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Anesthesia Flashcards

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1
Q

Name (3) forms of opiod receptors that are used by endogenous and exogenous opiods

A

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

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2
Q

alpha, beta, and gamma endorphins (endogenous opiods) bind to _ receptors

A

alpha, beta, and gamma endorphins (endogenous opiods) bind to Mu receptors

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3
Q

Enkephalins (endogenous opiods) bind to _ receptors

A

Enkephalins (endogenous opiods) bind to delta receptors

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4
Q

Dynorphins (endogenous opiods) bind to _ receptors

A

Dynorphins (endogenous opiods) bind to kappa receptors

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5
Q

Codeine, morphine, hydrocodone, oxycodone, etc are examples of [class drugs]

A

Codeine, morphine, hydrocodone, oxycodone, tramadol, etc are examples of full MOR agonists
* MOR = mu opiod receptor

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6
Q

Buprenorphine and nalbuphine are exogenous opiods which are [drug class]

A

Buprenorphine and nalbuphine are exogenous opiods which are partial MOR agonists

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7
Q

Methylnaltrexone is a drug that acts as [drug class]

A

Methylnaltrexone is a drug that acts as peripherally acting MOR antagonist
* Other PAMORAs include alvimopan, naldemedine, naloxegol, pentazocine

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8
Q

_ and _ are two inverse agonists of MOR

A

Naloxone and Naltrexone are two inverse agonists of MOR

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9
Q

A drug from [drug category] or [drug category] class would be used for opioid reversal

A

A drug from neutral antagonist or inverse agonist class would be used for opioid reversal

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10
Q

Inverse MOR agonists are extremely effective becuase they inhibit _

A

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

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11
Q

Opiods _ the ascending pain pathways and _ descending modulatory pathways

A

Opiods inhibit the ascending pain pathways and stimulate descending modulatory pathways

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12
Q

Pre-synpatically, opioids act on _ channels

A

Pre-synpatically, opioids act on Ca2+ channels (inhibiting them)
* This inhibits NT release and transmission of ascending pain signal

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13
Q

Post-synaptically, opioids act on _ channels

A

Post-synaptically, opioids act on K channels (opening them) –> hyperpolarization
* * This inhibits NT release and transmission of ascending pain signal

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14
Q

Opiods act on the pre-synapse of modulatory pain neurons to _ the release of _ and turn on the modulation

A

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

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15
Q

Opioids act on the _ synapse to essentially stimulate the descending modulatory pathway and induce analgesia

A

Opioids act on the presynapse to essentially stimulate the descending modulatory pathway and induce analgesia

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16
Q

The glucuronidated forms of many opioids have slower _ and longer _

A

The glucuronidated forms of many opioids have slower renal clearance and longer durations of action

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17
Q

[Opioid] gets converted into morphine

A

Codeine gets converted into morphine
* Morphine and its derivatives can be neurotoxic

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18
Q

All opioids can cause _ and _ as CNS toxicities

A

All opioids can cause sedation and respiratory depression as CNS toxicities
* This is ultimately what causes opioid overdose death

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19
Q

Because Mu receptors are found all throughout the GIT, opioids can cause [toxicity]

A

Because Mu receptors are found all throughout the GIT, opioids can cause constipation
* We inhibit neuron firing in the gut and slow GI motility

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20
Q

[Drug class] can be used to treat opioid induced constipation

A

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

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21
Q

Because opioids inhibit GABA release to turn on the descending modulatory pathway, they additionally induce [toxicity]

A

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

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22
Q

_ is a good drug option for patients with opioid addiction because its properties treat physical and psychological dependence

A

Buprenorphine is a good drug option for patients with opioid addiction because its properties treat physical and psychological dependence

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23
Q

Buprenorphine is (more/less) potent than a full MOR agonist

A

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

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24
Q

NSAID works as an anti-inflammatory, non-opioid analgesic via [receptor action] and [downstream effect]

