Anesthesia Flashcards
Name (3) forms of opiod receptors that are used by endogenous and exogenous opiods
Name (3) forms of opiod receptors that are used by endogenous and exogenous opiods
1. Mu
2. Delta
3. Kappa
All exogenous opiods activate MOR to produce analgesia
alpha, beta, and gamma endorphins (endogenous opiods) bind to _ receptors
alpha, beta, and gamma endorphins (endogenous opiods) bind to Mu receptors
Enkephalins (endogenous opiods) bind to _ receptors
Enkephalins (endogenous opiods) bind to delta receptors
Dynorphins (endogenous opiods) bind to _ receptors
Dynorphins (endogenous opiods) bind to kappa receptors
Codeine, morphine, hydrocodone, oxycodone, etc are examples of [class drugs]
Codeine, morphine, hydrocodone, oxycodone, tramadol, etc are examples of full MOR agonists
* MOR = mu opiod receptor
Buprenorphine and nalbuphine are exogenous opiods which are [drug class]
Buprenorphine and nalbuphine are exogenous opiods which are partial MOR agonists
Methylnaltrexone is a drug that acts as [drug class]
Methylnaltrexone is a drug that acts as peripherally acting MOR antagonist
* Other PAMORAs include alvimopan, naldemedine, naloxegol, pentazocine
_ and _ are two inverse agonists of MOR
Naloxone and Naltrexone are two inverse agonists of MOR
A drug from [drug category] or [drug category] class would be used for opioid reversal
A drug from neutral antagonist or inverse agonist class would be used for opioid reversal
Inverse MOR agonists are extremely effective becuase they inhibit _
Inverse MOR agonists are extremely effective becuase they inhibit basal MOR activity
* MOR receptors signal in the absence of agonist
* Drugs like naloxone can turn off the agonist-independent signaling and antagonize the natural agonist
Opiods _ the ascending pain pathways and _ descending modulatory pathways
Opiods inhibit the ascending pain pathways and stimulate descending modulatory pathways
Pre-synpatically, opioids act on _ channels
Pre-synpatically, opioids act on Ca2+ channels (inhibiting them)
* This inhibits NT release and transmission of ascending pain signal
Post-synaptically, opioids act on _ channels
Post-synaptically, opioids act on K channels (opening them) –> hyperpolarization
* * This inhibits NT release and transmission of ascending pain signal
Opiods act on the pre-synapse of modulatory pain neurons to _ the release of _ and turn on the modulation
Opiods act on the pre-synapse of modulatory pain neurons to inhibit the release of GABA and turn on the modulation
* They disinhibit the descending modulatory pathway
Opioids act on the _ synapse to essentially stimulate the descending modulatory pathway and induce analgesia
Opioids act on the presynapse to essentially stimulate the descending modulatory pathway and induce analgesia
The glucuronidated forms of many opioids have slower _ and longer _
The glucuronidated forms of many opioids have slower renal clearance and longer durations of action
[Opioid] gets converted into morphine
Codeine gets converted into morphine
* Morphine and its derivatives can be neurotoxic
All opioids can cause _ and _ as CNS toxicities
All opioids can cause sedation and respiratory depression as CNS toxicities
* This is ultimately what causes opioid overdose death
Because Mu receptors are found all throughout the GIT, opioids can cause [toxicity]
Because Mu receptors are found all throughout the GIT, opioids can cause constipation
* We inhibit neuron firing in the gut and slow GI motility
[Drug class] can be used to treat opioid induced constipation
Peripherally acting mu opioid receptor antagonist (PAMORAs) can be used to treat opioid induced constipation
* They do not cross the BBB to interfere with opioid analgesia
Because opioids inhibit GABA release to turn on the descending modulatory pathway, they additionally induce [toxicity]
Because opioids inhibit GABA release to turn on the descending modulatory pathway, they additionally induce dopamine release
* Increase DA release into the nucleus accumbens via the mesolimbic pathway –> addiction
_ is a good drug option for patients with opioid addiction because its properties treat physical and psychological dependence
Buprenorphine is a good drug option for patients with opioid addiction because its properties treat physical and psychological dependence
Buprenorphine is (more/less) potent than a full MOR agonist
Buprenorphine is more potent than a full MOR agonist
* Although it is less effective, it is more potent so it outcompetes any full agonist that may be co-administered
NSAID works as an anti-inflammatory, non-opioid analgesic via [receptor action] and [downstream effect]
