Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Chapter 24: Pain > Flashcards

Chapter 24: Pain Flashcards

(68 cards)

Start Studying
1
Q

Major contributors to the onset of pain

A

arthritis, back pain, cancer, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

most common prescription meds used for pain relief

A

NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Acute pain

A

nocioceptive pain that is a result of actual or pending tissue damage

duration is short

resolves with healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

chronic pain

A

Perception is a function of a person’s personality and character traits, cultural/ethnic backgound, presence of support systems, work/home satisfaction, and motivation

lasts longer than 3 months

cause is hard to identify

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

removing barriers that render pain management ineffective

A

stigma attached to certain medications like morphine

patient prefernce on strength

provider concerns about DEA reprisal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

consequences of poorly managed pain

A

impaired function and quality of life

depression

polypharmacy from treated manifestations of pain (agitation, etc)

uncontrolled acute pain leading to chronic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

properly assess pain before prescribing any drug

A

detailed history and physical

idetify the source of the pain

discuss realistic goals

re-examine and adjust therapy as needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

remeber the goal of using medications to manage acute pain

A

restore function as soon as possible

prevent the development of chronic pain syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

use different prescribing algorythms for mild, moderate, and severe acute pain

A

mild - NSAIDs and acetominophen with adjunct medications like capscaicin creams or topical salicylates (Ben-gay)

moderate - hydrocodone/APAP, hydrocodone/ibuprofen, oxycodone/APAP, or codeine

severe - pure opiates with dosages limited to less than 200mg morphine equivalent/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

use different algorythm when prescribing for chronic pain

A

usually requires adjunctive use of other medications for neuropathic component

comes about through hyperstimulation of NMDA receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

remeber there is a role for adjunctive medications

A

drugs used to manage pain but whose primary action is ot analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

medications used to treat pain are generally grouped into what 2 categories

A

opioid and nonopioid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

opiates

A

naturally occuring opium alkaloids or synthetic derivatives of them

multiple opiate receptor types throughout body to relieve pain

function as either agonists, partial agonists, or antagonists at one or more types of receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which opiate receptors are most snesitive and most important for managing general anethesia

A

Mu1 and Mu2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

conscientious prescribing of opiates

A

equivalencies of using one opiate over another are approximate

when switching from oral to subQ or IV use 70-75% of dose

dose may be decreased d/t limited cross-tolerance

appropriate dose is the one that relieves pain with least side effects

schedule around the clock, not prn, especially for chronic pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

treatment of myoclonus reltaed to pain medication

A

change opioid or treat with lorazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

typica dose of Narcan for overdose

A

0.2-0.8mg IV

up to 2mg is often given

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

prototype agent for antagonist agonist opiate analgesics

A

Morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

morphine mechanism of action

A

have activity at pre- and post-synaptic mu receptors as well as pre-synaptic kappa and delta receptors

reduces neurotransmitter release from nociceptive primary afferent terminals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

antagonist agonist opiate analgesic (morphine)

pharmacokinetics

A
  • Absorption: oral, subQ, and IV absorbed well. Fentanyl not given orally because it is broken down by mucosal and hepatic P450 and 3A4
  • Distribution: widely into CNS and other tissues, especially lipophillic
  • Metabolism: morphine/hydromorphone by glucuronidation, fentanyl by P450 and 3A4, most others by P450 2D6 isoenzyme
  • Excretion: urine
  • Half-life: 2-3 hours, prolonged with hepatic impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

opiate adverse reactions

A
  • CV: ortho hypotension, decreased BP
  • DERM: occasional allergic rash/pruritus
  • EENT: visual changes
  • GI: constipation, n/v, abdominal cramps, dry mouth
  • GU: urine retention
  • META: decreased appetite, increased urine glucose
  • NEURO: sedation, diaphoresis, flushing, somnolence, dizziness
  • PUL: overdose=respiratory depression with skeletal muscle flaccidity, cold/clammy skin, cyanosis, extreme somnolence progressing to seizures, stupor, coma, death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

