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N552 Patho > Pain > Flashcards

Pain Flashcards

0
Q

Dysesthesia

A

Any abnormal sensation described as unpleasant by the patient

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1
Q

What is pain?

A

What Dr. E puts us through everyday.

An unpleasant sensory and emotional experience associated with actual/potential TISSUE damage, a protective mechanism

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2
Q

Hyperalgesia vs. Hyperpathia vs. Hyperesthesia

A

Hyperalgesia: Exaggerated pain response from a normally painful stimulus, usually includes aspects of summation with repeated stimulus of constant intensity and after-sensation
Hyperpathia: Abnormally painful and exaggerated reaction to a painful stimulus, related to hyperalgesia
Hyperesthesia: Exaggerated perception of TOUCH stimulus

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3
Q

Allodynia

A

Abnormal perception of pain from a normally non-painful stimulus, usually has elements of delay in perception

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4
Q

Anesthesia vs. Analgesia?

A

Anesthesia: reduced perception of sensation (touch)
Analgesia: reduced perception of pain stimulus

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5
Q

Hypoalgesia

A

Decreased sensitivity and raised threshold to painful stimuli

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6
Q

Pallanesthesia vs. Paresthesia?

A

Pallanesthesia: loss of perception of vibration
Paresthesia: mainly spontaneous abnormal sensation that is not unpleasant, “pins and needles”

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7
Q

Causalgia

A

Burning pain in the distribution of one or more peripheral nerves

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8
Q

Protopathic vs. Epicritic sensation?

A

Protopathic: noxious, painful
Epicritic: non-noxious, ex. pressure, light touch, temperature discrimination

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9
Q

Fast pain vs. slow pain: myelination, which fibers

Note: all pain receptors are non-adapting (or adapt very little)

A

Fast: thinly myelinated A-delta fibers, 0.1 sec to feel, ex: sharp, pricking, electric pains
Slow pain: unmyelinated C pain fibers, felt after 1 sec and increases slowly over seconds to minutes, felt in the deeper tissue, this pain is associated with tissue destruction, ex: slow burning aching, throbbing, chronic

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10
Q

Mechanical vs. thermal vs. chemical: are these pathways of fast pain or slow pain or both?

A

Mechanical: both
Thermal: both
Chemical: slow only
Chemicals that cause pain: bradykinin (the most painful), acetylcholine, prostaglandins, substance P, and proteolytic enzymes, by increasing permeability to ions such as K

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11
Q

Nociception: What are Transduction, Transmission, Modulation, Perception?

A

Transduction: noxious stimuli converted to electric activity at sensory nerve endings
Transmission: propagation of impulses along A-delta and C fibers to the dorsal horn of the spinal cord and to the brainstem, thalamus, and cortex
Modulation: physiologic process of suppressing or facilitating pain, can happens in the brain but can also happen in the spinal cord (interneuron signals)
Perception: what is perceived as pain using these 3 interactions

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12
Q

First order neurons vs. second order neurons vs. third order neurons in the ascending (afferent) pathway

A

First order neurons send axons to the spinal cord via the dorsal (sensory) root, may synapse with second order neurons, inter-neurons, SNS neurons, or ventral horn (motor) neurons
Second order neurons are in the gray matter of ipsilateral dorsal horn, they cross midline
Third order neurons are in the thalamus and send fibers to somatosensory areas in the parietal cortex and superior wall of the sylvian fissure. These neurons are responsible for perception and localization of pain

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13
Q

What is an alternate pain pathway that can cause insomnia due to pain?

A

Spinoreticular tract

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14
Q

What alternate pain pathway activates anti-nociceptive, descending pathways?

A

Spinomesencephalic (recognizes your own opioids)

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15
Q

What do the spinohypothalamic and spinotelencephalic tracts do?

A

These are stimulated by the slow pain pathways, they activate the hypothalamus and evoke emotional behavior

16
Q

What happens in the neospinothalamic tract?

A

This is the FAST pain pathway. First order neurons on A-delta fibers enter lamina I and V of the dorsal horn of the spinal cord. They synapse with second order neurons which cross the midline through the anterior white matter and pass up the anterolateral (spinothalamic) column. Some fibers terminate on reticular formation, but most travel to the Ventrobasal Complex of the thalamus. Third order neurons go to the somatosensory cortex (perception happens).

17
Q

What is the Paleospinothalamic pathway?

