Pain Management-Intro through Non-opioids Flashcards
Indication for Acetaminophen
Tx of mild to moderate pain
Adverse effects of Acetaminophen
usually well tolerated; hepatotoxicity, analgesic neuropathy, anemia, blood dyscrasias, rare skin rxns.
Non-opioid analgesics
Acetaminophen, NSAIDS (Nonsalicylates and salicylates)
MOA for Acetaminophen
Analgesic; inhibits prostaglandin synthesis in CNS and peripherally blocks pain impulse generation
How does Acetaminophen Hepatotoxicity Occur
A small amount of APAP is metabolized via CYP450 to a hepatotoxic metabolite;
Usually glutathione binds to NAPQI to allow excretion of non conjugates, but when Acetaminophen is misused/OD it depletes glutathione and NAPQI isn’t detoxified
MOA for NSAIDS
Nonselective NSAIDS inhibit both COX 1 and COX 2
Partially selective NSAIDS inhibit COX 2 more than COX1
Selective COX 2 inhibitors only inhibit COX 2
NSAID adverse effects
Cardiovascular Hematologic Toxicity CNS (high doses cause sedation/decreased cognition) Hepatotoxicity GI complications (mucosal damage) (Renal) Nephrotroxicity Skin (SJS/TEN) Pneumonic = CH CH GRS
Indication for Acetylated Salicylates
Mild to moderate pain; prevention of MI, CVA
MOA for acetylated salicylates
Analgesic: Inhibit both COX 1 and COX 2
Antipyretic: Inhibition of hypothalamic heat-regulating center
Adverse Effects for acetylated salicylates
Reye’s syndrome
ASA sensitivity (asthma, bronchospasm, andioedema, urticaria)
platelet inhibition
PNEUMONIC = RAP
Adverse Effects for nonacetylated salicylates
less GI toxicity than NSAIDS no antiplatelet effects same AE as N-NSAIDs occasional cross reactivity in ASA sensitive pts Reye's syndrome
What are nociceptors stimulated by?
Leukotrienes, prostaglandins, and histamine
What are the 3 endogenous endorphins used in the brain to modulate pain
Beta-endorphins, Enkephalins, Dynorphins
Think BED
4 types of pain
Nociceptive, inflammatory, neuropathic, functional
PQRST characteristics of pain
Palliative/Provocative Quality Radiation Severity Temporal factors
WHO Step 1: levels of pain and treatment
Mild pain (1-3/10)
+ non-opioid
+/- adjuvents
WHO Step 2: levels of pain and treatment
Moderate pain (4-6/10)
weak opioid
+ non-opioid
+/- adjuvents
WHO Step 3: levels of pain and treatment
Severe pain (7-10/10)
strong opioid
+ non-opioid
+/- adjuvent
Difference in effects between Acetaminophen and NSAIDS
NSAIDS have anti-inflammatory effect and Acetaminophen do not
Reason for NSAID mucosal damage
Due to direct or topical irritation of gastric epithelium OR systemic inhibition of endogenous GI mucosal prostaglandin synthesis
High Risk Patients for NSAID caused ulcer
Prior PUD or UGI bleed Age >60 NSAID (high dose or more toxic ) concurrent corticosteroid, bisphosphonate, or SSRI use anticoagulant use or coagulopathy Chronic illness (ex. CV disease) antiplatelet use (ex. ASA, clopidogrel)
PNEUMONIC: PANCACA
Risk factors for Nephrotoxicity with NSAID use
older age HF renal insufficiency ascites volume depletion diuretic therapy
Reason for Nephrotoxicity with NSAID use
NSAID decrease renal prostaglandins that usually help increase renal blood flow and maintain renal function, but NSAIDs decreases it.
How does ASA and non-selective NSAIDs differ in their hematologic effects.
ASA inhibits platelet aggregation for the lifetime of the platelet (7-10 days)
Other non-selective NSAIDs affect platelet aggregation to a lesser degree and only when the drug is on board
