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Advanced Pharm For NA 1 > Exam 1 Study Guide > Flashcards

Exam 1 Study Guide Flashcards

1
Q

Pharmacology:

A

study of the effect of chemicals on the living body

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2
Q

Pharmaceutics:

A

the FORMULATION and prep of drugs

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3
Q

Pharmacoeconomics:

A

study of economic impact of drugs

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4
Q

Toxicology:

A

study of the harmful effects of chemicals; pharm of WRONG doses

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5
Q

Pharmacognosy:

A

study of medicinal use of NATURALLY occurring compounds

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6
Q

Pharmacy:

A

the prep and dispensing of drugs

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7
Q

Pharmacogenetics:

A

genetic influences by and of drugs

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8
Q

Pharmacoepidemiology:

A

study of the use and effect of drugs on a large group of people

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9
Q

Pharmacokinetics:

A

study of absorption, distribution, metabolism, and excretion of the drug
What the body does to the drug

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10
Q

Pharmacodynamics:

A

physiological and biochemical mechanisms of action of drugs
What does the drug do to the body

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11
Q

Receptor Theory (pharmacodynamics)

A

there are receptors that recognize the presence of chemicals and postulate a response

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12
Q

Drug receptors are _ _ which act as the site for a drug

A

macromolecular complexes

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13
Q

Drug receptors are usually made of _ that are involved in production of normal cellular function

A

proteins

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14
Q

Drug receptors include:

A

carrier proteins
protein channels
ion channels
enzymes
nucleic acids

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15
Q

True or false: A drug can’t make the body do anything it can’t already do

A

TRUE

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16
Q

If a receptor is a lock, then the _ is the key

A

LIGAND; a drug becomes a ligand when it connects to a receptor

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17
Q

Properties of receptors:

A

sensitivity
selectivity
specificity

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18
Q

Drug response occurs from a _ _ (sensitivity) produced by _ _ chemicals (selectivity) and the response is the same bc the cell determines it. (specific)

A

low concentration
structurally similar

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19
Q

True or false: A desired response only occurs when the drug receptors are completely saturated

A

FALSE

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20
Q

Occupancy Theory:

A

-opposite of spare receptor theory, there is a linear relationship b/t receptors occupied and response
magnitude of a drug effect is proportional to the number of receptors occupied
-tissue response happens when sufficient receptors have been occupied

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21
Q

Spare-Receptor Concept:

A

there is a non-liner relationship between the number of receptors stimulated and the response
-max response can be stimulated by only a fraction of the receptors

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22
Q

Agonist:

A

bind to receptor and STIMULATE the function that receptor serves

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23
Q

The agonist _ the action of the endogenous ligand.(hormone, neurotransmitter in body)

A

MIMICS

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24
Q

In adequate concentrations, an agonist can cause max activation of all receptors and this is known as a _ _

A

full agonist

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25
Q

Antagonist have _ for a receptor but no _.

A

affinity for the receptor but no efficacy

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26
Q

An antagonist binds to a receptor and _ the endogenous function that the receptor serves.

A

blocks

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27
Q

Antagonists have a _ affinity for a receptor than agonists do.

A

HIGHER

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28
Q

Agonists and Antagonists compete with the _ _ for binding sites

A

endogenous transmitter

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29
Q

Competitive Bonding is _ for most drugs

A

REVERSIBLE; drug binds then wears off once conc of blood exceeds conc of drug in plasma

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30
Q

Noncompetitive Bonding is _ for drugs

A

NONREVERSIBLE; once it binds, it’s there forever until body replaces the structure the receptor is attached to
-EX) platelets and aspirin

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31
Q

Antagonists have receptor _ but lack intrinsic activity AKA _.

A

affinity, efficacy

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32
Q

Antagonists with weak affinity=

A

competetive

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33
Q

Antagonists with strong affinity=

A

noncompetetive

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34
Q

Antagonists cause a _ward shift in the drug-dose response curve, which means?

A

RIGHTWARD; more drug is needed to cause the same effect due to increased affinity; how far the shift depends on # of available receptors occupied by antagonist

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35
Q

The strongest type of bond is a _ bond and is _.

A

covalent, nonreversible

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36
Q

The weakest type of bond is a _ bond and is _.

A

Van Der Waals, reversible

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37
Q

The bonds of receptors are as follows in order of strongest to weakest:

A

covalent, ionic, hydrogen, hydrophobic, van der waals

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38
Q

A _ _ activates a receptor but can’t elicit max response

A

Partial Agonist

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39
Q

A partial agonist may not elicit max response because:

A

-it may partially block effects of the full agonist
-possess both agonist and antagonist properties
-has lower efficacy than full agonist

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40
Q

_ _ are drugs that bind to a receptor causing an opposite reaction to an agonist

A

Inverse Agonists
NOT antagonists

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41
Q

Inverse Agonists bind with inactivated receptors and could be more beneficial than antagonists in disease states that occur from _ of receptor activity

A

upregulation

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42
Q

Dose Response Curve is the relationship among _, _, and _ _ as they relate to a typical sigmoidal dose or concentration versus response curve

A

efficacy, potency, and individual variability

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43
Q

Affinity/Potency is used to differentiate between different agonists that activate the same receptor and produce the same _ _ but at _ concentrations

A

max response (efficacy), different concentration;
-most potent drug required smallest dose