A

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

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25
_ and _ are the prostaglandins that mediate pain receptors
**PGE2** and **PGF2a** are the prostaglandins that mediate pain receptors
26
? --> COX --> prostaglandins
**Arachidonic acid** --> COX --> prostaglandins
27
[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)*
28
_ is the only "selective" NSAID on the market
**Celecoxib** is the only "selective" NSAID on the market * *Specific to COX-2*
29
_ 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)
30
NSAIDs can lead to hypertension via [mechanism (hint kidneys)]
NSAIDs can lead to hypertension via **reducing GFR --> decreasing Na+/ H2O excretion --> increased blood volume**
31
COX-1 inhibition leads to [toxicity]
COX-1 inhibition leads to **inhibition of gastric mucus production** * *Increases risk of upper and lower GI bleeding*
32
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)
33
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*
34
_ 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*
35
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**
36
Celecoxib increases MI risk via blocking [prostaglandin] preferentially
Celecoxib increases MI risk via blocking **PGI2** preferentially
37
_ 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*
38
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**
39
All local anesthetics work via [mechanism]
All local anesthetics work via **inhibition of Na+ channels**
40
Local anesthetics come in either [chemical form] or [chemical form]
Local anesthetics come in either **amide** or **ester** form
41
Procaine, chloroprocaine, cocaine, and tetracaine are all [structure] local anesthetics
Procaine, chloroprocaine, cocaine, and tetracaine are all **esters** (local anesthetics)
42
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*
43
All local anesthetics are [acid/base status]
All local anesthetics are **weak bases**
44
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*
45
[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
46
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
47
Areas of infection can have _ pH, making local anesthetic _
Areas of infection can have **low (acidic)** pH, making local anesthetic **slower to onset**
48
Hydrophobic drugs are (more/less) potent
Hydrophobic drugs are **more** potent
49
Hydrophobic drugs have (shorter/longer) durations
Hydrophobic drugs have **longer** durations
50
Hydrophobic drugs have (shorter/longer) onset times
Hydrophobic drugs have **longer** onset times * *Due to binding to extracellular proteins*
51
Local anesthetics must be in _ form to bind Na+ channel
Local anesthetics must be in **hydrophilic** form to bind Na+ channel
52
Which is more sensitive to local anesthetics, small unmyelinated or large myelinated?
**small unmyelinated** small myelinated > small unmyelinated > large myelinated > large unmyelinated
53
Neurons that rapidly fire are (more/less) sensitive to local anesthetics
Neurons that rapidly fire are **more sensitive** to local anesthetics * ie nociceptors
54
_ 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*
55
_ can treat local anesthetic overdose
**IV lipid emulsion** can treat local anesthetic overdose * *To redistribute to muscle and liver*
56
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*
57
Drugs that potentiate GABA-A action promote _
Drugs that potentiate GABA-A action promote **Cl- influx --> hyperpolarization --> reduced neuronal firing --> unconsciousness**
58
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**
59
In general, inhaled anesthetics are not cleared by the liver, they are cleared just by _
In general, inhaled anesthetics are not cleared by the liver, they are cleared just by **exhalation**
60
The MAC represents the _
The MAC represents the **concentration of inhaled drug in the alveoli that produces a lack of response to surgical stimulation in 50% of patients**
61
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*
62
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
63
The onset time has to do with the inhaled general anesthetic's [characteristic]
The onset time has to do with the inhaled general anesthetic's **blood solubility** * *Also called the blood/gas partition coefficient*
64
The potency has to do with the inhaled general anesthetic's [characteristic]
The potency has to do with the inhaled general anesthetic's **lipophilicity/ L-G partition coefficient**
65
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*
66
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*
67
_ 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*
68
_ is the drug of choice to treat malignant hyperthermia
**Dantrolene** is the drug of choice to treat malignant hyperthermia
69
Dantrolene works to treat MH via [mechanism]
Dantrolene works to treat MH via **inhibiting Ca2+ flow through the ryanodine receptor**
70
Propofol (IV) has a rapid recovery due to _
Propofol (IV) has a rapid recovery due to **rapid redistribution to adipose tissue**
71
_ 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*
72
_ is a GA that works by glutamate antagonism
**Ketamine** is a GA that works by glutamate antagonism * *Blocks NMDA receptors*
73
Ketamine toxicity includes _ and _
Ketamine toxicity includes **dissociative effects** and **psychotomimetic effects**
74
Dexmedetomidine is a GA with [mechanism]
Dexmedetomidine is a GA with **alpha2 receptor agonist that activates the VLPO nucleus**
75
_ GA has maintains a relatively stable blood pressure and respiratory rate
**Etomidate** has maintains a relatively stable blood pressure and respiratory rate
76
Ketamine can cause [BP]
Ketamine can cause **hypertension** * *Whereas most others can cause hypotension*
77
_ 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"*
78
Non-depolarizing NMBA drugs work by [Moa]
Non-depolarizing NMBA drugs work by **competitively blocking Ach binding and channel opening**
79
Succinylcholine works by [Moa]
Succinylcholine works by **perisistently opening Nm channels and exhausting the muscle cell**
80
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*
81
"-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**
82
NMBAs can be reversed with [drug]
NMBAs can be reversed with **neostigmine** * *Acetylcholinesterase inhibitor*
83
In addition to neostigmine, NMBAs should be reversed with _
In addition to neostigmine, NMBAs should be reversed with **glycopyrrolate** * *M2/M3 antagonist to prevent parasympathetic toxicities*

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