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APEX > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

Loading dose

A

(Vd x desired Cp)/ bioavailability

Bioavailability=1 when directly injected into blood stream

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2
Q

Vd

A

Amount of drug/desired plasma concentration

Assumes- drug is instantly available, no elimination before fully circulating

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3
Q

Distribution of H2O in 70 kg patient

A 
TBW= 40L
ECF= 14 L
Plasma= 4 L
Instestitial fluid= 10L
ICF= 28L
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4
Q

Low Vd

A 
Less than 0.6 L/kg or 42L
Hydrophilic
Not into fat
Lower dose for higher plasma concentration
Ex: NMB’s
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5
Q

High Vd

A 
>0.6 L/kg or 42 L
Lipophilic
Distributes into fat
Higher dose for plasma concentration
Ex: prop
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6
Q

Clearance

A

Volume of plasma cleared per unit time
Directly proportional- clearing organ, extraction ratio, drug dose
Inversely proportional- half life, drug conc in central compartment

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7
Q

Steady state

A

Rate of administration=rate of elimination

Achieved after 5 half times

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8
Q

2 part compartment model

A

A- redistribution with steep slope, steeper slope=larger Vd=lipophilic, t 1/2 alpha
B- elimination, t 1/2 beta

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9
Q

Ionization and pharmacology

A 
Water- hydrophilic, lipophilic
Not active
Less likely hepatic bio transformation 
More likely renal elimination 
Can’t diffuse across lipid bilayer
(Opposite for unionized)
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10
Q

Acid and bases in solution

A

Acid wants to donate protons
Base wants to accept protons
Like dissolves like (are more unionized in like solution)

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11
Q

Weak acid in preparation

A

Paired with a positive ion
Ex: Na, Ca, Mg
Sodium thiopental

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12
Q

Weak base in perpetration

A

Paired with negative ion
Ex: chloride, sulfate
Lidocaine hydrochloride, morphine

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13
Q

Fetal ion trapping

A 
Fetal pH= slightly acidotic 
Weak base (LA) is mostly unionized in mom
Travels into baby and becomes ionized in acidic fetus 
Cause my maternal ALKALOSIS and fetal ACIDOSIS
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14
Q

Percent change

A

((New value-old value)/ old value) x 100

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15
Q

Albumin

A 
Most plasma protein
Determines plasma oncotic pressure
T 1/2 = 3 weeks
- charge
Binds acidic drugs mostly 
Decreased- liver and renal disease, old age, malnutrition, pregnancy
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16
Q

A1 acid glycoprotein

A

Binds basic drugs
Increase- surgical stress, MI, chronic pain, RA, age
Decreased- neonates, pregnancy

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17
Q

Beta globulin

A

Binds basic drugs

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18
Q

Zero order kinetics

A

Constant amount of drug per time
More drug than enzyme
Linear graph
Ex: aspirin, phenytoin, alcohol, warfarin, heparin, theophylline

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19
Q

1st order kinetics

A

Constant fraction of drug per time
Less drug than enzyme
Logarithmic = curved graph
Majority of drugs are 1st order

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20
Q

Phase 1

A

Modification (oxidation, reduction, hydrolysis)
Increases polarity of molecule
Most carried out by P450 system

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21
Q

Phase 2

A

Conjugation
Adds on endogenous, highly polar, water soluble substrate to molecule
Enterohepatic circulation into bile happens after conjugation, ex: diazepam

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22
Q

Phase 3

A

Excretion/elimination
ATP dependent Carrie protons transport drugs across cell membranes
In kidney, liver, and GI tract

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23
Q

Goal of metabolism

A

Change a lipid soluble, pharmacologically active compound into a water soluble, pharmacologically inactive byproduct

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24
Q

Perfusion dependent hepatic elimination

A

ER > 0.7
Dependent on liver blood flow
Fentanyl, lidocaine, propofol

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25
Q

Capacity dependent hepatic elimination

A

ER < 0.3
Changes in hepatic enzyme activity or protein binding have profound impact on clearance
Diazepam, rocuronium

