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Pharmacology > E's intro to Anesthetics > Flashcards

E's intro to Anesthetics Flashcards

1
Q

what type of anesthesia provides numbness to a small area limited to where local anesthetic is injected?

A

Local Anesthesia

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2
Q

What type of anesthesia provides numbness to a much larger areas, such as epidurals, spinals, and peripheral nerve blocks?

A

Regional Anesthesia

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3
Q

What type of anesthesia uses sedatives and other agents, but the patient is responsive and can breathe on their own?

A

MAC- monitored anesthesia care

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4
Q

What type of anesthesia is a deep state of sleep where the patient loses consciousness and sensation and usually (not always) requires assisted ventilation?

A

General Anesthesia

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5
Q

What type of anesthesia can be referred to as “IV sedation”?

A

Monitored anesthesia care

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6
Q

What is the major difference between monitored anesthesia care and general anesthesia?

A

MAC patient can still move (like for bronchoscopy and EGD; sedative)
General anesthesia the patient CANT MOVE/ no longer responds to stimulus

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7
Q

Distinguish the effects of Minimal sedation (vs moderate, deep, and general anesthesia)

A

(anxiolysis) patient can respond to verbal commands; cognitive function and coordination may be impaired; CV and Ventilatory functions are UNaffected

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8
Q

Distinguish the effects of moderate sedation/ analgesia (vs. minimal, deep, and general anesthesia)

A

(Conscious Sedation) patient responds purposefully to verbal commands, either alone or with tactile stimulation; adequate spontaneous ventilation; CV usually maintained. easily aroused

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9
Q

Distinguish the effects of deep sedation (vs. minimal, moderate, and general anesthesia)

A

NOT easily aroused; respond purposefully to repeated PAINFUL stimuli; ventilatory function and patent airway may be impaired; CV function usually maintained

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10
Q

Distinguish the effects of General anesthesia (vs. minimal, moderate, and deep sedation)

A

NOT arousable even with painful stimuli; IMPAIRED ventilatory function–>requires ventilatory assistance for patent airway; PPV may be required; CV function may be impaired (elderly may have CV issues, vasodilated…etc)

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11
Q

What is General Anesthesia?

A

generalized, reversible CNS depression

  • NO sensory perception (all senses are gone)
  • Loss of consciousness
  • No recall of events
  • Immobiity
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12
Q

What are other potential effects of general anesthetics and adjuncts? (4)

A
  • muscle relaxation
  • suppression of autonomic reflexes (good and bad: decreases the stress response, but knocks out ability to compensate BP etc.)
  • Analgesia (NOT ALWAYS with general Anesth. ie. with EGD dont need pain relief)
  • Anxiolysis
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13
Q

What are the steps of General Anesthesia with an ETT template? (7)

A
  • Pre-op medications/ sedation
  • Induction Drug
  • Neuromuscular blockade
  • inhalation drug
  • opioids/ local anesthetics etc.
  • Antiemetic
  • Neuromuscular Blockade reversal agent
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14
Q

What is the purpose of pre-op medication/sedation in the GA with an ETT template? (4)

A

patient comfort, reduce anxiety, prevent aspiration, antibiotics per surgeon request (usually benzos/versed)

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15
Q

What is the purpose of the induction drug in the GA with an ETT template?

A

to induce anesthesia (DUH!!!)–> can be IV (usually) or inhaled

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16
Q

What is the purpose of the neuromuscular blockade in the GA with ETT template?

A

to facilitate intubation and optimize surgical conditions (remember, you dont have to!! like you could give propofol)

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17
Q

What is the purpose of the inhalational drug in the GA with ETT template?

A

to maintain general anesthesia (can also be IVV gtt agent like propofol)

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18
Q

What is the purpose of opioids/local anesthetics etc. in the GA with ETT template?

A

to minimize physiological effects of pain and to promote comfort at emergence (ppl can feel pain on anesthetics! so give them the juice!)

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19
Q

What is the purpose of the antiemetic in the GA with ETT template?

A

to prevent nausea likely with opioids/inhalational agents “ain’t nobody got time for that”

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20
Q

Whats the purpose of giving a neuromuscular blockade reversal agent?

A

to reverse the paralyzing effects of neuromuscular blockade (dont have to with the half-times of drugs….)

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21
Q

What are the 5 pharmacologic effects of Benzodiazepines?

