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Drug Action III > Pain and Neuropathy (Physiology) - Block 2 > Flashcards

Pain and Neuropathy (Physiology) - Block 2 Flashcards

1
Q

What is pain?

A

Unpleasant sensory and emotional experence associated with actual or potential tissue damage
* subjectively defined

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2
Q

How does pin initiate a stress response?

A
  1. hormonal and metabolic change
  2. HPA axis and sympathetic NS
  3. Neuroendocrine response induces catabolic state
  4. Increases oxygen delivery and organ perfusion
  5. Increased plasma glucose, proteins , and free fatty acids
  6. Water retention by kidnes
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3
Q

What are the negative effects of stress response?

A
  1. HTN and tachycadia
  2. Hyperglycemia, negative nitrogen, immunosuppression
  3. Hypercoag state
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4
Q

What is nociceptive pain?

A

Physiologic response to heat, cold, viration, stretch, or chemicals released from damaged cels that may cause tissue damage
* a protective biological response

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5
Q

What is the difference between somatic and visceral pain?

A

Somatic: aching, throbbing, dull pain from skin, muscle, and joints
Visceral: squeezing, cramping, dull, and deep pain from organ

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6
Q

What is neuropathic pain?

A

Nerve cell dysfunction in the PNS and/or CNS

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7
Q

What is the difference between acute and chronic pain?

A

Acute: hours-weeks
Chronic: occurs after resolution of an acute infury or inflammation

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8
Q

What is transduction?

A

COnversion of noxious thermal, mechanical, chemical stimulus into a nerve impulse

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9
Q

What is transmission?

A

Transfer of a noxious peripheral stimulus to the CNS

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10
Q

What is modulation?

A

Peripheral and central neurotransmitters and other substances that enhance or dampen the transduction and transmission of noxious stimulus

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11
Q

What is perception?

A

Cognitive appreciation of a noxious stimulus

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12
Q

What is the function of afferent neurons?

A

Detection of a noxious thermal, mechanical, or chemical stmulus

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13
Q

What is a nociceptors?

A

Free peripheral endings of sensory neurons

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14
Q

What is the difference between somatic and visceral nociceptors?

A

Somatic: Respond to thermal, mecanical, chemical stimulus
Visceral: Stimulated by inflammation, ischemia, dilation, stretch, and spasm

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15
Q

What is the function of afferent nociceptive fibers with VGSCs?

A

Transmission of noxious stimulus to the CNS

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16
Q

What are A delta fibers?

A

Large myelinated fibers that have a low stimulation threshold and a fast conduction velocity

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17
Q

Differentiate the typws of A delta fibers?

A

Type 1: High-threshold mechical nociceptors that respond to both chemical and mechanical stimuli (first and fast and ends when the stimulus is removed)
Type 2: Low-heat threshold and high mechanical threshold (fast for heat stimulus)

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18
Q

What are C fibers?

A

Smaller unmyelinated, polymodal, mechno-heat-responsive nociceptors that have a slow conduction velocity (second or slow pain such as throbbing, burning, aching)

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19
Q

What happens if a pain threshold of fibers is reached?

A

Action potetial is generated

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20
Q

How is an action potential produced by nociceptors?

A
  1. Nociceptor carries the noxious stimulus to the CNS
  2. Conscious percepton of pain
  3. Nociceptors show no adaptation and depolarize in portion to the intensity and frequency of the stimulus
  4. Activation of:
    * VOltage gated sodium and potassium channels -> generation and conduction of action potential
    * VOltage gated calcium channels -> release of neurotransmitters for transmission of pain or mediation
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21
Q

What is the roles of upregulation of calcium channels in C fibers?

A

Hyperalgesia: exaggerated and prolonged response to pain
Allodynia: perception of pain from a stimulus that doesn’t usually cause pain

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22
Q

Describe the structure of a-delta and c afferents?

A
  1. cell bodies from the trunk and limbs located in the dorsal root ganglion
  2. cell bodies from the fce are located in the trigeminal ganglion
  3. Both have a peripheral branch and central axonal branch
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23
Q

What are the layers of gray matter in the spinal cord called?

A

Rexed laminae
* dorsal horn contains laminae I-VI

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24
Q

What are the first-order neurons invlved with transmission of pain?

