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NMSP II Exam 1 > Drugs for Pain (Wolff) > Flashcards

Drugs for Pain (Wolff) Flashcards

1
Q

What are 4 common classes of adjuvant therapy for pain (T/S/AC/TA)?

A
  1. TCAs
  2. SNRIs
  3. anticonvulsants
  4. topical anesthetics
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2
Q

Aspirin

What is its MOA, what is it used for, and what are 4 common toxicities it can cause in patients (U/B/RS/SC)?

A

MOA: IRREVERSIBLY inhibits COX-1 AND COX-2 (platelet inhibition lasts its lifetime)
- administered orally, rectally

  • used for a variety of painful issues

T: ulcers, inc. risk of BLEEDS, Reye Syndrome (<18 yo w/chicken-pox or flu), and inc. Serum Creatinine

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3
Q

How does Aspirin/Salicylate lead to Metabolic Acidosis?

A
  • salicylates uncouple the mitochondrial oxidative phosphorylation in CNS, which the respiratory center registers as HYPOXEMIA due to dec. ATP
    • causes patient to HYPERVENTILATE
  • hyperventilation leads to dec. CO2, causing respiratory alkalosis which causes kidney to deplete bicarbonate
  • organic acids accumulate because ATP is no longer generated = inc. lactic acidosis –> life-threatening metabolic syndrome
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4
Q

Ibuprofen

What is its MOA, what are its 2 common uses, and what are 3 serious toxicities of use (O/MI/B)?

A

MOA: REVERSIBLY inhibits COX-1 AND COX-2
- administered orally

  • used for reduction of fever and pain management

T: Oligohydramnios (also premature ductus arteriosus closure) in pregnant women, inc. risk of MI/stroke, GI BLEEDING

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5
Q

How is Naproxen different than Ibuprofen?

A
  • naproxen has a longer half-life (t1/2 - 12-17 hrs) than ibuprofen (t1/2 - 2 hrs)
  • naproxen is available for ONCE DAILY dosing
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6
Q

Celecoxib

What is its MOA, what is it used for, and what are 3 serious toxicities of use (O/M/GI)?

A

MOA: inhibits prostaglandin synthesis by COX-2 BUT NOT COX-1

  • administered orally (capsule)
  • prolonged absorption = low solubility
  • used for acute pain management

T: Oligohydramnios/closure of ductus arteriosus, inc risk of MI/stroke, and serious GI RISKS (bleed/ulceration/perforation

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7
Q

Why are Thrombotic events like MI and Stroke more of a problem with COX-2 inhibitors, like Celecoxib, than with COX-1 and COX-2 inhibitors?

A
  • COX-2 inhibitors do NOT inhibit thromboxane synthesis in platelets, meaning that thrombotic events are MORE likely to develop than if patient was using dual COX inhibiting drugs
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8
Q

What are two conditions that Aspirin is very useful in helping treat?

A
  1. Rheumatoid Arthritis

2. Chronic Inflammatory Conditions

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9
Q

What are two things that should be done to help minimize the risk of aspirin-induced ulceration in patients?

A
  1. test for/eliminate H.pylori infections BEFORE starting therapy
  2. give a Proton Pump Inhibitor in addition
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10
Q

When should non-aspirin NSAIDS, like ibuprofen and naproxen, be taken when also using aspirin and why?

A
  • should be taken 2 hours AFTER aspirin use
  • non-aspirin NSAIDS antagonize the antiplatelet actions of aspirin, thus dec. protection against MI and STROKE

non-aspirin NSAIDS should be used at LOWEST effective dosage for SHORTEST possible time possible

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11
Q

Which NSAID is recommended for use in patients with Cardiovascular Complications that REQUIRE therapy?

A

Naproxen

- has long half-life and is relatively non-selective

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12
Q

What are 5 common contraindications for NSAID use (C/U/C/A/A)?