opiate interactions

A

anything that causes respiratory depression

medications that prolong QT interval if using methadone or buprenorphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

mixed/partial agonist-antagonist analgesics

4 available agents

A

buprenorphine (Buprenex, Subutex)

pantazocine (Talwin)

nalbuphine (Nubain)

butorphanol (Stadol)

can precipitate withdrawal symptoms in patients taking chronic opiates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

clinical use of buprenorphine

A

alters emotional perception of pain

sed as an alternative to methadone in opioid detox because of slow dissociation from mu receptor

antagonist at delta and kappa receptors

low analgesi activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
clinical use for pentazocine (Talwin) and nalbuphine (Nubain)
treat mod-severe pain higher rate of hallucinations, nightmares, and anxiety than other opioids Talwin is used as a supplement to surgical anethesia or pre-surgical sedative
26
clinical use of butorphanol (Stadol)
available as nasal spray and IV treat mod-severe pain (migraines) supplement anethsesia pain during labor
27
synthetic opiate antagonists
bind to same opioid receptors as morphine but with higher affinity so it blocks effects of opioid precipitates withdrawal symptoms in opioid-dependency no effect on non-addicts
28
naloxone (Narcan)
fast onset (minutes) will antagonize post-op analgesics
29
Narcan mechanism of action
high affinity for mu sites antagonistic effects at delta and kappa sites
30
clinica use of Narcan
opioid overdose
31
Narcan pharmacokinetics
* Absorption: very poor from GI tract, well absorbed when given SC or IV * Distribution: rapidly to all tissues, crosses placenta * Metabolism: glucuronide conjugation in the liver * Excretion: urine * Half-life: 1-2 hours
32
Narcan adverse reactions
* CV: HTN, hypotension, v-fib, tachycardia * GI: n/v * MISC: severe opiate withdrawal
33
methylnaltrexone (Relistor)
no risk for abuse/dependency peripherally acting mu opioid receptor antagonist does not cross blood brain barrier
34
Relistor clinical uses and contraindication
treats opioid induced constipation (counteracts opioid effects like constipation and itching without effecting analgesia because it doesn't cross the blood brain barrier) contraindicated in GI obstruction
35
Relistor pharmacokinetics
* Absorption: admin SC w/ peak concentration in 30 minutes * Distribution: moderate * Metabolism: slightly via methylation in the liver * Excretion: 85% unchanged, half in urine, half in feces * Half-life: 8 hours
36
Reistor adverse reactions
* DERM: hyperhidrosis * GI: abdominal pain, gas, nausea, severe and/or persistent diarrhea * NEURO: dizziness
37
nalmefene (Revex) and naltrexone (ReVia, Trexan)
similar chemical structures used to decrease craving for opioids naltrexone: used in "rapid detox" for opiate addicts and alcoholics nalfmefene: long-acting injectable used to prevent alcoholic from relapsing
38
examples of nonopiate analgesics
tramadol (Ultram) ziconotide (Prialt) tapentadol (Nucynta)
39
tramadol (Ultram)
centrally acting synthetic agent with analgesic properties used for mod-moderatly severe pain can be subject to abuse
40
tramadol (Ultram) mechanism of action
binds to mu receptors in CNS and inhibits reuptake of serotonin and norepinephrine to modify the acending pathways of pain
41
tramadol pharmacokinetics
* Absorption: good absorption through GI tract * Deistribution: widely * Metabolism: liver * Excretion: urine * Half-life: 6-8 hours
42
tramadol adverse effects
* CV: flushing * DERM: rash * EENT: burry vision, miosis * GI: nausea, constipation * MISC: flu-like symptoms * NEURO: dizziness, headache, insomnia, somnolence, weakness, and possible seizures
43
tramadol contraindications
seizure disorders or concomittent use with medications that lower seizure threshold
44
ziconotide (Prialt)
used for severe chronic pain when IT (intrathecal) therapy is warranted administered directly into CSF for patients who are intolerant of or refractory to other treatments