A
  • Anxiolysis** especially with major surgeries like CV
  • Sedation
  • Anterograde Amnesia (From when you give it until its gone, so introduce yourself before!)
  • Anticonvulsant Actions
  • Muscle Relaxation (Spinal Level)– decreases muscle spasms
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22
Q

What is the prototype benzodiazepine?

A

Diazepam (Valium!)

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23
Q

What is the MOA of Benzodiazepines?

A

Potentiates binding of GABA to GABAa receptor; Increases GABA potency times 3 at the site

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24
Q

What happens due to the binding of GABA to GABAa receptors with respect to ions (3)….for benzodiazepines?

A
  • increases chloride influx
  • hyperpolarization
  • Decreased neuronal excitability
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25
Q

What are the uses of Benzodiazepines in anesthesia? (5)

A
  • pre-medication
  • IV sedation
  • GA induction (rare)
  • GA maintenance (rare)
  • post-op anxiolysis
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26
Q

What are the adverse effects and precautions of benzodiazepines?

A
  • Dose dependent decrease in ventilation
  • Hypoxemia and hypoventilation enhanced in presence of opioid
  • decreases in SVR at induction dosage (only with large doses)
  • BP consequently decreases especially with hypovolemia (BP generally stable except in large doses!)
  • contraindicated in pregnancy
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27
Q

What are the pharmacological effects of opioids in supraspinal and spinal analgesia?

A

activation of endogenous pain suppression system

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28
Q

What are the opioid receptors and where does it act at the synapse?

A

agonist acts at the mu receptors- activates pain modulating systems
-acts at pre and post synaptic sites

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29
Q

What happens with neurotransmission when opioids bind to the receptor?

A

decreased neurotransmission

  • increased K conductance– hyperpolarization
  • Ca2+ channel inactivation
  • Immediate decrease in neurotransmitter release (Substance P)
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30
Q

What are the uses of opioids in anesthesia? (4)

A
  • pre-medication (unless in the OR, dont premedicate with versed/fentanyl b/c synergistic and will stop breathing!)
  • Intra-operative pain management (IV, epidural, spinal)
  • General anesthesia (at very high doses)
  • Post-op pain management
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31
Q

What is the prototype for opioids?

A

Morphine

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32
Q

How do opioids affect the CV system?

A

VERY CARDIAC STABLE!

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33
Q

What are the adverse effects and precautions of opioids? (7)

A
  • bradycardia
  • respiratory depression
  • miosis
  • urinary retention
  • constipation
  • physical dependence
  • sedation (in higher doses, synergistic with other drugs)
34
Q

What happens in respiratory depression with opioids regarding respiratory rate and tidal volume?

A

decreased respiratory rate and increased tidal volume (breathe deep and slow)

35
Q

What is the MOA of Barbiturates? (4)

A
  • decreases the rate at which GABA dissociates from its receptor–> increases duration of GABA activated Cl- channel opening (enhances GABA activity)
  • Mimics GABA at the receptor site (direct activation of Cl- channels)
  • produces function inhibition of the post-synaptic neuron
  • Depresses RAS–> sleep
36
Q

Where in the synapse do barbiturates work?

A

POST synaptic neuron

37
Q

What is the prototype drug for barbiturates?

A

Thiopental

38
Q

What are the uses of barbiturates? (4)

A
  • sedation and hypnosis
  • Cerebral protection (decreases cerebral blood flow and CMrO2)
  • Anti-seizure (better effects than benzos)
  • Anesthetic Uses
39
Q

What are the anesthetic uses of barbiturates?

A
  • induction of general anesthesia (useful in patients with increased ICP and/or focal brain ischemia
40
Q

What are the adverse effects and precautions of Thiopental (barbiturates?) (6)

A

-“hang-over” effect (distrib. quickly but hangs out in the plasma for a long time)
-depression of medullary vasomotor center & decreases SNS outflow from CNS (peripheral vasodilation-> preload decreases->
- SBP decreases, compensatory HR increases
- if SNS not intact OR hypovolemia OR large doses given to reduce ICP, will see significant decreases in BP and myocardial depression
- Ventilatory depression
- Intraarterial injection (can result in gangrene/ nerve damage)
~MASSIVE decrease in BP (but propfol is worse)

41
Q

What can result from intraarterial injection of barbiturates?

A

gangrene/ nerve damage

42
Q

What are the adverse effects and precautions of barbiturates? (5)

A
  • Hepatic enzyme induction with chronic use (phenobarb is MOST potent inducer!)
  • increases metabolism of oral anticoagulants, phenytoin, TCAs, corticosteroids, and Vit. K
  • Accelerated production of heme by stimulation of enzyme: D-aminolevulinic acid synthetase- Avoid in patients with porphyria
  • Allergy 1:30,000, HIGH mortality
  • readily crosses placenta!
43
Q

What is the classification of Propofol/Diprivan?

