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SEE/NCE Boards Core Concepts > SEE BASIC SCIENCES: PHARMACOLOGY REVIEW > Flashcards

SEE BASIC SCIENCES: PHARMACOLOGY REVIEW Flashcards

1
Q

Rate of change proportional to amount of drug at any given time is PROPORTIONAL to the concentration present

A

FIRST-ORDER KINETIC

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2
Q

Constant amount of drug elimination over a specific amount of time

A

Zero order kinetic

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3
Q

A drugs that undergoes first order kinetic: increase drugs concentration will

A

lead to a larger amount of drugs elimination

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4
Q

What are determinant of drug tissue uptake include?

A 
Blood flow
BBB
Ionization
lipid solubilty 
Protein binding
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5
Q

4 methods of Drug metabolism are

A

Oxidation
Reduction
Hydrolysis
Conjugation

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6
Q

3 methods prepare for the fourth one with drug metabolism

A

Oxidation, reduction and hydrolysis prepare for conjugation

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7
Q

Effect on MAC: GENDER

A

No change in MAC

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8
Q

Effect on MAC: woman with red hair

A

Increased MAC

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9
Q

Effect on MAC: Pregnancy

A

Decrease MAC

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10
Q

Effect on MAC: Chronic ETOH abuse

A

Increase MAC

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11
Q

Effect on MAC: BP means greater than 40mmHg

A

No change in MAC

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12
Q

Effect on MAC: Alpha 2 agonists

A

Decrease MAC

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13
Q

Effect on MAC: Hyperthermia

A

Increase MAC

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14
Q

Effect on MAC: Drugs that increase CNS catecholamines

A

Increase MAC

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15
Q

Effect on MAC: Lidocaine

A

Decrease MAC

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16
Q

Effect on MAC: Hypernatremia

A

Increase MAC

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17
Q

Effect on MAC: acute alcohol intoxification

A

Decrease MAC

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18
Q

When do pharmacokinetics interactions occur

A

When a drug alters the ADME of another drug

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19
Q

Drugs with identical mechanism lead to ____Effects

A

Additive (2 effects leads to a greater effect of the 2 drugs combined

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20
Q

Inducer of hepatic drug metabolism (RPP CSC)

A 
Rifampin
Phenytoin
Phenobarbital
Carbamazepine
Smoking
St John's Wort 
Barbiturates 
Tobacco
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21
Q

What is the alveolar anesthetic concentration that blunts ADRENERGIC RESPONSE to noxious stimuli in 50% of patients?

A

MAC-BAR

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22
Q

MAC BAR is the

A

MAC required to blunt adrenergic response in 50% patients

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23
Q

Goals of drug combination

A

Decrease toxicity

Increase and maintenance of efficacy

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24
Q

Most important organ for metabolism

A

Liver

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25
Q

Hepatic drug clearance depends on

A

Hepatic blood flow
Extent of binding of the drug to blood
intrinsic ability of the liver to Metabolize the drug

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26
Q

Vd: is greater with lipophillic or lipophobic?

A

lipophillic

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27
Q

Dose response curve can determine pharmacodynamics?

A

no

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28
Q

What does the dose response curve tell you?

A

Response observed to a quantity of a drug.

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29
Q

Which of the following requires energy provided by the hydrolysis of ATP ?

A

Active transport

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30
Q

What is the phase II reaction?

A

Drug molecules who underwent reduction , hydrolysis or oxidation are assimilated- CONJUGATED into compounds more readily removed from the body.

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31
Q

Occurence of plasma concentration of a drug exceeding the capacity of metabolizing enzymes

A

Zero order kinetics.

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32
Q

Prolonged exposure of receptors leads to

A

lower drug effect at the target site

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33
Q

Prolonged receptor inactivity results in production of a

A

Relative maximal or super-maximal effect at the receptor

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34
Q

Chronically denervated NMJ will _____the specific receptors in an attempt to produce a signal in the face of lower concentration of agonists

A

Up regulate

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35
Q

Drugs that are incapable of producing a MAXIMAL effect even at very high concentration are called?

A

Partial agonist (only a limited response)

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36
Q

During a constant infusion , plasma steady state drug concentration reaches 90%

A

3 half lives.

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37
Q

When a steady state is achieved when

A

The quantity of a drug administered is equal to the quantity of drug that is eliminated via metabolism

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38
Q

and

A

50% of steady state

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39
Q

After 2 half-lives, you will have reached

A

75% of steady state,

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40
Q

After 3 half-lives you will have reached

A

87.5% of steady state.

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41
Q

The rule of thumb is that steady state will be achieved after

A

5 half-lives (97% of steady state achieved)

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42
Q

What % of IV -administered drug remains after after 5 elimination half-times have passed ?

A

3%

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43
Q

How to calculate 5 half lives

A

50x50x50x50x50 = 312500000 x 100 = 3.125

100- 3.125= 96.