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44
Q

Efficacy is its ability to produce the desired response _ by _ of a receptor

A

expected, stimulation
-The magnitude of response with respect to the given dose

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45
Q

There will always be some _ in the dose response curve

A

variability

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46
Q

Intrinsic Activity is the _ _ effect obtained when comparing compounds in a series

A

relative max

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47
Q

Quantal Drug Response=

A

quantifies the actions of the drugs and expresses them as the effective dose (ED50), toxic dose (TD50), and lethal dose (LD50)

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48
Q

ED50=

A

effective dose in 50% of the population

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49
Q

TD50=

A

toxic dose in 50% of the population

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50
Q

LD50=

A

lethal dose in 50% of the population

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51
Q

LD50/ED50=

A

Therapeutic Index (bigger the better)

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52
Q

TD50/ED50=

A

Therapeutic Window (pharmaceutical window)

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53
Q

Therapeutic Index=

A

LD50/ED50, safety measure of a drug; how much it takes to kill someone

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54
Q

Therapeutic Window=

A

TD50/ED50; index used to estimate drug dose to treat disease effectively WHILE IN SAFETY RANGE and not causing significant adverse effects

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55
Q

Therapeutic Range ( Margin of Safety)=

A

range of doses that produce concentrations between toxicity and subtherapeutic thresholds

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56
Q

The top end of the therapeutic range is the toxic threshold which is the _ _ _ which is derived from _

A

minimum toxic concentration, TD50

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57
Q

The bottom end of the therapeutic range is the subtherapeutic threshold which is the _ _ _ which is derived from _

A

minimum effective concentration, ED50

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58
Q

Receptors not only initiate regulation of physiological and biochemical functions but themselves are also subject to many _ and _ controls

A

regulatory and homeostatic

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59
Q

Down Regulation AKA Desensitization=

A

diminished response

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60
Q

Effects of down regulation on cell:

A

-receptors decrease in number
-each receptor is less stimulated (decreased sensitivity -> tolerance)

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61
Q

Increased doses of a drug are needed to achieve same effect is the result of _ _

A

down regulation

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62
Q

Down regulation is caused by:

A

continued stimulation of the cell by AGONISTS
-Ex) bronchodilators for asthma

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63
Q

Up Regulation=

A

number and sensitivity of receptors increase

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64
Q

Effects of up regulation on cell:

A

-increase in number of receptors
-receptors are more sensitive to a drug

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65
Q

A patient developing tolerance requiring higher doses of an antagonist to counteract the increased receptor number is the result of _ _.

A

up regulation

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66
Q

Up regulation is caused by:

A

chronic administration of an ANTAGONIST
-Ex) beta adrenergic receptors up regulating in presence of antagonists and down regulate in presence of agonist

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67
Q

Tolerance=

A

increased concentration of a drug is needed for a response

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68
Q

Drug Tolerance (pharmacodynamic tolerance)=

A

a change in tissue sensitivity due to an adaptive mechanism

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69
Q

Dispositional Tolerance (pharmacokinetic tolerance)=

A

a change in the drug level due to an adaptive change in absorption, distribution, metabolism, or excretion of the drug
-Ex) enzyme induction or inhibition

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70
Q

Tachyphylaxis=

A

rapid development of tolerance with acute drug administration

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71
Q

Ceiling Effect=

A

dose beyond which there is no increase in effect, additional dosing leads to adverse effects

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72
Q

Interaction=

A

alteration in the therapeutic action of a drug by concurrent administration of other exogenous chemicals

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73
Q

Addition=

A

the combined effect of 2 drugs acting via the same mechanism is EQUAL to that expected by simple addition of their individual actions;
1+1=2

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74
Q

Synergism=

A

The combined effect of 2 drugs is GREATER than the algebraic sum of their individual effects
1+1=3

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75
Q

Potentiation=

A

The enhancement of the action of 1 drug by a second drug that has no detectable action of its own
1+0=3
Ex) penicillin (1) + probenicin (0) = prevents drugs from being excreted but has no effect on infection

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76
Q

Antagonism=(in terms of reactions)

A

action of one drug opposes the action of another
1+1=0
Ex) opioids + narcan, protamine + heparin, NMBD + suggamadex

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77
Q

Pharmacokinetics (4 things)

A

absorption
distribution
metabolism
excretion

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78
Q

The effect of size on pharmacokinetics:

A

the smaller a molecule is the more able it is to cross membranes

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79
Q

Degree of Ionization/ Lipid Solubility:

A

drugs are either weak acids or bases;
-higher the ionization the less likely a drug will pass thru a membrane
-measured with pKa

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80
Q

Ionized drugs are:

A

-charged
-water soluble
-unable to pass thru cell membranes

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81
Q

Non-ionized drugs are:

A

-non-charged
-lipid soluble
-able to diffuse across cell membranes

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82
Q

Bioavailability=

A

% of a drug that enters the systemic circulation in an unchanged form after administration of the product

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83
Q

The extent to which a drug reaches its effect after its introduction into the circulatory system is its _.

A

bioavailabiliity

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84
Q

The rate at which the systemic absorption occurs establishes a drug’s _ and _.

