patho exam 3

Question 1

What is pain?

Answer 1

-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

Question 2

Pathophysiology of pain

Answer 2

-neurophysiologic basis of painful sensations
-Nociceptive pain vs. neuropathic pain

Question 3

Nociceptive pain

Answer 3

results from injury to tissues
two forms:
-somatic pain: injury to somatic tissues (bones,joints,muscles)
-visceral pain- injury to visceral organs (small intestines)

Question 4

Neuropathic pain

Answer 4

-results from injury to peripheral nerves
-responds poorly to opioids

Question 5

Pain impulses are enhanced by

Answer 5

Prostaglandins, substance P (make the nerve endings more sensitive to pain)

Question 6

Brain suppresses pain by using

Answer 6

endogenous opioid compounds (endorphins/enkephalins)

Question 7

The brain receives pain sensations

Answer 7

-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)

Question 8

Midbrain and mesolimbic area

Answer 8

-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

Question 9

acute pain

Answer 9

-sudden onset
-usually subsides once treated

Question 10

chronic pain

Answer 10

-persistent or recurring
-lasts 3 to 6 months
-often difficult to treat
-tolerance
-physical dependence

Question 11

Classification of Pain

Answer 11

-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

Question 12

Dermatomes

Answer 12

-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

Question 13

visceral pain

Answer 13

-arises from internal organs such as the intestine, bladder, and the heart
-tumor involvement or obstruction

Question 14

analgesics

Answer 14

drugs that relieve pain without causing the loss of consciousness

Question 15

opioids

Answer 15

are the most effective pain relievers available

Question 16

non-opioids

Answer 16

-acetaminophen and NSAIDS
-effective for mild to moderate pain
-may be used in conjunction with opioids=opioid-sparing
-most available without a prescription

Question 17

analgesic ceiling

Answer 17

-increasing the dose beyond the upper limit provides no greater analgesia
-they do not produce tolerance or physical dependence

Question 18

acetaminophen

Answer 18

-most widely used nonopioid analgesic
-analgesic
-anti-pyretic-lowers febrile body temperatures by acting on hypothalamus, takes 71 mins to lower temperature

Question 19

acetaminophen contraindications

Answer 19

known allergy and severe liver disease
FDA limits daily dose to no more than 4000mg/24 hours

Question 20

acetaminophen MOA

Answer 20

blocks peripheral pain impulses by inhibition of prostaglandin synthesis in CNS. Does not suppress platelet aggregation

Question 21

acetaminophen route, onset of action, peak, etc.

Answer 21

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

Question 22

Acetaminophen interactions

Answer 22

-Alcohol the most dangerous
-chronic heavy alcohol abusers at risk of liver toxicity
drug interactions:
-phenytoin
-barbiturates
-warfarin
-isoniazid,rifampin
-beta-blockers
-anticholinergic drugs

Question 23

Acetaminophen interactions
alchohol & warfarin

Answer 23

-alcohol can increase a toxic metabolite
-warfarin may inhibit warfarin metabolism

Question 24

acetaminophen therapeutic uses
+ action

Answer 24

-analgesic, antipyretic
-does not have any antiinflammatory or antirheumatic actions

action: inhibits prostaglandin synthesis in CNS

Question 25

acetaminophen toxicity/overdose

Answer 25

-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

Question 26

adverse effects of acetaminophen

Answer 26

-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)

Question 27

First-generation NSAIDS
ibuprofen

Answer 27

-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

Question 28

NSAIDS

Answer 28

-23 different NSAIDS in the US
-large and chemically diverse group of drugs with analgesic, anti-inflammatory, and antipyretic effects

Question 29

NSAIDS indications

Answer 29

-osteoarthritis, rheumatoid arthritis, fever, mild to moderate pain
-gout, bursitis, tendonitis, juvenile rheumatoid arthritis
-chronic pain syndromes from cancer or lower back pain

Question 30

Ibuprofen

Answer 30

-NSAIDS
-anti-inflammatory, antipyretic, and analgesic effect
-propionic acid derivative

Question 31

ibuprofen MOA

Answer 31

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)

Question 32

Ibuprofen route, onset of action, etc.

Answer 32

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

Question 33

NSAIDS adverse effects

Answer 33

-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

Question 34

Classification of Drugs that Act at Opioid Receptors

Answer 34

-basic pharmacology of the opioids
-pure opioid agonist (morphine/codeine)
-pure opioid antagonists (naloxone)

Question 35

opium poppy-papaver somniferum

Answer 35

-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

Question 36

opioid receptors

Answer 36

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

Question 37

what are opioids?

Answer 37

opioid receptor Mu, Kappa, Delta
(+) activity at brain MU receptors leads to euphoria, sedation, decrease BP & RR, constricted pupils, itching, analgesia

Question 38

opioid MOA

Answer 38

-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