pain management Flashcards

(62 cards)

1
Q

what are the 3 distinct families of endogenous opioid peptides

A

endorphins
enkephalins
dynorphins

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2
Q

what are common side effects of Mu receptor activation

A

sedation and respiratory depression

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3
Q

antagonists don’t produce ____

A

analgesia

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4
Q

antagonists are primarily used to treat….

A

opioid overdoses
addiction

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5
Q

what is the primary agent used to treat opioid overdose

A

naloxone

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6
Q

strong agonists are used to treat…

A

severe pain

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7
Q

morphine is an example of

A

strong agonist

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8
Q

mild-to-moderate agonists are used to treat….

A

moderate pain

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9
Q

codeine, hydrocodone and oxycodone are what type of agonsit

A

mild-to-moderate

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10
Q

mixed agonist-antagonists strength

A

less risk of side effects with Mu receptors

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11
Q

mixed agonist-antagonist weaknesses

A

may produce psychotropic effects
maximal analgesic effect may not be as strong

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12
Q

spinal effects/mechanism of opioids

A

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)

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13
Q

opioid receptors are linked via _________ to signaling pathways

A

G proteins

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14
Q

supraspinal effects/mechanism of opioids

A

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)

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15
Q

increased activity of descending pathways travel through the ventromedial medulla (VMM) to reach the ______

A

dorsal horn of the spinal cord

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16
Q

neurons in descending pathways release _____ and _____ onto _______ to inhibit pain impulses to the brain

A

serotonin
norepinephrine
dorsal horn synapses

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17
Q

orthostatic hypotension

A

when you get up too fast and get dizzy

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18
Q

2 mechanisms of opioid tolerance

A
  1. receptor down-regulation
  2. loss of communication between opioid receptors and G proteins
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19
Q

when do withdrawal symptoms become evident, when is the peak, and how long do they last for?

A

evident: 6-10 hours
peak: day 2-3
last for: 5 days

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20
Q

some symptoms of physical dependence to pain medicine include

A

body aches
diarrhea
fever
insomnia
irritability
stomach cramps
vomiting/nausea

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21
Q

opioid-induced hyperalgesia

A

failure to respond to opioids
could increase pain sensitivity

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22
Q

methadone function

A

offers milder withdrawal symptoms

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23
Q

peripheral effects/mechanism of opioids

A

the exogenous opioids assist the endogenous peptides in stopping the transmission of pain

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24
Q

2 types of corticosteroids

A
  1. glucocorticoids (cortisol)
  2. mineralocorticoids (aldosterone)
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25
what corticosteroid affects carbohydrate and protein metabolism
glucocorticoids (cortisol)
26
what corticosteroid regulates electrolyte and water metabolism
mineralocorticoids (aldosterone)
27
glucocorticoids __(increase/decrease)___ blood glucose and liver glycogen
increase
28
glucocorticoids act on macrophages, lymphocytes, and endothelial cells to inhibit the expression of __________
inflammatory proteins (cytokines)
29
how do glucocorticoids reduce inflammation
1. inhibits inflammatory proteins (cytokines) 2. reduces lymphocytes and eosinophils 3. inhibits adhesion molecules so leukocytes can't promote inflammation 4. reduces vascular permeability by suppressing histamine and kinins
30
in order to reduce vascular permeability, ____ and ___ must be produced (think endogenous)
histamine and kinins
31
what are the main functions of glucocorticoid medications
decrease inflammation immunosuppression replacement for adrenal insufficiency
32
the main adverse symptom of prolonged corticosteroids in the ENDOCRINE system
hyperglycemia
33
the main adverse symptom of prolonged corticosteroids in the CARDIOVASCULAR system
fluid retention/edema
34
the main adverse symptoms of prolonged corticosteroids in the IMMUNE system
increase risk of infections activates latent viruses masks infection
35
the main adverse symptoms of prolonged corticosteroids in the MUSCULOSKELETAL system
osteoporosis bone fractures
36
the main adverse symptoms of prolonged corticosteroids in the GASTROINTESTINAL system
peptic ulcers GI bleeding gastritis nausea
37
the main adverse symptoms of prolonged corticosteroids in the NERVOUS system
insomnia mood changes
38
-prazole
proton pump inhibitor helps with gastric ulcers
39
-idine
histamine H2-receptor blockers helps with gastric ulcers
40
-amide
oral antidiabetics (sulfonylurea group) helps with type 2 diabetes (antidiabetics)
41
-dronate
bisphosphonates helps with osteoporosis
42
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
43
prostaglandin
a group of lipid-like compounds that are produced by all living cells (except RBCs)
44
leukotriene
pro-inflammatory and mediates airway inflammation
45
increased PGE2 causes
inflammation
46
how do eicosanoids promote fever
altering thermo-regulatory set-point
47
dysmenorrhea
painful cramps that accompany menstruation
48
eicosanoids cause
pain fever dysmenorrhea thrombus formation inflammation
49
how do eicosanoids cause thrombus formation
TXA2 causes platelet aggregations that result in the blood clot formations
50
what do aspirin and other NSAIDs inhibit
Cyclooxygenase (COX)
51
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
52
COX1 function
gastric protection platelet function
53
COX2 function
pain fever bone formation
54
what is aspirin good at preventing
pain/inflammation fever vascular disorders cancer prevention
55
what is the primary NSAID used in treating fever in adults
aspirin
56
2 main adverse effects of aspirin-like drugs
1. gastrointestinal problems 2. cardiovascular problems
57
aspirin is linked to causing _______ in children
reye syndrome
58
benefit of COX-2 selective drugs
because COX1 is untouched, the chance of gastric irritation is much lower
59
what does NSAID stand for
Nonsteroidal anti-inflammatory drugs
60
which COX drug (1 or 2) may increase the risk of serious cardiovascular events like heart attack/stroke
COX-2
61
is acetaminophen an NSAID drug? why or why not?
no because it lacks anti-inflammatory and anti-coagulant properties
62
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