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Anesthesia Pharm > Exam 3 Part IV > Flashcards

Exam 3 Part IV Flashcards

1
Q

what patients would be especially vulnerable to an increase in PVR 2/2 N2O use

A
  1. pts with pulmonary htn 2. neonates with bronchopulmonary dysplasia and/or RSV 3. those with congenital heart defects (–> R-to-L shunt)
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2
Q

respiratory effects of N2O

A
  1. mild decrease in Tv 2. mild increase in RR 3. hypoxic respiratory drive decreased 4. ventilatory response to increased CO2 affected
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3
Q

renal/hepatic effects of N2O

A
  1. no significant effects on kidney 2. mild decrease in hepatic blood flow
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4
Q

neuromuscular effects of N2O

A
  1. does NOT provide significant muscle relax 2. increased muscle tone with high concentrations 3. does NOT trigger MH
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5
Q

hematologic effects of N2O

A
  1. inhibits enzymes that are vitamin B12 dependent (methionin synthetase) 2. leads to bone marrow suppression 3. peripheral neuropathies 4. & pernicious anemia
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6
Q

T/F: N2O causes increase uterine smM contractility

A

false; no effect on uterine smM

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7
Q

fetal effects of N2O

A
  1. increased incidence of spontaneous abortion with chronic exposure to N2O 2. may be hazardous to fetus esp during 1st trimester
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8
Q

what anatomical areas are “compliant spaces” and would have an increase in volume with the use of N2O

A
  1. GI tract 2. pneumoperitoneum 3. pneumothorax 4. air emboli
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9
Q

principle objective of inhlational anesthesia

A
  1. achieve a constant and optimal partial pressure of the agent
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10
Q

partial pressure gradients that guide INH anesthetic uptake

A
  1. anesthesia machine 2. alveolar 3. blood 4. brain
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11
Q

the goal with INH partial pressure gradients is for the _______________ to = ______________

A

inspired pressure; alveolar pressure

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12
Q

input of INH agent into alveoli is dependent on

A
  1. anesthesia machine 2. inspired partial pressure 3. alveolar ventilation
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13
Q

uptake of INH agent from alveoli to blood is dependent on

A
  1. solubility of the gas 2. CO 3. alveolar to venous partial pressure gradient
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14
Q

order of pressure gradients for inhalational agents

A

Pressure device (PD) - pressure inspired (PI) - Pressure alveoli (PA) - pressure arterial (Pa) - pressure brain (Pbr) same order with fraction

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15
Q

doubling the CO _________________ the time to uptake of INH agent

A

doubles

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16
Q

Et of INH agent = ________________ of the agent

A

partial pressure

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17
Q

pt will have awareness at a MAC < ___________

A

0.7

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18
Q

factors that influence tissue uptake of INH agent

A
  1. tissue solubility 2. tissue blood flow 3. Pa-Pbr partial pressure difference
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19
Q

you should have equilibration of INH agent Pa with VRG within _______________min

A

8-Apr

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20
Q

you should have equilibration of INH agent Pa with muscle and skin group (MG) within ___________________

A

1-4 hours

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21
Q

you should have equilibration of INH agent Pa and fat group within ____________

A

> 24 hours

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22
Q

your MAC should not get below ___________ without reversing your muscle relaxant

A

0.7

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23
Q

elimination of INH agent is determined by?

A
  1. length of administration of agent 2. solubility of agent (elim time decreased with less plasma soluble agents)
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24
Q

rate of decrease of INH in Pbr is reflected by the ____________

A

PA

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25
Q

what is the effect of N2O is discontinued abruptly

A
  1. reversal of partial pressure gradients –> reverse concentration effect 2. high volume of N2O enters the alveoli from capillary flow –> displacing O2 from alveoli –> decreasing PaCO2 3. dilutes PaCO2 –> decreased stimulus to breathe all leads to diffusion hypoxia
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26
Q

how can you avoid diffusion hypoxia with N2O

A

filling lungs with 100% FiO2 at the end of a case

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27
Q

Tec6 heats the vaporizer to _______________ creating VP = ___________atm

A

39 C; 2

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28
Q

what is the MOA of all local anesthetics?

