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NS_BTRAN > Unit2_PharmaFrench+Dell'Acqua > Flashcards

Unit2_PharmaFrench+Dell'Acqua Flashcards

1
Q

Acute pain is primarily _______ (with somatic more common than
visceral), although it may also be neuropathic in nature in relation to the levels of pathology.

A

nociceptive

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2
Q

Chronic Pain: ?

A

Chronic Pain: pain that persists for longer than would be expected as the healing process reduces
the pain-producing stimuli; an arbitrary threshold for chronicity (e.g., 1 month) is generally not useful.

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3
Q

What are the subtypes of chronic pain?

A
  • Pain that persists beyond the normal healing time for an acute injury
  • Pain related to a chronic disease (e.g., osteoarthritis)
  • Pain without identifiable organic cause (e.g., fibromyalgia)
  • Pain, chronic and acute, associated with cancer- multiple etiologies
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4
Q

“Normal” pain resulting from activation of nociceptive nerve fibers is what type of pain?

A

Nociceptive Pain

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5
Q

Nociceptive Pain:

Somatic pain?

Visceral pain?

A

Somatic pain (arising from skin, bone, joint, muscle, or connective tissue) is often due to musculoskeletal conditions, inflammation, or mechanical/compressive problems. Described as throbbing and well-localized.

Visceral pain (arising from internal organs) can manifest as arising from other structures (referred) or be well-localized

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6
Q

What type of pain is distinct from nociceptive pain - persists and has become disengaged from noxious stimuli or the healing process; often described in terms of chronic pain.

A

Neuropathic Pain / Functional Pain.

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7
Q

______1______ = result of nerve damage (postherpetic neuralgia, diabetic neuropathy).

______2______= abnormal operation of the nervous system. Syndromes include: fibromyalgia, irritable bowel syndrome, tension type headache.

A
  1. Neuropathic pain

2. Functional

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8
Q

What is the drug that blocks TRANSDUCTION in the acute Nociceptive pathway?

A

NSAIDs–COX inhibition

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9
Q

What is the drug that blocks TRANSMISSION in the acute Nociceptive pathway?

A
  • Local anesthetics (lidocaine): block of voltage-sensitive sodium channels (VSSC) –> reducing nociceptive stimuli action potential
  • NMDA receptor antagonists (ketamine): block glutamate receptor depolarization at 2nd order neuron –> decreased transmission of nociceptive stimuli
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10
Q

What is the drug that blocks MODULATION OF TRANSMISSION in the acute Nociceptive pathway?

A

μ-opioid receptor agonists (morphine): block glutamate-substance P release from primary neuron plus hyperpolarize 2nd order neuron → attenuation of afferent-evoked excitation of 2nd order neuron → decreased transmission of nociceptive stimuli.

  • α2-adrenergic receptor agonists (clonidine): block glutamate-substance P release from primary neuron –> attenuation of afferent-evoked excitation of 2nd order neuron -> decreased transmission of nociceptive stimuli
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11
Q

What is the TX principles of Acute Pain Management for MILD PAIN (pain scale 1-3)?

A

treated with a non-opioid (e.g., NSAID or acetaminophen) ± adjuvant analgesics (agents that are useful, but not typically classified as analgesics)

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12
Q

What is the TX principles of Acute Pain Management for MODERATE PAIN (pain scale 4-6)?

A

treated with immediate-release, short-acting opioids with slow titration, + non-opioid, ± adjuvant analgesics

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13
Q

What is the TX principles of Acute Pain Management for SEVERE PAIN (pain scale 7-10)?

A

treated with immediate-release, short-acting opioids with rapid titration, + non-opioid, ± adjuvant analgesics (most commonly local anesthetics). Commonly managed with multimodal analgesia approach.

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14
Q

What is the Prophylaxis for Migraine Headaches?

A

B-blockers, anticonvulsants, antidepressants, Ca2+ channel blockers, NSAIDs, 5-HT2 receptor antagonists

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15
Q

What is the Prophylaxis for Cluster Headaches?

A

Lithium, methysergide, verapamil

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16
Q

What is the Prophylaxis for Tension Headaches?

A

TCADs (amitriptyline), SSRIs

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17
Q

What is the Abortive therapy for Migraine Headaches?

A

DHE, ergotamine, isometheptene, NSAIDs, tramadol, triptans

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18
Q

What is the Abortive therapy for Cluster Headaches?

