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2 Review Course > Pharmacology 1 > Flashcards

Pharmacology 1 Flashcards

1
Q

What is primary site of anesthetic action?

A

membrane receptors

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2
Q

What are the three common properties of receptors?

A

specificity, sensitivity, selectivity

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3
Q

Arrange the bonds between drug and receptor from weakest to strongest.

A

van Der walls, hydrophobic, hydrogen, ionic, covalent

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4
Q

What are the prominent forces that help agonist drugs align with its receptors?

A

van Der walls and ionic bonding

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5
Q

How do volatile anesthetics bind to their cell receptors?

A

nonspecific hydrophobic bonding

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6
Q

Which proteins mainly bind acidic drugs?

A

albumin

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7
Q

What proteins mainly bind basic drugs?

A

a1-acid glycoprotein and beta-globulin

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8
Q

Acetylcholine and sodium transduce a _____ signal.

A

excitatory

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9
Q

GABA and chloride ions transduce a ____ signal.

A

inhibitory

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10
Q

What is the occupancy theory?

A

the magnitude of a drugs effect is proportional to the number of receptors it occupies.

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11
Q

When the therapeutic safety margin is ___ the risk of drug-induced death is ____, and the margin of therapeutic safety is ____.

A

When the therapeutic safety margin is large the risk of drug-induced death is small, and the margin of therapeutic safety is wide.

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12
Q

What value can be used to compare the potency of drugs in a class?

A

ED50

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13
Q

What phrase describes drug onset time and magnitude of drug response?

A

pharmacokinetic analysis

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14
Q

What phrase describes the duration of the tissue response of a drug?

A

drug elimination kinetic analysis

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15
Q

Antagonist drugs lack ___ but have ____

A

Antagonist drugs lack intrinsic activity or efficacy but have receptor affinity.

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16
Q

What type of antagonist can be displaced by the agonist?

A

competitive

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17
Q

What type of antagonist have a strong affinity for the receptor protein and cannot be displaced by an agonist.

A

noncompetitive

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18
Q

Continued stimulation of cells with agonists can result in what?

A

down-regulation

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19
Q

Chronic administration of an antagonist leads to what type of response to receptors?

A

up regulation

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20
Q

How does molecular size affect molecules crossing lipid bilayers?

A

the smaller the molecule the easier it crosses membranes and tissues

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21
Q

What range of molecular weights prevents molecules from crossing membranes?

A

100-200

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22
Q

What is antiport transportation?

A

exchange of one molecule for another agonist a concentration gradient

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23
Q

What is symport transportation?

A

transportation of two molecules together in the same direction against a concentration gradient

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24
Q

For a given pKa what part of the drug is charged and uncharged?

A

charged, ionized, water soluble

uncharged, nonionized, lipid soluble

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25
Q

What is the pKa formula for basic drugs?

A

pKa = pH = log (HA/A)

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26
Q

What is the pKa formula for acidic drugs?

A

pKa = pH = log (A/HA)

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27
Q

A acidic drug into a more acidic pH =
A acidic drug into a more basic pH =
A basic drug into a more acidic pH =
A basic drug into a more basic pH =

A

A acidic drug into a more acidic pH = nonionized
A acidic drug into a more basic pH = ionized
A basic drug into a more acidic pH = ionized
A basic drug into a more basic pH = nonionized

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28
Q

What plasma proteins bind to acidic drugs? To basic drugs?

A

albumin binds acidic drugs

alpha-1 acid glycoprotein, and beta globulin bind basic

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29
Q

What proteins bind cyclosporin and corticosteroids?

A

lipoproteins bind cyclosporin

transcortin binds corticosteroids

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30
Q

How does protein binding affect the drug acting on the tissues?

A

high protein binding prevents the drug from entering the tissues

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31
Q

How does ionization affect protein binding?

A

the more lipid soluble (nonionized), the more highly protein bound the drug will be.

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32
Q

What are drugs that have protein binding greater than 90%?

A

warfarin, phenytoin, propranolol, propofol, fentanyl and analogs, and diazepam

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33
Q

What type of drugs are highly absorbed in the stomach?

