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Intro to Pharmacology > Introduction to Pharmacodynamics > Flashcards

Introduction to Pharmacodynamics Flashcards

1
Q

Pharmacokinetics 2 vs. Pharmacodynamics 2

A

Pharmacokinetics (PK)
“What the body does to a drug”

Involves movement of drugs to get to the site of action
ADME
Absorption
Distribution 
Metabolism 
Excretion

Pharmacodynamics-what the drug does to the body

Interaction at the effective site to produce pharmacologic activity
Ex: How a drug interacts with a specific receptor and triggers a change in biological regulation

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2
Q

What are receptors?

What are most receptors and what are they made of?

A

Molecular targets where drugs interact to produce an effect
Most are proteins
Made of amino acids and subunits

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3
Q

Where are they located?

A

Some imbedded in the lipid bilayer of cell membranes (transmembrane)
Others located intracellularly

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4
Q

Describe the types of protein strcutrures?

A 
Primary
-Amino acid sequence of protein
Secondary
-Microstructures due to attractions between amino acids
Tertiary
-Global shape due to secondary structure
Quaternary
-Only with multiple, distinct molecules
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5
Q

Why are receptors important?

A
  1. Selectivity of drug action
  2. Affinity depends on the properties of the drug
    - Shape, charge, size
  3. Determines the relationship between dose and the pharmacological effects of the drug
  4. Responsible for pharmacologic actions of agonists and antagonists
    - When drugs bind to receptors, what action occurs (inhibition or excitation)
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6
Q

4 major types of interactions between drugs and receptors

A
  1. Transmembrane ion channels
  2. Transmembrane receptor-enzymes
  3. Transmembrane G-protein coupled receptors (GPCRs)
  4. Cytosolic-nuclear receptors
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7
Q

Examples of gated ion channels?

3

A

Gaba receptors-benzodiapenes-seizure medication- inhibitor

Nicotinic- ach

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8
Q

What do receptor-enzymes?

A

causes a conformational change.

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9
Q

What activates GPCRs?

A

ligand binds and activates

Then GPCR exchanges GTP for GDP

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10
Q

What does the activated G protein allow?

A

dissociation of the alpha subunit. The alpha subunit is then free to move into the cytoplasm and signal

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11
Q

When does signal transduction occur?

A

after a drug binds to a specific receptor

Changes within the cell in response to a drug

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12
Q

Why are receptors in the plasma membrane so important for drugs?

A

Most drugs are positively and negatively charged so they are unable to diffuse directly through the membrane. They need receptrs and channels

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13
Q

What does drug affinity depend on?

A

depends on the properties of the drug

-Shape, charge, size

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14
Q

Cells recieve multiple stimulatory and inhibitory signals simultaneously. How are they interpreted?

A

second messengers

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15
Q

Another defintion for pharmacodynamics?

A

Induce changes within the cell to produce a biochemical or physiologic response

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16
Q

What do second messengers do?

A

Help in translating the message from the bound drug into a cellular response

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17
Q

Examples of second messengers?

A

Cyclic adenosine monophosphate (cAMP)
Cyclic guanosine monophosphate (cGMP)
Inositol trisphosphate (IP3)

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18
Q

What does inositol triphosphate do? (IP3)

A

Aids in release of calcium from within the cell

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19
Q

Where do the drug and recepetor pair in the cytosolic-nuclear receptors and where do they go?

A

they bind in the cytosol and move into the nucleus. When they get there they bind to DNA and create RNA making specific proteins.

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20
Q

Examples of cytosolic-nuclear receptors?

A

glucocorticoids and sex hormones

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21
Q

Drugs compete for selective receptor sites

Favorability of the interaction is based on what?

A 
Chemistry
Biochemical affinity (attraction)
Intermolecular interactions (compatibility)
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22
Q

What does affinity refer to ?

A

Chemical forces that cause the drug to associate with the receptor
Bond Forces

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23
Q

If there is a higher affinity how does that affect the drug and receptor interaction?