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26
Q

extraction ratio

A

How much drug is delivered and how much is removed by that organ
(Arterial concentration- venous concentration)/arterial concentration
1 means 100% of what is delivered is being cleared
0.5 means 50% of what is being delivered is being cleared

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27
Q

Cyp 3A4 drugs

A

Opioids- fent, alfent, student, methadone
Benzodiazepines- midazolam, diazepam
LAs- lido, bupi, topi

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28
Q

Cyp 3A inducers and inhibitors

A

Inducers- alcohol, rifampin, barbs, tamoxifen, carbamazepine, St. John’s wart
Inhibitors- grapefruit, cimetidine, erythromycin, anole antifungals, SSRI’s

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29
Q

CYP 2D6 drugs

A

Codeine to morphine
Oxycodone
Hydrocodone

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30
Q

CYP 2D6 inducers and inhibitors

A

Inducer- disulfiram

Inhibitors- isoniazid, SSRI’s, quinidine

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31
Q

Organic anion and cation transporters

A

In proximal renal tubules
OAT- lasix, thiazides, penicillin
OCT- morphine, meperidine, dopamine

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32
Q

Urine pH

A 
AAA= acidic drugs are better absorbed in an acidic medium
BBB= basic drugs are better absorbed in a basic medium
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33
Q

Altering urine pH

A

Acidifying urine- ammonium chloride and cranberry juic
Helps eliminate basic drugs

Alkalizing urine- sodium bicarb and acetazolamide
Helps eliminate acidic drugs

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34
Q

Pseudocholinesterase

A

Succ
Mivacurium
Ester LA’s

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35
Q

Nonspecific esterases

A

Remi
Esmolol (RBC esterase)
Etomidate
Atracurium

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36
Q

Alkaline phosphatase

A

Fospropofol

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37
Q

Hoffman elimination

A

Ph and temp dependent
Cisatracurium
Atracurium

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38
Q

Pharmacodynamics

A

Relationship between effect site concentration and clinical effect
What the drug does to the body

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39
Q

Pharmacokinetics

A

Relationship between drug dose and plasma concentration

What the body does to the drug

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40
Q

Pharmacobiophasics

A

PK and PD together

Relationship between plasma concentration and effect site concentration

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41
Q

Potency

A

Dose require to achieve a clinical effect
On X axis
Affected by absorption, distribution, metabolism, elimination, and receptor affinity
ED50 and ED90

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42
Q

Efficacy

A

Intrinsic ability of drug to elicit a clinical effect

On Y axis- heigh of plateau

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43
Q

Therapeutic index

A

LD 50/ED 50

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44
Q

Chirality

A

Typically tetrahedral bonding of carbon binding to 4 different atoms

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45
Q

Enantiomers

A

Chiral molecules that are non superimposable mirror images of each other

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46
Q

Meds prepared as single enantiomers

A

Levobupivacaine

Ropivacaine

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47
Q

Examples of enantiomers being different

A

S-bupivacaine (levobupivacaine) less cardiotoxic than R or racemic mixture
S ketamine is less likely to cause emergence delirium than R- also more potent

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48
Q

Propofol

A

GABA A agonist
Induction: 1.5-2.5 mg/kg IV
Infusion: 25-200 mcg/kg/min
Liver P450 and extra hepatic clearance in lungs
Antipruiritic and anti emetic (10-20 mg with 10mcg/kg/min inf)
Generic preparation can cause bronchospasm

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49
Q

Prop effects

A 
Decreased BP, SVR, contractility 
Less sensitive to CO2
Decreased CMRO2, CBF, ICP, IOP
No analgesia 
Green urine= phenol excretion
Cloudy urine= uric acid excretion
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50
Q

