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Ty's Neuro Domain Cards > Neuro Domain - Pharmacy of Pain > Flashcards

Neuro Domain - Pharmacy of Pain Flashcards

1
Q

Nociceptive Pain

A

Via activation of peripheral nociceptors (mechanical, chemical, thermal sensory stimuli)

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2
Q

Inflammatory Pain

A

associated with tissue damage and resulting infiltration of immune cells; SENSITIZATION of nociceptors either peripherally or centrally

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3
Q

Neuropathic Pain

A

associated with damage to CNS or PNS

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4
Q

TRPV1

A

receptor channel on peripheral sensory afferent terminal (nerve ending)

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5
Q

Hyperalgesia

A

increased response to noxious stimuli (aka “pain” stimuli hurts even more… like a needle poke feeling like a gun shot)

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6
Q

Allodynia

A

pain response to innocuous stimulus (aka “pain” from something that normally wouldn’t be painful like a gentle touch)

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7
Q

Sensitization

A

repeated exposure to a stimulus results in progressive amplification of a response… occurs in inflammatory pain!

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8
Q

Central sensitization

A

increased membrane excitability and synaptic efficacy and reduced inhibition

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9
Q

peripheral sensitization

A

reduced threshold and amplification in responsiveness of nociceptors

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10
Q

Role of microglia in sensitization of nociceptors

A

primary peripheral nociceptor afferents come back to dorsal horn and activate microglia… the microglia then release pro-inflammatory cyto/chemokines that modulate pain by

1) enhancing pre-synaptic release of neuroTs
2) enhancing post-synaptic excitability

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11
Q

Nerve sprouting in sensitization

A

when fibers from touch receptors synapse on dorsal horn neurons that normally only receive nociceptive input! (allodynia?)

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12
Q

(Substance P + Glutamate)-combo in sensitization

A

COMBINED release of substance P + Glutamate from primary afferents in dorsal horn causes excessive activation of NMDA receptors

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13
Q

TrkA receptors in sensitization

A

Nerve growth factor (NGF) and tumor necrosis factor (TNF) released by injured tissue is picked up by TrkA receptors in nerve terminals and retrogradely transported to DRG cell bodies causing altered gene expression!

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14
Q

Role of Nerve growth factor in sensitization (2 of em)

A

NGF increases production of Substance P and converts non-nociceptive neurons to nociceptive neurons!!! (phenotypic change!)

ALSO influences expression of “nociceptive-specific” sodium channel “Nav 1.8” in DRG

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15
Q

Nav 1.8

A

sodium channel that is specific to nociceptive neurons in DRG!!!

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16
Q

Capsaicin

A

TRPV1 agonist… thus it activates TRPV1 nerve terminals and “depletes/exhausts” the supply of Substance P so that other painful stimuli have a decreased outcome

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17
Q

Ambroxol

A

selectively blocks Nav 1.8 channels.

used to treat oral and pharyngeal cavities

(lidocaine and mexiletine are also thought to work this way which is why some dentists use lidocaine)

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18
Q

Ketamine (aka “special K”)

A

NMDA receptor antagonist

when used in combination with opioids, may decrease tolerance to opioids!

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19
Q

Gabapentin/Pregabalin

A

Anti-Convulsant

GABA analogues (GABA is an inhibitory NeuroT)

acts on V-gated CALCIUM channels

treatment of **“neuropathic & inflamm pain” **like fibromyalgia (old people have it… and old people need “calcium” for their bones)

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20
Q

Carbamazepine

A

Anti-Convulsant

blocks V-gated SODIUM channels

Gold-standard for treating trigeminal neuralgia

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21
Q

Valproic Acid (Valproate)

A

Anti-Convulsant

blocks V-gated SODIUM channels

Treatment of Migraines

22
Q

Topiramate

A

Anti-Convulsant that potentiates GABA transmission

MOA: block V-gated SODIUM channels AND blocks AMPA/kainate Glutamate receptors

Treatment of migraines

23
Q

Amitriptyline, desipramine etc.

A

Examples of tricyclic anti-depressants

can manage pain by activating endogenous opioid system by activating the descending 5-HT (serotonin) pathway

24
Q

Name 4 strong opioid receptor agonists

A

1) morphine
2) Methadone
3) Meperidine
4) Fentanyl

25
Q

Methadone

A

slightly more potent than morphine and equally efficacious

  • bioavailability exceeds morphines
  • tolerance and abstinence develop slower than morphine
  • used to treat opioid tolerance and dependence
  • Can also block NMDA and monoaminergic reuptake transporters (thus explaining ability to relieve difficult-to-treat pain)
26
Q

Meperidine

A

1/10th potency of morphine and LESS efficacious

pronounced anti-shivering vs other opioid analgesics

may accumulate in kidney with renal insufficiency

27
Q

Fentanyl

A

One of the most widely used opioid analgesics

100X more potent then morphine as an analgesic

highly lipophilic with high first pass rate

***can cause muscle rigidity thus should use neuromuscular blocking agent in conjunction

28
Q

Name 2 Partial/Weak opioid receptor agonists

A

1) oxycodone

2) codeine

29
Q

codeine

A

1/10 analgesic of morphine (from which it is synthesized)

converted to morphine by CYP 2D6

-used as an antitussive

30
Q

Oxycodone

A

Used in combo with acetaminophen (percocet) or aspirin (percodan) for oral use

used in controlle-release tablets (oxycontin)

