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Pharmacology > Non opioid analgesics > Flashcards

Non opioid analgesics Flashcards

1
Q

what are analgesics used for

A
  • relief of acute and chronic dental/facial pain
  • non opioid
  • preoperative pain
  • postoperative pain to reduce expected pain after the dental procedure
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2
Q

what is pain

A
  • common symptom
  • body uses it as a defence mechanism: avoid damaging situation and encourage to see medical help
  • perception and reaction are individualized: sensory (the actual painful stimulus) and reactionary (the emotional response to pain)
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3
Q

where does the sensory response to pain and the emotional response to pain stem from

A
  • sensory: response to the actual stimulus comes from the peripheral nervous system
  • emotional: originates in the central nervous system
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4
Q

what are the 4 types of pain

A
  1. fast/first pain
  2. slow/second pain
  3. acute pain
  4. chronic pain
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5
Q

what is neuropathic pain

A
  • due to direct injury to nerves
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6
Q

what is nociceptor pain

A
  • pain due to injury to tissues (somatic pain, visceral pain)
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7
Q

what is somatic pain

A
  • pain that comes from the skin, muscles and soft tissues
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8
Q

what is visceral pain

A
  • pain that comes from internal organs
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9
Q

what are the 2 types of sensory fibers in nociceptors

A
  1. a fibers: myelinated, sharp pain

2. c fibers: unmyelinated, dull pain

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10
Q

what is substance p

A
  • a neurotransmitter for pain perception in the spinal cord

- continues or stops the message

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11
Q

what can help control substance p that’s non pharmacological

A
  • endogenous opioids released from the CNS

- decrease pain

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12
Q

examples of non-pharmacological management of pain

A
  • acupuncture
  • biofeedback
  • massage
  • heat or cold packs
  • meditation
  • relaxation therapy
  • art or music therapy
  • imagery
  • chiropractic manipulation
  • hypnosis
  • therapeutic touch
  • healing touch
  • transcutaneous electrical nerve stimulation (TENS)
  • energy therapies (Reiki, Qi gong)
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13
Q

examples of non steroidal anti-inflammatory drugs (NSAIDs)

A
  • ibuprofen, naproxen
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14
Q

examples of narcotic (opioid) drugs

A
  • codeine, morphine, diluadid, demerol, etc
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15
Q

what can we use to treat chronic neuropathic pain

A
  • gapapentin (anti-epileptic drugs enhance neuronal stability, which results in pain relief)
  • 5% lidocaine patch
  • tricyclic antidepressants
  • narcotics are not approved for chronic neuropathic pain*
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16
Q

what is the purpose of the inflammatory process

A
  • defense mechanism
  • necessary for the body to heal itself (contain the injury or destroy the foreign agent)
  • can be acute or chronic
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17
Q

what can cause inflammation

A
  • infection
  • allergic reactions
  • physical injuries
  • exposure to toxic chemicals
  • extreme heat
  • death of cells
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18
Q

what is chronic inflammation

A
  • can arise from acute case or an injury
  • last years, worsen over time
  • causes damage to affected sites or internal organs
  • body heals - scar tissue forms (can alter normal workings of the body system)
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19
Q

symptoms of inflammation

A
  • redness
  • swelling
  • heat
  • pain
  • loss of function
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20
Q

what is the inflammatory process

A
  • damage to tissue

- chemical mediators released

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21
Q

what chemical mediators are released during the inflammatory process

A
  • vasodilation (redness, heat)
  • vascular permeability (swelling)
  • cell infiltration (pus)
  • thrombosis (clots)
  • stimulation of nerve endings (pain)
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22
Q

what are prostaglandins

A
  • group of lipids made at sites of tissue damage or infection that are involved in dealing with injury and illness
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23
Q

what do prostaglandins do

A
  • stored and released by mast cells
  • increase capillary permeability
  • attract white blood cells to site
  • cause pain
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24
Q

what is cyclooxygenase and what are the 2 forms

A
  • enzyme that synthesizes prostaglandins
  • found in all tissues
  • two forms: COX-1 and COX-2
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25
Q

what does COX-1 do

A
  • takes care of normal functions
  • protects gastric mucosa
  • promotes platelet aggregation
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26
Q

what does COX-2 do

A
  • found at tissue injury sites
  • sensitizes receptors to pain
  • mediates inflammation
  • affects fever and pain perception
  • takes care of pain and discomfort
27
Q

what are some examples of first line pain drugs

A
  • acetaminophen

- aspirin/NSAIDs

28
Q

what are some examples of 2nd line/pain out of control pain drugs

A
  • opioids (sustained-release of immediate-release)