A

tighter drug binding to the receptor

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24
Q

What does drug efficacy refer to?

A

Extent of functional change imparted to a receptor upon binding of a drug

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25
Q

What is the benefit of having a better knowledge of a receptor structure?

A

increased ability to design a drug selective for a certain receptor this could perhaps cause fewer side effects

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26
Q

Describe basal activity and what is another name for it?

A
  • Also called constitutive activity
  • Activity of a cell in the absence of a ligand (either endogenous or exogenous)
  • Or the “natural” activity of a cell
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27
Q

How does an agonist affect activity?

What mediums?

A

increases activity

Natural ligand
Exogenous compound (drug)
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28
Q

How does an inverse agonist affect activity?

A

Decreases activity

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29
Q

Describe the process of agonism?

3

A
  1. Drug binds to receptor
  2. Interaction activates signal cascade
  3. Leads to function within the cell
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30
Q

Describe epinephrines role with beta-1 receptors in cardiac tissue?
3 steps
5 things total to remember

A

Its an alpha/beta receptor agonist so….
1. Epi attaches to beta-1 receptors →
2. increases calcium level in the cell →
3. increases force of contraction of cardiac muscle
Useful in cardiac arrest

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31
Q

What are partial agonists?

A

Drug that cannot produce a full response, regardless of the concentration

32
Q

What are some factors that make agonists partial agonists?

2

A

number of receptors on the cell membrane

Drug history

33
Q

What is Buprenorphine?

A

opioid analgesic used to treat acute and chronic pain

34
Q

What is Buprenorphine role as a partial agonist?

A

Partial agonist of mu receptor in central nervous system → pain relief
Used to deccrease withdrawl symptoms

35
Q

Whats can partial agonists be used for?

A

utilized in opioid treatment programs to decrease withdrawal symptoms in patients but not provide as much euphoria as a full opioid agonist (Ex: Heroin)
Can be displaced from receptor by opioids with higher affinity

36
Q

What are inverse agonists?

A
  • Drug that can stabilize receptors in the inactive state

- Binding to a receptor by an inverse agonist produces an effect opposite that of an agonist

37
Q

Examples of inverse agonists?

A

diphenhydramine

Gaba receptors

38
Q

How does an anti-histamine work as a inverse agonist?

3

A
  • Anti-histamine is an inverse agonist for the H1-receptor
  • Blocks the release of histamine from mast cells
  • Decreases symptoms caused by histamine release
39
Q

How does a GABA receptor work as an inverse agonist?

A
  1. When bound by natural ligand (GABA) →
  2. allows chloride into the cell, which causes sedation
  3. Inverse agonist of GABA receptor will cause anxiety and seizure
40
Q

Look at illustrations for agonists in the slide show

A

More agonists binding = more saturation = more active unbound drug

41
Q

What is ED50?

A

The point where 50% of patients have a therapeutic effect from the medication
-directly in between threshold and and ceiling levels

42
Q

What is potency?

A

Dose of drug necessary to produce a specified effect

43
Q

What determines potency?

A
  1. receptor density,
  2. efficiency of the stimulus-response mechanism
  3. affinity
  4. efficacy
44
Q

What is intrinsic efficacy?

And what is it determined by?

A

Power of a drug to induce a response

Number of receptors in the target tissue

45
Q

How do you determine if one drug is more potant than the other?

A

If it requires less drug to get the same effect

46
Q

How os relative potency calculated?

A

ED50b/ED50a

47
Q

What is a competitive antagonist?

2

A
  1. Drug that binds to a receptor but does not initiate a response
  2. Compete for active sites with agonists
48
Q

What is an active site?

aka?

A
  • Site where the drug recognizes and binds to the receptor

- Also called substrate binding site

49
Q

How does propranolol act as a competitive antagonist?
3

Whats its end result on the heart?

Look at competitive antagonists picture slides and explain them

A
  1. Its a beta-blocker so it binds to beta1 receptor preventing epinephrine, a beta agonist, from binding to the same receptor
  2. Does not initiate a response
  3. Blocks epinephrine from initiating its response → decreasing rate and contractility in the heart
50
Q

What is a non-competitive antagonist?

