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Coexisting Test 3 > Pain cards from patho > Flashcards

Pain cards from patho Flashcards

1
Q

What is WHO’s definition of pain?

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage

pain is a protective mechanism

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2
Q

What is dyesthesia?

A

any abnormal sensation described as unpleasant by the patient

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3
Q

What is hyperalgesia?

A
  • Exaggerated pain response from a nromally painful stimulus
  • usually includes aspects of summaiton with repeated stimulus of constant intensity and aftersensation
    • people on chronic opioids can develop hyperalgesia
    • theory- with nerve propagation, can’t stack signalts (or response isn’t as great)but in these patients, propagation is continuous and there’s no dampening of pain signals
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4
Q

What is hyperesthesia (hypesthesia)

A

exaggerated pereception of touch stimulus

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5
Q

What is allodynia?

A

abnormal perception of pain from a normally non-painful mechanical or thermal stimulus; usually has elemtents of delay in perception

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6
Q

What is hypoalgesia

A

decreased sensitiivty and raised threshold to painful stimuli

(patient with no pain sensation in OR)

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7
Q

What is paresthesia?

A

mainly spontaneous abnormal sensation that is not necessarily unpleasant; usually described as pins and needles

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8
Q

What is causalgia

A

burning pain in the distribution of one or more peripheral nerves

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9
Q

What are the 4 physiological processes to nociceptive stimuli?

A
  • Transduction- noxious stimuli
    • converted to electric activity at the sensory nerve endings
  • Transmission- propagation of impulses through the sensory nervous systme
  • Modulation- process of transmission modified by neural influenced
  • Perception- above 3 interact with the psychology of the pt ot create what is perceived as pain
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10
Q

What happens during transduction of pain?

A
  • Noxious stimuli causes cell damage with the release of sensitizing chemicals
    • prostaglandins
    • bradykinin
    • serotonin
    • substance P
    • histamine
  • These substances activate nociceptors and lead to generation of action potential
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11
Q

What happens during transmission of pain?

A
  • Action potential continues from
    • site of injury to spinal cord
    • spinal cord to brainstem and thalamus
    • thalamus to cortex for processing
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12
Q

What happens at perception of pain?

A

conscous experience of pain

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13
Q

What happens durign modulation of pain?

A
  • Neurons originating in the brainstem descend to the spinal cord and release substances (eg endogenous opioids) that inhibit nociceptive impulses
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14
Q

What are pysiologic responses to acute pain?

A

Neuroendocrine resposne

  • increase secretion of catabolic hormones
  • stress response
  • decrease anabolic metabolism
    • decrease anabolic metabolism, insulin, testosterone
    • ACTH release
    • Hyperglycemia
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15
Q

What is cardiac resposne to pain?

A
  • Increase HR, BP, SVR, CO
  • MI, CHF, Dysrrhythmias
  • decrease myocardial oxygenation- secondary pulmonary dysfunction-atelectasis
  • coronary artery constriciton- high catecholamines
    • release of serotonin may induce coronary vasopasm
  • increase plama viscosity- platelet induced occlusion
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16
Q

What is pulmonary response to pain?

A
  • increase in total body o2 consumption
  • increase CO2 production
  • increase minute ventilation
    • decrease in TV, VC, FRC- most detrimental alteration in post surgical lung volume
      • FEV1, also decrease
    • as FRC decreases, resting lung volume approaches closing volume, as it continues, atelectasis results, V/Q mismatch, and hypoxemia ensues
      • most detrimental alteration in post surgical lung volume
    • Increase in RR
  • pulmonary function decreases with abdominal or thoracic incisions (splinting)
17
Q

Other responses from vascular system with pain?

A
  • Stress mediated due to platlet adhesion and hyper-coagulability
    • dvt, pulmonary edema
18
Q

Other response from GI and urinary systems in response to pain?

A
  • visceral pain is referred to somatic sites
  • GI and urinary systmes increase sympathetic tone, increase sphincter tone, decrease gastric motility, promoting ileus and urinary retention
  • nausea and vomiting common
  • stress ulcers can occur– increase gastric juices
19
Q

What response do muscles have to pain?

A
  • muscle spasms- periosteal and somatic irritation initiates reflex motor resposne, leading to muscle spasm
  • anxiety and anger- if lack of pain control
20
Q

What is chronic pain?