A

highly acidic drugs. Because They are more nonionized, so they are absorbed more.
somach pH is 1.5-2.5

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34
Q

What is pre systemic elimination?

A

when the drug is eliminated before it reaches the systemic circulation

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35
Q

What are the mechanisms that cause pre systemic elimination?

A

stomach acid hydrolyzes the drug, digestive enzymes deactivate the drug, liver biotransforms the drug

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36
Q

What is the first pass hepatic effect?

A

when the liver biotransforms the drug before it reaches its clinical effect site

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37
Q

What is the ideal route of administration of Nitroglycerin?

A

sublingual

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38
Q

Insertion of a drug into which part of the rectum leads to more predictable circulatory levels?

A

Distal rectum

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39
Q

What determines systemic absorption of intramuscular and subcutaneous injections?

A

capillary blood flow, and lipid solubility

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40
Q

Requirements for a transdermal medication include
molecular weight:
dosage:
pH:

A

molecular weight: < 1000
dosage: < 10mg
pH: 5-9

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41
Q

What impacts the bioavailability of a drug?

A

lipid solubility, solubility in aqueous and organic solvents, molecular weight, pH, pKa, blood flow

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42
Q

What is the volume of distribution

A

the amount of drug in the body compared to the serum concentration

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43
Q

How are drugs with a low Vd and high Vd described?

A

Low: < 0.6mL/kg or < 42L
high: > 0.6mL/Kg or > 42L

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44
Q

What affects a drugs Vd?

A

lipid solubility, plasma protein binding, and molecular size

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45
Q

What are some isomers?

A

cisatracurium, levobupivicaine, ropivicaine, dexmedetomidine

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46
Q

what occurs during phase 1 reactions?

A

oxidation, reduction, hydrolysis.

The molecule becomes more polar and ready for elimination

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47
Q

What occurs during phase 2 reactions?

A

conjugation.
a drug or metabolite is conjugated with an endogenous substrate like glucuronic acid, sulfuric acid, acetic acid, glycine, and a methyl group

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48
Q

What do you get when you add water to an ester?

A

acid and alcohol

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49
Q

What do you get when you add water to an amide?

A

acid and amide

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50
Q

What is another name for the P450 system?

A

mixed-function oxidase system

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51
Q

Genetic variation of CYP2D6 causes changes in metabolism of what class of drugs?

A

B-blockers

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52
Q

What are the enzyme inducers?

A

alcohol, phenobarbital, phenytoin, rifampin, and carbamazepine

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53
Q

What effect do enzyme inducers have on half life?

A

decrease half life

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54
Q

What drug does erythromycin inhibit the metabolism of?

A

theophylline

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55
Q

What is the context sensitive half time?

A

time required to decrease the drug dose by 50% after stopping an infusion

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56
Q

What is drug clearance?

A

the volume of plasma that is cleared of drug per unit time

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57
Q

What is clearance directly proportional to?

A

dose
extraction ratio
blood flow to the clearing organ

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58
Q

What is clearance inversely proportional to?

A

half life

drug dose in the central compartment

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59
Q

What are the two main clearing organs?

A

liver and kidneys

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60
Q

What determines rate of clearance?

A

blood flow to the clearing organ

the organs ability to extract the drug from the bloodstream

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61
Q

What is the formula for clearance?

A 
Clearance = Q x E
q= blood flow, e= extraction ratio
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62
Q

What are three examples of drug that undergo perfusion dependent elimination?

A

verapamil, morphine, lidocaine

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63
Q

How does protein binding effect capacity dependent drug clearance?

A

decreased protein binding increases clearance

increased protein binding decreases clearance

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64
Q

What are two drugs that undergo capacity dependent elimination?

A

diazepam and theophylline

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65
Q

The excretion of drugs involves:
____ glomerular filtration
____ tubular secretion
____ reabsorption

A

passive glomerular filtration
active tubular secretion
some reabsorption

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66
Q

What substances are actively secreted from the kidneys?

A

morphine, meperidine, furosemide, penicillin, and quaternary ammonium compounds

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67
Q

What determines the amount of drug available for renal elimination?