A

DHE, ergotamine, glucocorticoids, lidocaine, oxygen, sumatriptan

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19
Q

What is the Abortive therapy for Tensions Headaches?

A

NSAIDs, Acetaminophen

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20
Q

What is the first phase of Migraine?

A

First phase: cerebral vasoconstriction + ischemia.

Serotonin (5-HT) released from neurons/platelets = peripheral mechanism

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21
Q

What is the second phase of Migraine?

A

cerebral vasodilation + pain.

Trigeminal neurovascular system releases vasoactive peptides (substance P + calcitonin) → vasodilation, neuroinflammation of pial and dural vessels = sensory nerve discharge → stimulate nociceptive fibers of trigeminal nerve that cause pain

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22
Q

What phase of Migraine has cerebral vasoconstriction + ischemia?

A

First Phase

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23
Q

What phase of Migraine has cerebral cerebral vasodilation + pain.

A

Second Phase

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24
Q

What are the first line drug for moderate/severe migraines?

A

“-triptans” (sumatriptan / zolmitriptan)

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25
Q

What is the MOA of “-triptans” (sumatriptan / zolmitriptan):

A

Agonist activity at 5HT-1B/1D receptors →

1) Vasoconstriction of cerebral vessels → reverse vasodilation-induced throbbing headache.
2) Inhibit release of vasodilatory, neuroinflammatory, and pain causing peptides.
3) Prevent activation of pain fibers in trigeminal nerves.

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26
Q

How can you administer “-triptans” (sumatriptan / zolmitriptan)?

A

PO, Nasal, SC

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27
Q

What is the DOA of “-triptans” (sumatriptan / zolmitriptan)?

A

t ½ = 2-4 hours

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28
Q

What are ADRs of “-triptans” (sumatriptan / zolmitriptan)?

A
  1. Tingling, flushing dizziness, drowsiness, fatigue
  2. Coronary vasospasm, angina MI, cardiac arrhythmia–Heaviness/tightness/pressure in chest
  3. Stroke and death
  4. Avoid use in patients with uncontrolled HTN, cerebrovascular, coronary, or arterial disease
  5. DO NOT use within 24 hrs of ergot alkaloid or concurrently with MAOI→ vasoconstriction additive
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29
Q

What would you use to Tx mild/moderate episodes of migraine without nausea or disabling symptoms?

A

NSAIDS (ibuprofen / naproxen)

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30
Q

What is the MOA of NSAIDS (ibuprofen / naproxen)?

A

interrupts inflammatory mediator synthesis/release initiated by CGRP.

(COX-i)

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31
Q

What is the route of Administration of NSAIDS (ibuprofen / naproxen)?

A

oral

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32
Q

What is the DOA of NSAIDS (ibuprofen / naproxen)?

A

4-6 or 8-12 hours

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33
Q

What are the side effects of NSAIDS (ibuprofen / naproxen)?

A

should be avoided in patients with acute gastritis, peptic ulcer disease, renal insufficiency, and bleeding disorders

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34
Q

What drug is best used in terminating moderate/severe migraine attacks?

A

Ergot alkaloids (dihydroergotamine)

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35
Q

What is the MOA of Ergot alkaloids (dihydroergotamine)?

A

agonist at 5HT-1B/1D receptors (Similar to triptans)

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36
Q

What is the route of admin of Ergot alkaloids (dihydroergotamine)?

A

Nasal, parenteral

37
Q

What is the DOA of Ergot alkaloids (dihydroergotamine)?

A

agonist at 5HT-1B/1D receptors.

Similar to triptans

38
Q

What are the side effects of Ergot alkaloids (dihydroergotamine)?

A

a. More toxic and less effective than triptans - NOT FIRST LINE.
b. Mild effects = nausea, vomiting → treat concurrently with antiemetic.
c. Serious effects = vascular occlusion and gangrene due to stimulation of a1-adrenergic receptors.
d. AVOID USE WITH non-selective B-blockers or other vasoconstrictors (→ peripheral ischemia).

39
Q

What are the major classes of Migraine Prophylaxis? (4)

A
  1. Beta-Blockers (First-line)
  2. CCBs (Third-line)
  3. Anti-Depressants (Second-line)
  4. Anti-Convulsive (First-line)
40
Q

Prophylaxis of migraines, Beta-Blockers: ?

