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443 - Pharmacology & Toxicology > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

What is the aim of drug therapy?

A

Rapidly deliver and maintain therapeutic yet nontoxic levels of the appropriate drug in the target tissue so that the disease is treated without adversely affecting the patients.

In other words, maximize efficacy and minimize adverse effects.

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2
Q

How the drug is delivered will affect…

A

how much of the drug reaches its target and how long it remains in the animal.

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3
Q

What questions should be asked before prescribing a drug?

A
  • Which drug?
  • What dose?
  • How often?
  • What route?
  • How long should it be used for?
  • What is the benefit?
  • What are the adverse effects?
  • How quickly does the drug leave the body? (production animals)
  • Are drug combinations appropriate?
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4
Q

What is the risk-benefit analysis for drug use?

A

The need of the patient, the predicted efficacy, and their relative safety.

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5
Q

T/F: No drugs are completely safe or without risk.

A

True

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6
Q

What are the three approaches used to make drug decisions?

A
  1. A pathophysiological approach
  2. An evidence-based approach
  3. An anecdotal approach
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7
Q

Which is the preferred approach to follow for making decisions?

A

The evidence-based approach

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8
Q

What is an evidence-based approach to making drug-related decisions?

A

An approach where there is scientific evidence and clinical trials to back therapeutic decisions.

In vet med, often this info is not available for all cases or animals.

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9
Q

What is the pathophysiological approach to making drug-related decisions?

A

Known information about the drug, the disease, and its pathophysiological mechanisms are used to make rational decisions on therapeutic choices.

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10
Q

What is the anecdotal approach to making drug-related decisions?

A

Using recommendations from colleagues based on what has worked for them in the past.

Worst method but commonly used.

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11
Q

What is empirical therapy?

A

Drug selection based on prior experience with the specific situation.

OR

When the diagnosis is not confirmed but patient is treated to see the outcome.

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12
Q

What is rational therapy?

A

Drug selection that is based on the risk, cost, and benefit considerations for the specific patient or population.

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13
Q

What are the different names for a drug?

A
  • Brand name: Commercial name, commonly recognized by this name (ex. Tylenol, Metacam, Advil).
  • International non-proprietary name: Generic drug name. Identifies the pharmaceutical substances or active ingredients. Globally recognized.
  • Chemical name: Long, complex, rarely used.
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14
Q

What are generic products?

A

Generic products are copies of a drug that is no longer patent-protected. (Drugs are patent-protected for a few years when first introduced).

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15
Q

Do all drugs have generic names and generic products?

A

No, all drugs do have a generic name but not all drugs have generic products.

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16
Q

T/F: Brand names for drugs are the same everywhere.

A

False, only the generic names are the same globally.

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17
Q

What is extra-label drug use?

A

Using a drug for a species, condition, or route of administration that is not on the drug’s label.

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18
Q

What changes when the drug formulation is different?

A

The base of the drug is the same but the diluent, carriers, or salts may be different.

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19
Q

With a change in formulation, the _____ properties stay the same but the _____ may change.

A

With a change in formulation, the pharmacodynamic properties stay the same but the pharmacokinetics may change.

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20
Q

Define pharmacodynamics.

A

What the drug does to the body (how drugs interact with biological systems).

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21
Q

What is the structure-activity relationship?

A

The relationship between the chemical/3D structure of a drug and its biological activity.

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22
Q

What does the structure-activity relationship influence?

A

How a drug interacts with its target.

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23
Q

What are the 8 principles of pharmacodynamics?

A
  1. Drugs act primarily through molecular targets
  2. Receptor types determine the response to many drugs
  3. Receptors can be turned on or off
  4. Multiple mechanisms of antagonism exist
  5. Efficacy and potency are not the same
  6. Receptors are not static
  7. Selectivity is important
  8. The body tries to maintain homeostasis
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24
Q

What do all receptors have?

A

Endogenous ligands (naturally occurring molecules in the body that bind and activate them).

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25
Q

What are drug targets?

A

Call surface or intracellular proteins that receive and transduce a signal.

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26
Q

What is affinity?

A

The strength with which a drug binds to its target.

27
Q

List the receptor types in order of fastest response to slowest response.

A
  1. Ligand-gated ion channels (fastest)
  2. G-protein coupled receptors
  3. Enzyme-linked receptors
  4. Intracellular receptors (slowest)
28
Q

Which receptors alter gene expression?

A

Intracellular receptors (ex. steroid receptors).

29
Q

What is the MOA of ligand-gated ion channels?

A

Changes in membrane potential or ion concentration within the cell.

30
Q

What is the MOA of G-protein coupled receptors?

A

Once the G-protein is activated, GDP is converted to GTP which either results in activation of an ion channel (quick) or activation of an enzyme that generates a second messenger (slower)

GPCRs amplify the signal!!!

31
Q

What is the MOA of enzyme linked receptors?

A

Enzyme-linked receptors have a large extracellular binding site linked to an intracellular enzyme. When ligands bind to both receptors they form a dimer. This activates an enzyme which phosphorylates the relay proteins that mediate the response
to the receptors and activate signal transduction.

