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Pharmacology > Pharmacodynamics (Exam 1) > Flashcards

Pharmacodynamics (Exam 1) Flashcards

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1
Q

Agonist

A

Activator

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2
Q

Antagonist

A

Inhibitor

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3
Q

Endogenous

A

Naturally made

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4
Q

Xenobiotics

A

Synthetically made

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5
Q

Drug Targets

A
  1. Receptors
  2. Enzymes
  3. Ion Channels
  4. Transports/Carriers/Pumps
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6
Q

Types of Receptors

A

Ligand-Gated Ion Channels (LGIC)
G-Protein Coupled Receptors (GPCR)
Enzyme-Linked Receptors
Intracellular Receptors

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7
Q

Affinity

A

Strength of attraction between drug and its binding site

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8
Q

Covalent

A

Strong and in many cases not reversible
Least Common

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9
Q

Electrostatic

A

Vary from relatively strong linkages to weaker hydrogen bonds to van der Waals
Most Common

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10
Q

Hydrophobic

A

Important for highly lipid soluble drugs

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11
Q

Drug Response

A

Result of chemical interactions between a drug and binding site

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12
Q

Receptors

A

Transmembrane proteins located within cell membrane

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13
Q

How do receptors work?

A

Bind to ligand and propagate a signal leading to effect/response

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14
Q

Ligand

A

Molecule which produces a signal by binding to a site on receptor

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15
Q

Receptor Mediated Messenger System

A

First Messenger - ligand
Signal Transducer - receptors
Effector - enzymes activated by signal transduction
Second Messenger - Signaling molecules that activate other targets, allows for signal amplification

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16
Q

Autocrine Signaling

A

Ligand originates from same cell

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17
Q

Autoreceptor

A

Receptors whose purpose is to bind their own ligand as negative feedback mechanism

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18
Q

Paracrine Signaling

A

Ligand originates from nearby cell

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19
Q

Endocrine Signaling

A

Ligand originates from distant cell and travels through bloodstream

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20
Q

Hormones

A

Ligands of endocrine system

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21
Q

Ligand Gated Ion Channels (LGIC)

A

Ligand binding causes conformational change that opens channel allowing ions (Na+, Ca2+, K+, Cl-) to pass through

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22
Q

LGIC for Na+ and Ca2+

A

Excitatory
Make cell more positive, closer to threshold potential

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23
Q

LGIC for Cl- and K+

A

Inhibitory
Make cell more negative, farther from threshold potential

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24
Q

Acetylcholine (LGIC)

A

Nicotinic Receptor
LGIC (Na+)