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44
Q

Why is IV loading dose use ?

A

To achieve effective target concentration (therapeutic plasma concentration) immediately

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45
Q

For anaphylaxis to occur what must have happened?

A

Prior exposure is needed for sensitization . UPon subsequent exposure, the IgE antibodies form during the initial exposure

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46
Q

Type I hypersensitivity reaction

A

Mediators release from mast cells and basophils after antigen binding to IgE antibodies on cell membrane

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47
Q

Type II hypersensitivity reaction (2 cells)

A

Antibody dependent, cell mediated cytotoxic hypersensitivity: IgG or IgM mediated

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48
Q

Type III hypersensitivity reaction

A

Circulating soluble antigens and antibodies bind to form iNSOLUBLE complexes that deposit in vasculature

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49
Q

Type IV hypersensitivity reaction I

A

interaction with sensitized cytotoxic ells.

DElayed hypersensitivity reaction I

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50
Q

Type IV hypersensitivity reaction I

A

interaction with sensitized cytotoxic ells.

DElayed hypersensitivity reaction

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51
Q

Anaphylaxis is what type of hypersensitivity reactions?

A

Type I

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52
Q

ABO incompatibility is what type of hypersensitivity reactions?

A

Type II

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53
Q

Serum sickness after SNAKE BITE what type of hypersensitivity reactions?

A

Type III

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54
Q

Contact dermatitis is what type of hypersensitivity reactions?

A

Type IV

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55
Q

Vasoactive mediators release during anaphylaxis are

A

HIstamine
Leukotrienes
Prostaglandins

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56
Q

Vasoactive mediator that releases endothelium derived factor Nitric oxide from vascular endothelium?

A

Histamine

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57
Q

Vasoactive mediators that releases endothelium derived factor Nitric oxide from

A

HIstamine

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58
Q

All vasoactive mediators do that

A

Increased capillary permeability

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59
Q

Vasoactive mediator that contracts vascular smooth muscle and airway

A

Histamine

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60
Q

Vasoactive mediator that cause intense bronchoconstriction

A

Leukotrienes

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61
Q

Vasoactive mediator that causes NEGATIVE INOTROPY

A

Leukotrienes

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62
Q

Vasoactive mediator that causes coronary artery vasoconstriction?

A

Leukotrienes

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63
Q

Vasoactive mediator that is synthesized after mast cell activation through Lipoxygenase pathway? (LL)

A

Leukotrienes

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64
Q

Vasoactive mediators that causes Pulmonary HTN and bronchospasm

A

Prostaglandins

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65
Q

Vasoactive mediator that is synthesized after mast cell activation through cyclooxygenase pathway?

A

Prostaglandins

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66
Q

What lab provide immediate proof of anaphylaxis?

A

Serum Tryptase level (within 60-120 mins)

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67
Q

Tryptase and anaphylaxis

A

Stored in mast cells, an is an integral component, and released into the systemic circulation when anaphylaxis occur but NOT DURING ANAPHYLACTOID

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68
Q

Primary treatment of anaphylaxis should include

A

Airway support
100% O2
stopping all drugs
IV fluids and EPINEPHRINE

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69
Q

Responsible for MOST INTRAOPERATIVE anaphylactic reactions?

A

Muscle relaxants (not ABT)

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70
Q

Patient with which allergies have a cross-sensitivity to LATEX (BAK)

A

Bananas
Avocados
Kiwis

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71
Q

Pharmacodynamic interaction when

A

Drug alters the sensitivity of a target receptor or tissue to the effects of a second drug. (differ from pharmacokinetics which is when one drugs alter ADME)

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72
Q

An example of Pharmacodynamic interaction?

A

Second gas effect

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73
Q

What is the second gas effect?

A

Administration of Nitrous along with VA results in an additive effect by both agents

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74
Q

Drug that activates or stimulates a receptor

A

Agonist

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75
Q

Absorption, distribution, metabolism and excretion of inhaled or injected drugs

A

pharmacokinetics

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76
Q

Responsiveness of receptors to drugs, and the mechanims by which drugs causes these effects to occur?

A

Pharmacodynamics

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77
Q

A drug that binds to receptors to prevent exogenous or endogenous substances from activating them

A

Antagonists

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78
Q

An effet produced by 2 drugs acting together that is greater than would occur with each drug alone

A

Synergistic

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79
Q

Calculation by which a dose of a drug is administred by IV and is divided by the plasma concentration to reflect the apparent volume of the drug into various intercellular compoenents

A

Volume of distribution

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80
Q

Transmembrane protein macromolecule that acts as a mechanism for a drug to being to and exert its effect?

