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Advanced Pharm > Non-opioid analgesics > Flashcards

Non-opioid analgesics Flashcards

1
Q

At what dose do ASA and Acetaminophen reach their ceiling affect?

How does that compare to other NSAIDS?

A
  • between 650-1300 mg
  • NSAIDS other than aspirin may have a higher ceiling
  • Exceeding the ceiling dose will result in increased adverse effects, no added efficacy
  • tolerance does not develop to the analgesic effects of these drugs
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2
Q

How does Acetaminophen work?

What is it a good choice to treat?

A
  • We dont really know how it works
  • Central anti-prostaglandin effect
  • antipyretic
  • Lacks peripheral activity
  • weak anti-inflammatory (not a true NSAID)
  • Good choice to treat:
    • PUD
    • pediatric patients
    • pts who need well funtioning platelets
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3
Q

Acetaminophen

PO dose

IV dose

When was IV dose FDA approved?

A
  • PO dose: 325-650 mg q4-6 hours
    • similar potency as ASA; same time-effect curve for single analgesic doses
  • IV dose: 1 g over 15 min q 4-6 hours, not to exceed 4,000 mg in 24 hours
    • make sure no other sources of acetaminophen
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4
Q

How is acetaminophen metabolized?

Describe the plasma concentration chart comparing IV acetaminophen to PO

A
  • Conjugated and hydroxylated to inactive metabolites; very little excreted unchanged by kidneys
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5
Q

How does an acetaminophen overdose injure the liver?

A
  • Liver can only metabolize a limited amount of the hepato-toxic metabolite N-acetyl-p-benzoquinone with glutathione
  • When the glutathione is outnumbered during an OD, hepatic injury occurs
  • Max safe dose 4,000mg/day
    • lower with ETOH abuse
    • lower with isoniazid
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6
Q

What can be used to substitute for glutathione in the case of an acetaminophen OD?

What is the time frame for administration?

A

Acetylcusteine

within 8 hours of OD

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7
Q

How does acetaminophen cause renal toxicity?

What has higher risk of renal toxicity, NSAIDS or acetaminophen?

A
  • Renal papillary accumulation of metabolites can cause renal cell necrosis
    • may be responsible for some cases of ESRD
  • NSAIDS have higher risk of renal toxicity
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8
Q

Arachadonic acid is released from phospholipids by the enzyme phospholipase A2.

What can it be immediately metabolized by? (3 enzymes)

What will it form with these different metabolizations?

A
  • Cyclooxygenase
    • prostaglandins
    • prostacylcin
    • thromboxanes
  • Lipoxygenase
    • Leukotrienes
    • Lipoxins
  • Epoxygenase
    • 4 types of Epoxyeicosatetraenoic acids that regulate inflammation; further research necessary
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9
Q

What is aspirin used for?

A
  • most mild to moderate pain
    • HA, muscle pain, arthritis
    • antipyretic
    • MI/stroke prevention; protection during MI
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10
Q

How does aspirin differ from other NSAIDS?

A
  • irreversible inhibition of COX
    • single dose inhibits platelet function for the lifetime of the platelet (8-10 days)
    • large doses can also decrease prothrombin
  • zero order kinetics
  • does NOT induce ESRD with chronic use
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11
Q

What are some other effects of aspirin?

A
  • Can increase LFTs (usually reversible)
  • Single dose can cause asthma problems in aspirin-sensitive pts
  • cross-sensitivity with other NSAIDS
  • Can cause GI bleeding, PUD
  • CNS stimulation
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12
Q

Aspirin dosing:

analgesic/antipyretic

anti-inflammatory

A
  • analgesic/antipyretic: 325-650 mg
  • anti-inflammatory: 1,000 mg (3-5 g/day)
    • increase dose gradually
    • follow serum salicylate levels
    • rarely used d/t GI side effects
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13
Q

How is aspirin cleared?

A
  • Hepatic clearance
  • E1/2t is 15020 minutes for aspirin and 2-3 hours for the active metabolite salicylic acid
  • overdose will cause metabolic acidosis and tinnitus
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14
Q

What makes nonacetylated salicylates more favorable than aspirin?

A
  • They do not interfere with platelet aggregation
  • rarely associated with GI bleeding
  • well tolerated by asthmatic patients
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15
Q

Why should aspirin not be used in children/teens with viruses?

A

Risk of Reye’s syndrome (encephalopathy)

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16
Q

What is the MOA of NSAIDS?

absorption?

PB?

VD?

metabolization?

half lives?

A
  • Cyclooxygenase (COX) inhibition
    • blocks conversion of arachidonic acid to prostaglandins
    • decreases production and release of prostaglandins
  • weak acids, well absorbed
  • >95% PB
  • Small volume distribution
  • extensively metabolized and excreted in urine
  • half lives vary from <6 to >12 hours
17
Q

How do NSAIDS affect platelets?

A
  • Reversible inhibition of platelet aggregation
    • inhibition of COX-1 blocks synthesis of thromboxane A2 which inhibits platelet aggregation
18
Q

What are some of the RARE adverse effects of NSAIDS?

Can they be taken during pregnancy?

A
  • Rare adverse effects:
    • hepatic injury
    • aseptic meningitis
  • Pregnancy
    • best avoided but category B if necessary
    • Avoid in 3rd trimester, Category D d/t premature closure of DA
19
Q

What are some GI adverse effects of NSAIDS?

What are the risk factors for these GI SEs?

