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clinical neuroscience 2 > Pharm- 17 > Flashcards

Pharm- 17 Flashcards

1
Q

What is the role of the limbic system in pain?

A

Responsible for emotion, social behavior, autonomic control, perception of pain, and memory

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2
Q

What happens in the descending pain modulation?

A

An ↑ or ↓ of the sensation of pain, possibly due to a 2º neural pathway

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3
Q

What is the fxn of N-type Ca channels?

A

Plays a strong role in controlling the release of neurotransmitters
AP’s generated in primary afferents induce neurotransmitter release at the dorsal horn of the spinal cord

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4
Q

What happens if u block N-tpye voltage gated Ca channels?

A

analgesia

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5
Q

Which receptors are between the C-fiber and secondary projection nuerons?

A

glutamate R’s (NMDA and AMPA)

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6
Q

What is the roles of cannabinoid receptors?

A

These have regulatory roles in the spinal cord and both are G protein-coupled

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7
Q

What is the fxn of CB1 receptors?

A

expressed in brain, spinal cord, and sensory neurons; mediator of analgesia following a stressor

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8
Q

What is the fxn of CB2 receptors?

A

largely expressed in nonneural tissue; especially immune cells including microglia. Up-regulated in spinal cord microglia after peripheral nerve injury

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9
Q

Where is substance P at?

A

dorsal horns

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10
Q

What is the fxn of substance P?

A

to aid in the signaling response to stimuli of particularly high intensity because they require higher frequency and longer-lasting action potential trains than release of glutamate-containing vesicles.

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11
Q

What is the fxn of B-endorphin, enkapalins, and dynorphins (mu, k, and d receptors) in the CNS?

A

inhibit synaptic transmission to the brain (reducing pain sensed; analgesia) and are released at several CNS sites in response to pain stimuli

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12
Q

What are the effects of opioid receptor stimulation?

A

reduced presynaptic calcium conductance (↓ Presynaptic Nt release), enhanced postsynaptic potassium conductance (↓ post-synaptic excitability), and reduced adenylyl cyclase activity. Gi crap.

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13
Q

True or False: Norepinephrine, serotonin (5-HT), glycine, and GABA are major inhibitory neurotransmitters in the dorsal horn of the spinal cord

A

True

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14
Q

What is the fxn of the NE/5-HT system for pain?

A

These systems can limit transfer of incoming sensory to the brain and descending information from the brainstem to the dorsal horn

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15
Q

What is the role of the NE receptors in the spinal cord?

A

it works on a2 receptors –> Gi mediated inhibition of pain excitation

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16
Q

What is the role of 5-HT3 ligand-gated channels in the spinal cord?

A

excitatory actions of serotonin in the spinal cord

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17
Q

What is the role of 5-HT G protein-coupled receptors in the spinal cord?

A

mediate the inhibitory actions of 5-HT

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18
Q

How does the GABA R work?

A

by hyperpolarizing the membrane by opening K+ or Cl- channels and causing an influx of Cl- or an efflux of K+ .

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19
Q

What are the 2 types of different pain perceptions can result from peripheral sensitization?

A

alldynia (noninjurous pain) and hyperalgesia

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20
Q

What causes the peripheral sensitization?

A

peripheral stimuli which induce primary afferents to lower their activation THRESHOLDS thereby making them more sensitive/responsive

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21
Q

What are the mediators to peripheral sensitization?

A

bradykinin, protons, histamine, prostaglandin E2 (EP receptors), and nerve growth factor (NGF; TrkA receptors)

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22
Q

What types of receptors do the mediators to peripheral senstization act on?

A

G-protein coupled or receptor tyrosine kinase on nociceptors

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23
Q

What is the first-line drug for peripheral sensitization?

A

NSAIDs

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24
Q

What is the mechanism of action of NSAIDs?

A

inhibits COX → ↓ prostaglandins → ↓ local inflammatory response and peripheral sensitization

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25
Q

celecoxib, rofecoxib, and valdecoxib block which COX?

A

COX2

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26
Q

celecoxib, rofecoxib, and valdecoxib have an increased risk of what?

