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BIOM*3090 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

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1
Q

How are drugs categorized?

A

Based on safety concerns, abuse potential, patient understanding, prescribing practices, and dispensing methods

Drug categorization is crucial for regulating access and ensuring patient safety.

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2
Q

What is the role of NAPRA in drug scheduling?

A

Provides schedules for drug categorization

NAPRA stands for the National Association of Pharmacy Regulatory Authorities.

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3
Q

What is required for drugs in NAPRA I?

A

Prescription needed for sale by pharmacist; includes prescription drugs, narcotics, controlled substances, and targeted substances

Example: Fentanyl patch.

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4
Q

What characterizes NAPRA II drugs?

A

Prescription not required; must be dispensed by pharmacist, e.g., insulin

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5
Q

What is the distinction of NAPRA III drugs?

A

Client may obtain at pharmacy without need of pharmacist, e.g., ranitidine (Zantac®)

These drugs are typically less potent and safer.

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6
Q

What defines unscheduled drugs?

A

Client may obtain at retail stores as well as pharmacy, e.g., naproxen (Aleve®)

These are often over-the-counter medications.

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7
Q

Define a drug (ligand).

A

Any substance that brings about change in biological function through chemical actions

Drugs can alter various physiological processes.

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8
Q

What are pharmacodynamics?

A

The actions of drugs on the body

This includes the effects that drugs have once administered.

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9
Q

What are pharmacokinetics?

A

The actions of the body on drugs

This encompasses the absorption, distribution, metabolism, and excretion of drugs.

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10
Q

What properties must useful drugs have?

A

Must enable transport from site of administration to target site (termed “biophase”) and be inactivated and excreted at a reasonable rate

This ensures drugs do not remain active in the body longer than necessary.

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11
Q

What state are most drugs in at room temperature?

A

Solid, e.g., aspirin

Some drugs may also be liquids or gases.

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12
Q

What is the most important type of receptor for drugs?

A

Proteins

Proteins interact with drugs to produce physiological effects.

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13
Q

What is a signal transduction pathway?

A

The receptor, its cellular target, and any intermediary molecules

This pathway is crucial for understanding how drugs exert their effects.

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14
Q

What is affinity in drug-receptor interactions?

A

Favorability of a drug-receptor binding interaction

Higher affinity indicates a more effective interaction.

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15
Q

What is the lower size limit for drug molecules?

A

100 daltons (Da)

This is the minimum size needed for specificity of action.

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16
Q

What is the upper size limit for drug molecules?

A

1000 daltons (Da)

Larger molecules may have difficulty moving to sites of action.

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17
Q

What type of bonding is strongest in drug-receptor interactions? List the types of bonding in order from most to least strong.

A

Covalent > ionic > hydrogen > van der Waals

Covalent bonds are usually irreversible.

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18
Q

What are enantiomers?

A

Optical isomers that can exist for drugs with chiral centers

One enantiomer is usually more potent due to better fit with the receptor.

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19
Q

What is a racemic mixture?

A

A 50:50 mix of both enantiomers of a drug

These mixtures can have different pharmacological effects. Ie: One can be stronger than the other

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20
Q

What defines the selectivity of an ideal drug?

A

Interacts only with molecular targets producing desired therapeutic effects

Minimizes adverse effects by avoiding non-target interactions.

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21
Q

All drugs act on receptors, True or False?

A

False: antacids for example, directly neutralize HCl in the stomach

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22
Q

What type of bond is USUALLY irreversible?

A

covalent

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23
Q

What are the two major functions of physiological receptors?

A
  1. Ligand binding via ligand-binding domain
  2. Message propagation via effector domain
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24
Q

What are the four ways a drug can modify cellular function after binding to receptors?

