Pharm Chp 6

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  1. What are the two parts to pain:
    sensory and reactionary
  2. What is the sensory part of pain and where does it originate from
    • The actual painful stimulus
    • comes from the PNS.
  3. What is the reactionary part of pain and where does it originate from
    • The emotional response to pain
    • originates from the CNS
  4. Acute pain has a
    short time course. Usually simple to evaluate and treat
  5. Chronic pain has a
    undetermined time course, more complex evaluation, treatment not as successful
  6. Orofacial pain is classified into:
    • Nociceptive pain
    • Neuropathic pain
  7. Nociceptive pain is
    pain arising from a stimulus such as injury to tissue, bone, joint muscle or connective tissue outside of the CNS. A scaler/currette
  8. Neuropathic pain
    also called neuralgia. Originates in a damaged or compromised nerve
  9. Nociceptive pain can be ______ or _______
    somatic or visceral
  10. Somatic pain is
    sharp, well-localized sensations
  11. Visceral (deep) pain is ________ associated with a phenomenon called _______
    • a generalized dull, throbbing or aching, poorly localized pain.
    • referred pain, which detects the painful stimulus in areas removed from the site where the pain originated
  12. Nociceptive pain is pain that occurs when _______ (located on the ends of nerves transmitting stimuli) are stimulated by _______
    • nociceptors
    • noxious stimuli
  13. What are some examples of Neuropathic Orofacial Pain
    trigeminal neuralgia, postherapeutic neuralgia, burning mouth, burning tongue syndrome
  14. Drug therapy for Neuropathic Orofacial Pain includes what class of drugs and what specific drugs
    • tricyclic antidepressants, analgesics, and anticonvulsants
    • gabapentin (Neurontin) (antiepileptic drug that enhances neuronal stability, which results in pain relief)
    • 5% lidocaine patch
    • Tricyclic antidepressants
  15. Narcotics are NOT FDA approved for
    chronic neuropathic pain
  16. Drug Therapy for Nociceptive Pain include
    • Nonnarcotic (nonopioid) analgesics–Nonsteroidal anti-inflammatory drugs (NSAIDs)
    • Narcotic (opioid) analgesics–Ex. codeine, hydrocodone
  17. Non narcotics analgesics include:
    • salicylates (Aspirin)
    • acetaminophen (Tylenol)
    • Nonsteroidal anti-inflammatory drugs (NSAIDs)including selective COX2 inhibitors
  18. Trauma to a nerve fiber following tissue trauma/damage stimulates ______, which causes _______ to break off from _________
    • phospholipase A
    • arachidonic acid
    • phospholipids on cell membrane
  19. Arachidonic acid follows two paths: Interactions with _____ or ______
    • lipoxygenase
    • Cyclooxygenase (COX) I and II enzymes
  20. Interaction of arachidonic acid with lipoxygenase creates ________ which leads to _______
    • Leukotrienes
    • bronchoconstriction (in asthma) and other localized allergic reactions
  21. Interaction of arachidonic acid with cyclooxygenase creates _______, ______, and _______
    Prostaglandins, Prostacyclin and Thromboxane A2
  22. Prostaglandins are _______ that are made in _______ and serves what purposes
    • Fatty acids found in all tissues
    • cell during inflammation
    • Promote pain, inflammation, and fever
    • Protect lining of stomach from damaging acid
    • Cause uterine contractions during labor
    • Maintain renal (kidney) blood flow
  23. ________ is a potent mediator of inflammation. High levels are found in ________
    • Prostaglandin E2 PGE2
    • inflammatory periodontitis
  24. Thromboxane A2 is synthesized and found in _______ and functions to ______
    • platelets
    • Prevents bleeding; potent vasoconstrictor which induces platelet aggregation for clotting
  25. Prostacyclin (PGI2) is found in _______ and functions to _______
    • blood vessel cell walls
    • Prolongs bleeding; vasodilator (opposite function of thromboxane A2), prevents platelet aggregation
