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Pharm > Pain Management Meds > Flashcards

Pain Management Meds Flashcards

1
Q

Pain meds

A

NON-OPIOIDS;
nonsteroidal anti-inflammatory drugs(NSAIDs)
Acteminophen
Antiepileptics, local anesthetics
OPIOIDS

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2
Q

NSAIDS

A

~ for mild to moderate pain, associated with inflammation, and temporary reduction of FEVER ( children)
~No evidence for management of neuropathic pain
~Some have other non-pain related indications ( aspirin is used for 2nd prevention of MI)
~ Remember: choice of agen depends on several factors; comorbidities, risk for bleeding
Recommendation Rx the lowest effective dose for each pt for the shortest pd.

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3
Q

COX-1

A
  1. constitutive “HOUSEKEEPING ENZYME” particularly in STOMACH
  2. Inducible activity (2-4X)
  3. Major product is thromboxane, induces platelet aggregation
  4. Inhibition of platelet COX-1 explains why aspirin effectively reduces cardiac events
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4
Q

COX-2

A
  1. Inducible enzyme in the INFLAMMATORY RESPONSE
  2. Inducible activity (10-20X)
  3. Kidney , lungs and inflammatory cells (macrophages)
  4. Both NSAIDs and GLUCOCORTICOIDS inhibit COX-2 gene expression; help reduce inflammation
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5
Q

NSAIDs MEDS (8)

A
  • acetylated salicylates (aspirin
  • non-acetylated salicylates (diflunisal),
  • propionic acids (ibuprofen, naproxen),
  • acetic acids (indomethacin, diclofenac),
  • anthranilic acids (meclofenamate, mefenamic acid),
  • enolic acids (meloxicam, piroxicam),
  • naphthylalanine (nabumetone), and
  • selective COX-2 inhibitors (celecoxib, etoricoxib).
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6
Q

NSAIDs MOA

A

Primary: inhibition of cyclooxygenase enzyme -> inhibiting prostaglandin synthesis
most inhibit both COX isoforms with little selectivity
Higher affinity to one or another (apirin, & coxibs) will exert anti-inflammatory, analgesic, and antipyretic effects at different degrees.
Low doses of aspirin= antiplatelet effect
High doses = analgesic effects

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7
Q

NSAIDS ADRs

A

-GI : Nausea, anorexia, dyspepsia, abdominal pain, ulcers, gastrointestinal hemorrhage, perforation, constipation, diarrhea **
-Cardiovascular: Hypertension, decreased effectiveness of anti- hypertensive medications, myocardial infarction, stroke, and thromboembolic events (last three with selective COX-2 inhibitors); inhibit platelet activation, propensity for bruising, and hemorrhage.
-Renal: Salt and water retention, deterioration of kidney function, edema, decreased effectiveness of diuretic medications, decreased urate excretion, hyperkalemia, analgesic nephropathy **
-CNS: Headache, dizziness, vertigo, confusion, depression, lowering of seizure threshold, hyperventilation (salicylates)
-Hypersensitivity: Vasomotor rhinitis, asthma, urticaria, flushing, hypotension, shock.
-Hepatotoxicity**

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8
Q

NSAIDs CI

A
  • HYPERSENSITIVITY is only major CI for NSAID use*
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9
Q

NSAIDS conditions demand AVOIDANCE, temporary SUSPENSION, or CAUTION

A

age >50 y.o
family hx of GI bleed/disorders
uncontrolled HTN
Renal disease
IBS, IBD
coronary artery & gastric bypass surgery
PREGNANCY => placental abruption
Stroke, TIA, MI ; excluding apirin

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10
Q

NSAIDS drug interaction with ACE inbitiors

A

severity: MODERATE
ADR: may decrease antihypertensive & natriuretic effects
Recommendation: monitor BP & cardiovascular function

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11
Q

NSAID drug interaction w/ LITHIUM

A

Severity: MODERATE
ADR: may increase Li plasma levels & decrease its clearance renally
Recommend: Monitor for lithium toxicity

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12
Q

NSAID drug interaction w/ WARFARIN

A

Severity: MODERATE
ADR: may result in increase risk of bleeding
Recommend: MOnitor PT & INR

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13
Q

NSAIDs drug interaction w/ METHOTREXATE

A

Severity: SEVERE
ADR: may result in increase risk of methotrexate toxicity
Recommend: DONT administer NSAIDS within 10 days of hihg dose methotrexate

