Week 7 Flashcards

1
Q

A conscious experience that results from brain activity in response to noxious stimulus and engages the sensory, emotional, and cognitive processes of the brain.

A

Pain

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2
Q

The process that information about a noxious stimulus is conveyed to the brain.

A

Nociception

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3
Q

A physiological process whereby a noxious mechanical, chemical, or thermal stimulus in transducer via specialized receptors on primary afferents into an electrical impulse up to the brain.

A

Transduction

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4
Q

Once transduced and generated, nerve impulses are conducted to the CNS, using specific sodium channels.

A

Transmission

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5
Q

The process by which a noxious event is recognized as pain by a conscious person.

A

Perception

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6
Q

Inhibition of nociception impulses. Descending input from the brain stem influences central nociceptive transmission in the spinal cord. Neurons from the brain stem release 5HT and norepinephrine.

A

Descending modulation

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7
Q

These enhance normal modulation by interfering with reputable of 5HT and NE. In turn decreases the perception of pain.

A

Tricyclic antidepressants

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8
Q

Referred, colicky, diffuse pain in organs such as gall bladder, liver, intestines. Squeezing, cramping, bloating
Examples: UC, cholecystitis, peptic ulcer

A

Visceral pain

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9
Q

Well-localized pain caused by tissue damage to skin, soft tissue, muscle, or bone. Stabbing, aching, sharp
Examples: trauma, arthritis

A

Somatic

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10
Q

Injury or inflammation of nerves. Often coexists with somatic or visceral pain. Radicular, stocking like, burning, numb, electric, tingling
Examples: phantom limb syndrome, diabetic neuropathy, postherpetic neuralgia

A

Neuropathic

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11
Q

When is nociceptor pain functional in a fetus?

A

24 weeks

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12
Q

When is sucrose given and what age is it most effective?

A

Should be given 2 minutes before painful procedure

Most effective under 1 month of age

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13
Q

OLDCART:

A
Onset
Location
Duration
Characteristics
Aggravating factors
Relieving factors
Treatment
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14
Q

Step 1 of WHO analgesic ladder:

A

Treat with non-opioid (Tylenol, Motrin)

+- adjuvant (gabapentin)

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15
Q

Step 2 of WHO ladder:

A

Moderate to severe pain or if fail step 1:
Use oral opioid + nonopioid (Percocet)
+- adjuvant

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16
Q

Step 3 of WHO ladder:

A

Severe pain or if fail step 2:
Treat with opioid for severe pain without nonopioid (oxycodone/ OxyContin)
Practice ATC dosing
Adjuvant medications

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17
Q

Tylenol MOA:

A

Believed to inhibit the synthesis of prostaglandins in the CNS and work peripherally to block pain impulse generation.

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18
Q

What is max Tylenol dose per day:

A

4g with monitoring

3g without monitoring

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19
Q

FDA recommends that no prescriber gives form of Tylenol that exceeds ___ mg/tablet

A

325

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20
Q

Pediatric Tylenol dosing:

A

10-15 mg/kg/dose every 4-6 hours

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21
Q

Side effects of Tylenol:

A

Skin rash, increased ALT/bilirubin

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22
Q

Tylenol contraindicated in:

A

Liver impairment

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23
Q

NSAIDs MOA:

A

Reversibly inhibits Cox 1 and Cox 2 enzymes, which results in decreased formation of prostaglandin precursors.

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24
Q

NSAIDs max dose per day:

