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Human basic neuroscience > Lecture 17, 18: Pain > Flashcards

Lecture 17, 18: Pain Flashcards

1
Q

Discriminative pain

A

Ability to perceive and localize

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2
Q

Affective pain

A

Behaviors and emotions that affect mood and motivation

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3
Q

Pain information is carried in which spinal tract? Which fibers? What thalamic nuclei?

A

Spinothalamic; Ad and C fibers; VPL and VPM (face)

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4
Q

Affective pain nuclei in pons

A

Parabrachial nucleus (ACh cells)

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5
Q

Affective pain nuclei in midbrain

A

Periaquaductal gray

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6
Q

Affective pain nuclei in thalamus

A

VM and MD (recieves a lot of limbic information, relays to PFC)

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7
Q

Affective pain nuclei in forebrain

A

Amygdala (fear), globus pallidus (mediates decision making)

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8
Q

Affective pain nuclei in hypothalamus

A

VMH

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9
Q

MD projects to…

A

Cingulate (and PFC)

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10
Q

VM projects to…

A

S1 and insula

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11
Q

Limbic system contributes what to pain? What structures?

A

Emotional content; amygdala/cingulate

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12
Q

Motor/cognitive systems contribute what to pain? What structures?

A

Motivation; GP, insula, cingulate, S1

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13
Q

Hypothalamus contribute what to pain? What structures?

A

Generation of appropriate beavhiors to threats; VMH

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14
Q

Descending systems contribute what to pain? What structures?

A

Transmission of nociceptive info back down to dorsal horn of spinal cord; amygdala, VMH, PAG, rostroventral medulla (parabrachial, LC, raphe)

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15
Q

What structure directly projects to the descending systems of the spinal cord?

A

PAG

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16
Q

Raphe and LC nuclei project to what kind of dorsal horn neuron? What do these projects to? Effect?

A

Local circuit inhibitory endogenous opioid neurons; Ad or C axons AND dendrites of neurons rising up the spinothalamic tract; diminish pain signal

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17
Q

General types of pain disorders (4)

A

Nociceptive, inflammatory, dysfunctional, neuropathic

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18
Q

Nociceptive pain

A

Physiological pain produced by noxious stimuli that achieves high-threshold nociceptor neurons, protective

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19
Q

What fiber mediates first pain? Second pain?

A

Ad; C

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20
Q

Why is visceral pain able to generate referred pain?

A

Cutaneous and visceral neurons carrying pain information converge on the same neuron in dorsal horn

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21
Q

Inflammatory pain; always require stimulus?

A

Pain hypersensitivty due to peripheral inflammation, adaptive and reversible (protects during healing); NO, pain at baseline AND a not necessarily a painful stimulus can worsen (allodynia and hyperalgesia)

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22
Q

Allodynia and how? (pathway)

A

Normally non-painful stimuli becomes painful (sunburn); Ab fibers and C fibers can both synapse on the same inhibitory local circuit neuron, which then synapses on spinothalamic system

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23
Q

Hyperalgesia and how? What is this phenomenon called?

A

Exaggerated response to a normally painful stimulus; enhanced synaptic signaling in dorsal horn between Ad/C fibers and spinothalamic tract; central sensitization

24
Q

Dysfunctional pain; always require stimulus?

A

Same features as inflammatory pain, but w/out evidence of inflammation, neither protects nor supports healing (fibromyalgia); NO (can be spontaneous)

25
Q

Neuropathic pain; always require stimulus?