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14
Q

NSAIDS nursing assessments

A

MONITOR:
NO need for routine monitoring of acute administration in healthy pts
*use chronically and pts at risk for toxicity should have evaluation including CBC, renal, & hepatic function test as a minimum
Most OD case are asymptomatic or develop insignificatnt self limiting GI symptoms
SERIOUS COMPLICATIONS: confusion, HA, nystagmus, drowsiness, blurred vision, diplopia, tinnitus, convulsion, matabolic acidosis, acute renal or liver failure, GI bleed, & coma

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15
Q

Acetaminophen (Tylenol)

A

~mild to moderate pain, moderate to severe pain, temporary reduction of FEVER
~ shouldnt be used for neuropathic pain there is no documented effect
~ Dose for ADULTS 650mg to 1000 mg Q4-6H, max of 4g/day*
Children dose 15mg/kg Q6H, up to 60mg/kg/day
~Administered PO, Rectally, IV

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16
Q

Acetaminophen MOA

A

Unclear to date, lacks anti-inflammatory properties & does not bind to the active site of either COX enzymes
HYPOTHESIS: inhibits a different variant of COX-1 AKA COX-3, remains uncomfirmed in human studies
~Diminished activity of the COX pathway leads to decreased prostaglandin synthesis in the central nervous system, thus inducing analgesia (serotonergic inhibitory pathways) and antipyresis (hypothalamic heat-regulating center)

17
Q

Acetaminophen ADRs

A

Depends on route of administration
IV: Nausea, vomiting, pruritus, constipation, and abdominal pain.
Oral or rectal: acetaminophen may cause any of the following:
Rash or hypersensitivity reactions (toxic epidermal necrolysis, acute generalized exanthematous pustulosis, and SJS)
Hematological: anemia, leukopenia, neutropenia, pancytopenia
**Nephrotoxicity **
Metabolic and electrolyte disorders: Decreased serum bicarbonate, Hyponatremia, Hypocalcemia, Hyperammonemia, Hyperchloremia, Hyperuricemia, Hyperglycemia, Hyperbilirubinemia, Elevated alkaline phosphatase

18
Q

Acetaminophen Considerations

A

Hypersensitivity to acetaminophen or any of its excipients, **severe hepatic impairment, or severe active hepatic disease. **
Pregnancy is not a contraindication for acetaminophen administration.

19
Q

Acetaminophen Toxicity

A

develops at 7.5 g/day to 10g/day or 140mg/kg
* large amounts may cause severe liverdamage leading to liver
* Poisoning more frequent in children
* Adults present w/ more serious & fatal presentations
* serum levels must be drawn 4-24hrs since estimated time of ingestation to determine treatment modality
* Toxicity tool used is Rumack-Matthew Nomogram
* level greater than 140 mcg/ml at 4hrs from ingestation requires treatment w/ N-acetyl-cysteine (NAC)
* Activated charcoal avidly binds to acetaminophen & may be used w/in 1st hrs DONT administer to pts w/ increase risk of airway obstruction.

20
Q

Neuropathic Med

(4)

A

Known for analgesic properties through MOA of lowering neurotransmitter release or neuronal firing.
* Gabapentin
* Pregabalin
* Oxcarbazepine
* Carbamazepine

21
Q

Gabapentin treats…

A

Postherpetic neuralgia in adults & neuropathic pain

22
Q

Pregabalin treats

A

neuropathic pain associated w/ diabetic peripheral neuropathy or spinal cord injury, postherpetic neuralgia and fibromyalgia.

23
Q

Oxcarbazepine & Carbamazepine treats

A

trigeminal or glossopharyngeal neuralgia

24
Q

Gabapentin & Pregabalin

MOA

A

Both are ligands to the αδ subunit of the voltage-dependent calcium channels, which overexpress in patients with neuropathic pain.
Reducing this calcium dependent release of excitatory neurotransmitters => decreases neuronal excitability.

25
Q

Gabapentin & Pregabalin

ADRs

A

Gabapentin: The most common side effects are dizziness, somnolence, ataxia, peripheral edema, and confusion. Among other, more serious adverse effects are anaphylaxis, suicidality, depression, fever, infection, steven-Johnson syndrome, angioedema, erythema multiforme, and rhabdomyolysis.
Pregabalin: Dizziness, somnolence, headache, peripheral edema, nausea, weight gain, disorientation, blurred vision, increased risk of suicidal thoughts

26
Q

Gabapentin & Pregabalin

Considerations

A

Hypersensitivity
dose adjustment for pts with compromised RENAL FUNCTION
Evaluate baseline creatinine levels before and during the treatment for patients under treatment for either gabapentin or pregabalin.
Screen for depression, behavioral changes, and suicidality
Gabapentin: Gabapentin does not carry the risk of overdose or addiction as other pain management medications (eg., opioids). However, gabapentin may increase a euphoric state caused by opioids.
Pregabalin: The highest documented accidental overdose occurred during clinical research and was 8000 mg.
No specific antidote.

