Pain Management Flashcards
Pathophysiology of Pain
Stimulation
- Receptors (nociceptors) are activated by stimuli
- May differ for different painful conditions
- Neurotransmitters and ions are released:
- Serotonin
- Norepinephrine
- Baradykinin
- Prostiglandin
- Histamin
- Substance P
- Neurokinin
- Potassium and hydrogen
- Release of these substance in the periphery “activates” further neurons reducing the threshold for further inputs
Pathophysiology of Pain
Transmission
- Process by which pain signals ascend throught the spinothalamic tract
- Primary neurotransmitters involved are:
- glutamate/aspartate
- substance P
Pathophysiology of Pain
Perception
- the process that occurs in the cortex allowing an awareness of the experience of pain
- nonpharmacological therapies are based on modifying the patient’s perception of his or her pain
- CBT
- meditation
Pathophysiology of Pain
Modulation
- process of modification of pain signals
- can occur through the ascending or descending pathway
- endogenous systems of modulation include inhibitory neurotransmitters/receptors
- Endogenous opioids
- Blockade of NMDA (N-methyl-D-spartate)
- Serotonin
- GABA (Gamma- aminobutyric acid
Pathophysiology of Pain
Centralization or central sensitization
- an amplification of pain signals originating in the periphery.
- this amplification over time imprints or sustains the pain in the CNS
- thought to explain pain syndroms such as phantom limb pain, reflex sympathetic dystrophy, and hyperalgesia
Pathophysiology of Pain
Allodynia
presence of pain from stimuli that are not normally painful
e.g. a patient with diabetes who experieces pain when placing socks on feet
Pathophysiology of Pain
Hyperalgesia
- normal pain stimuli produce exaggerated pain responses in patients with peripheral or central sensitization
e. g. an immunization in the deltoid muscles cuases patients to experience extreme pain for many days, preventing them from lifting their arm. The injection site has no obvious erythema or signs of an injection site reaction
Acute Pain
1) pain is typically a result of an acute disease process (may be part of an mixed disease process - acute or chronic) and is typically managed as a symptom
2) Pathophysiology is primarily inflammation
3) Treatment goals include cessation of pain or substantial relief
4) Anticipatory anxiety may be involved - patients are worried that pain will worsen or that pain will reoccur when medication wears off.
Chronic Pain
1) a physiologic cause may not be determinable. Chronic pain should be managed as an independant disease state with a monitoring and treatment plan apart from other plans
2) Most types of chronic pain are mixed - somatic and neuropathic
3) Treatment goals include a reduction in pain and an improved quality of life. Patients do not usually achieve remission of their pain. Realistic expectations should be discussed
4) Anxiety and depression are often (30-50%) comorbidities of pain. Most patients develop a tolerance to and dependence on medications
Acute Pain Management
Mild
- manage with acetaminophen or NSAIDs
- consider around the clock dosing
- may require adjuvants in certain situations
- monitor and reassess
Acute Pain Management
Moderate
- manage with acetaminophen or NSAIDs in combination with low dose opioids
- consider around the clock dosing
- may require adjuvants in certain situations as well as potentially agents for breakthrough pain
- monitor and reassess
Acute Pain Management
Severe
- long acting opioid analgesics and combinations with breakthrough medications
- around the clock dosing
- may require adjuvants in certain situations as well as potentially agents for breakthrough pain
- monitor and reassess - patients are at higher risk for adverse effects and require stricter monitoring
Chronic Pain Therapies
Arthritis
Pharmacotherapy:
- first-line agents: acetaminophen, oral and topical NSAIDs, intraarticular steroids
- Tramadol
Nonpharmacotherapy
- aquatic, aerobic, and resistance exercise
- weight loss
Chronic Pain Therapies
Diabetic Neuropathy
Pharmacotherapy:
- primary goal - maintain diabetic control. Agent with highest level of evidence: Pregabalin - most common side effect weight gain
- Second tier agents/therapy - all are considered acceptable agents with weak levels of evidence and showed a significant number of adverse effects in trials
- Gabapentin
- Duloxetine
- Sodium valproate
- Venlafaxine
- Dextromethorphan
- Morphine sulfate
- Tramadol
- Oxycodone
- Capsaicin
Nonpharmacotherapy
- Percutaneous electrical stimulation
Diabetic Neuropathy adjuvants
Pregabalin
Dose: 300- 600mg
Common adverse effect: Sedation, weight gain
Diabetic Neuropathy adjuvants
Gabapentin
Dose: 1800 - 3600mg
Common adverse effect: Sedation, weight gain
Comment: dose should be reduced in renal dysfunction
Diabetic Neuropathy adjuvants
Duloxetine
Dose: 60-120mg
Common adverse effect: nausea, increase blood pressure, headache
Comments: Should not be used if CrCl<30; use with extreme caution with other serotonergic agents, rare LFT changes
Diabetic Neuropathy adjuvants
Venlafaxine
Dose: 75-225mg
Common adverse effect: hypertension
Comments: dose adjustment necessary if CrCl<50
Diabetic Neuropathy adjuvants
Desipramine, Nortriptyline
Dose: 25-150gm
Common adverse effect: Sedation, anticholinergic
Comments: Doses effective for pain may not be therapeutic for depression