NSAID works as an anti-inflammatory, non-opioid analgesic via inhibiting COX-2 receptors and blocking prostaglandin synthesis
* Most are non-selective and block COX-1 and COX-2
_ and _ are the prostaglandins that mediate pain receptors
PGE2 and PGF2a are the prostaglandins that mediate pain receptors
? –> COX –> prostaglandins
Arachidonic acid –> COX –> prostaglandins
[COX receptor] is constitutive while [COX receptor] is induced
COX-1 is constitutive while COX-2 is induced
* Meaning COX-1 is always on in the background for homeostatic functions while COX-2 is only used for inflammatory functions when necessary (pain, fever, etc)
_ is the only “selective” NSAID on the market
Celecoxib is the only “selective” NSAID on the market
* Specific to COX-2
_ and _ are two important prostaglandins that act as vasodilators (especially important in the kidney)
PGE2 and PGI2 are two important prostaglandins that act as vasodilators (especially important in the kidney)
NSAIDs can lead to hypertension via [mechanism (hint kidneys)]
NSAIDs can lead to hypertension via reducing GFR –> decreasing Na+/ H2O excretion –> increased blood volume
COX-1 inhibition leads to [toxicity]
COX-1 inhibition leads to inhibition of gastric mucus production
* Increases risk of upper and lower GI bleeding
Non-aspirin NSAIDs may increase clotting risk due to preferential inhibition of [prostaglandin] synthesis (which normally inhibits platelet activation)
Non-aspirin NSAIDs may increase clotting risk due to preferential inhibition of PGI2 synthesis (which normally inhibits platelet activation)
Aspirin preferentially blocks [prostaglandin] which normally promotes platelet activation
Aspirin preferentially blocks thromboxane A2 which normally promotes platelet activation
* Therefore it can lower MI and stroke risk
_ is a possible toxicity of aspirin in children who have a viral infection
Reye’s syndrome is a possible toxicity of aspirin in children who have a viral infection
* This is why sick kids should take acetaminophen or ibuprofen instead
Although celecoxib decreases anti COX-1 toxicities (GI upset), it carries an increased risk of _
Although celecoxib decreases anti COX-1 toxicities (GI upset), it carries an increased risk of MI
Celecoxib increases MI risk via blocking [prostaglandin] preferentially
Celecoxib increases MI risk via blocking PGI2 preferentially
_ is a COX-1/2 inhibitor that is not anti-inflammatory but is anti-pyretic
Acetaminophen is a COX-1/2 inhibitor that is not anti-inflammatory but is anti-pyretic
* It does act in the CNS and periphery
One toxicity of acetaminophen (especially in alcoholics) is liver toxicity due to build up of [toxic metabolite]
One toxicity of acetaminophen (especially in alcoholics) is liver toxicity due to build up of NAPQI
Procaine, chloroprocaine, cocaine, and tetracaine are all [structure] local anesthetics
Procaine, chloroprocaine, cocaine, and tetracaine are all esters (local anesthetics)
Articaine, lidocaine, mepivacaine, bupivacaine, etidocaine, levobupivacaine, ropivacaine are all [structure] local anesthetics
Articaine, lidocaine, mepivacaine, bupivacaine, etidocaine, levobupivacaine, ropivacaine are all amides
* Alll amide drugs have “i” early in their name
All local anesthetics are [acid/base status]
All local anesthetics are weak bases
The fewer the VG Na+ channels the easier the axonal action potential is blocked, such as in _ axons
The fewer the VG Na+ channels the easier the axonal action potential is blocked, such as in myelinated axons
* Small, myelinated axons are easiest to block
[Drugs] must enter the neuron in order to access the Na+ channel from within
Local anesthetics must enter the neuron in order to access the Na+ channel from within
Only _ form of the local anesthetic can pass through the plasma membrane
Only the uncharged, hydrophobic form of the local anesthetic can pass through the plasma membrane
Areas of infection can have _ pH, making local anesthetic _
Areas of infection can have low (acidic) pH, making local anesthetic slower to onset
Hydrophobic drugs are (more/less) potent
Hydrophobic drugs are more potent
Hydrophobic drugs have (shorter/longer) durations
Hydrophobic drugs have longer durations
Hydrophobic drugs have (shorter/longer) onset times
Hydrophobic drugs have longer onset times
* Due to binding to extracellular proteins
Local anesthetics must be in _ form to bind Na+ channel
Local anesthetics must be in hydrophilic form to bind Na+ channel
Which is more sensitive to local anesthetics, small unmyelinated or large myelinated?