A

Receptor

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81
Q

Reflect the concentration of an inhaled anesthetic measureed at 1 atm in the body to prevent skeletal muscel movement in response to a srugical incision

A

MAC

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82
Q

Difference in slope, efficacy and individual responses, , depics relationship between the dose of a drug administered or plasma concentration, and the resulting pharmacological effect

A

Dose-response curve

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83
Q

Enantiomers are

A

Chemical substance of exact bu opposite shape, mirror images of each other

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84
Q

When 2 enantiomers are present in 50:50 portion, subtances are known as

A

Racemic mixtures

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85
Q

Define competitive antagonism

A

Competitive antagonism is based on the principle that an agonist or antagonist can bind to the same recognition site(s) on the receptor, and when both agonist and antagonist are present concomitantly, they can compete for such sites. Increasing concentration of an antagonist drugs (such as NDNMB, progressively inhibit the responses to an unchanging concentration of an agonists

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86
Q

Simple competitive antagonism definition?

A

increase in the available concentration of an agonist cannot overcome the effect produced by the antagonist.

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87
Q

A drug that activate a receptor by binding to it

A

Agonist

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88
Q

Define Non-competitive antagonism?

A

After administration of an antagonist, even high concentrations of an agonists cannot completely overcome the antagonism

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89
Q

A drug that bins to the receptor without activating the receptor and at the same time prevents an agonist from stimulating the receptor

A

Antagonist

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90
Q

What does HOFFMAIN ELIMINATION rely on to degrade CISATRACURIUM?

A

Normal body temperature

pH

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91
Q

What is therapeutic Index?

A

relates the dose of a drug required to produce a desired effect to the dose that produces an undesired effect.

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92
Q

Formula for TI

A

LD 50/ ED 50

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93
Q

Where are the hepatic microsomal enzymes that participates in metabolism of many drugs found? (GHAK)

A

GI tract
Hepatic smooth ER
Adrenal cortex
Kidneys

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94
Q

How many half lives to eliminate 97 % of the drugs?

A

5

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95
Q

CYP 450 3 A4 composes what % of CYP 450 activity?

A

40-45

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96
Q

Responsible for the largest portion of drug metabolism in the body?

A

CYP 450

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97
Q

Name ending “tron” associated with

A

Serotonin blockers

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98
Q

Serotonin blocking drugs act on the

A

5HT3 receptor

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99
Q

Name 3 serotonin blockers

A

ondansetron
dolesetron
granisetron

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100
Q

Name ending “pril” associated with

A

ACEI

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101
Q

Name ending “dipine” associated with

A

CCB exception verapamil, cardizem

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102
Q

Name ending “tidine” associated with

A

H2 receptors blockers (antagonists)

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103
Q

Phase I reactions are (everything except conjugation)

A 
Methylation
Oxidation
Reduction
Dealkylation
Deamination
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104
Q

What is the significance of phase II reactions?

A

Compound can be readily eliminated from the body

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105
Q

Phase II reaction involves conjugation of the drug with

A

Glucuronide
Sulfate
Taurine
Glycine

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106
Q

Is phase II always required to complete drug metabolism ?

A

NO

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107
Q

Does phase II always follow phase I

A

NO

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108
Q

Physiological stimuli responsible for stimulating the release ADH include?

A

Stress and anxiety
Hyperthermia
Presence of histamine-releasing stimulus

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109
Q

Pharmacological stimuli that stimulates the release of ADH

A

PPV of the lungs

Beta adrenergic stimulation

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110
Q

ADH secreted by

A

Posterior pituitary

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111
Q

Increased serum osmolarity indicates

A

Insufficient water content

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112
Q

What is the target site for ADH ?

A

Collecting tubules of the kidney

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113
Q

Primary goal of ADH is to e prevent

A

water loss thereby decrease serum osmolarity and increasing circulating volume.

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114
Q

To minimize risk of Compound A production during SEVOFLURANE administration which of the following actions may be taken?

A

Run lower levels of sevoflurane
Use hydrated soda lime absorbent
Maintain gas flows equal to or greater than 2L/min

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115
Q

What are the factors that increase the risk of compound A formation ?

A

Low gas flow states
Increased levels of sevoflurane
Dry or warm CO2 absorbents

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116
Q

Which inhaled anesthetic is associated with the greatest production of heat in dessicated Co2 absorbent? how?

A

Sevoflurane; loss of moisture into the CO2 absorbent, facilitates an exothermic reaction between sevo and the absorbent. CAN lead to fire in the circuit

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117
Q

Which of the inhaled anesthetic is associated with the highest production of CO in dessicated CO2 absorbent?

A

Desflurane; Results in the production of the greatest amount of CO

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118
Q

Does higher doses of opioid decrease the MAC requirements of VA?

A

NO. MAC of VA is influenced to only a small degree so even higher amount of opiods analgesics won’t affect MAC

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119
Q

VP of desflurane is (high/low)

A

High

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120
Q

Halogenated anesthetics least metabolized?

A

Desflurane

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121
Q

The speed of an inhaled anesthetic action is determined by its solubility and expressed as which of the following?

