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PHAR232 > Module 1: Principle Of Pharmacology > Flashcards

Module 1: Principle Of Pharmacology Flashcards

1
Q

What is. Pharmacology?

A

The study of drugs and poisons

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2
Q

What is a drug?

A

Any substance used to exert a biological effect

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3
Q

What impacts the ease & rate of uptake of drug into the body?

A

The route of administration (ie oral, IV, etc)

The absorption

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4
Q

What are the 2 main tissue reservoirs?

A

Body fat

Blood proteins

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5
Q

What are the 2 main divisions of pharmacology?

A

Pharmacokinetics (movement around the body)

Pharmacodynamics (examination of drug interactions)

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6
Q

What is specificity and selectivity?

A

Specificity - drug having a single action at a tissue or organism level

Selectivity - ability of drug to affect one type of cell above others

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7
Q

What is an agonist?

A

Activator, Causes a shape change in the receptor.

Can be true agonist, partial agonist OR inverse agonist (causes a shape change AWAY from the active conformation)

In they key/lock metaphor - the agonist is the key that opens the lock

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8
Q

What is affinity?

A

Ability of drug to bind receptor.

Occupation is governed by affinity

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9
Q

What is efficacy?

A

Ability to activate receptor to elicit effect. (Only agonists have efficacy)

Activation is governed by efficacy

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10
Q

What is potency?

A

Range of concentrations required to have an impact

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11
Q

What is biased agonism?

A

Where different agonists can bind to the same receptor but cause different responses.

In other words, the shape change induced by the agonist can favour one signalling cascade over another

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12
Q

What are the 2 possible mechanisms for action of partial agonists?

A
  1. That the partial agonist only elicits a partial conformational change
  2. That the partial agonist elicits a full conformational change, but not all of the time
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13
Q

What is an inverse agonist?

A

Drug that interacts with a receptor to create a non-active conformational change. So it IS still a shape change, but in the opposite direction to the active form.

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14
Q

What is an antagonist?

A

An anti-agonist - it prevents the action of an agonist. It can bind to a receptor but not change it’s conformation.

It has affinity, potency but does not have efficacy

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15
Q

What are the 3 main categories of antagonist?

A
  • Competitive antagonist (competes against agonist for same site on receptor)
  • non-competitive antagonist (ie straight jacket when trying to raise your arm - binds to a different site on the receptor that stops the agonist)
  • irreversible antagonist (binds to same site on receptor, but can’t be removed)
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16
Q

What is the difference between Antagonist and antagonism?

A

Antagonist is the compound

Antagonism is the process

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17
Q

What is chemical antagonism?

A

An agonist itself becomes chemically bound to a chemical antagonist (ie bind to the agonist rather than receptor)

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18
Q

What is pharmacokinetic antagonism?

A

Changing the agonist half-life in the body by promoting elimination or altering its distribution/uptake

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19
Q

What is physiological antagonism?

A

Competition between 2 opposing systems in the body, ie when 2 drugs administered that affect opposing systems and effects cancel out.

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20
Q

What is the purpose of a receptor?

A

To translate an incoming signal into a cellular response

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21
Q

What are the primary groupings of receptors?

A

Ionotropic (ion channels)

Metabotropic (rely on metabolic event)

Kinase linked receptors

Nuclear receptors

22
Q

What response scales can you expect with ionotropic and metabotropic receptors?

A

ionotropic - milliseconds

Metabotropic - seconds

23
Q

How do ligand-gated Ion Channels avoid accidental activation?

A

It will often require 2 simultaneous events to activate the channel (ie binding of 2 ligand molecules)

24
Q

Where are ligand-gated ion channels located?

A

In electrically excitable cells (ie heart, brain, nerves, skeletal muscles)

25
Q

What effects can ligand-gated ion channels cause in a cell?

A

A change in membrane potential of the cell - can have a flow on effect on voltage-gated ion channels.

Either stimulators (influx of + ions) = depolarisation

Or Inhibitory (influx of - ions) = hyperpolarisation

26
Q

What are GPCRs?

A

G Protein coupled receptors

27
Q

what category of receptor does GPCR fall into?

A

Metabotropic

28
Q

What is the basic structure of GPCRs?

A
  • 7 transmembrane domains (can form a circle for binding pocket to nestle into)
  • Extracellular N terminus
  • Intracellular C terminus

The 3rd intracellular loop and the C terminal tail shift their position and act like “chopsticks” to “pick up” the G protein

29
Q

What is a PAR and what type of receptor is it? And what is it’s role?

