Opioids And Analgesics Flashcards

1
Q

What are nociceptors

A

They are first order neurons.

Sensory ends are located at skin, joints, or where the injury would occur. The dendrites are the sensory end of the nociceptor.

The sense travels up the neuron and transmitted to where the axon terminals are (neuro transmission) which is the second motor neuron

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2
Q

What is the second order neuron

A

Dorsal horn of the spinal cord, crossed over to the opposite side of the spinal cord and travels up the lateral spinothalamic tract to the thalamus

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3
Q

Third order neuron

A

Synapse between second and third neurons in the thalamus and that impulse gets distributed to multiple areas of the brain including motor, emotional, somatic area

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4
Q

What includes a family of peptides that are widely distributed in the cns and the peripheral nervous system and they function as neuro modulators, neurotransmitters, and neurohormones?

A

Endogenous opioids. Endorphins, enkephalins, and dynorphins.

They allow the body to damp down pain sensations

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5
Q

What is the “pain gate”

A

Descending inhibitory pathways release endorphins that dampen pain response. Occurs at second

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6
Q

What do Presynaptic opioid receptors activate ?

A

They activate signal transduction pathways that inhibit the n-type voltage-dependent calcium channels which blocks exocytosis and the release of excitatory neurotransmitters (like glutamate and substance p)

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7
Q

What do postsynaptic opioid receptors activate?

A

They activate Signal transduction pathways that open potassium channels which hyperpolarize membranes and block the formation of action potentials that are essential for transmitting pain sensations

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8
Q

What are mu (u1) (MOR) receptors

A

Induce analgesia, euphoria, physical dependence

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9
Q

What are mu (u2) (MOR) receptors

A

Cause sedation, bradycardia, and respiratory depression

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10
Q

What are delta (d)(DOR) receptors ?

A

Mediate spinal anesthesia and the development of tolerance to opioids

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11
Q

Kappa (k) (KOR) receptors

A

Mediate spinal anesthesia, miosis, and sedation a

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12
Q

The long term treatment of pain associated with cancer is compromised by the development of tolerance to opioid medications. How could the combined use of delta receptor antagonist and a mu receptor agonist address this problem?

A

If we block the delta receptors we could block the tolerance while still getting relief by agonizing the mu’s

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13
Q

Tissue injury/pain flow chart

A

Tissue injury (chemical injury, mechanical injury, inflammation, deprivation of oxygen) - rupture of cellular membranes- 1. release of arachidonic acid- cox makes prostaglandins- sensitize nociceptor- 2. Release of autocloids (self remedy) (histamines, bradykinin) that activate nociceptors- then pain transmission flow neurotransmission by nociceptor (first order)- neurotransmission through spinal cord(second order)- pain impulse transmission through brain (third order) cerebral cortex- perception and emotional response to pain

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14
Q

What are two ways nociceptors are sensitized ?

A

Prostaglandin e and autocloids(histamine, bradykinin, serotonin)

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15
Q

What are two types of cannabinoids that are found naturally in the resin of the marijuanna (cannabis) plant

A

Tetrahydrocannabinol (thc) and cannabidiol (cbd)

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16
Q

What are two synthetic cannabinoids

A

Dronabinol (Marinol)
Nabilone (cesamet)

17
Q

Difference between broad spectrum and full spectrum CBD

A

No THC
Full spectrum - small THC

may test positive for thc if using full spectrum product

18
Q

THC therapeutic effects

A

Analgesic effects, increases appetite, changes emotional and cognitive processes,

Reports suggest anticonvulsant, muscle relaxant, anxiolytic, antiphyscotic and anti inflammatory activity

19
Q

CDB therapeutic Effects

A

Analgesic, anticonvulsant, muscle relaxant, anxiolytics, antipsychotic, neuro protective, anti inflammatory, and antioxidant activity

20
Q

Nabilone (cesamet) MOA

A

Synthetic THC, cb1 and cb2 receptor agonist that has been used for the treatment of chemo induced nausea/vomiting, treatment of chronic pain (fibromyalagia) and anorexia associated with hiv infections

21
Q

Phamacotoxicology of THC

A

Sedation, ataxia, dizziness, lethargy, mental clouding, impaired memory, paranoia, hallucinations, euphoria, anxiety, depression, withdrawal reactions, tolerance, tremors, additive effects with other cns depressants

22
Q

What is the most endogenously produced in our body?

A

Anandamide

23
Q

Cb1 receptors target ?

A

Motor activity, thinking, motor coordination, appetite, short term memory, pain perception, immune cells

24
Q

Cb2 receptors target what in body?

A

Much broader and influence most of the body compared to cb1 Gut, kidneys, pancreas, adipose tissue, skeletal muscle, bone, eyes, tumors, reproductive system, immune system, respiratory tract, skin, cns, cardiovascular systems, liver

25
Q

Does cbd act through cb 1 and 2 receptors ?

A

No. Just THC. Cbd modulates intracellular calcium in excitable neurons and adenosine mediated signaling

26
Q

gabapentin use and MOA

A

Neuropathic pain, increases GABA levels in the cns an inhibits calcium channels

27
Q

Similarity and difference between local anesthetic procaine and lidocaine

A

MOA are sodium channel blockers that inhibit formation of action potentials and block nerve impulse conduction by nociceptors

Procaine has 1 minute half life bc it is ester-type that is quickly metabolized by plasma pseudocholinesterases
Lidocaine has 10 minute half life bc it is a amide-type anesthetic metabolized by hepatic cyp enzymes

28
Q

Propofol MOA

A

May enhance release of GABA, inhibiting sodium channels, or activating endocannabinoid system through CNS

29
Q

Isoflurane and etomidate MOA

A

Activating gaba receptors (inhibitory neurotransmitter) through cns

30
Q

Ketamine moa

A

Acts on many receptors but mostly NMDA antagonist (subtype of an excitatory receptor for glutamate) which blocks perception of pain

Short version- nmda receptor antagonist that blocks the perception of pain

31
Q

Propofol, isoflurane, etomidate short version MOA

A

GABA agonists at level of the cerebral cortex and block emotional and perception of pain.

32
Q

Naloxone and naltrexone MOA

A

Opioid receptor antagonist- inhibit cns depressant effects caused by narcotics.

33
Q

Lofexidine

A

Alpha 2 adrenergic agonist used to alleviate withdrawal symptoms

34
Q

Amitriptyline

A

Tricyclic antidepressant, elevates 5-HT

Prophylactic treatment of migraines

35
Q

Propranolol

A

Prophylactic treatment of migraines
Beta2 antagonist non selective

36
Q

Divalproex

A

Anti seizure med, prophylactic migraine med

37
Q

NSAIDs

A

Treatment of ongoing migraine condition

38
Q

Treatment of on going migraine

A

NSAIDs, ergotamine- alpha 1 agonist (causes vasoconstriction, sumatriptan- selective serotonin (5-ht) 1b/1d receptor agonist, telcagepant- oral crcp (calcitonin gene related proteins) antagonist