45
Prialt mechanism of action
blocks excitatory neurotransmitter release and reduces their sensitivity to painful stimuli
46
Prialt contraindications
history of psychosis, schizophrenia, clinical depression, bipolar disorder and seizures
47
Prialt pharmacokinetics
* Absorption: administered directly into CSF * Distribution: 50% bound to protein * Metabolism: by several enzymes inmultiple organs degrade it to peptide fragments and free amino acids * Excretion: urine * Haf-life: 2.9-6.5 hours
48
Prialt adverse reactions
* EENT: abnormal vision * GI: nausea, anorexia * NEURO: dizziness, confusion, headache, hypertonia, ataxia, somnolence, unsteadiness, memory impairment most severe are hallucinations, suicidal idation, new/worsening depression ans seizures
49
Tapentadol
similar to tramadol similar to oxycodone inits ability to relieve severe pain, but very inexpensive
50
NSAIDs
several available with similar pain alleviating effects and adverse reaction profiles
51
NSAID mechanism of action
* inhibit COX, resulting in decresed formation of prostaglandin precursors (PGE2, prostacyclin, and thromboxane) and an inhibition of phospholipids * may also inhibit lipoxygenase * extent of inhibition varies with each chemicla category * produces vasodilation by acting on the heat-regulation center of the hypothalamus
52
Clinical uses of NSAIDs
pain relief reduce inflammation reduce fever
53
NSAID contraindications
active peptic ulcers chronic inflammation of the GI tract GI bleeding history of ulceration history of sensitivity to ASA or other NSAIDs
54
NSAID pharmacokinetics
* Absorption: rapidly from GI tract * Distribution: 90% via protein binding * Metabolism: in liver to water soluble metabolite * Excretion: urine * Half-life: most are 2-4 hours
55
NSAID adverse reactions
* CV: edema * DERM: itiching, rash * ENDO: fluid retention * GI: abdominal pain. cramps, heartburn, constipation, gas, decreased appetite * NEURO: dizziness, headache, nervousness
56
NSAID interactions
inhibits alpha blockers, ACE inhibitors, ARBs, beta blockers, and diuretics decreased platelet aggregation with anticoagulants decreased clearance with aminoglycosides GI bleed with corticosteroids
57
NSAID conscientious considerations
watch for hypersensitivity reactions and renal impairment do not use in last trimester stop one week before elective surgery high doses do not increase effect
58
ASA properties
analgesic, antipyretic, anti-inflammatory, antiplatelet higher doses required for anti-inflammatory effect
59
ASA antiplatelet effect
significantly reduces risk of MI and CVA mearurable prolongation of bleeding time inhibitory platelt aggregation effect lasts up to 8 days
60
ASA mechanism of action
inhibits prostaglandin and thromboxane synthesis
61
salicylism
mild, chronic salicylate intoxication after repeated administration of high doses symptoms: headache, dizziness, tinnitus, hearing loss, mental disturbances, sweating, thirst, hyperventilation, n/v, occasional diarrhea IMMEDIATE treatment required
62
treatment of salicylism
gastric lavage activated charcoal to absorb drug left in stomach
63
ASA and Reye's syndrome
association exists in children no ASA under 16yo
64
acetominophen mechanism of action
exact site and mechanism not known possibly inhibits nitric oxide pathway mediated by multiple neurotransmitter receptors, most notable substance P and NMDA blocks production and release of PGEs into CNS and blocks their effects in the heat-regulating areas of the anterior hypothalamus
65
clinical uses of acetominophen
analgesic, antipyretic, mild arthritis, analgesic in those taking anticoagulants or children (not associated with Reyes syndrome)
66
acetominophen contraindications
liver disease allergy
67
acetominophen conscientious considerations
risk for hepatotoxicity in malnourished and alcohol abusers any drug that increases action of liver enzymes may nullify effect safe in pregnancy and lactation
68

Pharmacology (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions