Module 9.1 - Pain Flashcards

1
Q

What is acute pain?

A
  • Duration is short- usually < 6 months
  • Treatment is definitive due to clear source of injury (i.e. surgery)
  • Generally resolves on its own as healing process occurs
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2
Q

What is chronic pain?

A
  • Usually > 6 months duration,
  • Rarely resolves on its own
  • Examples: RA, OA, post-herpetic neuralgia, diabetic neuropathy, back pain
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3
Q

What is somatic pain?

A

Pain that arises from bone, muscle, joint, skin, connective tissue; tends to be throbbing or aching in nature and well-localized

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4
Q

What is visceral pain?

A

Pain that arises from the visceral organs, i.e. GI tract, pancreas or liver; tumor involvement or pain in hollow organ; may be vague and often dull in nature.

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5
Q

What is neuropathic pain?

A
  • Results from abnormal processing by the peripheral and central nervous systems; can be from disease (such as DM) affecting the somatosensory system
  • Characterized by unusual burning, tingling sensations, electric shock-like quality to pain and may be triggered by a very light touch
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6
Q

What are the 2 types of neuropathic pain?

A
  1. Centrally generated pain: involving the dysregulation of the peripheral, central or autonomic nervous system (phantom limb pain, burning pain below spinal cord lesion)
  2. Peripherally generated pain: involving pain along the distribution of nerves, or an injury to the peripheral nerves (diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia or nerve entrapment)
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7
Q

What are some adverse physiologic and psychological consequences associated with acute pain?

A
  • Reduced tidal volume
  • Excessive stress response
  • Progression to chronic pain
  • Inability to comply with rehabilitation
  • Patient suffering and dissatisfaction
  • Acute pain is more difficult to manage if permitted to become severe in nature
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8
Q

What are the treatment goals for chronic pain?

A
  • Chronic pain is often debilitating and associated with significant physical, emotional and social issues.
  • Treatment should address social and psychological consequences of pain as well as any physical pathology
  • Assessment should include the patient’s acceptance of their condition, their motivation to participate in treatment and the ability to follow-through with recommendations; as well as, available time and resources

Main goals:

  1. Diminished suffering including pain and associated emotional distress
  2. Restore or increase physical, social and recreational function
  3. Optimize health and well-being
  4. Improve coping ability
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9
Q

How do you manage patients with chronic pain?

A

1. Use a multi-modal therapy approach:

  • Medications from different classes (combination drug therapy)
  • Rehabilitative therapies: physical therapy, occupational therapy
  • Regional anesthesia: nerve blockade
  • Interventional pain management: trigger point or steroid injections

2. Medical Management

  • Differs from acute pain management in that in chronic pain management there is greater use of adjuvant analgesics
  • Chronic pain reflects a greater frequency of neuropathic pain that has a reduced responsiveness to traditional analgesics
  • EBP recommendations: Clinical trials support the use of anti-depressants, antiepileptic medications (Gabapentin) and local anesthetics as first line approaches to the treatment of chronic pain.

3. Non-Pharmacological Management

  • Reconditioning (physical therapy/occupational therapy) reduces pain and promotes physical and psychological rehabilitation; thereby empowering the patients
  • Biofeedback and relaxation can relax muscles and reduce autonomic nervous arousal.
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10
Q

How do you treat patients with chronic arthritis pain? What non-opioids, opioids, or adjuvant analgesics would you use?

A

Non-opioids:

  • Acetaminophen, NSAIDs, Selective COX-2 inhibitors​

Opioids:

  • Short term mild opioids for flare-ups​

Adjuvant Analgesics:

  • Corticosteroids (oral for RA, injections for OA and RA); topical capsaicin and diclofenac and lidocaine patches
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11
Q

How do you treat patients with chronic lower back pain? What non-opioids, opioids, or adjuvant analgesics would you use?

A

Non-opioids:

  • Acetaminophen, NSAIDs, Selective COX-2 inhibitors

Opioids:

  • Short term opioids for mild to moderate flare-ups

Adjuvant Analgesics:

  • Muscle relaxants (short term)
  • Topical anesthetics: lidocaine patches, capsaicin
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12
Q

How do you treat patients with chronic fibromyalgia? What non-opioids, opioids, or adjuvant analgesics would you use?

