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Pharm Flashcards

1
Q

phase 1 reactions

A

oxidation, reduction, hydrolysis

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2
Q

phase 2 reactions

A

conjugation

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3
Q

oxidation and reduction occur via what

A

cytochrome p450

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4
Q

how does cytochrome p450 work

A

hydroxylation, dealkylation, deamination, desulfuration, epoxidation, dehalogenation

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5
Q

inducers p450

A

phenobarbital and phenytoin

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6
Q

inhibitors p450

A

amiodarone and CCB

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7
Q

what is conjugation

A

conjoins hydrophobic drug molecules with polar moities to increase solubility and renal clearence

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8
Q

morphine metabolism

A

metabolized in liver to form M3G and M6G
M3G inactive, M6G is potent and can’t be cleared in renal disease

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9
Q

Rate of metabolism

A

rate = Q(Cin - Cout), Q blood flow to liver

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10
Q

hepatic extraction ratio

A

ER = Cin-Cout/Cin

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11
Q

clearence equation

A

Q * ER

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12
Q

if a drug has a high extractino ratio, what does clearance depend on

A

Q, blood flow to liver
GA decreases hepatic blood flow
less important in drugs that have low extraction ratio

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13
Q

examples of tissue clearance

A

esmolol, succ, remi - ester hydrolysis in tissue and plasma

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14
Q

drugs that undergo butylcholinesterase/pseudocholinesterase metabolism in plasma

A

succ, mivacurium, chloroprocaine

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15
Q

what undergoes nonspecific ester hydrolysis in muscle and intestine

A

remi, atracurium

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16
Q

hofmann degradation

A

plasma, cis

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17
Q

major protein binding for anesthesia drugs

A

albumin and alpha 1 acid glycoprotein

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18
Q

free fraction

A

ratio of unbound drug to total amount of drug,
free raction of 1 means 100% of drug is free in plasma - would not be impacted by changes in protein conc
decrease in protein binding results in an increase in the conc of free form of drug, artifically decreased Vd

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19
Q

zero order kinetics

A

occurs at constant rate, rate independent of conc of drug

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20
Q

first order kinetics

A

dose dependent, rate of clearance proportional to conc, log

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21
Q

3 compartment model

A

body has central plasma compartment, rapid equilibrating comp (vessel rich like brain and GI) and slow equilibrating compartment (vessel poor like fat)
IV injection –> all in plasma —> rapid distribution phase, down conc gradient into surrounding tissue –> slow distribution phase, equilibrate with slow uptake tissue –> elimination

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22
Q

where do epidural opioids have site of action

A

outside of epidural space in dorsal horn

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22
Q

two main processes that interfere w opioid ability to reach CSF from epidural space

A

clearance of drug into plasma, partioining of drug into other tissues
dependent on lipid solubility

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23
Q

highly lipid soluble drugs (fentanyl, sufentatil) reach ____ peak concentrations in CSF

A

lower, compared to hydrophilic drugs like morphine
lipophilic drugs partition into epidural fat, more rapidly cleared into plasma which occurs in dura matter
epinephrine reduces clearance rate bc reduces dural blood flow

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24
Q

why don’t spinal lipophilic opiates cause resp depression

A

move out of CSF into epidural fat so limited bioavail at spinal cord rostral to site

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25
Q

intrathecal bioavailability of epidurall administered LA ____ with lipophilicity

A

increase , opposite of opioids

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26
Q

hyperbaric solutions, how to make them denser

A

greater density than csf, glucose
achieve considerable spread
travel to most dependent part of spines

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27
Q

isobaric

A

limited subarachnoid spread , not affected by gravityu
more profound motor block and more prolonged duration

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28
Q

three most important factors in determining neuraxial spread

A

baricity, position, dose

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29
Q

drug tolerance refers to changes in what 2 things

A

potency (higher effective dose)
effectiveness (decreased maximal effect)