  26. Cox 1 is a _________ found inside ________ such as the ______ and functions to _______
    • "Housekeeping enzyme”
    • most cells in the body
    • GI tract, kidney, platelets
    • Protect the lining of the stomach from stomach (gastric) acids, maintain normal platelet function, and regulate renal blood flow
  27. COX-2 is produced only
    during inflammation
  28. Aspirin is also known as
    acetylsalicylic acid
  29. Aspirin inhibits _______ and _______ but predominately _________ thus causes many problems such as ________
    • COX-1 and COX-2
    • COX-1
    • GI problems –Bleeding, ulcer
  30. What are the therapeutic effects of aspirin
    • Analgesia
    • Anti-inflammatory
    • Antipyretic
    • Antiplatelet effects
  31. Aspirin has analgesic effects due to
    Due to inhibition of prostaglandins and bradykinin (bradykinin, an inflammatory mediator, sensitizes nociceptor peripheral terminals) reducing pain threshold
  32. What is the ceiling effect
    Increasing dose beyond a point does not increase analgesia
  33. Aspirin has anti-inflammatory effects due to
    –blocking formation of PGE2
  34. Aspirin has antiplatelet effects due to
    inhibiting thromboxane A2
  35. Low dose aspirin ___mg is used for ______ and primarily inhibits _______
    • 81
    • prophylactic treatment for heart attacks and stroke
    • thromboxane A2
  36. Normal strength aspirin is ____ mg
    325
  37. Primary prevention is using low dose aspirin to _______ while secondary prevention is using low dose aspirin to ________
    • prevent a first cardiovascular event for most patients who are at moderate risk
    • prevent cardiovascular or cerebrovascular events in patients with a history of heart conditions
  38. Reye’s syndrome is
    primarily a children’s disease. Children are at increased risk to develop Reye’s Syndrome if they take aspirin to treat viral illnesses including chicken pox or flu
  39. Patients taking aspirin with nasal polyps and allergic rhinitis are at risk of
    developing bronchoconstriction and anaphylaxis
  40. What are some adverse effects of aspirin
    • Gastrointestinal upset–Reduces some with enteric-coated tablets
    • Bleeding
    • Salicylism (toxicity)
    • Nausea/vomiting
    • Renal dysfunction
    • Excessive doses stimulate the depth and rate of respiration (hyperventilation)
  41. What drugs have an interaction with aspirin and what is that reaction
    • Oral antidiabetic: increases Hypoglycemic response of oral antidiabetic drugs
    • Angiotensin-converting enzyme (ACE) inhibitors: decreases effectiveness of the hypertensive drug
    • Other aspirin-containing OTC drugs: increases Aspirin effects
    • Thiazide or loop diuretics: decreases Actions of diuretic
    • Anticoagulants (e.g., warfarin): increases Bleeding
    • Alcohol: increases GI irritation and bleeding
    • Herbs (dong quai, chamomile, ginseng, ginger, and red clover): Increased bleeding
  42. In a child toxicity is seen with _____ , and a lethal dose is _____g
    • 1 g (1000 mg)
    • 10 g
  43. Diflunisal (______)
    • Dolobid
    • –Derivative of salicylic acid but is not converted to salicylic acid
    • –It is a more potent anti-inflammatory than aspirin, and it is an inhibitor of cyclooxygenase.
    • It does not have antipyretic activity because it penetrates poorly into the CNS
    • –Anti-inflammatory for arthritis and for dental pain
    • –Less intense gastrointestinal and antiplatelet effects than aspirin
    • Good for dental pain
    • Use loading dose of 500-1000mg followed by 250-500mg q8-12h
  44. Prototype for NSAID's is __________(________)
    • ibuprofen
    • Advil, Motrin
  45. What is the action of NSAID's
    • Block the COX enzymes and reduce prostaglandins throughout the body
    • Ongoing inflammation, pain, and fever are reduced
    • –Reduces protection of gastric mucosa Ulcers
    • NSAIDs differ in how strongly they inhibit COX-1 and thus their tendency to cause ulcers and bleeding is less than aspirin
  46. What are the indications of NSAIDs
    • Analgesia –Dental pain – very effective.
