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Pharmacology > Week 2 Acute Pain Pharma > Flashcards

Week 2 Acute Pain Pharma Flashcards

1
Q

describe the mechanism of acute pain

A

you have an injury to the tissue, which causes inflammation and then a mediator response. This will stimulate the nociceptor, and will send a signal up the spinothalamic tract to the thalamus and then the somatosensory cortex.

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2
Q

what are the two most common substances in a chemically mediated response to pain

A

prostaglandins and substance P

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3
Q

is the described mechanism the reality of how we feel pain?

A

no, it is very complex, with various mechanisms

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4
Q

what is The WHO pain ladder

A

you try adjuvant and nonopioids at the first level. Then you move to opioids and more opioids

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5
Q

what is nocioceptive pain

A

noxious peripheral stills that affects the structure, like mechanical, chemical, heat and cold,

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6
Q

what is the difference between somatic and visceral nocioceptive pain

A

somatic is injury to the bone or skin

visceral comes from organs, compression or dissension. This can be things like pancreatitis and cancer pain

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7
Q

what is neuropathic pain

A

more in chronic, and damage to the PNS or CNS. things like burning types of pain

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8
Q

what are some ways we can assess intensity

A

word scales, VAS, Wong-Baker FACES pain scale

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9
Q

what are some descriptive terms for pain

A

throbbing, aching, cramping= nocioceptive

burning, tingling, stabbing, shocking = neuropathic.

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10
Q

when do you use acetaminophen

A

with mild or moderate pain, or for more moderate to severe pain if you mix it with an opioid

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11
Q

what is Percocet

A

oxycodone and acetaminophen

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12
Q

what is Vicodin

A

hydrocodone and acetaminophen

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13
Q

TF: acetaminophen is commonly used to reduce fever

A

true

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14
Q

acetaminophen has a mild adverse effect profile, but what is a big concern with taking high doses

A

liver damage/toxicity

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15
Q

TF: acetaminophen is preferred for things like OA when you have GI sensitivity

A

true

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16
Q

what are NSAIDS examples

A

non-steroidal anti-inflammatory drugs

  • aspirin
  • COX1 inhibitor
  • COX 2 inhibitor
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17
Q

what do prostaglandins lead to

A

inflammation and pain when injury occurs,

18
Q

what does cyclooxygenases do

A

converts arachidonic acid to prostaglandins, which is responsible for inflammation and pain when an injury occurs.

19
Q

how do NSAIDS work

A

they block the COX enzymes, which converts the arachidonic acid to prostaglandins, which is then blocking pro-inflammatory things.

20
Q

what are eicosinoids

A

local hormones like prostaglandins, thromboxanes and leukotrienes

21
Q

what is the relationship between prostaglandins and the GI tract

A

prostaglandins are protective in the stomach and the GI tract, so taking these can cause stomach irritation

22
Q

more COX2 selective means what for the GI tract

A

less stomach upset and bleeding

23
Q

what does COX1 help to protect

A

the stomach lining because of prostaglandins

24
Q

what is the relationship between COX 2 and cardiac risk

A

COX 2 selective drugs shift the balance of platelet activity to favor increased clotting by inhibiting prostacyclin (which promotes vasodilation and prevents platelet occlusion in the carotid arteries). but continues to allow thromboxane (which promotes platelet aggregation)

25
Q

what are the 4 actions of NSAIDS

A

analgesic, anti-inflammatory, anti-pyretic, anticoagulant.

26
Q

what are the risk factors for an increased risk of Gia bleeding

A

advanced age, multiple NSAIDS, high doses of NSAIDS, history of ulcers, alcoholism, use of other agents (like anticoags and steroids)

27
Q

side effects of NSAIDS

A 
drowsiness
dizziness
blurred vision 
bleeding 
anemia
dermatologic rash
renal toxicity 
hyperkalemia
CV event (MI, stroke)
GI event (GI irritation, inflammation, ulceration bleeding
28
Q

difference between opium, opiate and opioid

A
  • opium is anything derived from the poppy seed
  • opiate is anything derived from opium (morphine)
  • opioid is endogenous and exogenous substances that act on opioid receptors
29
Q

what are the 4 steps of nocioceptive pain

A
  1. stimulation of the nocioceptoos
  2. transmission of the signal on afferent fibers to the dorsal horn of the spinal cord, then to the cortex via the thalamus
  3. perception is when the information reaches the somatosensory cortex and pain is felt, or perceived
  4. modulation is when we tolerate pain and reduces endogenous opiates
30
Q

what are endorphins and what are their other names

A

Mu of (u), in acute and chronic pain, facilitates reward and abuse, and causes sedation, euphoria, respiratory depression, miosis, vomiting and constipation

31
Q

what are enkephalins

A

delta, they are in moderate to chronic pain, and facilitate reward and abuse. works for sedation, antidepressant, and neuroprotective

32
Q

what are dynorphines

A

kappa, they are for hyperalgesia, and inhibit reward and abuse. they also cause sedation and dysphoria

33
Q

what is the mechanism of action for the following drugs: fentanyl, hydromorphone, oxymorphone, oxycodone, hydrocodone, morphine, codeine,

A

they are mu agonists, and at higher doses may agonize kappa and delta

34
Q

what can excessive opioid exposure lead to

A

hyperalgesia (paradoxical increase in pain sensitivity, and and increased painful response)
allodynia (pain from a normally non-painful stimuli)

35
Q

what might help with opioid induced hyperalgesia

A

N-methyl-D-aspartate (NMDA) receptor antagonists like ketamine, and dextromethorphan

36
Q

what is naloxone used for

A

opioid overdose, and as a mu receptor antagonist

37
Q

what is buprenorphine and naloxone used for

A

opioid dependence, and buprenorphine agonizes mu and kappa receptors

38
Q

what is naltrexone

A

used to treat alcohol and opioid dependence, and mu receptor antagonist. blocks the euphoric feeling associated with opioid use.

39
Q

how can you administer opioids orally

A

either for an immediate response, or an extended release. can take 1 tablet per day or BID in extended release formulations to prevent pain, and can used immediate release PRN for breakthrough pain (but if they get too much, must adjust).

40
Q

how can we administer transdermal opioids

A

extended pain control, swallowing issues, cognitive impairment

41
Q

how can we administer transmucosal opioids

A

fentanyl lollipops, and absorbed through the mucosa.

Pharmacology (1 decks)

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