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Orthopedics and Rheumatology > Pain Management > Flashcards

Pain Management Flashcards

1
Q

Pathophysiology of Pain Transmission

A

Pain transmission starts at nociceptors, which are stimulated by leukotrienes, prostaglandins, and histamine

Nerve fibers of the spinal cord initiate pain sensation by exciting pain transmission neurons.

Pain is modulated by nerve fibers in the spinal cord that inhibit spread of action potentials caused by nociceptors. Also modulated by the brain by the endogenous opiate system made up of 3 kinds of endogenous endorphins: enkephalins, dynorphins, and beta-endorphins.

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2
Q

Types of Pain

  • Nociceptive
  • Inflammatory
  • Neuropathic
  • Functional
A

Nociceptive

  • Transient pain in response to noxious stimulus at nociceptors that are located in cutaneous tissue, bone, muscle, connective tissue, vessels and viscera
  • prevents further tissue damage due to autonomic withdrawal reflex

Inflammatory
- Contributes to pain hypersensitivity to prevent contact or movement of injured part until healing is complete, thus reducing further damage

Neuropathic
- Spontaneous pain and hypersensitivity associated with damage to PNS

Functional
- Pain hypersensitivity due to an abnormal processing or functioning of the CNS

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3
Q

Classification of Pain

acute 
chronic 
chronic malignant 
chronic nonmalignant
neuropathic
A

Acute
- occurs as result of injury or surgery and is usually self-limited, subsiding when injury heals

Chronic
- persists beyond the time of the expected healing and serves no useful physiologic purpose

Chronic Malignant
- associated with progressive disease that is usually life threatening (i.e. CA)

Chronic Nonmalignant
- not associated with life threatening disease and lasting more than 6 months beyond the healing period

Neuropathic
- a type of chronic nonmalignant pain involving disease of the central and peripheral nervous systems

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4
Q

Incorrect assumptions/attitudes/pain assessment that lead to the undertreatment of pain

A

There is a correct amount of pain for a given injury

People become easily addicted to narcotics (Truth: people are more likely to become addicted when they are inadequately tx’d)

Pain is necessary and builds character or using analgesics builds character

Inadequate assessment fosters undertreatment because prn dosing is based on pts report of need for analgesics

Pain is difficult to evaluate in young children and elderly with dementia

Limited information on pain management in medical training

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5
Q

Predictors of Inadequate Pain Management

A

Age
Non-Caucasian
Low cognitive performance
Multiple other medications

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6
Q

Principles of Effective Pain Assessment

A

Measure pain using self report +/- behavioral observation tools
- interpret behaviors cautiously (people in chronic pain will have fewer behavioral/physiologic changes)

Use physiologic measures only as adjuncts to self report and behavioral observation

Tailor assessment to developmental level and situation

Pain is 5th vital sign

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7
Q

Principles of Effective Pain Management (4)

A

Assess pain intensity and relief at regular intervals

Respect pt preferences (not necessarily drug seeking)

Evaluate effectiveness of pain management and medication side effects and adjust as needed

Suspect pain – pt may not be able to report

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8
Q

Nonpharm Therapy

Psychological interventions and PT

A

Psychological Interventions

  • Acute: controlled mental imagery, controlled attention or distraction
  • Chronic: relaxation training, biofeedback, cognitive behavioral therapy, psychotherapy, support groups, spiritual counseling

Physical therapy
- US therapy, TENS, massage, therapeutic exercises, heat, cold

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9
Q

Steps for treating acute pain

A

Step 1:

  • mild pain (1-3/10)
  • +non-opioid +/- adjuvants

Step 2:

  • moderate pain (4-6/10)
  • weak opioid + non-opioid +/- adjuvants

Step 3:

  • severe pain 7-10/10
  • strong opioid + non-opioid +/- adjuvents
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10
Q

Acetaminophen

Indication
MOA
Usual/Max Dose
AE (6)

A

Indication

  • tx mild-moderate pain
  • analgesic effect = ASA

MOA
- inhibits pg synthesis in CNS and peripherally blocks pain impulse generation

Usual dose 325-650 mg q4-6hrs
Max dose 4000 mg/day

AE

  • usually well tolerated
  • hepatotoxicity
  • analgesic nephropathy
  • anemia
  • blood dyscrasias
  • rare skin rxns (SJS/TEN)
  • OD ==> serious/fatal hepatotoxicity

Hepatotoxicity Mechanism

  • small amount of APAP is metabolized by CYP450 into NPAQI, a hepatotoxic metabolite
  • NPAQI is usually bound by glutathione and excreted, but OD/misuse leads depletes glutathione
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11
Q