A

Non-opioids:

  • Acetaminophen, NSAIDs, Selective COX-2 inhibitors
  • Pregabalin (Lyrica) - works to reduce electrical activity a/w overactive nerve impulses

Opioids:

  • Short term opioids for mild to moderate flare-ups
  • Tramadol

Adjuvant Analgesics:

  • Muscle relaxants (short term)
  • Tricyclic antidepressants: amitriptyline and imipramine
  • Second generation antidepressants: Duloxetine, fluoxetine, etc.
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13
Q

How do you treat patients with chronic peripheral neuropathy? What non-opioids, opioids, or adjuvant analgesics would you use?

A

Non-opioids:

  • Acetaminophen, NSAIDs

Opioids:

  • Short term

Adjuvant Analgesics:

  • Anti-epileptics: Gabapentin, pregabalin, tegretol
  • Topical anesthetics: Lidocaine patches, capsaicin topically;
  • Muscle relaxants: tizanidine
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14
Q

What are some characteristics of NSAIDS?

A
  • Do NOT cross the blood-brain barrier
  • 95-99% are bound to albumin
  • Act mainly on the periphery, but may have a central effect
  • Extensively metabolized by the liver and have a low renal clearance
  • Regular NSAIDs inhibit the synthesis of Thromboxane A2 (TXA2) by inhibiting COX-1 & thus inhibits COX-2 (inhibits prostaglandin G/H synthase enzymes, known also as COX; thereby inhibiting the synthesis of prostaglandin E, prostacyclin, and thromboxane. )
    *
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15
Q

What are some adverse effects associated with NSAIDS?

A

Since NSAIDs inhibit the production of not only COX-2, but also COX-1 (which synthesizes prostaglandins):

  • NSAIDS can affect the kidneys because prostaglandins help to maintain GFR and blood flow.
  • Prostaglandins also contribute to the modulation of renin release, excretion of water, and tubular ion transport.
    • In patients with normal renal function NSAID-induced renal dysfunction is extremely rare.
  • NSAIDS can affect platelets because platelets are very susceptible to COX inhibition, which also inhibits the endogenous pro-coagulant thromboxane. Long-term use of standard NSAIDs produces a consistently prolonged bleeding time, but the prolongation is mild and values tend to remain below the upper limits of normal.
  • NSAIDS can cause GI toxicity (ulcer formation)
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16
Q

What are some side effects associated with opioid use?

A
  • Most common opioid prescribed in the U.S. is hydrocodone
  • Extremely high doses of morphine and related opioids can produce seizures, presumably by inhibiting the release of GABA (at the synaptic level) - Demerol
  • Opioids produce a dose-dependent respiratory depression by acting directly on the respiratory centers of the brainstem
  • Therapeutic doses of morphine decrease minute ventilation by decreasing respiratory rate
  • Opioids depress the ventilator response to carbon dioxide
  • The apneic threshold is decreased and also the increase in ventilatory response to hypoxemia is blunted by opioids
  • Naloxone can effectively and fully reverse the respiratory depression from opioids
17
Q

How do you treat opioid addiction?

A
  • Buprenorphine (Suboxone) is a semisynthetic opioid and is used in out-patient facilities to treat opioid addiction
  • It is a sublingual film to take under the tongue.
  • Other formulations of Suboxone includes a combination Naloxone/Suboxone sublingual tablet (Zubsolv)
  • These medications are usually taken once a day.
  • Doses are titrated to response.
  • Stopping suboxone may cause withdrawal symptoms, such as hot or cold flushes, restlessness, teary eyes, runny nose, sweating, chills, muscle pain, vomiting or diarrhea.
18
Q

In what patients and with what combination should benzodiazepines be avoided in?

A
  • Avoid in geriatric patients
  • Avoid in combination with opioids
19
Q

What are some risk factors for NSAID induced renal dysfunction?

A
  • Prolonged and excessive NSAID use
  • Older patients
  • Chronic renal dysfunction
  • Congestive heart failure
  • Ascites
  • Hypovolemia
  • Treatment with nephrotoxic drugs