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Pharmacology > Lecture 4-5 Pharmacodynamics > Flashcards

Lecture 4-5 Pharmacodynamics Flashcards

1
Q

What is the component of a cell to which a drug binds to initiate the chain of events that leads to a biological response

A

Receptor

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2
Q

Most receptors are ___, some are ___

A

Proteins, nucleic acids

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3
Q

For most drugs the duration of action is directly related to the __ the drug is bound to the receptor

A

Time

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4
Q

As the drug is cleared from the blood stream its action will be ___

A

Terminated

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5
Q

What are some drugs that are exceptions to the relationship between time bound to receptor and action

A

Corticosteroids, MAO inhibitors, omperazole, aspirin, DFP

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6
Q

How do corticosteroids persist for several weeks after the drug has been cleared from the body

A

Act on nuclear receptors and alter the expression of genes

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7
Q

How does the effect of MAO inhibitors, omeprazole, aspirin and DFP persist for a long period of time even without lots of free drug in the plasma

A

Irreversibly bind to and inhibit enzymes and their effects

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8
Q

What are the 5 drug-receptor interactions

A
  1. Electrostatic interactions
  2. Hydrogen bonds
  3. Van der waals
  4. Hydrophobic interactions
  5. Covalent binding
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9
Q

Which drug-receptor interactions have low energy bonds and therefore break easily

A

Electrostatic interactions, hydrogen bonds, van der waals, hydrophobic interaction

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10
Q

Which drug-receptor interactions have high energy bonds and therefore are irreversible

A

Covalent binding

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11
Q

Why type of receptors regulate gene expression

A

Intracellular receptors

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12
Q

How do intracellular receptors work/interact with hormone or drug

A

Hormone or drug crosses the plasma membrane, stimulates intracellular receptor.

Then stimulates gene transcription

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13
Q

Effect on intracellular receptors occurs after ___ period and ____over time

A

Lag period and persists over time

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14
Q

What some examples of molecules/hormones that can act on intracellular recpetors

A

Corticosteroids, mineralcorticoids, sex steroids, Vitamin D, and thyroid hormone

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15
Q

Can steroid hormones that act on intracellular receptors be stored

A

No, except for thyroid hormone

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16
Q

Why can’t steroid hormones be stored

A

They must be very lipid soluble to cross plasma membrane and interact with intracellular receptor and considering storage vesicles are made of lipids they would just diffuse out

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17
Q

How do allosterically regulated transmembrane proteins work

A

Ligand binds causing receptors to associate, stimulating tyrosine kinase, phosphorylating receptors and other downstream proteins

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18
Q

What enzymes can be used in allosterically regulated trans membrane signaling

A

Tyrosine kinase, serine kinase, guanylyl cyclase

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19
Q

What are some molecules that can active protein tyrosine kinases

A

Insulin, epidermal growth factor and platelet derived growth factor

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20
Q

How do ligand gated ion channels work

A

Binding of neurotransmitter or drug opens the channel, causing influx of ions either depolarizing or hyperpolarizing the cell

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21
Q

Do nicotine acetylcholine receptors excite/depolarize or inhibit/hyperpolarize

A

Excite/depolarize

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22
Q

Do GABA-a receptors inhibit/hyperpolarize or excite/depolarize

A

Inhibit/hyperpolarize

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23
Q

What ion channel opens when ACh binds

A

Na+

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24
Q

What channel is always open at NMJ and why

A

K+ to establish membrane potential

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25
Q

Acetylcholine acts on what receptor to influx what ion

A

Acts on nicotinic receptor and influxes Na+

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26
Q

What receptor does GABA act on and what ion channel does it open

A

Acts on GABA-A receptor and opens Cl- channels

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27
Q

What receptor do benzodiazepines act on and what ion channel does it open

A

Acts on GABA-A receptor and opens Cl- channels

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28
Q

What ions does glutamate act on

A

Ca2+ and Na+

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29
Q

Why are benzodiazepines less toxic than phenobarbital

A

Benzos need to act on GABA-A receptor to open Cl- channels, meanwhile phenobarbital opens Cl- channels by itself so very limited therapeutic range

