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Pharm Unit 3 > Anesthetics I and II > Flashcards

Anesthetics I and II Flashcards

1
Q

Glutamate is the; GABA is

what can volatile anesthetics do to either?

A

major excitatory NT in the brain;
an inhibitory NT in the brain;

they can inhibit glutamate release; they can increase and decrease GABA release

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2
Q

Glutamate receptor is a; GABA A receptor is

A

tetrameric protein with structurally related subunits; going to have 5 non-identical subunits

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3
Q

NMDA receptors and some facts on it

A
  1. glutamate-activated ion channels
  2. They conduct Na, K, Ca, and modulate long term synaptic responses
  3. Volatile anesthetics might INHIBIT NMDA receptors
  4. Ketamine is a potent and SELECTIVE inhibitor of NMDA receptors
  5. N2O can selectively inhibit NMDA receptors
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4
Q

GABA-activated ion channels and facts

A
  1. Most important inhibitory NT in CNS
  2. GABA A receptor mediates postsyn response by selectively allowing Cl ions to enter, hyperpolarizing neurons
  3. Modulated by barbs, anesthetic steroids, benzos; propofol, etomidate; volatile anesthetics
  4. Barbs, propofol, volatile anesthetics increase freq/length of time Cl channels are open (CONFORMATIONAL change in GABA A receptor); they likely bind to different sites on receptor
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5
Q

Glycine-activated ion channels:

A

glycine most important inhibitory NT in the spinal cord and brainstem

  1. Cl selective ion channel
  2. volatile anesthetics potentiate glycine acttivated currents and increase receptor affinity for glycine (could contribute to ANESTHETIC action)
  3. Propofol, alphaxalone, pentobarb can do same as 2
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6
Q

Meyer-Overton rule; unitary theory of anesthesia:

A

potency of anesthetic gases directly related to their solubility in OLIVE OIL;
variety of structurally unrelated drugs obey rule, they MUST bind at same hydrophobic site

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7
Q

Potency of inhibition correlates with; what is luciferase?

A

potency of anesthetic;

water soluble protein inhibited by anesthetics, and likely the anesthetics bind to the HYDROPHOBIC pockets on proteins like luciferase

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8
Q

SE’s of halothane? methoxyflurane?

A

Dysrhythmogenic, liver toxicity, hypotension;

hepatic metabolism increases Fl and then nephrotoxicity

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9
Q

What is the boiling point of desflurane?

A

22.8 degrees C

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10
Q

Inhaled anesthetics and course of uptake and distribution?

A
  1. absorbed from alveoli into pulmonary capillary blood (uptake)
  2. DISTRIBUTED to site of action (brain) and RESERVOIRS (vessels, muscle, fat)
  3. Variably metabolized
  4. eliminated principally via lungs
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11
Q

Henry’s Law? Also a partition coefficient is

A

concentration of gas dissolved in solution is DIRECTLY PROPORTIONAL to partial pressure of gas above solution;

ratio of solubilities of a gas between two compartments, e.g. blood:gas, brain:blood, at EQULIBRIUM
THINK: insoluble agents need FEW mc’s present in blood to raise the agent’s partial pressure

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12
Q

Equilibration between two phases for an anesthetic gas means

A

same PARTIAL PRESSURE of gas exists in both phases; however, does NOT mean same concentration exists in both phases

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13
Q

______ propel anesthetic to brain

A

Partial pressure gradients (e.g. equlibration between alveolar, pulmonary capillary blood, and brain partial pressures!!)

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14
Q

What determines PA? Factors to increase it?

A

Delivery of anesthetic to alveoli minus uptake of anesthetic into the blood:
increase delivery to alveoli:
1. increase inhaled partial pressure of agent (concentration effect, 2nd gas effect)
2. Increased alveolar ventilation
3. Decreased FRC (the RESERVOIR)

decrease uptake by blood

  1. decrease blood solubility of agent
  2. Decrease CO
  3. Decrease gradient between PA and Pa
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15
Q

What happens with inhaled partial pressure by the time it reaches the alveoli? How do you deal with this?