A

duration and intensity

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85
Q

Factors that influence bioavailability:

A

-lipid solubility
-solubility in aqueous and organic solvents
-pH and pKa
-blood flow
-environment into which drug is introduced
-patient’s age, sex, pathology, temperature

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86
Q

Route of admin with HIGHEST bioavailability:

A

IV, 100% bioavailable, most rapid onset

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87
Q

Route of admin with LOWEST bioavailability:

A

PO and inhalation; 5-100% bioavailable,
-PO is most convenient but has SIGNIFICANT first-pass effect
-inhalation has a VERY rapid onset

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88
Q

Admin order of highest % of bioavailability:

A

IV, transdermal, IM, subcutaneous, per rectum, PO, Inhalation

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89
Q

Stomach pH

A

1-3

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90
Q

Duodenal pH (small intestine)

A

5-6

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91
Q

Colon pH (large intestine)

A

8

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92
Q

Ileum pH (rectum)

A

8

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93
Q

Blood plasma pH

A

7.4

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94
Q

CSF pH

A

7.4

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95
Q

Urine pH

A

4-8

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96
Q

pKa

A

pH at which a drug is 50% ionized and 50% nonionized; ionization constant

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97
Q

True or false: pKa is a measure of acid or base status

A

FALSE, it measures the extent of ionization

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98
Q

True or false: the ionized portion of the drug will stay in the blood but it sends the non ionized drug elswehere.

A

true

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99
Q

Drugs that are 100% _ will have no CNS effect because none is transferred to the brain

A

ionized

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100
Q

If any portion of the drug is _ it can pose potential for fetal harm

A

nonionized

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101
Q

_ soluble substances are excreted by the kidney at the _ _ .

A

water, distal tubule

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102
Q

The liver converts _ soluble substances into _ soluble substances most commonly with cytochrome oxidases AKA _ _ _.

A

fat, water, cytochrome enzyme P450.

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103
Q

Primary metabolizing enzymes include (4):

A

CYP450, microsomal enzymes, mixed function oxidase, an metabolizing enzymes

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104
Q

3 factors effecting liver metabolism:

A

-intrinsic ability of the liver to metabolize a drug
-hepatic blood flow
-extent o binding of the drug to blood components

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105
Q

Lipid synthesis happens with enzymes found in the _ _ _ and to some degree in the _ of the cell. (think parts of cell)

A

smooth endoplasmic reticulum and cytosol of the cell

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106
Q

Although it mostly occurs in the liver, there are still considerable levels of metabolization that happen in:

A

lungs, kidneys, GI and placenta

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107
Q

Phase 1 of metabolism in the liver includes the processes of:

A

oxidation, reduction, hydrolysis (more common)

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108
Q

Phase 1 of the liver metabolism forms products that are more _ and _ active

A

chemically and pharmacologically

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109
Q

Phase 1 of the liver metabolism often involves the _ system in which _ _ is involved

A

momooxygenase, cytochrome P450

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110
Q

CYP3A4 metabolizes about _% of clinically administered drugs

A

50%

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111
Q

CYP2D6 metabolizes about -% of clinically administered drugs

A

25%

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112
Q

Phase 2 of the liver metabolism includes the processes of:

A

conjugation and synthesis

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113
Q

Conjugation=

A

coupling the reactive drug molecule (from phase 1) to an endogenous group so the resulting product is more water soluble

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114
Q

If a drug takes too much energy to metabolize, the body will use _ _ so that when you excrete _ the drug is carried with it.

A

glucuronic acid, glucose

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115
Q

Some drugs are excreted via bile, reactivated in the _, and reabsorbed via _ circulation

A

intestine, enterohepatic

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116
Q

P450 enzymes can _ hepatic drug metabolism which increases the _ of drugs with _ metabolites

A

accelerate, toxicity, toxic

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117
Q

Enzyme Induction=

A

increases drug metabolizing effects in liver
- ex) alcoholics have high amts of liver enzymes and break drugs down more quickly

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118
Q

Enzyme Inhibition=

A

decreases drug metabolizing effects of liver
- ex) grapefruit juice inhibits enzyme CYP3A4 which means less if broken down and more is circulating in plasma, increasing effects

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119
Q

First Pass Effect AKA Hepatic Metabolism is a _-systemic metabolism in the liver or gut wall that reduces the _ of many drugs when given orally.

A

pre-systemic, bioavailability

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120
Q

True or false: upon ingestion, the drug first goes to the blood stream and from there to the liver.

A

False! Goes to liver first then bloodstream!

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121
Q

True or false: since some parts of a drug are metabolized by the liver this means there is less drug bioavailability for use

A

True

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122
Q

Drugs bind to _ _ because of their innate affinity to them

A

plasma proteins

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123
Q

Acidic drugs bind to the protein:

A

plasma albumin

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124
Q

Basic drugs bind to these 2 proteins:

A

B-globulin and A-acid glycoproteins

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125
Q

The degree of a protein binding to a drug is proportional to its _ solubility which means more _ soluble agents = more highly protein bound

A

lipid, lipid

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126
Q

True or false: A bound drug is free to act on receptors therefore protein binding doesn’t effect drug distribution

A

FALSE, they can’t act on receptors unless they are free

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127
Q

The drug-protein molecule is too large to diffuse through _ _ membranes and is trapped in the _ system which will cause high _ concentrations.