Propofol infusion syndrome

A

Increased long chain triglycerides impairs oxidative phosphorylation and fatty acid metabolism
Acute refractory bradycardia to asystole and one of these: met acidsosis, rhabdo, enlarged/fatty liver, renal failure, hyperlipidemia, lipemia
Prop dose > 4 mg/kg/hr for >48 hours
More in kids

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51
Q

Fospropofol

A

Aqueous solution- no burning or lipid bacteria growth
Prodrug- converted to prop by alkaline phosphatase
Slower and longer DOA
Bolus: 6.5 mg/kg
repeat bolus: 1.6 mg/kg not more than q4m
Causes genital/anal burning

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52
Q

Ketamine

A

NMDA antagonist
Racemic mixture
IV: induction 1-2 mg/kg, maintenance 1-3mg/min
IM: 4-8 mg/kg
P.O.: 10mg/kg
Liver P450 metabolism- induces its own metabolism
Norketamine- Active metabolite, less active, renal excretion

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53
Q

Ketamine effects

A

Increased SNS tone, CO, HR, SR, PVR- all effects from an intact SNS, depleted catecholamines= myocardial depressant
Bronchodilation, maintains resp drive, increased secretions
Increased CMrO2, CGF, ICP, IOP, EEG, nystagmus, emergence delirium
Relieves somatic pain
Off label depression use
Very little protein binding

54
Q

Etomidate

A

GAGA a agonist
Dose: 0.2-0.4 mg/kg
P450 and plasma esterases- awakening due to redistribution

55
Q

Etomidate effects

A 
Hemodynamics stability
Mild resp dep
Decreased CMRO2, CBF, ICP
CPP same
No analgesia 
Myoclonus- increased risk of seizures in patients with seizure history
PONV
56
Q

Etomidate and cortisol

A

Etomidate inhibits 11 beta hydroxylase (adrenal medulla) and 17 alpha hydroxylase
Suppresses adrenocortical function for 5-8 hours (up to 24)

57
Q

Thiopental

A 
Barbiturate
Water soluble, highly alkaline 
GABA A agonist 
Dose: adult 2.5-5 mg/kg, kid 5-6 mg/kg
P450- awakening due to redistribution
58
Q

Thiopental effects

A

Hotn, decreased preload, myocardial expression
Histamine release
Reflex tachycardia from baroreceptor
Respiratory depression an bronchoconstriction
Deceased CMRO2, CBF, ICP, EEG
No analgesia

59
Q

Acute intermittent porphyria

A

Defect in heme synthesis that promotes accumulation of heme precursors- due to induction of ALA synthase in heme precursor production
S/S: abdominal pain, psych symptoms, delirium, seizures, neuropathy, coma
Drugs to avoid (induce ALA synthase)- barbs, etomidate, glucocorticoids, hydralazine
Glucose and heme arginine reduce ALA synthase activity

60
Q

Dexmedetomidine

A

Alpha 2 agonist
Loading dose : 1mcg/kg over 10 min
Maintenance: 0.4-0.7 mcg/kg/hr
P450

61
Q

Dexmedatomidine effects

A

Bradycardia, hotn
Rapid administration—> htn from alpha 2 stim, short lived
No respiratory depression
Decreased CBF, no CMRO2 or ICP changes
Resembles natural sleep
Antishivering effect
Analgesia- alpha 2 stim in dorsal horn of SC

62
Q

Midazolam

A

Imidazole IMG- opens and increases water solubility in acidic pH
GABA a agonist- increases frequency of channel opening
1st pass metabolism=50% bioavailability
P450
1 hydroxymidazolam= active metabolism, 1/2 potency, prolonged in renal failure

63
Q

midazolam effects

A

Minimal with sedation, decreased BP and SVR with induction dose
Minimal resp with sedation, resp dep with induction dose (potentiated with opioids)
Anterograde amnesia
Anticonvulsant
No analgesia

64
Q

Diazepam

A

Enterohepatic recirculation
T 1/2 43 hours
Pain on injection due to propylene glycol