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30
Q

Describe the basic mechanism of GPCR’s

A

Molecule binds, activates Gq, Gs, or Gi subunits and acts on phospholipase C

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31
Q

Stimulation of G-proteins ___ the response to binding of agonist to the receptor

A

Amplifies

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32
Q

Do receptors linked to Gs stimulate or inhibit cAMP

A

Stimulate

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33
Q

Do receptors linked to Gi inhibit or stimulate formation of cAMP

A

Inhibit

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34
Q

What is the downstream signaling when an agonist activates a GPCR

A

Gs—> AC—> cAMP—> phosphorylation of various proteins

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35
Q

What breaks down cAMP

A

PDE

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36
Q

What happens if you phosphorylation K+ channels

A

Close channels and decrease membrane potential—> depolarization

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37
Q

What would happen if you phosphorylated Ca2+ channels

A

Open

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38
Q

What receptors does epinephrine act on through Gs GPCR

A

B1 and B2

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39
Q

What receptor does NE act on through Gs GPCR

A

B1

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40
Q

What receptor does isoproterenol act on via Gs GPCR

A

B1 and B2

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41
Q

What receptor does Dobutamine act on in Gs GPCR

A

B1

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42
Q

What receptor does histamine act on via Gs GPCR

A

H2

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43
Q

Does FSH and ACTH act through Gs or Gi pathway

A

Gs

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44
Q

What receptor does NE act on via Gi GPCR

A

Alpha-2

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45
Q

What receptor does Epinephrine act on via Gi GPCR

A

Alpha-2

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46
Q

What receptor does dexmedetomidine act on via Gi GPCR

A

Alpha-2

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47
Q

What receptor does acetylcholine act on in Gi GPCR

A

M2

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48
Q

What receptor does morphine act on in Gi GPCR

A

Mu, kappa, delta

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49
Q

What receptor does serotonin act on via Gi GPCR

A

5-HT1

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50
Q

Describe the steps in poylphosphoinositide signaling

A
  1. Agonist binds GPCR
  2. Gq activates PLC
  3. PLC hydrolyzes IP3 and DAG
  4. IP3 releases Ca2+ from intracellular stores
  5. DAG stimulates protein kinase C
  6. IP3 is dephosphorylated
  7. DAG is broken down
  8. Ca2+ is pumped out
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51
Q

What is the result of IP3 releases Ca2+

A

Ca2+ will bind calmodulin and activate myosin in smooth muscle leading to smooth muscle contraction

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52
Q

What neurotransmitters can stimulate GQ formation of IP3 and DAG

A

Acetylcholine, norepinephrine, epinephrine, phenylephrine, and serotonin

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53
Q

What receptor does acetylcholine act on in GQ stimulation of IP3/DAG

A

Muscarinic M1 and M3

54
Q

What receptor does NE and epinephrine act on in GQ stimulated formation of IP3 and DAG

55
Q

What receptor does phenylephrine act on in GQ stimulated formation of IP3/DAG

56
Q

What receptor does serotonin act on in GQ stimulated formation of IP3/DAG

57
Q

What are some examples of drugs that interact with body components that have non-receptor mediated effects on the body

A

Antacids and osmotic agents (mannitol, laxatives)

58
Q

Heparin can bind to what in order to inactive

59
Q

Is a drug-receptor interaction reversible or irreversible

A

Usually reversible

60
Q

The response to a drug is directly related to the # of

A

Receptors occupied

61
Q

The response to a drug is maximal when….

