pain management Flashcards

1
Q

pain

A

-unpleasant sensory and emotional experience that normally serves to alert an individual to actual or potential tissue damage”
-Causes of tissue damage which results in pain
-Exposure to noxious chemical, mechanical or thermal stimuli -> Acids, Pressure, Extreme heat
-Pathological process -> Tumor, Muscle spasm, Inflammation, Nerve damage

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

classification of pain

A

-acute- obvious cause, reversible, high HR and HTN
-chronic- not always obvious, not reversible, depression, withdrawal
-relation to cancer

-Pathophysiology (Nociceptive, neuropathic, visceral):

-Nociceptive – pain due to stimulation of nerve fiber by noxious stimulus (chemical, thermal, mechanical and/or ischemic)

-somatic: well localized to specific dermal, subQ or musculoskeletal tissue. Described as dull/aching pain. Can treat with opioids and non opioids

-Visceral : originates in thoracic or abdominal structures, poorly localized and distant from source of pain. Described as deep, aching and cramping. Treat with opioids/non opioids

-Neuropathic pain – usually caused by nerve damage to CNS or PNS. (nerve compression, diabetic neuropathy, post herpetic neuralgia) Often described as burning or stabbing and may radiate down arms and legs. Treatment w/ all forms of analgesics – variable and unpredictable.

-Idiopathic pain – often due to psychological factors with no known cause or origin

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

general anesthetics

A

-inhalational or parenterally to cause the loss of consciousness and prevent awareness of pain during surgery

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

local anesthetics

A

applied topically or locally to the site where the pain will originate to prevent transmission of pain impulse to spinal cord

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

analgesics

A

-Opioid analgesics – work primarily in CNS to inhibit the neurotransmission of pain

-non-opioid analgesics: Work primarily in peripheral tissues to inhibit formation of pain impulses from nociceptive stimuli. Inhibitors of prostaglandin synthesis. Also exert antipyretic and anti-inflammatory properties

-Aspirin

-NSAIDS

-Acetaminophen:
-no anti-inflammatory properties
-relatively safe
-can cause liver toxicity with high doses, prolonged use or in alcoholics. Limit dose to 3-4 grams/day

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

opioids

A

-Opium – extracts of opium poppy. Morphine was isolated from opium in 19th century
-Opioid Receptors – members of G protein-coupled receptor family.
-Activation of receptor: inhibition of membrane depolarization

-Types of opioid receptors
-mu-1 and mu-2 – mediates most of effects of morphine and strong opioid agonists
-sigma
-delta
-epsilon
-kappa – mediates effects of mixed opioid agonist-antagonists -> limits addiction

-D. Endogenous opioid peptides
1. enkephalins – smaller peptides, release from neurons throughout entire pain axis
2. endorphins – larger peptides
3. dynorphins – larger peptides

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

types of opioids (Narcotics)

A

-1.Full agonists:
-strong agonists vs. moderate agonists
-can also be subdivided based on chemical structure class (useful to know in case patient has allergic-type reaction to one particular agent):
-Phenanthrenes; codeine, morphine, oxycodone, hydromorphone, levorphanol
-Phenylpiperidines: meperidine, fentanyl
-Diphenylheptanes: methadone, propoxyphene

-2. Mixed agonist antagonists
-3. Pure antagonists

-important bc if someone is allergic to codeine you can try fentanyl or methadone

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

effects of opioid agonists

A

-CNS effects
-Analgesia – alters perception of pain and pts reaction to pain!
-Dysphoria/euphoria – floating sensation, free from anxiety!
-Inhibition of cough reflex – used as antitussives! (codeine)
-Miosis (except meperidine causes mydriasis) “pinpoint pupils”!
-Physical dependence
-Respiratory Depression – dose-limiting factor! -> benzos are hard to OD on bc of this
-Sedation – causes drowsiness and impairs thinking!

-CVS effects
-decrease myocardial oxygen demand
-vasodilation & hypotension

-GI/biliary effects
-Constipation – !due to decreased motility and HCl secretion. Tx/prevent with laxatives and stool softeners!
-Increased biliary sphincter tone & pressure – gall stones!
-Nausea and vomiting !stimulates CTZ!

