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PHY V > Pain And Temperature > Flashcards

Pain And Temperature Flashcards

1
Q

ALS

  1. 2 other terms
  2. Organization
A

Anterolateral System Pathway

  1. Aka spinothalamic tract or ventrolateral system
  2. Somatotopic organization
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2
Q

DCML vs. ALS in terms of:

  1. Fibers
  2. Velocity
  3. Spatial orientation
  4. Transmitted signal?
A
  1. Fibers
    DCML: Large, myelinated
    ALS: Small myelinated and unmyelinated
  2. Velocity
    DCML: 30-110 m/s
    ALS: few meters to 40 m/s
  3. Spatial orientation
    DCML: High degree
    ALS: Small degree
  4. Transmitted signal?
    DCML: Sensory info that must be transmitted rapidly with temporal and spatial fidelity
    ALS: Ability to transmit broad spectrum of sensory modalities
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3
Q

An unpleasant sensory (objective) and emotional (subjective) experience associated w/ an actual or potential tissue damage or described in terms of such damage

A

Pain

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4
Q

Define the ff:

  1. Nociception
  2. Allodynia
  3. Analgesia
  4. Anesthesia
  5. Hypo/hyperalgesia
  6. Hypo/hyperesthesia
  7. Paresthesia
  8. Neuralgia
A

Nociception  neural responses to traumatic or noxious stimuli
Allodynia  perception of non-noxious stimulus as pain
Analgesia  absence of pain
Anesthesia  absence of sensation
Hypo/hyperalgesia  diminished/increased response to noxious stimulation
Hypo/hyperesthesia  decreased/increased cutaneous sensation
Paresthesia  abnormal sensation perceived without an apparent stimulus
Usually described as numbness, tingling, pins and needles, or pricking
Usually arises from nerve compression or damage
Neuralgia  pain in the distribution of a nerve or a group of nerves

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5
Q

Types of Pain?

A

Fast

  • Felt w/in 0.1 second
  • Sharp, pricking, acute, electric
  • Felt in the skin and not felt in most deep tissues of the body

Slow

  • Begins after x > 1 s
  • Slow burning, aching, throbbing, nauseous, chronic
  • Felt in both skin and almost any deep tissue or organ
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6
Q

When we’re talking about pain, which type of receptor are we referring to?

A

Free nerve endings

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7
Q

Three types of stimulus? Which constitute the fast pain? Slow pain?

A
  1. Mechanical
  2. Thermal
  3. Chemical

Mech + Thermal = Fast Pain

Mech + Thermal + Chemical = Slow pain

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8
Q

Fast vs. Slow Pain Pathway?

A

What’s the difference between the two - fast and slow pain pathway?
Neospinothalamic pathway
>Utilized by your mechanical or thermal stimuli
>NT: Glutamate
>Observed by your Adelta fiber (which is said to be myelinated as compared to your C fiber)
>From the periphery, it will terminate in your lamina I (termed as lamina marginalis in your dorsal horn of your spinal cord). From the lamina I, it will then cross immediately to the other side to terminate to follow your ALS, your spinothalamic tract then it would terminate majority in your thalamus (or vertebrobasal complex) and a few fibers will terminate in your brainstem
>Accurate localization (pag sinampal, alam mo sinampal sa area na yun)

Paleospinothalamic pathway
>Paleo = slow
>Like dinosaurs na malalaki = slow gumalaw
>Usually, it’s your chemical stimuli
>NT: Glutamate & Substance P
>C fiber (small and unmyelinated)
>Terminates in lamina II and II
>From your periphery, it would terminate in your lamina II and III termed as your substantia gelatinosa. And then to your lamina V (which is also located in your dorsal horn). Then after terminating there, synapsing or making connections here, it would cross immediately to follow your spinothalamic tract then it would terminate widely in your brainstem and only a handful, 1/10 to ¼ will pass all the way to your thalamus (reticular areas located in your brainstem) directly.
>Localization imprecise (e.g. dysmenorrhea - can’t localize where exactly is the pain)
*Malaking dinosaurs, mabagal lumakad

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9
Q

What is “Double Pain Sensation”?

A

A painful stimulus stimulates both fast pain pathway and slow pain pathway.

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10
Q

4 Elements of Pain Processing

A

Elements of Pain Processing
Transduction
-What is transduction? This is where you transform your electrical, chemical, or mechanical stimulus to electrical kasi kailangan niya ma-transmit through your NS
-Your noxious stimuli are converted into an AP

Transmission

- Or conduction
- When you transmit that from the periphery towards your spinal cord through your nerve fibers
- In other books, hinihiwalay pa nila yan. You have conduction from the peripheral fibers then nagiging transmission siya pagdating sa spinal cord. Pero in other books, pinag-isa na lang nila yan. 		-Pinagkaiba lang nila (Conduction and Transmission): NT and location where the process is occuring (Yung isa spinal cord, yung isa sa peripheral fiber)

Modulation
-It alters your afferent neural transmission.
-Most common site: Dorsal horn (most common site)
-Ano nangyayari sa modulation? It can either Inhibit or augment that incoming signal
Perception
-Higher centers
-The final common pathway
-It integrates all information

