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Sedation > Pharmacology of moderate sedation > Flashcards

Pharmacology of moderate sedation Flashcards

1
Q

What are the most common type of receptors?

A

Cell membrane receptors

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2
Q

Are cell membrane receptors easy to isolate?

A

no

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3
Q

Types of cell membrane receptors

A
  • Cell wall
  • Cytoplasmic
  • Nuclear
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4
Q

The most significant portion of the plasma membrane

A

Phospholipid bilayer

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5
Q

Parts of transmembrane receptors

A

Intracellular

Extracellular

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6
Q

Types of receptors

A

Ion channel linked
G protein linked
Enzyme linked
Intracellular

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7
Q

What kind of receptors do local anaesthetics work on?

A

Ion channel linked

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8
Q

What are the kinds of Ion channel linked receptors?

A

Voltage gated

Ligand gated

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9
Q

What kind of receptor do sedatives work on?

A

G protein linked

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10
Q

What kind of receptor does insulin work on?

A

Enzyme linked

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11
Q

What kind of receptors do steroids work on?

A

Intracellular

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12
Q

Examples of voltage gated channel linked receptors

A

Sodium channels with LA

SA Node

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13
Q

How do ligand gated channels work?

A

They are activated after ligand-drug binding

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14
Q

G-protein-linked receptors aka

A

Metabotropic receptors

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15
Q

How do G-protein linked receptors work

A

They amplify biologic signal by G protein activation

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16
Q

What system is integral to the function of G protein linked receptors

A

Second messenger system

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17
Q

Activity of what enzyme triggers the second messenger system?

A

Adenyl cyclase

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18
Q

What enzyme causes increase in intracellular function?

A

Protein Kinase A

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19
Q

What receptors form half of ALL drug binding sites?

A

G protein linked receptors

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20
Q

Give an example of a drug that uses G-protein linked receptors

A

Epinephrine

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21
Q

Gs?

A

Stimulatory

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22
Q

Gi?

A

Inhibitory

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23
Q

What kinds of receptors are Beta 1 receptors?

A

Gs - G-protein linked stimulatory receptors

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24
Q

What works on Beta 1 receptors?

A

Norepinephrine

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25
Q

How do B1 receptors work?

A

Norepinephrine acts on B1 receptors to increase heart rate

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26
Q

Where are Beta 1 receptors located?

A

Heart

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27
Q

Give an example of a Gi Receptor

A

Alpha 2 receptors

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28
Q

Role of Alpha 2 receptors

A

Autoregulation of Norepinephrine —> vasoconstriction

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29
Q

Gq receptors - example

A

Alpha 1 receptors

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30
Q

Location of Alpha 1 receptors

A

Arterioles

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31
Q

What is the significance of G-protein linked receptors in dentistry?

A

LA activates Beta 1 receptors (Gs) and Alpha 1 receptors (Gq) leading to increased heart rate and increased vasoconstriction

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32
Q

What kinds of receptors act very quickly?

A

Enzyme linked receptors

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33
Q

How do enzyme linked receptors work?

A

Binding site on cell membrane activates cytoplasmic enzymatic activity

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34
Q

What receptors do cytokines work on?

A

Enzyme linked receptors

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35
Q

What receptors do growth factors work on?

A

Enzyme linked receptors

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36
Q

What kind of receptors act slowly?

A

Intracellular receptors

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37
Q

Why do intracellular receptors act slowly?

A

Their activation leads to increase in DNA activity

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38
Q

What kind of receptors do glucocorticoids work on?

A

Intracellular receptors

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39
Q

What kind of receptors do mineralocorticoids work on?

A

Intracellular receptors

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40
Q

What kind of receptors do sex steroids work on?

A

Intracellular receptors

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41
Q

What basic kinds of substances act on intracellular receptors?

A

Lipophilic substances

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42
Q

How long does it take for the effect of an orally administered drug to be evident when acting on intracellular receptors?

A

1 day

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43
Q

Duration required for evidence of action of IV administered drug to be apparent when acting on intracellular receptors

A

several hours

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44
Q

What drugs are receptor independent?