A

Nonbarbiturate Intravenous Anesthetic

44
Q

What is propofol supplied as?

A

1% soln in egg, soy, glycerol base (causes pain when administered!)

45
Q

What is added to propofol as a preservative to decrease bacterial growth?

A

Sodium metabisulfite vs. EDTA

46
Q

What is the MOA of Propofol?

A
  • Potentiates binding of GABA to GABAa receptor (B1 subunit)

- Decreases the rate of disassociation of GABA from the receptor

47
Q

What happens at the cellular level when propofol decreases the rate of disassociation of GABA from receptor? (3) hint….it has to do with an ion

A
  • increases chloride influx
  • hyperpolarization
  • decreased neuronal excitability
48
Q

What are the pharmacological effects of propofol? (5)

A
  • dose dependent sedation and hypnosis
  • antiemetic
  • antipruritic
  • anticonvulsant
  • attenuation of bronchoCONSTRICTION
49
Q

What is the attentuation of bronchospasm usually related to with regards to propofol?

A
  • usually related to the patient not being deep enough under anesthesia (ie. for asthmatics maintain a very deep level of sedation
50
Q

What are the anesthetic uses of propofol? (5)

A
  • intravenous sedation
  • induction of general anesthesia
  • maintenance of general anesthesia
  • part of balanced technique for maintenance of anesthesia
  • antiemetic (small doses)
51
Q

What are the adverse effects and precautions of propofol? (6)

A
  • dose dependent ventilatory depressant
  • dose dependent myocardial depression and vasodilation (similar decreases in SV, CO, and SVR)
  • Myoclonus (jerky movements that are not purposeful)
  • pain on injection
  • Lipidemia with long term infusion
  • Infection
  • Bronchospasm (b/c some of the sulphite preservatives in it can cause bronchoconstriction)
52
Q

What happens to heart rate when propofol is in use?

A

HR unchanged!

not good, more so because propofol is blocking baroreceptors from being able to compensate

53
Q

What does action potential mean?

A

depolarization of nerve terminal

54
Q

What are the Pre-synaptic events at the NMJ? (4)

A
  • action potential
  • Ca channels open
  • Ca diffuses down gradient to nerve terminal
  • Ach spills out into synaptic cleft
55
Q

What are the post-synaptic events at the NMJ? (5)

A
  • Ach combines with nicotinic receptors
  • after both nicotinic receptors occupied. Channels open Na+, Ca diffuse into cell and K+ diffuses out
  • motor end plate depolarizes
  • action potential created
  • skeletal muscle contracts
56
Q

Name 4 things regarding the acetylcholine receptor.

A
  • 5 protein subunits
  • central core for cation channeling
  • Ach must bind to both “a” subunits to open the core
  • “A” subunits are the site of agonism and antagonism
57
Q

What is the classification for succinylcholine?

A

Depolarizing neuromuscular blockade

58
Q

What is the MOA of succinylcholine?

A

binds to nicotinic receptors

  • channel opens, motor endplate depolarizes
  • single contraction occurs
  • Sch not metabolized by true acetylcholinesterases
  • channels stay open until Sch diffuses back into the circulation
  • further action potentials cannot be initiated
59
Q

What is the pharmacologic effect/anesthetic use of Succinylcholine?

A

Trauma setting/ Neuromuscular Blockade

  • optimize intubating conditions**
  • rapid sequence induction
  • treatment of life-threatening laryngospasm
60
Q

What are the adverse effects and precautions of succinylcholine? (7)

A
  • CARDIAC DYSRHYTHMIAS** esp. in kids
  • Hyperkalemia (increased susceptibility seen with burns, trauma, nerve damage, neuromuscular diseases, renal failure)
  • Muscle Pains (fasciculations)
  • Increased ICP
  • Increased IOP
  • ***POTENT MALIGNANT HYPERTHERMIA TRIGGERING AGENT
  • Avoid in patients with atypical acetylcholinesterase
61
Q

What is the drug classification for Vecuronium?

A

Non-depolarizing muscle relaxant; monoquaternary aminosteroid

62
Q

What is the MOA of Vecuronium?