A

Aδ fibers synapse with second-order neurons.

C fibers primarily synapse with interneurons that synapse with second-order neurons.

Aβ fibers may be involved in the transmission of chronic pain.

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25
Q

What are the second-order neurons invlved with transmission of pain?

A

nociceptive-specific neurons: small receptive fields and respond only to nociceptive stimuli
Wide dynamic range (WDR) neurons: Have complex receptive fields and respond to nociceptive and tactile input.
Excitatory neurotransmitters in the dorsal horn

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26
Q

What are the receptors used for glutamate signalling?

A

AMPA
NMDA

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27
Q

What is the inhibitory neurotransmitter?

A

GABA adn glycine

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28
Q

What are the excitatory neurotransmitters?

A

GLutamate, aspartate, VIP, substance P, CCK, CGRP

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29
Q

What are the tracts that ascend second-order neurons to the thalamus?

A
  1. Spinothalmic tract (STT)
  2. Spinoreticular tract (SRT)
  3. Spinomesencephalic (SMT)
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30
Q

What are thrid order neurons?

A

Transmit novious impulses from the thalamus to the primary somatosensory areas of the cortex for the perception of pain

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31
Q

What are the primary neurotransmitters?

A

NE, seratonin

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32
Q

What stimulates the releae of supraspinal and spinal endogenous opiods?

A

Descending tracts

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32
Q

What are the peripheral influences of modulaing pain?

A
  1. injuredtissue releases substance p and glutamate which activate nociceptors
  2. mediators are released to tissue -> inflammation
  3. peripheral sensitization -> primary heperalgesia
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33
Q

What are the functions of glial cells?

A

decreases the effectiveness of the inhibitory function of te descending tracts

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34
Q

What is central sensitization?

A

Increased excitability of the dorsal horn -> amplification of the novious stimulus

Excessive or continued activation of the dorsal horn -> abnormal response to sensory input and secondary hyperalgesia

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35
Q

What influences the perception of pain?

A
  1. Emotional or psychological stress
  2. Cultural and religious beliefs
  3. Prior experience with pain
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36
Q

What is a pain threshold?

A

The minimum intensity of a noxious therma, mechanical, or chemical stimulus that activates nociceptors and is perceived as painful

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37
Q

How is the pain threshold modulated in the periphery?

A

Increased release of chemical mediators that increase/decrease the threshold

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38
Q

How is the pain threshold modulated in the central?

A

Exictaory/inhibitory neuortransmitters that increase/decrease the threshold in the dorsal horn and thalamus

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39
Q

What is an increased excitability of neurons?

A

Sensitization

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40
Q

What is central sensitization?

A

Increased excitability of neurons in the CNS

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41
Q

What responses results from central sensitization?

A
  1. Tactile allodynia
  2. Secondary hyperalgesia
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41
Q

What is pain tolerance?

A

Amount of pain an individual can take or tolerate

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42
Q

How do you increase pain tolerance?

A

Activation of large somatic fibers

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43
Q

What is the gate control theory of pain?

A

Nnpainful input closes a pain gate to painful input in the dorsal horn and prevents the transmission of pain to the CNS

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44
Q

When there is no imput from A-delta and C fibers what happens?

A

inhibitory interneurons in the dorsal horn block activation of second-order neurons, closing the pain gate

45
Q

Why is it important for large somatic nerve fibers to activate inhibitory interneuorons?

A

To prevent smaller pain fibers from activating second-order neurons

46
Q

What type of pain is difficult to pinpoint?

A

Visceral pain

47
Q

What are the types of acute nociceptive pain?

A

Somatic and visceral

48
Q

What is a soft tissue injury?

A

Damages of muscles, ligaments tendons, joint structure (pain, swelling, bruising, damage)

49
Q

What are the types of soft-tissue injuries?

A
  1. Strains
  2. Sprains
  3. Contusions
  4. Bursitis
  5. Tendonitis
  6. Synovitis
50
Q

What is the difference between the strain and sprain?

A

Strain: Injury to muscle or muscle-tendon unit from overstretching (extend beyond capacity)
Sprain: ligaments around th joint are stretched or torn

51
Q

What is the most common site for strains?

A

Lower back and neck

52
Q

What is the most common site for sprains?