A

It’s been diluted b/c it mixes with gas in anesthesia circuit and gas in patient’s lungs;
INCREASE PI above what you need to induce anesthesia

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16
Q

2nd gas effect is what

A
  1. ability of high volume uptake of one gas (N2O) to accelerate rate of increase in PA of a second gas (your potent anesthetic agent)
  2. the large volume uptake of N2O increases concentration of remaining gases (O2 and anesthetic) in resulting SMALLER lung volume
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17
Q

Speed of anesthetic induction is determined by; poorly soluble agents

A

rate of rise of alveolar concentration of the anesthetic agent (FA/FI);
rapidly achieve a high alveolar concentration and induction occurs really quick (FA/FI = 1)

18
Q

MAC is; other facts?; site of action

A

concentration of inhaled anesthetic agent at which 50% of patients WON’T move in response to surgical incision (ED 50);
related to SOLUBILITY in olive oil;
MACs are additive;
to produce immobility is the spinal cord (depression of excitation, enhancement of inhibition) and LOSS OF AWARENESS and recall occurs at .4-.5

19
Q

What increases MAC? What decresaes it?

A
  1. Hyperthermia 2. Pheomelanin (red hair) 3. Increased CNS catecholamines 4. Cyclosporine 5. Hypernatremia 6. Increased central NT’s (MAOIs, cocaine, ephedrine, L-DOPA)
  2. Hypothermia 2. Increased age 3. Opposite of 3 above 4. Opioids, anxiolytics, alpha-2 agonists, lidocaine 5. hyponatremia 6. Pregnancy/post partum period
20
Q

N2O: class, mechs, thera, SE’s, other SE’s, misc

A

Class: -
Mech: NMDA receptor antagonist
Thera: Mask induction in children
Important SE’s: Post-operative nausea and vomiting; inactivates vitamin B (leading to abnormal embryonic development, abortion); accumulates in closed, air-containing spaces (bowel, middle ear, pneumothoraces, air emboli) because N2O insoluble in blood; adverse effects on EMBRYONIC development
Misc: No muscle relaxation; used with volatile agents for MAINTENANCE

21
Q

Isoflurane (Forane)

A

Class: Volatile anesthetic
Mech: Most potent
Thera: Gold standard for maintenance of anesthesia
Important SE’s: Pungent; dose dependent CNS depression (EEG, sensory evoked potentials, motor evoked potentials, cerebral metabolic rate), increase in cerebral blood flow and intracranial pressure; dose dependent decrease in systemic BP, decrease in respiratory function like TV and response to hypoxia or hypercarbia; relaxes skeletal muscle and airway smooth muscles; malignant hyperthermia in susceptible patients; more blood flow to brain, muscle skin, less to liver, kidneys, gut
Misc: Difficult for mask induction

22
Q

Desflurane:

A

Class: Volatile anesthetic
Mech: Least soluble, least potent (allows for rapid emergence from anesthesia)
Important SE’s: Most pungent (airway irritation symptoms: coughing, salivation, breath holding, laryngospasm); dose dependent CNS depression (EEG, sensory evoked potentials, motor evoked potentials, cerebral metabolic rate), increase in cerebral blood flow and intracranial pressure; dose dependent decrease in systemic BP, decrease in respiratory function like TV and response to hypoxia or hypercarbia; relaxes skeletal muscle and airway smooth muscles; malignant hyperthermia in susceptible patients;
can get reflex tachy sometimes; more blood flow to brain, muscle skin, less to liver, kidneys, gut;
increase in HR due to reflex tachy

23
Q

Sevoflurane (Ultane)

A

Class: Volatile anesthetic
Mech: Less soluble, less potent (but not irritating)
Thera: Mask induction in children and adults
Important SE’s: Can form CO if not combined with CO2 correctly by exposure to strong bases; dose dependent CNS depression (EEG, sensory evoked potentials, motor evoked potentials, cerebral metabolic rate), increase in cerebral blood flow and intracranial pressure; dose dependent decrease in systemic BP, decrease in respiratory function like TV and response to hypoxia or hypercarbia; relaxes skeletal muscle and airway smooth muscles; malignant hyperthermia in susceptible patients; more blood flow to brain, muscle skin, less to liver, kidneys, gut; also metabolized into inorganic Fl and compound A (latter a nephrotoxin in rats)

