Terms in this set (274)
what is the three compartment model of PK?
when drugs are injected, they first go to the well perfused (central) compartment of the body/parts of body that get the most blood flow (
brain, heart, kidney
) and then distributes to the rest of your body
_____ can cause dysphoria and feeling of dissociation
what is induction?
going from consciousness to unconsciousness
what is diversion of controlled substances?
when providers self-administer drugs that they prescribe to patients
what system do sedatives/hypnotics act on?
ascending arousal system
do drugs work once they leave the central compartment?
why is drug redistribution important?
because drugs don't work once they leave the central compartment (e.g. you'll wake up after a single dose of propofol in a few minutes even though it stays in your body for hours)
what terminates drug effect?
redistribution (out of central compartment)
what is context-sensitive half time?
half life of drug is dependent on how long it is administered (accumulation of drug in fat - create a deposit that can then refuse into the blood- the longer you infuse a drug, the longer it takes to eliminate)
how are drug redistribution and context-sensitive half time related?
redistribution from plasma --> fat during longer infusions causes longer CS half time
what is the contraindication for propofol administration?
how is propofol administered?
what is the most commonly used induction agent?
propofol (used in 95% of general anesthesia cases)
what are uses for propofol?
induction & maintenance of general anesthesia
procedural and ICU sedation
what are off label uses for propofol?
chronic headache therapy
drug withdrawal (expensive)
what is the redistrubution of propofol?
2-8 minutes (termination of effect of single dose)
what is the elimination half life of propofol?
what metabolizes propofol?
liver, kidney, lungs, intestines
most propofol is _____ or _____ prior to excretion
what happens to the central compartment as you age?
decreases in size (so drug doses are higher in children)
is dosage of propofol weight dependent?
what is the mechanism of propofol?
potentiates the effects of GABA (binds to beta subunit of GABA-A receptors)
what are the cardiac physiologic effects of propofol?
tension (due to vasodilation preload/afterload, decreased sympathetic tone, myocardial depression)
variable effects on heart rate (will see a change, but direction depends on autonomic tone)
what are the respiratory physiologic effects of propofol?
nea or apnea (due to decreased tidal volume- have same/increased respiratory rate)
decreased response to hypoxia/hypercarbia
what are the neurologic physiologic effects of propofol?
decreased cerebral metabolic rate (burst suppression)
decreased cerebral blood flow (brain relaxation)
what are the adverse effects of propofol?
pain on injection
propofol-related infusion syndrome (cardiovascular collapse/metabolic acidosis in kids and ppl with brain injury)
hypertriglyceridemia and pancreatitis
decreased PMN chemotaxis
what are relative contraindications for propofol use?
hemodynamic instability (hypotension)
awareness under anesthesia (TIVA)
what would you use for a patient with a history of awareness under anesthesia?
inhaled agents (bc they have standard doses, not weight dependent)
why does propofol have potential to be a drug of abuse?
increased dopamine concentrations in nucleus accumbens (like cocaine)
NOT scheduled by DEA
what is the major clinical use for etomidate?
induction of anesthesia in patients with known or anticipated hemodynamic instability/cardiac arrest (critical illness, cardiac anesthesia- NOT commonly use)
what is the mechanism of etomidate?
probably potentiates effects of GABA
also causes adrenocortical suppression (more likely under infusion circumstances)
does etomidate affect pain?
what is the redistribution rate of etomidate?
2-8 minutes (elimination is 3-5 hours, narrower than propofol)
what metabolizes etomidate?
liver, excretion in urine and bile (by ester hydrolysis or N-demethylation)
what are the physiologic effects of etomidate?
few. minimal to moderate hypotension and respiratory depression
why isn't etomidate used in neurosurgery?
can cause seizures
what are adverse effects of etomidate?
adrenal suppression, esp. in critically ill patients
increased post-op nausea/vomiting
what are the relative contraindications of etomidate?
critical illness, especially septic shock
history of post-op nausea/vomiting
what street drug is most similar to ketamine?
how do you administer ketamine?
what is the most widely used veterinary anesthesia?
what is commonly used for pediatric anesthesia?
what is ketamine's mechanism of action?