A

ankle

53
Q

Sx of strain?

A
  1. Immediate pain
  2. reduced ROM
  3. Musle spasm
  4. Edema
  5. Muscle weakness
  6. Partial tearing in muscle
54
Q

Sx of sprain?

A
  1. ROM severly hindered
  2. Pop or rip
  3. Bruising, pain, immediate swelling
  4. Pain exacerbated with movement
55
Q

What is a bursae?

A

Enclosed fluid-filled sacs that act as cushions between muscles, tendons, and bony prominences

56
Q

Inflammation of the bursa

A

Busitis

57
Q

What is a tendon sheath?

A

Elongated bursa that wraps around tendons

58
Q

What is inflammation of the tendon?

A

Tendonitis

59
Q

What is the synovial membrane?

A

Surrounds the inner lining of joints that creates synovial fluid for nourishment and lubrcation

60
Q

What is inflammation fo synovial mmbrane?

A

Synovitis

61
Q

What is the common areas of bursitis, tendonitis, synovitis?

A

Shoulder, hips, knees, elbows

62
Q

What are the causes of Bursitis, Tendonitis, and Synovitis?

A
  1. Overuse of joint, direct trauma to joint
  2. Constant friction between bursa and tissue around sac -> inflammation, irritation, and edema
63
Q

What are te sx of Bursitis, Tendonitis, and Synovitis?

A

Warm, red, swollen, tenderness, pain with extention and flexion

64
Q

How is a contusion formed?

A

Direct blow to the body that causes damage to the skin surface forcing BV to rupture

65
Q

What is chronic pain?

A

Pain that lasts longer than 12 weeks

66
Q

What are the types of chronic pain?

A
  1. Recurrent
  2. Intractable benign
  3. Progressive
67
Q

What is chronic recurret pain?

A

Repeated and intense episodes of pain separated by pain-free periods (migraine)

68
Q

What is chronic intractable benign pain?

A

Continuous pain with varying levels of intensity (low back pain)

69
Q

What is chronic progressive pain?

A

Continuous pain that increases in intensity (cancer pain)

70
Q

What is break through pain?

A

Occurs randomly and suddnely

71
Q

What is osteoarthritis?

A

Wear and tear on joints breaks down cartilage in joint , causing bone to rub on bone

72
Q

What is the most common site of OA?

A

Hands, knees, and hips

73
Q

What is the greatest risk factor of oA?

A

older age

74
Q

What are the forms of idiopathic OA?

A

Localized: affects one or two joints
Generalized: affects three or mor joints

75
Q

What is secondary OA?

A

OA caused by underlying conditions

76
Q

What are bone spurs?

A

Particles that break off joint to ittirate synovial tissue

77
Q

Describe the progression of OA?

A
  1. Chanes to joints synovium, subchondral bone, and cartilage slowly develop
  2. Joint no longer moves smoothly
78
Q

What are the manifestations of OA?

A
  1. Tenderness
  2. Effuion: swelling related to excess fluid
  3. Crepitus: crackling or grating of joint
  4. Bone spurs
  5. Decreaed ROM
79
Q

What is are the complications for OA?

A

Risk of falling from joint pain, stiffness, unsteady gair, and effects of medication

80
Q

What is the difference between neurtis and neuralgia?

A

Neuritis: inflammation of a nerve
Neuralgia: pain that follows the distribution of a nerve

81
Q

What is radiculopathy?

A

Pain or loss of sensory and/or motor function as a result of impaired conduction block in a spinal nnerve or its roots

82
Q

What is neuropathy?

A

a disease or disorder of the PNS or CNS

83
Q

What is peripheral neuropathy?

A

Constant or intermittent burning, aching, lancinating limb pain due to lesions or dysfunction of peripheral nerves
* Motor, sensory, autonomic fiber lesions or dysfunction

84
Q

What are central neuropathies?

A

Results from:
* Injury
* Stroke
* Disease
* Congenital condition in the brain or spinal cord

85
Q

What are the causes of neuorpathic pain?