A

Blood:gas solubility coefficient

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122
Q

The speed with which a volatile anesthetic vapor enters the pulmonary circulation is represented by the

A

Blood: gas solubility coefficient

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123
Q

Which of the following are the 2 main organs involved with volatile agent metabolism?

A

Lunger

Liver

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124
Q

The main elimination of volatile anesthetics via the

A

lung on exhalation

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125
Q

Responsible for a small amount of VA metabolism

A

Cytochrome isoenzymes

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126
Q

Vapor pressure refers to

A

Pressure of the vapor resulting from vaporization . Pressure at which molecules of a volatile liquid escape the liquid phase.

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127
Q

What are the 2 most soluble volatile anesthetics

A

Isoflurane

Halothane

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128
Q

Rate of uptake is dependent on

A

1) alveolar ventilation rate 2) partial pressure of gas (concentration effect) 3) breathing system

129
Q

For poorly soluble anesthetic agents (ex. N2O, desflurane), an increase in FA/Fi depends

A

very little on alveolar ventilation

130
Q

Enflurane has a blood/gas partition coefficient of 1.7. What does that mean?

A

if the gas is in equilibrium the concentration in blood will be 1.7 times higher than the concentration in the alveoli. Thus, it makes sense that a gas with a higher blood gas coefficient will require higher uptake of gas into the blood and induction will be slower.

131
Q

Higher partition coefficient = ______ipophilicity = _____potency = ______ solubility

A

higher; higher; higher

132
Q

MAC and Blood gas coefficient

A

MAC decreases as blood gas partition coefficient increases, generally speaking

133
Q

High solubility = more anesthetic needs to be dissolved =

A

slower onset

134
Q

Solubility represented by a higher blood:gas coefficient represents

A

The speed with which the agent is taken up into the pulmonary circulation

135
Q

The oil:gas partition coefficient is related to a volatile’s agent

136
Q

Potency and MAC relationship

A

Potency is inversely related to MAC

137
Q

The slowest induction is possible with which of the following

A

Halothane and INCREASED CO state

138
Q

The speed of an inhalation induction is inversely related to the

A

Blood: gas coefficient in the presence of increased CO.

139
Q

MAC decrease ______per decade of age

140
Q

Inhalational anesthetics on CBF and ICP

A

All inhalational anesthetics increase CBF and ICP

141
Q

Nitrous compared to volatile agents

A

Nitrous increase CMRO2, volatile agents do not

142
Q

NO has a blood:gas partition ratio of 0.47 and is thus

A

30 times more soluble in blood than nitrogen,

143
Q

Nitrous and volatile agents of seizure threshold

A

Increase the seizure threshold but only nitrous increase CMRO2

144
Q

Nitrous is a myocardial depressant or stimulant?

A

Nitrous is a sympathetic stimulant produce increase blood pressure, CO and HR

145
Q

Volatiles agents: myocardial depressant or stimulant?

A

VA are myocardial depressants

146
Q

What hemodynamics may be afffected with the use of Nitrous oxide?

A

Elevated RV EDP

147
Q

PVR and N2O

A

PVR is increased in the presence of N2O due to vasoconstriction of the pulmonary vasculature. Increase PVR results in increase RVEDP

148
Q

What is the B:G coefficient of Nitrous

149
Q

What is the B:G coefficient of sevo

150
Q

What is the B:G coefficient of Isoflurane

151
Q

What is the B:G coefficient of Desflurane

152
Q

Which inhalational agent is a halogenated alkane?

153
Q

Which inhalational agent is halogenated with FLUORINE

A

Desflurane

Sevoflurane

154
Q

Which agent results in an increased heart rate during

inhalational anesthesia?

A

Sevoflurane > 1.5 MAC

155
Q

Which inhalational agent is the least desirable
or a patient with chronic bronchitis and a 50-pack/
year history o smoking?

A

Desflurane

156
Q

Which agent increases the cerebral metabolic rate or

oxygen (CMRO2)?

157
Q

Which o the following halogenated agents potentiates

the effects of epinephrine the most?

158
Q

What is the recommended minimum liter flow to

avoid renal injury when using sevoflurane?

159
Q

T e patient is scheduled or a total knee arthroscopy
under general anesthesia. T e patient’s history includes
retina surgery using sulfur hexafluoride 2 months ago.
What will you avoid?

A

(A) Nitrous oxide Nitrous oxide expands the gas bubble and may cause intraocular hypertension

160
Q

Which o the following would be appropriate
anesthesia induction techniques or a severely hypertensive patient with coronary artery disease and moderate ventricular dysfunction?

A

(A) Inhalational induction with sevoflurane

161
Q

Which inhaled agent is most associated with emergence

delirium in children?

A

(A) Sevoflurane

162
Q

An inhalational induction with will likely cause catecholamine release, urther increasing blood pressure and heart rate?

A

desflurane

163
Q

What type of vaporizer contains desflurane?

A

Electronic

164
Q

When using evoked potentials, which o the ollowing

will you avoid?

