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BI316 > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

What is an important pre-requiste for proper drug action?

A

An important prerequisite for proper drug action is the non-uniform distribution of drugs within the body

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2
Q

Name and explain the 4 different levels which drugs act on

A
  • Molecular - biomolecules as immediate targets of drugs
  • Cellular - biochemical constituents in the process of transduction
  • Tissue - alteration of organ function
  • System - alteration of system function
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3
Q

What are most drug-receptor interactions mediated by?

A
  • Most drug-receptor interactions are mediated by NON-COVALENT bonds, which are reversible
  • In contrast to covalent bonds, there is no formation of a shared electron pair, but drugs attach to their site of action by multiple non-covalent contacts!
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4
Q

Drug-receptor interactions

A
  • Highly stable ion-ion electrostatic attraction
  • Partial charge dipole-ion electrostatic attraction
  • Partial charge dipole-dipole electrostatic attraction
  • Low strength van de Waals’ electrostatic attraction between apolar groups
  • Hydrophobic interactions of apolar molecules in an aqueous environment
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5
Q

How do most drug molecules produce their effects?

A

Most drug molecules produce their effects by binding to protein domains.

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6
Q

Name the four major groups of regulatory proteins involved as primary drug targets

A
  • Receptors
  • Ion channels
  • Enzymes
  • Carrier

look at slide 12

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7
Q

What does it mean when the specificity of drug action is reciprocal?

A
  • Individual classes of drugs bind only to certain molecular and cellular targets.
  • Individual molecular and cellular targets recognize only certain classes of drugs.
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8
Q

What does it mean when the specificity of drug action is dose-dependent?

  • specificity of drug action is usually strictly dose-dependent
A

Increasing the dose of drug (above its therapeutic range) will often affect molecular targets other than the principal pharmacological one, thus causing toxic side-effects.

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9
Q

Name examples of receptors (target) and its agonist (effector)

A

Nicotinic acetylcholine receptor - Nicotine
Beta-adrenoreceptor - Isoprenaline

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10
Q

Name examples of ion channels (target) and its modulator (effector)

A
  • Voltage-dep. Na+-channel - Lidocaine
  • Voltage-dep. Ca2+-channel - Nifedipine
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11
Q

Examples of Enzymes (receptor) and its inhibitor (effector)

A
  • Acetylcholinesterase - Neostigmine
  • Cyclooxygenase - Aspirin
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12
Q

Examples of carriers (target) and inhibitor (effectors)

A
  • Choline carrier - Hemicholinium
  • Na+/K+ pump - Ouabain
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13
Q

Agonist

A

Drug - that binds and activates its respective receptor
Drug D1 (agonist) D1 + R -> D1-R -> D1-R * -> Response

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14
Q

Affinity

A

Tendency of a drug to bind to a receptor.
Receptor occupation by drug is governed by affinity.

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15
Q

Efficacy

A

Tendency of a drug, once bound, to activate the receptor. Receptor activation by bound drug is governed by efficacy.

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16
Q

Antagonist

A

Drug that binds to receptor without triggering activation, thus preventing binding of agonist/physiological ligand.

Drug D2 (antagonist) D2 + R -> D2-R -> No Response

17
Q

Maximal pharmacological response

A

The maximal response on a particular receptor differs between chemically related agonists

18
Q

Maximal pharmacological Response

A

The maximal response on a particular receptor differs between chemically related agonists

19
Q

Maximal response

A
  • The largest response that a tissue is capable of giving, if triggered by a specific substance at high concentration.
  • Due to toxic side effects, the therapeutic dose might be considerably lower than the maximal response dose.
20
Q

Full agonist

A

A drug that can produce a maximal response

21
Q

Partial agonist

A

A drug that can only trigger a sub-maximal response

22
Q

When might a partial agonist act as a full agonist?

A
  • if a tissue contains a so-called ‘receptor reserve’ (due to poor intrinsic efficacy), then an otherwise partial agonist may act as a full agonist.
  • poor efficacy may be offset by activating a larger number of receptors, as would be required by a proper full agonist.

intrinsic efficacy = refers to the ability of a drug to produce a maximal biological response at a given receptor or target site

23
Q

Competitive Antagonist

A
  • Substance that has no intrinsic efficacy and binds reversibly with receptor.
  • Pharmacologically it dilutes the receptor concentration, causing a parallel shift of the dose-response curve.
  • Importantly, an increase of agonist dose can return tissue response to normal.
24
Q

Irreversible antagonist

A
  • Substance that triggers a blocking effect that cannot be reversed by increasing the agonist concentratoin
25
Q

Nicotinic acetylcholine receptor

A
  • Prototype of a ligand-gated ion channel of pharmacological importance
  • Part of a superfamily of neutrotransmitter-gated ion channels
  • 16 different cDNAs have been cloned from different species
26
Q

Competitive antagonst of nicotinic acetylcholine receptor

A

Tubocurarine
-Drug competes with native ligand, the neurotransmitter acetylcholine, for the receptor
-But drug does not initiate a biological response (nAChR ion channel opening)

27
Q

What are the 16 different types of cDNA that have been cloned from different species?

A
  • α-subunits 1 to 9
  • β-subunits 1 to 4
  • δ-subunits
  • γ-subunits
  • ε-subunits
28
Q

What are the three main branches of nAChr gene family?

A
  • Muscle nAChRs (NMJ)
  • Heteromeric neuronal nAChRs
  • Homomeric neuronal nAChRs
29
Q

Agonist of Nicotinic acetylcholine receptor

A

Suxamethonium
-Agonistic drug depolarizes the neuromuscular junction
-But does not dissociate rapidly from the nAChR complex causing a neuromuscular block

30
Q

Molecular approaches used in the structural analysis of pharmacologically important protein receptors

A
  • Protein purification and characterization
  • Affinity purification and characterization
  • Protein/peptide N-terminal sequence analysis
  • Mass spectrometric analysis of protein subunits
  • Cloning and sequencing of cDNA
  • High-resolution x-ray crystallography
  • High-resolution cryo-electron microscopy
  • Differential co-immuno precipitation methodology
  • Chemical cross-linking analysis
  • Native two-dimensional gel electrophoresis
  • Gel filtration analysis

BI316 (13 decks)

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