Test 4: Multimodal Acute vs Chronic Pain

Question 1

What is Acute Pain (basic definition)?

Answer 1

Pain caused by noxious stimuli due to traumatic injury (chemical, thermal, or mechanical), surgery, or acute illness.

Question 2

What is Chronic pain (basic definition)?

Answer 2

Pain with no apparent biological value that lasts longer than 3 months or beyond the normal course of healing.
-Associated with insomnia, lost work days, impaired mobility & emotional distress (anxiety, anger, fear, depression)
-Hyperexcitable state. Nerves are constantly activated from damage.
-Two general classifications: Malignant or Non-Malignant
-Challenging to treat (multimodal approach)

Question 3

What is Malignant pain?

Answer 3

Pain caused by or related to cancer and its treatment.

Question 4

What is Non-Malignant pain?

Answer 4

Neuropathic
Inflammatory
Musculoskeletal
Idiopathic
Combination of one or all of the above

Question 5

What triggers responses with acute pain?

Answer 5

SNS triggers neuroendocrine responses in response to surgical stress.

Question 6

What factors can impact the SNS response with Acute Pain?

Answer 6

SNS response impacted by:
-Size of the surgical field
-Number of nerve/pain receptors in the area
-Bleeding, infection, anxiety
-Coexisting diseases

Question 7

What are the Cardiovascular Effects associated with acute pain?

Answer 7

-Increases catecholamines from SNS and increases cortisol = inc HR, inc vascular resistance (peripheral, systemic, and coronary), increased myocardial oxygen contractility, and increased arterial BP.
-Leads to increase in Myocardial O2 demand & consumption (!)

-Potential for rupture of artherosclerotic plaque from vascular walls (further decreases O2 supply to tissues)
-Can lead to Dysrhythmias, angina, myocardial ischemia & infarct
-Risk of MI due to increased myocardial O2 demand/consumption (!)

Question 8

T/F: Aggressive pain management is essential to preventing post-op cardiac complications.

Answer 8

True (Blue Box!)

Question 9

What are the Respiratory Effects associated with acute pain?

Answer 9

-Most problematic for pts with trauma/surgery in the upper ABD area & thorax
-Pain ⬇TV due to ⬇thoracic and abdominal movement
-⬇Vital capacity, ⬇inspiratory capacity & ⬇FRC
-⬇ability to clear the airway due to pain
-Muscle spasms = ⬇limited respiratory muscle movement (dec ventilation)
-Poor cough, splinting ⇒atelectasis & pneumonia
-Effects are worse in pts with pre-existing pulm dysfunction (Asthma, COPD) or ⬇FRC at baseline (morbidly obese, elderly)

Question 10

How does acute pain increase the risk for DVT or PE?

Answer 10

Pain decreases/delays mobilization

Question 11

What physiological changes associated with acute pain do you need to know (basic overview)?

Answer 11

-Inc HR, PVR, and ABP: all things we assess to see if they’re experiencing pain
-Decreased VC, TV, and TLC
-V/Q mismatch, atelectasis, PNA
-Decreased ability to cough leads to hypoxia and hypercarbia
-Decreased gastric emptying, decreased intestinal motility
-Inc plt aggregation (thrombosis). compounded if they aren’t moving
-Decreased immune function (increased risk of infection)
-Inc urinary sphincter tone (urinary retention)

Question 12

What is Sensitization?

Answer 12

-Non-associative learning. Behavior toward a stimulus changes in the absence of any apparent associated stimulus or event (such as a reward or punishment)
-Repeated administration of a stimulus results in the progressive amplification of a response
-Often characterized by an enhancement of response to a whole class of stimuli in addition to the one that is repeated
-Post-op surgical pain can trigger chronic pain of a different kind

Question 13

What is Central Sensitization?

Answer 13

-Pain modulation is enhanced due to neuroplastic changes in the CNS
-Repetitive stimuli to injured nerves alters neurotransmitter levels
-Associated with chronic pain states

Question 14

What is Peripheral Sensitization?

Answer 14

-Environmental chemical changes of peripheral nerves
-Release of algogenic substances and neurotransmitters, such as Bradykinin, serotonin, Substance P, glutamate, etc.
-Enhanced excitability of nerves
-Reduces nociceptive thresholds
-High-threshold nerve endings become responsive to non-noxious stimuli

Question 15

How does acute pain transition to chronic pain?

