Chapter 24: Pain Flashcards Preview

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Flashcards in Chapter 24: Pain Deck (68):
1

 

 

Major contributors to the onset of pain

 

 

arthritis, back pain, cancer, headache

2

 

 

most common prescription meds used for pain relief

 

 

NSAIDs

3

 

 

Acute pain

 

 

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

duration is short

resolves with healing

4

 

 

chronic pain

 

 

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

5

 

 

removing barriers that render pain management ineffective

 

 

stigma attached to certain medications like morphine

patient prefernce on strength

provider concerns about DEA reprisal

6

 

 

consequences of poorly managed pain

 

impaired function and quality of life

depression

polypharmacy from treated manifestations of pain (agitation, etc)

uncontrolled acute pain leading to chronic pain

7

 

 

properly assess pain before prescribing any drug

 

 

detailed history and physical

idetify the source of the pain

discuss realistic goals

re-examine and adjust therapy as needed

8

 

 

remeber the goal of using medications to manage acute pain

 

restore function as soon as possible

prevent the development of chronic pain syndrome

9

 

 

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

 

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

10

 

 

use different algorythm when prescribing for chronic pain

 

usually requires adjunctive use of other medications for neuropathic component

comes about through hyperstimulation of NMDA receptors

11

 

 

remeber there is a role for adjunctive medications

 

 

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

12

 

 

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

 

 

opioid and nonopioid

13

 

 

opiates

 

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

14

 

 

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

 

 

Mu1 and Mu2

15

 

 

conscientious prescribing of opiates

 

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

16

 

 

treatment of myoclonus reltaed to pain medication

 

 

change opioid or treat with lorazepam

17

 

 

typica dose of Narcan for overdose

 

 

0.2-0.8mg IV

up to 2mg is often given

18

 

 

prototype agent for antagonist agonist opiate analgesics

 

 

Morphine

19

 

 

morphine mechanism of action

 

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

20

 

 

antagonist agonist opiate analgesic (morphine)

pharmacokinetics

  • 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

21

 

 

opiate adverse reactions

  • 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

22

 

 

opiate interactions

 

anything that causes respiratory depression

medications that prolong QT interval if using methadone or buprenorphine

23

 

 

mixed/partial agonist-antagonist analgesics

4 available agents

 

buprenorphine (Buprenex, Subutex)

pantazocine (Talwin)

nalbuphine (Nubain)

butorphanol (Stadol)

can precipitate withdrawal symptoms in patients taking chronic opiates

24

 

 

clinical use of buprenorphine

 

 

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

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