10. Non-narcotic Analgesics Flashcards
What are the NSAIDs (non-steroidal anti-inflammatory drugs) in the non-narcotic analgesics?
Aspirin Ibuprofen Celecoxib Rofecoxib Acetaminophen
What are the 2 drugs used for neuropathic pain?
TCAs
NSRIs
What are the 3 drugs used for trigeminal neuralgia?
Carbamazepine
Phenytoin
Lamotrigine
What are the 2 drugs used for fibromyalgia?
Pregabalin
TCAs
What are the 3 drugs used for gout?
Colchicine
Allopurinol
Probenecid
What are NSAIDs? (Non steroidal anti inflammatory drugs)
Act primarily by inhibiting the cyclooxygenase enzymes which block 1st step in prostanoid biosynthesis
Decreasing prostanoid biosynthesis is good and bad
Slides 4-5
What are prostaglandins role in pain, fever, and inflammation?
Prostaglandins sensitize nociceptors to many chemical mediators of pain such as bradykinin, cytokines, substance P and sensitize thermal and physical stimuli
PGs and prostacyclin (PGI2) increase blood flow to injured tissues which increases leukocyte formation (results in edema and inflammation)
What are the mechanisms and adverse effects of aspirin and ibuprofen?
Mechanisms- inhibit cyclooxygenase I and II (aspirin irreversibly) reducing prostaglandins and thromboxanes
Inhibit pain sensory transmission in peripheral CNS (spine/brain)
Reduce elevated body temps but don’t alter normal body temp
Not usually necessary to lower mild to mod fever
AEs: inhibits COX I which increases stomach protective mucus and GI irritation and ulceration, can cause GI perforation and severe GI bleeding in elderly, decrease renal blood flow in kidneys
Slides 7-8
What are the doses needed for analgesic activity and anti inflammatory activity?
The analgesic activity occurs at lower doses
Anti-inflammatory dose is higher, hepatic enzymes are saturated at this dose producing a zero order kinetic pattern
Slide 9
What are celecoxib and rofecoxib’s mechanisms of action and adverse effects?
Mechanisms- selective COX II inhibitors which reduces various mediators if the inflammatory process, but doesn’t alter GI mucosal defence or platelet aggregation
AE- found increasing clots and myocardial infarcts in orients with existing CV risk factors
Celec May cause rash
Slide 10
What is acetaminophen?
Mechanisms of action
Weak inhibition of prostaglandin formation in peripheral tissues
Lacks anti-inflammatory and antiplatelet actions
Analgesic and anti-pyretic actions aren’t comparable to aspirin (less GI stress than aspirin)
Slide 11
What is neuropathic pain?
Characteristics
Results from injury to the peripheral/central sensory nerves due to endocrine disease, connective tissue disease, viral infection, chemotoxicity
The primary afferent neurons are hyperactive discharging spontaneously (increase expression of Na channels) so use Na channel blockers and Ca channel blockers (carbamazepine, lamotrigine)
Characteristics:
Hyperalgesia- increase pain
Allodynia- pain caused by stuff not usually painful
Paresthesias- tingling, pins and needles
Dysethesias- burning, shooting, electric shock
Slide 12-13
What is trigeminal neuralgia?
Triggers
Disabling neuropathic shooting pain throughout distribution of trigeminal nerve (face)
Triggers: chewing, brushing teeth, wind on face
Na channel blocking drugs are helpful
Slide 14
What is fibromyalgia?
Chronic diffuse pain (increase painful response to pressure)
Increase sensitivity of brain to pain signals due to decrease pain threshold
May have fatigue sleep disturbance and depression
Slide 15
What is gout?
Inflammatory joint disease caused by increased uric acid in blood and deposition of uric acid crystals in joints
Uric acid is waste generated from purine metabolism (it normally dissolves in blood)
Often involves big toe
Extremely painful
Use NSAIDs and corticosteroids to decrease inflammation
Long term decrease uric acid through blocking hypoxanthine oxidase
