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Regional > Noception > Flashcards

Noception Flashcards

1
Q

How many neuronal pathways are there for pain? What are they?

A

Pain is conducted along three neuron pathways (first, second and third order neurons) that transmit noxious stimuli from the periphery to the cerebral cortex.

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2
Q

Where are the primary afferent neurons located?

A

Primary afferent neurons are located in the dorsal root ganglion which lie in the vertebral foramina at each spinal cord level.

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3
Q

Each neuron has a single axon that bifurcates, where are the two locates that the axon bifurcates to?

A

Each neuron has a single axon that bifurcates, sending one end to the peripheral tissues it innervates and the other into the dorsal horn of the spinal cord.

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4
Q

Where are the majority of the First order neurons?

A

The majority, enter the dorsal spinal root at each cervical, thoracic, lumbar, and sacral level

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5
Q

The pain fibers of the first order neurons in the head originate by which cranial nerves?

A

Pain fibers originating in the head are carried by the trigeminal (V), facial (VII), glossopharyngeal (IX), and vagal (X)

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6
Q

What is the pathway for the first order neurons in the head?

A

Each have specific ganglion which hold cell bodies of these nerves. The first order neurons in the ganglia (head) reach the brainstem and synapse with the second order neuron

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7
Q

How many rexed lamina does the spinal cord gray matter have?

A

Spinal cord gray matter is divided by Rexed into 10 lamina

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8
Q

What are the second order neurons??

A

Second order neurons are either nociceptive-specific or wide dynamic range (WDR)

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9
Q

What are the first six lamina of the dorsal horn?

A

First six makeup the dorsal horn, receive all afferent neural activity, represent the principle site for modulation of pain

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10
Q

What does Lamina I respond to?

A

Lamina I responds to nociceptive stimuli from cutaneous and deep somatic tissues

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11
Q

What does Lamina II contain?

A

Lamina II (substantia gelatinosa), contains many interneurons responsible for processing and modulating nociceptive input from cutaneous tissue. Major site of action for opioids

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12
Q

which Lamina is the major site of action for opioids and what is the most abundant receptor?

A

Lamina II aka substantia gelatinosa is the major site of action for opioids. Mu2 is the most abundant.

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13
Q

What does Lamina VII contain?

A

Lamina VII contains preganglionic sympathetic neurons

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14
Q

Which Lamina contains visceral afferents?

A

Lamina V and I contains visceral afferents

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15
Q

Which Lamina responds to both noxious and non noxious stimuli? and receives both somatic and visceral inputs?

A

Lamina V responds to both noxious and non noxious stimuli and receives both somatic and visceral inputs

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16
Q

What is the pathway of the Spinothalamic tract?

A

The spinothalamic tract Cross the midline to the level of origin to the contralateral side of the spinal cord

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17
Q

How many divisions are the spinothalamic tract divided into? what are they?

A

The spinothalamic tract are Divided into lateral and medial

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18
Q

What does the lateral spinothalmic tract project to?

A

Lateral spinothalmic tract projects—location,density,duration of pain in the ventral posteriorlateral nucleus of the thalamus

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19
Q

What does the medial spinothalmaic tract project to?

A

Medial spinothalamic tract projects—unpleasant emotional perception of pain in the medial thalamus

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20
Q

What is the Spinalreticular pain pathway?

A

Spinalreticular pain pathway- arousal and autonomic responses to pain

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21
Q

What is the Spinalmesencephalic pathway?

A

Spinalmesencephalic–anti-nociceptive descending pathways because of its projections in the periductal gray area

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22
Q

Where are the third order neurons located? were are they synapsed?

A

Third order neurons are Located in the thalamus

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23
Q

Where does the third order neurons send fibers to?

A

Send fibers to the somatosensory areas I and II in the post central gyrus of the parietal cortex and superior wall of the sylvian fissure

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24
Q

Which afferent nerve fibers are mylinated?

A

A and B fibers

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25
Q

Which afferent nerve fibers are nonmylinated?

A

C fibers

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26
Q

Which afferent nerve fibers are slow poorly localized?

A

C fibers

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27
Q

Which afferent nerve fibers are fast, sharp well-localized sensation?

A

A delta fibers

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28
Q

Afferent “A” nerve fibers are defined into what?