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11
Q

Chemical Mediators of Transduction and Transmission

A

Tissue damage -> release of algogenic substances -> vasodilation -> further release of plasma proteins -> senstizes receptor (lower threshold) -> 1’ Hyperalgesia

Pain pathway becomes excessively excitable (you lower the threshold for excitation)
1. Primary hyperalgesia
At the site of injury

  1. Secondary hyperalgesia
    Outside the area of injury
    And usually, lesions in the spinal cord or thalamus (diba dorsal horn)
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12
Q

Analgesia system

A
  • Body’s own mech to suppress pain.
  • Endogenous opioids utilizes 3 major pathways:
    1st: Signal originates from periaqueductal gray and PVN -> secrete your enkephalin

2nd: —> enkephalin would be received by raphe magnus nucleus (lower pons and upper medulla) and your nucleus reticularis paragigantocellularis (medulla) -> enkephalin
3rd: —> activate pain inhibitory complex (located in the dorsal horn) & the NT responsible for this is serotonin

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13
Q

Opioids

  1. 3 main receptors?
  2. Mechanism of action/s
  3. Derived from?
A
  1. Mu, delta, kappa
    2.
    A. Inhibit Ca2+ influx presynaptically -> decrease release of NTs and Neuropeptides

B. Enhances K+ efflux postsynaptically -> Hyperpolarization of the cell and dec in transmission

C. Activation of descending inhibitory pain circuit via inhibition of GABAergic transmission in the brainstem

D. PERIPHERAL:
Inhibits release of pronociceptive and proinflammatory substances.

  1. Derived from 3 large proteins: Pro-opiomelanocortin, proenkephalin, prodynorpo
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14
Q

Stress-induced analgesia

A

Stressful situations may cause activation of the analgesia system and release of endogenous opioids. E.g. NorE and Endogenous Cannabinoids

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15
Q

Pain felt in a part of the body that is fairly remote from the tissue causing the pain. What is behind this effect?

A

Referred Pain.
2 theories:
1. Convergence-Projection
>Somatic + Visceral fibers synapse at the same location in your dorsal horn of your SC so no delineation where pain is from

  1. Convergence-Facilitation
    - Use the same model but receptors/impulses from visceral fibers facilitate somatic fibers as well
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16
Q

Visceral Pain.

  • When do you feel it? -Transmitted through?
  • Localized in?
A
  • Highly localized damage to the viscera seldom causes pain (only if whole organ or stimulus is diffused!!!)
  • Transmitted through your small type C pain fibers
  • Localized in the dermatomal segment of origin
17
Q 
True Visceral vs. Parietal pathway?
In terms of:
1. Transmitted via?
2. Area
3. Characterization of pain
A

1.
True Visceral (TP): ANS
Parietal (P): Local spinal nerves

2.
True Visceral (TP): Referred to areas far from source
Parietal (P): Localized directly over the source of pain

3.
True Visceral (TP): Pain poorly characterized
Parietal (P): Pain well characterized
18
Q

Pain management is?

A

Multimodal.

19
Q

Surgical Stress Response

A

Neuroendocrine response due to stress causing an increase in the catabolic hormones leading to hyperglycemia, negative nitrogen balance, muscle wasting, poor wound healing, immunocompetency

Thus, we give meds to avoid this response.

20
Q

Gate control theory

A

-States that simultaneous non-painful tactile input suppresses painful input from the same area.
-Mechanism:
>Non-painful tactile stimulus leads to activation of your large A beta fiber which synapse with your C fiber (fiber for pain) in one location. Thus, if you do more of the non-painful tactile input simultaneously than the painful input, then you are flooding the gate. Also, the A beta fiber activates the inhibitory interneuron which inhibits the signal transmission coming from your C fiber.

21
Q

Temperature receptor types?
>Which is greater in number - cold or warmth?
>Which utilizes a definitive receptor?
>Fiber

A
  1. Cold receptors
    - greater in number (3-10x)
    - with a definitive cold receptor
    - A beta nerve endings + some type C free nerve endings
  2. Warmth receptors
    - fewer
    - presumed to be free nerve endings
    - Type C
  3. Pain receptors
    - stimulated by extremes
22
Q

Stimulation of Thermal Receptors?

A

> Different gradations of thermal sensations is determined by the relative degrees of stimulation of the different types of endings

(In degrees Celsius)
5-15 = combination of cold and pain
24 = no pain aspect
15-25 = becomes cold only
30 = combination of cold and warmth
40-45 = mainit
More than 45 = painful
23
Q

Adaptation and Summation of Thermal Receptors

A

Adaptation

  • Respond markedly to changes in temperature in addition to being able tor respond to steady states of temperature
  • Receptors adapt to a greater extent but never 100%

Summation
-The more receptors stimulated at the same time -> more you’ll feel the stimulus

24
Q

Mechanism of Stimulation

  1. Transmitted in?
  2. Mechanism?
A
  1. Pathways parallel to pain
  2. From the tract of Lassauer -> terminate mainly in laminae I-III of dorsal horns -> it’ll cross to the opposite ALS tract -> terminate in both reticular areas of the brainstem and ventrobasal complex -> few signals relayed to cerebral somatic sensory cortex from the vasobentral complex

PHY V (12 decks)

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