A
  1. Chronic Kidney Dz (creatine clearance < 60 mL/min)
  2. active duodenal/gastric ULCER
  3. Cardiovascular Dz (heart failure, uncontrollable HTN)
  4. NSAID Allergy
  5. ongoing ANTICOAGULANT treatment (Warfarin)
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13
Q

Acetaminophen

What is its MOA, what is it used for, and what are 2 major toxicities of use?

A

MOA: not fully understood but believed activation of descending serotonergic inhibitory pathways in CNS and inhib. of hypothalamic heat-regulating center
- administered orally and parenterally

  • used for temporary reduction of fever and pain, but does NOT SUPRESS INFLAMMATION

T: medication errors can lead to HEPATOTOXICITY with acute liver failure and DEATH

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14
Q

When does Acetaminophen become toxic and what is used as an antidote to Acetaminophen poisoning?

A
  • becomes toxic when GLUTATHIONE is depleted

- use N-acetylcysteine as an antidote

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15
Q

What 3 things does Acetaminophen NOT cause?

A
  • does NOT cause GI ulceration
  • does NOT suppress platelet aggregation
  • does NOT impair renal function
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16
Q

What drug does Acetaminophen block the metabolism of, leading to inc. risk of bleeding?

A

Warfarin

17
Q

Morphine

What is its MOA, what is it used for, and what are two toxicities of use?

A

MOA: binds to opioid receptors in CNS leading to inhibition of ascending pain pathway and alters perception of pain response
- 2nd line for treatment of Nociceptive pain

  • used for pain management and acute/chronic pain

T: respiratory depression and CNS depression

18
Q

What drugs are used in Management of Neuropathic Pain:

  1. First Line (C/S/T)
  2. Second Line (VA/O/T)
  3. Third Line (N/A/T/B)
  4. Fourth Line - ineffective analgesia (B/Z)
A
  1. calcium channel alpha2delta ligands, SNRIs, TCAs
  2. valproic acid, opioids, tramadol
  3. NMDA antag., analgesic combos, tizanidine/baclofen
  4. Botulinum toxin, intrathecal ziconotide
19
Q

Amitriptyline

What is its MOA, what two things is it used for, and what is a major toxicity of use (SI)?

A

MOA: tricyclic antidepressant (TCA) that inhibits NE/serotonin reuptake by presynaptic neuronal membrane pump (inc. synaptic concentrations)

  • used for Unipolar Major Depressive Disorder and Neuropathic Pain

T: inc. risk of suicidal thinking/behavior in children, adolescents, and young adults

20
Q

Duloxetine

What is its MOA, what is it used for, and what are two toxicities of use (SI/H)?

Who is this drug especially useful for?

A

MOA: SNRI that is potent inhibitor of serotonin/NE reuptake and is also a weak dopamine reuptake inhibitor

  • used for Neuropathic Pain associated with DM

T: suicidal ideations/behaviors and hyponatremia (SIADH)

especially useful for patients with Neuropathic Pain with concurrent depression

21
Q

Pregabalin (Gabapentin)

What is its MOA, what two things is it used for, and when are pain benefits usually seen?

A

MOA: binds to a2d subunit of voltage-gated calcium channels that does NOT bind to GABA receptors
- inhibits excitatory neurotransmitter release

  • used for Neuropathic Pain and seizures
  • pain benefits evident in the first week of use

do NOT discontinue abruptly due to increased risk of seizures

22
Q

What are the 4 approved indications for Pregabalin use?

NP/PN/S/F

A
  1. Neuropathic pain with diabetic neuropathy
  2. Postherpetic neuralgia
  3. seizures
  4. fibromyalgia

FIRST DRUG approved for use with fibromyalgia

23
Q

Tramadol

What is its MOA, what is it used for, and what are 4 toxicities of use (RD/A/C/WS)?