A

blood vessel, circulatory, plasma

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128
Q

Extensive protein binding can _ drug elimination via metabolism and excretion

A

SLOW

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129
Q

Clinical drug interactions rarely occur because of _ between drugs for _.

A

competition between drugs for proteins

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130
Q

When unbound drugs increase in plasma, _ increases as well, lowering the risk of toxicity

A

excretion

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131
Q

When plasma proteins are at lower level than normal, total drug concentrations are _ but unbound concentrations are _ _.

A

LOWER, NOT AFFECTED
-ex) warfarin, phenytoin, propranolol, propofol, fentanyl, diazepam

132
Q

Drug Elimination/Elimination Clearance=

A

ability for drug eliminating tissue to irreversibly remove drugs from the body

133
Q

The kidneys eliminate _ or _ _ drugs more readily.

A

hydrophilic or water soluble

134
Q

Elimination Half Life=

A

time needed for the plasma content of a drug to drop half of its prevailing concentration after a rapid bolus injection

135
Q

A drug is considered fully eliminated once _% has been excreted which is usually - half lives.

A

95%, 4-5 half lives

136
Q

First Order Kinetics or Dosage Independence states that most drugs leave the body at a _ rate.

A

constant

137
Q

At a half life of 0, _% of drug is eliminated and _% remains

A

0%, 100%

138
Q

At the 1st half life, _% of drug is eliminated and _% remains

A

50%, 50%

139
Q

At the 2nd half life, _% of drug is eliminated and _% remains

A

75%, 25%

140
Q

At the 3rd half life, _% of drug is eliminated and _% remains

A

87.5%, 12.5%

141
Q

At the 4th half life, _% of drug is eliminated and _% remains

A

93.75%, 6.25%

142
Q

At the 5th half life, _% of drug is eliminated and _% remains

A

96.875%, 3.125%

143
Q

Most drugs tend to be more _ than _ so they can pass thru cell membranes to their site of action

A

lipophilic than hydrophilic

144
Q

Highly lipophilic drugs have a _ onset of action because they _ diffuse into the highly perfused brain. They have a _ duration because of redistribution of the drug from CNS into the blood.

A

rapid, rapidly, short

145
Q

Lipophilic drugs have _ volumes of distribtions

A

greater

146
Q

An increase in the volume of distribution of a drug will _ its elimination half life.

A

increase

147
Q

An increase in elimination clearance will _ a drugs elimination half life.

A

decrease

148
Q

Distribution clearance of a drug is influenced by _ _ and regional _ _.

A

cardiac output and regional blood flow

149
Q

The autonomic nervous system works with _, _, and _ to respond to internal and external stressors.

A

renin, cortisol, and hormones

150
Q

Sympathetic Nervous System (SNS) =

A

amplification

151
Q

Parasympathetic Nervous System (PNS) =

A

limited targeted response

152
Q

_ and _ anesthetics can alter hemodynamics by influencing autonomic function

A

Inhaled and IV

153
Q

Beta-adrenergic blockade is important for prophylaxis for _ and as a therapy for _, _, and _.

A

ischemia, HTN, MI, and CHF

154
Q

SNS demonstrates both _ and _ adaptation to stress _ and _.

A

acute and chronic adaptation, pre and postsynaptically
-ex) biosynthesis, receptor regulation

155
Q

Presynaptic alpha receptors play a significant role in regulating _ release

A

sympathetic

156
Q

Many treatments for HTN target direct or indirect effects on the _.

A

SNS

157
Q

The _ _ is the superhighway of the PNS, accommodating ~75% of CNS traffic

A

vagus nerve

158
Q

Aging and other disease states (diabetes, SCI) come with important changes in _ function

A

autonomic

159
Q

Symp/Parasympatholytic=

A

blocks SNS/PNS

160
Q

Symp/Parasympathomimetic=

A

stimulates SNS/PNS

161
Q

Parasympathetic outflow occurs with the _ _ which extends all over the body

A

vagus nerve

162
Q

Sympathetic outflow occurs with the _ _.

A

Thoracolumbar region

163
Q

PREsynaptically both SNS and PNS secrete _ to bind with _ _ receptors

A

acetylcholine, nicotinic cholinergic receptors

164
Q

POST synaptically the SNS secretes _ to bind with an _ receptor and the PNS secretes _ to bind with a _ _ receptor.

A

SNS secretes norepinephrine, binds with adrenergic receptor
PNS secretes acetylcholine, binds with muscarinic cholinergic receptor

165
Q

Types of adrenergic receptors:

A

-alpha
-beta
-dopamine

166
Q

4 goals of anesthesia?

A

as stress free as possible
-amneisa
-anesthesia
-analgesia
-muscle relaxation via paralytic

167
Q

Amnesia=

A

loss of memory

168
Q

Anesthesia=

A

loss of consciousness

169
Q

Analgesia=

A

freedom from pain

170
Q

Muscle Relaxation via Paralytic=

A

relaxation or cessation of movement, certain reflexes

171
Q

Deepening stages of anesthesia correlate with apparent irregular _ paralysis of the CNS

A

descending
-ex) cortex, subcortical areas, lower cord, upper cord, medulla

172
Q

Changes in which 5 aspects define the different stages of anesthesia?

