Pain, Inflammation, Gout Drug Therapy Flashcards
pain
5th vital sign
warning of disease/infection/injury
part of healing process
analgesics
drugs to relieve pain
nociceptors
nerve endings that respond to injury and pain
substances that trigger nociceptors
prostaglandins, histamine, bradykinin, serotonin, substance p
two elements of pain
local irritation (stimulation of peripheral nerves) recognition of pain (CNS, anxiety and apprehension)
types of pain duration
acute and chronic
responses to pain
psychological-tired/irritable/insomina/anxiety/depression
physical- increased HR/decreased BP/weakened immune
opioid analgesics
derived from opium, act on opioid receptors scheduled, monitor for tolerance/dependance
nonopiod analgesics
NSAIDS, acetaminophen, silicates
treat mild pain
MOA of opioids
react on opiod receptors, mimic analgesic peptides, decrease CNS, inhibits substance P and glutamate and nociceptors
uses of opioids
moderate to severe pain, cough
pt teaching.SE of opioids
sedation, respiratory depression, changes in mood, decreased peristalsis causing constipation, may be unable to operate vehicle, miosis, muscle spams, orthostatic hypotension, oliguria, bradycardia, dry mouth, do not drink alcohol
MOA and use of narcotic “pure” agonists
block opiods from binding
used for addiction/overdose
MOA of narcotic “partial” agonists
produce respiratory depression/mild pain relief
uses for non-opioid analgesics
inflammation, arthralgia, HA, myalgia, fever, mild pain
arachidonic pathway
formation of arachidonic acid via enzyme conversion of phospholipids
COX form prostaglandins
MOA of salicylates
blocks COX 1 and 2, inhibit synthesis of prostaglandins, suppress heat center, inhibit aggregation of platelets
uses and pt teaching for salicylates
analgesic, antipyretic, anti-inflmmatory, anti-coagulation
reyes syndrome tinnitus
MOA of NSAIDS
treat inflammation by inhibiting pathway of prostaglandin synthesis, inhibit COX
pt teaching of NSAIDS
ulcers/GI upset, disrupts stomach lining
MOA of COX 2 selective inhibitor
alleviate pain and inflammation without gastric mucosal disruption
MOA of acetominophen (Tylenol®)
acts on regulation center, inhibits prostaglandin synthesis and formation in CNS, not anti-inflam
pt teaching of acetaminophen (Tylenol®)
hepatotoxicity, no alcohol
antidote for tylenol
acetylcysteine
combination drugs
narcotic + non narcotic
gout
inflammatory condition causing joint pain, accumlation of uric acid in joint fluid attacked by phagocytes
avoid alcohol/beer/wine/cheese etc
subcategories of drugs used for gout
acute anti-gout
hypouricemic agent
uricosuric agent
MOA of acute anti-gout
alters ability of phagocytes to attack uric acid crystals
prophylactic therapy- long term anti gout
hypouricemic agent
uricosuric agent
MOA of hypouricemic agent
inhibits enzyme to produce uric acid
MOA of uricosuric agent
enhances renal excretion of uric acid, prevents reabsoprtion of uric acid
rheumatoid arthritis
autoimmune condition of joints
steroids, NSAIDS, analgesics, DMARDS
MOA of local anesthetics
decrease NA influx, interfere with nerve conduction
MOA of general anesthetics
increase GABA, inhibit glutamate
caution of malignant hyperthermia