A

amount of free unbound drug

GFR

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68
Q

What induction agent is almost completely reabsorbed by the kidneys?

A

propofol

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69
Q

How does urine pH affect the elimination of drugs?

A

acidic urine eliminates basic drugs

basic urine eliminates acidic drugs

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70
Q

Are water soluble or lipid soluble agents more likely to accumulate in the elderly?

A

lipid soluble.

Their fat compartment is increased, therefore their Vd is larger.

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71
Q

Which gender is more sensitive to propofol?

Does should be reduced by how much?

A

males

30%

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72
Q

What is pharmacogenetics?

A

studies variations in genes suspected of affecting drug response

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73
Q

Does pharmacogenetics or pharmacogenomics aim to identify the genetic basis for variations in drug efficacy, metabolism, and transport?

A

genomics

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74
Q

What are polymorphisms?

Do polymorphisms affect phase 1 or phase 2 reactions more?

A

genetic variations in the DNA sequence

Phase 1

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75
Q

Functional polymorphisms occur in which four P450 isoenzymes?

A

2A6
2C9
2C19
2D6

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76
Q

Significant morbidity and mortality occur in which two patients populations receiving codeine, that are ultra rapid metabolizers of CYP2D6?

A

pediatric tonsillectomy

neonates of breast feeding mothers

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77
Q

What are two machine related factors that affect uptake of inhaled anesthetic?

A

solubility of anesthetic in the machine components

FGF

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78
Q

What gases are triggers for malignant hyperthermia?

A

all but N2O

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79
Q

How do you flush the anesthesia machine in a patient with a history or increased risk of malignant hyperthermia?

A

100% O2 at 10L/min for 20 minutes

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80
Q

What is an alternative to purging the AM to prevent malignant hyperthermia?

A

charcoal filters

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81
Q

blood:gas solubility and onset of anesthesia have what type of relationship?

A

inverse.

The lower the solubility the faster the onset of anesthesia

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82
Q

What is the ventilation effect?

A

The faster and deeper the patient breathes the faster the onset of an inhalation induction

83
Q

What is overpressurizing or the concentration effect?

A

delivering higher concentrations of anesthetic needed for maintenance, to speed the initial uptake

84
Q

Overpressurizing or the concentration effect is most effective with which agents?

A

Sevo and Iso, they are less soluble/ less potent

85
Q

What is the second gas effect?

A

Adding a fast agent (N2O) to a slower agent during inhalation induction to sleep the onset of the slower agent

86
Q

What relationship does oil:gas partition coefficient and potency have?

A

direct.
The higher the solubility the more potent the drug.
Iso has an oil:gas of 91, and its MAC is 1.4

87
Q

Which anesthetic gas onset is most affected by increased cardiac output?

A

Iso

88
Q

As the patients temperature falls, what happens to the anesthetic gases solubility and potency?

A

solubility and potency increase

89
Q

How does temperature affect inhaled induction?

A

decreased temperature slows induction

90
Q

What factors lead to a faster inhalation induction?

A

low B:G solubility, low CO, high Ve, high FGF, high concentration, second gas effect

91
Q

What factors lead to a slow inhalation induction?

A

high B:G solubility, high CO, low Ve, low FGF, low concentration, V/Q mismatch, hypothermia

92
Q

Arrange the gases from slowest to fastest emergence, when the anesthetic was delivered for 10 hours?

A

Iso, Sevo, Des, N2O

The longer an anesthetic is delivered the slower the patient emerges. Effect is greatest with most soluble Iso.

93
Q

Why are children anesthetized faster than adults?

A

They have a high alveolar ventilation per weight

94
Q

Are anesthetics more or less blood soluble in children compared to adults? What does this mean?

A

less blood soluble

they work faster

95
Q

What inhaled agent is most likely to cause emergence reactions and agitation in children?

A

sevo

96
Q

What are risk factors for children having increased agitation during emergence?

A

age 2-5
separation anxiety
anxiety and post-op pain

97
Q

What agents are ineffective in decreasing emergence agitation in children?

A

midazolam, serotonin antagonists, parental presence

Effective: fentanyl, precedex, propofol, ketamine

98
Q

How do right to left shunts affect inhalation induction?