A

NSAIDs

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45
Q

How do NSAIDs work?

A

They alter enzyme activity

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46
Q

How do receptor independent drugs work?

A

They work on enzymes to produce natural ligands for receptors

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47
Q

Demonstrate downstream effect with NSAIDs

A

NSAIDs —> Inhibit COX —> inhibit production of prostaglandins —> inhibit inflammatory response

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48
Q

Where does arachidonic acid come from?

A

Cell wall

49
Q

Types of receptor independent drugs

A
  • Alteration of enzyme activity
  • Chemically reactive
  • Physically active
  • Counterfeit biochemical substances
50
Q

Example of physically active drug

A

Hydrogen peroxide

51
Q

Name agonists of BZD receptors

A

Diazepam, Lorazepam, Midazolam

52
Q

How does Flumazenil interact with BZD receptor?

A

Competitive antagonist

53
Q

What kind of drugs elicit responses that are the same as natural ligands?

A

Agonists

54
Q

Example of a full agonist

A

Dobutamine - epinephrine

55
Q

What is the difference between full agonists and partial agonists?

A

Full agonists don’t have a ceiling response

56
Q

What is the difference between partial agonists and partial antagonists?

A

Semantics

57
Q

What is the difference between agonists and antagonists?

A

Antagonists have no intrinsic activity

58
Q

A drug that blocks agonist or natural ligand is a….

A

An antagonist

59
Q

What are the different kinds of antagonists?

A

Competitive and non-competitive

60
Q

What are the most dangerous kinds of antagonists?

A

Non-competitive antagonists

61
Q

Examples of non-competitive antagonists

A

Serin nerve gas

Malathion

62
Q

Why are non-competitive antagonists so dangerous?

A

They bind and sit at the receptor forever - and are therefore lethal

63
Q

What kind of drug is used to reverse the toxic effects of an agonist?

A

Competitive antagonist, because it displaces the agonist or ligand.

64
Q

What kind of drug is flumazenil

A

it is the competitive antagonist of diazepam

65
Q

How do you treat diazepam toxicity?

A

Flumazenil

66
Q

IS standard dose the same for everyone?

A

No

67
Q

Why does standard dose vary?

A

Some people are super-responders and some are slow-responders

68
Q

How effective is titration of drug?

A

Very hard with orally administered drugs, easier with IV activity and Nitrous oxide.

69
Q

What is therapeutic index?

A

LD50 / ED50

70
Q

What does CSM Stand for

A

Certain safety margin

71
Q

How is TI related to the quality of the drug?

A

Greater the TI better the drug

72
Q

How are TI and CSM related?

A

High TI and low CSM for the same drug is bad because that means that the drug has an overlapping region for maximum efficacy and the beginning of the lethal dose

73
Q

Give an example of supra additive drugs

A

Benzodiazepines (valium, versad) and opioids (Fentanyl, Demirol, Morphine)

74
Q

Give an example of potentiation

A

Epinephrine and SNRI’s

75
Q

SNRI’s

A

Serotonin norepinephrine reuptake inhibitors

76
Q

Potentiation

A

Prevention of reuptake of drug from synapse leading to prolonged action

77
Q

Massive rebound hypertension

A

On stoppage of beta blockers after chronic usage, receptor downregulation leads to massive hypertension.

78
Q

What is the major mechanism of drug absorption

A

Passive diffusion

79
Q

Aquaporins

A

very small water soluble drugs

80
Q

How do lipid soluble drugs get absorbed?

A

Transcellular diffusion aided by thin capillary walls

81
Q

How do small hydrophilic drugs get absorbed?

A

Paracellular diffusion across intercellular clefts

82
Q

Specialty of the Blood brain barrier

A

Very tight endothelial junctions, meaning only lipophilic drugs can cross

83
Q

How are drugs transported away from the brain

A

Extensive transporter system to export drugs, prominently P-glycoprotein

84
Q

Which part of the placenta protects it from drug entry?