A

Isoflurane

165
Q

The patient is scheduled or laser removal of vocal

cord papilloma. What will you avoid?

166
Q

What is the Vapor pressure of isoflurane?

167
Q

What is the Vapor pressure of Desflurane?

168
Q

What is the Vapor pressure of Sevoflurane?

169
Q

What is the Vapor pressure of Nitrous oxide?

170
Q

Blood-gas Partition coefficient of Isoflurane

171
Q

Blood-gas Partition coefficient of Desflurane

172
Q

Blood-gas coefficient Partition of Sevoflurane

173
Q

Blood-gas coefficient Partition of Nitrous oxide

174
Q

Brain-Blood coefficient Partition of Isoflurane

175
Q

Brain-Blood coefficient Partition of Desflurane

176
Q

Brain-Blood coefficient Partition of Sevoflurane

177
Q

Brain-Blood coefficient Partition Nitrous Oxide

178
Q

MAC of Isoflurane

179
Q

MAC of Desflurane

180
Q

MAC of Sevoflurane

181
Q

MAC of Nitrous oxide

182
Q

What is the relationship between the partition coefficient with the rate of induction?

A

INVERSELY proportional

183
Q

What are the determinant of the speed of onset and offset ? BIAC2CG

A 
B/G partition coefficient
Inspired anesthetic concentration
Alveolar ventilation
Concentration effect
2nd gas effect
Cardiac output
Gradient between alveolar and venous blood
184
Q

The mechanism of action of nitrous oxide is thought to be attributed to ?

A

The antagonisms of NDMA receptors in the CNS

185
Q

The mechanism of action of Volatile anesthetics is thought to be attributed to what actions on what receptors?

A

GABAa, Glycine and glutamate receptors play a role

186
Q

What determines the speed of induction of general anesthesia?

A

The rate of the rise of the ration of FA/FI

187
Q

What are the 2 opposing processes that determine FA/FI at a given time?

A

Anesthetic delivery to and uptake from alveoli

188
Q

How does the blood gas partition coefficient affect the rate of rise of the FA/FI?

A

Lower solubility in blood will lead to lower uptake of anesthetic into the bloodstream, thereby increasing the rate of rise of teh FA/FI at a given time.

189
Q

2 patient condition that increases solubility of halogenated volatile anesthetics in blood

A

Hypothermia

Hyperlipidemia

190
Q

How does Alveolar Ventilation affect the rate of rise of the FA/FI?

A

Increasing MV increasing FA/FI

191
Q

What is the concentration effect?

A

As FI increases, the rate of FA/FI also increases. For a gas with a FI like nitrous , a large amount is taken up into blood and there is a large loss of the total gas volume. The remaining nitrous is concentrated and the addition of more anesthetic with the next breath will increase the concentration further.

192
Q

With the concentration effect the uptake of a large gas volume (such as nitrous) creates what?

A

draws more fresh what into the alveoli, thereby increasing FA and augmenting the inspired TV.

193
Q

What explains why the rate of FA/FI is faster for nitrousoxide than desflurane? (even though the blood-gas partition coefficient for desflurane is smaller)

A

The concentration effect.

194
Q

What is the 2nd gas effect?

A

It is a direct outcome of the concentration effect. When nitrous and a potent inhalation anesthetic are administered together, the uptake of nitrous oxide concentrates the second gas (such as isoflurane) and increases the input of additional second gas in the alveoli via the augmentation of inspired volume.

195
Q

How does CO affects the rate of rise of FA/FI?

A

An increase in cardiac output, and therefore pulmonary blood flow, will increase the anesthetic uptake and decrease the rate of rise in FA/FI?

196
Q

Mnemonic for FA/FI chart (FA on the left, time bottom)

197
Q

Explain how the gradient between alveolar and venous blood affect FA/FI?

A

The uptake of anesthetic into the bloodstream will decrease as the anesthetic partial pressure gradient between the alveolar gas and the venous blood decreases. This gradient is particularly large early in the course of anesthetic administration.

198
Q

Distribution of volatile anesthetics in the tissues: Rate of equilibration of anesthetic partial pressure between blood and a particular organ system depends on what factors?

A

Tissue Blood flow
Tissue solubility
Gradient between arterial blood and tissue

199
Q

Tissue blood flow affect rate of equillibration of anesthetics partial pressure, explain.

A

Equillibration occurs first in the tissue with increase perfusion. VESSEL RICH GROUP of highly perfused organs system, which receives about 75% of the CO . Remainder of the CO goes to muscle and fat

200
Q

Anesthetic agents with high-tissue solubility are ______(slower/faster) to equillibrate?

201
Q

Gradient between arterial blood and tissue: Until equillibration is reached between the anesthetic partial pressure in the blood and a particular tissue, a _______exist that leads to the uptake of anesthetic by the tissue. The rate of uptake will (decrease/Increase) _____as the gradient decreases

A

gradient ; decrease

202
Q

What is the predominant route of elimination of VA?