-Genitourinary effects
-Increased bladder sphincter tone
-Prolongation of labor
-Urinary retention

-Neuroendocrine system effects
-Inhibition of release of LH & FSH – !decrease ovarian and testicular fn!
-Stimulation of release of ADH and prolactin

-Immune system effects
-Suppression of function of natural killer cells

-Dermal effects
-Flushing
-Pruritis
-Urticaria (hives) or other rash

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

therapeutic uses of opioids

A

-analgesics
-acute myocardial infarction (for pain and anxiety)
-antitussives
-Tx of acute pulmonary edema
-antidiarrheals
-adjunct to anesthesia (given in combo with anticholinergic prior to surgery. Anticholinergic will decrease tracheal and bronchial secretions)

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

contraindications and precaution for opioids

A

-Contraindications for Opioid Use:
-Severe respiratory depression – can get respiratory failure!
-acute/severe asthma – b/c of respirator depression!
-increased ICP
-SR products if GI obstruction

-Precautions for Opioid Use::
-Avoid mixed agonist/antagonist in pts on full agonists !May precipitate withdrawal syndrome! -> limiting
-Head injuries
-Pregnancy (Chronic use during pregnancy may result in a dependent offspring)
-if underlying respiratory dysfunction, respiratory failure can occur
-Half-lives increased in patients with hepatic or renal dysfunction

-ADRs:
-Tolerance – usually after 2-3 weeks of nl therapy!!

-Physical dependence - after few weeks w/ withdrawal symptoms if drug abruptly d/c
-Psychologic dependence

-Constipation - !non pharm prevention!! Fluids and exercise!
-Prevention: Docusate + Senna or Bisacodyl PO
-can cause straining -> tear sutures -> observe in hospital
-Tx: MOM, Lactulose, Magnesium Citrate, Bisacodyl suppositories, phosphate soda enemas

-N/V – Can use metoclopramide, odensetron, prochlorperazine or trimethobenzamide short term.
-Respiratory depression – usually develop tolerance. With overdose -> pinpoint pupils -> Treat w/ naloxone (opioid antagonist)
-sedation, confusion, dizziness – usually with initiation or with dose increases. May last 2-3 days or until dose decreased -> tolerance should develop.
-Itching – occurs secondary to histamine release.
-hallucinations: rare

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

strong opioid agonists

A

-becomes cat D with prolonged use or high doses at term
-Used for mod - severe pain
-Dosing – no ceiling dose, no max dose
-Depending on agent being used - can be given PO, PR, SL, Buccal, IV, IM,SC, spinally (epidural and intrathecal) and transdermal.
-Controlled Substance category CII

-morphine
-methadone
-oxycodone
-fentanyl
-hydromorphone
-meperidine
-tapentadol

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

moderate opioid agonists

A

-Less potent than strong opioid agonists
-Do not produce max analgesia at doses that are well tolerated -> therefore given in submaximul doses for tx of mild-moderate pain and given in conjunction with non-opioid analgesic like aspirin or acetaminophen to enhance effects.
-Remember to monitor total dose of non-opioid analgesic as well. (i.e. APAP should be less than 3-4 grams/day)

-codeine
-codeine with APAP
-hydrocodone/APAP
-oxycodone/APAP
-oxycodone/ASA
-tramadol

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

morphine

A

-INJ (IV/IM/SC), PO, PR
-Principal alkaloid of opium poppy
-Kinetics – well absorbed PO, but -> significant first pass -> Need higher doses PO
-INJ:PO ratio is 1:6 or 1:3 w/ chronic use -> 6x higher dose for oral compared to INJ
-Indications – GOLD STANDARD -> DOC for cancer pain
-Also used for severe pain assoc w/ trauma and MI

-INJ (IV/IM/SC) – in several doses
-Epidural or intrathecal – must use preservative-free IV solutions (Duramorph) to prepare
-PO – (MS Contin, Kadian, Avinza) – long acting or sustained release
-PO – (MSIR) – immediate release, short acting, used PRN for breakthrough pain in combo with MS Contin around the clock
-PO solution immediate release – comes generic in various concentrations (10mg/5ml, 20mg/5ml or 20mg/ml) and brand name Roxanol (20mg/ml or 100mg/5ml). Caution when prescribing and administering
-Suppository immediate release – (RMS) 5mg, 10mg, 20mg, 30mg

-Dosing in cancer – use around the clock (ATC) w/ long acting form and PRN for breakthrough pain with immediate release
-PRN total daily dose should be half total daily dose of ATC regimen
-Ex. MS Contin 200mg Q 8 hrs (total dose 600mg/day) & Morphine Sulfate Immediate Release 60mg q 4h prn, MDD 5/day (300mg/day) -> 900mg a day

