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PHRM 845: Therapeutics III > Pain: Barker > Flashcards

Pain: Barker Flashcards

1
Q

What are the classifications of pain?

A
  • Acute and Chronic
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2
Q

What is Acute pain?

A
  • Refers to an injury or post-operative faire
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3
Q

What is Chronic pain?

A
  • Pain that last more than 3 months
  • Nociceptive [Somatic; Inflammatory], Neuropathic, Visceral [Inflammatory], Mixed
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4
Q

what is the basic function of pain?

A
  • Bodies warning system [1st warning]
  • Aid in repair [Hypersensitivity]
  • Can be maladaptive [further damage]
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5
Q

How does pain act as an alarm system?

A
  • Tissue Damage: releases cytokines and chemical mediators that increase vascularization and sensitizes somatosensory
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6
Q

What is Allodynia?

A
  • Spontnaeuos or breakthroug pain
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7
Q

What are some way that we can characterize pain?

A
  • Temporal [WHEN?], Intensity, Location [WHERE?], Quality [HOW DOES IT FEEL?]
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8
Q

What is Referred Pain?

A
  • Pain that is in one area that can lead to other areas of the body
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9
Q

What are some of the ways the chronic pain may appear?

A
  • Inflammatory Pain [Arthritis], Neuropathic Pain [Diabetes], Verceral Pain [Cancer], Breakthrough Pain, Fibromyalgia [Allodynia], Migraine, Phantom [Amputation]
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10
Q

What is the etiology of Chronic pain?

A
  • Tissue Injury leading to the release of Active factors [PG, BK, K]
  • Persistent activiation and sensitization of Ay/C
    -Activity in ascending pathway [Peripheral sensitization]
  • Output for the input
  • Ongoing pain [Central sensitization]
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11
Q

What are the peripheral receptors and channels that are involved in pain signaling?

A
  • Temperature, Acid, Chemical Irritant Sensitive
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12
Q

What are the Temperature Sensitive receptors for pain?

A
  • Transient receptor Potential Cation Channel
  • TRPV = Hot
  • TRPM = Cold
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13
Q

What are the Acid Sensitive receptors for pain?

A
  • Acid Sensing Ion channels [ASIC]
  • Activated by H+ and Conducts Na+
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14
Q

What are the Chemical irritant receptors for pain?

A
  • Histamine and Bradykinin
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15
Q

What are the three different pain fibers?

A
  • Ab - Fibers
  • Ay - Fibers
  • C - Fibers
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16
Q

What are the Ab - Fibers?

A
  • Bigger and More Myelinated [Fastest]
  • Non-noxious [Touch and Pressure]
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17
Q

What are the Ay - Fibers?

A
  • Less myelinated
  • Pain and Cold
  • “First Pain” [Sharp and Prickly]
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18
Q

What are the C - Fibers?

A
  • Unmyelinated
  • Pain, Temperature, Touch, Pressure
  • “Second Pain” [Dull, Aching]
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19
Q

How does Substance P play an important role in heightening pain responses?

A
  • Repeated Stimuli that reduces the firing treshold
  • Causes: vasodilation, Degranulation, Histamine Release, Inflammation
  • Increase expression of pain
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20
Q

How is a sunburn temporary peripheral pain?

A
  • UV radation damages the skin = Inflammation
  • Involves TRPV4 [Temperature Sensitive]
  • Allodynia occurs
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21
Q

What is the pathway for spinal pain?

A
  • The release of Substance p and glutamte from the primary neuron to the secondary neuron
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22
Q

What is found within the pain ciruitray of the brain?

A
  • High expression of opioid receptors along the descending pathway [Opioids, GABA, NA, & 5-HT]
  • Mu Receptors
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23
Q

What are the two type of alkaloids found witin opioids?

A
  • Phenanthrenes [Morphine] & Benzylisoquinolines
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24
Q

What are Opiates?

A
  • Opioids that are naturally occurring
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25
Q

What are the structure relationships of Phenanthrenes in opioids?

A
  • 3 Position: substitution decreases potency [Codeine]
  • 6 Position: Increases activity [Hydromorphone or Hydrocodone from Codeine]
  • 14 Position: OH increases potency [Oxycodone]
  • N-allyl: Antagonist [Narcan]
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26
Q

What are the Pharmacokinetics or Morphine [Phenanthrenes]?

A
  • Metabolized in the Liver [Hepatic]
  • Bioavailability 25%
  • 2D6 and 3A4
  • Glucuronidation at 3’ and 6’
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27
Q

What are some of the Administration routes for Opioids?

