Analgesia Techniques Flashcards

1
Q

What are the classes/types we use for paraenternal analgesia?

A

NSAIDS

CRI drugs

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2
Q

What do we use for local/regional anestheisa?

A

select nerve blocks

Eipdural, lumbosacral caudal epidural

wound infusion catheters

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3
Q

List the 6 common NSAIDS

A
Carprofen
Deramaxx
Meloxicam
Robenacoxib
Phenylbutazone
Flunixin
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4
Q

What is Fentanyl?

A
Dogs, cats
Intra-Op analgesia
**Dose dependent/MAC sparing (up to 65%)
'one' dimensional analgesia
watchout for bradycardia
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5
Q

What is MLK?

A

Morphine, Lidocaine, Ketamine

multimodal analgesia

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6
Q

What pain pathways does morphine block?

A

Transduction
Modulation
Preception

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7
Q

What type of apin is morphine useful for?

A

Visceral pain

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8
Q

______ is the backbone of mist/all analgesic protocols

A

Morphine

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9
Q

Lidocaine blocks which pain pathways?

A

transduction, transmission, modulation

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10
Q

Why is lidocaine included in multimodal analgesia?

A

anti inflammatory, central analgesia properties with CRI

decrease cardiac/cerebral ischemia- reperfusion injury

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11
Q

How does lidocaine prevent cardiac/cerebral ischemia- reperfusion injury (mechanism)

A

prevents intracellular Na+ overload & through its anti-inflammatory properties

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12
Q

Ketamine blocks ____ pain from____

A

somatic pain from bones, joints, ligaments skin

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13
Q

Ketamine modualtes the spinal pathways via:

A

Blocks NMDA receptors

decreases central sensitization/wind up

Prevents secondary hyperalgesia

Chronic pain

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14
Q

Describe the mechanism of Ketamine central sensitization:

A

frequent/sever activation of Alpha-Delta nociceptors

increased exitatory neurotransmitters (glutamate/subs P)

activates NMDA, NK, AMPA receptors

increased signal molecules, gene expression, neuroplasticity

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15
Q

When the Alpha-Beta mechanoreceptors are activated, NON-painful stimuli contribute to the pain response, a condition known as _____

A

Secondary Hyperalgesia

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16
Q

How does Ketamine offer neuroprotection?

A

via NMDA blockade

decrease Ca influx =>
increased cell intergrity, survival, regeneration

17
Q

T/F MLK is commonly used at ISU, and given as a either a CRI or SQ Bolus

A

FALSE

DO NOT BOLUS THIS

18
Q

What is the CRI for MLK ?

A

Infuse @ 5mls/kg/hr for first hr

then reduce to 2.5 mls/kg/hr

19
Q

T/f MLK is not very effective at MAC sparing

A

FALSE
decreases the MAC of ISO by 45%
many patients on

20
Q

T/F Because of its MAC sparing effects, patients on MLK should be monitored closely

A

TRUE, monitor EtCO2

have IPPV available

21
Q

Describe how to recover animals from MLK

A

Wean from IPPV, monitor EtCO2
10 min O2 support after vaporizer off
Monitor SpO2, keep above >93-95% w/ o2 supplementation
+/- partial reversal if prolonged O2 dependence

22
Q

What reversal agent would you use for MLK?

A

butorphanol, given in 0.2 ml increments

23
Q

What is the difference between MLK and HLK

A

one letter dumb ass

Hydropmorphone

24
Q

What ‘benefits’ does hydromorphone offer in sedation

A

Clinical impression-

less sedation, more vocalization/dysphoria at recovery

25
Q

What is in the concoction F + LK?

A

Fentanyl, lidocaine, ketamine

26
Q

What is the benefit of F+LK

A

more control/titration of opiod dose

retain multi-multiple neuroprotective and/or anti-inflammatory effects of L&K

use Fentanyl in syringe pump, add LK to IV fluid