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30
Q

4 key characteristics of drug tolerance

A
  1. reversible, once exposure to drug dc
  2. dependent on dose and frequency of drug exposure
  3. variable time course and extent of tolerance development between different drugs
  4. not all drug effects develop same amt of tolerance
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31
Q

dispositional/metabolic tolerance

A

repeated use of a drug reduces amount of drug available at target tissue
alcohol, opiates, barbiturates
accelerated drug clearance due to induction of enzymes

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32
Q

reduced responsiveness tolerance

A

when repeated use of drug alters nerve cell function, days/weeks to develop
caffeine
increased receptor activation by agonistic drugs –> receptor downregulation
reduction in receptor activations due to antagonism results in receptor upregulation

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33
Q

behavioral tolerance

A

repeated drug use reduces effect in environemnt where administered, learned behaviors

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34
Q

tachyphylaxis

A

not dose dependent, neurotransmitter depletion

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35
Q

to be excreted drugs need to be more _____

A

hydrophilic

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36
Q

to be reabsorbed drugs need to be more ______

A

lipophilic

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37
Q

two types of biotransformation

A

phase I nonsynthetic and phase II synthetic

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38
Q

what are phase I reactions

A

oxidation, reduction, hydrolysis

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39
Q

what are phase II reactions

A

conugation reactions
glucuronyl transferase, sulfotransferase, transacylases, glutathione transferase, acetylases, ethylases, methylases

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40
Q

total clearance equation

A

clearance = volume * rate constant

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41
Q

three processes of renal excretion

A

glomerular filtration, active secretion, passive reabsoprtion

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42
Q

net renal excretion

A

equals amount filtered at glomerulus plus amount secrete minus amount reabsorbed
= U * V/P
U is concentration, v = volume of urine p=plasma conc

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43
Q

two ways drugs can alter by two main mechanisms

A

increasing or decreasing cardiac output, displacing the drug from protein binding sites

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44
Q

naloxone MOA

A

binds to opiate receptors and blocks effect of narcotics

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45
Q

flumazenil MOA

A

blocks effects of alc/benzos at GABA receptor

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46
Q

ACh inhibitors MOA

A

antagonize breakdown of Ach molecules

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47
Q

Opiate agonist-antagonist compounds MOA

A

agonists at kappa=opiate receptor and antagonists at mu opiate receptor

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48
Q

serotonin syndrome

A

mental status changes, muscle twitching, excessive sweating, shivering, fever

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49
Q

inhaled anesthestics are affected by ?

A

central catecholamine levels

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50
Q

anaphylaxis

A

antigen-antibody, type I hypersensitivity rxn, antigen binding to IgE antibodies on the surface of mast calls initials release of various chemical mediators

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51
Q

anaphylactoid rxns

A

resemble anaphylaxis but IgE does not mediate them , clinically indistringuishable

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51
Q

local anesthestic allergy

A

ester - common, amide - rare, usually related to PABA preservative

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52
Q

ephedra

A

potential interactions with cardiac glycosides, MAOIs, oxytocin, MI, stroke, hypertension, tachy, arrythrmias

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52
Q

echinacea

A

hepatotoxicity

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52
Q

feverfew

A

inhibit platelets

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53
Q

garlic

A

potentiate warfarin, heparin, aspirin

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54
Q

ginger

A

potentiate anticoagulant effects, inhibit thromboxane synthetase

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55
Q

ginkgo biloba

A

potentiate nsaids, warfarin, decrease effects of anticonvulsants, lower seizure threshold, hyphem and bleeds

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56
Q

ginseng

A

sleepiness, hypertonia, edema, hypoglycemia, tachy, HTN, mania, SJS, epistaxis, inhibition of platelet aggregation

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57
Q

goldenseal

A

paralysis, htn, electrolyte abnormalities

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58
Q

kava-kava

A

potentiate barbituates, benzos, ethanol, increased suicide risk, decreased mac, hepatotxicity, hallucinations

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59
Q

licorice

A

HTN, hypoK, edema, renal, hypertonia

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60
Q

saw palmetto

A

headaches, GI

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61
Q

st john’s wort

A

interact with MAOIs, prolonged anesthesia, photosensitivity, restlessness, dizziness, fatigue