A

[propanolol]

Firstline
Reduce frequency and severity of migraines

Side effects: fatigue, exercise intolerance, depression, orthostatic hypotension

41
Q

Prophylaxis of migraines, Calcium Ch. Blockers:?

A

[Verapamil]

Third line
Tolerance may develop
Do not use with B-blocker = increased potential for heart block

42
Q

Prophylaxis of migraines, Anti-Depressant: ?

A

[amitriptyline]

Second line.

Can prevent migraines, given as adjunct with other prophylactic agents.

Side effects: sedation, dry mouth, constipation, tachycardia, weight gain, urinary retention.

43
Q

Prophylaxis of migraines, Anti-Convulsive: ?

A

[topiramate]

First line

Possible mechanism of alteration of neuronal transmission in CNS

Side effects: paresthesias, language and cognitive impairment, weight loss, taste perversion, fatigue.

44
Q

What are the First-line Migraine Prophylaxis drugs?

A

Beta Blockers: propanolol
&
Anticonvulsants: topiramate

45
Q

What are the Second-line Migraine Prophylaxis drugs?

A

Antidepressants: amitriptyline

46
Q

What are the Third-line Migraine Prophylaxis drugs?

A

Calcium Channel Blockers: verapamil

47
Q

Should you use Ergot alkaloids as first line agents?

A

No.

They are more TOXIC than Triptans.

Serious effects = vascular occlusion and gangrene due to stimulation of a1-adrenergic receptors.

48
Q

What headache drug should you AVOID USE WITH non-selective B-blockers or other vasoconstrictors (→ peripheral ischemia)

A

Ergot alkaloids (dihydroergotamine)

49
Q

What drug class has Agonist Activity at 5’HT-1B/1D receptors?

A

“-triptans” (sumatriptan / zolmitriptan)

50
Q

“-triptans” (sumatriptan / zolmitriptan) have Agonist Activity at 5’HT-1B/1D receptors. What are the physiological results of this and how does it help with headaches? (3)

A

1) Vasoconstriction of cerebral vessels → reverse vasodilation-induced throbbing headache
2) Inhibit release of vasodilatory, neuroinflammatory, and pain causing peptides
3) Prevent activation of pain fibers in trigeminal nerves

51
Q

What class of headache drugs has the following ADRs:

○ Stroke and death

○ Avoid use in patients with uncontrolled HTN, cerebrovascular, coronary, or arterial disease

○ DO NOT use within 24 hrs of ergot alkaloid or concurrently with MAOI→ vasoconstriction additive

A

“-triptans” (sumatriptan / zolmitriptan)

52
Q

What headache drugs should be avoided in Pt. w/ acute gastritis, peptic ulcer disease, renal insufficiency, and bleeding disorders.

A

NSAIDS

(ibuprofen / naproxen / Celecoxib / ASA / Acetaminophen):

53
Q

What Drug should you use to Tx. mild/moderate episodes of migraine without nausea or disabling symptoms?

A

NSAIDS

(ibuprofen / naproxen / Celecoxib / ASA / Acetaminophen):

54
Q

What opioid has an indication for Diarrhea conditions?

A

Loperamide - local GI tract actor

55
Q

What are the effects of Opioids on the CV system?

A

Minimal. Can be used for pain in MI and decrease cardiac load.

56
Q

What is the MAJOR Opioid contraindication?

A

any Respiratory Dysfunction!

i.e. emphysema, asthma, sleep apnea, severe obesity

57
Q

List contraindications of Opioid use:

A
  • Suspected head injury (opioids cause cerebral vasodilation → problem if pt has increased ICP)
  • Hypotension → lower BP even more
  • Shock → makes shock worse
  • Histamine release
  • Hypothyroidism
  • Impaired hepatic function → increased bioavailability and accumulation of toxic metabolites
58
Q

Which one of the 4 behavior effects is due to the buildup of toxic metabolites?

A

Behavioral excitation (sign of acute toxicity)

59
Q

What are the 3 major Adverse Drug-Drug Interactions of opioids?

A

1) CNS Depressants:
Barbiturates: additive or synergistic CNS depression

Can increase metabolism of some opioids
2) Antipsychotics (Phenothiazines)
Increase opioid analgesia, but increase respiratory depression
Increase hypotensive effect of opioids
Some can reduce analgesia

3) MAO Inhibitors and Tricyclic Antidepressants:
Increase respiratory depression
Can induce CNS excitation, delirium, and seizures

60
Q

Morphine act at what receptor?

