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NEUROSCIENCE OF PAIN > LECTURE 8 > Flashcards

LECTURE 8 Flashcards

1
Q

LA MECHANISM

A

ACTS BY BLOCKING SENSORY AND MOTOR NERVE CONDUCTION TO PRODUCE A LOSS OF SENSATION W/O LOSS IN CONSCIOUSNESS (BLOCKS NA+V CHANNELS OF EXCITED CELLS)
VERY LIPOPHILIC AND HYDROPHILIC
I.E. BLOCKS CONDUCTION INTO SPINAL CORD (SENSORY) AND OUT OF SPINAL CORD (MOTOR)

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2
Q

AP FIRING

A
  1. ) RESTING MEMBRANE POTENTIAL - ALL NA+ AND K+ CHANNELS ARE CLOSED - INACTIVATION GATES OPEN
  2. ) DEPOLARIZATION - STIMULUS STRENGTH REACHES THRESHOLD, VOLTAGE-GATED NA+ CHANNELS OPEN, NA+ LEAVES
  3. ) REPOLARIZATION - NA+ CHANNELS INACTIVATE AND K+ CHANNELS OPEN
  4. ) HYPERPOLARIZATION - CELLS HYPERPOLARIZE UNTIL K+ CHANNELS CLOSE CAUSING RELATIVE REFRACTORY PERIOD INACTIVATION AND ACTIVATION GATES ARE RESET ON NA+ CHANNELS
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3
Q

LA EFFECT ON AP

A

REVERSIBLY BLOCKS IMPULSE CONDUCTION ALONG NERVE AXONS (BLOCKS NA+ INFLUX) AND CAUSES A SLOW PROPAGATION OF NERVE IMPULSES BY REDUCING THE RATE OF RISE OF THE AP AND REPOLARIZATION
THIS INCREASES THE THRESHOLD FOR CONDUCTION

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4
Q

LA CHARACTERIZATION

A

SEPARATED BY

  1. ) POTENTIAL TOXICITY
  2. ) STRUCTURE
  3. ) DURATION OF ACTION
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5
Q

LA FAVORS

A

1.) SMALLER RATHER THAN LARGER NERVES
IT IS EASY TO DIFFUSE THROUGHOUT ENTIRE NERVE IF IT IS SMALLER
2.) MYELINATED NERVES RATHER THAN UNMYELINATED NERVES
MYELINATED NERVES ONLY LEAVE NODES OF RANVIER TO DEACTIVATE WHEREAS, UNMYELINATED NERVES LEAVE THE ENTIRE NERVE
3.) ACTIVE NERVES RATHER THAN RESTING NERVES
NAV CHANNELS HAVE TO BE OPEN FOR LA TO BIND INTRACELLULARLY
I.E. DELTA FIBERS NUMBED BEFORE C FIBERS, SENSORY FIBERS ARE NUMBED BEFORE MOTOR NERVES, CNS IS MORE ACTIVE THAN PNS

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6
Q

LA STRUCTURE

A

LIPOPHILIC (AROMATIC) TAIL
INTERMEDIATE CHAIN (DIFFERENTIATES LAs INTO ESTER/AMIDE-BASED STRUCTURES)
HYDROPHILIC HEAD
WEAK BASES - PARTLY LIPID/WATER SOLUBLE - IMPORTANT B/C OF LOCATION OF INTRACELLULAR RECEPTOR

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7
Q

LA DoA

A

ESTERS -
PROCAINE < COCAINE < TETRACAINE
AMIDES -
LIDOCAINE < BUPRIVICAINE

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8
Q

LA METABOLISM

A

ESTERS - BROKEN DOWN BY PLASMA CHOLINESTERASE
AMIDES - BROKEN DOWN BY LIVER MICROSOMAL ENZYMES*
*THIS ALLOWS FOR POTENTIAL DRUG-DRUG INTERACTIONS, LIVER DISEASE PROLONGS T1/2 OF LA AS WELL AS DECREASED HEPATIC BLOOD FLOW
BOTH ARE EXCRETED IN THE URINE