A

Exhalation ; After the VA is turned off, the anesthetics tissue and alveolar partial pressure decrease

203
Q

What is the predominant route of metabolism of VA?

A

VA undergoes degrees of hepatic biotransformation

204
Q

What is the predominant route of Anesthetic loss?

A

Skin or/and visceral membranes

205
Q

CV effect and nitrous oxide

HR, BP, SNS

A

Mild sympathetic NS stimulant

HR and BP unchanged usually

206
Q

Resp effect and nirous oxide

A

May increase PVR

Mild resp depressant

207
Q

VA and CNS effects: low doses

A

Alpha, delta and slow oscillation are present at lower does of iso, des, and sevo.

208
Q

VA and CNS effects: high doses

A

theta oscillation appears follwed by burst suppression

209
Q

VA on SSEPs (remember dail)

A

DAIL
Decrease amplitude of SSEPS
Increase latency of SSEPS

210
Q

VA on CBF and CMRO2

A

Increase CBF and decrease CMRO2: uncouple autoregulation of CBF

211
Q

VA on Cardiovascular system?

A

Dose dependent Myocardial depression and systemic Vasodilation
HR unchanged

212
Q

Action of desflurane on CV

A

Increase SNS stimulation
Tachycardia
Hypertension
Usually on induction, or when the concentration is abruptly increased.

213
Q

What can VA do to the myocardium?

A

May sensitize the myocardium to the arrhythmogenic effects of catecholamines, which is a concern during infiltration of epi-containing solutions, or administration of sympathomimetic agents.

214
Q

What are the RESP effects of VA?

A

Dose dependent respiratory depression with decrease TV, increase RR and increase arterial CO2 pressure

215
Q

VA, light anesthesia and resp

A

May precipitate coughing, laryngospasm, or bronchospasm particularly in patients with asthma or COPD

216
Q

What makes sevo more suitable for use as an inhalation agent?

A

Lower pungency

217
Q

VA on bronchioles

A

Bronchodilatory effects EXCEPT desflurane which has mild bronchoconstricting activity

218
Q

What are the effects of VA on HPV?

A

Inhibit HPV which may contribute to pulmonary shunting.

219
Q

Neuromuscular system and VA

A

Dose dependent decrease in skeletal muscle tone’

May lead to MH

220
Q

VA and hepatic system

A

Halothane can lead to hepatitis

221
Q

VA and renal system

A

Decrease RBF through decrease in MAP or increase in renal vascular resistance

222
Q

3 adverse effects of NITROUS OXIDE

A

Expansion of closed gas spaces
Diffusion hypoxia
Inhibition of tetrahydrofolate synthesis

223
Q

Nitrous and explansion of closed gas spaces, explain?

A

Because nitrous oxide is 35 times more soluble in blood than nitrogen , closed air space will expand as the amount of nitrous oxide diffusing into these spaces is greater than the amount of nitrogen diffusing out.

224
Q

What is the predominant constituent in closed gas-contraining spaces in the body ?

225
Q

Spaces that nitrous oxide can diffuse to?

A

Pneumothorax
occluded middle ear
Bowel lumen
Pneumocephalus

226
Q

ETT cuff and the use of N2O

A

Nitrous oxide will diffuse into the cuff of an ETT and may increase the pressure within the cuff. The cuff pressure should be assessed intermittently and if necessary , adjusted.

227
Q

Diffusion hypoxia with which gas? explain

A

Nitrous oxide; After you d/c nitrous oxide , its rapid elimination from the blood into the lung may lead to a low partial pressure of O2 in the alveoli, resulting in hypoxia and hypoxemia with supplemental oxygen is not administered.

228
Q

Caution of nitrous oxide administration in patient with this deficiency ? why?

A

B12 ; because nitrous inhibits methionine synthase, a vitamin B12 dependent enzyme necessary for the synthesis of DNA. It should be use with caution with pregnant patients and those deficient in vitamin B12

229
Q

Desflurane can be degraded to

A

CO in CO2 absorbents (especially baralyme). More likely when absorbent is new or dry.

230
Q

Sevoflurane can be degraded to

A

Fluoromethyl 2-2 difluoro-1-vinyl ether (compound A) which shows that it can lead to renal toxicity in animal models

231
Q

Compound A concentration increase at

A

low fresh gas rates.

232
Q

Mechanism of action of barbiturates? on RAS, neurotransmitters

A

Depresses the Reticular activating system
Depression of NDMA in a concentration dependent manner
Depression of Excitatory neutrotransmitters (glutamate and nicotinic)
Enhance Inhibitory neutrotransmitters

233
Q

The sodium salts of barbiturate in solution are (acidic/basic; stable/unstable)

A

Alkaline (pH>10)

Relatively unstable

234
Q

Are sodium salts of barbiturates water soluble?