    • Anti-inflammatory
    • Antipyretic
  47. What is the mechanism of action of NSAIDs
    • Inhibition of COX-1 also inhibits the production of thromboxane A2, which prevents platelet aggregation
    • NSAIDs do not covalently bind to the cyclooxygenase enzymes and do not irreversibly inhibit platelet function as does aspirin
  48. What are some adverse effects of NSAIDs
    • –Due to COX-1 inhibition, which decreases GI mucosal defense mechanisms and increases gastric acid secretion, which leads to ulceration
    • Take with food or milk
    • Kidney function –Depressed due to inhibition of prostaglandin synthesis, which plays a protective role in kidney function
    • All NSAIDs can lead to the onset of new hypertension or worsening of preexisting disease
  49. Patients with a Hypersensitivity to NSAIDs include patient with
    asthma and nasal polyps
  50. What are the drug interactions of NSAIDs
    • Counteracts the antihypertensive effects of angiotensin converting enzyme inhibitors (ACE inhibitors) and beta-blockers 
    •  increases Lithium levels by decreasing renal excretion of lithium (can cause lithium toxicity)
    • increases bleeding with anticoagulants
    • increases Hypoglycemic effects with oral antidiabetic drugs
  51. _________ is the only COX-2 inhibitor currently available and has a black box warning of the potential for ________
    • Celecoxib (Celebrex)
    • increased risk of cardiovascular events as well as serious and potentially life-threatening gastrointestinal bleeding
  52. What is the mechanism of action of celebrex
    • Only inhibits cyclooxygenase-2Inhibits prostaglandin synthesis
    • Analgesic
    • Antipyretic
    • Anti-inflammatory
    • Antiplatelet–Not used for prevention of strokes/heart attacks because it reversibly binds to the platelets
  53. The major advantage of acetaminophen (__________) compared to other NSAIDs is
    • Tylenol
    • its lack of effect on platelet function and less or no gastric irritation
  54. After ingestion Acetaminophen reaches peak blood levels in ______ minutes
    30 to 60
  55. What are the adverse effects of acetaminophen and what is an overdose treated with
    • Hepatotoxicity (liver necrosis)
    • acetylcysteine
  56. Maximum dose of acetaminophen is
    3 to 4 g
  57. What are the drug interactions of acetaminophen
    • Alcohol–Increase liver damage (hepatotoxicity)
    • Carbamazepine (Tegretol), phenytoin (Dilantin), and rifampin (Rifadin)–Increase liver damage (hepatotoxicity)
  58. Acetaminophen has a __ pregnancy category
    B
  59. OPIOID ANALGESICS act on _______ of pain and act as agonists and affect specific binding sites called _______ in the _____
    • central components
    • opiate receptors
    • CNS
  60. What is the mechanism of action of opioids
    • Enkephalins and endorphins are released from neurons in the brain and activate opioid receptors, thereby blocking the transmission of pain impulses
    • These substances are the body’s natural opiates that inhibit painful stimuli
  61. What are the three main opioid receptors
    • Mu (μ)
    • Delta (δ)
    • Kappa (κ)