- NSAID’s

29
Q

what are some examples of refractory pain medications

A
  • spinal/epidural opioids
  • selective nerve blocks
  • neuroablative procedures
  • total sedation
30
Q

what are opioids

A
  • morphine like

- narcotic

31
Q

what does acetaminophen do

A
  • reduces pain by unknown mechanism
  • reduces fever by direct action at level of hypothalamus
  • causes dilation of peripheral BV -> dissipation
  • no anti-inflammatory action
  • mild to moderate pain and fever in children
  • major advantage is lack of effect on platelet function and less or no gastric irritation
  • NOT and NSAID
32
Q

side effects of acetaminophen

A
  • safe
  • no effect on blood coagulation
  • no GI irritation
  • no malnutrition -> acute toxicity -> renal failure
  • hepatotoxicity (liver necrosis)
33
Q

what are signs of acute toxicity

A
  • nausea, vomiting, chills, abdominal discomfort
34
Q

what is the maximum dose of acetaminophen in 24 hours

A
  • 4g, with higher doses increasing the risk of liver damage (not more than eight 500 mg tablets in 24 hours)
35
Q

how are overdoses treated for acetaminophen

A
  • with acetylcysteine
36
Q

how does acetaminophen react with alcohol

A
  • increases liver damage (hepatotoxicity)
37
Q

what are the negative effects of inhibiting COX-1

A
  • gastric erosion
  • ulceration
  • bleeding
  • renal damage
38
Q

what do first generations of NSAIDs do

A
  • inhibit COX-1 and COX-2

- decrease in inflammation, pain, fever

39
Q

what do second generation NSAIDs do

A
  • COX-2 selective
  • reduce inflammation
  • reduce pain
  • reduce fever
  • without side effects of COX-2 inhibition
40
Q

what do NSAIDs do

A
  • inhibit cyclooxygenase: prostaglandins not formed, prostaglandins cannot activate nociceptors
  • for mild to moderate pain, inflammation and fever
41
Q

what are some advantages to NSAIDs

A
  • over the counter and inexpensive
  • different formulations
  • safe
42
Q

what is acetylsalicylic acid

A
  • ASA/aspirin
  • originally derived from the bark of willow tree
  • today made synthetically
  • inhibits both COX-1 and COX-2 (but predominately COX-1), thus many GI problems (bleeding, ulcers)
43
Q

what is analgesia and what causes it

A
  • the process of reducing pain
  • due to inhibition of prostaglandins and bradykinin
  • relieves mild to moderate pain (dental)
  • ceiling effects (increasing dose beyond a point does not increase analgesia)
44
Q

what causes the anti-inflammatory process

A
  • drug or substance that reduces inflammation

- due to blocking formation of PGE2 (prostaglandin E2)

45
Q

what is antipyretic

A
  • used to prevent or reduce fever

- reduces abnormal fever

46
Q

what are the antiplatelet effects of aspirin

A
  • inhibits lately aggregation (clotting)
  • irreversible inhibition of cyclooxyrgenase activity (anticlotting effects last the lifetime of a platelet, which is about 7 days. inhibits clotting -> causes bleeding)
47
Q

should patients stop taking aspirin before dental surgery due to clotting effects