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62
Q

valerian

A

barbituates, benzo withdraw syndrome, prolonged effects of anesthesia

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63
Q

mechanism of anesthetic gases

A

enhance inhibitory receptors (GABA and glycine) and dampen excitatory pathyways (nicotinic and glutamate)
suppresiom of nociceptive motor responses w/in spinal cord and supraspinal suppresion causing amnesia

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64
Q

MAC increases (decreases in potency)

A

hyperthermia, stimulants, chronic alcohol, infants aged 6-12m

65
Q

mac decreases

A

hypothermia, hypoNa, opioids, barbituates, alpha 2 blockers, ca2 blockers, acute alcohol, pregnancy, prematurity, aging

66
Q

____ partition coefficient = ____ solubility = ____ rate of induction

A

____ partition coefficient = ____ solubility = ____ rate of induction

67
Q

blood gas coefficient for des

A

0.4

68
Q

blood gas coefficient for sevo

A

0.6

69
Q

blood gas coefficient for iso

A

1.4

70
Q

speed of induction slowest to fastest

A

iso –> sevo –> des

71
Q

solubility highest to lowest

A

iso –> sevo –> des

72
Q

boiling point highest to lowest

A

sevo/en > halothane > iso > des > nitric

73
Q

vapor pressure highest to lowest

A

Nitrous > des > halothane > iso > en > sevo

74
Q

MAP ____ with use of all volatile agents except halothane

A

decreases, decreases SVR
nitrous unchanged or increased MAP

75
Q

HR ____ with all volatile agents at a MAC of 0.25 for iso, 1 for desflurane, 1.5 for sevo

A

increases

76
Q

all volatile anesthestics sensitize myocardium to ____ and _____ myocardial contractility

A

epi and depress contractility

77
Q

effect of gas on TV and RR and MV

A

decrease TV, increase RR, little effect on MV
PaCO2 increases
blunt vent stimulation caused by hypoxemia and hypercarbia
decrease FRC, cause bronchodilation

78
Q

gas effect on cerebral blood flow and CMRO2

A

increase blood flow, decrease cerebral metabolic rate for oxygen (except nitrous with increases CMRO2)
but inhibit autoregulation (iso maintains it the best)

79
Q

Iso effect on CSF

A

no effect on CSF production, decreases resistance to CSF absorption

80
Q

des effect on CSF

A

increases CSF production without affect absoprtion

81
Q

ICP with volatile

A

increased ICP, counteracted by hypocapnia
blunted by narcotics

82
Q

gases ____ amplitude and ____ latency of SSEPs

A

decrease and increase

83
Q

EEG tracings with gas

A

more gas, more amplitude and synchrony of EEG

84
Q

ED50/MAC

A

50% do not move in response to stimulus, 1 SD is about 10% of the MAC value

85
Q

iso mac

A

1.15

86
Q

sev mac

A

2

87
Q

des mac

A

6

88
Q

pain is transmitted by a what system

A

3-neuron system

89
Q

At periphery, noxious stimuli mainly received and tramsitted by

A

A beta, A delta, C fiber
First order neurons

90
Q

first order neurons synapse with 2nd order neurons where

A

dorsal horn spinal cord

91
Q

second order neurons travel up spinal cord via

A

dorsal column and spinothalamic tract and synapse with 3rd order in thalemus —> cerebral cortex —> pain

92
Q

bradykinin

A

macrophages and plasma kininogen, activates nociception

93
Q

serotonin

A

from platelets, activates nociception

94
Q

histamine

A

from platelets and mast cells - vasodilation, edema, pruritis

95
Q

prostaglandin

A

COVX pathway, sensitizes nociception

96
Q

leukotriene

A

LOX pathway, sensitizes nociception

97
Q

H+ ions

A

tissue injury, ischemia, hyperalgesia

98
Q

cytokines/TNF/interleukins

A

from macrophages, snesitive nociception

99
Q

adenosine

A

from tissue injury, activates nociceptors, hyperalgesia

100
Q

glutamate

A

injured nerve terminals, activates nociceptors

101
Q

substance P

A

injured nerve terminals, activates macrophages and mast cellsn

102
Q

nerve growth factor

A

macrophages, stimulates histamine and serotonin release

103
Q

major receptors activated by opioids

A

mu, delta, kappa
G protein coupled receptors - cAMP
located at periphery, dorsal horn, brainstem and cortex