A

Mu

61
Q

What is the Endogenous agonist for the Mu receptor?

A

B-endorphin

62
Q

Which opioid receptor does NOT have a clinical use?

A

Delta

63
Q

What is the Endogenous agonist for the kappa receptor?

A

dynorphin 1-17

64
Q

Pentazocine acts at what opioid receptor?

A

kappa

65
Q

What is the major pharmacological response of kappa receptor?

A

Pharmacological response: spinal analgesia

66
Q

What is the major pharmacological response of Mu receptor?

A

analgesia (central) and respiratory depression

67
Q

Can Tolerance be Tolerance can “generalize” to similar drugs (all mu agonists)?

A

YES.

Therefore all Mu-receptor Opioid drugs will be tolerated by the Pt. in similar manner.

Tolerance reverses following withdrawal

68
Q

What is Withdrawal with respect to Opioids?

What are the Sx of Withdrawal?

A

Occurs with cessation of opioid following prolonged use.

Sx of withdrawal: OPPOSITE to those caused by acute opioids
“Flu-like”, dilated pupils, insomnia, restlessness, yawning, rhinorrhea, sweating, diarrhea, nausea, cramps, chills
Withdrawal not life-threatening with opiates

69
Q

What drug can you use to Tx the Sx of Opiate Withdrawal?

A

Clonidine (a2-agonist)

“get closer to the alpha-2-agonist effects of: can’t see, can’t pee, can’t shit, can’t spit”

70
Q

Where do Opioid drugs act in the gut?

A

myenteric plexus (side effect-complication)

71
Q

Where do Opioid drugs act to produce analgelsia?

A

1) Periaqueductal gray (descending pain)
2) Medulla nuclei (side effect respiratory depression)
3) Spinal cord dorsal horn (ascending pain)

72
Q

Where do Opioid drugs act in the CNS?

A

Limbic and motor CNS regions:
Amygdala, hippocampus, striatum (affective response to pain)

“Reinforcement” Regions in CNS:
Ventral tegmentum, nucleus accumbens (addiction-abuse)

73
Q

What are the classes of endogenous opioids? (4)

A
  • Enkephalins
  • Endorphins
  • Dynorphin
  • Endomorphins
74
Q

Describe the endogenous opioid known as Enkephalins.

A

neurotransmitter at synapses in neurons throughout brain and spinal cord

75
Q

Describe the endogenous opioid known as Endorphins.

A

neurotransmitters and “neurohormones”.

Mostly in hypothalamic neurons and pituitary

76
Q

Describe the endogenous opioid known as Dynorphin.

A

???

77
Q

Describe the endogenous opioid known as Endomorphins.

A

opioid peptides with μ-receptor selectivity

78
Q

Which endogenous opioid is a neurotransmitter at synapses in neurons throughout brain and spinal cord?

A

Enkephalins

79
Q

What are the major μ agonists drugs? (7)

A
  • Morphine
  • Heroin
  • Hydrocodone
  • Oxycodone
  • Codeine
  • Tramadol
  • Fentanyl
80
Q

What opioid is 100x more potent than morphine?

A

Fentanyl

81
Q

What Drug is a Mu receptor agonist, but also blocks monoamine (serotonin) uptake to potentiate descending pain pathway?

A

Tramadol

82
Q

List popular Combination Opioid + NSAIDs: (5)

A
  • Codeine-acetaminophen
  • Codeine-ASA
  • Hydrocodone-acetaminophen
  • Hydrocodone-ibuprofen
  • Oxycodone-acetaminophen (aka Percocet)
83
Q

Buprenorphine is what special class of opioid?

A

Partial μ agonist

84
Q

What Opioid Drug is used as an Antitussive?

A

Antitussives: Dextromethorphan (Robitussin DM)

85
Q

What Opioid Drug is used as an Antidiarrheals?

A

Loperamide (oral)

86
Q

What drug is a μ ANTAGONIST?

A

Naloxone (Narcan)

[Competitive antagonist]

87
Q

What is Naloxone (Narcan) used for?

A

Tx of OD with long-acting agonists

88
Q

What are some drugs used to Tx constipation side effects of opioid use?

A
  • Bisacodyl-senna (stimulant laxative)
  • Docusate (stool softener)
  • Magnesium hydroxide (osmotic laxative)
  • Polyethylene glycol (osmotic laxative)

NS_BTRAN (21 decks)

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