-Advantages: lots of dosage forms available, easy to titrate, generics available, easy conversion from IV to PO
-Disadvantage: M6 active metabolite – Can cause excessive sedation

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

methadone

A

-PO, INJ
-Low TI
-Used for pain but more for detox and maintenance tx of opiate dependence (heroin addiction)
-must closely monitor inventory and observe pt taking drug!
-use liquid form so pt can not cheek drug!
-never trust methadone pt telling you their dose -> give small amount and give rest of dose once confirmed

-Advantages:
-inexpensive, no active metabolite -> good in renal/hepatic dysfunction
-Use in morphine allergy

-Disadvantage:
-Difficult dosing/titration: Long half life for euphoric affect, but analgesic effect is 4-8 hours
-Titrate dose q5-7 days
-!!!Usually administered as q8h but can give extra dose for breakthrough pain -> usually ends up QID drug.
-Conversion more complex b/c cross tolerance is incomplete, will explain when go over charts!!!

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

oxycodone

A

-PO
-Available immediate release as tabs or oral solution. Also available as controlled/sustained release (Oxycontin).
-When given alone, considered strong agonist, when combined with APAP as in Percocet, can be used for mild-moderate pain although still CII controlled drug

-Advantages: no active metabolite !good in elderly or renal dysfunction!
-Disadvantages: no IV form

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

fentanyl

A

-INJ, transdermal patch, buccal-oral lozenge/lollipop
-Used for pain control and as adjunct to regional and general anesthesia!
-Oral Transmucosal Fentanyl Citrate (Actiq)- lollipop -> good if cant swallow
-Used for management of breakthrough cancer pain in pts with cancer who already have opioid therapy and are tolerant
-Advantage: Rapid onset. Good if can not swallow tabs. Can use if “morphine” allergy.
-Disadvantage: Expensive, short doa, accidental poisonings in kids

-Transdermal system:
-Good for chronic pain management
-Start w/ 25mcg/hr patch if no previous opiate use, otherwise use conversion chart
-Patch changed every 3 days -> Some patients require every 2 days!!
-conversion from morphine to transdermal fentanyl (Fentanyl dose in mcg/hr = ½ total daily dose of morphine PO)

-Advantages: Can use in morphine allergy. Less constipation than PO narcotics. Good if patients are NPO or if have severe stomatitis
-Disadvantages: Hard to titrate, Onset is 12 hours.

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

hydromorphone

A

-PO, PR, INJ
-very potent
-often used as PCA pump (pt controlled)
-advantages- less ADRs when used as epidural
-post op
-very well tolerate

-high addiction risk!

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

meperidine

A

-PO, INJ
-Not recommended for cancer pts b/c of short analgesic half-life of 3 hrs and irritates tissue -> can cause severe muscle fibrosis
-No long acting form available.
-Metabolite-Normeperidine has seizure activity and may cause neurological adverse effects
-!!!Can get grand mal seizures.
-!!!Metabolite has longer half life than parent compound -> stay in body longer than analgesic activity
-!!Metabolite excreted via kidney -> accumulates if renal dyfunction -!!!Hydroxyzine and promethazine may increase risk of neurological effects
-use within 14 days of MAOI (Tranylcypromine, Phenelzine, Isocarboxazid) -> life-threatening DDI like HTN crisis -> !!!(severe h/a, palpitations, n/v, sweating, choking sensation, increased temp, agitation, shivering, visual disturbances) !!!!
-Tachycardia or bradycardia and chest pain may occur
-Intracranial hemorrhage has also been reported

-NOT REALLY USED BC METABOLITES

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

tapentadol

A

-PO
-Unique MOA – mu receptor agonist and NE reuptake inhibitor
-Similar to tramadol but more potent and CII controlled substance. Used for moderate to severe pain
-Analgesic Potency similar to oxycodone, but with less GI ADRs
-Precautions: Similar to other opioids. Also - Seizures, Serotonin Syndrome

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

codeine

A

-PO, INJ
-C-II
-Better bioavailabilty than morphine
-!!Metab to morphine but has more ADRs. Used still b/c can call it in as verbal order w/ 6mo supply!!
-Good choice for anti-tussive