*major drug of abuse

31
Q

Name 2 opioid receptor mixed agonist-antagonists

A

1) nalbuphine

2) buprenorphine

32
Q

nalbuphine

A

strong MOP antagonist and KOP agonist

**parenteral use only

respiratory depression a problem, and difficult to reverse with naloxone

33
Q

buprenorphine

A

partial MOP agonist but antagonist at DOP & KOP

  • used in management of opioid dependence
  • admin sublingually to avoid first pass effect

as effective as methadone in detoxification of heroin abusers and may be safer also reduces craving for alcohol but costs 10X as much as methodone

34
Q

Tramadol

A

NON-opioid analgesic

  • synthetic codeine analog
  • major MOA = inhibition of serotonin reuptake transporter
35
Q

Name 2 opioid receptor antagonists

A

1) naloxone

2) naltrexone

36
Q

Naloxone

A

competitive antagonist at MOP, DOP, & KOP

rapidly blocks agonist effects of morphine! (ie reverses resp. depression, coma etc)

Major use is to treat an acute overdose of opioid analgesics *given IV

37
Q

Naltrexone

A

Competitive antagonist at MOP, DOP, & KOP

subject to rapid first pass metabolism

blocks effects of heroin for up to 48 hours (thus longer lasting than naloxone)

***used to help prevent relapse in chronic alcoholics; may act by releasing Beta-endorphins

38
Q

MOA of local anesthetics

A

Blockade of voltage-gated sodium channels (unmyelinated, small nerve fibers are more susceptible to the effect aka those like A-delta and C-fibers for pain)

Also have a higher affinity for more active nerve fibers vs those at rest

39
Q

Name 5 local anesthetics listed

A

1) Cocaine (ester-like)
2) Tetracaine (ester-like)
3) Bupivacaine (amide-like)
4) Lidocaine (amide)
5) Mepivacaine (amide)

40
Q

Name the 5 major goals of a generalized Anesthetic

A

1) analgesia
2) muscle relaxation
3) stable CV and resp. function
4) amnesia
5) loss of consciousness

41
Q

MOA of general anesthetics (inhaled and IV)

A

GABA-A mediated inhibition… they don’t need to bind to GABA-A receptors as “agonists” but simply sensitize the GABA-A receptors to endogenous GABA which leads to an influx of chloride ions and thus hyperpolarization preventing nociceptive action potential formation

42
Q

What are the 2 general anesthetics that are exceptions to GABA-A mediated inhibition and name their MOA

A

1) Ketamine
2) Nitric Oxide
Work by inhibiting the glutamate-gated cation channel in NMDA receptors

43
Q

Neural pathways blocked during anesthesia

A

even low [ ] of anesthetics inhibit transmission of nociceptive input to neurons in substantia gelatinosa in dorsal horn and in the spinothalamic tract neurons

44
Q

How do general anesthetics cause sedation?

A

Via suppression of reticular activating system of the brainstem

45
Q

How are anesthetics similar to sleep?

A

anesthia modulates endogenous sleep regulating pathways such as the ventrolateral preoptic nucleus and tuberomammillary nuclei.

46
Q

How do anesthetics cause amnesia?

A

via actions in the hippocampus

47
Q

definition of Minimum alveolar concentration (MAC)

A

the avleolar concentration of anesthetic such that 50% of patients do not move in response to a noxious stimulus

48
Q

what does blood:gas coefficient measure and why is it important?

A

it is a measure of solubility of a gas… the higher the number, the easier the gases dissolve in the blood.

A higher solubility also means a less rapid increase of partial pressure in the arteries thus there won’t be a big change in arterial tension. (low solubility results in a fairly rapid increase in arterial tension)

49
Q

What are the 2 differences between induction and recovery phases of anesthesia?

A

1) You can enhance movement of anesthesia into lungs by increasing the concentration of drug into the air the pt. is breathing… but in recovery, manipulation of concentration of drug cannot be altered
2) In recovery you can have variations of arterial tension in different tissue whereas in induction the arterial tension due to anesthetic is zero (as it hasn’t entered yet)

50
Q

Name 4 inhaled anesthetics and one fun fact about them

A

1) desflurane (increase HR)
2) Isoflurane (increase HR)
3) Sevoflurane (no change in HR and is a bronchodilator thus is DOC for pts with pulmonary probs) also commonly used in ped. pts.
4) Nitric oxide – usually combined with others not used on its own

51
Q

Name 4 IV general anesthetics with fun facts and speed of onset

A

1) Ketamine (CV stimulant; increased cerebral blood flow) –moderately rapid post-op illusions and vivid dreams aka emergence phenomena*
2) Midazolam(benzodiazepine) – CV stability – SLOW onset
3) Propofol – RAPID induction and maintenance only with less post-op nausea
4) Thiopental (barbituate) – standard induction; CV depressant. rapidly crosses the BBB

Ty's Neuro Domain Cards (13 decks)

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