A

Drug that binds to receptor and does not produce an effect

Binds to a different site other than the drugs active site but that binding creates a conformational change in the binding of the active site.

51
Q

What is the site called that a non-competitive antagonist binds to?

A

an allosteric site

52
Q

Describe the steps in non competitive antagonists processes?

3

A
  1. Antagonist binds to this site ➔
  2. changes the conformation of the receptor ➔
  3. impossible for an agonist to bind
53
Q

What is chemical antagonism?

Example?

A

Drug (antagonist) interacts directly with the agonist drug and renders it inactive
Example: Digibind® - binds to the drug digoxin

54
Q

What is Functional/Physiologic Antagonism?

Example?

A

Antagonist acts through a completely different mechanism to counteract the effect of the agonist
Example: Calcium channel blockers reduce effects of epinephrine

55
Q

Describe the selectivity of aspirin?

A

Not very selective. It does it job by inhibiting COX1 and COX 2 receptors to stop inflammation but also interfers with other processes like platelet, kidney function, and stomach issues

56
Q

Describe the selectivity of Celecoxib or Celebrex?

A

Pretty selective. It only inhibits COX2 and works primarily at the site of inflammation. It also has fewer side effects

57
Q

Why is drug selectivity an important concept to understand when selecting drug therapy for patients?

A

Mitigate side effects of drugs being used

58
Q

What does cellular regulation accomplish?

A

Prevention of over-stimulation that could lead to cellular damage

59
Q

What are the four kinds of cell regulation?

A

Up regulation
Down regulation
Desensitization or (tachyphylaxis)
Refractory

60
Q

What is up regulation?

A

Cells may add receptors to the cell membrane

61
Q

What is down regulation?

A

Repeated stimulation of receptor → cell begins to remove receptors from the cell membrane

62
Q

What is Desensitization or (tachyphylaxis)?

A
  • not getting the same effect that you used to
  • Diminished effect of drug over time
  • Decreased ability of drug to stimulate receptor

Like caffeine if you drink too much

63
Q

What is refractory regulation?

A

Period of time during receptor simulation before another interaction can produce an effect

64
Q

What are the two borders of the acceptable therapeutic range?

A

Minimum Toxic Concentration
(MTC) -top border

Minimum Effective Concentration
(MEC)- bottom border

65
Q

Therapeutic Window/Range can best be described as?

A

Doses of a drug which elicit a therapeutic response without unacceptable toxicity

66
Q

What does the Therapeutic index provide?

2

A
  1. Method for quantifying therapeutic window

2. Provides a relative safety margin of a drug

67
Q

How does the TI affect the safety of the drug?

2

A

Greater the TI the safer the drug

Greater degree of dosage flexibility means more convenience

68
Q

Why does warfarin require a lot of monitoring?

A

It has a small therapeutic window.

If the INR is below two then risk of clotting. If INR is above 3 then they are at risk of bleeding.

69
Q

Describe penicillin’s therapeutic window?

A

Large therapeutic window. Toxic level is high

70
Q

What is the LD50?

A

LD 50-50% of patients die(or experience toxic effects) from this dose

71
Q

What is the equation for figuring out the TI?

A

LD50/ED50

72
Q

Examples of TI equations?
Diazapam?
Digoxin?

A 
TI = 100/1 = 100
TI = 2/1 = 2
73
Q

Example of digoxin TI calculations:
Therapeutic range at 0.6_1.5ng/mL
Toxic concentration at 1.5 ng/mL
TI?

A

TI = (toxic concentration / therapeutic range) = 2.5

74
Q

What three drugs have very narrow theraeutic windows that we talked about?

A

Warfarin
Digoxin
Lithium

75
Q

Drug A has a TI of 100 and drug B has a TI of 14. Based on therapeutic index alone, which is the safer drug?

A

Drug A

Intro to Pharmacology (6 decks)

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