Which agents is most affected by this?

A

slow induction

Desflurane

99
Q

What is the structure of ethers?

A

R - O - R

100
Q

What is the number of carbons used on the commonly used anesthetics?

A

maximum 4

101
Q

What are the two categories of the commonly used anesthetics?

A

ethers or aliphatic hydrocarbons (straight chain or branched nonromantic hydrocarbons)

102
Q

What is the consequence if the anesthetic molecule exceeds 4 or 5 carbons?

A

the anesthetic won’t produce immobility

103
Q

Halogenation of hydrocarbons and ethers is the addition of what molecules?

A

Flourine, chlorine, bromine, iodine

104
Q

How does potency affect MAC?

A

decreased potency, increase MAC

Des has a partition coefficient of 0.42 but a MAC of 6%

105
Q

How does halogen atoms affect cardiac dysrhythmias?

A

the more halogens the more likely dysrhythmias will occur

106
Q

what is the Meyer-overton theory?

A

lipid solubility is proportional to potency

107
Q

where do volatile anesthetics produce immobility?

A

spinal cord and supraspinal

108
Q

Where do inhalation agents produce unconsciousness?

A

cortex, thalamus, and brainstem

109
Q

Where do inhalation agents produce amnesia?

A

amygdala and hippocampus

110
Q

Where do inhalation agents produce analgesia?

A

spinothalamic tract

111
Q

Where do inhalation agents produce immobility?

A

spinal cord central pattern generators

112
Q

What MAC awake/MAC ratio is considered to be a potent anesthetic?

A

0.3-0.4

113
Q

What is MAC-bar?

A

MAC that prevents adrenergic response to skin incision

114
Q

What is the “triple low state” that increases 30 day mortality?

A

MAP of 75, MAC < 0.8, BIS < 45

115
Q

How do volatiles affect CMRO2?

A

decrease

116
Q

How do volatiles affect CBF and cerebral vessel diameter?

A

increase CBF by causing cerebral vasodilation

117
Q

How does N2O affect CMRO2 and CBF?

A

increases both

118
Q

How can we manipulate the increase in CBF that N2O causes if used on a patient with reduced intercranial compliance?

A

hyperventilation

119
Q

How do volatiles affect EEG activity?

A

Overall decrease

120
Q

Which evoked potential are the most and least affected by the volatiles?

A

Visual is most

Brainstem is least

121
Q

Which volatile augments seizure activity?

A

Sevo

122
Q

What did the PANDA trial determine?

A

Anesthesia in infants does not affect IQ score later in childhood

123
Q

Which two anesthetic agents are most likely to cause emergence delirium in preschool children?

A

des and sevo

124
Q

How do the volatiles affect hemodynamics?

A

Decrease MAP by decreasing SVR. Decreased CO and CI.

N2O increases SVR

125
Q

Which volatile supports cardiac index the best in a wide range of MAC values?

A

Des

126
Q

What mechanisms do anesthetics affect HR?

A

decrease SA node automaticity
modulate baroreceptor reflex
SNS activation

127
Q

What is coronary steal? What is another name for coronary steal?

A

Blood flow is stunted from diseased cardiac tissue to more healthy tissue.
Reverse Robinhood effect

128
Q

What is preconditioning caused by volatile anesthetics?

A

a cascade of intracellular events that help protect the myocardium from ischemic and reperfusion insult, potentially limiting infarct size.

129
Q

How do the volatiles affect the Qt interval?

A

they increase the Qt interval

130
Q

How do volatiles prolong the Qt interval?

A

inhibition of the delayed rectifier K current

131
Q

How does N2O affect PVR?

A

increases

132
Q

How do volatiles affect pulmonary artery pressure?

A

decrease

133
Q

How do volatiles affect Vt and RR?

A

decrease Vt and increase RR

134
Q

How do volatiles shift the CO2 response curve?

A

to the right. Less responsive to PaCO2

135
Q

Impairment of the hypoxic ventilatory response by volatile anesthetics is not abated by what two mechanisms?

