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42 Cards in this Set

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For receptor time-response, place the following in order of response: G-protein, Ion channel, Enzyme linked , DNA transcriptional contol (milisec, sec, min, hours)
milisec: ion channel… Seconds: G-protein… Minutes: Enzyme Linked… Hours: DNA transcriptional control
Give the equation for the binding affinity constant: Ka
Ka = k1/k2
Give the equation for the dissociation constant: Kd
Kd = k2/k1 = [D][R]/[DR]
When 50% of receptors are bound, what is the value of [R] (receptors)? And what is the value of Kd?
Given that Kd = [D][R]/[DR]… At 50% receptor saturation, [R]=[DR]… thus Kd=[D]
If Kd is low, what is the receptor/drug affinity?
High
If the Kd is high, what is the receptor/drug affinity?
Low
Give the formula for determining the amount of bound drug to receptors
B=(Bmax X [D])÷(Kd + [D])
Given the fomula for BOUND DRUG:

B=(Bmax X [D])÷(Kd + [D])

Define B, Bmax, [D] and KD
For B=(Bmax X [D])÷(Kd + [D])

B is the amount of bound drug…

Bmax is the maximum amount of specific binding sites
[D] is the amount of free drug at equilibrium

Kd is the equilibrium dissociation constant
None
When does the Kd = [D]?
when 50% of the receptors are bound to drug
Given a saturation for curve specific binding that shows Bmax (and 1/2-Bmax), how do you determine the equilibrium constant (KD)?
KD is found along the X-axis where Bmax = 50%
None
What does EC50 represent?
EC50= [D] when 50% of the max effect (Emax) is seen...

Or

EC50 is the [drug] that produces half of the maximal effect
None
Are Kd and EC50 the same?
not necessarily
What does Kd represent?
Given that Kd=[R][D]÷[DR]

Kd determines the fraction of receptors bound to Drug at a given [D], independent of the [B].
None
Which cannot be saturated by excess drug, specific binding or non-specific binding?
non specific binding
None
How do you determine the number of specific binding, given the total number of binding and the total number of non-specific binding?
Specific Binding = total binding - non-specific binding
What does cell sensitivity to drug dependent upon?
Affinity (Kd) and degree of spareness
Give the formula for the effect of a drug and define the terms: E =?
Effect of a drug:

E=(Emax x [D])÷ (EC50 + [D]

where Emax is the maximum effect of a drug at highest concentration…

[D] is the concentration of free drug…

EC50 is is the concentration of drug that produces 1/2 of the maximum effect
None
Given a graph that shows the maximum effect of a drug at highest concentration (Emax) and 50% of Emax, where would you determine EC50? (the concentration that produces 1/2 of the maximum effect)
EC50 is the point along the X-axis where Emax is at 50%
how can the maximal biological effect of a drug occur with only a fraction of receptors being occupied?
Spare receptors
how is it that spare receptors increase the sensitivity of a receptor to its ligand?
there is a greater likelihood of the ligand binding with more receptors, therefore, since there is an excess of receptors, activation requires less ligand (drug)
What is an antagonist?
binds to receptor but does not produce a response
How would you reverse the effects of a competitive antagonist?
apply a higher concentration of agonist so as to out-compete the antagonist
What is a non-competitive antagonist?
Cannot be reversed by any concentration of agonist
Is an irreversible antagonist always non-competitive?
yes
Is a non-competitive antagonist always irreversible?
No
Graphically, which antagonist resembles a partial agonist? A competitive or non-competitive antagonist?
graphically, a non-competitive antagonist resembles a partial agonist, because in both cases the full effect cannot be attained regardless of how much agonist is applied
If a receptor without a drug is mostly in an inactive state and a receptor that is bound to an agonist is mostly in an active state, what state is a partial agonist in?
only partially active
what is a partial agonist?
bind and produces response , but not = in response to full agonist
What does a partial agonist look like on a graph?
like an agonist combined with an non-competitive antagonist
None
what affect does a partial agonist have on a full agonist?
act somewhat like a non-competitive antagonist
None
What is an inverse agonist?
Inverse agonists stablize a receptor in its "off" state: So it binds to a receptor and produces a response that is opposite to an agonist
Of the following, (parial agonist, antagonist, inverse agonist)which will have the greatest NEGATIVE affect on a circuit that is on (due to an agonist)? (Hint: place in order)
Greatest to lowest negative effect: inverse agonist > antagonist > partial agonist
Of the following, (partial agonist, agonist, inverse agonist), which will have the most POSITIVE affect on the circuit that is off (due to an antagonist)? (Hint: place in order from greatest to lowest positive effect:
Greatest to lowest positive affect: Agonist > partial agonist > inverse (no positive effect)
Define Efficacy and Potency
Efficacy: the extent of the biological response to a drug (a infinite concentration)… Potency: the amount of drug needed to produce a biological effect (where more potent drugs require less concentration to have an effect - albeit not necessarily a maximal effect)
On a drug response curve how is a) greater potency demontrated… b) greater efficacy demonstrated?
a) more potent the curve is to the left… b) greater efficacy goes higher in reponse
On a curve that shows 3 drugs, one has NO cooperativity and the other two have either positive cooperativity and negative cooperativity, how is demontrated?
Postive cooperativity has a steeper curve… where negative cooperativity is a shallower curve… both relative to the "no cooperativity" curve
Do cooperative curves show Michaelis Menton?
no
Define desensitization, homo desensitization, and hetero desensitization.
Desensitization: decreased response to an agonist over a short period of time… Homologous D: only the stimulated receptor is desensitized… Heterologous D: other receptors are alos desensitized even though they are not stimulated by the initial agonist.
what does a quantal dose effect curve show?
response is reduced to "plus" or "minus", and a fraction of individuals who respond is plotted vs dose
What is the usefulness of quantal dose curves?
They are useful in determining therapeutic indices.
what are three potential mechanisms for therapeutic vs toxic effects?
(1) one DR interaction--> one effector, which can have a therapeutic or toxic toxic effect… (2) one DR interaction --> two effectors: on effector has a therapeutic effect the other receptor has a toxic effect… (3) D+R1 and D+R2 --> each effects a different effector, one effector has a therapeutic effect and the other effector has a toxic effect
Give the equation for the therapeutic Index
therapeutic index = TD50/ED50… where TD50 is the dose at which a toxic effect is seen in 50% of individuals… ED50 is the dose at which a efficacy is seen in 50% of indivduals
None