  62. Morphine has an affinity for _____ and ______receptors.
    mu and kappa
  63. Mu receptors are involved in the _______ effects
    analgesic, respiratory, depressant, and euphoric effects
  64. Kappa receptors are involved with
    respiratory depression, miosis (pupil constriction), and sedation
  65. What are the Opioid Adverse effects
    • CNS
    • –Respiratory depression
    • –Cough suppression
    • –Nausea/vomiting
    • GI
    • –Constipation
    • Tolerance can develop
  66. What are the Drug Interactions with Opioids
    • Antihistamines, sedative/hypnotics, alcohol, and psychotropics
    • –Increased CNS effects (e.g., sedation)
  67. Opioids are readily absorbed from the
    GI tract, nasal mucosa, and lungs (smoke)
  68. What are the three classifications of opioids
    • Full agonists: Strong or moderate in producing an analgesic (relief of pain) effect
    • Mixed opioid agonist/antagonists: Analgesic effect with some antagonist activity
    • Pure antagonists: No analgesic effects; used in opioid overdose
  69. What drug is the prototype for Opioid Agonists
    Morphine
  70. What are the Central Actions of Morphine
    • Analgesia
    • Drowsiness and sleep
    • Cough suppression
    • Vomiting (due to stimulation of chemoreceptor trigger zone in the brain)Hypotension
    • Miosis (papillary constriction)
    • Respiratory depression (high doses) –Major toxic effect and cause of death because no tolerance is developed to respiratory depression
    • Euphoria (ecstasy; develop tolerance rapidly to euphoric actions)
    • Increased release of ADH (antidiuretic hormone), which causes urinary retention
  71. What are the Peripheral Actions of Morphine
    • Constipation (due to stimulation of cholinergic activity in the GI tract)
    • Body warmth/flushing/itching (due to histamine release)
  72. Methadone
    • Long-acting synthetic morphine derivative used orally in the treatment of opioid (usually heroin) addiction
    • “Wean” patients off narcotics because it does not produce euphoria (ecstasy).
  73. Meperidine (Demerol)
    is a less effective analgesic than morphine with half the duration of action (75 mg meperidine IM [intramuscular injection] = 10 mg morphine IM)
  74. What are some adverse effects of Oxycodone and Hydrocodone
    Respiratory depression, antitussive, constipation, and dependence
  75. Hydrocodone is a Schedule ____ drug
    III
  76. hydrocodone + APAP (acetaminophen) =
    Vicodin
  77. hydrocodone + aspirin =
    Lortab
  78. hydrocodone + ibuprofen =
    Vicoprofen
  79. Oxy + APAP (acetaminophen) =
    Percocet / Tylox
  80. Oxy + aspirin =
    Percodan
  81. Oxy + ibuprofen =
    Combunox
  82. OxyContin is the brand name for
    pure oxycodone HCl extended release for long term pain control
  83. Codeine is a naturally occurring narcotic agonist obtained from the ______ but in lesser amounts than _______
    • opium poppy
    • morphine
  84. What drug is more orally active than other opioids
    codeine
  85. What are the effects of Codeine and what is it usually combined with
    • Less respiratory depressant and constipation and has less dependence potential
    • other nonnarcotic drugs such as acetaminophen (Tylenol) for the relief of acute nociceptive mild to moderate dental pain
    • Antitussive–Cough syrups (Schedule V)
  86. What are some Guidelines for Patients Taking Codeine
    • Monitor patient for dry mouth; fluoride rinses if indicated.
    • Monitor vital signs because of potential effects on the heart and respiratory system.
    • Causes drowsiness/sedation
  87. Dextromethorphan
    • –Opioid without any analgesic activity
    • –High antitussive effects
    • Cough medicines: Some trade names are Benylin, Delsym, and Vicks
  88. Loperamide (________)
    • Imodium
    • –Opioid without analgesic effects
    • –Increases smooth muscle tone in the gastrointestinal tract and is used as an antidiarrheal
  89. Diphenoxylate
    • –Antidiarrheal
    • –Combined with atropine in a product called Lomotil
    • It can cause severe respiratory depression, coma, and death after overdose in children
  90. Tramadol (_______)
    • Ultram
    • –Unique analgesic having both opiate and central acting adrenergic qualities 
    • Not a controlled substance
    • FDA approved for moderate to moderately severe pain
    • Can cause serious neurotoxicity and is not the first-line drug of choice

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Author:
haitianwifey
ID:
327915
Filename:
Pharm Chp 6
Updated:
2017-02-04 21:43:31
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Pharm Chp
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Pharm Chp 6
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