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25
Serotonin (LGIC)
5HT3 Receptor LGIC (Na+)
26
Glutamate (LGIC)
NMDAR Receptor --> LGIC (Ca2+) AMPAR Receptor --> LGIC (Na+)
27
GABA (LGIC)
GABA-A Receptor LGIC (Cl-)
28
G-Protein Coupled Receptors (GPCRs)
Receptor bound to G-protein and leads to G-protein activation
29
Gs GPCRs
Activates adenylyl cyclase (AC)
30
Gi GPCRs
Inhibits adenylyl cyclase (AC)
31
Gq GPCRs
Activates phospholipase C (PLC)
32
What determines if receptor is Gs, Gi, or Gq?
The alpha subunit of G-protein
33
Gs Signaling Pathway
AC is activated and converts ATP to cAMP cAMP acts as second messenger --> activates cAMP dependent protein kinases Kinases phosphorylate other proteins
34
Gi Signaling Pathway
AC is inhibited Sometimes K+ channels opened
35
Gq Signaling Pathway
Phospholipase C (PLC) is activated and converts PIP2 into DAG and IP3 DAG and IP3 act as second messengers DAG activates PKC which activates other enzymes IP3 causes Ca2+ release from intracellular storage Ca2+ activates calmodulin --> other enzymes
36
Acetylcholine (GPCR)
M1, M3, M5 Receptor --> GPCR Gq M2, M4 Receptor --> GPCR Gi
37
Norepinephrine/Epinephrine (GPCR)
alpha-1 receptor --> GPCR Gq alpha-2 receptor --> GPCR Gi beta1-3 receptor ---> GPCR Gs
38
Dopamine (GPCR)
D1, D5 Receptor --> GPCR Gs D2, D3, D4 Receptor --> GPCR Gi
39
Serotonin (GPCR)
5HT1, 5 Receptor --> GPCR Gi 5HT2 Receptor --> GPCR Gq 5HT4, 6, 7 Receptor --> GPCR Gs
40
Endogenous cannabinoids (GPCR)
CB1, CB2 Receptor --> GPCR G1
41
Endogenous opioids (GPCR)
Mu, delta, kappa Receptors --> GPCR Gi
42
Which receptor works quicker? GPCR or LGIC
LGIC because there's no second messenger system
43
Activation of which receptor leads to increase in cAMP?
Gs coupled receptors
44
Enzyme-Linked Receptors
Linked to an enzyme that mediates downstream signaling Alter gene expression to produce effects --> slow onset and long duration
45
Receptor Tyrosine Kinases
Enzyme within receptor Ligand binds to receptor --> Conformational change leads to dimerization --> Activates tyrosine kinase function --> phosphorylation of tyrosine residue -> receptor becomes activated and phosphorylates downstream proteins
46
Which ligand uses receptor tyrosine kinases?
Insulin
47
Cytokine receptors
Enzyme as separate protein Enzyme binds non-covalently and becomes activated following ligand binding and dimerization
48
Which ligand uses cytokine receptors?
Growth hormone
49
Intracellular/Nuclear Receptors
Ligand must be lipid soluble to cross cell membrane Nuclear receptors bind to DNA and regulate gene expression Contain ligand binding domain (LBD) and DNA binding domain (DBD)
50
Type 1 Nuclear Receptors
In cytosol but enter nucleus after ligand binding
51
Type 2 Nuclear Receptors
Remain in nucleus and ligand must enter to bind
52
Which ligands use Type 1 Nuclear Receptors?
Sex hormones and glucocorticoids
53
Which ligands use Type 2 Nuclear Receptors?
Vitamin D and thyroid hormone
54
Onset and Duration of LGIC
Onset: Milliseconds Duration: Seconds
55
Onset and Duration of GPCR
Onset: seconds to minutes Duration: minutes to hours
56
Onset and Duration of Kinase-Linked Receptors
Onset: 30 mins to an hour Duration: Hours to days
57
Onset and Duration of Nuclear Receptors
Onset: 30 mins to hours Duration: Hours to days
58
Regulation of Recepetors
Overstimulated receptor leads to decreasing sensitivity or number of receptors Can occur due to high levels of endogenous ligand or drug
59
Competitive inhibitor
Bind to enzyme at same site as substrate
60
Noncompetitive inhibitor
Bind to enzyme at different site and block reaction from occurring
61
Uncompetitive inhibitor
Bind only to enzyme-substrate complex and block reaction form occurring
62
Intracellular Enzyme
Phosphodiesterase (PDE) - responsible for breaking down cAMP and cGMP
63
What is an example of competitive inhibitor of PDE5?
Sildenafil Used to treat ED and pulmonary arterial hypertension
64
Extracellular Enzyme
Acetylcholinesterase (AChE) - responsible for breaking down acetylcholine in synapse
65
What is an example of competitive inhibitor of AChE?
Donepezil Treatment of Alzheimer's disease
66
Voltage Gated Ion Channels (VGICs)
Change in voltage causes conformational change that opens channel and allows ions to pass through Rapid Signaling
67
VGIC fo Na+ or Ca2+
Excitatory More positive cell and closer to threshold potential
68
VGIC for Cl- or K+
Inhibitory More negative cell and farther from threshold potential
69
Ca2+ VGIC in Vasculature
Blocked by some blood pressure lowering drugs
70
Na+ VGIC on Neurons
Blocked by some drugs used to treat epilepsy
71
Transporters/Pumps/Carriers
Proteins that help bring small molecules across biological membranes
72
Why are transporters different than channels?
Transporters have binding sites for transported molecules Channels are simultaneously open to inner and outer membrane
73
Serotonin Transporter
Uptake of serotonin from synapse into presynaptic neuron (SSRIs) block transporter and increase serotonin levels in synapse
74
A drug binds to receptor located in the cytosol. Then, the drug-receptor complex travels to nucleus and enhances transcription. What kind of receptor is this?
Nuclear Receptor
75
Drug Receptor Theory
Formation of drug-receptor complex leads to biological response
76