NMDA receptor antagonist, but also effects many other receptor types (GABA A, 5HT-3, opiate receptors- excitatory; nicotinic Ach-R- inhibitory)
why is ketamine used as an analgesic?
agonist for opiate receptors in brain and spinal cord
what phase of ketamine gives desired effects?
S phase (is a racemic mixture)
what drug is a potent bronchodilator?
does ketamine preserve respiration?
what happens in the R phase of ketamine?
undesirable effects (salivating, lacrimation, sympathetic stimulation --> increased myocardial work, increased ICP)
what is the redistribution rate of ketamine?
11-16 minutes (elimination 2-3 hours)
what are adverse effects of ketamine?
sympathetic stimulation - tachycardia, hypertension
why is ketamine administered with a benzo?
to minimize uncomfortable sensation of dissociation
what are relative contraindications for ketamine?
psychosis (loopy + loopy)
extremely compromised myocardial function (low ejection fraction, infarct)
inability to tolerate tachycardia/hypertension (brain bleeds)
what are the indication for ICU sedation?
intolerance of mechanical ventilation
open abdomen (repeat procedures)
status epilepticus (in seizure state)
to decrease metabolic demand (lung disease/bad oxidation)
how are ICU sedation drugs administered?
what are the most common ICU sedation drugs?
dexmedetomidine (A-2 agonist)
what are issues with ICU sedation?
ICU-acquired weakness (atrophy)
tachyphylaxis (drugs work less well)
why do sedative-hypnotics also have anti-emetic activity (anti nausea)?
impact serotonin, dopamine, histamine
review slide for IV anesthetics
what is the target of benzodiazepines?
what is the target of clonidine/dexmedetomidine?
what drugs are dopamine antagonists?
what are melatonin agonists?
melatonin and ramelteon
what is general anesthesia?
behavioral phenotype of drug induced reversible unconsciousness that can be induced by a diverse array of agents
does the behavioral state of general anesthesia reflect a
no, collection of states that share a phenotype
what are the elements of general anesthesia?
akinesia (reduced muscle tone)
how do we know that general anesthesia isn't the same as sleep?
not all anesthetics share the same patterns of neural activity as slow wave sleep
sleeping person would wake up during surgery
what types of anesthesia share some cortical and subcortical patterns of neural activity with slow wave sleep?
(EEG with diffuse slowing, decrease in global cerebra; metabolic rate)
what anesthetics do NOT share neural activity patterns with sleep?
what has a similar EEG pattern to general anesthesia?
is post-operative cognitive decline attributable to general anesthesia?
no, just as likely to come from the procedure itself
what is unique about the therapeutic index of general anesthetics?
very low (4-8, while most drugs have a ratio of over 1000)
why are general anesthetics used at much higher concentrations that other drugs?
weak interactions with receptors (van der waals forces)
do general anesthetics have an effect on all eukaryotes?
yes (even plants)
are there any antagonists for general anesthetics?
what actions can general anesthetics have at a synapse?
alter NT release by acting at
alter NT release by acting
how can general anesthetics impact action potentials?
affect sodium and potassium channels to affect generation and propagation of action potentials
can general anesthetics impact neuronal networks?
yes (e.g. changes in ca2+ conductance can change long term potentiation- observed in altered network properties)
where in the brain do hypnotic anesthetics act?
CNS structures that govern sleep, arousal, and information gathering
1. ascending arousal system: locus coeruleus, ventral tegmental area, basal forebrain
2. sleep active centers (preoptic area)
3. thalamic nuclei that control arousal
4. cortex (enhance inhibitory cortical interneurons, suppressing cortical activity)
are general anesthetics specific?
yes (bind everywhere in the brain, but to very specific molecular targets; sometimes drugs have similar targets)
what are the chemical classes in inhaled anesthetics?
nitrous oxide is a ____ onset/offset drug of hypnotic action
is nitrous oxide soluble?
what receptor does nitrous oxide affect?