A

Alpha, Beta, Gamma, and Delta

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29
Q

Each afferent nerve fibers innervation provides a specific function and the classification of these fibers are based on diameter and velocity of conduction. TRUE or FALSE?

A

TRUE.

Each afferent nerve fibers innervation provides a specific function and the classification of these fibers are based on diameter and velocity of conduction.

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30
Q

Which afferent nerve fibers are sympathetic preganglionic?

A

B fibers

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31
Q

Which afferent nerve fibers are sympathetic post ganglionic??

A

C fibers

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32
Q

Which afferent nerve fibers are muscle spindle motor to skeletal?

A

A alpha fibers

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33
Q

Which nerve fibers are touch and pressure afferents?

A

A Beta fibers

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34
Q

Which afferent nerve fibers are motor to muscle spindle?

A

A gamma fibers

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35
Q

Which afferent nerve fibers are mechanoreceptors and nociceptors?

A

A delta and C fibers

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36
Q

Which afferent nerve fiber has the fastest velocity?

A

A alpha with a mean velocity of 100m/sec

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37
Q

Which afferent nerve fiber has the slowest velocity?

A

C fibers with a mean velocity of 1m/sec

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38
Q

Which afferent nerve fiber has the greatest diameter?

A

A alpha fibers

39
Q

Which afferent nerve fiber has the smallest diameter?

A

C fibers

40
Q

What do Mechanonocicieptors respond to?

A

Mechanonociceptors– respond to pinch and pinprick

41
Q

What do Silent Nociceptors respond to?

A

Silent nociceptors—respond to inflammation

42
Q

What doe Polymodal mechohear nocicieptors respond to?

A

Polymodal mechoheat nociceptors—respond to heat and pressure

43
Q

What do the free nerve endings of nociception sense?

A

Free nerve endings sense heat, mechanical, and chemical damage

44
Q

What are considered alogens?

A

bradykinin,histamine,serontonin,5-HT,K+, some prostaglandins, and possibly ATP

45
Q

What do Somatic nocicpetors include?

A

Somatic nociceptors include: muscle tendon, fascia, bone

46
Q

The cornea and thooth pulp are innervated by which fibers?

A

Cornea and tooth pulp are innervated by A delta and C fibers

47
Q

Visceral organs are innervated by which fibers

A

Visceral organs—silent nociceptors

48
Q

Nociceptive C fibers travel from the esophagus, larynx, and trachea with the vagus nerve to enter the nucleus solitarius in the brainstem

A

Nociceptive C fibers travel from the esophagus, larynx, and trachea with the vagus nerve to enter the nucleus solitarius in the brainstem

49
Q

Where is substance P released?

A

Substance P—released by first order neurons both peripherally and in the dorsal horn

50
Q

What facilitates transmission of the pain pathway?

A

Substance P transmission in pain pathways via NK-1 receptor activation

51
Q

Chemical mediators of pain sends collaterals to what parts of the body?

A

Sends collaterals to blood vessels, sweat glands, hair, mast cells in the dermis

52
Q

What does chemical mediators of pain do?

A

Degranulates histamine and serotonin from platelets, is a vasodilator, chemoreactor for leukocytes

53
Q

What are the peripheral modulation of pain?

A
  • Release of alogens from damage tissues
  • Histamine from mast cells, basophils,platlets
  • Serontonin from mast cells, platelets
  • Factor XII allows the release of bradykinin
54
Q

How does arachidonic cascade begin?

A

Glutamine and asparate wind-up activation of NMDA and non-NMDA receptors—this increases intracellular calcium in spinal neurons and activates phospholiapaseA2

Phospholipase A2 on phospholipids produce prostaglandins and form arachidonic acid and the cascade begins

55
Q

What converts arachidonic acid to prostacylcin?

A

Cyclooxygenase coverts arachidonic acid to prostacyclin and PGE2

This potentiates the edema from bradykinin

56
Q

What converts arachidonic acid to leukotrines?

A

Lipoxygenase pathway converts Arachidonic acid into leukotrienes

57
Q

What inhibits prostaglandin production?

A

Corticosteriods inhibit prostaglandin production through blockage of phospholipase A2 activation

58
Q

What inhibits cyclooxygenase?

