Pain & Mgmt Flashcards

1
Q

Acute nociceptive pain w/ normal physiological activity in normal pain receptors can last up to ____

A

3 months (the time it normally takes for the tissue to heal)

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2
Q

Somatic pain

A

It is localized, and typically described as aching, stabbing, squeezing or throbbing

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3
Q

Visceral pain

A

Pain is localized or generalized and described as cramping, or gnawing.
It may be referred to the skin of the dermatome innervated by the same nerve as the viscus

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4
Q

All ____ fibers are unmyelinated.

A

sympathetic postganglionic

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5
Q

Describe Neuropathic pain

A
  • Neuropathic Pain occurs when there is CNS +/or PNS dysfunction.
  • Causes are numerous—nerve compression, ischemia, inflammation, infiltration, metabolic
  • This pain is disproportionate to injury, & may outlast it
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6
Q

Peripheral C‐fibers: myelination?

A

• Unmyelinated (slow)

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7
Q

Peripheral A‐δ fibers: myelination?

A

Thinly myelinated (medium speed)

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8
Q

Peripheral C-fibers: type of pain?

A

Spontaneous, diffuse burning/aching

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9
Q

When primary afferents of pain pathway are activated, they release __a__ at synapses in dorsal horn (fast excitation).
They also release __b__ & __b__, which produce
a slower and longer-lasting excitation.

A

a) Glutamate

b) Substance P and Calcitonin gene-related peptide

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10
Q

The area to which visceral pain is referred corresponds to what?

A

The dermatome innervated by the spinal segment to which the visceral afferents project

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11
Q

Anatomic basis for referred pain?

A

The convergence of visceral and somatic pain fibers in a given dorsal root on the same pain-transmission neurons i.e. the neurons whose axons will cross the midline and form the spinothalamic tract.
The common explanation is the idea that spinal neurons are most often activated by inputs from the skin, so the brain “mislocalizes” activity evoked by input from deep structures to a place that roughly corresponds with the region of skin innervated by that segment.

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12
Q

What surgical procedure?
- the classic ablative surgery. Afterwards patients often report that the pain is just the same but now they don’t seem to care…

A

Cingulotomy

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13
Q

DBS for pain control would target what brain structure?

A

Periaqueductal gray stimulation
or
PAG plus somatosensory thalamus

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14
Q

If a painfully hot stimulus is applied to a normal subject, fMRI shows somewhat increased activity (blood flow) in the ___a___.
b. What happens if subject is asked to go to their “happy place” & not pay attention to painful stimuli?

A

a) Periaqueductal Gray
b) Blood flow in this area is increased
even more and the stimuli are reported to be
less unpleasant

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15
Q

What are the 2 effects of periaqueductal gray axons stimulating the serotonin-containing neurons of Raphe Nuclei?

A

The 5HT-containing neurons of Raphe Nuclei:
• Inhibit DRG pain axons directly (presynaptic)
• Inhibit neurons whose axons form the spinothalamic tract (either directly or via small interneurons in the substantia gelatinosa)

(descending pain control)

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16
Q

Functions of the serotonin cell bodies of the Raphe Nuclei?

A

Impulse control, Pain Modulation, Mood stability

  • Help control arousal & aggression (in forebrain)
  • Help modulate pain-related signals (in SC)
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17
Q

List some inputs to the Periaqueductal Gray Matter

A
  • Hypothalamus
  • Amygdala
  • Many cortical areas include limbic and prefrontal cortex
  • Spinothalamic tract axons (Input about level
    of noxious stimulation)
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18
Q

Damage to the descending pain modulating circuits will affect the action of what type of drugs?

A

In animals, lesions in this pathway reduce the effect of opioid drugs given systemically

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19
Q

Neuropathic pain- cause & outcome?

A

Neuropathic pain is produced by direct damage to or dysfunction of peripheral or central pathways for pain (nerve compression, ischemia, inflammation, infiltration, metabolic)

Typically patients have loss or impairment of pain sensation AND spontaneous pain

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20
Q

What to include in taking the pain history of a patient?

A

PQRST

  • P‐‐provocative/palliative measures, including treatments previously tried (what makes it better or worse?)
  • Q—quality – patient’s own words. Their story is often more helpful than tests.
  • R—region and radiation (where pain starts and moves to)
  • S‐‐severity‐‐how bad is it at its worst, best and now? How does it affect their life? Analog scales
  • T‐‐temporal course—acute, chronic or recurrent, look for history of trauma or new activity, how does it change during the day?
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21
Q

Assessment & Management of pain in a patient?

A

Identify anatomic structures that may be causing or worsening the pain‐‐correct underlying pathology if possible, or explain etiology
– Physical examination: Inspection (posture, pain behaviors) palpation (for masses, guarding), vitals, signs of sympathetic dysfunction (sweating, tachycardia, trophic skin changes)

Assess effect of pain on patient
– physical comfort , including sleep
– ability to carry out usual daily activities
– emotional toll on patient & family

Negotiate treatment strategy as appropriate.
– What meds or treatment are appropriate, acceptable to patient
– Psychosocial Hx important for prior substance abuse (drugs or alcohol) especially in chronic pain

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22
Q

Initial Drug Management for Pain ‐‐ how many pain meds to start off w/?

