Chapter 6_2 flashcards

(53 cards)

1
Q

Neuropathic Pain: Origin [cite: 1]

A

Originates from injury or dysfunction in peripheral nerves or the central nervous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Neuropathic Pain: Common Characteristics [cite: 2]

A

Burning, tingling (paresthesia), shooting, stinging, or “pins-and-needles” sensations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Neuropathic Pain: Common Locations [cite: 2]

A

Often occurs in feet, legs, back, thighs, or toes, but can be in upper body too.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neuropathic Pain: Associated Conditions [cite: 3]

A

Can result from conditions like diabetic polyneuropathy, postherpetic neuralgia, spinal nerve radiculopathy, postsurgical pain syndromes, Complex Regional Pain Syndrome (CRPS).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Neuropathic Pain: Classification Note [cite: 4]

A

Not typically classified as acute or chronic in the same way as nociceptive pain; can occur in waves of frequency and intensity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Somatic Pain (Deep Somatic Pain): Origin [cite: 5]

A

Arises from ligaments, tendons, bones, blood vessels, and nerves themselves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Somatic Pain (Deep Somatic Pain): Characteristics [cite: 5]

A

Often described as dull or aching and is typically well-localized; longer duration than cutaneous pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Visceral Pain: Origin [cite: 6]

A

Emanates from deep organs, usually resulting from disease processes (e.g., distention of hollow organs, inflammation like cystitis or pancreatitis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Visceral Pain: Characteristics [cite: 6]

A

Often poorly localized, vague, and may be described as pressure-like, deep squeezing, dull, or colicky. Can be accompanied by nausea or other autonomic symptoms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phantom Limb Pain: Definition [cite: 7]

A

Pain perceived in a limb or part of a limb that has been amputated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Phantom Limb Pain: Cause [cite: 8]

A

Caused by continued neuronal activity in the brain (neuromatrix theory explains this as brain’s perception of the body/neurosignature) or spinal cord, despite absence of sensory input from the missing limb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Simple Reflex Arc: Protective Function [cite: 9]

A

A protective response that occurs without initial brain involvement, allowing for immediate action.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Simple Reflex Arc: Neural Pathway [cite: 9, 10]

A

Afferent neuron carries sensory input into the dorsal horn of the spinal cord[cite: 9]; connects to an interneuron in the substantia gelatinosa[cite: 10]; interneuron then connects to an efferent neuron, which sends motor output via the ventral horn to enact motor activity[cite: 10].

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Simple Reflex Arc: Brain Interpretation [cite: 11]

A

Brain interpretation is not required for the initial reflex action to occur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acute Pain: Characteristics [cite: 11, 12]

A

Sudden onset, short-term (hours to days)[cite: 11]. Usually linked to new tissue injury, inflammation, or surgery[cite: 12]. Resolves as healing occurs[cite: 12]. Serves a biologically protective role.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Chronic Pain: Characteristics & Associated Symptoms [cite: 12, 13]

A

Persists for more than 6 months[cite: 12]. May occur with or without apparent tissue damage[cite: 13]. Often associated with fatigue, irritability, depression, and sleep disturbances[cite: 13]. Debilitating and does not serve a protective function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

WHO Pain Ladder Approach: Step 1 [cite: 13]

A

For mild pain: Non-opioids (e.g., acetaminophen, aspirin, NSAIDs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

WHO Pain Ladder Approach: Step 2 [cite: 13]

A

For mild to moderate pain persisting or increasing: Weak opioids (e.g., codeine, tramadol) ± Step 1 drugs ± adjuvants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

WHO Pain Ladder Approach: Step 3 [cite: 13]

A

For moderate to severe pain persisting or increasing: Strong opioids (e.g., morphine, fentanyl, oxycodone) ± Step 1 drugs ± adjuvants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

WHO Pain Ladder Approach: Application for Tension Headaches [cite: 14]

A

For tension-type headaches, non-opioid treatments (Step 1) are typically tried first.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Fibromyalgia: Characteristics [cite: 14]

A

Characterized by widespread musculoskeletal pain, presence of multiple tender points upon palpation, fatigue, sleep disturbances, headaches, anxiety, depression. [cite: 14]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Fibromyalgia: Cause [cite: 14]

A

Cause is unknown, but believed to involve central pain sensitization (abnormal pain processing by the CNS).

23
Q

Spinal Nerve Radiculopathy: Definition & Pain Pattern [cite: 15, 16]

A

Involves compression or inflammation of a spinal nerve root[cite: 15]. Pain is typically localized to a specific dermatome supplied by that nerve (e.g., sciatica - pain radiating down posterior leg from L4-S1 impingement), not usually widespread[cite: 16].