-Codeine w/ APAP (PO) (CIII or CV if liquid form)
-Tylenol #2 – 15mg codeine
-Tylenol #3 – 30mg codeine
-Tylenol #4 – 60mg codeine
(all have 300 or 325 mg APAP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

hydrocodone/APAP

A

-vicodin (C-III)
-not available alone!!
-good for moderate pain but not severe pain bc dose is limited by APAP content!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

oxycodone/APAP

A

-percocet (C-II)

23
Q

oxycodone/ASA

A

-percodan (C-II)

24
Q

tramadol

A

-PO (C)
-mild to moderate pain
-Manufacturer is aiming for the NSAID population
-has no anti-inflammatory activity.
-MOA – Mu agonist. NE and 5HT reuptake inhibitor
-not really a opioid but if you take enough it works

-!Abuse potential- avoid in pts with a tendency to opioid abuse or dependence. Cases of abuse, dependence and withdrawal upon d/c of drug have been reported!!!!

-Precations: Seizures !!Esp in pts with predisposition to seizures or if taking drugs which lower seizure threshold (MAO-Is, TCAs, psych drugs)!!!!
-Serotonin Syndrome
-no more than 3 days use

-structurally unrelated to opiates -> but is “atypical” opiate -> can cause anaphylactoid rxn in pts with hx of opiate allergy
-contraindicated in opiate allergy

25
Q

equianalgesic dose conversions

A

-30mg of oral morphine what is hydromorphone dose 3 of hydromorphone
-90mg of morphine -> need higher dose of methadone

-doesnt want us to memorize ? -> but will ask on the test ? -> chart given??

26
Q

miscellaneous opioid agonists: dextromethorphan

A

-(“DM” in cough & cold preparations)
-little analgesic activity
-significant antitussive activity
-cough syrup

27
Q

miscellaneous opioid agonists: diphenoxylate

A

-(with atropine = Lomotil) and Loperamide (Imodium) -> limiting
-Activate opioid receptors in GI smooth muscle
-used to treat diarrhea
-DO NOT USE IN INFECTIOUS DIARRHEA

28
Q

mixed agonist/antagonists and partial agonists

A

-Mixed agonists are Pentazocine, Butorphanol and Nalbuphine
-!!!Partial narcotic agonists include: Buprenorphine and Dezocine -> plain version is usually only for pregnant pts (females of reproductive age) bc you dont want them to go into withdrawal
-Buprenorphine w/ naloxone (Suboxone)- males or menopausal women

-Unlike opiates -> analgesic ceiling effect
-!!!Can precipitate withdrawal and loss of pain control if given to pts who have repeatedly received opiates!!!

-May produce psychomimetic rxns -> feelings of unreality, depersonalization, dysphoria, nightmares, vivid daydreams, hallucinations, delusions and panic.

-Indications – Parenteral forms for preop and post op analgesia and obstetric analgesia during L&D
-Oral forms for moderate to severe pain.
-Buprenorphine alone (Subutex) or in combo with naloxone (Suboxone) now used as alternative to methadone for heroin addiction

29
Q

opioid antagonists

A

-INJ
-Naloxone (Narcan) (INJ) and Naltrexone (PO, IM)
-competitive antagonists that rapidly reverse effects of morphine
-Used for tx of opioid OD and prevention and tx of opioid dependence and addiction
-Naltrexone also been used in tx of alcohol dependence

30
Q

patient controlled analgesia (PCA)

A

-IV administration where pt can self-administer preset amounts of analgesic via a syringe pump with timed device.
-May not be suitable in elderly or right after surgery b/c use of pump depends on pts ability to activate device
-Can be given with or w/o local anesthetics -> anesthetic allows for smaller doses of narcotic and less ADRS.
-Anesthetics -> lidocaine or bupivicaine
-May cause infection and urinary retention
-make sure pt can feel their legs! -> fall risk

-high pt satisfaction

31
Q

adjuvant drugs

A

-enhance analgesic efficacy of opiates, treat concurrent symptoms that exacerbate pain, and provide independent analgesia for specific types of pain.
-can be used in all stages of the step wise approach to pain mgt
-They do not replace opiates for pain mgt.

-antidepressants
-benzo
-corticosteroids
-anticonvulsants
-psychostimulants
-biphosphonates
-pimozide
-capsaicin cream
-ziconotide
-lidocaine patch
-clonidine
-muscle relaxants

32
Q

antidepressants

A

-TCAs: amitriptyline, imipramine
-Use (night) HS dosing – minimizes ADRs (dry mouth, blurred vision, etc)
-Also produces sedation

-SSRIs (fluoxetine)

-Dual reuptake inhibitors
-venlafaxine (Effexor)
-duloxetine (Cymbalta)

33
Q

benzodiazepines

A

may be useful to treat anxiety. Short acting is best, such as Lorazepam or Alprazolam.