A

CNS arousal or acute pain

136
Q

What serum concentration of methoxyflurane causes vasopressin resistant polyuric renal insufficiency?

A

50mmol/L

137
Q

What are the FDA recommendations for Sevo to prevent formation of compound A?

A

Sevo exposure should not exceed 2 MAC hours at flow rates of less than 1-2L/min

138
Q

N20 is an antagonist at ____ receptors, causing a potential decrease in ____ pain post-op.

A

NMDA, chronic

139
Q

Which anesthetic gases is ok to use in a MH susceptible patient?

A

N2O

140
Q

What is the chemical name of propofol?

A

2,6 - Diisopropyl phenol

141
Q

What is the pH and pKA of propofol?

A

pH: 7-8.5
pKa: 11

142
Q

What are the preservatives of branded and generic propofol?

A

branded: EDTA
generic: metabisulfite (bronchoconstriction, benzyl alcohol (avoided in infants)

143
Q

What is the elimination half life of propofol?

A

1-2 hours

144
Q

What are three factors that decrease protein binding?

A

decreased lipid solubility, increased drug concentration, competition to binding sites with other drugs

145
Q

What are two factors that increase protein binding?

A

increased pH (<8.0), increased protein concetration

146
Q

How does propofol work?

A

it stimulates the inhibitory GABA receptor. Causing Chloride to move into the cells and cause hyperpolarization.

147
Q

What is one of the major inhibitory receptors in the CNS?

A

GABA, glycine, and K channels

148
Q

How does propofol affect the CNS?

A

decreases CMRO2, ICP, CBF, and CPP

149
Q

What is the effect of Propofol on EEG activity?

A

causes Delta waves, can cause burst suppression with higher doses

150
Q

What are the predictors of hypotension from induction doses of propofol?

A

age > 50, ASA 3-4, baseline MAP < 70, high doses of fentanyl

151
Q

What are the primary reasons for propofol induced hypotension?

A

decreases sympathetic tone and vasodilation

152
Q

What are the preferred induction agents of the patient with asthma?

A

ketamine and propofol

153
Q

One absolute contraindication to propofol is allergy to what?

A

sulfite. dont use generic

154
Q

What is propofol infusion syndrome?

A

Metabolic derangements that occur from multiple days of high infusions of propofol. Common in the ICU not anesthesia.

155
Q

What are risk factors for propofol infusion syndrome?

A 
Dose > 4mg/kg/hr
Duration > 48 hours
critically ill
high fat low carb intake
catecholamine infusion
steroid administration
156
Q

What is one common denominator for propofol infusion syndrome?

A

impaired systemic microcirculation with tissue hypo perfusion and hypoxia

157
Q

What drug is (1- [1-phenylethyl]-1H-imidazole-5-carboxylic acid ethyl ester)

A

Etomidate

158
Q

What are some of the negative side effects of etomidate?

A

pain on injection, increase nausea, adrenal cortical suppression, myoclonia,

159
Q

What is the pH and pKa of etomidate?

A

pH 8.1

pKa 4.2

160
Q

How is etomidate metabolized?

A

hepatic enzymes and plasma esterases

161
Q

What is the elimination half life of etomidate?

A

2-5 hours

162
Q

How does etomidate affect CMRO2 and CBF?

A

decreases both

163
Q

Pretreatment with which drugs can decrease the incidence of myoclonus from etomidate?

A

dexmedetomidine, midazolam, roc, and lidocaine

164
Q

How does etomidate affect the evoked potential monitors?

A

BAEP: decreased amplitude, and increase latency
EEG: prolonged epileptic activity after ECT
SSEP: enhanced amplitudes
MEP: suppressed amplitudes

165
Q

How does etomidate affect respiratory dynamics?

A

decrease Vt but increase RR

166
Q

Which induction agents cause histamine release?

A

Propofol,

167
Q

Adrenal cortical suppression caused by etomidate inhibits which enzymes?

A

11-B hydroxylase
17-A hydroxylase
causing a decrease in cortisol, aldosterone and corticosterone levels

168
Q

What are porphyria?

A

a deficiency in the enzyme involved in the synthesis of heme

169
Q

What is the rate limiting enzyme in the biosynthesis pathways of porphyrins?

