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Exam 2 > Pharmacodynamics > Flashcards

Pharmacodynamics Flashcards

1
Q

Drug

A

Any substance that when administered to a living organisms produces a biological affect

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2
Q

Pharmacology

A

Study of how function of living systems is affected by chemical agents

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3
Q

Pharmacokinetics

A

Study of absorption, distribution, metabolism, and a excretion of drug

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4
Q

Pharmacodynamics

A

Study of effects of drugs and their mechanisms of action

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5
Q

Toxicology

A

Study of adverse effects of drugs.

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6
Q

Drug receptor

A

Component of organism with which the drug interacts. Sometimes called drug target.

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7
Q

What types of ion channels can drugs act upon?

A

Voltage gate and ligand gated

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8
Q

For ligand gated channels, what is an example of ligands?

A

Neurotransmitters (acetylcholine) or an intracellular mediator (cAMP and second messengers)

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9
Q

What two drugs classes act by altering the conductance of ion channels?

A

Local anesthetic and benzodiazepines

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10
Q

How do local anesthetics work?

A

Block voltage gated sodium channels in neurons that transmit pain information from the periphery to the CNS. this prevents action potential propagation and pain perception.

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11
Q

How do benzodiazepines work?

A

Bind to the GABAa receptor in neuronal membranes in the CNS. GABAa functions as a chloride ion channel and is activated by GABA (inhibitory neurotransmitter). This enhances the ability of GABA to open the chloride channel, hyperpolarizing the neuron.

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12
Q

On which receptor do most prescription drugs act?

A

G protein linked receptors

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13
Q

Albuterol

A

Beta-2 agonist use for asthma

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14
Q

Propranolol

A

A beta antagonist used for hypertension

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15
Q

Bethanechol

A

Muscarinic (acetylcholine receptor) agonist used for atonic bladder

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16
Q

Ipratropium

A

Muscarinic antagonist used for asthma

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17
Q

what are the three components of G protein linked receptors?

A

Cell surface receptor, G protein, effector (enzyme or an ion channel)

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18
Q

G protein effectors

A

G proteins can either directly control ion channels or they can interact with enzymes which leads to the production of second messengers

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19
Q

What are the most frequent target enzymes for G proteins?

A

Adenylyl cyclase and phospholipase C

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20
Q

What was Gs do?

A

Increase adenylyl cyclase

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21
Q

What does Gi do?

A

Decrease adenylyl cyclase and open potassium channels by decreasing cAMP

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22
Q

What does Gq do?

A

Increases the amount of phospholipase C

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23
Q

What does IP3 do?

A

releases calcium from the ER, which allows calcium to control many enzymes

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24
Q

What are some calcium meditated responses?

A

Smooth muscle contraction, increased force of contraction of cardiac muscle, secretion from exocrine glands, neurotransmitter release, hormone release

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25
Q

What are the ligand regulated transmembrane enzymes?

A

Tyrosine kinase, serine/threonine kinase, and guanylyl cyclase

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26
Q

What are the receptors for tyrosine kinase?

A

Insulin receptor, epidermal growth factor receptor, platelet derived growth factor, and nerve growth factor receptor

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27
Q

What can gain of function mutations in tyrosine kinase receptors cause?

A

Cancer, because tyrosine kinase receptors play an important role in cellular growth and differentiation

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28
Q

Imatinib

A

Tyrosine kinase inhibitor that is effective for leukemia

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29
Q

Cytokine Receptors

A

Respond to peptide ligand like growth hormone, prolactin, erythropoietin, and interferons. Have no intrinsic enzymatic activity. Bind to an intracellular tyrosine kinase from the Janus-kinase (JAK) family.

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30
Q

What usually makes up intracellular receptors?

A

Nuclear receptors, enzymes, structural proteins

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31
Q

Nuclear Receptors

A

Ligand activated transcription factors, contain binding sites for ligands and DNA. Regulate the expression of genes. May be in the nucleus or the cytoplasm.

32
Q

Statins

A

Drugs that act on enzyme receptors-specifically the HMG-CoA receptor that is used in the rate limiting step for cholesterol synthesis. This leads to less intracellular cholesterol, leading to LDL up regulation and LDL clearance in the blood.

33
Q

Vinca Alkaloids

A

Drug that acts on structural proteins. It binds to tublin and prevents the polymerization of tublin to microtubules which leads to there being a lack of cell division. Cells are arrested in metaphase. Cancer drug.

34
Q

ACE

A

Extracellular enzyme that converts angiotensin I to angiotensin II (which is a potent vasoconstrictor)

35
Q

Transporters

A

Membrane transported are targets for many psychiatric drugs.

36
Q

SSRIs

A

Selective serotonin reuptake inhibitors that act by blocking serotonin reuptake.