NMDA receptor, inhibition
what is the primary use for nitrous oxide?
what is unique about the dosage of nitrous oxide?
provides significant analgesia at
what shares a common frontal EEG pattern from nitrous oxide's EEG?
what are the most common drugs for
what are halogenated ethers a derivative of?
when do you use sevoflurane (ether) to
patients who can't tolerate needles
why can't desflurane and isoflurane (ether) be used on awake patients?
they are mild airway irritants
what is the molecular target of halogenated ethers?
enhanced GABAergic signaling
what is seen on EEG for halogenated ethers?
pronounced slowing and increased amplitude of signaling
is elemental xenon safe?
yes, but use limited by extreme cost
what is the molecular target of elemental xenon?
NMDA receptor inhibition
is elemental xenon used in the US?
what is unique about the EEG for xenon?
patterned like GABAergic halogenated ethers with large slow waves, even though it acts through inhibition of the NMDA receptor
what is another potential use for xenon?
neuroprotection after a stroke
what types of anesthetics are usually used for induction?
intravenous (due to PK - rapidly reach peak plasma concentrations)
what types of anesthetics are usually used for maintenance?
inhalation (due to PK- steady levels after a slower increase due to continuous inhalation)
what can speed up inhaled anesthetic induction (rate of change of blood levels)?
low solubility in blood
increased respiratory rate
increased inhalation of anesthetic
low cardiac output (not significant)
what can slow inhaled anesthetic induction?
high solubility in blood
decreased respiratory rate
decreased inhalation of anesthetic
high cardiac output
what is the relationship between anesthetic agents and partial pressure in alveoli?
increased uptake of anesthetic by the blood creates a bigger difference between inhaled and alveolar concentrations, leading to a
rate of induction
what factors affect anesthetic uptake?
alveolar blood flow (cardiac output)
difference in partial pressure between alveolar gas and venous blood
what reflects the potency of an inhaled anesthetic?
minimum alveolar concentration (MAC)
what is MAC?
alveolar concentration when 50% of the
move with surgical incision
does MAC relate to unconsciousness?
NO (relates to movement in reaction to pain)
what are uses for MAC?
comparing potencies of different drugs
predicting combined effects of different drugs
providing a standard for evaluation
how does MAC relate to brain partial pressure?
mirrors it (reflects an actual, measurable value)
anesthetic's potency directly correlates with.....
affinity for olive oil in a water and oil mixture (meyer-overton correlation)
inhibition of firefly luciferase
where on a protein do general anesthetics bind?
membrane bound lipophilic portion (proteins have large hydrophobic portions)
is there population variability of hypnotic response to inhaled agent?
what is the multi-target theory of inhaled anesthetics?
multi-site mechanism of drug action that explains the odd properties of inhaled anesthetics (lack of inhibitors/adaptation of resistance/conservation of action)
inhaled anesthetics are _______ligands
promiscuous - has a lot of targets (bind specifically to 1-2% of the proteome)
why are there so many side effects from inhaled anesthetics?
have many non therapeutic targets (therefore have low therapeutic ratios)
what is a serious side effect of nitrous oxide?
pernicious anemia (anemia, red tongue, numbness/weakness/paresthesias/unsteady gait/cognitive impairment)
what underlies nitrous oxide pernicious anemia?
oxidation of colbamin atom in vitamin B12 inhibits methionine synthase
why are there neurologic symptoms in NO pernicious anemia?
what are cardiovascular adverse effects of ethers/alkanes?
decreased systemic vascular resistance
through relaxation of vascular smooth muscle leading to hypotension (limiting factor for tolerance of drug)
what are respiratory adverse effects of ethers/alkanes?
decreased hypoxic drive/dependence on CO2 to drive respiratory rate and bronchodilation (but means it can be useful for asthema)
what are renal adverse effects of ethers/alkanes?
decreased renal blood flow, GFR, and urine output
what are GI side effects of ethers/alkanes?
nausea and vomiting
what is the serious metabolic side effect of ethers/alkanes?