A

consciousness
respiration
skeletal muscle tone
eye signs
sequential loss of reflexes

173
Q

Stage 1 of anesthesia (analgesia)=

A

time between normal wakefulness(induction) and the loss of consciousness(hypnosis) due to an anesthetic agent
-mild analgesia; 3 planes

174
Q

Planes of stage 1 anesthesia

A

i-no amnesia or analgesia
ii-total amnesia and partial analgesia
iii-total amnesia and total analgesia (incision is felt as a blunt instrument across skin)

175
Q

Stage 2 of Anesthesia (excitatory or delirious)=

A

loss of consciousness to onset of automatic rhythmicity of vitals

176
Q

Things you will see in stage 2 of anesthesia:

A

-loss of awareness and recall (amnesia)
-combativeness
-cardiovascular instability
-excitation
-deconjugate ocular movements
-emesis, vocalizations
-breath holding/retching
-nystagmus
-increased muscle tone, jaw sets

177
Q

Disinhibition=

A

brain has both excitatory(dopamine) and inhibitory(GABA) receptors, induction drugs typically depress inhibitory receptors first

178
Q

Stage 3 (surgical anesthesia); 4 planes=

A

a state where movement in response to pain is suppressed, initiated by the cessation of respiration

179
Q

Stage 3 Plane 1=

A

-full regular respirations
-coordinated thoracic and diaphragmic muscular activity
-pupillary constriction
-eyes moist and slow, decreasing activity, loss of lid/lash reflex
-BP and HR normal

180
Q

Stage 3 Plane 2=

A

-diminished and regular respirations
-mixed midline and dilated pupils
-loss of corneal and laryngeal reflexes
-BP and HR near normal

181
Q

Stage 3 Plane 3=

A

-continued diaphragmic movement but diminished thoracic movement/intercostal paralysis
-RR increases, TV low
-further pupil dilation
-no reflexes
-hypotension and tachycardia

182
Q

Stage 3 Plane 4

A

-respirations jerky and shallow
-thoracic paralysis, very diminished diaphragmic activity
-significant pupillary dilation
-complete muscle relaxation
-hypotension and tachycardia

183
Q

Stage 4 (Medullary Paralysis or Death)

A

cessation of spontaneous respiration and medullary cardiac reflexes that may lead to death
-from cessation of respiration to death
-no reflexes
-flaccid paralysis, marked hypotension, weak irregular pulse

184
Q

True or false: the body’s reflexes get stronger the more superficial on the body you go.

A

FALSE; DEEPER = STRONGER,
lungs’ reflexes are stronger than lips’

185
Q

Reflexes go out in this order:

A

-swallowing (first air reflex)
-retching/gagging
-vomiting
-lid/lash (first eye reflex)

186
Q

Nystagmus=

A

seen in stage 2 of anesthesia, cerebral cortex depression

187
Q

Phase 1/3 of Emergence

A

from when anesthetic turned off and drugs reversed
-apnea-irregular breathing-regular breathing
-increased alpha and beta activity on EEG

188
Q

Phase 2/3 of Emergence

A

where mostly everything comes back, EXTUBATE HERE IF POSSIBLE
-increased HR and BP, return of ANS and muscle tone, + pain response
- + salivation, tearing, grimacing, swallowing, gagging, coughing, defensive psoturing

189
Q

Phase 3/3 of Emergence

A

EXTUBATE ASAP ROCKY
-eye opening
-responds to commands
-awake patterns on EEG

190
Q

Uptake and Distribution of inhaled anesthetics are influenced by 4 main things:

A

-machine
-lungs
-blood
-tissues

191
Q

Fa/Fi=

A

the uptake of anesthetic into lungs

192
Q

Machine factors influencing uptake/distribution:

A

-liter flow
-absorption into plastic

193
Q

Lungs’ factors influencing uptake/distribution (6 items):

A

-ventilation (volume)
-concentration
-blood gas solubility of drug
-V/Q problems (decrease admin rate esp. for LOW blood/gas soluble drugs)
-2nd gas effect (pulls slower anesthetics in faster)
-N20 diffusion into closed spaces (can cause expansion issues)

194
Q

Blood’s factor influencing uptake/distribution:

A

cardiac output (decreased rate of administration especially for HIGH blood/gas soluble drugs)

195
Q

Tissues’ factors influencing uptake/distribution 7 items:

A

-oil/gas solubility (high coefficient, slow in/slow out and vice versa)
-metabolism
-diffusion hypoxia (N20 must be washed out with 100% O2)
-pediatrics (need higher dose and affects them longer)
-pregnancy (high CO and high MV[minute vent] cancel each other out=unpregnant person during induction)
-obesity (no change in induction but more lipid mass so anesthetic stays in longer/longer to wake)
-hypothermia (faster induction from decreased MAC)

196
Q

What is MAC?

A

minimum alveolar concentration required to achieve surgical anesthesia in 50% of patients exposed to noxious stimuli

197
Q

What is MAC-Awake?

A

the minimum alveolar concentration that inhibits responses to commands in 50% of patients; less than regular MAC

198
Q

What is MAC-BAR?