37
Q

Antacids

A

Not mediated by binding to receptors, but neutralize gastric acid.

38
Q

Mesna

A

Not mediated by binding to receptors. Reacts in bladder with acroleine (a metabolite of the anti cancer drug cyclophosphamide) preventing hemorrhagic cystitis

39
Q

Mannitol

A

Increases the osmolarity of various body fluids. Can promote increase in urine of reduction of cerebral edema

40
Q

Cholestyramine, colestipol, and colesevelam

A

Bind bile acids in the intestinal lumen and prevent their reabsorption. Used to treat hyperlipidemia. Does not bind to receptor.

41
Q

Dimercaprol

A

Chelates heavy metals. Does not bind to a receptor.

42
Q

Graded Dose-response Curves

A

Hyperbolic curve that shows relationship between the drug concentration and effect

43
Q

What does a high Kd represent?

A

Low binding affinity of drug to receptor

44
Q

Spare Receptors

A

Spare receptors can be seen when 50% of the max affect can be achieved by binding with 50% of the available receptors. You have “spares” that aren’t being used

45
Q

Efficacy

A

Maximal effect a drug can produce

46
Q

Potency

A

Measure of the concentration or amount of drug necessary to produce and effect of a given magnitude.

47
Q

What value determined potency?

A

EC50

48
Q

What value determines efficacy?

A

Emax

49
Q

What determines the clinical effectiveness of a drug?

A

Maximal efficacy

50
Q

Agonist

A

Drug that binds to and activates a receptor in a way that brings about an effect

51
Q

Antagonist

A

Inhibits the action of an agonist, but has no effect in the absence of the agonist

52
Q

Receptor Antagonism

A

Receptor antagonist binds to the same receptor to which the agonist binds

53
Q

Competitive Antagonism

A

Competitive antagonist bind to the agonist binding site on the receptor, preventing the binding of agonist to the receptor.

54
Q

Reversible Competitive Antagonism

A

Increases the amount of agonist required for a given response. Can be overcome with high concentrations of agonist. Emax remains the same.

55
Q

Irreversible Competitive Antagonism

A

Receptor cannot respond to the binding of an agonist. Emax is reduced, and the antagonism cannot be surmounted by adding more agonist

56
Q

Noncompetitive Antagonism

A

Allosteric antagonism. Antagonist bind to the receptor as a site different from the agonist binding site, reducing the action of the agonist. Insurmountable. Emax is decreased.

57
Q

NonReceptor Antagonism

A

Does not bind to the receptor where the agonist binds, but still inhibits response to agonist.

58
Q

Indirect Antagonism

A

Antagonist binds to a macromolecule in the pathway that links the receptor to the effect

59
Q

Physiological Antagonism

A

One agonist opposes another, but through different receptors. Example of using epinephrine when histamine has increased and there is bronchoconstriction

60
Q

Chemical Antagonism

A

Reacts chemically with an agonist to form an inactive product

61
Q

Effect of protamine

A

Protamine is a protein which is positively charged and counteracts that effects of heparin, a negatively charged anticoagulant

62
Q

Full agonist

A

Produced maximal response

63
Q

Partial Agonists

A

Produce a submaximal response

64
Q

Partial Agonist Inhibition

A

Partial agonist can act as a competitive antagonist in the presence of a full agonist by competing with the full agonist for receptor occupancy, reducing the response to the full agonist

65
Q

Inverse Agonist

A

Reverse the constitutive activity of the receptor.

66
Q

Constitutive Agonist

A

Activity in the absence of an agonist due to a fraction of the receptors being in the active state always

67
Q

Drug Selectivity

A

A drug is selective if there is a10-fold difference between its binding affinity for the first target (therapeutic effects) and its second target (adverse effects)

68
Q

Desensitization and tachyphylaxis

A

Synonymous terms used to describe the diminishing effect of drugs when given continuously or repeatedly

69
Q

tolerance

A

Gradual decrease in responsiveness to a drug, taking weeks or days to develop

70
Q

Refractoriness

A

Loss of therapeutic efficacy

71
Q

What can cause rapid desensitization?

A

Activation of ion channel receptors and G-protein receptors

72
Q

Quantal Dose Effect Curves

A

Plots fraction of the population that responds to a given dose of drug as a function of the drug dose. Defined as present or not present.

73
Q

Median Toxic Dose

A

Dose required to produce a particular toxic effect in 50% of animals

74
Q

Median Lethal Dose

A

The dose required to cause death in 50% of animals

75
Q

Therapeutic Index

A

Ratio of the TD (toxic dose) to the ED50

76
Q

The larger the toxic dose…

A

The safer the drug

Exam 2 (10 decks)

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