104
Q

three major mechanisms of action of opioids

A

inhibiton of presynaptic Ca2+ influx (depolarizes, inhibits release of neurotransmitters)
increases postsynaptic K+ efflux deploarizes and inhibits cellular signal transmission
activation of descending inh pain pathway via inihibito of GABAergic receptors in brainstem

105
Q

peripheral Mu

A

decreased GI secretions, biliary spasm, pruritis, muscle rigidity, urinary retention

106
Q

mu1

A

supraspinal
decreased GI transit, prolactin release, catalepsy

107
Q

mu2

A

spinal and supraspinal, resp depression, decreased GI transit, cardiovascular effects

108
Q

Mu3

A

decreased inflammation

109
Q

kappa peripheral

A

decreased ADH, sedation

110
Q

kappa1

A

spinal, antipruritic

111
Q

kappa3

A

supraspinal

112
Q

delta peripheral

A

resp depression, decrease GI transit, urinary retention

113
Q

delta1 and 2

A

1 - spinal, 2 - supraspinal, 1 - dopamine turnover

114
Q

MOA barbituates

A

depress nerve synapses in reticular activating system, inibit excitatory neurotransmission (acetylcholine and NMDA) and enahnce inhibitor neurotransmission like GABA

115
Q

GABA receptor is a ____ channel

A

chloride ion channel, increases chloride ion conductance when GABA binds and membrane hyperpolarizes

116
Q

barbituates on cerebral physiology

A

dose dependent cerebral vasoconsition and cerebral metabolic rate
reduce ICP and blood flow
preserve autoregulation
dose dependent EEG depression
minimal effect on SSEP and MEP
dose dependent depression of BAEP
neuorprotection for focal cerebral ischemia (not global)

117
Q

barbituates good for this type of surgery

A

space occupying cranial lesions

118
Q

barbituate effect CVS

A

depression of medullary vasomotor center vasodilates periphery
decreased preload
decrease contractility
tachycardia

119
Q

resp effects barbituates

A

resp depression, decreased MV, decreased response to hypercap and hypoxia, airway obstruction, bronchospasm/laryngospasm

120
Q

contraindication barbituates

A

porphyria

121
Q

hypnotic effects propofol

A

agonism of beta subunit of GABA in CNS
inhibits Ach release in hippocampus and prefrontal cortex
inhibit NMDA subtype of glutamate receptors

122
Q

propofol effect on ICP

A

decrease 30-50%, decreases CMRO2 and CBF

123
Q

propofol effect on myocardial blood flow and oxygen consuption

A

decreases both so supply and demand remains the same

124
Q

euphoria mechanism propofol

A

increased dopamine in nucleus accumbens

125
Q

etomidate mechanism

A

potentiation of GABAa receptors, increases cl ion conduction leading to neuronal hyperpolarization and depression of reticular activating system

126
Q

etomidate endocrine side effects

A

inhibits 11-beta-hydroxylase (cholesterol to cortisol), can lead to adrenal insufficiency for up to 8 hours after dose

127
Q

etomidate CNS effects

A

reduces CBF and ICP due to cerebral vasoconstriction
can look like seizures on EEG
decreased IOP

128
Q

etomidate and heme effects

A

inhibits platelet function

129
Q

benzo MOA

A

enhance inhibitory neurotransmission via GABA receptors
alpha 1 - sedation, amnesia, anticonvlusion
alpha 2 - anxiolysis and muscle relaxation

130
Q

benzo receptor affinity

A

lorazepam > midaz > diazepam

131
Q

ketamine MOA

A

within thalamus and limbic system, binds NMDA receptors, nonceompetitive antagonism
catalepsy, high amplitude slowing of EEG

132
Q

where else can ketamine bind

A

my opioid receptor
sigma opioid resulting in dysphoria
miscarinic and nicotinin receptors producing dose dependent potentiation of paralytics