A

Ibuprofen 3200 mg/day

Naproxen 1250 mg/day

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25
Peds Motrin dosing:
5-10 mg/kg/dose every 4-6 hours (max 2400 mg/day)
26
Side effects of NSAIDs:
Edema, skin rash, epigastric, heartburn, ulcers
27
Monitoring parameters of NSAIDs:
Renal panel, CBC
28
Caution in NSAIDs:
HTN, renal disease, blood disorders, Avoid in pregnancy
29
Topical eutectic mixture of lidocaine and prilocaine that anesthetizes skin before painful procedures
EMLA
30
Indicated for acute pain related to sprains, strains, and OA
Voltaren gel (NSAID type gel)
31
How many times a day can you use Voltaren gel?
Four
32
Adjuvants to pain medication include:
SNRIs TCAs Anticonvulsants
33
SNRI examples:
Cymbalta and Effexor
34
SNRI MOA:
Potent inhibitor of neuronal serotonin and norepinephrine reuptake and a weak inhibitor of dopamine reuptake.
35
Side effects of SNRIs:
Ha, nausea, drowsiness, xerostomia
36
Clinical indication of SNRIs in pain:
Neuropathic pain, chronic musculoskeletal pain
37
TCAs MOA in pain:
Central inhibition of norepinephrine and serotonin reuptake
38
TCAs side effects:
Sedation, anticholinergic effects, postural hypotension, cognitive impairment
39
Example of TCA and when to give?
Amitriptyline and give at night
40
Avoid what population for TCAs?
The elderly: check EKG for conduction abnormalities prior to initiation
41
Clinical indications for TCAs and pain:
Neuropathic pain and chronic pain
42
Gabapentin MOA:
High affinity binding sites are located throughout the brain; sites correspond to the presence of voltage gates calcium channels which may modulate the release of exciting neurotransmitters which participate in nociception.
43
Side effects of gabapentin:
Dizziness, drowsiness, ataxia, fatigue, peripheral edema Give at night due to drowsiness
44
Clinical indication for gabapentin and pain:
Neuropathic pain
45
Pregabalin (lyrics) MOA:
Exerts antinociceptive and anticonvulsant activity; may also affect descending noradrenergic and serotonergic pain transmission pathways from the brain stem to the spinal cord
46
Side effects of lyrica:
Peripheral edema, dizziness, drowsiness, ha, fatigue
47
Monitoring parameters lyrica:
Sedation, weight gain, suicidality
48
Indications for lyrica in pain:
Neuropathic pain
49
Tramadol is for:
Moderate pain option that is a nonopioid that works on the opioid receptor.
50
Tramadol MOA:
Bonds to mu-opiate receptors in the CNS causing inhibition of ascending pain pathways, altering the perception of and response to pain. Also, inhibits the reuptake of norepinephrine and serotonin.
51
Side effects of tramadol:
Can lower seizure threshold, flushing, dizziness, ha, nausea, constipation
52
Monitoring parameters of tramadol:
Sedation and suicidal ideation
53
Caution with tramadol:
Risk for serotonin syndrome when combined with TCAs, SSRIs, SNRIs, and Triptans
54
When stopping tramadol:
It needs to be tapered after chronic use
55
Opioid MOA:
Bind to opioid receptors in the CNS, causing inhibition of ascending pain pathways, altering the perception of and response to pain; produces generalized CNS depression
56
Primary opioid receptor:
Mu
57
Opioid side effects:
Sedation, respiratory depression, nausea, vomiting, constipation, urinary retention, pruritus, confusion, and hypotension
58
What opioids have active metabolites that can accumulate in renal impairment
Morphine, dilaudid, and codeine
59
What opioid should not be used in opioid naive patients?
Fentanyl
60
Pure opioid antagonist that competes and displaces opioids at opioid receptor sites
Naloxone
61
Dose of naloxone:
0.4-2mg IV, IM, subQ, every 2-3 minutes
62
Side effects of naloxone:
Flushing, HTN, tachycardia, agitation
63
Caution with naloxone:
Patients with CV disease
64
Monitoring parameters of naloxone:
RR, HR, BP, temperature, level of consciousness, ABGs, pulse ox
65
When prescribing opioids patients must also have a:
Bowel regimen of motility focused laxatives
66
What are options for bowel regimen with opioids?
Senna Dulcolax Miralax (Promotility)
67
What should be avoided for bowel regimen with opioids?
Bulk forming laxatives including Metamucil and citrocel
68
Psychological dependence on the drugs. Often associated with drug seeking behaviors.
Addiction
69
Expected effect of chronic opioid use. Presents as decreased duration of analgesia.
Tolerance
70
Expected effect of chronic use. Not a sign of addiction. Withdrawal symptoms when opioid dose is markedly decreased.
Physical dependence