Assumptions of Drug Receptor Theory
Reversible manner Increase in drug concentration increase response, visa versa Max response achieved when receptors saturated Drugs competing with endogenous ligand
77
What receptor does norepinephrine activate?
Beta1 receptors on the heart leading to increase in heart rate
78
What receptor does acetylcholine activate?
M2 receptors in the heart leading to a decrease in heart rate
79
Full agonist
Produces same maximum response as endogenous ligand
80
Partial agonist
Produces lower maximum response than endogenous ligand
81
A partial agonist acts as net agonists when...
...endogenous ligand concentrations are low
82
A partial agonist acts as net antagonists when...
...endogenous ligand concentrations are high
83
Competitive antagonist
Competes with endogenous ligand for binding site
84
Non-competitive antagonist
Does not compete with endogenous ligand Binds to allosteric site
85
Reversible Antagonist
Binds reversibly to the receptor
86
Irreversible Antagonist
Binds covalently to the receptor
87
Inverse agonist
Reduces receptor activity below basal levels Decrease constitutive activity
88
Constitutive (Basal) Activity
Low levels of basal activity, even when there is no ligand present
89
Positive Allosteric Modulators (PAM)
Bind to receptor at allosteric site and either increase receptor affinity OR increase receptor efficacy
90
Negative Allosteric Modulators (NAM)
Bind to receptor at allosteric site and either decrease receptor affinity OR decrease receptor efficacy
91
An ion channel has constitutive activity of 5 Ca2+ ions per second. The endogenous ligand for an ion channel causes the influx of 20 Ca2+ per second. If drug A binds to ion channel and cause the influx of 2 Ca2+ per second, what best describes drug A?
Inverse agonist
92
Dose-response curve
Describes relationship between the dose/concentration of drug molecule and specific effect/response
93
Efficacy
Measure of the maximum biological response produced by the drug
94
Intrinsic Activity (IA)
Drug's maximal efficacy as a fraction of maximal efficacy produced by endogenous ligand
95
Saturation Binding Curve
Drug concentration versus number/percentage of receptors bound Determine affinity
96
Key parameters of saturation binding curve
Bmax and KD
97
Dose Response Curve
Drug concentration/dose versus effect/response Determine efficacy and potency
98
Key parameters of dose response curve
Emax and EC50
99
Bmax
Concentration of receptor sites (total number of receptors)
100
KD
Drug concentration at which 50% of receptors are bound
101
Relationship between KD and affinity
Smaller KD will have a higher binding affinity Inversely proportional
102
Emax
Maximum possible response that a drug can produce
103
Relationship between Emax and Efficacy
Larger Emax will have higher efficacy Directly proportional
104
EC50/ED50
Amount of drug needed to produce 50% of the maximum response
105
Relationship between EC50 and Potency
Smaller EC50 will have higher potency Inversely proportional
106
Relationship between slope and sensitivity
Steeper slope means higher sensitivity
107
A shift to the right of dose response curve means...
...competitive antagonist
108
A downward shift of the dose response curve means...
....non-competitive or irreversible antagonist Changning Emax
109
Spare receptor
When possible to elicit a maximal response at a concentration of agonist that does not result in occupancy of all available receptors
110
Reasons for Spare Receptors
1. Number of receptors may be greater than number of available downstream signaling molecules 2. Duration of activation of signaling molecules is much greater than duration of drug-receptor interaction
111
Selectivity
Degree to which drug acts on a specific tissue or target relative to others
112
Tissue Selectivity
When receptor or target is only found in one type of tissue Direct application may provide some selectivity
113
Target Selectivity
Antibody drugs usually have high selectivity for target
114
Temporal relationship between drug binding and effect
Drug remains bound: persistent effect until complex is destroyed or new molecules produced Drug dissociates from target: Terminate drug action, may persist due ti coupling molecule being active
115
Idiosyncratic
Rare and unpredictable drug response
116
Hyporeactive
Patients who have lower degree of drug response
117
Hyperreactive
Patients who have higher degree of drug response
118
Tolerance
Diminishing drug efficacy over time
119
Tachyphylaxis
Tolerance that occurs rapidly after use of a drug
120
Quantal Dose-Response Curve
Dose of drug versus percentage of individuals experiencing specific effect
121
Therapeutic Index (TI)
Relationship between dose of drug that causes toxicity versus the dose that causes therapeutic effects TI = TD50 / ED50
122
Which of the following drugs would be considered the safest, based on therapeutic index?
Drug with TD50 of 20mg and ED50 of 1mg 20 / 1 = 20
123
Therapeutic Window
Dose or concentration range which can treat disease effectively without having toxic effects Larger the therapeutic window the safer the drug
124
Therapeutic Drug Monitoring
Plasma concentrations are monitored to ensure serum concentrations within therapeutic window

Pharmacology (18 decks)

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