A

Protease-activated receptor. It is a type of GPCR. This is the “smoke alarm” warning system of the cell.

30
Q

How are PARs different from other types of GPCRs?

A

Same basic structure, but it has a tethered ligand that is cleaved to activate the receptor. This means they are “1 use only”

31
Q

What are 3 new GPCR types?

A

Proton-sensing and lysolipid-sensitive G protein coupled receptors

  • activated by protons or lipids
  • associated with cancer

Calcium-sensing receptors
- important role in suppressing parathyroid hormone secretion

32
Q

What are G proteins?

A

Heterotrimeric compounds composed of α, β and γ proteins in combination. They interact with GPCRs.

33
Q

How does the G protein α subunit activity differ from the β and γ subunits?

A

the α subunit is a GTPase. At rest it is bound with GDP, then when activated (binds with GTP instead), the GPCR receptor is activated and can interact with G protein.

The enzyme part of α subunit can then cleave a phosphate to become GDP again (inactive form).

Different types of α subunits have different effects on adenylate cyclise activity (activate or inhibit)

34
Q

What is the action of β-γ subunits of G proteins?

A
  • acts as signalling molecules once liberated from α subunit

- appears to always function together

35
Q

What are the steps of G protein signalling?

A
  1. GPCR inactive. G protein subunits together, α subunit bound to GDP.
  2. GPCT receptor activated by ligand, conformational change in positioning of 3rd intracellular loop & C terminus tail allowing interaction with G protein. α subunit exchanges GDP for GTP and dissociates from βγ.
  3. Both α and βγ active at specific target effectors.
  4. α subunit cleaves phosphate to reform GDP, collapses in and rejoin βγ to form G protein again.
36
Q

What are RGSs and what is their job?

A

Regulators of G-protein signalling.

Their job is to regulate α subunit activity

37
Q

What are the 3 types of RGS?

A
  1. GAPs (GTPase-Activating Proteins)
    - promotes enzyme of activity to turn GTP to GDP which reduces action time of α.
  2. GEFs (Guanine Nucleotide Exchange Factors)
    - encourages α subunit to drop GDP and uptake GTP, increases signalling of α.
  3. GDIs (Guanine Nucleotide Dissociation Inhibitors)
    - prevents activation of G proteins
38
Q

What is the impact of RGSs?

A
  • some neurodegenerative disorders associated with alterations to these
  • represent targets for drugs
  • activity of some poisons require inactivation of these
  • cancers proposed to include mutations of these
39
Q

Why is cAMP important?

A

It regulates many proteins either directly or through activation of PKA

40
Q

What is cAMP

A

Cyclic AMP - made by adenylate cyclase from ATP

41
Q

What is the activity of a protein kinase?

A

Moving phosphate molecules. As a result, critical to kinase cascades

42
Q

What are RTKs

A

Receptor tyrosine kinase

43
Q

What is the key summary of RTK activity?

A 
Monomers form dimer
Dimer self phosphorylation
That attracts other proteins
They get phosphorylated
They trigger cascades
Really important for gene transcription
44
Q

What is special about nuclear and cytoplasmic receptor transcription factors?

A

They are a receptor and also a transcription factor (rather than being a receptor that then activates a separate transcription factor)

45
Q

What are the classes of nuclear receptors?

A

Class I - move from cytoplasm into the nucleus, homodimer
hybrid class - nucleus only, heterodimer with retinoid receptor
Class II - nucleus only, heterodimer for all except retinoid receptor

46
Q

What are the 2 phases of gene transcription from nuclear receptors?

A

Primary response - direct regulation of small number of genes, within 30min

Secondary response - gene transcribed in primary response are transcription factors that transcribe additional genes

47
Q

What are 2 primary types of signalling?

A

Neuronal - punctual & rapid

Hormonal - can have a short-lived signal with long-lived response

48
Q

What is desensitisation?

A

Loss of sensitivity of a receptor to continuing stimulation by agonist.

Loss of response due to ongoing treatment with a drug.

49
Q

What is arrestin and what does it do?

A

A compound that can recognise receptors that have gone through repeated cycles of phosphorylation/dephosphorylation. It binds and removes the receptor from the membrane.

This is in the process of homologous desensitisation.

50
Q

What is homologous and heterozygous desensitisation?

A

Homologous: only the receptor that is in a constantly-activated state is regulated

Heterologous: All receptors of a certain type are regulated (whether activated or not)

51
Q

What is remodelling?

A

Process by which cells adapt to continued presence of a drug to change the response of the entire network or organ

PHAR232 (5 decks)

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