A
  1. Initiation
  2. Enhancement
  3. Diminishment
  4. Termination (by blocking)
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25
What are the four major types of drug receptors?
1. Ion Channels 2. G-protein Coupled Receptors (GPCRs) 3. Transmembrane Receptors with Enzymatic Cytosolic Domains 4. Intracellular Receptors
26
Membrane lipid bilayers are largely impermeable to ____
polar ions
27
Where are the major ligand gated channels found?
CNS
28
What type of receptor is the nicotinic acetylcholine receptor? Give a description of how it works
Ligand-Gated: * channel pore occluded by bulky amino acids in closed state * full opening occurs with binding of 2 ACh molecules to the alpha subunits inducing a conformational change
29
What type of channel initiates action potentials in the acons of nerves and muscle cells? Give a description of how they work.
Voltage-Gated Ion Channels (specifically Na+ channels!) * Activation induces depolarization * channel then becomes inactivated (refractory) and cannot open until repolarized
30
How can drugs influence voltage-gated ion channels?
Drugs can have greater affiinity for certain conformations (ie: local anaesthetics bind to channel to prolong refractory period)
31
What is the SUR1 receptor?
* sulfonylurea receptor * Regulates ATP-dependent K+ channel in pancreatic beta cells * sulfonylurea class oral hypoglycemics facilitate closure of the channel and secretion of insulin by binding SUR1
32
What is the most abundant class of receptors in the body?
GPCRs
33
What are GPCRs activated by?
neurotransmitters, eicosanoids, peptide hormones, opioids
34
Give the steps of GPCR activation
1. Agonist binding to GPCR 2. GDP exchanged for GTP on G protein, activating it 3. alpha subunit of G protein (that is bound to GTP) diffuses to the effector and activates it 4. Agonist unbinds from receptor 5. GTP is hydrolyzed -> GDP by inherent GTPase activity of alpha subunit 6. Heterotrimeric G protein is reconstituted
35
What is the role of effector molecules that are activated by G proteins?
production of second messengers (ie: cAMP)
36
What is the action of G-stimulatory protein?
Activation of Ca2+ channels, activates adenylyl cyclase
37
What is the action of G-inhibitory proteins?
Activation of K+ channels, inhibits adenylyl cyclase
38
What is the action of Go proteins?
inhibition of Ca2+ channels
39
What is the action of Gq proteins?
activation of phospholipase C
40
What is the action of G12/13 proteins?
Diverse ion transporter interactions
41
What are the endogenous ligands of B-adrenergic G protein receptors? What is their action?
* Catecholamines (NE/E) * stimulate cAMP production and cellular effects based on tissue localization
42
What are the actions of transmembrane receptors with intracellular linked enzymatic domains?
* Roles in cell metabolism and differentiation (tonic activation can cause tumors) * Add/remove phosphate groups from specific aas
43
What is the largest group of transmembrane receptors with enzymatic cytosolic domains?
Receptor Tyrosine Kinases
44
What is the difference between Receptor Tyrosine Kinases and Tyrosine Kinase-Associated Receptors?
Receptor Tyrosine Kinases have intrinsic enzymatic activity, Tyrosine Kinase-Associated Receptors have no intrinsic enzymatic activity
45
What is an example of an effector associated with receptor tyrosine kinases?
SH2 domains on signaling molecules like Grb2
46
What is an example of an effector associated with tyrosine kinase-associated receptors?
dimerization of the receptor allows for binding of an intracellular tyrosine kinase (JAK) which can then phosphorylate other proteins (STAT) which translocate to the nucleus
47
How do nuclear hormone receptors work?
Circulating steroid hormones are lipophilic and can diffuse through the plasma membrane to bind transcription factors and modify nuclear events
48
What are the two binding domains on nuclear hormone receptors?
ligand binding domain, DNA binding domain
49
What are the three isoforms of NO synthase
1. endothelial (eNOS) 2. inducible (iNOS) 3. neuronal (nNOS)
50
How does NO synthase/Guanylyl cyclase work? What are the effects?
* NO produced by NOS binds to N-terminal domain of soluble guanylyl cyclase and enhances its activation of cGMP * cGMP induces vascular smooth muscle effects (mainly due to its actions of PKG - vasodilation from reduced intracellular calcium levels)
