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Advanced Pharmacology > Pain management > Flashcards

Pain management Flashcards

1
Q

Transduction

A
  • pain stimulus converted into nerve impulse

- impulses travel from nerve endings toward the CNS

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2
Q

Transmission

A

-impulse is carried to brain via Neospinothalamic or Paleospinothalamic pathways

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3
Q

Perception

A
  • messages from periphery are interpreted by brain

- influenced by neural circuitry and psychosocial factors

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4
Q

Modulation

A
  • brain sends signals to suppress or amplify pain signals

- gate control theory of pain

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5
Q

Fast pain receptors

A
  • felt within 0.1 secs of stimulus
  • sharp, prickling, acute, electric
  • not felt in deeper tissues
  • associated with tissue destruction
  • to stimulate brain to remove tissue from injurious agent
  • Delta A fibers
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6
Q

slow pain receptors

A
  • felt >1 sec of stim
  • increases slowly over many seconds
  • burning, aching, throbbing, nauseous
  • to remind you to allow the area to recoup
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7
Q

Types of pain stimuli

A
  • mechanical
  • thermal
  • chemical
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8
Q

What substances are released from damaged tissue that stimulate pain receptors?

A
  • Bradykinin
  • Serotonin
  • Histamine
  • K+ ions
  • Acids
  • Prostaglandins
  • Substance P
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9
Q

Neospinothalamic tract

A
  • Type A delta pain fibers (fast pain receptors)
  • mechanical and thermal pain
  • nerve fibers travel all the way to thalamus
  • pain can be localized precisely
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10
Q

Paleospinothalamic tract

A
  • Type C pain fibers (slow pain receptors)
  • Terminates widely in brainstem (pons)- signal must pass thru additional short fibers
  • chemical pain
  • not well localized, important for suffering
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11
Q

What impact does reticular formation have?

A

strong arousal on nervous activity in the brain when in severe pain- hard to sleep

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12
Q

what are the primary neurotransmitters involved in pain suppression?

A

Enkephalin and Serotonin

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13
Q

Name NSAIDs

A 
Aspirin
Diclofenac
Diflunisal
Etodolac
Fenoproten
Ibuprofen
Celecoxib
Ketorolac
Nabumetone
Naproxen
Piroxicam
Salsalate
Sulindoac
Tolmetin
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14
Q

What is the mechanism of action of NSAIDs

A
  • Covalently modifies COX1 and COX2 pathways => inhibits prostaglandin synthesis => interrupts transduction of pain
  • COX1 is found in blood vessels, stomach, kidneys, plts, and intestines (physiologic stimulation)
  • COX2 is induced by cytokines and mediators during inflammation
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15
Q

When are NSAIDs indicated?

A
  • musculoskeletal disorders
  • chronic post op pain d/t inflammation
  • pain d/t inflammation
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16
Q

Side effects of NSAIDs

A
  • d/t COX-1 inhibition
  • GI intolerance/ulcers
  • blockage of plt aggregation- stroke & MI
  • inhibited renal function- Na & H2O retention, HTN, AKI
  • prolonged gestation
  • vasomotor rhinitis
17
Q

NSAID drug interactions

A
  • potentiates anticoagulation
  • increased lithium and methotrexate toxicity
  • decreased effectiveness of antihypertensives
18
Q

What lab is important to monitor for NSAIDs

A

K+ (hyperkalemia d/t decreased renal perfusion)

19
Q

Acetaminophen

A
  • COX inhibitor (perhaps COX3 or very selective COX2)
  • better for kidneys
  • works well for fever
20
Q

What is the mechanism of action for opioids?

A
  • binds to mu receptors => inhibits nociceptive (pain) receptors in CNS
  • acts as synthetic enkaphlins
21
Q

What are other effects of opioids beyond pain management?

A
  • directly suppresses resp. and cough centers
  • stimulates chemoreceptor trigger zone (CTZ)
  • decreases HCl secretion in stomach
  • decreases biliary, pancreatic, and intestinal secretions
  • enhances nonpropulsive contractions and inhibits propulsive contractions in sm intest.
  • augments anal sphincter tone
22
Q

Side effects of opioids

A
  • N/V
  • constipation
  • urinary retention
  • mental clouding
  • dizziness
  • hypotension
23
Q

Tapentadol (Nucynta)

A
  • synthetic mu-agonist and norepi reuptake inhibitor
  • for neuropathic pain
  • ER version- for diabetic periph neuropathy
24
Q

Tramadol (Ultram)

A
  • very selective, weak mu-opioid receptor agonist
  • norepi reuptake inhibition
  • poteniates serotonin release
  • can produce physical addiction
  • risk of seizure with recreational use
25
Q

Hysingla ER

A
  • long-acting hydrocode - once daily

- abuse deterrant- cannot be chewed or crushed, thick gel that can’t be injected

26
Q

How do antidepressants help with pain

A

pain centers located very close to mood centers in the brain

27
Q

Which antidepressants are used in treating pain?

A

TCAs- esp. amitriptyline

SNRIs- duloxetine used for DPN

28
Q

How do antiepileptics help with pain?

A
  • similar chemical structure to TCAs
  • decreases synaptic transmission of pain by potentiating GABA or inhibiting glutamate
  • helpful for neuropathic pain
29
Q

Which AEDs are indicated for diabetic neuropathy?

A

Carbamazepine
Gabapentin
Pregabalin
Lamotrigine

30
Q

What medications are used as abortive therapy for migraines?

A
  • NSAIDs
  • Isometheptene
  • Ergotamine
  • “triptans”- rescue drug
  • Dopamine antagonists- last resort
  • Dihydroergotamine mesylate (DHE)
31
Q

What medications are used as prophylactic therapy for migraines?

A
  • Beta blockers
  • TCAs
  • Calcitonin gene-related peptide (CGRP) inhibitors
  • GABA inhibitors
32
Q

What agents are used as first-line therapy for migraines

A
  • Beta blockers, TCAs

- both attenuate variability in vascular tone

33
Q

CGRP inhibitors

A
  • Erenenumab (Aimovia)
  • Fremanezumab (Ajovy)
  • Galcanezumab (Emgality)
  • monoclonal antibodies
  • well tolerated, favorable adverse effect profile
34
Q

GABA inhibitors

A

Gabapentin
Topiramate
Valproic acid

Advanced Pharmacology (9 decks)

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