65
Q

Lorazepam

A

6 hours

Slow onset so not useful as anticonvulsant

66
Q

Flumazenil

A 
Competitive GABA a receptor antagonist
Reverses benzo overdose
Initial dose:0.2 mg IV
Titration in 0.1 dose increments 
Short DOA (30-60 min)
Reverses sedative more than amnestic effects
67
Q

Alkylphenol

A

Prop, fosprop

68
Q

Arlcyclohexlamine

A

Ketamine

69
Q

Imidazole

A

Etomidate, dex

70
Q

Identifying volatiles

A

Iso- 5 fluorine and 1 chlorine (increases potency), chiral carbon, methyl ethyl ether
Des- 6 fluorines, chiral carbon, fully fluorinated, methyl ethyl ether
Sevo- 7 fluorines, no chiral carbon, methyl isopropyl ether

71
Q

Vapor pressure

A

Pressure exerted by a vapor in equilibrium with its liquid or solid phase in closed container
Directly proportional to temp

72
Q

Partial pressure

A

Vol% x total gas pressure= partial pressure of gas
Determines depth of anesthesia, NOT vol percent
Leads to under dosing of des above sea level

73
Q

Sevo physiochemical properties

A 
Vapor pressure- 157
Boiling point- 59
Molecular weight (g)- 200
Unstable in CO2 absorber
Forms compound A
74
Q

Des physiochemical properties

A 
Vapor pressure- 669
Boiling point- 22
Molecular weight (g)- 168
Stable in hydrated absorber
Unstable in dehydrated absorber
Carbon monoxide
75
Q

Iso physiochemical properties

A 
Vapor pressure- 238 mmHg
Boiling point- 49
Molecular weight- 184
Stable in hydrated absorber
Unstable in dehydrated absorber
Carbon monoxide
76
Q

N2O physiochemical properties

A

Vapor pressure- 38,770
Boiling point- -88
Molecular weight- 44
Stable in absorber

77
Q

Solubility

A

Ability of gas to dissolve into blood and tissues
Polar solute= hydrophilic
Nonpolar solute= hydrophobic

78
Q

Sevo solubility coefficients

A

Blood gas- 0.65

Oil gas- 47

79
Q

Des solubility coefficients

A

Blood gas- 0.42

Oil gas- 19

80
Q

Iso solubility coefficients

A

Blood gas- 1.46

Oil gas- 91

81
Q

N2O solubility coefficients

A

Blood gas- 0.46

Oil gas- 1.4

82
Q

FA/FI

A 
FA= partial pressure of anesthetic inside the alveoli
FI= concentration of anesthetic exiting vaporizer
83
Q

Solubility and FA/FI

A

Low solubility —> less uptake in blood —> increased rate of rise —> faster equilibration of FA/FI —> faster onset

84
Q

Increased FA/FI

A

Faster onset and curved pushed up

High FGF and alveolar ventilation
Low FRC, time constant, and anatomic dead space
Low solubility, CO, and Pa-Pv difference

85
Q

Decreased FA/FI

A

Slower onset and curve pushed down

Low FGF and alveolar ventilation
High FRC, time constant, anatomic dead space
High solubility, CO, and Pa-Pv difference

86
Q

Uptake is dependent on:

A

Tissue blood flow
Solubility of anesthetic in the tissue
Arterial blood: tissue partial pressure gradient

87
Q

Vessel rich group

A

CO= 75%, body mass=10%
Heart, brain, kidney, liver, endocrine glands
First to equilibrate with FA

88
Q

Muscle and skin

A

CO= 20%, Body mass= 50%

89
Q

Fat

A

CO= 5%, Body mass= 20%

High capacity to store large amounts due to lipid solubility of agents

90
Q

Vessel poor group

A

CO < 1%, body mass=20%
Tendons, ligaments, cartilage, and bone
Doesn’t really contribute to uptake

91
Q

How inhaled agents exit body

A

Elimination from lungs- exhalation
Hepatic biotransformation
Percutaneous loss- minimal, not clinically significant