Answer 15

Pain goes from Nociceptive to Neuropathic.
1) Initiated by either peripheral or central mechanisms:
-Peripheral Sensitization
-Central Sensitization
2) Hyperexcitable nerve endings:
-Changes resulting from direct nerve injury
-Sprouting of new nerve endings. Fire ectopically
3) Neuroma formation:
-Abnormal growth or tumor of the nerve
-Abnormal mechanosensitivity
4) Damaged nerves have reduced pain thresholds:
-Respond to non-noxious stimuli

Question 16

What is Neuropathic pain?

Answer 16

-Initiated or caused by changes in the PNS or CNS
-“shooting” “burning” “stinging”
-Accompanied by hyperalgesia and allodynia.

Question 17

What is Mechanosensitivity?

Answer 17

Physiological foundation for the senses of touch, hearing and balance, and pain is the conversion of mechanical stimuli into neuronal signals.

Question 18

What is “Wind Up”?

Answer 18

Sensitization of the Wide Dynamic Range (WDR) neurons in the posterior column of the spinal cord.
-With chronic stimulation, these increase cellular calcium, increase release of inflammatory substances (ex: Substance P, Bradykinins, and Glutamate), and produce cyclooxygenase.
-Prostaglandins are also synthesized, which are responsible for the reduction of our neuropathway inhibition (reduction of inhibition = excitability)
-Sustained stimulation of afferent C Fibers leads to a longer sustained depolarization. Afferent input sensitizes low threshold afferents, increasing the neuronal field.
-Increased neurologic pathway excitation and formation of hyperalgesia = “Wind Up”.
-Very hard to treat this. Complex.

Question 19

What is Glutamate?

Answer 19

Theorized to play a key role in the development of “Wind Up”.
-The primary excitatory neurotransmitter
-Released by Primary afferents in the dorsal horn (A Delta & C fibers)

Acts on receptors within the Dorsal Horn:
-Metabotropic
-Kainite
-AMPA
-NMDA

Question 20

What occurs when Glutamate stimulates the NMDA Receptor?

Answer 20

-Activation of the receptor
-Released of 2nd messengers: Kinases and Lipases

Question 21

What causes upregulation of 2nd Messengers?

Answer 21

Substance P and Calcitonin Gene Related Peptide.
-Produces hyperexcitability of the NMDA Receptors.
-Leads to long term neuronal plasticity, excitability, and eventually produces gene transcription changes.
-Contributes to central sensitization and chronic pain states.

Question 22

What are the different techniques used in treating acute pain?

Answer 22

-Preemptive analgesia
-NSAIDS (Ketorolac, Acetaminophen (not rly a NSAID), and Celecoxib)
-Opioids
-NMDA Antagonists
-Alpha2 Adrenergic Agonists
-Local Anesthetics
-PCA

Question 23

What are different techniques to treat Chronic pain?

Answer 23

-Anticonvulsants
-Antidepressants
-Corticosteroids
-Methadone

Question 24

Why are Anticonvulsants used to treat Chronic pain?

Answer 24

2nd gen Anticonvulsants: Gabapentin and Pregabalin
-Inhibit neuronal excitation and stabilize nerve membranes
-Decrease repetitive neural ectopic firing (neuropathic pain). Used in the tx of postherpetic neuralgia, diabetic neuropathy, and trigeminal neuralgia.

Question 25

Why are Antidepressants used to treat Chronic pain?

Answer 25

-Ex: TCAs, SSRIs, SNRIs
-Descending inhibitory pathway is altered in central sensitization.
-Antidepressants increase the availability of inhibitory neurotransmitters
-Can also act on other sites.
-Dose is lower than normal recommended antidepressant doses (effects may not occur until 4-10 days)

Question 26

What other sites do Antidepressants work on?

Answer 26

-Blocking of sodium and calcium channels
-Decreasing PGE2 and TNF-α
-Blocking NMDA receptors
-Enhancing opioid receptors

Question 27

What Tricyclics (TCAs) are used in chronic pain treatment?

Answer 27

-Ex: amitriptyline (Elavil), nortriptyline
-C/I in recent MI, prolonged QT, dysrhythmias, unstable CHF
-Used to treat postherpetic neuralgia, headaches, fibromyalgia

Question 28

What SNRIs are used in chronic pain treatment?

Answer 28

-Ex: duloxetine (Cymbalta), venlafaxine (Effexor)
-Preferred for pts with cardiac disease

Question 29

What SSRIs are used in chronic pain treatment?

Answer 29

-Ex: Prozac, Paxil, Celexa, Zoloft, Lexapro
-weak data