A

MOA: partial agonist at mu-opiate receptors in CNS and inhibits NE/serotonin reuptake

  • used for altering perception of/response to pain (pain relief)

T: respiratory depression, addiction, CYP450 inducer, withdrawal syndrome

low abuse potential but used for suicide

24
Q

Tapentadol

What is it and who is it reserved for?

A
  • moderate-strong opioid agonist that also blocks NE reuptake
  • reserved for patients who are not effectively treated with other non-opioids and opioids
25
Q

Ketamine

What is its MOA, what is it used for, and what is a major toxicity of use?

A

MOA: noncompetitive NMDA receptor antagonist that causes dissociation from pts. surrounding environment
- given IV

  • used for induction/maintenance of general anesthesia and sub-doses for acute/chronic pain/analgesia

T: prolonged emergence from anesthesia (carefully monitor)

helps reduce amount of morphine needed for pain control

26
Q

Dexmedetomidine

What is its MOA, what is it used for, and how is it administered?

A

MOA: selective a2-adrenoreceptor agonist with sedative properties due to receptor activation in brainstem
- inhibits NE release; causes periph. vasoconstriction

  • used for sedation of ventilator patients in the ICU and procedural sedation
  • administered IV (unlike clonidine)
27
Q

What is Clonidine used for (H/P) and how is it administered vs Dexmedetomidine?

A
  • a2 adrenergic agonist used for HYPERTENSION and severe PAIN RELIEF
  • administered as continuous infusion through EPIDURAL CATHETER (vs Dexmedetomidine = IV)

treats severe cancer pain in those not treated effectively with opioid alone

28
Q

Ziconotide

What is its MOA, what is it used for, how is it administered, and what are two toxicities of use (PS/PH)?

A

MOA: selective N-type voltage-sensitive Ca channels on nociceptive afferent nerves of DORSAL HORN that blocks excitatory neurotransmitter release
- dec. painful stimuli sensitivity

  • used for severe chronic pain in patients requiring INTRATHECAL THERAPY that are INTOLERANT/REFRACTORY to other therapies

T: psychiatric symptoms, inc. risk of significant patient harm when used in error

29
Q

How do these Topical Anti-Pain Agents work:

  1. Capsaicin
  2. Camphor
  3. Menthol
  4. Lidocaine
A
  1. stims TRPV1 –> depletes substance P (heat from red pepper)
  2. stims TRPV1 –> heat similar to Capsaicin
  3. stims TRPM8 –> causes cooling sensation
  4. topical Na channel blocker in Aspercreme
30
Q

Sumatriptan

What is its MOA, what is it used for, and what are 3 toxicities of use (TdP/MI/S)?

A

MOA: selective 5-HT1B/HT1D agonist causing vasoconstriction and dec. neurogenic inflammation

  • used for migraine of moderate-severe intensity and cyclic vomiting syndrome (SubQ has most availability)

T: Torsades de Points, MI (vasospasm), stroke (HTN)

31
Q

Lasmiditan

What is its MOA, what is it used for, and how is it administered?

A

MOA: high-affinity selective 5-HT1F agonist

  • used to treat migraine WITHOUT causing vasoconstriction
  • administered by PO tablets
32
Q

Ubrogepant

What is its MOA, what is it used for, and how is it administered?

A

MOA: calcitonin gene related peptide (CGRP) receptor antagonist that inhibits pathologic dilation of intracranial arteries WITHOUT reflexive VASOCONSTRICTION

  • used for migraine with/without aura in adults
  • administered by PO tablets
33
Q

Dihydroergotamine

What is its MOA, what is it used for, and what is its major toxicity?

A

MOA: ergot alkaloid binding to multiple receptors that constricts BVs and can cause behavioral disturbances and distal gangrene

  • used as LATE TREATMENT for migraine, as well as cluster headaches

T: contraindicated w/inhibitors of CYP3A4 due to inc. risk of vasospasm –> cerebral ischemia and ischemia of extremities

NMSP II Exam 1 (6 decks)

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