A
  • pain which persists one month longer than expected
  • chronic pain was originally defined as pain that has lasted 6 months or longer. It is now defined as the disease of pain
  • associated with musculoskeletal disorders, chronic visceral disorders, lesions of peripheral nerves, nerve roots, dorsal root ganglia (including causalgia, phantom limb pain), lesions of the CNS and cancers invading the nervous system
  • may be due to nociception, neuropathic pain, but in which psychological and behavioral factors often play a major role
  • acute pain is a symptom of disease, but chronic pain is itself a disease
    • no protective mechanism for chronic pain
  • chronic pain has no time limits, often has no apparent cause and serves no apparent biological purpose
  • chronic pain can trigger multiple psychological problems that confound both patient and HCP, leading to feeling sof helplessness and hopelessness
  • the most common causes of chronic pain include low-back pain, HA, recurrent facial pain, CA pain, arthritic pain. sometiems chronic pain can have psychosomatic or psychogenic cause
21
Q

All main causes/theories of chronic pain?

A
  1. Psychological mechanism
  2. peripherla mechanism
  3. reflex role
  4. peripheral- central mechanism
  5. circle mechanism
  6. chronic nerve compression
  7. central pain mechanism
  8. psychophysiologic mechanism
  9. learned mechanism
22
Q

What are effects of chronic pain?

A
  • serotonin and endorphins become depleted so minor injuries become intolerable
  • psychological profiles- the chronic pain patient shows significant differences on the MMPI, neuroticism. however, when the pain is relieved, the neurotic features dissipate
    • the longer the duration of the pain, the greater the psychological changes
23
Q

What is treatment for chronic pain?

A
  • must not only remove the pain and the cause of the pain, but also rehabilitate the patient and family physicallyh and psychosocially and psychologically
  • examples of pain contorl include
    • steroid epidural injection with or without trigger point injections
    • peripheral nerve blocks with neurolytics
    • acupuncture
  • note- often require more analgesics
24
Q

What role does peripheral-central mechanism, circle mechanism, chornic nerve compression and central pain mechanism have in chronic pain?

A
  • peripheral-central mechanism- lesions of peripheral nerves, dorsal roots or dorsal ganglion cells
    • found in causalgia, and other reflex sympathetic dystrophy, phantom pain
  • Circle Mechanism- suggests that intense stimulation of nerve fibers in the cord activate internuncial neurons creating an abnormal reverberatory activity in a closed loop
    • interneurons firing when they shouldn’t
  • chronic nerve compression- nerve being compressed, causign chronic pain
  • central pain mechanism- found in lesions to the thalamus and spinal cord injury as in paraplegia
    • supratentorially in brain
25
Q

What role does psychophysiologic mechanisms and learned mechanisms have in causing chronic pain?

A
  • Psychophysioligc mechnism- severe stress, usually seen in chronic tension headaches and chronic pain d/t muscle spasm in the shoulder, back and chest
  • learned mechanism- secondary gian. these patients frequently develop reactive depression and hypochondriasis
26
Q

What is the peripheral mechanism involved in acute pain physiology?

A
  • Information about noxious stimuli arrives from periphery along A-delta and C fibers
  • Substance P and excitatory amino acids (EAAs) ie glutamate are released
  • activation of neurokinin-1 (NK-1) receptors by substance P and activation of amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors by EAAs cause transient depolarization of pain neurons
27
Q

What is central mechanism to pain cellular physiology (chronic)

A
  • The information is relayed to higher brain areas
  • N-methyl-d-aspartate (NMDA) linked channels are inoperative as they are chronically plugged by magnesium ions
  • in response to intense and/or prolonged barrages of incoming nociceptive information, the neurons become sensitized and over-respond to subsequent incoming nociceptive signals
  • this barrage depolarizes the neuron such that the magnesium ions exist the NMDA-linked channel
  • results in influx of calcium ions- acitvates nitric oxide synthas (cNOS), causing conversion of L-arginine to nitric oxide (NO)
    • because it is a gas, NO rapidly diffused out of the nneurons
  • this NO acts presynpatically to cause exaggerated release of substance P and EAAs
  • postynaptically, NO causes the neurons to become hyperexcitable, releasing substance P, ACh, etc

EAAs= excitatory amino acids, ie glutamate

Coexisting Test 3 (8 decks)

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