pharmacokinetics can be referred to as "PKPD". Pharmacokinetics is the study of what the body does to a drug.
Pharmacodynamics is the study of what a drug does to the body. A drug's pharmacodynamics can be affected by physiologic changes due to disorders, aging, or other drugs. Disorders that affect pharmacodynamic responses include genetic mutations, thyrotoxicosis, malnutrition, myasthenia gravis, Parkinson's disease, and some forms of insulin-resistant diabetes mellitus. These disorders can change receptor binding, alter the level of binding proteins, or decrease receptor sensitivity.
Contents |
Effects on the body
The majority of drugs either (a) mimic or inhibit normal physioloical/biochemical processes or inhibit pathological processes in animals or (b) inhibit vital processes of endo- or ectoparasites and microbial organisms.
There are 4 main drug actions:
- depressing
- stimulating
- destroying cells
- replacing substances
Desired activity
The desired activity of a drug is mainly due to one of the following:
- Cellular membrane disruption
- Chemical reaction
- Interaction with enzyme proteins
- Interaction with structural proteins
- Interaction with carrier proteins
- Interaction with ion channels
- Ligand binding to receptors:
- Hormone receptors
- Neuromodulator receptors
- Neurotransmitter receptors
General anesthetics were once thought to work by disordering the neural membranes, thereby altering the Na+ influx. Antacids and chelating agents combine chemically in the body. Enzyme-substrate binding is a way to alter the production or metabolism of key endogenous chemicals, for example aspirin irreversibly inhibits the enzyme prostaglandin synthetase (cyclooxygenase) thereby preventing inflammatory response. Colchicine, a drug for gout, interferes with the function of the structural protein tubulin, while Digitalis, a drug still used in heart failure, inhibits the activity of the carrier molecule, Na-K-ATPase pump. The widest class of drugs act as ligands which bind to receptors which determine cellular effects. Upon drug binding, receptors can elicit their normal action (agonist), blocked action (antagonist), or even action opposite to normal (inverse agonist).
In principle, a pharmacologist would aim for a target plasma concentration of the drug for a desired level of response. In reality, there are many factors affecting this goal. Pharmacokinetic factors determine peak concentrations, and concentrations cannot be maintained with absolute consistency because of metabolic breakdown and excretory clearance. Genetic factors may exist which would alter metabolism or drug action itself, and a patient's immediate status may also affect indicated dosage.
Undesirable effects
Undesirable effects of a drug include:
- Increased probability of cell mutation (carcinogenic activity)
- A multitude of simultaneous assorted actions which may be deleterious
- Interaction (additive, multiplicative, or metabolic)
- Induced physiological damage, or abnormal chronic conditions
Therapeutic window
The therapeutic window is the amount of a medication between the amount that gives an effect (effective dose) and the amount that gives more adverse effects than desired effects<ref>freepatentsonline.com</ref>. For instance, medication with a small pharmaceutical window must be administered with care and control, e.g. by frequently measuring blood concentration of the drug, since it easily loses effects or gives adverse effects.