92
Q

Hepatic biotransformation numbers

A

DIS (alphabetical order), rule of 2’s
Des- 0.02%
Iso- 0.2%
Sevo: 2-5%

Nitrous- 0.004%

93
Q

Liver metabolism halogenated agents

A

P450 system- CYP2E1
Des and iso- metabolized to inorganic fluoride ions and trifluoroacetic acid (TFA)
Halothane- up to 40% liver metabolism —> halothane hepatitis (immune mediated)
Sevo- metabolized to inorganic fluoride ions (no TFA), concerns of high output renal failure

94
Q

High output renal failure

A

Comes from sevo metabolism
Unresponsive to vaso
S/S- polyuria, hypernatremia, hyperosmolarity, increased plasma creatinine, inability to concentrate urine
Doesn’t actually happen

95
Q

Sodalime and breakdown of halogenated anesthetics

A

Sevo- compound A in soda lime, desiccated soda lime increases production
Des and iso- carbon monoxide in desiccated soda lime

96
Q

Concentration effect

A

Concentrating effect

Augmented gas flow

97
Q

Concentrating effect

A

Higher concentration of agent to alveolus = faster onset
Only relevant with N2O
Concentrating effect and augmented gas inflow

98
Q

Augmented gas flow

A

Breath after concentrating effect has increased anesthetic in tracheal gas to replace lost alveolar volume
Causes increased alveolar ventilation and augments FA
Temporary

99
Q

Ventilation effect

A

Greater alveolar ventilation leads to greater Fa/Fi rise

Spontaneous ventilation- alveolar ventilation decreased with deepening anesthetic depth, protective mechanism

100
Q

2nd gas effect

A

Rapid uptake of N2O
Alveolus shrinks and alveolar volume decreases
Relative increase in concentration of 2nd gas
Other gas concentration is higher than if it was given alone
Transient

101
Q

Diffusion hypoxia

A

Large volume of N2O from body into alveoli quickly
Dilutes O2 and CO2- causes temporary diffusion hypoxia and hypocarbia
100% O2 for 3-5 min when N2O turned off

102
Q

Right to left shunt

A

Blood leaving R heart bypasses lungs - doesn’t pick up O2 or inhalation agent
Volatiles- lower solubility agents more affected, desflurane impacted most
IV agents- faster IV induction, blood bypasses lungs and travels to brain faster

103
Q

R to L shunt examples

A 
Tetralogy of Fallot
Foramen ovale
Eisenmengers syndrome
Tricuspid atresia
Epstein’s anomaly
104
Q

Left to right shunt

A

Volatiles- no meaningful effect

IV agents- slow IV induction, agent recirculates to lungs

105
Q

Nitrous in closed air spaces

A

N20 34x more soluble than N2
Compliant airspace- N2O increases volume, will convert to a fixed airspace
Fixed airspace- increases pressure of space

106
Q

Ocular bubbles

A

SF6- discontinue N2O 15 min before, avoid for 7-10 days after
Air- avoid for 5 days
Perfluoropropane- 30 days
Silicone- can use N2O

107
Q

N2O and vitamin B12

A

Irreversibly inhibits B12 which inhibits methionine synthase (required for folate metabolism and myelin)

108
Q

MAC

A

Measure of potency
MAC awake- 0.4-0.5, where patient can open their eyes, typically where awareness is prevented
Mac bar- 1.5 MAC, block autonomic response

109
Q

Increasing MAC

A 
Chronic alcohol use
Increased CNS neurotransmitters- acute meth, acute cocaine, MAOIs, ephedrine, levodopa
Hypernatremia
Infants 1-6 months
Hyperthermia
Red hair
110
Q

Decreasing MAC

A 
Acute alcohol intoxication
IV anesthetics
N2O
Opioids
Alpha. Agonists
Lithium
Lido
Hydroxyzine
Hyponatremia
Old age (6% per decade after 40)
Prematurity
Hypothermia
Hotn
Hypoxia/anemia
Bypass
Met acidosis 
Pregnancy
PaCO2 > 95 mmHg
111
Q