A
  • IV, Intra-axial, IM, Oral, Topical
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28
Q

Which opioids create active metabolites?

A
  • Herion, Codeine, Tramadol = Prodrugs
    [Morphine, O-Hydroxy-oxymorphone, Morphine]
  • Fentanyl and Methadone DO NOT
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29
Q

What does CYP3A4 make within Opioids?

A
  • Makes the “NOR”
30
Q

What does CYP2D6 make within Opioids?

A
  • Other active metabolites
31
Q

What are the metabolizers for 2D6?

A
  • PM, IM, EM, UM
  • UM: Higher blood concentration; higher SE
  • PM: NO therapeutic effect
32
Q

What are the types fo opioid receptors?

A
  • G Protein [Gi, GRIK], Mu [Morphine], Kappa [Ketocyclazocine], Delta [Defernes], Nociceptin, Sigma [NOT opioid]
33
Q

What is the signal transduction within the opioids receptors?

A
  • Presynpatic: Inhibition of Ca2+ channel [Gi] decreases the neurotransmitters release
  • Postsynaptic: Activation of GIRK channels [Gby] causing an efflux of K+ =>hyperpolarization
34
Q

What are the endogenous opioids contained within the human genome?

A
  • Pro-opiomelanocortin [POMC]
  • Preproenkephalin
  • Preprodynorphin
  • Nociceptin/Orphanin FQ
35
Q

What is important to know for the MU opioids receptors?

A
  • Linked to Beta-Endorphins
  • Uses: Analgesia [NOT Chronic], Sedation, Antitussive [Suppression of cough]
36
Q

What are some of the opioid induced side effects?

A
  • ON TARGET EFFECTS
  • Respiratory depression, Constipation, Itch [NOT allergic reaction], Addiction, Urinary retention, Nausea & Vomiting, Miosis
37
Q

What is important to know about the KAPPA opioid receptors?

A
  • Linked to Dynorphins
  • Activation is dysphoric [Negative feelings]
  • Treatment for addiction [Decreases dopamine]
38
Q

What is important to know about the DELTA opioid receptor?

A
  • Linked to Enkephalins
  • Reduces Anxiety, depression
  • Treats Alcoholism
  • SEIZURES
39
Q

What is opioid induced hyperalgesia and how is it different than tolerance?

A
  • Tolerance: INCREASE in dose to get the same effect
  • Hyperalgesia: INCREASED sensitivity toward pain; increasing the does makes that pain worsen
40
Q

What are some of the clinically used opioids for?

A
  • Cough/antitussive & Anti-Diarrheal
41
Q

What are some of the Cough/Antitussive opioids used?

A
  • Codeine [C-II]
  • Dextrometorphan [Limited Opioid activity; opens receptors in the brain stem]
42
Q

What are some of the Anti-Diarrheal opioids that are used?

A
  • Diphenoxylate with atropine [Lomotil]
  • Loperamide [Strong P-glycoprotein; pumps out of brain]
  • Eluxadoline [Mu/Kappa Agonist, Delta Antagonist
43
Q

What opioids are used within the hospital setting?

A
  • ALL ARE C-II
  • Agonist: Sufentanil, Remifentanil, Alfentanil [Breakdown by plasma esterases]; Fentanyl, [lollipop], Hydromorphone, Oxymorphone, Morphine, Hydrocodone, oxycodone
44
Q

What are the Non-Phenanthrene opioids?

A
  • Tramadol, Tapentadol [SNRI like; 5HT & NET inhibitor]
  • Meperidine [Toxic Metabolite: Normeperidine]
45
Q

What opioids are able to block the NMDA receptors?

A
  • Methadone [used for opioids dependence; QTc PROLONGATION, NMDA antagonist]
46
Q

What are some of the opioids that are used in MOR and KOR?

A
  • Pentazocine [k agoinst, mu antagonism]
  • Nalbuphine [Full k agonist, mu antagonist]
  • Buprenorphine [Partial mu agonist, weak k agonist & y antagonist]
47
Q

What are the types of NASIDS?

A
  • Salicylates [Aspirin]
  • Arylpropionic Acids [Ibuprofen, Naproxen]
  • Arylacetic Acids [Indomethain, Diclfenac…]
  • Enlic Acids [Piroxicam, Meloxicam]
48
Q

What is the therapeutic applications for NSAIDs?

A
  • Analgesic [Chronic Pain, Inflammatory Pain]
  • Anti-Inflammatory [Arthritis]
  • Antipyretic [Fever]
  • Reduce Myocardial Infarction
49
Q

What contributes to the Inflammatory pain?