A

Competitive antagonist at PRE and POST neuromuscular junction nicotinic AcH receptors
-occupies alpha subunits of ACH receptor without inducing a conformational change
-AP can not be initiated
(BLOCKS ACTION POTENTIALS)

63
Q

What are the pharmacological effects/anesthetic uses of Vecuronium?

A

Muscle relaxation/Paralysis
-facilitate endotracheal intubation
-optimize surgical condictions*****
~for us and the surgeons, not for the patient

64
Q

What are the adverse effects and precautions of Vecuronium? (7)

A
  • Prolonged/ unpredictable effects with: liver and kidney disease, neuromuscular disease, hypothermia and electrolyte imbalances, antibiotics: aminoglycosides (metabolized similarly so it can prolong the action of vecuronium)
  • resistance in burn patients
  • be on the look out for residual neuromuscular blockade in all patients
  • in theory, at higher risk for recall if inadequate general anesthesia given
65
Q

What is the drug class of Isoflurane?

A

Inhalational anesthetic; halogenated methyl ethyl ether

66
Q

What determines onset, duration, etc. for isoflurane?

A

Lipid solubility!!! (potency and how long it lasts)

67
Q

How are inhalational agents, Isoflurane, eliminated?

A

almost entirely by the lungs, contemporary inhaled agents minimally metabolized by the liver or eliminated via kidney

68
Q

What are the pharmacological effects and anesthetic uses of isoflurane (inhaled anesthetics)? (2)

A
  • bronchodilator
  • general anesthesia (sedation, hypnosis, partial muscle relaxation)–> induction (usually sevo only) and maintenance of anesthsia
69
Q

What are the adverse effects and precautions of isoflurane (inhaled anesthetics)? (5)

A
  • Respiratory effects: higher rates, lower volumes
  • cardiac effects: depression- dcreased CO, and BP and causes vasodilation
  • **Malignant Hyperthermia (1st sign is increasing CO2): Ca2+ channel interference, muscle rigidity, increased temp, and increased CO2
  • Aspiration (RISK; airway reflexes are abolished)
  • OR Pollution
70
Q

What is MAC: Mean Alveolar Concentration?

A

of a volatile anesthetic to which a 50% of patients do not move to noxious stimulus (ie. dose at which 50% of people will not move)

  • describes potency
  • tells us how much of a specific gas to administer
71
Q

What is the minimum alveolar concentration of Isoflurane?

A

1.2% (so, if I had the patient on 100% oxygen and dialed my isoflurane vaporizer to 1.2%. The patient would be breathing the following gas mixture: 98.8% oxygen molecules and 1.2% isoflurane molecules

72
Q

What is the only inhaled agent that will not by itself provide 100% anesthesia, and what is its MAC?

A

Nitrous oxide, and its MAC is 104%

73
Q

What is the MOA of local anesthetics? (3)

A

-local anesthetics block impulse conduction during the depolarization phase of the action potential

74
Q

What causes the blockade by local anesthetics?

A

-blockade is caused by the inhibition of the influx of SODIUM ions

75
Q

What condition regarding sodium channels must occur for local anesthetics to cause blockade?

A

blockade ONLY occurs when Na channels are in the INACTIVATED closed state

76
Q

What is the drug prototype for local anesthetics?

A

Lidocaine

77
Q

What are the pharmacologic effects of local anesthetics?

A

Blocks afferent nerve transmission to produce analgesia and anesthesia without loss of consciousness

78
Q

What 3 types of blockade occur from local anesthesia?

A
  • autonomic blockade
  • somatic sensory blockade
  • somatic motor blockade
79
Q

What is the drug classification of lidocaine?

A

AMIDE local anesthetics

80
Q

What does the typical local anesthetic molecule consist of ?

A
  • lipophilic head (an aromatic ring)
  • intermediate chain (containing either an amide (NH) or an ester (COO-)
  • hydrophilic tail (a tertiary amine)
81
Q

What are the CNS adverse effects and precautions of local anesthetics?

A

CNS TOXICITY!

  • circumoral/tongue numbness, tinnitus, vision changes, dizziness, slurred speech, restlessness
  • seizure followed by CNS depression, apnea, hypotension
82
Q

What are the cardiovascular adverse effects and precautions of local anesthetics? (4)

A

Cardiovascular instability

  • more resistant to toxic effects than CNS
  • hypotension, myocardial depression, reduced SVR and CO
  • Bupivacaine- arrhythmias, AV heart block, hypotension and arrest may occur
  • Cocaine overdose manifests as massive sympathetic outflow, coronary vasospasm, MI, dysrhythmias including V-fib

Pharmacology (23 decks)

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