A

they block voltage gated sodium channels

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29
Q

uses of local anesthetics

A
  1. local infiltration (hernia repair) 2. peripheral/regional blocks 3. neuraxial blocks 4. acute or chronic pain 5. IV injection for arrhythmias
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30
Q

all currently available LA consists of a _______________ ring + ___________

A

lipophillic phenyl ring; tertiary (majority)/quaternary amine

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31
Q

what determines whether a LA is an amide or an ester

A

the bond btween the benzene ring and the carbon group

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32
Q

tertiary amine LA have more _______________ effects than those that are quaternary

A

toxic CNS

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33
Q

which LA are esters

A
  1. procaine (novicaine) 2. chloroprocaine** (nesacaine) 3. tetracaine (pontocaine) 4. cocaine 5. benzocaine**
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34
Q

_______________ is available commercially as ambesol and origel

A

benzocaine

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35
Q

which LA are amides

A
  1. lidocaine (xylocaine)** 2. mepivacaine (carbocaine) 3. prilocaine 4. bupivacaine** (marcaine, sensorcaine) 5. levobupivicaine (chirocaine) 6. ropivicaine (naropin)** 7. articaine
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36
Q

which LA has the highest risk of toxicity

A

bupivicaine

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37
Q

metabolism of ester LA

A
  1. catalyzed by plasma tissue cholinesterases via hydrolysis 2. occurs throughout the body in the blood 3. rapid metabolism
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38
Q

which ester is NOT metaboized by plasma and tissue cholinesterases

A

cocaine

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39
Q

what is the longest acting ester

A

tetracaine

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40
Q

DOA of ester LA

A

short due to rapid metabolism

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41
Q

which category of LA is more likely to have allergic potential

A

esters; and is due to metabolism into PABA

42
Q

if someone has an allergy to an amide LA, it is probably an allergy to what _______________

A

preservatives

43
Q

an allergy to one ______________ is an allergy ALL, but an allergy to one ____________ is NOT an allergy to all

A

ester; amide

44
Q

what are your low potency, short DOA LA

A
  1. procaine (novocaine) 2. chloroprocaine (nesacaine)
45
Q

what are your intermediate potency, intermediate DOA LA

A
  1. mepivacaine (carbocaine) 2. lidocaine (xylocaine)
46
Q

what are your high potency long DOA LA

A
  1. tetraine (pontocaine) 2. bupivicaine (marcaine) 3. ropivacaine (naropin)
47
Q

which LA have a fast onset

A
  1. chloroprocaine 2. mepivacaine 3. lidocaine
48
Q

which LA have a slow onset

A
  1. procaine 2. tetracaine 3. bupivacaine 4. ropivacaine
49
Q

DOA of procaine

A

60-90 min

50
Q

DOA of chloroprocaine

A

30-60 min

51
Q

DOA of mepivacaine

A

120-240 min

52
Q

DOA of lidocaine

A

90-120 min

53
Q

DOA of tetracaine, bupivacaine, and ropivacaine

A

180-600 min

54
Q

all LA are _______________ (weak acid, weak base, strong acid, strong base)

A

weak bases

55
Q

what is pKa

A

the pH at which 50% of the drug is ionized (water soluble form) and 50% in non-ionized (lipid soluble) form

56
Q

LAs are mostly ionized at a pH that is signifcantly ___________ its pKa

A

less

57
Q

LA with increased pKa have _________ ionization at normal pH

A

increased (which slows the onset)

58
Q

decreased pKa = ______________ onset

A

faster

59
Q

what is the exception to pKa with LA onset

A

chloroprocaine, has a fast onset, but due to the dose not the pKa

60
Q

rate of diffusion of LA depends on:

A
  1. chemical structure 2. lipid solubility 3. state of ionization (**most important characteristic)
61
Q

a base in a in an alkaline environment is _______________, ___________, & ______________ across the bilipid membrane

A

non-ionized, lipid soluble, and easily diffusible

62
Q

T/F: if the tissue you are trying to inject LA into is infected, the block will be potentiated

A

false; block will not work because infected tissue = acidic environment

63
Q

T/F: the further away the pKa is from physiologic pH the more it will be ionized at injection

A

TRUE

64
Q

LA provide analgesic as long as they __________________________

A

are in the site of deposition

65
Q

target site of action of LA

A

NAME?

66
Q

potency of LA is related to _____________

A

lipid solubility (which is dependent on pH and pKa)

67
Q

onset of LA depends on ________ & _______

A

route and dose

68
Q

DOA of LA depends on ____________ & ____________

A

protein binding; vascular uptake

69
Q

increased protein binding of LA = __________ DOA; increased vascular uptake = _____________ DOA

A

increased; decreased

70
Q

how does epi affect DOA of LA

A

they vasoconstrict which slows the vascular uptake rate, just prolonging the DOA

71
Q

epidural requires ____________x more of the dose of LA to produce the dense block achieved with a spinal

A

10

72
Q

a ________________ block has no nerve sheaths, has direct access to the nerves thus gives a fast onset

