Anesthetics Flashcards

1
Q

Routes of Local Anesthesia

A

Topical
Infiltration
Epidural
Spinal

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2
Q

Epidural

A

High dose
Slow onset
Multiple dosing possible
Given at various points in backbone

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3
Q

Spinal

A

Low dose
Fast onset
Single dose only
Can only be given at specific site in backbone to avoid damage

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4
Q

Cocaine

A

First LA

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5
Q

LA Charecteristics

A

Potency- as lipophilicity increases so does potency

Onset of action- decreasing pKa speeds onset

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6
Q

General classes of synthetic cocaine derivates

A

Aminoesters- procaine, chloroprocaine

Aminoamides- Lidocaine, bupivicaine

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7
Q

MOA of LA

A

State dependent block of NA channels

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8
Q

Nociceptors

A

C fibers- slower sense pain

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9
Q

Black Mamba

A

Venom contains:
a-dendrotoxin (work on K+ Channels)
Mambaglins- which block ASIC ~type of NA channel opened by acid

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10
Q

Cone Snail

A

Prialt- specific blocker of Cav2.2 N-Type channels
Intrathecal analgesiac
Used for pain in morphine tolerant/Addict pts

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11
Q

GA Charecteristics

A

Modes of delivery: Inhalation/Injection

Sedation/hypnosis (loss of consciousness-ideally)
Immobility (but breathing)
Analgesia- no pain
Amnesia- dont want to remember the process

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12
Q

Measuring Inhaled anesthesia

A

MAC-moinimum alveolar concentration. Meausres the response of pts to a surgical stimulus. The lower the mac, the more potent the anesthetic.

Factors that can effect it- hair color, age lifestyle, medications.

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13
Q

MAC trends

A

More potent- more lipophillic

Less potent- less lipophillic

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14
Q

Are sleep an anesthesia equivalent?

A

No! Sleep is arousable, sedation can be arousable, GA is unarousable!

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15
Q

Partition trends

A

Lower # will be easier to partition (travel) to other parts of body. From alveoli, to blood, to brain

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16
Q

Ether

A
The first GA.
No longer recommended by WHO
MAC of 3.2
B/G partition of 12- v high
MOA: PAM at GABA
Agonist at GABA at high doses
17
Q

NO

A

MAC over 100!
B/G Partition 0.46
Has to be used 50/50 with O2, can be used as an adjunct to other anesthetics

MOA:
weak PAM at GABA and Glycine
weak activator of K2P channels
Weak blocker of NMDA, AMPA, Kainate

18
Q

Halothane/Isoflurane

A
Low macs, and good B/G partitioning
MOA:
Agonist at GABA and Glycine
Antagonist at NMDA and NA channels
Activates K2P channels

Isoflurane>Halothane due to hepotoxcity of halo.

19
Q

Sevoflurane

A

Good mac and good B/G
Widely used- more expensive though

PAM at GABA
NMDA antagonist
K2P channel activator

20
Q

Injectable anesthetics

A

More potent
Are often sedative hypnotics agents, used to induce anesthesia
TIVA can be used, with some precautions- though not often.

21
Q

Main uses of injectable anesthetics

A

Thiopental- not commonly used anymore due to capital punishment, made it hard to get
Methohexital- ECT, lowers seizure thresholds
Propofol- most common induction agent
Ketamine- trauma, or unclear history. Will raise BP/HR
Etomidate– less commonly used, unless pt is hemodynamically unstable

22
Q

Thiopental

A
Rapid onset (20-45s)
Short acting <10 minutes, peak dose within ~1min
Increases open time of GABA receptors
Used to break status epilepticus
23
Q

Methohexital

A

Rapid off-rate= fast recovery
Lowers seizure threshold ECT
Other sedatives/anesthetics must be used to break the seizure
Increases open time of GABA A receptor channels

24
Q

Propofol

A

Rapid onset, anti emetic, anti seizure
Used to break status epilepticus
PAM at GABAa
NAv channel blcoker

25
Q

Etomidate

A

Rapid onset, used in pt where history is unclear, or BP unstable

PAM at B2,B3 GABA, becomes an agonist at higher concentrations

26
Q

Ketamine

A

Trauma
NMDA antagonist main MoA
SA’s

27
Q

Esketamine

A

For MDD

Non competitive antagonist at NMDA

28
Q

Xenon

A

High MAC!
Good B/G partition
Antagnoist at NMDA, however minimal SA’s compared to ketamine
Expensive, can we recycle it?

29
Q

MOC etomidate

A

Maintain the Rapid onset of etomidate, and hemodynamic charecteristics.
Removes the decrease in cortisone.