24
Q

Trigeminal Neuralgia (Tic Douloureux): Affected Nerve & Symptoms [cite: 16, 17]

A

Affects the trigeminal nerve (cranial nerve V)[cite: 16]. Symptoms include intense, stabbing, electric shock-like facial pain, usually unilateral, often around eye, cheek, lower face[cite: 17]. Triggered by touch, sounds, common activities.

25
Nociception Processes (Gate Control Theory)
1. Transduction: Conversion of painful stimuli into neuronal impulses at nociceptor. 2. Transmission: Travel of impulse along afferent nerve axon to spinal cord dorsal horn. 3. Modulation: Influence of interneurons (and descending/ascending pathways) on pain signal at spinal cord "gate". 4. Perception: Conscious awareness/interpretation of pain in the brain.
26
A-delta Fibers vs. C Fibers (Pain Transmission)
A-delta fibers: Larger diameter, myelinated, conduct impulses rapidly; cause first, short-lived, sharp, acute pain. C fibers: Smaller diameter, unmyelinated, conduct impulses slowly; cause longer-lasting, persistent, dull, throbbing, or burning pain.
27
Spinothalamic Tract & Corticospinal Tract (Pain Pathways)
Spinothalamic Tract: Ascending tract directing sensory (including pain) impulses from spinal cord up through brainstem to thalamus and cortex. Axons cross over in spinal cord. Corticospinal Tract: Descending motor tract from brain's sensorimotor cortex, crossing over mainly in medulla, to control muscles.
28
Sensitization (Wind-Up)
Repeated or excessive stimulation of C fibers sensitizes afferent neurons, so even mild stimulation may be perceived as painful. Exaggerates excitement of nerve fibers and impairs inhibitory influences.
29
Gate Control Theory: Detailed Mechanism
Pain impulses from periphery via A-delta/C fibers (first neuron) synapse with interneuron (second neuron, the 'gate') in spinal cord's dorsal horn. Interneuron's activity is modulated by other peripheral inputs (e.g., large fiber stimulation like rubbing closes gate) and descending pathways from brain (e.g., endorphins, distraction close gate). Third neuron projects to brain for perception.
30
Neuromatrix Theory: Detailed Mechanism for Chronic/Phantom Pain
Brain contains a genetically determined, experience-shaped neural network (body-self neuromatrix). Sensory inputs create characteristic neurosignatures impressed on this matrix. Brain can generate pain based on these neurosignatures even without ongoing peripheral nociceptive input, explaining phantom limb pain or pain without obvious pathology.
31
Referred Pain: Mechanism & Example
Pain perceived at a distance from actual pathology. Nerve fibers from regions of normally low sensory input (viscera) and high sensory input (skin) converge on same spinal cord levels. Brain misinterprets visceral pain as originating from the somatic area with a stronger neurosignature. Example: Myocardial infarction pain referred to left arm/chest (C4-T4).
32
Colicky Pain: Characteristics & Cause
Pain that occurs in waves; builds to a peak and then declines. Caused by spasmodic contraction of hollow organs (e.g., intestine in gastroenteritis, gallbladder in cholecystitis with gallstone).
33
Acute Abdomen Pain: Peritoneal Inflammation Signs
Intense pain from inflammation of peritoneal membrane. Signs: Abdominal muscle rigidity (guarding), rebound tenderness, pain aggravated by movement (jumping, coughing).
34
Catastrophizing (Pain Perception)
An exaggerated negative orientation toward actual or anticipated pain experiences; misinterpretations of pain leading to avoidance, disuse, and disability. Common in chronic pain.
35
Opioid Pharmacology: Controlled Substance Schedules
Schedule I: High abuse, no accepted medical use (e.g., heroin). Schedule II: High abuse, severe dependence risk, accepted medical use (e.g., morphine, oxycodone). Schedule III: Moderate abuse, moderate/low physical or high psychological dependence (e.g., codeine products). Schedule IV: Low abuse potential (e.g., tramadol, benzodiazepines). Schedule V: Lowest abuse potential (e.g., cough preps with limited codeine).
36
Morphine: Prototypical Opioid & Effects
Effective for visceral/somatic pain. Produces analgesia, euphoria, sedation. Can cause respiratory depression, constipation, nausea, miosis. Most effective given preemptively to prevent central sensitization.
37
Naloxone: Mechanism & Use in Opioid Overdose