A

dose of anesthesia needed that blocks adrenergic and CV response to noxious stimuli in 50% of patients; blunts autonomic response (pain with incision);
-is 1.6 x MAC

199
Q

Sevoflurane AKA Ultane (MAC, BG Partition Coefficient)=

A

2%, 0.6
50 OG, POTENT

200
Q

Isoflurane AKA Forane (MAC, BG Partition Coefficient)=

A

1.15%, 1.4
99 OG ,VERY POTENT

201
Q

N20 (MAC, BG Partition Coefficient)=

A

105%, 0.47
1.4 OG NOT POTENT AT ALL

202
Q

Desflurane AKA suprane (MAC, BG Partition Coefficient)=

A

5.8%, 0.42
18.7 OG, NOT VERY POTENT

203
Q

Halothane AKA fluothane (MAC, BG Partition Coefficient)=

A

0.75%, 2.3
224 OG, VERY POTENT

204
Q

When giving anesthetic, never give less than _% O2, remaining _% is up to us.

A

30%, 70%

205
Q

True or false: at any point in time lung concentration = brain concentration of anesthesia

A

TRUE

206
Q

MAC and potency are _ proportional

A

INVERSELY

207
Q

How ventilation influences uptake/distribution

A

ventilation rate increases, the Fa/Fi ratio which increases more rapidly
-faster you breathe faster you go to sleep

208
Q

How liter flow rates influence uptake/distribution:

A

higher the flow, faster gas admin; lower the flow, slower gas admin
-usually 1-2 mins for gas to get thru circuit

209
Q

How absorption into plastic influences uptake/distribution:

A

gas can absorb into circuit tube/ machine
-VERY bad for people at high risk for to MH bc volatile anesthetics trigger MH, must do a complete washout of machine/tubes

210
Q

How alveolar concentration influences uptake/distribution:

A

higher the dose (more you give) the faster it works
-Fa/Fi is how fast gas rises into lungs to reach inspired gas level

211
Q

How blood/gas solubility of drug influences uptake/distribution:

A

lower the coefficient= faster anesthetic rises in lungs; faster induction + emergence
higher the coefficient= slower anesthetic rises in lungs; slower induction + emergence

212
Q

How V/Q deficits influence uptake/distribution: which drugs are effected most?(3)

A

less than normal lungs go to sleep slower than normal lungs
-there is a decrease in onset rate especially for LOW blood/gas coefficient or more INSOLUBLE drugs-N2O, SEVO, DES
-sports care slows down much faster than old beater can

213
Q

How 2nd gas effect influences uptake/distribution:

A

using N20 at a high concentration with another gas briefly to RAPIDLY produce effects quicker than either by themselves
-N20 is low solubility and not very potent when given with agent with higher solubility works very quickly

214
Q

Implementing 2nd gas effects violate _ ‘s Law of partial pressure.

A

Dalton’s; gases aren’t working independently

215
Q

How N20 Diffusion influences uptake/distribution:

A

N20 expands closed gas spaces due to difference in solubility of nitrogen it replaces and its high concentration that is required
-pressure changes at a rate dependent on perfusion of tissue around it and compliance of space it’s in

216
Q

N20 Diffusion is contraindicated in bowel obstruction because:

A

risks perforation from obstruction blocking bowel

217
Q

N20 Diffusion is contraindicated in pneumothorax because:

A

makes pneumothorax larger

218
Q

N20 Diffusion is contraindicated in inner ear surgery because:

A

can make eardrum bulge and harder for surgeon to reattach it

219
Q

N20 Diffusion is contraindicated in neurosurgical procedures with air injections such as:

A

craniotomy-too much air

220
Q

N20 Diffusion is contraindicated in air embolism at the level above the heart such as:

A

carotid endarterectomy-worsens

221
Q

N20 Diffusion is contraindicated in laparoscopy _ .

A

rarely, won’t be able to close belly from distention from intestines

222
Q

N20 Diffusion is contraindicated within 4 weeks of use of sulfur hexafluoride gas injection into ocular surgery such as:

A

retinal detachment repair

223
Q

How CO influences uptake/distribution:

A

If CO increases, onset of all anesthetics SLOW
-affects SLOW drugs more than FAST drugs bc of Fa/Fi ratio-increased CO removes drug at quicker rate
-ISO

224
Q

Vessel rich group % consumption of CO and % body mass (organs)

A

75% of CO
10% body mass

225
Q

Muscle group % consumption of CO and % body mass (skeletal, muscle, skin)

A

20% of CO
50% body mass

226
Q

Fat group % consumption of CO and % body mass

A

5% of CO
20 body mass

227
Q

Vessel Poor group % consumption of CO and % body mass (bone, tendons, cartilage)

A

0% of CO
20% body mass

228
Q

How oil/gas solubility influences uptake/distribution:

A

describes potency; if highly potent it is slow to go in, slow to come out; halothane most potent, N20 least
-high OG solubility = more potent
-low OG solubility = less potent

229
Q

How metabolism influences uptake/distribution:

A

certain drugs have different amounts of metabolites that are toxic so we limit those in high amounts
-sevoflurane most toxic (5-7%), N20 is the least with trace toxins

230
Q

How diffusion hypoxia influences uptake/distribution:

A

opposite of 2nd gas effect; N20 leaves body so fast floods lungs and dilutes other gases including O2
-we give 100% O2 at end of case for ~5 mins to wash out N20 and prevent displacement of O2

231
Q

How pediatrics influences uptake/distribution:

A

kids need higher doses but it lasts longer in them
-have factors that WOULD make onset slower but kids’ increased minute ventilation overrides the other factors