24
Q

Barbituates qualities:

A
  1. prepared as aqueous solutions of Na salt
  2. Rapid onset, short duration of action
  3. ONLY hypnosis/sedation
  4. Hypnotic effect terminateed by drug redistribution from brain to muscle and fat
  5. Metabolized by liver
  6. Dosing based on lean body mass
  7. Used to induce ANESTHESIA
  8. Hyponosis by enhancing inhibitory NT’s (bind GABA A receptors to enhance Cl conductance; direct agonist at higher concentrations) and inhibiting actions of excitatory NT’s (target NMDA receptors)
  9. Barbs and propofol produce dose dependent decreases in BP due to vasodilation and also dose dependent respiratory depression; also NEGATIVE inotropes
25
Q

Propofol (Diprivan)

A

Class: Alkylphenol (a fatty acid)
Mech: GABAa and glycine receptor agonist to depress spinal cord neurons, antagonist of NMDA-glutamate receptor; some a2 receptor activity for sedation maybe; rapid onset and offset; metabolized in liver and lung, metabolites leave by kidney
Thera; Most commonly used IV anesthetic; anti-emetic at low doses; induction and maintenance of general anesthesia; sedation in ICU, procedural sedation
Important SE’s: Propofol infusion syndrome: being given for several days leads to metabolic acidosis, rhabdomyolysis, renal failure, lowering of BP, bradycardia, and death (likely due to fatty acid oxidation)
Other SE’s: Painful injection site; supports bacterial growth
Misc: Administered IV in a lipid emulsion (cause of pain); be aware of allergies (egg and soy in emulsion); no malignant hyperthermia

26
Q

Etomidate (Amidate)

A

Class: Carboxylated imidazole
Mech: GABAa receptor agonist (only D-isomer)
Thera: Hypnosis; no analgesic activity
Important SE’s: Pain on administration (due to solvent, propylene glycol); involuntary myoclonic movements due to subcortical disinhibition (not a seizure); post-operative nausea and vomiting; single dose inhibits cortisol synthesis
Misc: Minimal cardiorespiratory depression (good agent in patients with minimal cardiac reserve)

27
Q

Ketamine (Ketalar)

A

Class: Phencyclidine
Mech: NMDA receptor antagonist, kappa opiate agonist; leads to dose-dependent unconsciousness, amnesia, analgesia
Thera: Sedative/anesthetic for pediatric/developmentally delayed patients; excellent bronchodilator; induction in patients with reactive airway disease, hypovolemia (trauma patients), cardiac disease; with propofol for IV procedural sedation; adjuvant during and after surgery to reduce opiod use; part of multimodal pain therapy regimen; depression treatment
Important SE’s: Stimulates sympathetic nervous system outflow; increases systemic and pulmonary vascular resistance; increase HR, cardiac work; increases cerebral blood flow, ICP; emergence delerium; nystagmus, lacrimation, salivation, and dissociative anesthesia
Misc: Racemic mixture (S more potent); metabolized by P450 (norketamine, a third to a fifth as effective); great bronchodilator; contraindicated in CAD, patients with intracranial lesions;

28
Q

Dexmedetomidine (Precedex)

A

Class: a2 adrenergic agonist
Mech: Binds a2a and a2b in locus coeruleus and spinal cord (produces sedation, sympatholysis, and analgesia); metabolized by liver, excreted in urine and feces
Thera: Awake intubations, awake craniotomies; adjunct to general anesthesia in patients susceptible to narcotic-induced post-op respiratory depression; withdrawal/detoxification
Important SE’s: Limited respiratory depression (wide safety margin)
Misc: Since GABA not hit, sedation is easier to wake from and is similar to non-REM sleep; FDA approved only for ventilation of ICU patients for under 24 hours

29
Q

Why do we need NMB’s?

A

They give hypnosis, amnesia, analgesia, attenuation of autonomic reflexes, and muscle relaxation, but NOT ENOUGH of the latter for surgical anesthesia!!