A
  • controversial

- recommend continuing use to prevent emboli, myocardial infarction, or stroke

48
Q

how long after taking aspirin does platelet inhibition become evident

A
  • within 1 hour
49
Q

what is the primary use of aspirin

A
  • prevention of a first cardiovascular (eg heart attach) or cerebrovascular (eg stroke) event for most patients who are at moderate rose (use low-dose – 81 mg – aspirin daily)
50
Q

what is the secondary use of aspirin

A
  • low-dose aspirin to prevent cardiovascular or cerebrovascular events in patients with a history of heart conditions (eg stroke, engine, or acute coronary syndrome)
  • reduction of pain, inflammation and fever
51
Q

what are some contraindications of aspirin

A
  • children less than 17 years of age (eye’s syndrome)
  • nasal polyps and allergic rhinitis (hay fever/allergic reactions) to aspirin are at risk of developing bronchoconstriction and anaphylaxis)
  • about 10% of patients with asthma are intolerant to aspirin and other NSAIDs
  • ulcers
52
Q

what are some adverse effects of aspirin

A
  • GI upset (enteric coated tablets and buffered available)
  • bleeding
  • salicylism (toxicity)
  • nausea/vomiting
  • renal dysfunction
  • doses stimulate the depth and rate of respiration
53
Q

questions to ask patients that are taking aspirin

A
  • ask patient why he or she is taking aspirin
  • ask patient if his or her physician knows he or she is taking the aspirin
  • ask patient if he or she is taking 81 mg or regular-strength aspirin (325 mg)
  • determine if aspirin will cause increased bleeding during the dental procedure
  • remind patient not to put aspirin directly on the tooth or gums
  • consult patient’s physician regarding discontinuing use 7 days prior to dental surgery)
54
Q

what does ASA do

A
  • inhibits prostaglandin synthesis (pain and inflammation)
  • mild to moderate relief of fever
  • anticoagulant activity (do not give with other anticoagulants)
  • reduce risk of colorectal cancer
  • high doses -> GI discomfort and bleeding
  • not to be given during 3rd trimester
55
Q

what drugs interactions might we see with aspirin

A
  • oral anti diabetic (increased hypoglycaemic response)
  • angiotensin-converting enzyme (ACE) inhibitors (lowers effectiveness of the hypertensive drug)
  • other aspirin-containing over the counter drugs (higher aspirin effects)
  • thiazide or loop diuretics (lowers actions of diuretic)
  • anticoagulants (increase bleeding)
  • alcohol (increase GI irritation and bleeding)
  • herbs (increased bleeding)
56
Q

what do NSAIDs do

A
  • block the COX enzymes and reduce prostaglandins throughout the body (also prevents platelet aggregation)
  • 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
57
Q

what are some indications of NSAIDs usage

A
  • analgesia (dental pain)
  • anti-inflammatory
  • antipyretic
58
Q

what are NSAIDs not used for

A
  • the prevention of strokes and heart attacks
  • all NSAIDs can lead to the onset of new or worsening of preexisting disease
  • limit use of naproxen and other NSAIDs therapy to the lowest effective dose for the shortest possible duration to minimize risks (MI, bleeding)
59
Q

what are some adverse effects and contraindications for use of NSAIDs

A
  • GI effects: due to COX-1 inhibition -> decreases GI mucosal defense mechanisms and increases gastric acid secretion -> leads to ulceration. take with food
  • kidney function: inhibition of prostaglandin synthesis -> depress kidney function
  • asthma
  • nasal polyps
  • hypersensitivity to NSAIDs
60
Q

what are some drug interactions we may see with NSAIDs

A
  • angiotensin converting enzyme inhibitors (ACE inhibitors) and beta blockers (counteract the antihypertensive effects)
  • lowers lithium levels
  • increases bleeding with anticoagulants
  • increases hypoglycaemic effects with oral anti diabetic drugs
61
Q

directions for taking NSAIDs

A
  • take the pill with a full glass of water and with food

- do not take with aspirin; can take with acetaminophen

62
Q

what does naproxen do

A
  • inhibit prostaglandin synthesis

- non selective inhibition of COX-1 and COX-2

63
Q

what are some side effects of naproxen

A
  • not serious
  • GI upset (reduced if taken with food)
  • dizziness
  • drowsiness
  • caution with patients with bleeding disorders because prolongs bleeding time
64
Q

what is celebrex

A
  • causes selective inhibition of COX-2

Pharmacology (21 decks)

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