27
Q

Local Anesthesia

what does it do, administered & used

A
  • Effectively reduce or eliminate sensation
  • Can be administered topically, by local injection, or intrathecal infusion (e.g. epidural)
  • effective in treating acute pain(e.g., labor pain, post-surgical pain, trauma)
  • can be used to manage chronic pain(most often in combination with an opioid or NSAID)
  • intraoperative anesthesia (topical or epidural) (dental, ophthalmic, podiatry, abdominal, etc)
  • aid in minor procedures (topical) (blood draws, etc)
28
Q

2 types of anesthesia

A

Esters & Amides

29
Q

Esters

(5) (have _ i)

A

(ONE i) -degraded by plasma esterases
* benzocaine
* procaine
* tetracaine
* novacaine
* cocaine

29
Q

Amides

(7) (have _ i)

A

(TWO i’s) - degraded by hepatic enzymes
* Lidocaine, procaine
* bupivacaine
* mepivacaine
* ropivacaine
* dibucaine, lidocaine

29
Q

Lidocaine MED

MOA, Presentations, ADR, CI

A
  • Lidocaine is among the most commonly used* FDA approved for postherpetic neuralgia and recommended for peripheral neuropathic pain
  • MOA : Lidocaine stabilizes the neuronal membrane by inhibiting sodium ion channels on the internal surface of nerve cell membranes.
  • Thus, pain conduction through nerve impulses becomes impaired at the site of action, which contributes to the absence of systemic effects
  • Presentations include skin patches, topical solutions, creams, gels, ointment, and lotions.
  • Adverse effects: Application-site pain, pruritus, erythema, and skin irritation
  • Contraindications: History of sensitivity. Application of lidocaine patches should only be to intact skin
30
Q

Lidocaine nursing education

A

Narrow therapeutic index
Patients with severe hepatic impairment, under prolonged infusions, or with broken or inflamed skin should be monitored for increased plasma levels.
Lidocaine toxicity usually presents at lidocaine blood concentrations above 5 mcg/mL.
* Symptoms progress from slurred speech, tinnitus, paresthesias, and dizziness to loss of consciousness, seizures, cardiac arrhythmias, and cardiorespiratory arrest.
* Management is supportive (oxygen, IV fluids, and inotropes)
* If with refractory cardiovascular collapse, intravenous lipid emulsion is indicated

30
Q

Opiates

what are they, used for, Rx, administrations

A

Most effective and widely used drugs in **treating severe pain. **
Have potential for **addiction, tolerance, and side effects. **
CDC guidelines recommends that only if the expected benefits for both pain and function outweigh the risks
Clinicians should prescribe opioids at the **lowest effective dose and for the shortest expected duration **to treat the pain severe enough to require opioids
Dosage forms to use for several routes of administration: oral, transdermal, intramuscular, intravenous, subcutaneous infusion, rectal, epidural, intrathecal, intranasal, and transmucosa

31
Q

Opiotes

MOA

A

act on G protein-coupled receptors (3): kappa, delta, & sigma
Mojority act primarly at “mu receptors” & are considered **“mu agonist” **
depending on receptor activated different physiologic effects occur
exert effects on both presynaptic & postsynaptic neurons

32
Q

Presynaptically opioids

moa

A

block calcium channels on nociceptive afferent nerves, thus inhibiting the release of neurotransmitters such as substance P and glutamate.

33
Q

Postsynaptically opioids

moa

A

enhance the activity of potassium channels, thus hyperpolarizing cell membranes and increasing the required action potential to generate nociceptive neurotransmission.

34
Q

Opioids ADRs

9

A
  1. sedation – drowsiness, and impaired cognitive function
  2. constipation – activation of mu-opioid receptors in gut; basis
  3. respiratory suppression – primary cause of death
    • results from a desensitization of
      medullary respiratory center to CO2 (i.e., a larger rise in CO2 is needed to stimulate respiration); truncal rigidity (increased tone of core muscles) also contributes to reductions in respiration
  5. euphoria – mu-opioid effect; contributes to abuse-liability
  6. dysphoria – k-opioid effect
  7. nausea / vomiting – activation of chemoreceptor trigger zone
  8. physical dependence – develops with
    chronic use; contributes
  9. to continued use/abuse
35
Q
A

Pharm (8 decks)

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