235
Q

Prompt awakening from a a single dose of thiopental or methohexital reflects ?

A

Redistribution

236
Q

What is the determining or limiting factor for the duration of action of a barbiturate?

A

redistribution the barbiturate undergoes

237
Q

CV effects following barbiturate administration?

A

Increase HR
Decrease Venous return
Decrease BP

238
Q

Barbiturates on CBF , CMRO2 and iCP

A

Decrease CBF, CMRO2 and ICP

239
Q

Barbiturates are neuro____

A

protective

240
Q

Names 2 barbiturates

A

Thiopental

Methohexital

241
Q

Onset of action of barbiturates

A

30-45 seconds, f/b rapid termination of effects due to redistribution

242
Q

How are barbiturates metabolized?

A

Hepatic metabolism

243
Q

With hepatic metabolism, thiopental vs methohexital which one has higher clearance?

A

Methohexital

244
Q

Prolonged infusion of barbiturates effects

A

Prolonged sedation and unconsciousness due to reduced rate of consciousness , return of the drug to the central compartment and hepatic metabolism

245
Q

The context senstive half time of thiopental is

A

long even after short infusion

246
Q

Barbiturates on cerebral vascular bed

A

Dose-dependent cerebral vasoconstriction decrease CBF and CMRO2, and ICP

247
Q

Do barbiturates affect cerebral autoregulation?

A

NO, Cerebral autoregulation remains unaffected.

248
Q

Thiopental and EEG

A

At high does will produce isoelectric EEG

249
Q

Methohexital and seizures

A

Methohexital can elicit seizure activity

250
Q

Barbiturates on SSEPs, MEPs,

A

Minimal effects

251
Q

Barbiturates on BAEPs

A

Dose dependent depressio

252
Q

Barbiturates on CV

A

Venodilation and depress myocardial contractility , leading to dose-dependent decreases in BP and CO especially for patient who are preload dependent.

253
Q

Barbiturates on baroreceptors

A

Remain intact; so hypotension will still lead to tachycardia.

254
Q

Barbiturates on RESP

A

Dose dependent decrease in RR and TV

255
Q

Barbiturates on ventilatory response

A

Ventilatory responses to hypoxia and hypercabia are depressed.

256
Q

Barbiturates: after induction what occurs

A

Apnea result for 30-90 seconds.

257
Q

Barbiturates compared with propofol

A

Laryngeal reflexes remain intact with barbiturates, so the incidence of cough and laryngospasm is higher,

258
Q

Reduce dose of barbiturates in those kind of patients?

A

Hypovolemic
elderly
Hemodynamically compromised patients

259
Q

Barbiturates admnistration caution

A

Do not mix with drugs with lower pH solution such as succinylcholine and cause precipitation of other drugs such as VEC. Therefore, use free running IV and avoid simulataneously injection with other drugs.

260
Q

Thiopental have histamine release

261
Q

Absolute contraindications of barbiturates

A

Acute intermittent Porphyria

262
Q

Why no barb in porphyria?

A

Barb induce porphyrin synthetic enzymes such gamma-aminolevulinic acid synthetase

263
Q

Barbiturates and IV

A

May cause pain at the site of administration due to venous irritation.

264
Q

Thiopental injection what can it cause? How do you treat?

A

Can cause severe pain and tissue necrosis if injected extravascularly or intra-arterialy . Treat with PHENTOLAMINE (alpha blocker) heparin, vasodilators, and regional sympathetic blockade.

265
Q

Often seen during induction with methohexital

A

Myoclonus

Hiccups

266
Q

Barbiturates protect agains focal ischemia or global?

267
Q

Barbiturates and EEG

A

High does can cause electrical silence on the EEG.

268
Q

Anticonvulsant activity of a barbiturate is structurally related to

A

PHENYL GROUP (the methyl group does not have anticonvulsant property)

269
Q

What can lead to higher concentration of thiopental in the brain?

A

When the central component is reduced(hypovolemia)’
When albumin is decreased (Liver disease)
When there is increased non-ionized fraction of the drug (acidosis)

270
Q

Thiopental and elimination

A

Prolonged in the elderly because with increasing age the time for the drug to go from the central compartment via redistribution increases.

271
Q

When using methohexital , full recovery of psychomotor function after the single dose is more rapid compared to thiopental why?

A

ENHANCED METABOLISM; hepatic extraction of methohexital occurs at a rate 3-4 times greather than that for either thiopental or thiamylal.

272
Q

How is methohexital excreted?

273
Q

The only opioid receptor that produces respiratory stimulation ?

A

sigma receptor

274
Q

The sigma opioid receptor produces

A

Respiratory stimulation

275
Q

What are the endogenous peptide that bind to opioid receptors?

A

Endorphin
Enkephalin
Dynorphin

276
Q

What is the principal effect of opioid receptor activation ?

A

Decrease in release and response to excitatory neurotransmitters.

277
Q

What happens when opiate receptors are activated?