A

Maladaptive plasticity caused by lesion/disease that alters nociceptive processing, can affect every stimulus in pain pathway, difficult to treat; NO

26
Q

Phantom limb pain arises from…

A

Maladaptive reorganization of connections (plasticity/sprouting) in CNS centers, particularly S1

27
Q

Treatments of neuropathic pain (4)

A

Antidepressants (enhances monoamine descending inhibitory control); anticonvulsants (block ectopic discharge and transmitter release); opioids (enhances endogenous opioid systems); cannabiniods (reduces pain-related activity in amygdala/cingulate); topical therapies (blast NTs out of pain pathways for temporary relief)

28
Q

Difficulties in treating neuropathic pathways (2)

A

Synapses throughout CNS and PNS make targeting treatment difficult and opioids can co-opt reward pathways leading to addiction

29
Q

Structural features of local anesthetics (3)

A
  1. Aromatic group (lipophilic); 2. Amino group (ionizable); 3. Linker region (amide vs ester)
30
Q

Duration of local anesthetics depends on…

A

Lipophilicity (more lipophilic/longer chain, longer action)

31
Q

How does benzocaine’s structure make it unique?

A

Non-ionizable, only topical

32
Q

Molecular target of local anesthetics…Structure? Where does the drug bind and how?

A

VG-Na+ Channel; four domains w/ 6 transmembrane channels, S4 helices are voltage sensors that open w/ depolarization; binds w/in pore of channel from INTRACELLULAR side

33
Q

What form of local anesthetic has higher affinity for Na+ pore?

A

Ionized

34
Q

Most LAs are weak/strong bases/acids with pKas between…

A

Weak bases, 7.5 - 9

35
Q

If the tissue pH is lower, what is the effect on LAs?

A

Less drug will be in the lipophilic form (less potent)

36
Q

About what percent of LAs passe into the membrane? What route?

A

10%; “Intracelluar Route”

37
Q

If a drug is only in uncharged form, what route? Major/minor? Require activity of cell?

A

Can diffuse INTO (not through) lipid bilayer and enter binding site = “Membrane Deliminated”; minor; cell does not have to be active

38
Q

LAs require the cell to be…This is called?

A

Active (firing APs = open Na+ channel); “Use-dependent blockade”

39
Q

T/F: Is the axon cell membrane the only barrier to the therapeutic binding site?

A

No! Epi/peri/endoneurium must also be transversed (requiring many transformations)

40
Q

Relate potency and hydrophobicity

A

More hydrophobic accumulate in lipid bilayer = more potent (but slower)

41
Q

What fiber type is the most sensitive to LAs?

A

C-type AND sympathetic post-ganglionic fibers (alpha receptors leading to vasodilation); Ad fibers also sensitive

42
Q

Why is a vasoconstrictor administered with a LA?

A

Increases duration of effect and reduce systemic adverse effects

43
Q

Esters are hydrolyzed by…why is this important? What are they metabolized into? Why is this important?

A

Pseudocholinesterases; metabolized locally so low risk of systemic effects; PABA = common hypersensitivty drug

44
Q

Amides are hydrolyzed by what and where? Why important?

A

P-450 enzymes, liver (so require systemic circulation); greater risk of systemic effects, bad for pts with liver disease

45
Q

Adverse effects of LAs: CNS

A

Sedation –> seizures and loss of consciousness

46
Q

Adverse effects of LAs: cardiac

A

Block of cardiac Na+ channels (arrhythmias: AV-block; ventricular arrest)

47
Q

T/F: Cadiac effects before CNS

A

False! CNS before cardio

48
Q

Routes of administration of LAs

A

Topical, inject near a nerve (infiltration, field block, nerve block, epidural, spinal), regional block

49
Q

Cocaine

A

Topical use on mucous membrane anesthetic, vasoconstrictor

50
Q

Procaine (novocaine)

A

Infiltrate w/ low potency, slow onset, short duration

51
Q

Tetracaine

A

Spinal block/topical w/ slow onset, but more potent/longer acting

52
Q

Benzocaine

A

Non-ionzable, only surface

53
Q

Lidocaine

A

Most common local anesthetic w/ rapid onset and high extraction by liver

54
Q

Prilocaine

A

Side effect: methemoglobinemia (Fe3+ –> Fe2+ in hemoglobin)

55
Q

Bupivacaine

A

Blocks sensory > motor neurons (good for labor)

56
Q

Ropivacaine

A

Correct isomer of bupivacaine

Human basic neuroscience (68 decks)

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