NSAID Efficacy

A

Most nonselective NSAIDs are more effective than full dose ASA or APA

Some have greater than or equal to analgesic effect of oral opioid combos

Some pts respond better to one NSAID than another

Celecoxib is less effective than ibuprofen or naproxen

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12
Q

NSAID Adverse Effects

Broad Categories

A 
GI
Renal
Hematologic 
Cardiovascular
Hepatotoxicity - rare
CNS - high doses can cause sedation and dec'd cognition in older adults 
Derm - rare SJS or TEN
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13
Q

NSAID GI Side Effects

MOI
High Risk Patients
Spectrum of GI toxicity

A

MOI

  • direct irritation of gastric epithelium
  • systemic inhibition of endogenous GI mucosal PG synthesis

High Risk Patients

  • > 60 y.o.
  • Prior PUD or UGI bleed
  • High dose or more toxic NSAIDs
  • concurrent corticosteroid, bisphosphonate, or SSRI use
  • Anticoagulant use or coagulopathy
  • Antiplatelet use (e.g ASA or clopidogrel)
  • Chronic illness

Spectrum of GI toxicity
ibuprofen < naproxen < ketorolac

Diclofenac/Misoprostol available to prevent PUD

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14
Q

NSAIDs and Nephrotoxicity

MOI
RFs

A

MOI

  • NSAIDs decrease renal blood flow
  • more pronounced in pts with pre-existing kidney disease

Risk factors

  • older age
  • HF
  • renal insufficiency
  • ascites
  • volume depletion
  • diuretic therapy
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15
Q

NSAIDs and Hematologic Toxicity

A

MOI
- may prolong bleeding times due to anti-platelet affects

ASA inhibits platelet aggregation for lifetime of platelets (7-10 days)

Other N-NSAIDs affect platelet aggregation to a lesser degree and only when drug is on board

These do not affect INR, but do increase bleeding risk when used with anticoagulants

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16
Q

NSAIDs and Cardiovascular Toxicity

A

May increase CV risk (depends on type)

Risk is greater with higher doses, prolonged duration, and greater COX-2 selectivity

Selective inhibition of COX-2 may decrease endothelial production of prostacyclin, leaving platelet thromboxane A2 mediated by COX-1 relatively unopposed, which may increase vasoconstriction, platelet aggregation, and thrombosis

Highest CV with celecoxib; naproxen is lowest

All NSAIDs can inhibit ASA’s antiplatelet effect

  • *NSAIDs also inc BP b/c decreased renal perfusion
  • *Avoid NSAIDs after MI indefinitely
17
Q

Acetylated Salicylates

Representative drug
Indication
MOA
AE

A

Aspirin

Indication

  • mild-moderate pain
  • prevention of MI, CVA

MOA
- same as N-NSAID

AE

  • platelet inhibit for life of platelet
  • ASA sensitivity (asthma, bronchospasm, urticaria) related to COX-1 inhibition–> inc leukotriene production –> inc histamine release
  • Do not use in pts with angioedema and bronchospasm with ASA
  • Reye’s Syndrome (don’t use in <19 y.o. esp with flu/mono)
18
Q

Nonacetylated Salicylates

A

Salsalate, Trisalicylate

AE:

  • less GI toxicity than N-SAIDs
  • no antiplatelet effects
  • otherwise same as N-NSAIDs
  • occassional cross-reactivity with ASA sensitive pts
  • Reye’s syndrome
19
Q

Opioid MOA and AE

A

MOA: stimluates opioid receptors (mu, kappa, and delta) in the CNS

Most common:

  • somnolence–>drowsiness
  • stimulation of CTZ–>N/V
  • decreased GI motility–>constipation (docusate)
  • histamine release –> pruritis

Most severe
- respiratory depression

20
Q

Opioid Withdrawal Symptoms

A

Minor

  • rhinorrhea
  • lacrimination
  • excessive yawning
  • mild irritability or restlessness
  • mild N/V

Major

  • increasing restlessness or irritability
  • tremors
  • abdominal cramps
  • anxiety
  • persistent N/V
  • increased HR, BP, hot or cold flashes, fever
21
Q

Opioids and Receptor Activity

A

Agonists
- best analgesic effect by binding mu receptor

Partial agonists
- submaximal response at the receptor even at high doses

Agonists/antagonists

  • mu agonist, kappa antagonist
  • lower abuse potential, ceiling effect on respiratory depression
  • only used in certain populations

Antagonists
- reverse or inhibit the effect of agonists by preventing receptor access

22
Q

Opioids for Moderate Pain (6)