No effect on MAC

A 
K changes
Mag changes
Thyroid changes
Gender
PaCO2 15-95
Htn
112
Q

Meyer Overton rule

A

Lipid solubility directly proportional to potency of inhaled anesthetic
Greater solubility = lower MAC

113
Q

Unitary hypothesis

A

All anesthetics share similar MOA but may work at different site

114
Q

Inhalation agent stimulation and inhibition

A

Stimulates inhibitory pathways- GABA A, glycine, K

Inhibits stimulatory pathways- NMDA, nicotinic, Na, dendritic spine function and motility

115
Q

Volatiles in brain

A

GABA A
Stimulates it
Increas Cl influx and hyperpolarizes neurons

116
Q

Volatiles in SC

A

Immobility in ventral horn

Glycine, NMDA, and Na

117
Q

N2O and xenon receptors

A

NMDA antagonism

K 2P channel stimulation

118
Q

Blood pressure

A

Decreased dose dependently
Decreased intraceullar Ca in vascular smooth muscle

Sevo causes least SVR decrease

119
Q

Heart rate

A

Direct decrease dose dependently- decreased SA node automaticity and conduction velocity, increased repolarization time cause prolonged QT
Des (and iso) can increase heart rate- pulmonary irritation causing SNS activation

N2O activates SNS and increases HR

120
Q

Contractility

A

Small decrease but preload responsive

121
Q

Coronary vascular resistance

A

Increases blood flow in excess of O2 demand

122
Q

Coronary seal

A

With increased O2 demand, vessels dilate
O2 extraction ratio= 75% so increase blood flow to increase O2
Stenotic vessels maximally dilated beyond stenosis- cant dilate further
Directs blood flow towards healthy tissue at expense of diseased tissue
Example of revere Robin Hood effect

123
Q

Pulmonary effects of volatiles

A 
Decreased TV
Increased RR
Decreased response to CO2 and increased apneic threshold (usually 3-5 mmHg below patients normal PaCO2)
Upper airway obstruction
Decreased FRC
Bronchodilators
124
Q

CO2 response curve

A

Right shift- MV les than predicted for given PaCO2 (respiratory acidosis), ex: GA, opioids, metabolic alkalosis
L shift- MV greater than predicted for given PaCO2 (respiratory alkalosis), ex: anxiety, stimulation metabolic alkalosis, increased ICP

125
Q

PaO2 sensing

A

Peripheral chemoreceptors in carotid bodies- monitor for hypoxemia
Carotid bodies- glossopharygeal nerve, sensitive to change in arterial gas tensions
Aortic bodies- vagus nerve, sensitive to BP changes

126
Q

PaO2 changes

A

Impaired chemoreceptor response for several hours

Greatest biotransformation impacts hypoxic drive the most (halothane>sevo>iso>des)

127
Q

Neurological effects

A

Reduce CMRO2 (N2O increases it)
Sevo can produce seizure activity- more with hypocapnia and peds inhalation inductions
increased CBF, blood volume, and ICP
cerebral autoregulation normally 50-150mmHG, decreased in dose dependent fashion so CBF dependent on BP

128
Q

SSEP

A

Integrity of dorsal column (medial leminiscus)

Perfused by posterior spiral arteries

129
Q

MEPs

A

Monitor corticospinal tract

Perfused by anterior spinal artery

130
Q

Components of monitored potentials

A

Amplitude- strength of response

Latency- speed of conduction

131
Q

Monitored potential changes with agents

A

Decreased amplitude- by 50%
Increase latency- by 10%

TIVA
Less than 0.5 MAC agent with no N2O
No muscle relaxants with MEPs

132
Q

Brain auditory and visual evoke

A

Brain auditory- most resistant to anesthetics

Visual- most sensitive

APEX (6 decks)

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