chemistry

Pharmacodynamics

Pharmacodynamics is a chemistry topic covered in the lgStudy science library. This page brings together a partial reference excerpt, illustrations, worked examples, real-world applications and a short study plan, so you can understand Pharmacodynamics rather than just read about it. In short: Pharmacodynamics (PD) is the study of the biochemical and physiologic effects of drugs (especially pharmaceutical drugs). The effects can include those manifested within animals (including humans), microorganisms, or combinations of organisms (for example, infection).

Key takeaways

Pharmacodynamics belongs to chemistry; place it in that map before memorising details.
Learn the definition first, then one example that makes the definition concrete.
Connect Pharmacodynamics to a quantity you can measure, compute or draw — that is where exam questions come from.
Reproduce the core statement of Pharmacodynamics from memory before moving on to harder problems.

Reference excerpt

Pharmacodynamics (PD) is the study of the biochemical and physiologic effects of drugs (especially pharmaceutical drugs). The effects can include those manifested within animals (including humans), microorganisms, or combinations of organisms (for example, infection). Pharmacodynamics and pharmacokinetics are the main branches of pharmacology, being itself a topic of biology interested in the study of the interactions of both endogenous and exogenous chemical substances with living organisms. In particular, pharmacodynamics is the study of how a drug affects an organism, whereas pharmacokinetics is the study of how the organism affects the drug. Both together influence dosing, benefit, and adverse effects. Pharmacodynamics is sometimes abbreviated as PD and pharmacokinetics as PK, especially in combined reference (for example, when speaking of PK/PD models). Pharmacodynamics places particular emphasis on dose–response relationships, that is, the relationships between drug concentration and effect. One dominant example is drug-receptor interactions as modeled by

L + R ↽ − − ⇀ LR {\displaystyle {\ce {L + R <=> LR}}}

where L, R, and LR represent ligand (drug), receptor, and ligand-receptor complex concentrations, respectively. This equation represents a simplified model of reaction dynamics that can be studied mathematically through tools such as free energy maps.

Basics There are four principal protein targets with which drugs can interact:

Enzymes – (e.g. neostigmine and acetyl cholinesterase) Inhibitors Inducers Activators Membrane carriers – [Reuptake vs Efflux] (e.g. tricyclic antidepressants and catecholamine uptake-1) Enhancer (RE) Inhibitor (RI) Releaser (RA) Ion channels – (e.g. nimodipine and voltage-gated Ca2+ channels) Blocker Opener Receptor – (e.g. Listed in table below) Agonists can be full, partial or inverse. Antagonists can be competitive, non-competitive, or uncompetive. Allosteric modulator can have 3 effects within a receptor. One is its capability or incapability to activate a receptor (2 possibilities). The other two are agonist affinity and efficacy. They may be increased, decreased or unaffected (3 and 3 possibilities).

NMBD = neuromuscular blocking drugs; NMDA = N-methyl-d-aspartate; EGF = epidermal growth factor.

Effects on the body The majority of drugs either There are 7 main drug actions:

stimulating action through direct receptor agonism and downstream effects depressing action through direct receptor agonism and downstream effects (ex.: inverse agonist) blocking/antagonizing action (as with silent antagonists), the drug binds the receptor but does not activate it stabilizing action, the drug seems to act neither as a stimulant or as a depressant (ex.: some drugs possess receptor activity that allows them to stabilize general receptor activation, like buprenorphine in opioid dependent individuals or aripiprazole in schizophrenia, all depending on the dose and the recipient) exchanging/replacing substances or accumulating them to form a reserve (ex.: glycogen storage) direct beneficial chemical reaction as in free radical scavenging direct harmful chemical reaction which might result in damage or destruction of the cells, through induced toxic or lethal damage (cytotoxicity or irritation)

Desired activity The desired activity of a drug is mainly due to successful targeting of one of the following:

Cellular membrane disruption Chemical reaction with downstream effects 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 that bind to receptors that 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 Overstimulation or Inhibition of receptors- lead to harmful physiological changes Development of tolerance - reduce their responsiveness, requiring higher doses of drug. Induced pathological conditions - long term structural or functional changes Disturbed homeostasis Functional selectivity (biased Agonism) - preferentially activate certain pathways over others, potentially leading to off-target or unanticipated effects.

Therapeutic window

… excerpt ends here. Continue reading the full article.

Illustrations

Worked examples

Example 1 — a first encounter with Pharmacodynamics

Start with the simplest possible case. Write down what Pharmacodynamics claims or describes in one sentence, then invent the smallest concrete situation in which that sentence is true. In chemistry, the smallest case is usually a single object, a single equation or a single measurement. Check that every symbol or term in your sentence has a meaning in that case.

Example 2 — changing one variable

Take the situation from Example 1 and change exactly one quantity: double it, halve it, or set it to zero. Predict what should happen to Pharmacodynamics before you calculate. Comparing your prediction with the result is the fastest way to find out whether you understand the idea or only the words.

Example 3 — an exam-style question

Typical questions about Pharmacodynamics ask you to (a) state it precisely, (b) apply it to given data, and (c) explain a limitation. Practise writing all three answers in under five minutes; the third part is what separates a full-mark answer from an average one.

Applications of Pharmacodynamics

In research: Pharmacodynamics appears in chemistry research whenever the underlying quantities have to be modelled precisely. Papers usually cite it as a starting assumption and then explore where it breaks down.
In technology and industry: Engineering practice reuses Pharmacodynamics in design rules, simulations and safety margins. Knowing the idea lets you read a specification sheet and understand why the numbers look the way they do.
In the classroom: Pharmacodynamics is common in secondary-school and first-year university syllabi. It links to neighbouring topics Life sciences industry, Medicinal chemistry, Pharmacodynamics, so understanding it makes those chapters shorter.
In everyday life: Look for Pharmacodynamics outside the textbook — in sport, cooking, traffic, electronics or the sky above you. An example you found yourself is remembered far longer than one you were given.

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How to study Pharmacodynamics in 20 minutes

Read the reference excerpt below once, without taking notes.
Close the page and write down what Pharmacodynamics means in your own words.
Compare your version with the excerpt and mark what you missed.
Work through the three examples above with pen and paper.
Explain Pharmacodynamics out loud to somebody else — or to Teacher Smith in the lgStudy chat.

Frequently asked questions

What is Pharmacodynamics in simple terms?

Why does Pharmacodynamics matter?

Because it connects several chemistry ideas at once: it gives you a definition you can apply, a quantity you can calculate, and a way to check whether a result is plausible.

How should I study Pharmacodynamics?

Read the excerpt, restate it from memory, then work through the examples and applications listed on this page. The five-step study plan above takes about twenty minutes.

What does this page cover?

It gives you a compact reference excerpt plus original lgStudy explanations, examples, applications and study material on Pharmacodynamics.