232
Q

How pregnancy influences uptake/distribution:

A

high CO and high MV[minute vent] cancel each other out so onset is like nonpregnant person

233
Q

How obesity influences uptake/distribution:

A

no change in induction but more lipid mass so anesthetic stays in longer/longer to wake
-longer case the longer it takes to wake bc more soluble with adipose

234
Q

How hypothermia influences uptake/distribution:

A

decreased MAC of anesthetic from low temp requires less to fall asleep but will take longer due to decreased metabolism
-wake up more slowly from poor circulation and vasoconstriction

235
Q

(3)Enzyme inhibition or activation Red Flag Drugs:

A

-grapefruit juice
-HIV antiretrovirals (avirs)
-certain antifungals (azoles)

236
Q

Heavy Protein Bound Drugs:

A

-COUMADIN
-AMIODARONE
-FENTANYL
-DILANTIN
-methadone!!!
-PHENYTOIN
-propranolol!!!
-diazepam!!!
-LOCAL ANESTHETIC (lidocaine)!!!

237
Q

CYP3A4=

A

metabolizer of 50% of drugs

238
Q

CYP3A4 Strong Inhibitors=

easy as 1,2,3
1)GIVEN
2) abx
3) you know

A

-protease INHIBITORS

-ciprofloxacin
-clarithromycin

-AZOLE ANTIFUNGALS**
-GRAPEFRUIT JUICE**
-HIV ANTIRETROVIRALS (-navir)**

239
Q

CYP3A4 Strong Inducers=

A

-PHENYTOIN
-barbiturates
-RIFAMPIN
-CARBAMAZEPINE
-ANTICONVULSANTS

240
Q

CYP3A4 Substrates=

A

-FENTANYL/ alfentanil
-OXYCODONE
-METHADONE
-LIDOCAINE
-dalasetron
-ONDANSETRON/ZOFRAN
-HALDOL

241
Q

CYP2D6=

A

metabolizes 25% of drugs

242
Q

CY2D6 Strong Inhibitors=

A

-AMIODARONE
-BUPROPION

-kava**
-goldenseal**

-FLUOXETINE**/ paroxetine

-QUINIDINE
-RITONAVIR**
-sertraline/ZOLOFT

243
Q

CYP2D6 Strong Inducers=

A

-RIFAMPIN
-dexamethasone
-oritavancin

244
Q

CYP2D6 Substrates=

A

-HYDROCODONE
-OXYCODONE
-CODEINE
-METHADONE
-merperidine
-dalasetron

245
Q

Ultra-Rapid Metabolizers (UM)=

A

carry multiple copies of functional alleles leading to excessive activity (high enzyme activity)

246
Q

Extensive Metabolizers (EM)=

A

have 2 normal or “wild type” alleles and have a normal metabolism

247
Q

Intermediate Metabolizers (IM)=

A

carry 1 normal and 1 nonfunctional OR 2 reduced functional alleles (reduced enzyme activity)

248
Q

Poor Metabolizer (PM)=

A

have 2 mutated alleles with very limited or completely lost enzymatic activity (reduced or absent enzyme activity)

249
Q

ProDrug=

A

needs metabolism to activate/work
-ex) codeine

250
Q

Active Drug=

A

metabolism inactivates drug, changes it into inactive
-ex)omeprazole, fentanyl

251
Q

Prodrug + PM or IM=

A

-metabolizes inactive drug too slowly, doesn’t make enough active drug
-poor drug efficacy
-subtherapeutic

252
Q

ProDrug (Codeine)+ UM=

A

-metabolizes inactive drug too quickly making too much active drug
-high drug efficacy
-accumulation of active drug increases risk of side effects

253
Q

Active Drug + PM or IM=

A

-slow metabolism doesn’t inactivate the active drug fast enough, needs lower dosage
-high drug efficacy
-accumulation of active drug increases risk of side effects

254
Q

Active Drug + UM=

A
  • fast metabolism inactivates the active drug too quickly, needs higher dosage
    -poor drug efficacy
    -subtherapeutic
255
Q

Fast or slow induction: Low B/G Solubility?

A

fast

256
Q

Fast or slow induction: High B/G Solubility?

A

slow

257
Q

Fast or slow induction: Low CO?

A

fast

258
Q

Fast or slow induction: High CO?

A

slow

259
Q

Fast or slow induction: High FGF rate?

A

fast

260
Q

Fast or slow induction: Low FGF rate?

A

slow

261
Q

Fast or slow induction: High minute ventilation?

A

fast

262
Q

Fast or slow induction: Low minute ventilation?

A

slow

263
Q

Fast or slow induction: High concentrations?

A

fast

264
Q

Fast or slow induction: V/Q Disfunction?

A

slow

265
Q

Fast or slow induction: Low concentrations?

A

slow

266
Q

Fast or slow induction: Hypothermia?

A

slow

267
Q

Fast or slow induction: 2nd Gas Effect?

A

fast

268
Q

Fast or slow induction: Children?

A

faster

269
Q

Fast or slow induction: Obesity?

A

no difference- SLOWER to WAKE

270
Q

Fast or slow induction: Pregnancy?

A

No difference- High Vm and High CO factors cancel each other out

271
Q

A high CO affects slow or fast drugs more?

A

Slow anesthetics

272
Q

A V/Q Problem affects slow or fast drugs more?