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9
Q

DIFFERENT TYPES OF SPINAL BLOCKS

A

1.) EPIDURAL - NEAR DURA; HOWEVER, DOES NOT ENTER THE SPINE
SPINAL NERVES ARE ANESTHITIZED AS THEY LEAVE THE CORD
DEADENS SENSORY PAIN AND LEAVES A LITTLE MOTOR ABILITY GIVING THE ANESTHESIOLOGIST A LOT OF CONTROL
2.) SPINAL BLOCK - ENTERS THE DURA AND INTO THE CSF
BLOCKS ALL IN- AND OUT-GOING SIGNALS
LA IS ABLE TO DIFFUSE UP, DOWN, AND AROUND SITE OF INJECTION
3.) CAUDAL BLOCK - BLOCKS CONDUCTION IN ALL NERVES COMING OUT OR GOING IN AT THE BOTTOM OF THE SPINE

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10
Q

LA CHOICE IS BASED HEAVILY ON…

A

DURATION OF ACTION (WOULD RATHER HAVE 1 INJECTION OF LONG-ACTING LA THAN 2 SHORT-ACTING INJECTIONS… COULD CAUSE TACHYPHYLAXIS)

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11
Q

ADVERSE EFFECTS OF LA

A

USUALLY W/IN THE CNS
LIGHT HEADEDNESS, SEDATION, RESTLESSNESS, NYSTAGMUS, CONVULSIONS, COMA, RESPIRATORY DEPRESSION, DEATH
WANT TO KEEP LA OUT OF CNS BY ADDING EPINEPHRINE OR NOREPINEPHRINE (VASOCONSTRICTORS WHEN THEY TRIGGER ALPHA-1 IN BLOOD VESSELS)

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12
Q

ESTER LAs

A

PROCAINE - LOW POTENCY, SLOW ONSET, SHORT ACTION (LIMITS USE)
COCAINE - INCREASES VASOCONSTRICTION AND ACTS AS AN LA ON ITS OWN, MEDIUM DURATION, SCHEDULE II DRUG
TETRACAINE - LONG DURATION, POTENT BUT TOXIC ABILITIES (USED FOR SPINAL ANESTHESIA)
BENZOCAINE - TOPICAL ONLY, SUSTAINED ACTION W/ NO SYSTEMIC ABSORBANCE, METHEMOGLOBINEMIA

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13
Q

AMIDE LAs

A

LIDOCAINE - MOST WIDELY USED, MANY APPLICATIONS FOR INTERMEDIATE DURATION
BUPIVICAINE - LONG DURATION, POPULAR FOR POST-OPERATIONAL PATIENTS AND LABOR
PRILOCAINE - LITTLE VASODILATION - LESS TOXIC THAN LIDOCAINE, METABOLITE => METHEMOGLOBINEMIA

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14
Q

NEUROPATHIC PAIN

A

MAINTAINED ECTOPICALLY (FIRING ON ITS OWN DUE TO EXTREME SENSITIZATION) DUE TO A DYSFUNCTION IN ACTIVITY OF TISSUE NOCICEPTORS AND/OR BY ABNORMAL PAIN SIGNALING IN THE CNS

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15
Q

TREATMENT OPTIONS OF NEUROPATHIC PAIN

A

ANTICONVULSANTS
ANTIDEPRESSANTS
PHYTO- AND ENDO-CANNABINOIDS

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16
Q

ANTICONVULSANTS

A

BLOCK ECTOPIC NEURONS FROM CONTINUALLY FIRING BY ATTACKING NA+ CHANNELS

17
Q

ANTICONVULSANTS ACT BY

A
  1. ) BLOCKING LOW THRESHOLD CA2+ CHANNELS
  2. ) ENHANCING GABA YIELDING AN INCREASE IN INHIBITION
  3. ) DECREASING GLUTAMATE RELEASE WHICH YIELDS A DECREASE IN EXCITATION
  4. ) LONGER REFRACTORY PERIOD AND SLOWS THE PROCESS OF REPOLARIZATION
18
Q