A
  1. Traumatic injuries
  2. Surgical procedures
  3. Repetitiatve stress
  4. Metabolic and endocrine disords
  5. Autoimmune diseases
  6. Chemo
  7. Viral/bacterial infections
  8. Deficiencies
  9. Alcohol
  10. Environmental exposures
86
Q

A pathologic disorder that occurs without obvious tissue injury or disease and serves no protective biological function.

A

Neuropathic pain

87
Q

What are the sx of neuropathic pain?

A
  1. Paresthesias
  2. Allodynoa
88
Q

What is paresthesias?

A

Numbness, tingling, pricking sensation

89
Q

What is allodynia?

A

Area of the body become abnormally sensitive
* innocuous stimulus
* Sensitzation of peripheral nocicetors

90
Q

What are descriptors of neuropathic pain?

A
  1. Burning
  2. Electric shock
  3. Shooting
  4. Numbness
  5. Throbbing
91
Q

Diminished pain response to a normally painful tactile and/or thermal stimulus.

A

Hypoalgesia

92
Q

Unpleasant sensation?

A

Dysesthesia

93
Q

Increased sensitivity to tactile or thermal stimulation.

A

Hyperesthesia

94
Q

Decreased sensitivity to tactile or thermal stimulation?

A

Hypoesthesia

95
Q

What is the characteristic of pain in the PNS and CNS?

A

Neuroplasticity

96
Q

What is the result of lesions or damage of primary sensory neurons?

A

Increased number of abnormal sodium channels that spontaneously or ectopically depolarize

97
Q

What are the manifestations of neuropathic pain?

A
  1. Loss of sensory input to the dorsal hron from increase neurotransmission and input from C fibers results in windup
  2. Release of inflammatory cytokines from central flial cells
  3. INcreased growth of alpha-adrenoreceptors on nociceptors
98
Q

What is the most frequent form of peripheral neuorpathy?

A

Diabetes

99
Q

What is diabetec PN?

A

Progressive loss of nerve fibers in both autonomic and peripheral NS from diabetes

100
Q

What is the cause of diabetic PN?

A

Microvascular complications
Windup of the WDR neurons in lamina V

101
Q

What are the manifestation of diabetic PN?

A
  1. Pain and paresthesia
  2. Dyin back pattern
  3. Stocking glove pattern
  4. Vasomotor changes: pallor, cyanosis, mottling
102
Q

Wht are the branches of trigeminal neuralgia?

A

Opthalmic: supplies sensation to the scalp, forehead, and the front of the head
Maxillary: supplies sensation to the cheek, upper jaw, top lip, teeth, gums
Mandibular branch: supplies snsory and motor innervation to the lower jaw, teeth, gums, bottom lips

103
Q

What is the cause of trigeminal neuralgia?

A

Pathophysiology involves segmental demyelination of trigeminal sensory fibers in the nerve root or brainstem:

Compression of the nerve root -> demyelination -> ephaptic communication stimulates trigeminal nerve

104
Q

What are the manifestations of trigeminal neuralgia?

A
  1. Sudden burning or shock-like paroxysms of facial pain
  2. Pain in motor activities: chewing, speakig, yawning, eating, brushing teeth
  3. Unilateral pain in V2 and V3 branches
105
Q

What is postherpetic neuralgia?

A

Painful peripheral neuralgia that is a sequela of herpes zoster infection

106
Q

What is herpes zoster?

A

Shingles caused by varicella zoster virus

107
Q

What is the cause of postherpetic neuralgia?

A

Reactivated herpes zoster

108
Q

What are the manifestations of postherpetic neuralgia?

A
  1. Thoracic dermatomes innervated by the T1-L2 ganglia and ophthalmic branch of the trigeminal nerve
  2. Hyperesthesia
  3. Allodynia
  4. No reliable predicotr ofprogression
109
Q

What are the RF of postherpetic neuralgia?

A
  1. Older age
  2. Compromised immune system
110
Q

What is the most common cause of widespread musculoskeletal pain?

A

Fibromyalgia

111
Q

What is FM?

A

widespread areas of tenderness distributed symmetrically on the trunk and proximal limbs
* Sympathetically mediated and sensitive to catecholamines
* Tender points
* Central sensitization

112
Q

How do you diagnose FM?

A
  1. 3 month duration
  2. 7 of the 18 trigger points
  3. Fatigue
  4. Absence of other disorders

Drug Action III (23 decks)

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