L38→↑↓ Drugs Used in Anesthesia Flashcards

1
Q

Nitrous Oxide (N2O)

A

Prolonged use interferes with vitamin B12

Analgesia and sedation

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2
Q

Isoflurane

A
Color code: purple
→Anesthesia but NOT analgesia
→ Decreases BP and increases HR
→ Decreases respiratory volume but increases rate
→ Moderate respiratory irritant
→ Increases bronchial secretions
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3
Q

Desflurane

A

Color code: blue
→ Anesthesia but NOT analgesia
→ Dose-dependent cardiovascular depression
→ May get tachycardia at higher concentrations
→ Dose dependent respiratory depression
→ Respiratory irritant
→ Increases bronchial secretions

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4
Q

Sevaflurane

A
Color code: yellow
→ Anesthesia but NOT analgesia
→ Decreases BP and HR
→ Dose-dependent depression of respiratory rate
→NOT irritant to airways
→→ Suitable for inhalational induction
→ Eliminated predominantly via the lungs; 5% metabolized by
cytochrome P450
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5
Q

Types and name of I.V. Induction Agents

A

Rapidly acting

Barbiturates
→thiopental

Phenols
→propofol

Imidazoles
→etomidate

Slow acting
Phencyclidine derivatives
→ ketamine
Benzodiazepines
→midazolam
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6
Q

Drugs Used in TIVA

A

Hypnotics
Propofol, etomidate,

Analgesics (opioid class)
Fentanyl, remifentanil,

Muscle relaxation
→ Atracurium, vecuronium

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7
Q

Drug combination for TIVA

A

Propofol and remifentanil

Propofol and fentanyl

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8
Q

Mechanism, Contraindication, S/E of Propofol

A

A free radical scavenging agent
MoA
→ It decreases the rate of dissociation of the GABA from the receptor, thereby increasing the duration of the GABA-activated opening of the chloride channel with resulting hyperpolarization of cell
membranes.

Adverse (side) effects:
→ Pain on injection
→ Bacterial growth

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9
Q

Mechanism, Contraindication, S/E of Etomidate

A

MoA
It binds at a distinct binding site associated with a Cl- ionophore at
the GABAA receptor, increasing the duration of time for which the
Cl- ionophore is opened

Maintains a good cardiopulmonary function

Adverse (side) effects:
→ Suppresses the production of cortisol
→ High concentration of propylene glycol in etomidate preparation causes hemolysis resulting in hemoglobinuria

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10
Q

Mechanism, Contraindication, S/E of Ketamine

A

Non-competitive antagonism at the NMDA receptor Ca2+ channel
pore
→ It reduces the presynaptic release of glutamate
→ Interaction with opioid receptors (Mu and Kappa), but NOT antagonized
by naloxone
→ Antagonistic interaction with monoaminergic, muscarinic and
nicotinic receptors

Adverse (side) effects:
→ Blurred vision
→ Dizziness
→ Drowsiness
→ Nausea and vomiting
→ Loss of appetite
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11
Q

MOA of Local Anesthetics

A

→Blockade of voltage-gated sodium channel conductance
→→ Prevents the initiation and propagation of the nerve impulse by
reducing the passage of Na+ ions through voltage-gated Na+ channels

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12
Q

Mechanism, Contraindication, S/E of

Lidocaine

A

used multipurpose LA

combination with epinephrine (adrenaline) – why?
→ Epinephrine binds to q1 receptors located on the blood vessels, which causes vasoconstriction
→→prolongs the duration of local anesthesia several-fold and may improve the frequency of successful nerve block
→→minimizes systemic toxicity of the local
anesthetic by reducing the peak blood concentration of the local anesthetic agent
→→When local anesthetic solutions are given by infiltration, epinephrine tends to reduce blood loss associated with
surgical procedures

→ In combination with an opioid in intrathecal or epidural
anesthesia

At normal therapeutic doses
→Dizziness
→ Paraesthesia – a burning or prickling sensation
→ Euphoria

At higher doses
→ Confusion
→ Vertigo
→ Tinnitus

Severe toxicity may precipitate seizures

 Overdose toxicity
→ Cardiac arrhythmias
→ Lowering blood pressure
→ Coma
→ Respiratory arrest
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13
Q

Classification of Local anesthetics

A

Amide group
Lidocaine
Prilocaine

Ester group
cocaine
procaine

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14
Q

Systemic Toxicity

A

→LAs absorbed into systemic circulation

→Most effects are dose-dependent

 Methemoglobinemia
→Hepatic metabolism of prilocaine
→Can also be induced by
→→ Benzocaine (ester type)
 Central nervous system toxicity
→ seizures
→ initially light headedness and dizziness

→ Cardiovascular system toxicity
→→cause vasodilation in area
of injection

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15
Q

Drug interaction

A

→Local anesthetics potentiate nondepolarizing muscle relaxant
blockade

→Succinylcholine and ester group local anesthetics depend on
pseudocholinesterase for metabolism

→ Pseudocholinesterase inhibitors can prolong the metabolism
of ester local anesthetics

→ Histamine (H2) receptor antagonists (blockers) and non-
selective  receptor antagonists (blockers)(e.g. propranolol) decrease hepatic blood flow and lidocaine clearance

→a2-Adrenergic agonists (e.g. clonidine) potentiate local
anesthetic analgesia produced after peripheral nerve block injection

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