small unmyelinated
small myelinated > small unmyelinated > large myelinated > large unmyelinated
Neurons that rapidly fire are (more/less) sensitive to local anesthetics
Neurons that rapidly fire are more sensitive to local anesthetics
* ie nociceptors
_ can be adminstered with local anesthetics in order to decrease clearance, bleeding, systemic effects
Epinephrine can be adminstered with local anesthetics in order to decrease clearance, bleeding, systemic effects
* Helps to keep the effect local
_ can treat local anesthetic overdose
IV lipid emulsion can treat local anesthetic overdose
* To redistribute to muscle and liver
Most general anesthetics (inhaled and IV) work by [mechanism]
Most general anesthetics (inhaled and IV) work by potentiating GABA-A receptors
* Ex: nitrous oxide, isoflurane, etomidate, propofol, thiopental
* Be careful, they are not agonists, they work indirectly as potentiators
Drugs that potentiate GABA-A action promote _
Drugs that potentiate GABA-A action promote Cl- influx –> hyperpolarization –> reduced neuronal firing –> unconsciousness
The potency of inhaled general anesthetics has to do with the drug’s [characteristic]
The potency of inhaled general anesthetics has to do with the drug’s hydrophobicity
The more hydrophobic the inhaled anesthetic, the _ the MAC
The more hydrophobic the inhaled anesthetic, the lower the MAC
* MAC = minimum alveolar concentration
* MAC and lipophilicity are inversely related
The lower the MAC, the _ the potency
The lower the MAC, the higher the potency
* Low MAC = high L/G coefficient = most lipophilic = most potent
The IGA with the _ will have the fastest onset time
The IGA with the lowest blood solubility will have the fastest onset time
* Since you have to saturate the blood before it can spill over to the brain
Less water-soluble drugs saturate the blood _
Less water-soluble drugs saturate the blood faster
* More water soluble drugs take longer and therefore have longer onset time
_ general anesthetics have a higher risk of post-operative nausea/vomiting
Inhaled general anesthetics have a higher risk of post-operative nausea/vomiting
* It is less common with IV anesthetics
Dantrolene works to treat MH via [mechanism]
Dantrolene works to treat MH via inhibiting Ca2+ flow through the ryanodine receptor
Propofol (IV) has a rapid recovery due to _
Propofol (IV) has a rapid recovery due to rapid redistribution to adipose tissue
_ is a GA with a toxicity of decreased cortisol synthesis and adrenal crisis (especially in elderly patients)
Etomidate is a GA with a toxicity of decreased cortisol synthesis and adrenal crisis (especially in elderly patients)
* It blocks 11-dehydroxylase
_ is a GA that works by glutamate antagonism
Ketamine is a GA that works by glutamate antagonism
* Blocks NMDA receptors
Dexmedetomidine is a GA with [mechanism]
Dexmedetomidine is a GA with alpha2 receptor agonist that activates the VLPO nucleus
Ketamine can cause [BP]
Ketamine can cause hypertension
* Whereas most others can cause hypotension
_ is a depolarizing NMJ Nm receptor inhibitor
Succinylcholine is a depolarizing NMJ Nm receptor inhibitor
* All of the others are non-depolarizing drugs, “-curium” and “-curonium”
Succinylcholine works by [Moa]
Succinylcholine works by perisistently opening Nm channels and exhausting the muscle cell
Because succinylcholine persistently depolarizes, it is associated with [toxicity]
Because succinylcholine persistently depolarizes, it is associated with hyperkalemia
* Also can lead to malignant hyperthermia in sensitive patients
“-Curium” drugs undergo a non-enzymatic chemical breakdown which means it is still cleared effectively even in patients with _
“-Curium” drugs undergo a non-enzymatic chemical breakdown which means it is still cleared effectively even in patients with liver and renal insufficiency
