Pain Management Quiz #3 Flashcards Preview

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Flashcards in Pain Management Quiz #3 Deck (17)
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1

Chronic Pain definition.

-Pain that has no apparent biologic value
-Lasts longer than 3 months duration or beyond the normal course of healing
-Often associated with insomnia, lost work days, impaired mobility and emotional distress (anxiety, depression, anger, and fear)

2

What are the 2 classifications of chronic pain?

1. Malignant: related to cancer and its treatment
2. Non-malignant: neuropathic, inflammatory, musculoskeletal, and idiopathic...or combination

3

Focus of chronic pain treatment

-Reducing pain
-improving activities of daily living
-Enhancing functioning
-using an interdisciplinary approach: pain management specialist, psychologist, physical therapist, OT, and patient

4

Chronic Pain Physiology: Peripheral mechanisms

-Transition from acute to chronic pain can be initiated or maintained by peripheral and/or central mechanisms

-Peripheral exposure:
1. enhanced excitability of the nerves
2. reduced nociceptive thresholds
3. renders high-threshold nerve endings responsive to normally non-noxious stimuli
-This process is termed peripheral sensitization and may contribute to chronic pain states
-Clinically manifested as hyperalgesia: due to nerve injury resulting in the sprouting of new hyper-excitable nerve endings, which fire ectopically

-Despite the sequelae regarding chronic inflammation and its effects on nerve excitability and alteration in stimulus threshold, changes can also occur directly to nerve endings when nerve injury is present. May result in:
1. sprouting of new hyper excitable nerve endings
2. a neuroma may form causing abnormal mechanosensitivity
3. regenerated and/or damaged nerves also have reduced thresholds

5

List Algogenic substances found in the periphery

-bradykinin
- serotonin
-prostaglandins
-NT substanceP and glutamate

6

Chronic Pain Physiology: Neuropathic pain

-Despite the sequelae regarding chronic inflammation and its effects on nerve excitability and alteration in stimulus threshold, changes can also occur directly to nerve endings when nerve injury is present. May result in:

1. sprouting of new hyper excitable nerve endings
2. a neuroma may form causing abnormal mechanosensitivity
3. regenerated and/or damaged nerves also have reduced thresholds

-Pain that is initiated or caused by changes in the peripheral or central nervous system is defined as neuropathic pain
-Shooting, burning, or stinging sensations that are accompanied by hyperalgesia and allodynia

7

Chronic Pain Physiology: Central mechanisms.

-Continuous effects of chronic inflammation with hyper excitability and sensitization of 2nd order neurons in the dorsal horn
-Sensitization of WDR neurons as well as an increase in the release of excitatory neurotransmitters, specifically GLUTAMATE, results in the phenomenon termed WIND UP
-Glutamate is the primary excitatory NT in wind up, and is released by primary afferents in the dorsal horn
-Acts at several receptor sites in the dorsal horn
-The hyperexcitability of NMDA (an ionotropic receptor that remains closed at rest due to a magnesium plug) receptors is a significant contributor to central sensitization and chronic pain states

8

Activation of NMDA receptors.

-Involves simultaneous binding of glutamate after repeated firing of signals
-Magnesium plug is displaced
-Causes an influx of Ca inside the cell
-Results in an increase in 2nd messengers such as protein kinases and phospholipases
-Are resistant to a stimulus-agonizing receptor mainly by the presence of the MAGNESIUM PLUG

9

T or F: When a skin incision is made (as in acute pain), there are pockets of glutamate that are released from nociceptive nerve terminal and they agonize/combine with AMPA receptors.

-True
-AMPA are sensitive to weak signals, very easy to excite them

10

Chronic Pain Analgesics and Adjuncts: Anticonvulsants

-AKA antiepileptics
-Commonly used in Neuropathic pain syndromes when treatment is refractory to traditional analgesics
-Inhibit neuronal excitation and stabilize nerve membranes in an effort to decrease repetitive neural ectopic firing, which is common in neuropathic pain

1st generation: carbamazepine and phenytoin
-have been used for years, but more recently the 2nd gen. are more widely used

2nd generation: gabapentin and neurontin
-inhibit neuronal excitation and stabilize nerve membranes in an effort to decrease repetitive neural ectopic firing
-used to treat post-herpetic neuralgia, diabetic neuropathy, trigeminal neuralgia as well as others
-mechanism of action: block alpha 2 delta subunit of the PRE-synaptic voltage-gated Ca channels in the CNS, thereby preventing excitatory NT release
-exhibit anticonvulsant, anxiolytic, and effects
-SIDE EFFECTS: dose dependent, dizziness, somnolence, peripheral edema, and weight gain
-Neither drug undergoes hepatic metabolism
-Unchanged form of drug is excreted by kidneys
-Dose modification is necessary in the renal compromised patient
-Great multimodal agents (not limited to chronic pain syndromes)
-Patients need to continue taking throughout the perioperative period!!!