A

MI

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27
Q

What happnens in central sensitization?

A

Hyperalgesia and allodynia can extend beyond the primary area of inflammation and tissue damage resulting in secondary hyperalgesia/allodynia; this depends on changes in sensory processing in the dorsal horn of the spinal cord.

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28
Q

Why does central sensitization occur?

A

occurs with repetitive high-intensity stimuli; synaptic transmission activates intracellular signal transduction cascades in the dorsal horn neurons that enhance the response to subsequent stimuli.

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29
Q

What are the receptors invovled with central senstiization?

A

AMPA, NMDA, glutamate, substance P receptor NK1 and the neutrophin receptor TrkB

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30
Q

How can drugs like Ketamine and Dextromethorphan treat central sensitization if it doesn’t self resolve?

A

they are NMDA receptor blockers used to oppose the activation of sensitized NMDA receptors

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31
Q

Which channels are upregulated in neuropathic pain?

A

Na-channels (1.3) in primary sensory neurons

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32
Q

What are the 2 Na-channel blockers to treat neuropathic pain?

A

carbazepine and carbamazepine

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33
Q

What is the progression of events to cause the cortical spreading depression for migranes?

A

a region of neuronal inactivation spreads across the Ca → release of mutliple peptides in the dural vasculature → trigeminal afferents from vasculature activated and sensitized → ↑activity in trigeminal afferent → secondary central sensitzation with hyperalgesia and tactile alldynia

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34
Q

What is an effetive Tx for migranes?

A

the triptan class of serotonin receptor agonist such as sumatriptan (selective for 5-HT1B & 5-HT1D receptors) and NSAIDs

35
Q

What type of migranes are triptans good at treating?

A

acute Sx but not recurring attacks

36
Q

How do ergot alkaloids treat migranes?

A

vasoconstriction

37
Q

How do full agonists to opioid receptors work?

A

produce both analgesia and other effects by acting on μ-opioid receptors and resulting in inhibition of neurotransmission

38
Q

What are some drugs that are full opioid agonists?

A

morphine, codeine, oxycodone, hydrocodone, tramadol

39
Q

What are synthetic opioid agonists?

A

utilize the μ-opioid receptors; result in inhibition of neurotransmission

40
Q

What are some example sof synthetic opioid agonists?

A

Phenlyheptylamines (methadone) and phenylpiperidines (fentanyl and meperidine)

41
Q

What do partial and mixed opioid agonists do?

A

utilize both μ & κ agonist; partial μ-receptor agonist and a κ-agonist with partial μ-receptor antagonist activity

42
Q

What are some partial/mixed opioid agonsts?

A

μ-agonist butorphanol and buprenorphine, as well as nalbuphine, a κ-agonist with μ-antagonist activity

43
Q

What do pure opioid antagonists do?

A

antagonists of μ- opioid receptors, thereby blocking endogenous and exogenous opioid effects

44
Q

What are some exampoles of pure opioid antagonists?

A

Naloxone & Naltrexone; Alvimopan & Methylnaltrexone

45
Q

What types of receptors are opioid receptors?

A

G proteins

46
Q

What are the intraceullular events that occur once an opioid receptor is activated?

A

Close voltage-gated Ca2+ channels on presynaptic nerve terminals and thereby reduce transmitter release

Hyperpolarize and thus inhibit postsynaptic neurons by opening K+ channels

47
Q

What are the physiological responses to μ receptor activation?

A

Supraspinal and spinal analgesia; sedation; inhibition of respiration; slowed GI transit; modulation of hormone and NT release

48
Q

What are the physiological responses to δ receptor activation?

A

Supraspinal and spinal analgesia; modulation of hormone and NT release

49
Q

Which drug classes act on μ and δ receptors?

A

endorphins > enkephalins > dynorphins

50
Q

What are the physiological responses to κ receptor activation?

A

Supraspinal and spinal analgesia; psychotomimetic effects; slowed GI transit

51
Q

Which drug classes act on κ receptors?