34
Q

corticosteroids

A

-decrease inflammation and edema
-treating pain due to nerve compression and brain metastases and for bone pain.
-Prednisone and Dexamethasone are MC used.
-Taper doses due to risk of hypothalamic-pituitary-adrenal (HPA) axis suppression
-decrease inflammation and make the other meds work better

35
Q

anticonvulsants

A

(Carbamazepine, Phenytoin, Valproate Gabapentin, Pregabalin, etc) are utilized for treating neuropathic pain.

36
Q

psychostimulants

A

-include Dextroamphetamine (Dexadrine), Methylphenidate (Ritalin) and Pemoline (Cylert)
-may decrease sedation from narcotics and potentiate their analgesic effects.
-Low doses enhance pt’s sense of well-being and provide enough energy to increase food consumption.
-Avoid HS since it may produce insomnia

37
Q

biphosphonates, Calcitonin, Gallium Nitrate and Strontium-89

A

-effective adjuvants for treatment of BONE PAIN associated with malignancy.

38
Q

pimozide and mexiletine

A

-used for tx of neuropathic pain such as trigeminal neuralgia and diabetic neuropathy.
-Pimozide’s ADRs include acute dystonia and akathisias.

39
Q

capsaicin cream

A

-Activates peripheral nociceptors on primary sensory neurons
-Produces burning sensation initially then analgesic effect

-it is pepper / oil
-if you dont wash your hands -> it will go everywhere

40
Q

ziconotide

A

-Non-opiod analgesics: N-type CCB
-Recently received FDA-approval for management of severe chronic pain in pts who intrathecal (IT) therapy is warranted, and who are intolerant of or refractory to other tx, such as systemic analgesics, adjunctive therapies or IT morphine
-MOA: targets and blocks N-type calcium channels on nerves that ordinarily transmit pain signals.
-Warnings: Can cause severe psychotic symptoms and neurological impairment and meningitis

41
Q

lidocaine patch

A

-mostly used for allodynia (!painful hypersensitivity!) and postherpetic neuralgia
-Apply directly to painful area
-!May contain conducting metal so it should be removed prior to MRI!
-!Can cut patches!

42
Q

clonidine

A

epidural infusions

43
Q

muscle relaxants

A

-Centrally-acting agents; All agents have CNS depressive side effects

-Baclofen (Lioresal) - MOA - Inhibits transmission of synaptic reflexes at spinal cord level → relieves muscle spasticity
-Methocarbamol (Robaxin) -MOA – unclear, general central depressant effects
-!!Cyclobenzaprine (Flexeril) - MOA - Reduces tonic somatic motor activity influencing both alpha and gamma motor neurons. Chemical structure very similar to diazepam (Valium) -> best choice
-Carisoprodol (Soma) - MOA – unclear, general central depressant effects
-Metaxalone (Skelaxin) - MOA – unclear, general central depressant effects

44
Q

NSAIDS MOA

A

-Inhibit prostaglandin (PG) synthesis from arachidonic acid by inhibiting the enzyme cyclooxygenase (COX)
-NSAIDS are nonselective -> they affect both COX 1 and 2

-COX-1
-Always present (constitutive) in various tissues
-Involved in synthesis of cytoprotective PGs (in GI tract)
-Catalyzes the formation of TXA2 (platelet aggregation and hemostasis)

-COX-2
-Levels normally low, induced via inflammation
-NOT involved in synthesis of cytoprotective GI protaglandins -> COX2 inhibitor less likely to cause GI bleeds and PUD
-Catalyzes the formation of Prostacyclin (antithrombotic)

-May also inhibit B and T cell proliferation by mechanisms not involving COX and PG formation

45
Q

NSAIDS properties and indications

A

-Onset of action is faster for analgesia than anti-inflammatory
-DOA is shorter for analgesia than anti-inflammatory
-Dose is lower for analgesia& anti-pyresis than anti-inflammatory
-Vary greatly in potency and half-life.
-No one NSAID proven more effective than others
-Patient variability
-Categorized based on chemical structure – see chart

-Therapeutic Uses:
-mild to moderate pain
-fever
-arthritis & inflammatory diseases
-gout & hyperuricemia