A

fast anesthetics

273
Q

Slow drugs have a _ B/G Solubility.

A

High

274
Q

Fast Drugs have a _ B/G Solubility.

A

Low

275
Q

Fast anesthetics are _ dissolved into blood and are _ ready in a gas state to bind to cells in tissues.

A

LESS, MORE

276
Q

Slow anesthetics are _ dissolved into blood and are _ ready in a gas state to bind to cells in tissues.

A

MORE, LESS

277
Q

Increase or Decrease MAC: Old age

A

decreasse

278
Q

Increase or Decrease MAC: hypothermia

A

decrease

279
Q

Increase or Decrease MAC: Giving other sedatives

A

decrease

280
Q

Increase or Decrease MAC: Giving other anesthetics

A

decrease

281
Q

Increase or Decrease MAC: Opiods

A

decrease

282
Q

Increase or Decrease MAC: Acute Ethanol Consumption

A

decrease

283
Q

Increase or Decrease MAC: Young age

A

increase

284
Q

Increase or Decrease MAC: Hyperthermia

A

increase- NOT MH tho :)

285
Q

Increase or Decrease MAC: Pregnancy

A

decrease

286
Q

Increase or Decrease MAC: Hypoxemia

A

decrease

287
Q

Increase or Decrease MAC:Hyponatremia

A

decrease

288
Q

Increase or Decrease MAC: Anemia

A

decrease

289
Q

Increase or Decrease MAC: Hypotension

A

decrease

290
Q

Increase or Decrease MAC: Lithium

A

decrease

291
Q

Most potent anesthetic:

A

Halothane, Isoflurane is 2nd

292
Q

Least potent anesthetic/gas:

A

N2O, 2nd least is Desflurane

293
Q

Fastest anesthetic/gas:

A

N20, 2nd is Desflurane

294
Q

Slowest anesthetic:

A

Halothane, 2nd slowest is Isoflurane

295
Q

True or false: The partial pressure of anesthetic stops rising in fat after halting delivery of anesthetic:

A

False, it continues rising for a while

296
Q

Fast or slow emergence: High B/G solubility

A

slow emergence

297
Q

Fast or slow emergence: Low B/G solubility

A

fast emergence

298
Q

Increase or Decrease MAC: Alpha Agonists

A

decrease MAC

299
Q

Increase or Decrease MAC: Hyperthyroidism

A

increase MAC

300
Q

Increase or Decrease MAC: Red Headed Females

A

Increase MAC

301
Q

Increase or Decrease MAC: Chronic Alcohol Abuse

A

Increase MAC

302
Q

Increase or Decrease MAC: Acute Admin of CNS Stimulants (caffeine, adderall, etc.)

A

Increase MAC

303
Q

Increase or Decrease MAC: Hypocapnia

A

no difference

304
Q

Increase or Decrease MAC: Gender

A

no difference

305
Q

Increase or Decrease MAC: Hypertension

A

no difference

306
Q

Increase or Decrease MAC: Hypokalemia

A

no difference

307
Q

Increase or Decrease MAC: Hyperkalemia

A

no difference

308
Q

Increase or Decrease MAC: Duration of case

A

no difference

309
Q

Need Increase or Decrease MAC: Hypercapnia

A

no difference

310
Q

CpMax=

A

desired serum concentration

311
Q

Equation for loading dose=

A

(pt’s weight x Vd of drug) x CpMax

312
Q

Vd=

A

volume of distribution;
-degree of a drug going into tissue over plasma
-drug specific ratio, applied to pt’s specific weight
-high Vd = high amount of tissue distribution

313
Q

Order of main points of anesthesia leaving during anesthesia:

A

-amnesia/ memory
-consciousness /awareness
-mobility/ pain response
-autonomic reactions/ reflexes

314
Q

VRG (vessel rich group) is AKA=

A

central compartment

315
Q

Parasympathetic NS involves the _ nerve

A

vagus

316
Q

PNS and SNS secrete _ to the _ _ receptors pre-synaptically

A

Acetylcholine, nicotinic cholinergic

317
Q

Post-synaptically the PNS secretes _ that binds with a _ _ receptor

A

Acetylcholine, muscarinic cholinergic

318
Q

Post-synaptically the SNS secretes _ that binds with an _ receptor

A

norepinephrine, adrenergic

319
Q

Adrenergic receptors include _, _, and _ receptors and they bind with _ secreted by the nicotinic cholinergic receptor from the SNS.

A

dopa, alpha, and beta, norepinephrine

320
Q

Muscarinic Cholinergic receptors bind with _ that is secreted by the nicotinic cholinergic receptor from the _.

A

acetylcholine, PNS

321
Q

Sympathetic outflow come from the _ _ region

A

thoraco-lumbar

322
Q

Parasympathomimetic (give example)=

A

stimulates PNS
ex) neostigmine (for myasthenia gravis)

323
Q

Parasympatholytic (give example)=

A

blocks PNS
ex) atropine

324
Q

Sympathomimetic (give example)=

A

stimulates SNS
ex) catecholamines like epinephrine, dopamine, levophed

325
Q

Sympatholytic (give example)=

A

blocks SNS
ex) beta blocker

326
Q

LD=

A

(pt’s weight x Vd of drug) x CpMax

Advanced Pharm For NA 1 (4 decks)

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