- uncontrolled rise in myoplasmic calcium in response to volatile anesthetics or succinylcholine
what is the etiology of malignant hyperthermia?
genetic - mutation of ryanodine receptor RYR1 gene
(common, autosomal dominant)
how do you treat malignant hyperthermia?
dantrolene (direct inhibitor of ryanodine receptors)
what are the signs and symptoms of malignant hyperthermia?
increased CO2 production and O2 consumption
rhabdomyolysis (late in progression)
what are adverse CV effects of nitrous oxide?
myocardial depression in people with already bad hearts
what are adverse respiratory effects of nitrous oxide?
decreased hypoxic drive
what are adverse renal effects of NO?
decreased GFR and urine production due to decrease in renal blood flow
what are adverse metabolic side effects of nitrous oxide?
inhibits B12 dependent enzyme (e.g. methionine synthase that is necessary for DNA methylation)
what inhaled anesthetic is potentially teratogenic?
nitrous oxide (epigenetic changes with prolonged exposure in utero)
what is a potential issue with nitrous oxide diffusion?
diffuses into air filled space and causes expansion (would be bad in the chest)
what are adverse effects of xenon?
nausea and vomiting
moderate decrease in respiratory rate but no minute ventilation change
why do inhaled anesthetics promote nausea?
direct receptor effects e.g. 5-HT receptor stimulation
indirectly through neuronal and circuit-level effects
what coordinates the vomiting response?
what can be used to prevent and treat inhaled anesthetic induced vomiting?
target inputs to solitary nucleus
(5-HT antagonists, NK antagonists, Ach antagonists, H1 antagonists, D2 antagonists)
how do anesthetics open GABAA-R channels?
bind at subunit interfaces within the membrane that make pore easier to open
if anesthetics don't effect GABA, what receptors do they effect and how?
inhibit NMDA receptor (ca2+ flux plays role in long term potentiation and synaptic plasticity)
are anesthetics agonists or antagonists?
antagonists (either in ligand binding domain or direct pore interference)
how do anesthetics impact voltage gated ion channels?
bind the linkage region between voltage-sensor and pore domain to block depolarization and synaptic release
do anesthetics impact hyper-polarization activate channels (HCN)?
yes, inhibit channel functions
what are HCN channels?
non specific neuronal pacemakers that open with hyperpolarization rather than depolarization
contribute to resting membrane potential and generate action potentials; contribute to temporal summation of inputs and normalize synaptic inputs
how do anesthetics impact tandem pore potassium channels (K2P)?
increase flux through channels, causing membrane hyper-polarization and decrease in neuronal firing
what do anesthetics interact with on membrane bound ion channels?
proteins within the membrane domain (they are also hydrophobic, so they bind to the lipophilic portion!)
what is the role of the NMDA receptor signaling/Ca+ flux?
long term potentiation and synaptic plasticity (anesthetics block NMDA signaling)
what are the essential characteristics of local anesthetics?
reversibly block nerve conduction
act on every type of nerve fiber
do not cause structural damage to nerve cell
what nerves are targeted by local anesthetics?
what was the first local anesthetic?
what is the mechanism of action for local anesthetics?
