Pain Pathways (Exam II) Flashcards
(56 cards)
1
Q
Differentiate the sensory-discriminative & motivational-affective aspects of pain.
A
- Sensory-discriminative - Ascending pathways and the perception of pain (location, intensity, sensation, etc.)
- Motivational affective - responses to painful stimuli (Ex. arousal, reflexes, endocrine responses, and emotional changes)
2
Q
What is nociception?
A
- The experience of pain through a series of complex neurophysiologic processes.
3
Q
What are the four stages of pain perception?
A
- Transduction (tissue level)
- Transmission (via nerves)
- Modulation (via spinal cord)
- Perception (CNS)
4
Q
Where does the modulation of pain impulses occur?
A
- Dorsal horn of the spinal cord
5
Q
What drugs are used to affect the transduction of pain?
What specifically is being affected by these drugs?
A
- Local anesthetics & NSAIDs
- Peripheral nociceptors
6
Q
What drugs are used to affect the transmission of pain?
What specifically is being affected by these drugs?
A
- Local anesthetics
- Αδ and C fibers
7
Q
What drugs are used to affect the modulation of pain?
What specifically is being affected by these drugs?
A
- LA’s, opioids, ketamine, α2 agonists
- Afferent fibers of the dorsal horn
8
Q
What drugs are used to affect the perception of pain?
What specifically is being affected by these drugs?
A
- General anesthetics, opioids, α2 agonists
- Brain
9
Q
Where are nociceptors located?
A
- Skin
- Muscles
- Joints
- Viscera
- Vasculature
10
Q
What characterizes afferent C-fibers?
A
- Unmyelinated
- Pain from heat (burning) & sustained pressure
- Slow (less than 2 m/s)
11
Q
What characterizes Aδ fibers?
A
-Myelinated
- Type I: Aβ & Aδ (heat,mechanical, chemical)
- Type II: Aδ (heat)
- Fast (>2 m/s)
12
Q
What chemical mediators of pain are targeted with spinal anesthetics?
A
Peptides
- Substance P
- Calcitonin
- Bradykinin
- CGRP
13
Q
Which chemical mediator is released first in response to injury?
A
- Bradykinin
14
Q
What chemical mediators of pain are inhibited by NSAIDs?
A
Lipids
- Eicosanoids
- Prostaglandins
- Thromboxanes
Remember Pharm 1? Eicosanoids are lipid-based signaling molecules that are derived from arachidonic acid.
15
Q
What chemical mediators of pain are inhibited by cannabis?
A
Lipids
- Endocannabinoids
16
Q
What is sensitization?
A
- Decreased pain threshold (likely due to upregulation of receptors)
17
Q
Differentiate hyperalgesia and allodynia.
A
- Hyperalgesia - ↑ pain sensations to normally painful stimuli.
- Allodynia - perception of pain to things that aren’t normally painful.
18
Q
What characterizes primary hyperalgesia?
A
Hyperalgesia at original site of injury.
- Lower pain threshold
- Spontaneous pain
- Expansion of receptive field
19
Q
What characterizes secondary hyperalgesia?
A
- Sensitization of CNS → hyperalgesia from uninjured skin surrounding injury.
20
Q
What area of the brain accounts for the perception (location & intensity) of pain?
A
- Somatosensory Cortex I & II (SI & SII)
21
Q
What is the relay center for nociceptive and sensory activity?
How does sensory activity travel from this area to the cerebrum?
A
- Spinal Dorsal Horn
- Ascending pathways
22
Q
What areas of the brain may depress or facilitate the integration of painful information in the spinal dorsal horn?
A
- PAG - Peraqueductal Gray Matter
- RVM - Rostral Ventral Medulla
23
Q
Where are afferent C-fibers located in the spinal column?
A
- Dorsal horn: Lamina I (marginal layer) & II (substantia gelatinosa)
24
Q
What is another name for Lamina II?
What drugs work here?
A
- Substantia gelatinosa
- Opioids
25
What nerve fibers are associated with an "open-gate" for pain?
What nerve fibers can shut this gate?
- Aδ & C-fibers = **open**
- Aβ fibers = **closed**
## Footnote
Remember AP and Pharm1? Aβ fibers deliver information about pressure and touch (rubbing). This is our primary pain inhibition pathway so think Aβ=inhibition=closed pain gate
26
What receptors does ketamine target for pain modulation?
- NMDA
27
The excision of what structure would result in the complete loss of perception of pain?
Amygdala
* Bonus points if you just said the whole brain you degenerate.
28
What neurotransmitters propagate excitatory transmissions in the spinal column?
* 5 stated in lecture
- Glutamate
- Calcitonin
- Neuropeptide Y
- Aspartate
- Substance P
29
What is the primary excitatory impulse mediator discussed in lecture?
Glutmate
30
What neurotransmitters propagate inhibitory transmissions **in the spinal column**?
* 5 were stated in lecture
- GABAA
- Glycine
- Enkephalins
- NE
- Dopamine
31
What are the four ascending pain pathways?
- Spinothalamic
- Spinomedullary
- Spinobulbar
- Spinohypothalamic
32
What information is carried by the spinothalamic pathway?
What laminae are used?