A

ALA-synthetase

170
Q

Which induction agents are contraindicated in poryphrias?

A

Etomidate and barbiturates

171
Q

What drug is 2-(O-chlorophenyl)-2-(methylamino) cyclohexanone

A

Ketamine

172
Q

What is the ph and pKa of Ketamine?

A

pH: 3.5-5.5
pKa: 7.5

173
Q

What receptors does ketamine bind?

A

antagonist at NMDA receptors, blocking signals to the thalamus and cortex

174
Q

How does ketamine exert its anti-inflammatory and antihyperanalgesic effects?

A

inhibits TNF-a and IL-6

175
Q

How is ketamine metabolized?

A

P450 to norketamine

176
Q

Intramuscular ketamine reaches peak plasma concentrations at what time interval?

A

22 minutes

177
Q

How does ketamine affect the CNS?

A

increases CBF, CMRO2, ICP

178
Q

How does ketamine affect EEG wave recordings and BIS?

A

produces theta waves, increases BIS

179
Q

What should be given to reduce the incidence of emergence delirium from ketamine?

A

benzos- midazolam, lorazepam, diazepam

180
Q

How does ketamine affect the cardiovascular system?

A

increases HR, CO, contractility, SVR, and CVP

181
Q

What is the induction agent of choice in the patient with asthma?

A

ketamine

182
Q

What are the mechanisms that ketamine causes bronchodilation?

A

increased catecholamines, bronchial smooth muscle relaxation, vagolytic actions

183
Q

What antisialogogue is preferred to decrease secretions after ketamine administration?

A

atropine

184
Q

What are some considerations when giving ketamine during eye procedures?

A

it causes nystagmus and increases IOP

185
Q

Is ketamine safe to use in parturients?

A

yes, doses 0.5-1mg/kg do not compromise uterine tone, blood flow, or neonatal delivery status

186
Q

What is the induction agent of choice for children with a difficult airway or reactive airway disease?

A

ketamine

187
Q

How do benzos exert their action?

A

agonists of the GABA receptor. It increases the frequency of chloride channel opening causing hyperpolarization

188
Q

Rank the benzos from shortest to longest acting?

A

shortest - Midazolam
lorazepam
longest- diazepam

189
Q

Which benzo has the highest clearance rate?

A

midazolam

190
Q

Which benzo is not affected by enzyme inhibition or induction?

A

lorazepam, undergoes phase 2 conjugation

191
Q

How is diazepam metabolized?

A

hepatic microsomal enzymes. Demethylated to dimethyl diazepam

192
Q

Although not an antiemetic, which benzo is used in reducing chemotherapy-induced N/V?

A

lorazepam

193
Q

What is the most respiratory depressing benzo?

A

midazolam

194
Q

What class of alpha-2 agonists does dexmedetomidine fall under?

A

imidazole

195
Q

What are the primary effects of dexmedetomidine?

A

sedation, analgesia, anxiolysis, reduced post-op shivering and agitation, cardiovascular sympatholytic actions

196
Q

What are the main sites of action of dexmedetomidine?

A

pontine noradrenergic nucleus and locus coeruleus

197
Q

What is the effect of alpha-2 agonism on ions from dexmedetomidine?

A

inhibition of Ca channels, activation of K channels, modulation of the release of proteins. This leads to hyperpolarization of cells

198
Q

What drug is (S)-5-(1-(2,3-Dimethylphenyl)ethyl)-1H-imidazole hydrochloride?

A

dexmedetomidine

199
Q

What is the loading dose of dexmedetomidine?

A

1mcg/kg

200
Q

How does dexmedetomidine affect the CNS?

A

increases CMRO2 and decreases CBF (cerebral vasoconstriction). This results in uncoupling.

201
Q

Which IV anesthetic increases the analgesic effects of N2O?

A

dexmedetomidine

202
Q

What are the main side effects of dexmedetomidine?

A

HoTN and bradycardia

203
Q

Transient HTN can result, if dexmedetomidine induced bradycardia is treated with what medication?

A

glycopyrrolate

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