patho exam 3 Flashcards
What is pain?
-Unpleasant sensory and emotional experience associated with actual or potential tissue damage
-the most reliable method of assessing pain is to have the patient describe his/her experience
-pain is inherently personal and subjective
Pathophysiology of pain
-neurophysiologic basis of painful sensations
-Nociceptive pain vs. neuropathic pain
Nociceptive pain
results from injury to tissues
two forms:
-somatic pain: injury to somatic tissues (bones,joints,muscles)
-visceral pain- injury to visceral organs (small intestines)
Neuropathic pain
-results from injury to peripheral nerves
-responds poorly to opioids
Pain impulses are enhanced by
Prostaglandins, substance P (make the nerve endings more sensitive to pain)
Brain suppresses pain by using
endogenous opioid compounds (endorphins/enkephalins)
The brain receives pain sensations
-the parietal lobe of the cerebral cortex
integrates and interprets pain sensations
“that cinder block that I just dropped elicited
an excruciating pain on my left toe”
Cingulate gyrus- governs the emotional response to pain
“@#!!! that hurts!” (thalmus)
Midbrain and mesolimbic area
-thalamus-relay station (to and from the periphery) “ouch- that’s a 10 on the pain scale!!”
-hippocampus-learning and memory “don’t forget you did that, you idiot…”
-amygdala/nucleus accumbens- treating the excruciating pain with narcotics not only activates the pain control system but also activates the dopaminergic reward system
acute pain
-sudden onset
-usually subsides once treated
chronic pain
-persistent or recurring
-lasts 3 to 6 months
-often difficult to treat
-tolerance
-physical dependence
Classification of Pain
-visceral -location of pain
-superficial –>location assists in
identifying cause
and treatment
-deep
-referred (dermatomes) -localized
-neuropathic -all over
-phantom -referred or
radiated from
origin to different
-cancer site
Dermatomes
-areas of skin that send their sensory information into specific spinal cord segments
-visceral structures share these sensory afferents with skin areas
-maximal intensity of the visceral pain is retrosternal area/precordial area, up the neck, down the inner arm
visceral pain
-arises from internal organs such as the intestine, bladder, and the heart
-tumor involvement or obstruction
analgesics
drugs that relieve pain without causing the loss of consciousness
opioids
are the most effective pain relievers available
non-opioids
-acetaminophen and NSAIDS
-effective for mild to moderate pain
-may be used in conjunction with opioids=opioid-sparing
-most available without a prescription
analgesic ceiling
-increasing the dose beyond the upper limit provides no greater analgesia
-they do not produce tolerance or physical dependence
acetaminophen
-most widely used nonopioid analgesic
-analgesic
-anti-pyretic-lowers febrile body temperatures by acting on hypothalamus, takes 71 mins to lower temperature
acetaminophen contraindications
known allergy and severe liver disease
FDA limits daily dose to no more than 4000mg/24 hours
acetaminophen MOA
blocks peripheral pain impulses by inhibition of prostaglandin synthesis in CNS. Does not suppress platelet aggregation
acetaminophen route, onset of action, peak, etc.
Route: PO
Onset of action: 10-30mins
Peak: 30 minutes to 2 hours
Half-life: 1 to 4 hours
Duration of action: 3-4 hours
Acetaminophen interactions
-Alcohol the most dangerous
-chronic heavy alcohol abusers at risk of liver toxicity
drug interactions:
-phenytoin
-barbiturates
-warfarin
-isoniazid,rifampin
-beta-blockers
-anticholinergic drugs
Acetaminophen interactions
alchohol & warfarin
-alcohol can increase a toxic metabolite
-warfarin may inhibit warfarin metabolism
acetaminophen therapeutic uses
+ action
-analgesic, antipyretic
-does not have any antiinflammatory or antirheumatic actions
action: inhibits prostaglandin synthesis in CNS
acetaminophen toxicity/overdose
-hepatic necrosis
-hepatotoxicity-can be reversed with acetylcysteine
-works by preventing the hepatotoxic metabolites of acetaminophen from forming
-most effective if given within 10 hours of overdose
-bad-tasting with odor of rotten eggs
-vomiting of oral dose common
-available in IV
-longer term ingestion of large doses=severe hepatotoxicity
-may be irreversible
adverse effects of acetaminophen
-very few at normal doses
-stevens-johnson syndrme (SJS), acute generalized exanthematous pustulosis (AGEP), and toxic epidermal necrolysis (TEN)
hepatotoxicity:
-with overdose or in patients with liver failure
overdose:hepatic necrosis:
-signs and symptoms of hepatic failure, coma, death
-early symptoms: nausea and vomiting, diarrhea, sweating, abdominal pain
-treatment for overdose: acetylcysteine (mucomyst)
First-generation NSAIDS
ibuprofen
-inhibits cyclooxygenase and has antiinflammatory, analgesic, and atipyretic actions
-indications: fever, mild to moderate pain, arthritis
-generally well tolerated
-low incidence of adverse effects
-safety alert: all first-generation NSAIDS are associated with an increased risk of GI bleeding that can lead to hospitalization or death
NSAIDS
-23 different NSAIDS in the US
-large and chemically diverse group of drugs with analgesic, anti-inflammatory, and antipyretic effects
NSAIDS indications
-osteoarthritis, rheumatoid arthritis, fever, mild to moderate pain
-gout, bursitis, tendonitis, juvenile rheumatoid arthritis
-chronic pain syndromes from cancer or lower back pain
Ibuprofen
-NSAIDS
-anti-inflammatory, antipyretic, and analgesic effect
-propionic acid derivative
ibuprofen MOA
non-selective inhibitor of an enzyme called cyclooxygenase (COX), which is required for the synthesis of prostaglandins via the arachidonic acid pathway
(block prostaglandins which stops mucous, causing GI bleed bc mucous is a protective agen)
Ibuprofen route, onset of action, etc.
route: oral
onset of action: 30-60 minutes
peak: plasma concentration 1-2 hours
elimination half-life: 2-4 hours
duration of action: 4-6 hours takes 42 minutes to reduce fever
dosing maximum 1200-3200 mg/day divided 3-4x
NSAIDS adverse effects
-over 100,000 hospitalizations each year with 16,000 reported deaths
-more common adverse effect is the effect on GI tract
-heartburn
-ulceration and GI
bleeding
-most fatalities due to
GI bleed
-acute renal failure
-cardiovascular risk
-thrombotic events
-MI
-Stroke
Classification of Drugs that Act at Opioid Receptors
-basic pharmacology of the opioids
-pure opioid agonist (morphine/codeine)
-pure opioid antagonists (naloxone)
opium poppy-papaver somniferum
-the flower being described here is the opium poppy, and the natural product that this plant produces, known as opium/ or its main constituent: morphine
-this natural product not only has the power to alleviate intense pain, but also rapidly induces dependence and addiction
opioid receptors
three main classes of opioid receptors
-mu receptors: analgesia, respiratory depression, euphoria, sedation, decrease GI motility and physical dependence
-kappa receptors: analgesia, decrease GI motility and sedation
-delta receptors
(don’t do much)
opioid analgesics act by activating the mu receptors and to a lesser degree kappa
what are opioids?
opioid receptor Mu, Kappa, Delta
(+) activity at brain MU receptors leads to euphoria, sedation, decrease BP & RR, constricted pupils, itching, analgesia
opioid MOA
-someone had to find the molecules produced by the brain that interacted with the receptors
-that took a few more years and eventually 3 families of endogenous opioid-like peptides were discovered
Three families of peptides:
-endorphins, enkephalins, dynorphins