46
Q

NSAIDS ADRs

A

-1. GI side effects
-GI upset, PUD, GI bleed: Increased incidence with Ketorolac (Toradol) - limit use to < 5 days -> Ibuprofen has lowest risk.
-Risk factors: high doses, increased age, males, hx of PUD, dyspepsia, CVD and concurrent use of antiplatelet drugs or steroids
-Strategies to minimize GI effects:
-Uses COX-2 inhibitor if possible
-Add GI protective agents like misoprostol or PPIs
-Minimize dose and duration of NSAID if possible
-Counsel pt on sx

-2. Cardiovascular effects:
-HTN and CHF secondary to increased Na and H20 retention
-Increased risk of MI and stroke secondary to altering the balance of TXA2 and Prostacyclin (COX-2 inhibitors block production of prostacyclin leading to a pro-thrombotic state)
-VIOXX & Bextra Withdrawal (COX-2 inhibitors) - Withdrawn due to cardiovascular ADRs.
-How does this impact patient care?
->Reevaluate the need for the COX 2 inhibitor (Celecoxib is still available)
->What is the patient’s GI risk? Consider adding PPI or misoprostol to NSAID regimen
->What is the patient’s Heart disease risk?
->Can consider meloxicam (Mobic) as alternative to COX-2 inhibitor

-3. Cinchonism- ringing in ears -> symptom of OD

-4. Renal effects
-Na and H2O retention
-Renal failure
-Hyperkalemia
-interstitial nephritis
-Tubular necrosis

-5. Hematologic
-inhibits platelet aggregation – causes bleeding. Counsel patient to monitor for signs and symptoms of bleeding

-6. Allergic Reactions – Bronchospasm – Can be severe/life threatening
-More common pts with asthma (0.6-4.5) -> Rare in pts w/o asthma (< 1%)
-Frequency increases with age, nasal polyps and female gender
-Reaction may be assoc with rhinorrhea, flushing of head and neck and conjunctivitis
-Cross sensitivity between ASA and NSAIDs -> Don’t forget ASA is an NSAID!!!

-7. CNS
-Psychosis (rare), cognitive dysfunction and depression in elderly

-8. Hepatic
-May increase LFT, rarely causing hepatic necrosis/failure

-9. Pregnancy
-Can retard uterine contractions, DO not use in 3rd trimester
-acetaminophen is pref

47
Q

NSAIDS DDI

A

-Antacids – may minimize GI effects but can decrease absorption -> we tell pts to take it anyways bc GI upset -> try PPI
-Aspirin – NSAIDs may block the antiplatelet benefit of ASA (wither by occupying COX-1 binding sites or if COX-2 inhibition dominates)
-Anticoagulants – increased risk of bleeding. Monitor INR
-DMARDs – increased risk of BMS
-Diuretics and other antihypertensives – antagonize antihypertensive effects secondary to Na and H20 retention

48
Q

acetaminophen

A

-PO, PR (APAP)
-Therapeutic category – analgesic, antipyretic

-Therapeutic indications:
-1. mild-moderate pain reliever:
-Headaches
-Myalgia
-Post-partum pain
-Osteoarthritis

-2. Antipyretic

-Pharmacology & Kinetics
-MOA – reduces central prostaglandin synthesis by an unknown mechanism. Produces analgesia and antipyretic effects – but has NO ANTI-INFLAMMATORY properties.

-Absorption: Oral administration, Peak effect is 30-60 minutes
-Distribution: Plasma protein binding – some
-Metabolism: Hepatic metabolism to primarily inactive metabolites, but can result in toxicity if metabolized to highly active metabolite
-Elimination: Less than 5% excreted unchanged, not affected by renal function
-Half-life: 2-3 hours, increased in liver disease or toxicity

-PO and IV absorb the same and do the same amount of effect but the difference is TIME

49
Q

acetaminophen ADRs and dosage! exam

A

-Generally well-tolerated

-Hepatic effects:
-Increase in LFTs
-Hepatic damage – n/v/d, abdominal pain
-Severe hepatotoxicity, liver failure

-Dosage:
-Adults: Usual dose is 325-500mg q4h-q6h PRN pain or fever. DO NOT exceed 3-4 g/day (MDD depends on dosage form and pt’s PMH)
-Children: 10-15 mg/kg/dose q4h-q6h PRN, MDD = 5 doses/day
-Be aware that APAP is available in many combination RX and OTC products