A

dynorphins > endorphins . enkephalins

52
Q

Where are the opioid receptors to inhibit pain transmission?

A

Dorsal horn

53
Q

What is tolerance?

A

repeated use of a constant dose of a drug results in a decreased therapeutic effect; development of tolerance requires either a change of analgesic drug or an increase in the dose or frequency of administration to maintain analgesia

54
Q

What is physical dependence?

A

abrupt cessation of tx results in a characteristic withdrawal syndrome

55
Q

What is addiction liability?

A

physical dependence is accompanied by drug abuse or drug-seeking behavior; need to balance the risk of addiction and under-tx of pain

56
Q

What is cardio toxicity?

A

opioids can reduce sympathetic tone and lead to orthostatic hypotension; can also cause bradycardia

57
Q

What is torsade de pointes?

A

opioids (esp methadone) can cause QT prolongation and Torsade de pointes

58
Q

Acetaminophen- mech of action

A

non-specific COX inhibitor, acts only centrally, prevents PGE2-induced reduction in glycinergic inhibiton

59
Q

Celecoxib- mech of action

A

COX-2 inhibitor

60
Q

Aspirin- mech of action

A

acetylates both COX 1 & 2 active sites therefore it tx’s mild or moderate pain

61
Q

Ibuprofen- use

A

used for analgesia and anti-inflammatory action, antipyretic, and it has lower incidence of adverse effects.

62
Q

Tramadol- mech of action

A

centrally acting analgesic; its analgesic effect results from monoaminergic effect w/in the CNS.

63
Q

What other classes of drugs help treat pain, especially in chronic pain conditions?

A

Anti-depressants

64
Q

What are the 2 ways tricyclic antidepressants treat pain?

A
  1. blocking Na channels

2. increasing the activity of NE and 5HT projections.

65
Q

What are some examples of tricyclics?

A

Amitriptyline, nortryptiline, imipramine

66
Q

Desipramine and maprotiline are examples of what class of drug that can treat pain,but are not as strong as tricyclics?

A

selective NE reuptake inhibitors

67
Q

Paracoxetine,fluoxetine and citalopram are examples of what types of drugs to treat pain,but are the least effective?

A

SSRI’s

68
Q

Define: these 2 drugs are dual NE and 5HT ruptake inhibitors, used to Tx neuropathic pain and fibromyalgia.

A

Venlafaxine and duloxetine

69
Q

Generally, how can antiepileptic and antiarrhythmic drugs treat pain?

A

by reducing neuronal excitability

70
Q

What class of meds does gabapentin belong to?

A

Antiepileptic

71
Q

Gabapentin- mech of action

A

GABA agonist, binds to a2d subunit of Ca++ channels and reduces the trafficking of the channel to the membrane.

72
Q

Pregabalin- mech of action

A

GABA analogue

73
Q

Pregabalin- use

A

potent and predictable, analgesia with neuropathic pain and fibromyalgia

74
Q

Lamotrigine- mech of action

A

Na channel blocker

75
Q

Lamotrigine- use

A

reduces painful sensory Sx that can occur in neuopathy,stroke, MS and phantomlimb

76
Q

Carbamezapine- mech of action

A

Na channel blocker

77
Q

Carbamexapine- use

A

trigeminal neuralgia

78
Q

Oxcarbazepine- mech of action

A

blocks Na channels

79
Q

Oxcarbazepine- use

A

trigeminal neuralgia and doesnt have the risk of aplastic anemia which is associated with carbamazepine

80
Q

Mexiletine- class

A

antiarrhythmatic

81
Q

Lidocaine- mech of action

A

use-dependent Na channel blocker

82
Q

Lidocaine- use

A

local anesthetic, may be administered IV for blunting ANS for high-intensity painful stimuli

83
Q

How does NMDA antagonists treat tings like chronic paina nd post-op pains?

A

NMDA R’s play a critical role in the induction and maintenance of central sensitization

84
Q

Which adrenergic receptor can you target int he dorsal horn to provide anti-nociceptive effects?

A

alpha2

clinical neuroscience 2 (16 decks)

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