Opioid antagonist with extremely high affinity for opioid receptors. Competitively blocks opioid attachment, reversing CNS and respiratory depression in overdose. Will cause rapid withdrawal in opioid-dependent individuals.
38
Methadone & Buprenorphine in Opioid Use Disorder
Methadone: Synthetic opioid for withdrawal prevention/weaning; lacks euphoric effects of other opioids. Buprenorphine: Partial opiate receptor agonist; ameliorates withdrawal, less analgesia/euphoria than methadone, "ceiling effect", not a respiratory depressant, reduces effects of additional opioid use due to high mu receptor affinity.
39
Non-Opioid Analgesics: NSAIDs (Mechanism & Side Effects)
NSAIDs (aspirin, ibuprofen, naproxen): Block COX-1 and COX-2 enzymes, preventing prostaglandin (PG) release. Nonselective. Side effects from COX-1 inhibition: diminished gastric mucus (ulceration), decreased renal perfusion, diminished clotting.
40
Non-Opioid Analgesics: COX-2 Inhibitors (Mechanism)
Celecoxib selectively inhibits COX-2 enzyme pathway, blocking PGs that cause edema, inflammation, and pain, while sparing COX-1 (intended to reduce GI side effects).
41
Non-Opioid Analgesics: Acetaminophen (Mechanism)
Antipyretic & analgesic, not anti-inflammatory. Mechanism not fully understood: blocks PG synthesis, activates serotonin receptors, inhibits endocannabinoid reuptake in CNS.
42
Adjuvant Medications for Pain: Examples & Purpose
Amplify analgesic effect. Acetaminophen (in combinations). Antidepressants (TCAs, SNRIs for neuropathic pain). Anticonvulsants (gabapentin, pregabalin for neuropathic pain). Local anesthetics. Corticosteroids (injections for musculoskeletal/nerve root pain). Cannabinoids.
43
Capsaicin (Topical): Mechanism
Depletes substance P (neurotransmitter for painful impulses) from peripheral sites to CNS, providing analgesia.
44
Cannabinoids in Pain Management: Mechanism & Potential
Endocannabinoid system (ECS) modulates pain. Cannabinoids (plant-based, synthetic) have analgesic/anti-inflammatory effects, modulate neurotransmitters, interact with opioids. THC can stimulate endorphins. Potential for opiate-sparing effect, preventing opioid tolerance/overuse. Controversial, more research needed.
45
Cancer Pain: Mechanisms
Tumor pressure/destruction of tissue. Cancer cells secrete enzymes/inflammatory mediators (endothelin-1, PGs, substance P). Metastasis (especially bone pain). Treatment side effects (chemo-induced neuropathy/mucositis, radiation burns, surgical pain).
46
Diabetic Peripheral Neuropathy: Pathophysiology
Hyperglycemia -> increased intracellular glucose in nerves -> impaired axonal transport, structural nerve breakdown. Excess glucose reacts with nerve membranes -> advanced glycation end products (AGEs) -> disrupt neuronal integrity. Arteriosclerosis of small vessels -> diminished circulation -> worsens neuropathy.
47
Complex Regional Pain Syndrome (CRPS): Types
Type I (Reflex Sympathetic Dystrophy): No demonstrable nerve lesion. Type II (Causalgia): Evidence of obvious nerve damage.
48
Postherpetic Neuralgia: Cause
Persistent pain after shingles (herpes zoster reactivation of varicella zoster virus, which remains dormant in dorsal root ganglia after chickenpox). Virus reactivates along a nerve dermatome causing painful vesicular rash, then chronic neuralgia.
49
Fibromyalgia: Diagnostic Tender Points
Diagnosis often includes history of >3 months widespread pain AND pain/tenderness in at least 11 of 18 specific tender-point sites (e.g., back of neck, shoulders, sternum, lower back, hips, shins, elbows, knees).
50
Trigeminal Neuralgia: Treatment Considerations
Medications: Anticonvulsants (carbamazepine), muscle relaxers, TCAs. Botulinum toxin type A injections. Surgery to relieve nerve pressure.
51
Multimodal Analgesia for Postoperative Pain
Using more than one type of analgesic modality (pharmacological and nonpharmacological) to achieve effective pain control with fewer adverse effects. Examples: Preoperative NSAIDs/anxiolytics, intraoperative neuraxial analgesia, continuous local anesthetic, TAP block, IV acetaminophen, PCA.
52
Excitatory Neurotransmitters in Pain
Prostaglandins, Interleukins, Tumor Necrosis Factor, Leukotrienes, Bradykinins, Glutamate, Substance P. [cite: 35]
53
Inhibitory Neurotransmitters/Neurochemicals in Pain
Enkephalins, Endorphins, Acetylcholine (spinal cord), GABA (spinal cord & brain), Norepinephrine (spinal cord), Dopamine (spinal cord & brain), Serotonin (PAG to NRM). [cite: 35]