A

All available receptor sites are occupied or bound to the drug and further addition of the drug does not produce an additional response

62
Q

What can we determine from dose response curves

A

EC50- 50% effective concentration

63
Q

When can a graded dose response curve be used

A

When measuring in response to 1 unit is given

Ex: give increasing doses of NE and measure vasoconstriction

64
Q

Maximal effect is equivalent to

65
Q

Are more potent drugs on the left or right side of response curves

66
Q

When can you use quantal dose response curves

A

Measuring a population

67
Q

What does a quantal dose response curve related

A

Dosages of the drug to the frequency with which a designated response will occur within a population

68
Q

Does a graded or quantal dose response curve have an “all or none” response

69
Q

How is the quantal dose response curve displayed in graph

A

Frequency distribution

70
Q

What are quantal dose response curves used to determine

A

Therapeutic ratio

71
Q

How do quantal dose response curves determine therapeutic ratio

A

Give increasing doses of drug and measure ED50 to determine effective dose in 50% and LD50 to determine lethal in 50%

72
Q

What is the therapeutic ratio equation

A

Therapeutic index= (LD50)/(ED50)

73
Q

where on this graph would indicated therapeutic dose and why

A

B because it is the beginning of overlap with greatest therapeutic response and lowest lethal response

74
Q

What is affinity

A

Measures binding of drug to receptor

75
Q

What is Kd

A

Concentration needed to produce half maximal binding

76
Q

What is potency

A

Dose required to produce a given effect

77
Q

What is EC50

A

Dose required for half maximal effect

78
Q

What is efficacy

A

Degree of biological response produced by binding of a particular drug to the receptor, not related to potency

79
Q

What is intrinsic activity

A

Synonymous with efficacy, ability of a drug to initiate a response

80
Q

Do antagonists, agonists or partial agonists have affinity and intrinsic activity

81
Q

Do antagonists, agonists, or partial agonists have affinity but no intrinsic activity

A

Antagonists

82
Q

Do antagonists, agonists or partial agonists have affinity but lower intrinsic activity

A

Partial agonists

83
Q

Compare the potency and efficacy (intrinsic activity) of Drug X and Y and are these full or partial agonists

A

These are full agonists as they reach 100% effect but drug Y needs higher concentration. Therefore Drug Y and X have the same efficacy but drug Y is less potent

84
Q

compare and contrast drug X and Drug Y on their potency and efficacy (intrinsic activity) and are these full or partial agonists

A

These are partial agonists as they don’t reach 100% effect. Drug Y doesn’t even reach 50% so can’t compare ED/LD and Drug Y is less potent and has less efficacy

85
Q

What is an agonist

A

Binds the receptor and initiates a response, causes a maximum shift of receptors to the activated state

86
Q

What is an antagonist

A

Binds to the receptor, but does not initiate a response, will block response to agonist

87
Q

What is a partial agonist

A

Binds to the receptor and causes a response, response is lower than produced by full agonist, may block the response to the full agonist

88
Q

T or F: partial agonists can also function as antagonists

A

Yes- because they will compete for binding sites with a full agonist

89
Q

Is morphine an agonist, antagonist or partial agonist

90
Q

Is naloxone an agonist, antagonist or partial agonist

A

Antagonist

91
Q

Is buprenophine an agonist, antagonist or partial agonist

A

Partial agonist

92
Q

What are the 4 different ways a drug can function as an antagonist

A
  1. Competitive binding
  2. Non-competitive binding
  3. Functional/physiological
  4. Chemical
93
Q

What does a competitive antagonist do

A

Compete for receptor binding with agonist

94
Q

What is the intrinsic activity and efficacy of a competitive antagonist

95
Q

How do competitive antagonist impact affinity

96
Q

How do competitive antagonists shift dose response curve

A

To the right in a parallel fashion

97
Q

Do competitive antagonists affect the maximum response produced

98
Q

What is non-competitive antagonists do

A

Bind irreversibly to the receptor so agonist can’t bind or bind to secondary site so agonist can’t act