A

Trophoblastic membrane

85
Q

2 superfamilies of transporters (active transport)

A

SLC

ABC

86
Q

SLC transporters

A

Solute carriers

87
Q

ABC transporters

A

ATP binding cassette transporters

88
Q

Which drug is used in Parkinson’s to bypass the BBB?

A

Levodopa

89
Q

Which transporters are bidirectional?

A

SLC family - cotransport with Sodium potassium ATPase pump

90
Q

Which transporters are unidirectional?

A

ABC family - primary active transport using ATP

91
Q

Major plasma proteins to bind drugs

A

Albumin (over 200 ionised functional groups)

Alpha acid glycoprotein (basic drug binding)

92
Q

Protein binding of Diazepam

A

98%

93
Q

Protein binding of Midazolam

A

95%

94
Q

Protein binding of Fentanyl

A

85%

95
Q

Protein binding of Meperidine

A

60%

96
Q

Tissue reservoirs

A

VRG (vessel rich group)
Muscle
Fat
Vessel poor group

97
Q

Hangover effect

A

Clinical effectiveness of a drug is based on its tissue redistribution and not its metabolism

98
Q

Descending order of blood flow of tissue reservoirs

A

VRG (75% )> Muscle (19%) > Fat (6%) > Vessel poor group (<1%)

99
Q

Lipid solubility

A

Directly proportional to:

  1. Potency
  2. Speed of onset
  3. Fraction in CNS

Inversely proportional to:

  1. Peripheral toxicity
  2. Duration of action
100
Q

Phases of Hepatic drug metabolism

A 
Phase I:
Oxidation (CYP 450)
Reduction
Hydrolysis
Dehalogenation

Phase II:
Conjugation reactions

101
Q

What type of protein is cyp 450?

A

Hemoprotein

102
Q

CYP Isozymes

A

CYP3A > CYP2D6 > CYP2C > CYP1A2 > CYP2E1

103
Q

Drugs that can have an effect on CYP are of what types?

A
  1. Enzyme substrate
  2. Enzyme inducer
  3. Enzyme inhibitor
104
Q

What other reactions can be affected by drugs that affect CYP450?

A

None except glucuronidation

105
Q

Enzyme inducer

A

increases CYP enzyme activity

106
Q

List CYP 3A4 inhibitors

A
  • Antiarrhythmics
  • Antifungals
  • Antiinfectives
  • Calcium channel blockers
  • Proton pump inhibitors
  • Protease inhibitors
  • SSRI’s
  • Leukotriene modifiers
  • Cannabinoids
107
Q

Depending on prevalence of CYP2D6, classify people

A
  • Extensive metabolism
  • Ultrarapid metabolism
  • Intermediate metabolism
  • Poor metabolism
108
Q

What sedative drugs are at high risk of interaction with CYP3A4 inhibitors?

A

Midazolam and triazolam

109
Q

What sedative is not CYP metabolised and hence can be given alongside CYP inhibitors without adverse reaction?

A

Lorazepam

110
Q

What sedative drug is metabolised with multiple CYP enzymes?

A

Diazepam

111
Q

beta half life

A

time it takes for drug to leave body after equilibration has occurred

112
Q

alpha half life

A

redistribution half life

113
Q

Why are subsequent IV doses lesser than the first dose?

A
  1. Plasma Protein loading

2/ Residual receptor occupancy

114
Q

clinical sedation time vs residual sedation

A

Clinicall determined by redistribution and residual (hangover) based on elimination

115
Q

Drug interaction types

A

Pharmacodynamic (action of drug)
Pharmacokinetic (distribution of drug)
Pharmaceutical (mixture of drugs)

116
Q

Pharmacodynamic interactions

A
  1. Drug receptor interactions (agonist + antagonist)

2. Receptor independent actions (block reuptake or affect enzyme activity)

117
Q

How many doses at the end of each beta half life does it take for steady state drug concentration?

A

4

118
Q

Terminal elimination half time

A

6 half times required for close to 100% of the drug being eliminated

Sedation (3 decks)

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