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Pharmacology test 1 > Basic Pharm of Anesthetics > Flashcards

Basic Pharm of Anesthetics Flashcards

1
Q

Benzodiazepines 5 pharm effects and prototype

A 
1 Anxiolysis 2 Sedation 3 Anterograde Amnesia (from the min drug given until drug is gone) 4 Anticonvulsant Actions 5 Muscle Relaxation (Spinal Level, not muscle)
-Prototype: Diazepam(valium)
fyi: midazolam(versed)
lorazepam(ativan)

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2
Q

Benzodiazepines Mechanism of Action

A

enhances the affinity for GABA to bind to GABAa receptor
increases GABAs potencyX3
Causes greater frequency of channels to open:
-Increases chloride influx
-Hyperpolarization
-Decreased neuronal excitability (when AP comes along nothing happens)

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3
Q

Benzodiazepines uses in anesthesia

A

-Pre-medication
-IV sedation
-General Anesthetic induction (rare)
-General Anesthetic maintenance (rare)
-Post-op anxiolysis (rare)


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4
Q

Benzo adverse effects and precautions

A

-Dose dependent decrease in ventilation
-Hypoxemia and hypoventilation enhanced in presence of opioid (synergistic)
-Decreases SVR at induction dosage
-BP consequently decreases especially with hypovolemia
*Contraindicated in pregnancy


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5
Q

Opioids effect and prototype

A

Supra spinal(brain) and SpinalAnalgesia – activation of endogenous pain suppression system

  • analgesia without loss of touch or consciousness.
  • Prototype: Morphine
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6
Q

Opioid MOA

A
  • Acts at brainstem, spinal cord, and peripheral tissues-Agonist at stereospecific opioid receptors – activates pain-modulating systems
  • Binding at opioid receptor = decreased neurotransmission
  • Immediate decrease in neurotransmitter release
  • Acts at pre and post synaptic sites
  • -Increased K conductance – hyperpolarization
  • -Ca channel inactivation
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7
Q

Opioid uses

A

-Pre-medication
-Intra-op pain management (IV, epidural, spinal)
-General anesthesia (high doses)
-Post-op pain management


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8
Q

Opioid Adverse effect and Precautions (7)

A
  • Bradycardia (in cardiac surg, this is a good thing)
  • Respiratory Depression (decreased RR, increased tidal volume, but volume won’t off set slow rate)
  • Miosis
  • Urinary retention
  • Constipation
  • Physical dependence
  • Sedation (in higher doses, synergistic w/other drugs)
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9
Q

Barbiturates MOA

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 (direct activation of Cl- channels)
  • Produces functional inhibition of the post- synaptic neuron
  • Depresses Reticular Activating System → Sleep
    (basically: activates GABA and mimics GABA)
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10
Q

Barb uses and prototype

A

-Sedation and Hypnosis
-Cerebral Protection
-Anti–seizure (benzos > effective)
-Anesthetic Uses
—Induction of general anesthesia (useful in patients with increased intracranial pressure and/or focal brain ischemia)
* Thuiopental (no longer used)

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11
Q

Barbs Adverse effects (cardiac, and resp) and Precautions

A
  • “Hang-over”effect–elimination 1/2life is so long
  • Depression of medullary vasomotor center & decreased SNS outflow from CNS → peripheral vasodilation→ preload decreases→
  • SBP decreases, compensatory HR increase
  • If SNS not intact OR hypovolemia OR large doses given to reduce ICP, will see significant decreases in BP and myocardial depression
  • Ventilatory Depression
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12
Q

Barbs adverse effects and precautions

A

-Intraarterial injection (can result in gangrene/nerve damage)–drug has high pH so if in artery precipitates fast
-Hepatic enzyme induction with chronic use–phenobarb most potent inducer
-Increases the 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!


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13
Q

Propofol/Diprivan class, how it’s stored

A

-Classification: Nonbarbiturate IV anesthetic
-Supplied as: 1% Solution in egg, soy, glycerol
-Infection Control- EDTA (ethylenediamine tetraacetic acid)
• Preservatives-Sodium metabisulfite (caution use asthma) vs EDTA
*dont spike twice

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14
Q

Propofol MOA

A

-Enhances binding of GABA to GABAa receptor (B1 subunit)
-Decrease the rate of disassociation of GABA from receptor (increase how long GABA interacts with receptor)
• Increases chloride influx
• Hyperpolarization
• Decreased neuronal excitability


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15
Q

Propofol effects

A
  • Dose Dependent Sedation & Hypnosis
  • Antiemetic
  • Antipruritic
  • Anticonvulsant
  • decreases the effect of Bronchoconstriction (except with metabisulfite)
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16
Q

Propofol uses

A
  • Intravenous sedation
  • Induction of general anesthesia
  • Maintenance of general anesthesia (TIVA)
  • Part of balanced technique for maintenance of anesthesia
  • Antiemetic (small doses)
17
Q