Na+ ion channel stabilizers: block transmission of pain and other signals within the nerve fibers by preventing depolarization, propagation, and conduction along axons
(lesser affinity for blocking K+ channels)
what is use dependence?
degree of nerve blocking is proportional to the rate of stimulation- repeated depolarization increases the fraction of drug-bound channels (more drug molecules enter Na+ channels when they are open and cause more inactivation)
what is the relationship between axon diameter and nerve blockage?
greater diameter, longer it takes to block
what nerves are blocked first in local anesthesia?
small, unmyelinated nerves (Sensory/sympathetic)
what nerves are blocked later in local anesthesia?
large myelinated fibers (motor)
why do small/unmyelinated fibers get blocked first in local anesthesia?
generate long action potentials are high frequency (and blockade is frequency-dependent)
if nerve fibers are of a similar size, what gets blocked first?
are local anesthetics acids or bases?
what is the organic structure of local anesthetics?
lipophilic group/benzene ring + hydrophilic group (tertiary amine) connected by an ester or amide linkage (important for drug metabolism)
how are aminoamides named
with 2 Is (e.g. lidocaine)
how are aminoesthers named
one i (e.g. procaine)
what compound is responsible for allergic reactions to aminoester local anesthetics?
p-aminobenzoic acid metabolite (PABA)
how are aminoesters broken down?
RAPIDLY by plasma cholinesterase enzymes (none in CSF)
is there cross reactivity between local anesthetics?
how are aminoamides broken down?
SLOWLY by liver
which class of local anesthetics has increased risk of systemic toxicity?
which class of local anesthetic breaks down in heat/sun?
is onset of action slow or fast for aminoesters?
is onset of action slow or fast for aminoamides?
moderate to fast
what are the clinical uses of local anesthetic?
prevention and tx of cardiac arrhythmia
blunt stress response to direct laryngoscopy
management of increased ICP
treatment of neuropathic pain/chronic pain syndromes
are allergic reactions to local anesthetics common?
no (when they occur, most likely due to esters)
activity of local anesthetics is a function of what five things?
lipid solubility (potency)
affinity for protein binding (duration of action)
percent ionization at physiologic pH (pKa)
are ionized drugs lipid soluble?
why are local anesthetics weak bases?
more molecules will be in the unionized, soluble form with more rapid onset of action (lipid soluble)
how can you maximize the effect of a local anesthetic?
increase the pH by adding bicarbonate
why doesn't local anesthetic work around infection/abscess?
infection is an acidic medium (pKa)
what is fetal ion trapping syndrome?
baby pH is acidic so can trap anesthetic during delivery
how is local anesthetic drug potency related lipid solubility?
nerve membrane is almost entirely lipid, so lipid solubility improves movement across cell membrane
how is protein binding related to duration of drug action?
the more protein that is bound to the drug, the longer drugs can bind to neuronal membrane proteins--- this increases the duration of drug action
(protein provides depot for maintenance of neural blockage)
what drugs have 95% bound protein and in turn, longer duration of action?
what drugs have a 6% bound protein and therefore shorter duration of action?
what drugs have 55-75% bound protein and therefore an intermediate duration of action?
after injection of a local anesthetic for an incision and drainage of an abscess, the surgeon notes the patient is still uncomfortable. why?
local anesthetic cannot cross the nerve membrane
(ionized/acidic form is not lipid soluble)
what are possible toxicities of local anesthetic?
allergy to local anesthetic
what are the initial symptoms of CNS toxicity to local anesthetic?
visual and auditory disturbances (tinnitus, difficulty focusing)
what are the higher dose symptoms of CNS toxicity to local anesthetic?
muscle twitching, convulsions, unconsciousness
coma, respiratory depression and arrest
when do more serious symptoms of CNS toxicity to local anesthetic occur?
after initial CNS excitation (followed by
what can influence CNS toxicity to local anesthetic?
plasma concentrations (drug specific)
rate of injection
inverse relationship between PaCO2 and LA
hyperkalemia (promotes depolarization)
which local anesthetic is very cardiotoxic?
what cardiovascular toxicities can occur with local anesthetic agents?
negative inotropic effects on muscle causing hypotension
how do you treat cardiac toxicity?