51
What are NO synthase and Guanylyl Cyclase?
Guanylyl Cyclase is an intracellular receptor of NO gas produced by NO synthase
52
What roles do drug receptors that exist outside of the plasma membrane serve?
* communication (vasoconstriction by ACE inhibitors) and neurotransmitters * cell surface adhesion (cell-cell interaction for functions like inflammation and coagulation) * structural role (antineoplastics are microtubule inhibitors)
53
Desensitization
DEcreased ability of a receptor to respond to stimulation by a drug or ligand
54
Homologous desensitization
decreased response at a single type of receptor
55
Heterologous desensitization
Decreased response at 2+ types of receptors
56
inactivation
loss of ability of a receptor to respond to stimulation by a drug or ligand
57
Refractory
After a receptor is stimulated, a period of time is required before the next drug-receptor interaction can produce an effect
58
The affinity of a drug is most influenced by changes in the ____ state
Off
59
What is Kon?
Forward/Association rate - rate of receptor-ligand binding
60
What is Koff?
Reverse/Dissociation rate - rate of receptor-ligand unbinding
61
What is Kd?
* Dissociation Rate Constant * Koff/Kon
62
What does a lower Kd indicate?
stronger binding (Koff>Kon)
63
What does Kd correspond to in relation to ligand-receptor concentrations
Concentration of ligand where 50% of receptors are bound by ligand
64
What does [LR]=[R0] indicate?
maximum ligand receptor binding
65
Graded D-R
Dose-Response of an individual
66
Quantal D-R
Dose-Response of a population of individuals
67
Efficacy
maximal response produced by the drug at that receptor
68
Potency
Drug concentration which elicits 50% of the maximal response (Emax)
69
Therapeutic Index
estimate of relatice safety margin of a drug
70
ED50
population based median effective dose
71
TD50
population based median toxic dose
72
LD50
population based median lethal dose
73
more potent drugs have a _____ affinity for their receptors
greater (lower Kd)
74
more efficacous drugs (with a larger Emax) usually cause a _____ proportion of their receptors to be activated
greater
75
Full agonists
agonists that are capable of eliciting maximal responses at a given receptor
76
Partial Agonist
Agonists that are not able to achieve a maximal response at a given receptor even with increasing agonist concentration
77
True or False: a partial agonist can show greater potency than a full agonist
True (a partial agonist might have a greater effect at a lower dosage, but not able to reach the maximal effect that a full agonist can)
78
What is a possible explanation for why partial agonists are incapable of achieving the maximal response?
A receptor may have multiple unstable DR* configurations depending on the conformation of the receptor bound by agonist
79
Receptor Antagonist
inhibits action of agonist by preventing its binding to the receptor
80
Competitive Antagonist
binds reversibly to receptor active site
81
Does a competitive antagonist affect receptor efficacy and/or agonist potency?
* receptor efficacy - no, agonist can outcompete antagonist to produce maximal effect * Potency - yes, potency is decreased with competitive antagonism because antagonist increases the Kd for the agonist
82
Noncompetitive Receptor Antagonists
Bind the active site essentially irreversibly because of covalent binding
83
Does a non-competitive receptor antagonist affect receptor efficacy or agonist potency?
* Efficacy - yes, efficacy is decreased because agonist cannot outcompete the non-competitive antagonist * potency - yes, antagonist increases Kd for agonist therefore decreasing agonist potency
84
Give two examples of non-receptor antagonists and explain how they work
1. Chemical antagonist: inactivates agonist of interest via modification or sequestering of it 2. Physiologic Antagonist: Two drugs are physiologic antagonists of one another if they bind two different receptors and produce opposite effects
85
Allosteric Modulators
* bind to sites on the receptor distinct from the agonist * binding of the allosteric site either alters the Kd for the agonist binding or alters the conformational change needed for receptor activation
86

BIOM*3090 (13 decks)

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