A

ASA and NSAID inhibit cyclooxygenase

59
Q

What are the three points in central modulation?

A
  1. Wind up and sensitization of second order neurons—increase frequency of repetitive prolong discharge even after C fibers input has stopped
  2. Receptor field expansion—Dorsal horn neurons increase their receptive fields to become more responsive to stimuli (noxious or not)
  3. Hyperexcitability of flexion reflexes.
60
Q

What is the pathway of the descending tract in regards to the modulation of pain??

A

Impulses arising in the periventricular/periaquaiductal gray matter of the brainstem are transmitted through the raphe magnus to the substantia gelatinosa (lamina I and II) by way of the descending dorsolateral funiculus (responsible to modulating pain)

61
Q

What happens to the action potentials arriving at the substantia gelatinosa from the descending tract of pain modulation?

A

Action potentials arriving at the substantia gelatinosa activate enkephalin neurons. The release of enkephalin decreases the release of substance P, thereby reducing the number of pain impulses ascending in the lateral spinothalamic tract. Also, action potentials descending in the dorsolateral funiculus hyperpolarize cell bodies of the second neurons in the pain pathway, thereby decreasing the number of action potentials in the ascending lateral spinothalamic tract. The descending dorsolateral funiculus modulates pain.**

62
Q

With modulation of pain, what parts of the brain do IV opioids effect?

A

Intravenous opioids act in other sites in the brain(limbic system,hypothalamus,and thalamus) produce supra spinal analgesia is mediated primarily by mu-1 receptors

Opioids act in a complex fashion to decrease the perception of pain and decrease the response to pain

63
Q

How does IV opioids produce analgesia in the descending pathway?

A

Intravenous opioids produce analgesia in part by initiating action potentials in the descending dorsolateral funiculus.

Opioids act in a complex fashion to decrease the perception of pain and decrease the response to pain

64
Q

How does spinal analgesia work in the modulation of pain??

A

Spinal analgesia, mediated by mu-2 receptors, occurs when the number of pain impulses passing through the substantia gelatinosa is decreased.

65
Q

What does Preemptive analgesia accomplish??

A
  • Induces an effective analgesic state prior to surgical trauma
  • Infiltration of site with local anesthetic, central neural blockade, administration of effective opioids, NSAIDs, or ketamine
  • This attenuates (stops) peripheral and central sensitization to pain
  • The use of preemptive analgesia may reduce the postoperative analgesic requirements
66
Q

What is acute pain?

A

Defined as that which is caused by noxious stimulation due to injury, a disease process, or abnormal function of muscle or viscera. It is nearly always nociceptive.

67
Q

What are the two types of acute pain?

A

Two types of acute pain:
somatic and visceral

(A delta fiber, fast, mylinated)

68
Q

What are the types of somatic acute pain?

A

Superficial somatic and deep somatic

69
Q

what are the acute superficial somatic pain?

A

Superficial somatic -skin, subcutaneous, mucous membranes

Well localized-sharp, pricking, throbbing, burning

70
Q

What are the acute deep somatic pain?

A

Deep somatic – muscles, tendons, joints, bones

Less well localized, dull, aching

71
Q

What is the visceral acute pain?

A

Disease process or abnormal function of an internal organ or its covering (eg, parietal pleura, pericardium, or peritoneum).

72
Q

How many types of visceral acute pain are there? and what are they??

A

Four types:
true localized visceral,
true localized parietal, referred visceral, referred parietal

73
Q

What are true localized visceral acute pain?

A

True visceral is dull, diffuse, midline and is associated with abnormal sympathetic or parasympathetic activity (N/V, sweating, changes in B/P and HR )

74
Q

What are true localized parietal acute pain?

A

True parietal is sharp and localized

75
Q

Where is the acute pain from parietal surfaces of the peripheral diaphragm referred to?

A

parietal surfaces of the peripheral diaphragm” -> is referred to the chest or upper abdominal wall**

76
Q

Where is the acute pain from the peritoneum or pleura over the central diaphragm referred to?

A

the “peritoneum or pleura over the central diaphragm” -> is referred to the neck and shoulder

77
Q

Sympathetic activation increases efferent sympathetic tone to where? and releases catecholamines from what?

A

Sympathetic activation increases efferent sympathetic tone to all viscera and releases catecholamines from the adrenal medulla.

