Anesthetics Flashcards

1
Q

Drugs with increased solubility in lipids do what to the potency?

A

Increased potency = 1/MAC

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2
Q

What is the MAC?

A

minimal alveolar concentration (of inhaled anesthetic) required to prevent 50% of subjects from moving in response to noxious stimulus (i.e. skin incision)

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3
Q

N2O

A

Decreased blood and lipid solubility, and thus fast induction and low potency.

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4
Q

Halothane

A

Halothane has increased lipid and blood solubility and thus high potency and slow induction

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5
Q

What are the inhaled anesthetics?

A

Halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide

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6
Q

mech of inhaled anesthetics

A

mechanism unknown

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7
Q

What is the effect of inhaled anesthetics?

A

Myocardial depression, respiratory depression, nausea/emesis, increased cerebral blood flow (decreased cerebral metabolic demand)

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8
Q

Toxicity of inhaled anesthetics?

A

Hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), expansion of trapped gsa in a body cavity (nitrous oxide). Can cause malignant hyperthermia - rare, life-threatening hereditary condition in which inhaled anesthetics (except nitrous oxide) and succinylcholine induce fever and severe muscle contractions. Treatment: dantrolene

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9
Q

Describe the potency and lipid solubility of IV barbiturates (Thiopental)

A

high potency, high lipid solubility and therefore rapid entry into brain

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10
Q

What is the use of Thiopental?

A

Induction of anesthesia and short surgical procedures. Effect terminated by rapid redistribution into tissue (i.e. skeletal muscle) and fat. Decrease cerebral blood flow.

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11
Q

What is the most commonly used benzodiazepine for endoscopy?

A

Midazolam; used adjunctively with gasous anesthetics and narcotics.

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12
Q

What is the risk of Midazolam?

A

may cause severe postoperative respiratory depression, decrease BP (treat overdose with flumazenil), and anterograde amnesia

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13
Q

What is an Arylcyclohexylamine?

A

Ketamine

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14
Q

What is ketamine?

A

PCP analog that act as dissociative anesthetic. Block NMDA receptors. Cardiovascular stimulants. Cause disorientation, hallucination, and bad dreams. Increase cerebral blood flow

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15
Q

Which opiods are used during anesthesia?

A

Morphine, fentanyl

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16
Q

Propofol

A

Used for sedation in ICU, rapid anesthesia induction, and short procedures. Less postoperative nausea than thiopental. Potentiates GABA(A)

17
Q

What are the IV anesthetics?

A

Barbiturates (thiopental), Benzos (midazolam), ketamine, opioids (morphine, fentayl), propofol

18
Q

What are the two classifications of local anesthetics?

A

Esters and amides

19
Q

What are the Esters?

A

Procaine, Cocaine, Tetracaine

20
Q

What are the Amides?

A

lidocaine, mepivacaine, bupivacaine (amides have 2 I’s in name)

21
Q

What is the mech of local anesthetics?

A

Block Na+ channels by binding to specific receptors on INNER portion of channel. Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.

22
Q

How do the tertiary amines bind?

A

Penetrate membrane in uncharged form, then bind to ion channels as charged form

23
Q

What can be given with the local anesthetics to enhance local action?

A

vasoconstrictors (usually epinephrine) - decrease bleeding, increase anesthesia by decreasing systemic concentration.

24
Q

In infeted tissue, why must more anesthetic be delivered?

A

In acidic tissue, alkaline anesthetics are charged and cannot penetrate membrane effectively

25
Q

Order of Nerve blockade?

A

Small-diameter fibers > large diameter. Myelinated fibers > unmyelinated fibers. Overall, size factor predominates over myelination such that small myelinated fibers > small small unmyelinated > large yelinated fibers > large unmyelinated fibers

26
Q

Order of pain loss?

A

1) pain 2) temp 3) touch 4) presssure

27
Q

What is the clinical use of local anesthetics?

A

Minor surgical procedures, spina anesthesia. If allergic to esters, give amides.

28
Q

Toxicity of local anesthetics

A

CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine)

29
Q

What are the neuromuscular blocking drugs used for?

A

muscle paralysis in surgery or mechanical ventilation. Selective for motor (vs. autonomic) nicotinic receptor

30
Q

What are the Depolarizing neuromuscular blocking drugs?

A

Succinylcholine

31
Q

What is the mech of succinylcholine

A

strong Ach receptor agonist; produces sustained depolarization and prevents muscle contraction.

32
Q

Describe the reversal of blockade of succinylcholine:

A

Phase I: (prolonged depolarization) - no antidote. Block potentiated by cholinesterase inhibitors
Phase II: (repolarized but blocked; ACh receptors are available, but desensitized) - antidote consits of cholinesterase inhibitors

33
Q

What are the complications of Depolarizing neuromuscular blocking drugs?

A

Hypercalcemia, Hyperkalemia, and Malignant Hyperthermia

34
Q

What are the nondepolarizing neuromuscular blocking drugs?

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuronium

35
Q

What is the mech of the nondepolarizing neuromuscular blockers?

A

competitive antagonists - compete with ACh for receptors.

36
Q

What is the reversal of blockade for the non depolarizing neuromuscluar blocking drugs?

A

Neostigmine (must be given with atropine to prevent muscarinic effects such as bradycardia), edrophonium, and other cholinesterase inhibitors.

37
Q

Dantrolene mech

A

Prevents the release of Ca++ from the SR of skeletal muscle

38
Q

What is the clinical use of Dantrolene?

A

used to treat malignant hyperthermia and neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).