Intro to Pharmacodynamics Flashcards Preview

Neuro II Exam 1 > Intro to Pharmacodynamics > Flashcards

Flashcards in Intro to Pharmacodynamics Deck (20):

What is the difference between pharmacokinetics and pharmacodynamics?

Pharmacokinetics: the effect of the body on drugs; how the body absorbs, distributes, metabolizes, and eliminates drugs

Pharmacodynamics: the effect of drugs on the body; how the drug binds to drug receptors, its dose-response curve, and MOA


A specific molecule in a biological system that plays a regulatory role; it interacts with a drug and initiates the biochemical events leading to drug effects



Component of the biologic system to which a drug binds without changing any fx

A molecule that binds to a receptor

Inert binding site



What is a dose response curve?

Graphing the drug dose arithmetically on the x-axis with the drug effects on the y-axis creates a ____.

Graphing the logarithm of the drug dose vs. the drug effect creates a ____.

Quantitatively shows the relationship between a drug and its effect

Hyperbolic curve

Sigmoidal curve


What is the Emax?


The maximal effect that can be produced by the drug

The dose of drug that produces 50% of its maximal effect (mean effective dose)


_____ response curves answer the question of "how much". The magnitude of a response varies ____. Represents the ____ within a population.

A graded dose means that a slight increase of drug brings a small ____ in response.



Continuously (measured on a continuous scale)

Mean value


Heart rate


____ response curves answer the question of "does this response occur or not? And in how many?"

It requires a pre-defined response. And is used to examine the ____ of a response in a population.




Epileptic seizures


What is a non-cumulative quantal dose response curve?


The number of individuals responding at a dose of a drug and only at that dose

Number of individuals responding at a dose of a drug and at all doses lower



How do you calculate TI?

What does TI mean?

What is the therapeutic window?

Median effective dose
Median toxic dose
Median lethal dose

Therapeutic index (TI)= TD50/ED50

Higher the TI the safer the drug

The range of doses of a drug or of its concentration in a body system that provides safe and effective therapy


What is affinity?

What is the difference between high and low affinity?

How readily and tightly the drug binds to its receptor

High affinity: good drug-receptor interaction; less drug needed for a response

Low affinity: poor drug receptor interaction; more drug needed for a response


____ is a property of a drug determined by its affinities at various binding sites.

A more selective drug would affect ____ targets over a specific concentration range.




____ describes the ability of a drug to change a receptor fx and produce a physiological response upon its binding to a receptor.

____ binds to the receptor and stabilize it in a particular conformation producing a physiologic response. Have intrinsic activity.

____ binds to the receptor but does not change its fx. It prevents activation of the receptor in the presence of an agonist. NO intrinsic activity.

Intrinsic activity




What are the three types of agonist drugs?

Full agonists: produce maximal pharmacological effects at full receptor occupancy

Partial agonists: produce sub-maximal pharmacological effects at full receptor occupancy (lower Emax)

Inverse agonists: produce an effect opposite a full or partial agonist


What are the three types of antagonism?

Pharmacologic: action at the same receptor as endogenous ligands or agonist drugs

Chemical: when a chemical antagonist makes the other drug unavailable (non-receptor antagonist)

Physiologic: occurs between endogenous pathways regulated by different receptors (non-receptor antagonist)


Pharmacologic antagonists are receptor antagonists. Where are the two places they bind?

A ____ makes the agonist look less potent by shifting the dose-response curve to the right.

A ____ reduces the maximal response that an agonist can produce.

Agonist site binding: reversible -> competitive antagonist; irreversible -> noncompetitive agonist site antagonist

Allosteric site binding: reversible or irreversible -> noncompetitive allosteric antagonist

Competitive antagonist

Noncompetitive antagonist


____ mimic the actions of endogenous chemicals at receptors.


Full agonists

Activations of mu opioid receptors (normally used by endogenous opioids like endorphins) by opioid analgesics like morphine, codeine, and meperidine.


_____ block the actions of endogenous ligands at receptors.


Antagonists and partial and inverse agonists

Blockade of alpha1 adrenoreceptors by the antihypertensive drug prazosin


Beneficial and adverse effects can be mediated by the ____ on the same cell types.


How do you control this?

Same receptors/signal transduction pathway

Insulin: can lower blood glucose from hyperglycemia to normoglycemia; but can become toxic if it lowers it to hypoglycemia

Avoid systemic administration of the drug (beta2 agonist can cause relaxation of bronchial smooth m, vasodilation, and increased breakdown of glycogen


Beneficial and adverse effects can be mediated by ____.

Highly selective drugs have ____ side effects. Lower selectivity leads to ____ side effects.

Different types of receptors

Less; increased


The lower the KD the _____ the affinity of a drug for its receptor.

The higher the KD the ____ the affinity of a drug for its receptor.