Propofol adverse effects and precautions

A

Dose dependent ventilatory depressant, myocardial depression and vasodilation

  • Similar decreases in SV, C.O. and SVR
  • HR unchanged (? baroreceptor inhibition)
  • Bradycardia related death – 1.4/100,000 patients
  • Myoclonus (twitching)
  • Pain on injection (lido first, or give fast)
  • Lipidemia with long term infusion
  • Infection and bronchospasm
18
Q

Succinylcholine class, MOA

A

Classification: Depolarizing Neuromuscular Blockade
Mechanism of action:
-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

19
Q

Succinylcholine effect and uses

A
  • Neuromuscular Blockade
  • Optimize intubating conditions–Rapid sequence induction
  • Treatment of life-threatening laryngospasm
20
Q

Succinylcholine adverse effects and precautions

A
  • Cardiacdysrhythmias
  • Hyperkalemia (increased susceptibility seen with burns, trauma, nerve damage, neuromuscular diseases, renal failure)
  • Muscle Pains (fasciculations)
  • Increased ICP (avoid with head injuries)
  • Increased IOP
  • Potent Malignant Hyperthermia triggering agent
  • Avoid in patients with atypical acetylcholinesterase
21
Q

Vecuronium class and MOA

A

Classification: Non-depolarizing Muscle Relaxant; Monoquaternary aminosteroid

  • Mechanism of Action: Competitive antagonist at pre and post neuromuscular junction nACH receptors (prevent Ach from binding to receptor site—no AP)
  • Occupies alpha subunits of ACH receptor without inducing a conformational change
  • Action Potential can not be initiated
22
Q

Vecuronium effect and used

A
  • Muscle Relaxation/Paralysis
  • Facilitate endotracheal intubation (must test vent before giving muscle relaxant)
  • Optimize surgical conditions
23
Q

Vecuronium adverse effects and precautions

A
  • Prolonged/ unpredictable effect with:
  • -Liver and kidney disease
  • -Neuromuscular disease
  • -Hypothermia, electrolyte imbalances
  • -Antibiotics: aminoglycosides
  • Resistance in burn patients
  • Be on the look out for residual neuromuscular blockade in all patients (make sure completely recovered ex. all 4 of TOF)
  • In theory, at higher risk for recall if inadequate general anesthesia given
24
Q

Isoflurane class and MOA

A

Class: Inhalational Anesthetic; Halogenated methyl ethyl ether
Mechanism of Action:
**Lipid solubility very important (determines onset, duration, etc.)
-These agents eliminated almost entirely via the lungs, contemporary inhaled agents minimally metabolized by the liver or eliminated via kidney

25
Q

Isoflurane effects and use

A
  • Bronchodilator
  • General Anesthesia (sedation, hypnosis, partial muscle relaxation)
  • Induction (usually Sevoflurane only)
  • Maintenance
26
Q

Isoflurane adverse effects and precautions

A 
Respiratory effects:
--Depression: higher rates, lower volumes.
Cardiac effects:
--Depression: ↓C/O, and BP, cause vasodilation
Malignant Hyperthermia
--Ca++channelinterference
--Muscle rigidity
--↑ temperature
--↑ CO2
Aspiration
--Airway reflexes are abolished (NPO)
OR pollution
27
Q

MAC (not monitored…)

A

Mean Alveolar Concentration = MAC (of a volatile anesthetic to which a 50% of patients do not move to a noxious stimulus)

  • Describes potency (similar ED50)
  • Tells us how much of a specific gas to administer
28
Q

Isoflurance: MAC

A

MAC of isoflurane is 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
• 1.2% Isoflurane molecules

29
Q

Nitrous Oxide MAC

A

Nitrous oxide is the only inhaled agent that will not by itself provide 100% anesthesia – its MAC is 104%

30
Q

Local Anesthetics MOA and prototype

A

-Local anesthetics block impulse conduction during the depolarization phase of the action potential
-Blockade is caused by the inhibition of the influx of sodium ions (sodium channel blockade)
-Blockade only occurs when Na channels are in the inactivated closed state
Prototype: Lidocaine

31
Q

LA effect

A
  • Block afferent nerve transmission to produce analgesia and anesthesia without loss of consciousness
  • Autonomic blockade
  • Somatic sensory blockade
  • Somatic motor blockade
32
Q

Lidocaine class

A

Amide
molecule consist od lipophilic head (aromatic ring), and intermediate chain either an amide or ester and a Hydrophilic Tail
-the tail
the lipophilic head is what it can cross the BBB (CNS toxicity)

33
Q

LA adverse effects and precautions

A

CNS toxicity

  • Circumoral /tongue numbness, tinnitus, vision changes, dizziness, slurred speech, restlessness
  • Seizure followed by CNS depression, apnea, hypotension
  • pt must be awake to assess for this
  • will see CNS effects before cardiac
34
Q

LA adverse effects and precautions cardiac

A

More resistant to toxic effects than CNS!

  • Hypotension, myocardial depression, reduced SVR and C.O
  • 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 test 1 (4 decks)

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