133
Q

ketamine CNS effects

A

increase ICP, increase CBF

134
Q

precedex MOA

A

selective alpha 2 adrenergic agnoist
reduction of pain signaling in spinal cord, hypnosis at locus coeruleus, reduction of CNS sympathetic activity

135
Q

two groups of LA

A

esters and amides

136
Q

ester LA

A

benzocaine, 2-chloroprocaine, cocaine, procaine, tetracaine

137
Q

amide LA

A

bupi, etidocaine, lidocaine, mepivacaine, prilocaine, ropi

138
Q

highest to lowest absorption/vascularity LA

A

IV > trachea > intercostal > paracervical > caudal > epidural > brachial plexus > sciatic > subq

139
Q

protein binding and duration of action LA

A

greater protein binding, longer duration - free drug is slowly made available for metabolism

140
Q

amides LA elimination

A

liver by P450 microsomal enzymes (hydroxylation and N-dealkylation)
amides have longer half life

141
Q

ester LA metabolism

A

hydrolyzed by pseudocholinesterases

142
Q

LA are weak/strong acid/bases

A

weak bases

143
Q

LA MOA

A

inhibit electrical conduction through nerves by blocking voltage gated soidum channels with nodes of ranvier
must cross axonal membrane into cystosol of neuro by diffuseing through lipid bilayer
decrease rate of depol in response to excitation, preventing ahcievement of action potential
DO NOT alter resting potential or threshold potential

144
Q

are myelinated or unmyelinated nerves blocked first by LA

A

myelinated

145
Q

A alpha

A

myelinated, proprioception, large motor

146
Q

A beta

A

myelinated, small motor, touch, pressure

147
Q

A gamma

A

myelinated, muscle tone

148
Q

A delta

A

myelinated, pain, temp, touch

149
Q

B fibers

A

myelinated, preganlionic autonomic

150
Q

C fibers

A

unmyelinated, dull pain, temp, touch

151
Q

LA potency determined by

A

lipid solubility, directly proportional

152
Q

LA speed of onset determined by

A

pKA, closer Pka to tissue pH the more rpaid onset time

153
Q

LA that cause methemoglobinemia

A

prilocaine, benzocaine

154
Q

transient neurologic symptoms

A

transient direct neurotox of lumbosacral nerves, severe pain and dysesthesia in lower back, butt, lower extremities with 12-24hr after uneventful spinal
NO sensory loss, motor, bowel/bladder dysfxn
lidocaine, higher doses, lithotomy
resolve within a week
tx: NSAIDs

155
Q

cauda equina syndrome

A

direct neurotoxicity of sacral nerves

156
Q

tetracaine

A

slow onset, profound motor blockade, potential neurotoxicity when administered at high doses, spinal anesthesia for long cases

157
Q

chloroprocaine

A

can impair action of subsequent epidural bupi and opioids

158
Q

ropivicaine

A

S(-) enantiomer of bupi, less pronounced motor block, reduced cardiotoxicity probably bc of vasoconstriction

159
Q

prolong duration of succ

A

liver disease, pregnancy, malnutrition, malignancy, hypothyroid

160
Q

electrolyte abnormalities that prolong duration/potentiate muscle relaxants

A

magnesium, hypoK, hyperCa, resp acidosis, metabolic alkalosis

161
Q

drugs that potentiate muscle relaxants

A

volatiles, LA, CCB, BB, aminoglycosides, mag, lithium, chronic steroids, dantrolene

162
Q

myasthenia gravis effect on paralytics

A

resistant to succ, sensitive to nondepolarizing

163
Q

lambert eaton effect on paralytics

A

more susceptible to succ and nondepolarizing

164
Q

what are cholinesterase inhibitors

A

neostigmine, pyridostigmine, physostigmine, edrophonium

165
Q

cholinesterase inhibitors side effects (muscarinic side effects)

A

bradycardia, bronchospasm, secretions, cerebral excitation, GI spasm, increased salivation, increased bladder tone, pupillary constriction

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