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Pathophysiology > pain physiology > Flashcards

pain physiology Flashcards

1
Q

nociception of pain has 4 stages

A

transduction
transmission
perception
modulation

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2
Q

transduction

A

nociceptors convert painful stimuli to neuronal action potentials.
-physical and chemical mediators alter the membrane potential of the pain receptor

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3
Q

chemical mediators of transduction

A

K, H, lactate, histamine, serotonin, bradykinins, prostaglandins

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4
Q

Transduction and NSAIDS

A

cyclooxygenase is needed to convert arachidonic acid to prostaglandin form. Which can then be used as a chemical mediator for pain.
NSAIDs block cycloosygenase, unable to convert arachidonic acid

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5
Q

transmission

A

action potentials transmitted to the CNS by means of specialized sensory fibers

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6
Q

sensory fibers

A

a fibers

c fibers

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7
Q

a fibers

A

mylinated
10% of pain fibers
fast traveling
sharp, stinging, cutting, pinching

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8
Q

c fibers

A

unmyelinated
90% of pain fibers
slower traveling
dull, burning, aching

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9
Q

trasmission in spinal cord

A

enter through the dorsal horn, synapse on interneurones, cross the cord and project centrally in the anterolateral tract

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10
Q

anterolateral tract has 2 divisions

A

neospinothalmic tract

paleospinothalamic tract

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11
Q

neospinothalmic tract

A

carries A fiber input, projects to thalamus and then sensory cortex

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12
Q

paleospinothalmic tract

A

carries C fiber input, protects diffusely to the reticular formation, mesencephalon, and thalamus

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13
Q

sensory dermatome

A

brain can localize pain sensation to a particular part of the body because nociceptor pathways are kept in specific anatomic order in the cord and somatosensory cortex

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14
Q

perception

A

result of neural processing of pain sensations in the brain

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15
Q

pain threshold

A

level beyond which a pain stimulation causes pain:

-similar between people

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16
Q

pain tolerance

A

degree of pain an individual is willing to bear before seeking relief
- differs with people

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17
Q

modulation

A

alters synaptic transmission of pain signals
occurs within
- peripheral nociceptors
- spinal cord
- brain
– descending pathways from brain release neurotransmitters that can inhibit synaptic transmission of pain signals

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18
Q

endogenous opiods

A

enkephalins, endorphins
play important role in pain modulation
-have different effects depending on the types of receptors they activate

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19
Q

receptors with analgesic activities

A

mu (brain)

kappa (spinal cord)

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20
Q

gate control theory

A

rubbing, pressing, or shaking the painful area may reduce pain
-impulses carried by A fibers can close the gate on nociceptor impulses; pain signals would be blocked

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21
Q

types of pain

A

physiologic pain

pathologic pain

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22
Q

physiologic pain

A

when tissue injury has occured

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23
Q

pathologic pain

A

occurs after tissue injury, but longterm changes occur along sensory pathways

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24
Q

classification of pain

A

duration (acute, chronic)
source (cancer, neuropathic, ischemic)
location (referred pattern)

25
Q

Acute pain

A

results from tissue injury and resolves when the injury heals
-less than 3 months

26
Q

S/S acute pain

A

increase sympathetic activity

  • increased HR
  • increased RR
  • HTN
  • pallor
  • sweating
  • nausea
  • grimacing
  • crying or moaning
27
Q

pain relief with acute pain

A

nonopiod and opiod medicatoins

  • risk of becoming dependent minimal
  • try to not use opiods
28
Q

chronic pain

A

gradual in onset, persists beyond the time for normal healing: 3 months
allodynia
hyperalgesia

29
Q

Examples of chronic pain

A

headaches
low back pain
osteoarthritis
fibromyalgia

30
Q

tx of chronic pain

A

multimodal therapies

opiods are neither safe nor effective

31
Q

fibromyalgia

A

chronic widespread pain affecting all four extremities

32
Q

fibromyalgia s/s

A 
sleep disturbance/insomnia
difficulty concentrating
fatigue
depression
irritable bowl syndrome
33
Q

tx of fibromyalgia

A

antidepressant
restore sleep patterns
regular exercise
pregabalin to target pain pathways