A
  • Eicosanoids
50
Q

What are the Eicosanoids that are recruited in Inflammatory cells?

A
  • Arachidonic Acid Metabolites
  • Prostaglandins [Redness, Heat, Pain]
  • Thromboxanes
  • Leukotrienes [Swelling]
  • Cytokines [Pain]
51
Q

What are the two pathways for Arachidonic Acid?

A
  • COX-1 & COX-2
52
Q

What happens COX-1 pathway?

A
  • Induces platelet activity - TXA2
  • Protects the Stomach lining
53
Q

What happens COX-2 pathway?

A
  • Induces the anti-platelet activity - PGI2
54
Q

What is important to know about Aspirin in regards to COX?

A
  • IRREVERSIBLY COX-1/2 Inhibitor
  • Low Dose = COX-1 & High Dose = COX-2
55
Q

What is important to know about Other NSAIDs in regards to COX?

A
  • REVERSIBLE COX-1/2 Inhibitors
  • anti-flammatory too
56
Q

What is Aspirin’s main use?

A
  • Prophylactic for Anti-coagulation
  • NO tolerance development to analgesic effects
  • DO NOT use in children - Reye’s Syndrome
57
Q

What are the Pharmacokinetic Properties of Aspirin [Salicylates]?

A
  • Absorption: Rapidly Absorbed
  • Distribution: Most tissues and Fluids
  • Metabolism & Excretion: Half-life 6-20 hour; increased excretion with increased urinary pH
58
Q

What are some of the side effects that relate to Aspirin [Salicyism] Posioning?

A
  • Vertigo, Tinnitus, Respiratory Alakalosis [hyperventilating], Metabolic Acidosis [lowering blood pH]
59
Q

What is the treatment for Aspirin [Salicyism] Poisoning?

A
  • REDUCE salicylate load
  • Will cause an increase in urinary excretion
60
Q

What is important to know about the Enolic Acids NSAIDs?

A
  • Used to treat ARTHRITIS
  • Meloxicam at low doses is COX-2
61
Q

What are some of the adverse effects for NSAIDs?

A
  • Renal function: Decrease PGE2 = Edema
  • Inhibition of Platelets = Increase bleeding
  • Inhibition of Uterine Motility
62
Q

What is the therapeutic use of Acetaminophen?

A
  • Highly effective analgesic and antipryretic
  • NO GI TOXICITY
  • Could lead to Hepatic Necrosis
63
Q

What are the side effects of Acetaminophen?

A
  • Renal Toxicity > aspirin
  • Hepatic Necrosis [High risk with alcohol] because of an increase in toxic acetaminophen metabolites [NAPQI]
64
Q

What are some of the contraindications for NSAIDs?

A
  • AVOID: chronic kidney disease, poptic uler disease, history of GI Bleeds
  • Cardiovascular risks [with CAD]
  • Interfere with Bone Healing [high doses]
  • Cause Asthma Exacerbations [COX-2 less likely]
65
Q

What is another way that we are able to get analgesic effects?

A
  • Blocking sodium channels - NaV1.7`
66
Q

What are some Psychiatric drugs that are also NaV1.7 Blockers?

A
  • Lamotrigine, Cabamazepine, Amitriptyline
67
Q

What are some SNRIs that are also NaV1.7 Blockers?

A
  • Increase Norepi [acting on a2A-Adrenergic]
  • Duloxtine, Venlafaxine, Milnacipran [lacking]
68
Q

What are the controlled substance drug classifications?

A
  • C-I: NO MEDICAL USE [Marjiuana, THC, LSD…]
  • C-II: High Abuse [Cocaine, PCP…]
  • C-III: Moderate Abuse [Marinol; THC oil]
  • C-IV: Low Abuse [Benzos]
  • C-V: Cough Suppressant with small amout of codeine or Lomotil
69
Q

What are some substances of abuse that act INDIRECTLY on GCPRs?

A
  • Cocaine, Amphetamine [block DAT]
  • MDMA/Ecstasy [block DAT & SERT]
  • Alcohol
70
Q

What are some substance of abuse that act on Ion channels?

A
  • Nicotine [Acetylcholine: Agonist]
  • PCP, Ketamine [NMDA; Antagonist]
  • Benzo [GABAa; allosteric modulators]
71
Q

What are some of the important ares of the brain that drugs can affect causings abuse?

A
  • Frontal Cortex: Decision Making
  • Striatum: Reward
  • NUCLEUS ACCUMBENS: Pleasure
  • VTA: Dopamine Source
  • Hippocampus: Memory Learning

PHRM 845: Therapeutics III (25 decks)

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