Lecture 2 Pharmacology Flashcards

1
Q
  1. What are receptors?

2. What are typical drug targets? (4)

A

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2
Q

With each, explain how it works:

  1. Receptors: agonist/inverse agonist, antagonist
  2. Ion channels: blockers, modulators
  3. Enzymes: inhibitor, false substrate, prodrug
  4. Transporter: normal transport, inhibitor, false substrate
A

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3
Q
  1. What is KD?
  2. What if you are below/above KD?
  3. What’d the basic formula for KD?
A

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4
Q

How do these work:

  1. Ligand-gated ion channels
  2. G-protein coupled receptors
  3. Kinase-linked receptors
  4. Nuclear receptors
A

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5
Q
  1. What are agonists?

2. What do these three terms refer to: affinity, efficacy, potency

A

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6
Q
  1. What is occupation governed by?

2. What is activation governed by?

A

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7
Q

What is ec50 or ic50?

A
  1. Effective concentration at which you see half the receptors occupied. Inhibitory conc at which you inhibit half the receptors

ACTUALLY SLIDE 28 SAYS IT IS THE CONC REQUIRED TO PRODUCE 50% OF THE MAX RESPONSE.

The IC50 is the concentration of an inhibitor where the response (or binding) is reduced by half.

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8
Q

What is the concept of spare receptors about?

A

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9
Q
  1. What are antagonists?
  2. What is the affinity and efficacy of antagonists?
  3. What’s the difference between inhibitor and antagonist?
A

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10
Q

Competitive antagonists:

  1. What is it? For which one that dominates, what factors determine that?
  2. What two types of competitive antagonist binding happens?
  3. In the presence of the reversible competitive antagonists, what happens to the agonist concentration-effect curve? The extent of the shift is a measure of what? What does the right shift without a change in slope/maximum mean?
  4. Irreversible competitive antagonists - explain with terms: equilibrium, receptors number and concentration of agonist.
  5. What does the graph look for irreversible competitive antagonists?
A

That means you need more conc of agnost to have the effect it used to have. ec50 increasing

They are parallel. The efficacy doesn’t change. You just need more agnost bc it’s a comabt b/w ago and antago

The multiple increase in the agonist concentration required to achieve a given response is called the dose ratio

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11
Q

Uncompetitive antagonists:

1. What are they?

A

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12
Q
  1. What are partial agonists?
  2. What is their efficacy and affinity like?
  3. Why would you need a fully functional agonist to measure this?
  4. What does their graph look like for: response vs conc/occupancy
A

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13
Q
  1. What is constitutive activity and do all receptors have it?
  2. What are inverse agonists?
  3. Go study the graphs on page 23 - look at axis and the labels!
A

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14
Q
  1. What is the two-state receptor model?
  2. Usually when no ligand is present, where does the equilibrium lie?
  3. What state does the agonist stabilise? So what happens to the equilibrium?
  4. What state does the inverse agonist stabilise?
A

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15
Q
  1. Drug effect can finishing following what?
  2. What is desensitisation, tolerance and resistance?
  3. By what 5 mechanisms do they work?
A

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16
Q

Comping drugs - what three things are used and what is least used to compare? Why?

A

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17
Q

Tell me about drugs becoming a poison and side effects

A

Due to non-specific binding and affinities for different receptors, no drug is completely specific. Generally increasing the dose of a drug will cause it to affect an increasing number of targets – this leads to side effects.

Bc non-specific binding is a thing - dont want too high of a dose bc other ish being avtivated?

18
Q

What is therapeutic index? Formula?

A

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