A
  • Dyspepsia, GI bleeding, PUD
  • inhibition of prostaglandins that maintain normal gastric and duodenal mucosa
    • increases acid production
    • decreases mucous production and gastric blood flow
  • local irritation
    • lipid soluble at low pH- enters mucosal cells, lose lipid solubility and become trapped in cell (ion trapping)
  • risk factors:
    • high doses
    • prolonged use
    • previous GI ulcer or bleeding
    • excessive ETOH
    • elderly
    • corticosteroid use
20
Q

Which NSAIDS are low risk for GI issues?

moderate risk?

high risk?

A
  • Low risk
    • ibuprofen and naproxen at low doses
    • those selective to COX2 inhibition (Etodolac, sulindac, Celecoxib)
  • Moderate risk
    • ibuprofen and naproxen at moderate to high doses
    • Diclofenac, oxaprozin, meloxicam, nabumetone
  • High risk
    • Ketorolac, Tolmetin, piroxicam, aspirin, indomethacin
21
Q

What are some Renal adverse effects of NSAIDS?

Who is at risk?

A
  • decreased synthesis of renal vasodilator PGs (PGE2)
    • leads to decreased RBF
    • fluid and Na retention
    • may cause renal failure or HTN
    • interstitial nephritis (rare)
  • rarely an issue in healthy ppl
  • Ppl at risk are those who rely on PGs for renal perfusion:
    • elderly
    • CHF, HTN
    • DM
    • renal insufficiency
    • ascites
    • volume depletion
    • diuretic therapy
22
Q

What are some drug interactions seen with NSAIDS?

A
  • Displaces other highly protein-bound agents
    • increases levels of warfarin, phenytoin, sulfonylureas, sulfonamides, digoxin
  • reduces the effects of diuretics, Beta blockers, ACE inhibitors via suppression of renal PGs
  • increased risk of GI bleed when given in conjunction with anti-coagulants
  • Probencid increases levels of most NSAIDS
    • avoid with ketorolac
23
Q

Ketorolac

route of administration

how does it compare to morphine?

adverse effects?

A
  • Only IV NSAID in US
  • IM or IV comparable analgesic effect to mild opioids
    • similar time to pain relieve btw ketorolac and morphine
    • no ventilatory or cardiac depression
  • adverse effects similar to typical NSAID
24
Q

Ketorolac:

limitations of use

onset

E1.2t

DOA

PB

matab

dose

A
  • do not exceed 5 days of use
  • Onset 10 min
  • E1/2t = 5 hours, prolonged in elderly
  • DOA = 6-8 hours
  • 99% PB
  • conjugated in liver
  • dose
    • 30 mg IV x1 or q 6 hours
    • daily max dose 120 mg
    • elderly: if you use at all, cut dose in half
25
Q

What is the only selective NSAID available today?

What is the difference between inhibiting COX1 and COX2?

A
  • Celecoxib (Celebrex)- COX2 inhibitor
    • no more effective in reducing pain and inflammation than non selective NSAIDS
  • Cox1- gastric protection and production of thromboxane adn A2 (vasoconstrictor and platelet aggregator)
  • COX2- production of prostacyclin (vasodilator, platelet inhibitor)
26
Q

Celecoxib (celebrex)

dose

taken with ____

avoid in pts with _____

A
  • Use lowest effective dose <200 mg/day
    • 200 mg/day = 500 mg BID naproxen
  • weigh the risks vs benefits, taking into consideration pts risk for GI or CV events
  • Taken with food
  • Avoid in pts with a sulfonamide allergy
27
Q

What are the black box warnings for NSAIDS?

A
  • CV risk
    • increased risk of serious thrombotic evetns, MI, stroke
  • GI
    • increased risk of bleeding, ulceration, perforation of stomach and intestines
  • **same for selective and non selective NSAIDS
28
Q

What are the drugs of choice for neuropathic pain syndromes?

A
  • Antidepressnats and anticonvulsants
  • TCAs
    • diabetic neuropathy, postherpetic neuralgia, polyneuropathy, nerve injury or infiltration with cnacer
    • may improve underlying depression or insomnia
  • Venlafaxine (Effexor)-SSRI
    • Neuropathic pain, HA, fibromyalgia, postmastectomy pain
  • Duloxetine (Cymbalta)-SSRNI
29
Q

What are Gabapentin and Pregabalin used for?

How do they work to help with pain?

A
  • Diabetic neuropathy, postherpetic neuralgia, fibromyalgia
  • mechanism not well understood
    • may be related to Ca influx inhibition and inhibition of excitatory neurotransmitters in spinal and supraspinal pathways by binding to alpha 2 and delta 1 subunits of presynaptic voltage-gated channels in the CNS
30
Q

What are all the adjunct analgesics?

A
  • TCAs
  • SSRIs
  • gabapentin
  • pregabalin
  • carbamazepine
  • phenytoin
  • sodium valproate
  • clonazepam
  • topiramate
  • lamitrogen
  • hydroxyzine
  • corticosteroids
  • topicals
31
Q

What kind of pain is hydroxyzine used for?

Corticosteroids?

A
  • low dose hydroxyzine can add analgesic effect to opioids in cancer and postoperateive pain while reducing incidence of N/V
  • Corticosteroids can produce analgesia in some patients with inflammatory diseases or tumor infiltration of nerves
32
Q

What are the different topical agents and what do they help with?

A
  • 5% lidocaine- post herptic neuralgia
  • EMLA- cutaneous anesthesia
  • Capsaicin cream (Zostrix)- for neuropathic and osteoarthritic pain
    • doesn’t really work
  • Clonidine patch- may improve pain and hyperalgesia in sympathetically maintained pain
33
Q

Which Caneboid receptor has more to do with aneshesia?

Where is it found?

A
  • CB1-
  • found in interneurons and CNS
  • CB2- found in periphery, more to do with inflammation

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