NAv CHANNELS INVOLVED IN NEUROPATHIC PAIN

A

NAv 1.3, 1.7, 1.8 (9 IN TOTAL)
NAv 1.7 = LOSS OF FUNCTION MUTATION WHICH YIELDS INACTIVE CHANNELS (CONGENITAL INSENSITIVITY TO PAIN)
GAIN OF FUNCTION MUTATION YIELDS PAROXYSMAL EXTREME PAIN DISORDER (SEVERE RECTAL, OCULAR AND MANDIBULAR PAIN)
I.E. CARBEMAZEPINE, PHENYTOIN, VALPROIC ACID, TOPIRAMATE

19
Q

CAv CHANNELS INVOLVED IN NEUROPATHIC PAIN

A

CAv 2.2 CHANNELS ARE ACTED UPON BY GABAPENTIN AND PREGABLIN –> ALPHA-2 SUBUNIT OF CHANNELS BINDS THE DRUG AND PREVENTS NEUROTRANSMITTER RELEASE
CONOTOXIN PEPTIDE FROM CONUS MAGNUS PROVIDES RELIEF FROM THE SEVERE PAIN

20
Q

ANTIDEPRESSANTS

A

HIGH COMORBIDITY BETWEEN SLEEP DEPRIVATION, DEPRESSION AND CHRONIC PAIN

21
Q

5-HT ROLE IN ANTIDEPRESSANTS

A

5-HT NEURONS LOCALIZED TO RVM

ANALGESIA IN SPINE MEDIATED BY 5-HT 1ALPHA RECEPTORS BUT OTHER RECEPTORS EXIST TOO

22
Q

NE ROLE IN ANTIDEPRESSANTS

A

SPINAL ALPHA-2 RECEPTORS ALSO MEDIATE ANTINOCICEPTION

23
Q

3 TYPES OF ANTIDEPRESSANTS

A
  1. ) TRICYCLICS
  2. ) SNRIs
  3. ) SSRIs - MOST POPULAR AND SAFE
24
Q

TRICYCLIC MECHANISM

A

BLOCK REUPTAKE VERY WELL; HOWEVER, CAUSE A LOT OF SIDE EFFECTS (I.E. DRUG-DRUG INTERACTIONS)
BLOCK PUMPS FROM REUPTAKING 5-HT AND NE IN THE CLEFT AND LEAVING THEM THERE FOR A HIGHER POTENTIAL EFFECT POST-SYNAPTICALLY
AUTO-RECEPTORS STIMULATED (ALPHA-2, 5-HT-1-ALPHA) YIELD A DECREASE IN 5-HT AND NE NEUROTRANSMITTER RELEASE
EX. AMITRIPTYLINE, NORTRIPTYLINE, IMIPRAMINE, DESIPRAMINE

25
Q

ENDOCANNABINOIDS

A

ENDOGENEOUS REGULATORS AND BIND TO RECEPTORS
CB1 - BRAIN (HIGH, LEARNING, PAIN)*
CB2 - IMMUNE CELLS (INFLAMMATION)*
*THC BINDS TO BOTH

ACT AS ALLOSTERIC MESSENGERS - PRODUCED AT THE SITE OF MOST NEED WHERE THEY ARE RELEASED FROM A POST-SYNAPTIC CELL AND BIND TO A PRE-SYNAPTIC CELL
ACTIVATION OF GABA => SYNTHESIS OF ENDOCANNABINOIDS

26
Q

ENDOCANNABINOIDS BIND TO CB1R

A

CAUSES A…

  1. ) DECREASE IN PRESYNAPTIC ADENYLYL CYCLASE
  2. ) DECREASE IN cAMP
  3. ) DECREASE IN CA2+ INFLUX (DECREASES THE AMOUNT OF NEUROTRANSMITTER RELEASED)
  4. ) INCREASE IN K+ EFFLUX
27
Q

CLINICAL CANNABINOID AGENTS

A 
CANNABIS (MARIJUANA) => ENTOURAGE EFFECT
DRONABINOL (MARINOL) = DELTA-9-THC
AFFINITY FOR CB1/CB2
USES NATURALLY MADE THC
NABILONE - DELTA-9-THC ANALOGUE
USES SYNTHETICALLY MADE THC
SATIVEX - BUCCAL SPRAY 
AIDS IN SPASTICITY AND NEUROPATHIC PAIN REDUCTION - ASSOCIATED W/ MS AND CANCER PAIN REDUCTION

NEUROSCIENCE OF PAIN (8 decks)

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