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Course 662 > Chapter 3 > Flashcards

Chapter 3 Flashcards

1
Q

What is pharmacodynamics?

A

the study of what the drug does to the body: mechanisms of drug action that occur at the cellular level

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2
Q

What is pharmacokinetics?

A

the study of what the body does to a drug

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3
Q

What is the strength of ionic attachment of a drug to a receptor determined by?

A

the fit of the three-dimensional structure of the drug to the three-dimensional site on the receptor, the so-called “lock–and–key” relationship.

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4
Q

What is a receptor?

A

A fairly large molecule (usually a protein) at which endogenous transmitters or modulators produce their biological response

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5
Q

what is affinity?

A

Class: the readiness with which two molecules join together.

book: the strength of the attachment of a neurotransmitter or drug with a receptor

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6
Q

What are the main types of membrane spanning proteins relevant to drug action?

A
  1. Ion channel receptors
  2. G-Protein-Coupled Receptors
  3. Transporter (carrier) proteins
  4. Enzymes
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7
Q

What are Ion Channel Receptors?

A

cell membrane-spanning receptors that form an ion channel
i.e., the center of the receptor crosses the membrane of the neuron and forms a pore, which enlarges when a drug or neurotransmitter binds to it and allows the flow of a specific ion

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8
Q

What are the sections of an ionotropic receptor called?

What are they made of?

How many are there?

A
  1. Subunits
  2. each unit it composed of 4 helical coils
  3. five
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9
Q

What are G-Protein-Coupled Receptors?

A

a type of membrane-spanning receptor protein

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10
Q

what are G-Protein-Coupled Receptors also known as?

A

Metabotropic receptors

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11
Q

describe a g-protein coupled receptor

A

The molecular structure of G-protein-coupled receptors consists of a single protein chain of 400 to 500 amino acids arranged as seven transmem`brane alpha helices

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12
Q

what is the key difference between how g-protein-coupled receptors and ion channel receptors function?

A

ionotropic recpetors form a membrane spanning pore allowing the direct passage of ions wheras metabotropic receptors instead causes the release of an intracellular protien called the G protein which then controls enzyme functions

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13
Q

What are ion channel receptors also known as?

A

ionotropic recpetors

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14
Q

which receptors actions are faster - ionotropic receptors or metabotropic receptors? why?

A

ionotropic recpetors are faster because when they are activated they form a pore through which ions can travel director across the cell membrane, whereas when metabotropic receptors are activated they produce a g protein which either directly or indirectly opens and closes ion channels through a series of enzymatic reactions (or alters other processes) whicch takes more time

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15
Q

Describe the action of a g protein coupled receptor

A

activation casuses the receptor to change shape, which activates a g protein
inside the cell. this protein then travels along the cell membrane and either
1. directly activates an ion channel
2. activates an enzyme which produces a ‘second messenger’ that can go on to open a receptor channel or affect processes in other parts of the cell (including the nuleus) **NOTE produces many second messangers

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16
Q

what is the benfit of g protein receptors

A

This mechanism provides the significant benefit of increasing the strength of the original extracellular signal of the first messenger.

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17
Q

Whata re the 4 major classes of second messengers?

A
  1. Cyclic nucleotides (such as cAMP)
  2. Inositol trisphosphate (IP3) and diacylglycerol (DAG) 3. Calcium ions (Ca2+)
  3. Nitric oxide/carbon monoxide
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18
Q

what do transporter (carrier) proteins do?

A

transports small organic molecules (such as neurotransmitters) across cell membranes against concentration gradients

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19
Q

note

A

stopped on 165 to go back and look at the end of chapter 2

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20
Q

What are the possible mechanisms of action for psychotropic drugs? (5)

A
  1. Change in production of Neurotransmitters
  2. Interference with Neurotransmitter storage or release
  3. Direct interaction with pre and/or postsynaptic receptors
  4. Interference with Neurotransmitter reuptake or destruction
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21
Q

Name the different classes of drugs (5)

A
  1. Agonists
  2. Antagonists
  3. Competitive binding (direct)
  4. Non-competitive binding (indirect)
  5. Partial agonists/partial antagonists
22
Q

What are Agonists?

A

drugs that act like the natural ligand

23
Q

What are Antagonists

A

drugs that act as if the ligand’s action were effectively blocked

so binds to the receptor (which blocks the ligand from binding) but does NOT have an effect on the receptor

24
Q

What is Competitive binding ?