50
Q

tylenol toxicity

A

-One of MC drugs involved in suicide attempt and accidental poisonings
-How much is an overdose?
-Depends on patient
-100-200 mg/kg (kids) or 7 g (adult) is considered potentially toxic
-Mechanism of Tylenol Toxicity: image

-Initial symptoms are mild and nonspecific -> asymptomatic or GI upset

-24-36 hours after ingestion:
-Increased LFTs
-hypoprothrombinemia

-Severe cases: liver failure, hepatic encephalopathy, death

-Tx of Tylenol Toxicity
-Measurement of serum acetaminophen levels
-IF level > 150-200 mg/L after 4 hours – increase risk of liver injury
-Antidote: N-acetylcysteine (NAC) Dose: loading dose of 140 mg/kg followed by 70 mg/kg q4h for 17 doses

51
Q

approach to pain management

A

-Factors affecting the choice of treatment
-location, cause and severity of pain
-risk of producing drug dependence

-Pain assessment
-essential to adequately treat pain
-Various pain assessment tools/scales available

-Recommendations
-Opioid Prescribing Resources
-1. Treatment of Acute Pain (duration less than 1 month):
-Nonopioid therapies are at least as effective as opioids for many common types of acute pain.
-maximize use of nonpharmacologic and nonopioid pharmacologic therapies as appropriate for the specific condition and patient
-only consider opioid therapy for acute pain if benefits are anticipated to outweigh risks to the patient
-Before prescribing opioid therapy for acute pain, clinicians should discuss with patients the realistic benefits and known risks of opioid therapy.
-Risk of producing drug dependence is low
-Initial stages – give analgesics ATC to avoid wide swings in pain and sedation, then switch to PRN basis
-Can use PCA as well

-2. Sub-Acute & Chronic Pain
-Subacute Pain (duration between 1 to 3 months)
-Chronic pain (duration greater than 3 months):
-Nonopioid therapies are preferred for subacute and chronic pain.
-maximize use of nonpharmacologic and nonopioid pharmacologic therapies as appropriate for the specific condition and patient
-only consider initiating opioid therapy if expected benefits for pain and function are anticipated to outweigh risks to the patient
-Before starting opioid therapy for subacute or chronic pain, clinicians should !!discuss with patients the realistic benefits and known risks of opioid therapy!!, should work with patients to !establish treatment goals for pain and function!, and should consider how opioid therapy will be discontinued if benefits do not outweigh risks.
-Increased risk of opioid tolerance and dependence
-If associated with peripheral nerve or nerve root sensitization – use treatment with transcutaneous nerve stimulation (TENS) or local anesthetics

-3. Opioid Therapy when indicated
-Initiate with Immediate Release (IR) formulations
-Initiation in Opioid naïve (all types of pain)– use lowest dose possible
-Continuation in sub-acute & chronic
-use caution when prescribing opioids at any dosage

52
Q

tx of cancer pain

A

-usually requires administration of strong opioid agonist ATC with PRN breakthrough doses as well
-Non-opiates and adjuvants also utilized
-Patients should receive sufficient doses to control their pain, regardless of potential for dependence or tolerance

53
Q

acute vs chronic pain strat

A
54
Q

John Jones, a 50-year-old male, is about to be discharged from the hospital. He has stage IV lung cancer and was using Morphine 8 mg IM q4h ATC with Morphine 4 mg IM q2-4h PRN (MDD = 24mg/day). You want to convert him to Duragesic patch with Percocet PO for breakthrough pain.

A
  1. Calculate the dose for the Duragesic patch based on the total ATC dose of Morphine IM

-morphine 8mg x 6 = 48mg ATC x 3 = 150mg PO
-Fent mcg/hr = 1/2 total daily PO morphine dose
-150mg/2 = 75mcg/hr fentanyl patch

fentanyl 75mcg/hr # 10 - apply 1 patch every 3 days

  1. What dose of Percocet PRN would be most appropriate for this patient?

-4mg x 6 - 24mg prn morphine
-5mg morphine im / 10mg oxy PO= 24mg IM morphine / x mg oxy PO
-x= 48mg
oxy in 5mg /325 apap
48mg/5mg = 10 tabs/day
percecet 5mg/325mg take 1 to2 tabs every 4 to 6 hrs prn pain max daily dose = 10 tabs

  1. What information would you include in your “patient education?”

  1. Write the prescription for a one month supply of the Duragesic patch and the Percocet PRN