11

Chronic Pain Analgesics and Adjuncts: Antidepressants

-For neuropathic pain
-In the presence of central sensitization, the descending inhibitory pathway, which uses inhibitory NT (serotonin and norepi), is altered
-They block the reuptake of serotonin and norepi in the CNS, thereby increasing availability
-Block Na and Ca channels
-Decrease PGE2 and TNFa
-Block NMDA receptors
-Enhance opioid receptors (analgesic effects may not occur until 4-10 days after initiating treatment

Common Antidepressants used for chronic neuropathic pain:
*Tricyclics (TCA's): amitriptyline (elavil), Nortriptyline (pamelor), Imipramine (tofranil)
*Selective Serotonin Reuptake Inhibitors (SSRIs): Fluoxetine (prozac), Citalopram (celexa)
Selective Norepinephrine and Serotonin Reuptake Inhibitors (SNRIs): Venlafaxine (effexor), Duloxetine (cymbalta), Milnacipran (savella)

12

Tricyclic Antidepressants (TCA's)

-Commonly used to treat post-herpetic neuralgia, H/A, and fibromyalgia
-Side effects:
*muscarinic (dry mouth, blurred vision, urinary retention)
*histaminergic (sedation, appetite stimulation, weight gain)
*adrenergic (orthostatic hypotension, prolonged QT interval)

***Caution: recent MI, prolonged QT interval, funky rhythms, CHF

13

Selective Norepinephrine Reuptake Inhibitors (SNRIs)

-Less side effects
-Better tolerated than TCAs bc they lack affinity for adrenergic, cholinergic, and histaminergic receptors
-Ideal for patients with cardiac disease
-Side effects: nausea, dry mouth, somnolence, H/A's and sexual dysfunction
-Concomitant use of SNRIs with SSRIs or triptans is not recommended bc this may precipitate SEROTONIN SYNDROME (can be life-threatening)

14

Serotonin Syndrome

-Can be life threatening
-Acute toxicity of serotonin manifesting as anxiety, agitation, delirium, seizures, hyperthermia, diaphoresis, tachycardia, HTN, hypotension, hyperreflexia, myoclonus, and muscle rigidity

15

Selective Serotonin Reuptake Inhibitors (SSRIs)

-Still investigational
-Primarily used for the treatment of depression (analgesic is weak)
-Regardless of type of antidepressant being taken for chronic pain, they should be continued throughout the perioperative period!!!

16

Chronic Pain Analgesics and Adjuncts: Corticosteroids

Treatment for:
-Rheumatoid arthritis
-Osteoarthritis
-Herpetic neuralgia
-Chronic low back pain
-Chronic neck pain

Body effects:
-Autoimmune
-Anti-inflammatory
-Anti-edema
-Anti-allergic

Mechanism of Action:
-Prevent release of arachidonic acid by inhibiting phospholipase A2 on cell membranes
-Decreases inflammatory cytokines and prostaglandins

Epidurally:
-Block C fiber transmission
-Suppress ectopic firing of nociceptors in the presence of nerve injury
-Produces a direct membrane stabilizing effect

-Reflective of supra-physiologic doses that usually exceed the rate of endogenous steroid production, which is approximately 20mg per day of hydrocortisone or its equivalent

-Effects are dependent on the degree of hypothalamic-pituitary-adrenal axis (HPA) suppression
*attributed to: type of steroid, duration of use, frequency of ingestion, route of administration, and dosage
*a single epidural steroid injection can cause HPA suppression from 4-5 days of injection and lasting up to 5 weeks
*in the event of a major surgical procedure after the recent administration of an epidural steroid, it may be prudent to administer a dose of exogenous steroid

17

Chronic Pain Analgesics and Adjuncts: Methadone

-PROLONGS QT interval!!
-Synthetic opioid used for the treatment of opioid addiction in detox
-A racemic mixture of 2 enantimers: d-isomer (S-methadone) and I-isomer (R-methadone)
-D-isomer (S-methadone): antagonizes NMDA receptor and inhibits serotonins and norepi uptake which aids in the treatment of neuropathic pain, ovoid tolerance, and hyperalgesia
-I-isomer (R-methadone): responsible for binding to opioid receptors, thereby owing to its analgesic effect.

PO peak analgesic effect: 30-60 minutes
IV peak analgesic effect: 15-20 min
Half-life: 15-60 hours

Metabolism: Hepatic

-Any medications that inhibit (phenytoin, carbazepine) may dramatically alter methadone metabolism

Side effects: respiratory depression (occur later than analgesic effects), excessive sedation, QT interval prolongation

-An EKG should be obtained pre-treatment, 30 days after starting, and then annually
-If dosage exceeds 100 mg a day, get EKG
-A QT interval > 500 ms: reduce dose/discontinue

-No active metabolites, long 1/2 life, and low cost make it desirable for chronic nonmalignant pain management