32
Q

What is an agonist?

A

A molecule that binds to the receptor and activates signal transduction (acts like the endogenous ligand).

33
Q

What are competitive antagonists?

A

Molecules that bind at the same site that the endogenous ligand binds and prevents ligand binding while it is in that site.

The amount of binding depends on the concentrations of ligand and antagonist.

34
Q

What are non-competitive agonists?

A

Molecules that bind to a site that is not the ligand binding site but causes a conformational change that prevents ligand binding.

35
Q

What is the difference between full agonists, partial agonists, inverse agonists, and antagonists?

A

Full agonists fully activate a receptor

Partial agonists activate their receptor, but not to it’s full effect

Inverse agonists bind to their receptor and cause an opposite response from that of its agonist

Antagonists prevent receptor activation, often by blocking agonists binding. They do not cause any activation of the receptor themselves.

36
Q

What are the mechanisms of antagonism?

A
  • Competitive
  • Non-competitive
  • Irreversible
37
Q

What is irreversible antagonism?

A

The antagonist irreversibly binds to the receptor so the receptor needs to be replaced to get rid of the antagonist effect.

In this case, the effect becomes stronger over time as more of the drug binds to receptors.

38
Q

How does competitive antagonism impact the dose-response curve?

A

It is a parallel shift, the curve appears the same but is shifted to the right. This means that the max effect can still be attained if more agonist is present.

39
Q

Which type of antagonism is dose dependent?

A

Competitive antagonism is dose dependent.

In non-competitive antagonism, the drug cannot be out-competed by the ligand since they bind at different sites.

40
Q

How does non-competitive antagonism impact the dose-response curve?

A

There is a decrease in the maximum response with the presence of a non-competitive antagonist.

41
Q

What is physiological antagonism?

A

A type of drug interaction where a drug binds to a different receptor than an agonist and produces the opposite physiological response.

42
Q

What is chemical antagonism?

A

Chemical antagonism occurs when a drug reduces the concentration of an agonist by forming a chemical complex. This type of antagonism does not work at the receptor level, but instead is due to the interaction of two compounds that changes the effects.

43
Q

What is pharmacokinetic antagonism?

A

Occurs when a drug changes another drug or chemical in the body, resulting in it being eliminated more quickly or prevented from entering the body.

44
Q

What is efficacy?

A

How effective a drug is at producing a
response.

45
Q

What is potency?

A

The concentration of the drug required to
produce a response.

46
Q

What is the EC50?

A

The concentration of drug that gives a response equal to half of the maximal response.

47
Q

A drug’s EC50 indicates its…

A

potency.

48
Q

The magnitude of a drug’s maximal response indicates the…

A

efficacy.

49
Q

Which part of the dose-response curve provides information on the drug’s efficacy?

A

The y axis (% biological effect).

Efficacy increases

50
Q

Which part of the dose-response curve provides information on the drug’s potency?

A

The x axis.

Potency is higher when the EC50 is more to the left.

51
Q

Which drug is more potent? Which has a higher efficacy?

A

Red is more potent, black is more efficacious.

52
Q

What influences the dose of drug we choose, potency or efficacy?

A

Potency

53
Q

What influences which drug we choose, potency or efficacy?

A

Efficacy

54
Q

What is clinical efficacy?

A

Magnitude and percent of clinical response. i.e. size of blood pressure drop

55
Q

What is pharmacological efficacy?

A

Inhibition or activation of receptor activity.

56
Q

The potency and efficacy of a drug are dependent on what ___ and how ___.

A

The potency and efficacy of a drug are dependent on what effect you are interested in and how you are measuring it.

57
Q
  1. Which drug is most potent?
  2. Which drug is least potent?
  3. Which drug is least efficacious?
  4. Which drug is least likely to cause fatal apnea?
A
  1. Red
  2. Black
  3. Blue
  4. Blue
58
Q

What is meant by “receptors are not static”?

A

The amount and response of receptors (and other drug targets) can be altered by the presence of drugs, disease, environmental exposure, or genetics. This will then influence the response to drugs on a temporary or long-term basis, depending on the cause.

59
Q

What factors can affect the amount and response of receptors?

A
  • Drugs
  • Disease
  • Environmental exposure
  • Genetics
60
Q

What happens to receptors when they are continuously stimulated?

A

They may be down-regulated (amount of receptors goes down) or they may desensitized (usually means uncoupling from second messenger pathways).

61
Q

What is the term for when receptors are down regulated or desensitized?

A

Tolerance

62
Q

What does drug selectivity influence?

A

The therapeutic response and adverse effects.

63
Q

How does dose relate to adverse effects?

A

Higher dose = more adverse effects.

Generally, drugs will be selective for their primary target but as dose increases, the drug may bind more to other targets which causes secondary or adverse effects.

64
Q

What are mechanisms that the body uses to maintain homeostasis when drugs are administered?

A

Drug administration disrupts homeostasis!

Receptor down-regulation and desensitization are mechanisms the body uses to try to maintain homeostasis. Also, increases in activation of physiologically antagonistic receptors may occur with exogenous receptor activation.

443 - Pharmacology & Toxicology (9 decks)

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