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Pharmacology > Introduction to Pharmacology > Flashcards

Introduction to Pharmacology Flashcards

1
Q

What is Thermodynamics?

A

The effect a drug has on the body (biological effects and mechanisms)

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2
Q

What is Pharmacokinetics?

A

How the body responds to the drug.

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3
Q

Name X3 Drug Targets

A
  • Proteins
  • DNA
  • RNA
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4
Q

What are Agonistic Drugs?

A

Mimics a neurotransmitter and binds to a receptor to activate and produce a cellular response.

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5
Q

Explain the X3 step how an Agonistic drug functions.

A

1) Agonist binds to receptor, this is reversible. (Binding step)
2) Receptor undergoes a conformational. (Affinity Steps)
3) Change in receptor conformation which activates the receptor. This is temporary.

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6
Q

Are Agonistic and Antagonistic drugs effects reversible?

A

-YES

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7
Q

What X2 Features does Agonistic drugs have?

A
  • Efficacy

- Affinity

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8
Q

What is Efficacy?

A
  • The ability a drug has to evoke a cellular response

- (‘e’-effect)

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9
Q

What is Affinity?

A
  • This is attraction between receptors and ligand (drugs)

- Determined by the chemical bonds between ligands and receptors.

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10
Q

What are Antagonistic Drugs?

A

-1) Bind to receptors (reversible) and block them. DO NOT ACTIVATE

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11
Q

Why do Antagonists not have Efficacy?

A

-They do NOT evoke e cellular response because they bind rot the receptor and block binding-No response occurs

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12
Q

What x2 types of graphs can show relationship between concentration and dose?

A
  • Sigmoidal

- Hyperbolic- Logarithmic (more accurate)

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13
Q

Compare the Efficacies between Partial and Full Agonists

A

Partial-Low Efficacy

Full-High Efficacy

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14
Q

What is drug potency?

A

The amount of a drug that is needed to produce a given effect

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15
Q

What is Reversible Competitive Antagonism?

A

-When Antagonist drug blocking effect can be overcome by increasing the concentration of the Agonist drug.

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16
Q

What is the name of the site where Competitive Antagonists and Agonist drugs bind?

A

-Orthosteric Site

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17
Q

Where do Non-Competitive Antagonistic Drugs bind?

A
  • Separate site

- Allosteric site

18
Q

What X2 things happen to a curve graph when Competitive and Non-Competitive Antagonists bind?

A

Competitive- Parallel shift to RIGHT (competitive- always right :)
Non-Competitive- Depresses the slope

19
Q

What affect does increasing concentration of an Agonist?

A

-Shifts curve to the RIGHT

20
Q

What effect does increasing concentration of a Competitive Antagonist and Non-Competitive have?

A

Competitive-Shifts more to the right

Non-Competitive- Depresses slope further

21
Q

What do Hydrophilic Signalling Molecules include?

A

neurotransmitters, hormones, endogenous molecules, peptides etc.

22
Q

What are Ligand-Gated Ion Channels?

A

Open in response to ligand binding

-Transmembrane Proteins

23
Q

What are G-Protein Coupled Receptors (GPCRs)?

A

Targeted by ‘Therapeutic Agents’-drugs

  • Signal via Secondary Messenger Systems
  • inbox for messages in the form of light energy, peptides, lipids, sugars, and proteins.
24
Q

What are Kinase-Linked Receptors?

A

uses second messenger signaling that triggers a cascade of cellular events.

25
Q

What are Nucleated Receptors?

A
  • In nucleus
  • Slow timescale-hours/days
  • Alter gene expression
26
Q

What type of channel are Voltage Gated Ion Channels: ?

A
  • Ligand Gated

- Opne in response to voltage

27
Q

How do G-Protein Coupled Receptors control effector activity?

A

-Secondary Messenger Systems

28
Q

How are G-Protein Coupled Receptors linked to Secondary Messenger Systems?

A

-Intermediate-G-Proteins

29
Q

What type of protein are receptors?

A

-Integral

30
Q

What is the structure of a receptor’s polypeptide and what terminus to they possess?

A
  • NH2 and COOH Termini

- Single Polypeptide Chain

31
Q

Wha is the structure of a G-Protein Coupled Receptor?

A

Polypeptide chain is connected to X7 transmembrane spans- are 3 intracellular AND 3 extracellular connecting loops

32
Q

What is the result when G-Protein Coupled Receptors are activated and what is this process called?

A
  • Activation of G-Proteins

- G-Cycle

33
Q

What are the X3 G-Protein sub-units?

A

Alpha, Beta and Gamma

34
Q

What type of protein are G-Proteins?

A

-Peripheral (Outside)

35
Q

What do G-Proteins called and act as when activated?

A
  • Intermediate-G-Proteins

- Intermediate between G-Protein Coupled Receptors and Effectors

36
Q

Explain what happens in the G-Cycle

A

Active State:

  • Alpha sub-unit dissociates off from polypeptide
  • GTP binds to Alpha sub-unit
  • GDP dissociates off (not-needed)

Deactivation of GCPRs:

  • Agonist dissociates off from receptor
  • Signalling can continue because G-Protein has been already activated
  • Alpha sub-units acts as an enzyme and breaks the GTP that’s is attached > GDP +Pi
  • Signal now turned off
  • Alpha sub unit re-joins polypeptide
  • G Cycle is COMPLETE!
37
Q

Are receptors used as signalling pathways?

A
  • YES

- Bind to signalling molecules to form signalling pathway

38
Q

What type of signalling molecules are Steroid Hormones?

A

-Hydrophobic

39
Q

What type of cascade is formed by Kinase-Linked receptors once bound to hydrophilic signalling molecules-causing Phosphorylation ?

A
  • Phosphorylation cascade

- As kinase enzymes trigger phosphorylation

40
Q

How do Nucleated Receptors Signal?

A
  • This causes dissociation of Inhibitory HSP protein
  • Hydrophilic and receptor complex moves to the nucleus and form a ‘Dimer’ (two receptors joint) - and binds to HREs (Hormone Response Elements)
41
Q

What does ‘Transpressed’ and ‘Transactivated’ mean in Transcription?

A

-Switched on= Transactivated

Switched off =Transpressed

42
Q

What type of factors are Nucleated Receptors

A
  • Transcription Factors

- Control DNA Transcription

Pharmacology (4 decks)

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