30
Q

All NMB’s

A
  1. are structurally related to ACh
  2. contain quarternary ammonium structure N+
    • chargers attract them to muscarinic AND nicotinic ACh receptors
31
Q

Succinylcholine (Anectine)

A

Class: Depolarizing NMB
Mech: Divalent ACh molecule; attaches to all ACh receptors, overstimulating them (first seen as disorganized muscular contractions (fasiculations), then paralysis)
Thera: Skeletal muscle relaxant (intubation)
Important SE’s: Malignant hyperthermia; cardiac dysrhythmias, hyperkalemia, increased intraocular pressure, increased intracranial pressure
Other SE’s: Increased intragastric pressure, myalgias, masseter spasm
Misc: Hydrolyzed by pseudocholinesterase (in plasma); blockade cannot be reversed; only NMB with rapid onset and ultra-short duration of action; diffuses away from NMJ

32
Q

What factors affect reversal of NMB?

A
  1. Depth of blockade (should see some recovery from NMB prior to anti-cholinesterase admin)
  2. Duration of action of non-depolarizer (shorter acting NMBs more easily reversed)
  3. Choice and dose of anti-cholinesterase (edrophonium is fastest onset, neostigmine with more complete antagonism, pyridostigmine with longer duration of action)
33
Q

Train of Four regarding monitoring the NMB?

A
  1. reduction in muscle response during electrical nerve stimulus reflects type and degree of blockade
  2. in non-depol bloackde, you have TOF ratio (B/A) of <1
  3. Depol blockade has a TOF ratio of 1
34
Q

Only want ____ effects of neostigmine; how do you block the other receptor type’s effects?

A

nicotinic; use anti-muscarinic like glycopyrrolate or atropine

35
Q

Pancuronium (Pavulon)

A

Class: Amino steroid non-depolarizing NMB (bis-quaternary)
Mech: Competitive blockade of ACh (no depolarization); vagolytic
Thera: Skeletal muscle relaxant; avoid in patients with renal insufficiency
Important SE’s: Increase in HR
Misc: Only long acting non-depolarizing agent (60-90 min); supplied as liquid; 80% excreted unchanged in liver (low metabolism in liver); reverse with AChEI

36
Q

Vecuronium (Norcuron)

A

Class: Amino steroid non-depolarizing NMB (monoquaternary)
Mech: Competitive blockade of ACh (no depolarization)
Thera: Skeletal muscle relaxant
Important SE’s: No cardiovascular effects
Misc: Intermediate acting; supplied as a powder (reconstitute); hepatic metabolism, hepatic and renal excretion; reverse with AChEI

37
Q

Rocuronium (Zemuron)

A

Class: Amino steroid non-depolarizing NMB (monoquaternary)
Mech: Competitive blockade of ACh (no depolarization)
Thera: Skeletal muscle relaxant (can substitute succinylcholine in rapid sequence intubation)
Important SE’s: No cardiovascular effects
Misc: Intermediate acting; supplied as a liquid; hepatic metabolism, hepatic and renal excretion; can speed onset with higher dose; reverse with AChEI

38
Q

Sugammadex (Bridion)

A

Class: Selective relaxant binding agent
Mech: Complexes with rocuronium, rendering it inactive; no effect on AChesterase
Thera: Immediate reversal of rocuronium
Important SE’s: Decrease in blood presure, nausea and vomiting, dry mouth
Misc: Not yet FDA approved; interior cavity traps rocuronium; faster more complete recovery compared to neostigmine

39
Q

Atracurium (Tracrium)

A

Class: Isoquinoline non-depolarizing NMB
Mech: Competitive blockade of ACh (no depolarization)
Thera: Skeletal muscle relaxant; use in patients with liver or renal dysfunction
Important SE’s: Histamine release (especially if given as rapid IV bolus), with resultant hypotension and tachycardia
Misc: Undergoes spontaneous, non-enzymatic degradation (Hofman elimination); intermediate acting; reverse with AChEI

40
Q

Difference between cisatracurium and atracurium?

A

Unlike atracurium, no histamine release or downstream effects

Pharm Unit 3 (12 decks)

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