A

SLOW pain pathway. First order neurons via C fibers enter lamina 2 and 3 of the dorsal horns (substantia gelatinosa) synapse with second order neurons which make connections with lamina 4-8 without crossing. Some neurons join fibers from the fast pathways, crossing to the opposite side. They terminate in the thalamus, medulla, pons, tectal area and periaquaductal grey.

18
Q

How does localization differ between fast and slow pain?

A

Fast is localized easily, slow pain is poorly localized

19
Q

What is the role of the periaquaductal grey matter in pain?

A

It descends modulation of pain and also plays a role in defensive behavior (guarding)
It is the epicenter of analgesia
It is the cerebral aqueduct within the midbrain

20
Q

What is the role of the nucleus raphe magnus in pain?

A

It is afferently stimulated from axons in the spinal cord and cerebellum. The main function is pain MEDIATION, it sends projections to the dorsal horn of the spinal cord to inhibit pain (inhibits release of chemicals such as substance P or bradykinins)

21
Q

Glutamate and Substance P: are they chemical mediators involved in fast pain or slow pain?

A

Glutamate (excitatory neurotransmitter) is secreted at A-delta pain (fast pain) nerve fiber endings
Substance P is the slow-chronic neurotransmitter with type C nerve endings.

22
Q

How are NMDA receptors, AMPA receptors, and NK-1 receptors related to ACUTE pain?

A

NMDA channels are plugged by magnesium (mag can be given to relieve pain)
Chemical mediators are released with pain response. Substance P activates NK-1 receptors (slow pain) and glutamine activates AMPA receptors (fast pain), causing depolarization of pain neurons, relayed to higher brain areas

23
Q

How do NMDA receptors and nitric oxide relate to the physiology of CHRONIC pain?

A

In response to intense/prolonged pain, neurons become sensitized and over-respond to pain signals. This depolarizes neurons so that mg ions exit the NMDA channel. The influx of calcium activates nitric oxide synthase (converts L-arginine to nitric oxide). Nitric oxide diffuses out and acts presynaptically and postsynaptically to release Substance P, glutamine, and other painful chemicals.

24
Q

What is the neuroendocrine response to acute pain?

A

Stress response
Secretion of catabolic hormones, release ACTH
Decrease anabolic metabolism, insulin (leading to hyperglycemia), and testosterone

25
Q

What is the cardiac response to acute pain?

A

Increase HR, BP, SVR, CO
MI, CHF, dysrhythmias
Decrease myocardial oxygenation (due to atelectasis)
Coronary artery constriction at high catecholamine levels
Serotonin release may induce coronary vasospasm
Increase plasma viscosity- platelet induced occlusion

26
Q

What are pulmonary responses to acute pain?

A

Increased metabolic response leads to increased oxygen consumption and CO2 production
Increased RR and minute ventilation
Decreased TV, VC, and FRC, leading to atelectasis (resting lung volume approaches closing volume), V/Q mismatch, hypoxemia

27
Q

How does visceral pain lead to urinary retention and ileus?

A

Increased sympathetic tone, increased sphincter tone, decreased gastric motility

28
Q

What are muscle spasms caused by?

A

Periosteal and somatic irritation that initiates reflex motor response

29
Q

What are COX-1 and COX-2?

A

COX-1 is an enzyme widespread through the body
COX-2 is an enzyme only active at the site of inflammation
Both COX 1 and 2 speed up prostaglandin production
This is why we use Cyclooxygenase Inhibitors during surgery, to inhibit prostaglandin synthesis

30
Q

In chronic pain causes, what is the central mechanism vs. the circle mechanism?

A

Central mechanism: lesions of peripheral nerve or roots cause the chronic pain (causalgias, phantom pain)
Circle mechanism: intense stimulation of nerve fibers activate internuncial neurons creating an abnormal reverberatory activity in a closed loop

31
Q

In chronic pain, why do minor injuries become intolerable?

A

Serotonin and endorphins become depleted

32
Q

What does does the WHO recommend for cancer pain?

A
  1. Nonopioid analgesic (ASA, acetaminophen, NSAIDS)
  2. weak oral opioids: codeine, oxycodone
  3. Stronger opioids: Morphine, hydromorphone
33
Q

What are these common adjuncts to cancer pain management helpful with? Corticosteroids and antidepressants

A

Corticosteroids: prevent release of prostaglandins and stimulate appetite
Antidepressants: potentiate narcotic analgesics, block reuptake of serotonin

N552 Patho (13 decks)

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