A

subarachnoid block

73
Q

if you do a spinal block but your patient becomes hypotensive and nauseated, this is a sign of _____________

A

high spinal block

74
Q

describe the chemical structure effect on MOA: (starting with drug in the vial)

A
  1. weak LA + slightly acidic solution = ionized 2. inject LA into tissues (more basic solution) –> protonating (picking up charge) –> unionization 3. unionized LA crosses lipid bilayer 4. intracellular pH is lower –> ionization of LA (so it cannot leave) 5. antagonizes the voltage gated ion channel
75
Q

_____________ = extension of a centrally located neuron & is the functional unit of peripheral nerves

A

axon

76
Q

axolemma of axon

A

Specialized bilipid plasma membrane surrounding the axoplasm containing proteins and ion channels

77
Q

on the nerve cells where are the voltage gated ion channels located?

A

between the nodes of ranvier

78
Q

for a LA to block saltatory conduction __________ nodes of ranvier have to be blocked

A

3

79
Q

what are the three layers of connective tissue on the nerve that are barriers to LA

A
  1. endoneurium 2. perineurium 3. epineurium
80
Q

LA preferentially bind to the ___________ & ____________ states of the voltage gated sodium ion channel

A

open; inactivated

81
Q

resting membrane potential of a neural cell

A

-70 to - 90 mV

82
Q

axolemma is relatively permeable to outward diffusion of __________, but is impermeable to __________

A

K+; Na

83
Q

describe the action potential of a neural cell

A
  1. sodium channels are open (below threshold) 2. at threshold (~50 mV) potassium channels open 3. at peak sodium channels close (inactive) –> repolarization 4. potassium channels close just below - 50 mV
84
Q

what is the guarded receptor/modulated receptor hypothesis

A

that LA’s preferentially bind to both the open & inactivated states of the voltage gated Na channels

85
Q

if a LA goes through the pore interior to get to the binding site this is the ______________ pathway

A

hydrophillic

86
Q

if LA goes through the lipid membrane to get to the binding site this is the _______________ pathway

A

hydrophobic

87
Q

intracellular Na channel pore receptors have an increased affinity for the ____________ form of LA

A

ionized

88
Q

what is the use dependent (phasic block/inhibition) of LA

A
  1. LAs work faster as the voltage gated sodium channel is repetitively depolarized 2. leads to greater number of Na channels being in the inactivated & open state 3. increases the opportunity for LA binding = accumulation of LA bound Na
89
Q

describe the sequence of what gets blocked when you administer a LA (i.e. differential block)

A
  1. vasodilation –> autonomic function block 2. pain 3. touch 4. temperature 5. motor fx 6. proprioception
90
Q

T/F: with LA non-myelinated fibers are generally blocked before myelinated fibers

A

false; myelin increases the diffusion barrier, but only need to block 3 nodes of ranvier and NOT the entire length of the nerve like with unmyelinated

91
Q

T/F: there is a strong correlation btwn potency and lipid solubility of LA

A

TRUE

92
Q

characteristics of larger LA molecules

A
  1. more lipophillic/relatively water insoluble 2. highly protein bound –> prolonged DOA 3. less easily absorbed systemically 4. bind to Na channels with a higher affinity that lower soluble agents 5. increased incidence of CV toxicity 6. higher potency = lower dose
93
Q

duration of action of LA is determined by _______________ & ______________

A

protein binding; vascular uptake

94
Q

the more protein bound a LA is –>

A
  1. more CV effects 2. longer duration of Action 3. higher affinity for voltage gated sodium channels
95
Q

sx of horners syndrome

A
  1. miosis 2. ptosis 3. anhydrosis 4. epopthalamus
96
Q

rate the sites of LA absorption from greatest absorption to least (after LA is IV)

A
  1. interpleural (greatest) 2. intercostal 3. caudal 4. epidural 5. brachial plexus 6. femoral/subarachnoid 7. sciatic 8. subcutaneous
97
Q

factors that affect LA absorption (i.e. into vasculature away from site of injection)

A
  1. site of injection (greater vasculaturity = greater absorption) 2. dose 3. pKa 4. additives: epi & ketamine (decreases absorption via VC), alpha2 agonist and opioids (increase absorption via VD)
98
Q

lipid solubility effect of LA on systemic absorption

A

more lipid soluble decreased systemic solubility

99
Q

the safe & recommended dose for one type of block could result in ______________ for another type of block

A

systemic toxicity

100
Q

w/ LA the faster the (systemic) absorption = the ______________ the DOA and the the ________________ risk of toxicity

A

shorter; increased

Anesthesia Pharm (18 decks)

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