lipid emulsion bolus infusion for 30 minutes (IV, repeat if cardiac collapse, double rate if BP returns but remains low)
can propofol be used as an alternative for intralipid in resuscitation of La indued cardiac toxicity?
only in low doses (can further depress the myocardium)
what hematologic sign is reported in association with benzocaine and lidocaine use?
is methemglobinemia always symptomatic?
only at high levels (10-40%)
what are the clinical symptoms of methemoglobinemia?
cyanosis, tachypnea, exercise intolerence
fatigue, dizziness, syncope, weakness
how do you treat hematologic toxicity from LA?
what are the most common LAs to cause allergic reaction?
what is suggestive of a local anesthetic allergy?
rash, urticaria, laryngeal edema, hypotension, bronchospasm
why is epinephrine a common adjuvant of local anesthetics?
increases neuronal uptake (higher local concentration)
vasoconstrictor (reduces systemic absorption/blood levels)
when is the effect of epinephrine particularly significant?
when used with local anesthetics with immediate/short duration of action
why shouldn't you use epinephrine when there is a nerve injury?
inhibits nerve regeneration
what is the action of clonidine as an adjuvant to LA?
longer duration of drug action - alpha 2 receptor agonist
what local anesthetic has intrinsic sympathomimetic (sympathetic stimulation) activity?
why may dexamethasone prolong anesthesia?
longer sensory and motor block due to site-specific vasoconstriction, anti-inflammatory effects, and immunosuppressive effects
possible systemic effects
how does dexamethasone decrease nociception?
increases activity of inhibitory potassium channels on nociceptive C fibers, decreasing their activity
what is a liposome?
artificial drug carrier - has lipid layers surrounded by aqueous layers that can penetrate the stratum corneum b/c they resemble lipid bilayers of cell membrane
possible use as extended release pain management mechanism/prolongs duration of analgesia
what is methemoglobinemia?
heme toxicity of local anesthetic when hemoglobin is oxidized by O-toludine to methemoglobin, only symptomatic at high levels
why does epinephrine have a lesser effect on more lipid soluble LA agents (bupivacaine)?
lipid solubility of bupivacaine keeps them intrinsically in the local tissue site, so not necessary
what is an opiate?
narcotic opioid alkaloid found in natural products such as the opium poppy
what is an opioid?
natural or synthetic drug that is an
what is the natural source of morphine and codeine?
can the body produce morphine endogenously?
yes (a type of endorphin)
what compounds are the basis of synthetic opioids?
morphine or precursor compounds (e.g. fentanyl)
what is the function of the Mu opioid receptor?
what is the function of the Kappa opioid receptor?
dysphoria (unpleasant effect)
what is the function of the delta opioid receptor?
(pharmacological effects unclear)
do opiate receptors have subtypes?
yes, all have different pharmacological effects
what is the function of mu 1 receptors?
what is the function of mu 2 receptors?
reduced GI motility
what is the function of mu 3 receptors?
is there polymorphism in opioid receptors?
yes, different people have different receptors (e.g. 118AOG OPRM1 polymorphism carriers need more drugs for pain relief)
what is a pure agonist?
has affinity for receptor binding AND efficacy
what us a pure antagonist?
has affinity for binding but NO efficacy, so blocks the action of ligands
what is a mixed agonist-antagonist?
produces an agonist effect at one receptor, while producing an antagonist effect at another
what is a partial agonist?
has affinity for receptor binding but LOW efficacy
opioids are a major medication for ___________ pain
moderate and severe
patients usually receive opioids in the _______ period
perioperative (but people still have a lot of pain!)
do all patients get the same amount of pain relief, and side effects, from opioids?
no! not all opioids and patients are the same
what are major issues with opioid usage?
what is tolerance?
a diminished response to a drug's action (seen with many compounds)
what is the physiological basis of tolerance?
changes in binding of drug to receptor OR changes in receptor transduction processes related to the drug
what are the results of tolerance?