A

Codeine/APAP
- gastritis frequent; metabolized to morphine
Hydrocodone/APAP
- also antitussive; less gastritis than codeine
Oxycodone/APAP
- less hallucinations than morphine; CYP3A4 substrate–>black box warning

Others:

  • Meperidine (Dermerol)
  • Tramadol (efficacy = codeine/APAP)
  • Trapentadol
23
Q

Opioids for Severe Pain (5)

A 
Morphine 
 - gold standard
Hydromorphone 
 - high potency, terminal pain syndromes
Oxymorphone

Others:

  • Fentanyl
  • Methadone (only use if know how to dose)
24
Q

Mixed mu Agonists/Antagonistsm (2)

A

Butorphanol
- 2nd line for mod-severe pain
Nalbuphine
- 2nd line for mod-severe pain, but IV/IM only

25
Q

Mu Antagonist (1)

A

Naloxone

- reversal of respiratory depression; overdose

26
Q

Pseudoallergy

True Allergy

A

Pseudoallergy

  • flushing, itching, sweating, mild hypotension
  • give nonopioid instead
  • avoid codeine, morphine (strongly associated)
  • more potent opioid that are less likely to release histamine
  • if necessary give diphenhydramine

True Allergy

  • give nonopioid
  • opioid from different class
27
Q

Adjuvant Analgesics

A

Caffeine
- may enhance APA, ASA, ibuprofen

Hydroxyzine
- may add to effect of opioids in postop and CA pain while reducing N/V

Corticosteroids
- can produce analgesia in pts with inflammatory disease or tumor infiltration of nerves

28
Q

Signs and Sxs of Persistent Pain (3)

A

Big three: depression, anxiety, sleep disturbance

Also:
	Frustration 
	Anger
	dec self-esteem
	dec involvement in social activities
	Financial stresses and concerns
	dec libido
	Work issues
	Inactivity 
	Altered family dynamics
	Frequent use of meds
	Legal issues 
	inc number of health care visits
29
Q

Treatment Goals for Persistent Pain (6)

A

Inc tolerance for physical activity
Dec suffering and pain
Dec reliance on the health care system
Dec reliance on medications
Return to work or other functional role in society
Develop appropriate strategies for self-management

30
Q

General Strategies for Txing Persistent Pain

A

 Simultaneously address the various components of the problem
 Taper use of inappropriate meds while initiating appropriate therapy
 Provide education about chronic pain; correct any misconceptions
 Focus on inc function and physical activity
 Establish a time frame for achieving specific goals
 Remind your patient and yourself that chronic pain is not the same as acute pain
 Emphasize the multifactorial nature of chronic pain and avoid the distinction between physical and psychological causes

31
Q

Nonpharm for persistent pain (3)

A

TENS
Biofeedback
PT

32
Q

Pharm for persistent pain (4)

general

A

Nonopioids
Tramadol
Opioids
Adjuvant Analgesics

33
Q

Adjuvant Analgesics

TCAs
AEDs
SNRI
Local anesthetic

A

TCAs

  • amitriptyline
  • inhibit NE & 5-HT reuptake
  • onset: weeks
  • SE: sedation

AEDs

  • dec synaptic transmission
  • Gabapentin, Carbamazepine, valproic acid

SNRI

  • potent inhibit of NE and 5-HT reuptake
  • duloxetine (cymbalta)
  • tx: diabetic neuropathy, chronic m/s pain

Local anesthetic

  • lidocaine patch
  • 12h on, 12h off
  • good bridging option
34
Q

Pharm Mngmt of Chronic Noncancer Pain

Chronic low back pain
Fibromyalgia
Neuropathic Pain

A

Chronic low back pain
- Acetaminophen first; tramadol or opioids in selected patients; AEDs or TCAs if neuropathic symptoms (evidence weak)

Fibromyalgia
- Acetaminophen considered 1st (evidence weak); TCAs, AEDs, SNRIs (stronger evidence); tramadol better alternative than opioids; NSAIDs only with other agents

Neuropathic Pain
- TCAs, SNRIs, AEDs, 5% lidocaine patch considered 1st line, tramadol and opioids considered 2nd-line agents; capsaicins considered 3rd line

35
Q

Guidelines for an Adequate Drug Trial

A

 Discuss “trial and error” method with patient
 Titrate only one drug at a time
 Start at the low end of the dosing range and increase periodically (q3-7 days)
 Increase dose if pain relief is inadequate, side effects are tolerable, and blood level is below toxic range
 Weekly or biweekly communication with patient is needed to assure optimized trial and efficient titration
 Continue titration until patient is satisfied with pain control or side effects are intolerable

Orthopedics and Rheumatology (8 decks)

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