34
Q

cancer pain

A

infiltration of organs
compression of structures by an expanding tumor
cancer treatments

35
Q

cancer pain s/s

A

mixture of sympathetic NS and behavioral changes

36
Q

cancer pain tx

A

multifaceted approace and use of potent meds: opiods

37
Q

neuropathic pain

A

results from nerve damage or dysfunction
constant aching with intermittent burning or shock-like pain
results from alteration in any of the stages of nociception

38
Q

neuropathic pain s/s

A 
allodynia
hyperalgesia
atrophy of affected extremity
coldness in affected area
dystrophic changes
- hair loss, shiny skin
39
Q

neuropathic pain tx

A

antidepressants

anticonvulsants

40
Q

allodynia

A

hurts when it shouldn’t

- light touch

41
Q

hyperalgesia

A

hurts more than it should

42
Q

trigeminal neuralgia

A

sudden, momentary, excruciating sharp pains along the II and III divisions of the trigeminal nerve
compression of nerve causing demyelination and irritation

43
Q

trigeminal neuralgia tx

A

anticonvulsants
surgical nerve decompression
gamma knife radiosurgery

44
Q

postherpetic neuralgia

A

caused by peripheral nerve damage by the reactivation of the latent herpes zoster virus

  • burning follows a dermatomal pathway
  • pain lasts > 8 weeks
45
Q

postherpetic neuralgia tx

A 
early use of antiviral meds within 72 hours of rash can decrease risk for postherpetic neuralgia
liodcain
capsaicin crea
anticonvulsants
antidepressants
vaccine
46
Q

diabetic neuropathy

A

damage to the large peripheral nerves by inflammation and demyelination

47
Q

diabetic neuropathy s/s

A

burning pain
numbness, tingling
weakness
loss of vibratory sense and proprioception

48
Q

diabetic neuropathy tx

A

pt education for foot care and glucose control
antidepressants
anticonvulsants

49
Q

ischemic pain

A

sudden or profound loss of blood flow
chronic ischemic pain associated with atherosclerosis; intermittent claudication
- pain with activity and alleviated with rest
activates inflammatory response

50
Q

ischemic pain s/s

A

aching
burning
tingling

51
Q

ischemic pain tx

A 
improving blood flow and reducing tissue hypoxia
wt loss
smoking cessation
exercise
lipid-lowering meds
surgical bypass
vascular stents
52
Q

referred pain

A

perceived in an area other than the site of injury

result of convergence of visceral nociceptor activity with primary somatic afferents in the posterior horn

53
Q

physiologic responses to pain

A 
sympathetic nervous system activation during acute pain leads to
-dilated pupils
perspiration
pallor
increased HR and BP 
increased blood sugar
decreased GI motility
hypomotility of the bladder
increased RR
54
Q

Pain in young and elderly

A
  • pain perception doesn’t decrease with age, but communication and expression of main may vary
  • infants have pain perception
  • inadequate pain treatment in neonates and infants can result in persistent behavioral changes and physical changes in the CNS
55
Q

pain tx modality points

A

nociception
spinal cord
brain

56
Q

interrupting peripheral transmission of pain

A

NSAIDs: dec. prostaglandins
local anesthetic agents
- blocking sodium influx through fast channels

57
Q

modulating at spinal cord

A

cutaneous stimulation activates large sensory fibers that block the central progression of nociceptive transmission at the interneurons

  • TENS
  • massage
  • acupuncture
  • heat/cold
  • theraeutic touch
  • epidural and intrathecal analgesia
  • dorsal column stimulators
58
Q

altering pain perception in brain

A 
analgesics: NSAIDs
opiods
nonpharmacologic
- distraction
-guided imagery
-relaxation
-biofeedback
-hypnosis

Pathophysiology (80 decks)

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