- Pain, Temp, & Itch
- Laminae I, VII, and VIII (all afferent fibers)
33
What information is carried by the spinobulbar pathway?
What laminae are used?
- Behavior towards pain
- Laminae I, V, and VII
34
What information is carried by the spinohypothalamic pathway?
What laminae are used?
- Autonomic, neuroendocrine & emotional aspects of pain
- Laminae I, V, VII, & X.
35
What part of the suprapinal pathway differentiates where pain is coming from (location and intensity)?
S1 & S2 (Somatosensory cortex 1 & 2)
36
What supraspinal areas deal with the emotional/motivational aspects of pain?
- Anterior cingulate cortex (ACC)
- Insular Cortex (IC)
- Amygdala
## Footnote
Other general supraspinal nociception modulation occurs in
* Prefrontal cortex
* Thalamus
* Cerebellum
37
Where do the descending inhibitory tracts originate?
Where do they then synapse at?
- PAG (periaqeueductal gray matter)
- Synapse at dorsal horn
38
What neurotransmitters are increased with exercise?
- Endorphins
- Enkephalins
- Serotonin
39
How do inhibitory tracts inhibit the propagation of painful stimuli?
**Hyperpolarizing Aδ & C fibers**
- ↓ release of substance P
- open more K⁺ channels and inhibit Ca⁺⁺ channels
40
Where does the pain inhibiting impulse originate from in the descending inhibitory tracts?
PAG-RVM areas
41
When is pain considered chronic rather than acute?
- If > 3 - 6 months
- If pain persists beyond tissue healing
## Footnote
Unpleasant emotional experiences, affective qualities traverse the same pathways and can cause:
* anxiety, depression, cognitive deficits, emotional distress
42
What is neuropathic pain?
Who is at increased risk of neuropathic chronic pain?
NP Pain persists after the tissue has healed and can cause allodynia/hyperalgesia
- Cancer patients (d/t chemo and radiation therapy)
- Diabetics
43
What is the treatment for chronic neuropathic pain?
- Opioids
- Gabapentin
- Amitriptyline
- Cannabis
*All situation dependent*
44
How is visceral pain characterized?
What examples were given in lecture?
Also, what causes it?
- Diffuse and poorly localized
- Referred to somatic sites: muscle & skin
- Causes: ischemia, stretching of ligamentous attachments, spasms, distention
45
What is complex regional pain syndrome?
- Variety of painful issues **following an injury** (sponateous pain, hyperalgesia, edema, etc.)
46
When can babies begin to perceive pain?
23 weeks of gestation
## Footnote
Neonates and infants have a lower pain threshold & exaggerated pain responses
47
What are the pulmonary effects of chronic pain?
- ↑ total body O 2 condumption and CO 2 production. --> increased work of breathing
- Splinting
- Shallow breathing → **atelectasis, shunting, and pneumonia.**
- Impaired cough
48
How does pain affect the GI/GU system?
- ↑ SNS = ↑ sphincter tone and ↓ peristalsis = **N/V, constipation, ileus, distension, urinary retention** etc.
- Hypersecretion of acids can lead to stress ulcers and aspiration
49
How can the effects of pain in the cardiovascular system be summarized?
↑ SNS:
↑SVR, ↑HR, HTN, myocardial irritability
* If LV compromised, ↓CO and myocardial ischemia
50
What hormones experience a decrease in response to chronic pain?
**Anabolic Hormones**
- Insulin
- Testosterone
51
What hormones experience an increase in response to chronic pain?
**Catabolic hormones**
- Catecholamines
- Cortisol
- Glucagon
52
Aside from anabolic and catabolic hormonal disregulation, what other effects does chronic pain have on the endocrine system?
- Negative nitrogen balance
- Carbohydrate intolerance
- Increases renin, aldosterone, angiotensin
53
How does pain affect the Hematologic system?
Pain causes a stress-related response that leads to hypercoagulability via:
- Increased platelet adhesiveness
- Reduced fibrinolysis
54
Which of the following is **NOT** an opioid receptor type?
- Mu
- Sigma
- Delta
- Kappa
Sigma
55
Which of the following statements is/are TRUE concerning the actions of opioids?
- They lead to an increase in Ca++ permeability in the axon terminal of the **primary** neuron.
- They lead to a decrease in K+ permeability in the axon terminal of the **primary** neuron.
- They lead to an increase in K+ permeability in the dendrite of the **secondary** neuron.
- They lead to an increase in K+ permeability in the dendrite of the **secondary** neuron.
- K+ permeability is not affected in the **primary** neuron, just the dendrite of the secondary neuron. More K+ channels opening via GPCR binding lead to hyperpolarization and less pain signals being sent to the brain!
## Footnote
Opioids also **decrease** (not increase) permeability of Ca++ in the primary neuron axon terminal by closing Ca++ channels via GPCR, leading to less EPSPs (less glutamate and Substance P being sent to secondary neuron).
56
Which of the following is **NOT** a therapeutic or S/E of opioids?
- Analgesia
- Diarrhea
- Respiratory Depression
- Pupillary Depression
- Antidiuresis
Diarrhea
## Footnote
Mu2 receptors in the stomach slow peristalsis, leading to constipation not diarrhea.
