pain management Flashcards
what are the 3 distinct families of endogenous opioid peptides
endorphins
enkephalins
dynorphins
what are common side effects of Mu receptor activation
sedation and respiratory depression
antagonists don’t produce ____
analgesia
antagonists are primarily used to treat….
opioid overdoses
addiction
what is the primary agent used to treat opioid overdose
naloxone
strong agonists are used to treat…
severe pain
morphine is an example of
strong agonist
mild-to-moderate agonists are used to treat….
moderate pain
codeine, hydrocodone and oxycodone are what type of agonsit
mild-to-moderate
mixed agonist-antagonists strength
less risk of side effects with Mu receptors
mixed agonist-antagonist weaknesses
may produce psychotropic effects
maximal analgesic effect may not be as strong
spinal effects/mechanism of opioids
inhibits both presynaptic and postsynaptic membranes of pain-mediating synapses by “trapping” neurotransmitters
(basically is able to stop neurons from communicating to each other that there is pain)
opioid receptors are linked via _________ to signaling pathways
G proteins
supraspinal effects/mechanism of opioids
opioids bind to the midbrain’s gray matter (PAG) and sends signals down a pathway to the pain sight to slow the pain signals
(basically decreases pain by stopping the pain signals to the brain)
increased activity of descending pathways travel through the ventromedial medulla (VMM) to reach the ______
dorsal horn of the spinal cord
neurons in descending pathways release _____ and _____ onto _______ to inhibit pain impulses to the brain
serotonin
norepinephrine
dorsal horn synapses
orthostatic hypotension
when you get up too fast and get dizzy
2 mechanisms of opioid tolerance
- receptor down-regulation
- loss of communication between opioid receptors and G proteins
when do withdrawal symptoms become evident, when is the peak, and how long do they last for?
evident: 6-10 hours
peak: day 2-3
last for: 5 days
some symptoms of physical dependence to pain medicine include
body aches
diarrhea
fever
insomnia
irritability
stomach cramps
vomiting/nausea
opioid-induced hyperalgesia
failure to respond to opioids
could increase pain sensitivity
methadone function
offers milder withdrawal symptoms
peripheral effects/mechanism of opioids
the exogenous opioids assist the endogenous peptides in stopping the transmission of pain
2 types of corticosteroids
- glucocorticoids (cortisol)
- mineralocorticoids (aldosterone)
what corticosteroid affects carbohydrate and protein metabolism
glucocorticoids (cortisol)
what corticosteroid regulates electrolyte and water metabolism
mineralocorticoids (aldosterone)
glucocorticoids __(increase/decrease)___ blood glucose and liver glycogen
increase
glucocorticoids act on macrophages, lymphocytes, and endothelial cells to inhibit the expression of __________
inflammatory proteins (cytokines)
how do glucocorticoids reduce inflammation
- inhibits inflammatory proteins (cytokines)
- reduces lymphocytes and eosinophils
- inhibits adhesion molecules so leukocytes can’t promote inflammation
- reduces vascular permeability by suppressing histamine and kinins
in order to reduce vascular permeability, ____ and ___ must be produced (think endogenous)
histamine and kinins
what are the main functions of glucocorticoid medications
decrease inflammation
immunosuppression
replacement for adrenal insufficiency
the main adverse symptom of prolonged corticosteroids in the ENDOCRINE system
hyperglycemia
the main adverse symptom of prolonged corticosteroids in the CARDIOVASCULAR system
fluid retention/edema
the main adverse symptoms of prolonged corticosteroids in the IMMUNE system
increase risk of infections
activates latent viruses
masks infection
the main adverse symptoms of prolonged corticosteroids in the MUSCULOSKELETAL system
osteoporosis
bone fractures
the main adverse symptoms of prolonged corticosteroids in the GASTROINTESTINAL system
peptic ulcers
GI bleeding
gastritis
nausea
the main adverse symptoms of prolonged corticosteroids in the NERVOUS system
insomnia
mood changes
-prazole
proton pump inhibitor
helps with gastric ulcers
-idine
histamine H2-receptor blockers
helps with gastric ulcers
-amide
oral antidiabetics (sulfonylurea group)
helps with type 2 diabetes (antidiabetics)
-dronate
bisphosphonates
helps with osteoporosis
what is the first step of the eicosanoid biosynthesis and then what are the 2 pathway options
arachidonic acid is released then either goes the LOX or COX pathway
prostaglandin
a group of lipid-like compounds that are produced by all living cells (except RBCs)
leukotriene
pro-inflammatory and mediates airway inflammation
increased PGE2 causes
inflammation
how do eicosanoids promote fever
altering thermo-regulatory set-point
dysmenorrhea
painful cramps that accompany menstruation
eicosanoids cause
pain
fever
dysmenorrhea
thrombus formation
inflammation
how do eicosanoids cause thrombus formation
TXA2 causes platelet aggregations that result in the blood clot formations
what do aspirin and other NSAIDs inhibit
Cyclooxygenase (COX)
what does it mean to say that aspirin is a nonselective inhibitor? Why is this a bad thing?
it means that aspirin inhibits COX1 and COX2
This is bad because COX1 helps platelet function and gastric protection
COX1 function
gastric protection
platelet function
COX2 function
pain
fever
bone formation
what is aspirin good at preventing
pain/inflammation
fever
vascular disorders
cancer prevention
what is the primary NSAID used in treating fever in adults
aspirin
2 main adverse effects of aspirin-like drugs
- gastrointestinal problems
- cardiovascular problems
aspirin is linked to causing _______ in children
reye syndrome
benefit of COX-2 selective drugs
because COX1 is untouched, the chance of gastric irritation is much lower
what does NSAID stand for
Nonsteroidal anti-inflammatory drugs
which COX drug (1 or 2) may increase the risk of serious cardiovascular events like heart attack/stroke
COX-2
is acetaminophen an NSAID drug? why or why not?
no because it lacks anti-inflammatory and anti-coagulant properties
what is the main contraindication to taking acetaminophen
people who have pre-existing liver disease (or are alcohol abusers)
acetaminophen is filtered through the liver and can be especially toxic in these individuals