A

drug binds to the same site as ligand (fights with the natural ligand for the same receptor)

25
what is Non-competitive binding?
drug binds to different site than natural ligand
26
What is specificity?
the selectivity a drug molecule has for a specific receptor (does it bond to many different receptors or only 1?)
27
What are Autoreceptors? | Heteroreceptors?
Autoreceptors: receptors on the presynaptic neuron for the SAME neurotransmitter that neuron releases e.g., a serotonin recepter on a neuron that releases seratonin Heteroreceptors: receptors on the presynaptic neuron for a DIFFERENT neurotransmitter than the one neuron releases (e.g. a dopamine receptor on a neuron that releases serotonin
28
What are Partial agonists/partial antagonists
they bind to the receptor but activate it to a lesser extent than the natural ligand so this would work as an agonist if the levels of NT in that area are low but would be an antagonist if the levels of NT are high
29
What is a benefit of g protein receptors?
they can increase the strength of the original extracellular signal
30
What 3 ionic states can Transporter (carrier) proteins be in?
1. Open to the synapse 2. Occluded with the transmitter “trapped” inside 3. Open to the cytoplasm of the presynaptic neuron
31
What are isomers?
forms of a molecule that are mirror images of each other
32
Describe how isomers behave chemically and biologically
typically only one of the isomers is biologically active, but they behave the same way with receptors meaning they behave the same chemically but different biologically
33
what are enantiomers
Substances that show optical isomerism
34
What is a racemic mixture?
a drug that is produced as a 50/50 mixture of their two enantiomers
35
What is a dose response curve?
A dose–response curve is a function that describes the relationship between the dose of a drug and the magnitude of the drug’s effect
36
What are the 2 types of dose response curves?
1. Quantal: Curve obtained by plotting the dose of drug against the percentage of subjects showing a given response at any given dose 2. Graded: Curve obtained by plotting the dose of drug against the intensity of response observed in any single person at a given dose. The intensity of response is plotted as a percentage of the maximum obtainable response.
37
what is potency? how is it determined?
refers to the amount of drug required to produce a given effect it is determined by 1. the number of drug molecules at the receptor sites 2. affinity (the strength of the binding of the drug molecules to their receptors)
38
What is residence time?
how long the molecule is bound to its target
39
How is potency reflected in the dose response curve?
The location of the dose–response curve along the horizontal axis (horizontal axis being dose and vertical being intensity of response) **how far the curve is shifted to the left or the right on the graph
40
What does the peak of the dose response curve represent?
The peak of the dose–response curve indicates the maximum effect that can be produced by a drug, regardless of further increases in dose.
41
How could you counter the effect of a competitive antagonist? What would happen to the dose response curve?
by administering a competitive agonist because of the presence of the competitive antagonist, you would need to administer more of the compeititve agonist to get the same effect which would shift the dose response curve to the right and make the agonist seem less potent
42
How could you counter the effect of an irreversible, or noncompetitive, antagonist? What would happen to the dose response curve?
you can't. Because they aren't competing for the same receptor sites, administering more agnosit will not be helpful in displacing it and countering the effects as a consequence the dose response curve would get shorter (less effect)
43
What is the ED50?
The dose of a drug that produces the desired effect in 50 percent of the subjects
44
What is the LD50?
The dose of a drug that is lethal for 50 percent of the subjects
45
What is the therapeutic index?
ratio of LD50 to the ED50 Median lethal dose / median effective dose
46
What is the highest level of drug exposure that does not lead to toxicity called?
NOAEL | no observable adverse effect level
47
lowest level of drug exposure that leads to toxicity called?
LOAEL | lowest observed adverse effect level
48
What is LD1/ED99
Certain Safety factor a more useful indication of the margin of safety is a ratio of the lethal dose for 1 percent of the population to the effective dose for 99 percent of the population
49
What is Combining medications to improve therapeutic outcome called?
Polypharmacy
50
What are the 2 types of dose response curves?
1. Graded D-R curves | 2. Quantal D-R curves
51
What is a Graded D-R curve?
Curve obtained by plotting the dose of drug against the percentage of subjects showing a given response at any given dose
52
For the theraputic index what is a bad number? good?
1 is bad - means half dying and half responding we want large numbers (e.g. 20?)

Course 662 (10 decks)

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