A

Excitatory neurotransmitter release is inhibited presynaptically, while a decrease response to the transmitters occurs postsynaptically.

278
Q

Endorphins are agonists of which opioid receptor?

279
Q

The primary mechanism of action of opiates is via

A

µ-receptor agonism.

280
Q

Opioids location in the brain?

A

the dorsal horn (layers 4 and 5 of the substantia gelatinosa) of the spinal cord, which inhibits the transmission of nociceptive information;

281
Q

EnKEphalins are agonist of which opioid receptor?

A

DELTA (KEd)

282
Q

Dynorphins are agonists of which opioid receptor?

283
Q

What increases the amount of pulmonary uptake of lipid soluble opioids?

A

History of tobacco use.

284
Q

Advantage of the use of neuraxial opioids over IV opioids or regional anesthesia over local anesthetics

A

NO loss of proprioception
No SNS denervation
No skeletal muscle weakness

285
Q

What is the most common side effect of neuraxial opioids?

A

Pruritus (highest incidence of occurrence)

286
Q

What is the triad of opioid overdose? MHC

A

Miosis
Hypoventilation
Coma

287
Q

The primary sign of opioid overdose is

A

Respiratory depression that can progress to apnea

288
Q

Morphine cause supraspinal analgesia by acting on which opioid receptor?

289
Q

Morphine cause spinal analgesia by acting on which opioid receptor?

290
Q

How is morphine metabolized?

A

Hepaticallly and renally

291
Q

Morphine metabolims occurs by

A

glucoronic acid conjugation primarily in hepatic and renal (extra hepatic sites)

292
Q

What is the least protein-bound opioid agonist?

A

Morphine (35% only )

293
Q

Protein bound % of Meperine, sufentanyl and fentanyl

294
Q

Both analgesic and possess weak local anesthetic properties?

A

Meperidine (alteration of nerve conduction)

295
Q

What is the least-lipid soluble opioid agonist?

296
Q

In order of LEAST to most lipid soluble opiods : MR. MASF

A

Morphine < remifentanil< meperidine< alfentanil< sufentanily< fentanyl

297
Q

Morphine-6- Glucuronide is a ______Potent and_______-lasting opioid agonist than morphine

A

MORE ; LONGER

298
Q

What is the metabolite of morphine?

A

Morphine-6-glucuronide

299
Q

Which of the following patients would have a prolonged elimination half time of fentanyl?

A

Elderly (aging changes in the liver main cause)

Continuous infusion lasting longer than 2 hours

300
Q

What is the pharmacologically active metabolite of fentanyl?

A

No significant active metabolite.

301
Q

The context sensitive half time of fentanyl

A

Initially it is shorter than that of sufentanil, but after 2 hours of infusion its longer.

302
Q

When a continuous infusion of fentanyl last beyond 2 hours, the half life becomes become _____Than sufentanil

A

Greater than sufentanil

303
Q

How long does it take for plasma fentanyl concentration to plateau with the use of the transdermal patch?

A

12-18 hours

304
Q

What is the major obstacle to transdermal administration of a medication?

A

Stratum corneum

305
Q

How much of an initial IV fentanyl dose undergoes first pass pulmonary uptake? why?

A

75%; because it is highly lipid solubility

306
Q

Compared to fentanyl and sufentanil, alfentanil has a more ________onset of action? why?

A

rapid; high degree of nonionization

307
Q

At physiological pH, what % of alfentanil is in the non-ionized form?

308
Q

Compared to fentanyl, alfentanil is ______potent and has a ______ onset of action

A

less : more rapid

309
Q

Alfentanyl potency

A

10-20% of that of fentanyl strength, 1/3 of fentanyl duration

310
Q

What can alter the elimination half time of alfentanil? and why?

A

Cirrhosis of the liver; Because almost all of a dose of alfentanil is metabolized by the liver within an hour of administration. Therefore, disease of the liver alters the half life of alfentanyl

311
Q

What is the most potent analgesis?

A

Sufentanil

312
Q

The standard to which opioid are compared to ?

313
Q

Fentanyl potency

A

75-125 times more potent than morphine

314
Q

Sufentanil potency

A

5-10 times more potent than fentanyl

315
Q

Sufentanil is _____Protein bound than fentanyl, and it has a _______volume of distribution

A

more; smaller (sufentanil 92.5% PB, 79-87% proteinb for fentanyl)

316
Q

For a continuous infusion lasting more than 2 hours (fentanyl) and less than 8 hours (alfentanil) rank the following opioid agonists from shortest to longest context-sensitive half-time? SAF

A

Sufentanil< alfentanil< fentanyl

317
Q

Symptom of normeperidine toxicity ?

A

Seizures and myoclonic activity

318
Q

Most effective opioid for decreasing shivering?

A

Meperidine (NDMA receptor activity , NE inhibitor in central neurons)

SEE/NCE Boards Core Concepts (49 decks)

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