decreased effect from a constant dose of a drug
increase in minimum dose required to produce a given level of effect
what is dependence?
when a drug is necessary for normal physiological functioning
what are withdrawal reactions?
response to dependence with physiologic effects that are opposite to those produced by the drug
what is the recommendation for acute postop pain?
multi-modal analgesia (use of variety of medications, techniques, and non-pharmacological interventions)
what is recommended for parenteral post-operative pain control?
intravenous patient-controlled analgesia (PCA)
what should you never give to a patient on PCA?
basal infusion of opioids with IV (can lead to overdose)
what can be given pre-operatively as a pain treatment adjuvant?
oral celecoxib (COX-2 inhibitor
what is a good component for multi-modal analgesia?
calcium channel blockers (gabapentin/pregabalin)
what drug is good for open/laparoscopic abdominal surgery pain relief?
___________________________ can be used in adults and children for procedures with evidence of efficacy
site-specific regional anesthetic techniques
morphine is an __________ ligand
is morphine fast acting?
no. slow rise to peak effects, ~90 min (slow receptor binding)
what can generate adverse/non intended effects from drugs?
active metabolites (cause problems if they accumulate, esp if there is renal failure)
what is the active metabolite of morphine?
what is the rapid onset form of morphine?
hydromorphone (better lipid solubility, much more potent)
why don't you use morphine in asthma patients?
can release a lot of histamine
does hydromorphone have active metabolites?
why is hydromorphone a good choice for postoperative PCA?
why is fentanyl a commonly used drug?
no active metabolites
potent and efficacious
many forms of administration (can be absorbed by mucosa)
what slow onset drug is more potent than morphine?
why is Sufentanil used in neurosurgery?
rapid recovery, patients wake up quickly for evaluation
do fentanyl derivatives have active metabolites?
why is remifentanil quick action/short acting?
lipid solubility & ester metabolism
what population needs a lower dose of remifentanil?
why are morphine and hydromorphone used for PCA in the perioperative period?
can reach a relatively stable therapeutic dose
is methadone a good option for PCA?
no, it has a long half life and can accumulate to a steady state, making it difficult to titrate
what form of methadone is a mu opiate agonist?
L methadone (racemic mixture)
what form of methadone is an NMDA receptor antagonist?
R methadone (racemic mixture)
what is buprenorphine?
(partial agonist - mu opioid receptor
partial antagonist- kappa opioid receptor)
what can be used for addiction therapy besides methadone?
kappa opioid receptor antagonists
opioid pharmacokinetics depend on ______ and _________
are all opioids lipid soluble?
why can fentanyl cross the blood CSF barrier more rapidly to produce faster analgesic effects?
higher lipid solubility
what is the least lipid soluble mu agonist/opioid?
what is the most lipid soluble mu agonists/opioid?
______ opioids can be easily replaced by ________opioids
weak binding, strong binding
is buprenorphine easily replaced by other opioid ligands at binding sites?
no, has a very strong affinity with receptors
what is naloxone?
opioid receptor antagonist with quick onset of action to reverse respiratory depression and unconsciousness
what are the pros of using acetaminophen?
minimal anti-inflammatory effects peripherally
fewer adverse effects than other non-opioid analgesics
no effect on platelet function
what are adverse effects of acetaminophen?
risk for hepatotoxicity at high doses (increased risk with liver disease or chronic alcoholism)
what are the adverse effects of NSAIDs?
affects coagulation and GI function/toxicity, renal toxicity, bleeding diathesis
what is the mechanism of NSAIDs?
inhibits peripheral and central cyclo-oxygenase (COX1/2), reducing prstaglandin formation
are NSAIDs specific?
no, but is effective against pain related to inflammation
are the effects of NSAIDs dose dependent?
yes (both pain relief and side effects)
what are effective adjuvant analgesics?
Alpha-2 adrenergic agonists
NMDA receptor antagonists (ketamine)
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