Anaesthesia - Analgesics - Opiods And Las

Front 1

Define analgesia

Back 1

Absence of sensory perception of pain in the presence of normally painful stimuli

Front 2

Which areas of the brain cause analgesia when stimulated?

Back 2

Periaqueductal grey (PAG) area of midbrain and substantia gelatinosa (SG)

Both contain opiod receptors

Front 3

Where else in the body do opiod receptors hang out?

Back 3

Joints and peripheral nerve endings, in addition to the midbrain and spinal cord

Front 4

Define hyperalgesia

Back 4

An increased amount of pain assd with a mild noxious stimulus

Front 5

Define allodynia

Back 5

Pain provoked by a normally non-noxious stimulus

Like clothes on burned skin

Front 6

What chemical mediators are involved with pain?

Back 6

5-HT and histamine for inflammation
Kinins - pain-producing and release PG
PG - lowers pain threshold
Substance P and glutamate

Front 7

What are different groups of analgesics? (5)

Back 7

Opiods
NSAIDS
LA's
a2-agonists
NMDA antagonists (ketamine)

Front 8

MOA of opiods

Back 8

-Belong to GCPR family and inhibit adenylate cyclase, reducing intracellular cAMP
-Also affect ion channels by promoting opening of voltage-gated K+ channels (hyperpolarised mems) and inhibiting the opening of Ca channels...this reduces neuron excitability and xmitter release due to decreased Ca

Front 9

Method of opiod administration

Back 9

-PO route bad because of first-pass metab
-i/v route common
-also IM, SC

Front 10

Opiod effect on nociceptive path

Back 10

-inhibits xmission of nociceptive impulses thru dorsal horn
-suppresses spinal reflexes
-inhibits release of substance P

Front 11

The 4 opiod receptor types

Back 11

mu - responsible for most analgesic efx
delta - impt in periphery and spinal analgesia
kappa - spinal analgesia
sigma - not a true receptor, dysphoria

Front 12

Principle site of opiod action.

Back 12

Spinal cord
Inhibits xmission of nociceptive impulses and inhibition of substance P.

Front 13

Main effects of opiods

Back 13

-Sedation and euphoria
-Respiratory and cough suppression
-Reduced GIT motility
-Stimulate vom centre
-Histamine release causing hypotension

Front 14

Full mu opiod agonists (4)

Back 14

Morphine
Pethidine
Fentanyl
Methadone

Front 15

Partial mu opiod agonists (3)

Back 15

Butorphenol
Buprenorphine
Etorphine

Front 16

Opiod antagonists (2)

Back 16

Naloxone
Nalorphine

Front 17

Morphine
-control
-metab
-effects

Back 17

-schedule 2 controlled drug but not liscensed
-metab to active analgesic
-emesis, resp depression, decreased GIT motility

Front 18

Pethidine
-control
-effects
-onset/duration

Back 18

-schedule 2, liscensed
-spasmolytic, histamine release
-onset 10-15 min, lasts 60-90
Good for pre-emptive analgesia and spasmolic colic

Front 19

Fentanyl
-control
-kinetics
-extra

Back 19

-schedule 2 controlled, unliscensed
-onset rapid (30 sec), duration 15-20 min
-a rescue analgesia that is available in patches...can top up other opiods with this

Front 20

Buprenorphine
-control
-uses

Back 20

-schedule 3, licensed
-used for moderate, not severe, pain
-can be used for PARTIAL reversal of full mu agonist

Front 21

Butorphanol
-method
-spectrum
-uses
-kinetics

Back 21

-PO
-horses
-for mild pain and a potent anti-tussive (cough supression)
-onset in 15 min, lasts 2-4 hours

Front 22

What makes up LA immobilon?

Back 22

Etorphine and acepromazine

Front 23

What makes up SA immobilon?

Back 23

Etorphine and methotrimeprazine

Front 24

What makes up Hypnorm?

Back 24

Fentanyl and Fluanisone

Front 25

How do local anaesthetics work?

Back 25

Act mainly by blocking Na+ channels, reducing excitability, and by activating K+ channels

Front 26

What are the two categories of LA's?

Back 26

Ester-linked and amide-linked

Front 27

Why are amide-linked LA's better than ester-linked?

Back 27

Ester-containing compounds usu inactivated in plasma and tissues (liver) by non-specific esterases.

Amides are more stable and have longer plasma t 1/2

Front 28

Pharmacokinetics of LA's

Back 28

-i/v/, spray, cream, gel
-administered around nerves requiring block
-amides are metab by liver whereas esters are broken down by plasma esterases and excreted by kidneys

Front 29

Why must LAs be weak bases?

Back 29

To penetrate the nerve sheath

Front 30

What order do LAs block axons in?

Back 30

1. small myelinated axons
2. non-myelinated axons
3. large myelinated axons

This means that nociceptive and sympathetic xmission is blocked first, really good!

Front 31

What are LA's unwanted side efx?

Back 31

Tremors and convulsions
Respiratory depression
Reduced myocardial contractility
Vasodilation - low BP
Reduces tissue healing
Allergic rxn

Front 32

Name 4 amide-linked LAs

Back 32

Lidocaine
Bupivicaine
Mepivicaine
Proxymetacaine

Front 33

Name the main ester-linked LA

Back 33

Procaine

Front 34

Lidocaine
-type
-effects

Back 34

-amide linked
-infusion lowers MAC (animal anaesthetised on lower conc)
-adrenaline prolongs duration

Front 35

Bupivicaine
-type
-effects

Back 35

-amide linked
-long acting (8 hours)
-cardiac toxicity so DONT i/v!

Front 36

Mepivicaine
-type
-effects

Back 36

-amide linked
-less vasodilation than lidocaine
-less irritant to tissues
-EXPENSIVE

Front 37

Proxymetacaine
-type
-kinetics

Back 37

-amide linked
-toxic to corneal epithelium
-rapid onset (10 sec) with 10-20 min duration

Front 38

Procaine
-type
-effects

Back 38

-ester linked
-causes vasoconstriction, possible allergen, added to penicillin to reduce pain on injection

USED IN CATTLE