78
Q

What causes a response that results from an increased sympathetic tone and hypothalamic mediated reflexes?

A

The hormonal response results from increased sympathetic tone and hypothalamically mediated reflexes

79
Q

What happens to the cardiovascular system with acute pain?

A
  • hypertension, tachycardia, enhanced myocardial irritability, increased SVR
  • Increased CO, may be decrease with patients who have compromised ventricular function
  • Increased myocardial oxygen demand, therefore, pain can aggravate or precipitate myocardial ischemia
80
Q

What happens to the respiratory system with acute pain?

A

Increase in total body O2 consumption and CO2 production increases minute ventilation

81
Q

What happens to the gastrointestinal and urinary system with acute pain?

A
  • Enhanced sympathetic tone increases sphincter tone and decreases intestinal and urinary motility, promoting ileus and urinary retention
  • Hyper-secretion of gastric acid promotes stress ulceration, together with deceased motility, predisposes the patients to severe aspiration pneumonitis
82
Q

What happens to the endocrine system with acute pain?

A
  • increase in catabolic hormones (catecholamines, cortisol, and glucagon) and decrease in anabolic hormones (insulin and testosterone)
  • Develops a negative nitrogen balance, carbohydrate intolerance and increased lipolysis
  • Increase in cortisol with increase in renin, aldosterone, angiotensin, and antidiuretic hormone results in NA retention and water retention
83
Q

What happens to the immune system with acute pain?

A

Produces leukocytosis with lymphopenia, predisposes patients to infection

84
Q

What happens to the hematologic system with acute pain?

A

Increases in platelet adhesiveness, reduced fibrinolysis, and hypercoagulability

85
Q

What happens to perception with acute pain?

A

Anxiety, sleep disturbance—if duration of pain is prolonged depression and anger

86
Q

True or false?
MODERATE TO SEVERE ACUTE PAIN, REGARDLESS OF SITE, CAN AFFECT NEARLY EVERY ORGAN FUNCTION AND MAY ADVERSLY INFLUENCE POSTOPRATIVE MORBIDITY AND MORTALITY

A

True.
MODERATE TO SEVERE ACUTE PAIN, REGARDLESS OF SITE, CAN AFFECT NEARLY EVERY ORGAN FUNCTION AND MAY ADVERSLY INFLUENCE POSTOPRATIVE MORBIDITY AND MORTALITY

87
Q

What is Chronic pain?

A

Chronic pain is defined as that which persists beyond the usual course of an acute disease or after a reasonable time for healing to occur.

88
Q

What is the timeframe that classifies chronic pain?

A

This period varies between 1-6 months

89
Q

What can Chronic pain be?

A

Chronic pain may be nociceptive, neuropathic, or a combination of both

90
Q

What are some characteristics of Chronic pain?

A
  • Patients with chronic pain often have an attenuated or absent neuroendocrine response
  • Psychological mechanisms, sleep and affective disturbances
  • Neuropathic pain classically spontaneous, has a burning sensation, and is associated with hyperpathia
91
Q

What are some common forms of Chronic pain?

A

Musculoskeletal disorders, chronic visceral disorders, lesions of the peripheral nerves, nerve roots, dorsal root ganglia , phantom limb pain, lesions of the central nervous system (stroke, spinal cord injury, multiple sclerosis) and cancers invading the nervous system

92
Q

What are the peripheral-central and central mechanisms for chronic pain?

A
  1. Spontaneous self-sustaining neuronal activity in the primary afferent neuron (neuroma)
  2. Marked mechanosensitivity associated with chronic nerve compression3. Short circuits between pain fibers, following demyelination, activating nociceptors by nonnoxious stimuli
  3. Reorganization of receptor fields in the dorsal horn neurons
  4. Spontaneous electrical activity in the dorsal horn cells or thalamic nuclei
  5. Release of segmental inhibition in the spinal cord
  6. Loss of descending inhibitory influences that are dependent on normal sensory input
  7. Lesions of the thalamus or other supraspinal structures
93
Q

What are the treatments for chronic pain?

A

Treatment includes a wide variety of blocks, COX inhibitors, opioids, antidepressants, neuroleptic agents, anticonvulsants, corticosteroids and systemic local anesthetics

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