99
Q

How do non-competitive antagonists impact maximum response

100
Q

How do non-competitive antagonists impact EC50

A

May or may not change

101
Q

What is functional/physiological antagonism

A

Antagonist acts through a different receptor or mechanism to alter a physiological response, less specific and harder to control

102
Q

What is an example of functional/physiological antagonism

A

Anaphylaxis causes histamine release which acts on H1 receptors and decrease BP and to counteract give epinephrine to vasoconstrict and increase BP

**both act to increase BP but do not act in the same mechanism

103
Q

What is a chemical antagonist

A

Antagonist neutralizes drug or compound chemically

104
Q

What is an example of a chemical antagonist

A

Heparin neutralized by protamine

105
Q

___ agonists produce a response but with lower efficacy than full agonists

106
Q

What is tolerance

A

After chronic administration of many drugs effect of the drug decreases

107
Q

Pharmacokinetic tolerance

A

Drug induces its own metabolism and may increase metabolism of another drug (via P450)

108
Q

Barbiturates undergo ___ tolerance

A

Pharmacokinetic

109
Q

Pharmacodynamic tolerance

A

Usually due to a receptor down or up regulation

110
Q

Beta receptor agonists or antagonists and opioids undergo ___ tolerance

A

Pharmacodynamic

111
Q

How do beta blockers chemically induce super sensitivity or hyperactivity

A

Induce bradycardia and decrease BP but if you abruptly stop beta blocker it will result in increase BP and HR because new receptors are not being inhibited anymore

112
Q

How can surgically induced denervation cause super sensitivity or hyperactivity

A

Increase NMJ and give stimulators agent and will cause big effect

113
Q

How do antagonist increase super sensitivity or hyperactivity

A

Upregulate receptors to drugs

114
Q

How does a deficiency of degrading enzymes increase supersensitivity or hyperactivity

A

Increase lifespan of drug action

115
Q

What kind of physiologic synergism do NSAIDs provide

A

Additive or summation

116
Q

What type of physiological synergism do antihypertensives cause

117
Q

What type of physiologic synergism do cholinesterase inhibitors do

A

Potentiation

118
Q

How can one drug elicit multiple responses

A

Due to presence of multiple receptors being activated at different dose levels

119
Q

Drugs are ____ but rarely ___

A

Selective but rarely specific

120
Q

What are some examples of drugs that can act on multiple receptors and cause adverse effects

A
  1. Phenothiazines
  2. Antihistamines
  3. CNS depressants
121
Q

What is a dose dependent toxicity

A

If an adverse reaction is mediated by the same receptor-effector mechanism

122
Q

What are some common dose-dependent toxicities

A
  1. Excessive hypotension
  2. Arrhythmias
  3. Hypoglycemia
  4. Hemorrhage
123
Q

What organ specific toxicity does aminoglycosides cause

A

Renal and ototoxicity

124
Q

What organ specific toxicity does acetaminophen cause

A

Hepatotoxicity

125
Q

What organ specific toxicity does chloramphenicol cause

A

Aplastic anemia

126
Q

What organ specific toxicity does tetracycline cause

A

Retardation of bone growth

127
Q

What form of antagonism does the following graph show

A

Competitive- in order for drug A to have same efficacy in the presence of increasing concentrations of drug B it must also increase concentration to reach the same efficacy

128
Q

What type of antagonism does the following graph show

A

Competitive- acetylcholine by itself can be administered at a lower dose to reach maximum efficacy but when administered with atropine the dose of acetylcholine must be increased to reach same efficacy

129
Q

What type of antagonism is this graph showing

A

Non-competitive- bind irreversibly so adding dibenamine to epinephrine will inhibit epinephrine from reaching maximum efficacy even if you increase the dose of epi

130
Q

What type of antagonism is the graph showing

A

non-competitive because drug A in presence of non-competitive inhibitor drug B will never be able to reach maximum efficacy despite increasing dose of drug A

Pharmacology (14 decks)

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