A

Optimize relief w/ 1 drug before changing or adding a 2nd drug.
Note: some drugs have ceiling effects

Also: avoid simultaneous use of multiple drugs from same class, especially multiple opioids.

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23
Q

When to use long acting medications in pain relief?

A

Use long acting medications when pain is chronic or constant.

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24
Q

Often ____ plus opioid reduces opioid dose needed to give good analgesia

A

COX inhibitor

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25
Q

If using opioids always give _____

A

stool softeners

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26
Q

If pain is neuropathic, addition of ______ in Tx may be needed

A

an antidepressant or anticonvulsant

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27
Q

How long does “chronic pain” last?

A

Chronic pain lasts longer than 3 months

i.e. it outlasts time for tissues to heal normally

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28
Q

T or F? Chronic pain alone is a disease state.

A

True. Chronic pain is a disease state in and of itself, & serves no physiologic role.

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29
Q

Most common type/location of pain?

A

Primary back pain

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30
Q

Describe the pain transmission pathway

A

Noxious stimuli activate sensory peripheral ending of afferent nociceptor by transduction –> message

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31
Q

What is the “Positive Pain Phenomena”?

A

Occurs when there is abnormal increased function of the sensory system.
Pain may be spontaneous or stimulus induced.

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32
Q

Spontaneous Positive Pain Phenomena?

A

– Paresthesia‐‐abnormal sensation. Usually described as tingling, prickling, or asleep.
– Dysesthesia‐‐severe, distressing paresthesia

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33
Q

Stimulus-induced Positive Pain Phenomena?

A

– Allodynia‐‐stimulus induces another type of sensation‐‐touch is painful, for example
– Hyperalgesia or hyperpathia‐‐painful stimulus causes more than expected perceived pain

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34
Q

What is “Tic Doloreaux”? What is it seen in?

A

Patient winces involuntarily when pain occurs so it looks like a facial tic.

It is seen in Trigeminal Neuralgia

35
Q

Trigeminal Neuralgia pathology?

A

Demyelination‐‐ of nerve, or in trigeminal
ganglion or spinal trigeminal nucleus‐‐leads to
ephaptic (i.e. a short circuit!) transmission of
electrical impulses and a clinical pain
syndrome.

Compression by vascular structures is often
the cause of demyelination, especially in older
patients. In this patient there was a blood
vessel on top of the nerve

36
Q

Trigeminal Neuralgia Tx options?

A

Medical:
– Carbamazepine or Phenytoin
‐‐ slows recovery of voltage gated Na channels.
– stabilizes neuronal membrane.
– Baclofen
‐‐ GABA‐B receptor agonist
‐‐ increases inhibition by interneurons.
– Antidepressants
‐‐ block 5HT & NE reuptake in PAG matter

Surgical:
—ablation of Trigeminal Ganglion or Isolation of nerve from vessel

37
Q

Types of damage that may cause neuropathic pain?

A
  • Most common in PNS disease/injury (ex: the “burning feet” of diabetic neuropathy or the pain of trigeminal neuralgia)
  • But also seen in CNS damage, particularly when it involves the spinothalamic tract or the thalamus
  • Not common in lesions of cerebral cortex
38
Q

FICA Spiritual Assessment?

A

F: Faith or beliefs
- “Tell me something about your faith or beliefs.”

I: Importance & influence
- “How does this influence your health/well-being?”

C: Community
- “Are you part of a supportive community?”

A: Address or application
- “How would you like me to address these issues in your health care?”

39
Q

White matter damage causes what type of clinical implications?

A
  • Cognitive slowing, other cognitive deficits & mood changes
  • Typically include processing speed, sustained attention, memory retrieval, or executive dysfunction
  • May produce syndromes usually seen with cortical lesions
  • Frequently causes depression & irritability (Possibly from disruption of catecholaminergic fibers)
40
Q

Gray matter damage causes what type of clinical implications?

A
  • Focal neurobehavioral syndromes, cortical deficits, seizures
  • Prefrontal syndromes are common
41
Q

Symptoms of Dorsolateral damage?

A

(gray matter-type lesion)

  • Abulic, unmotivated
  • Apathetic
  • Psychomotor slowing
  • Poor problem solving
  • Occasional outbursts
  • “Pseudodepressed”
42
Q

Sx of Orbitofrontal damage?

A

(gray matter-type lesion)

  • Impulsive, disinhibited
  • Inappropriately jocular
  • May be hyperactive
  • Emotional lability
  • Frequent outbursts
  • “Pseudopsychopathic”
43
Q

Sx of Medial damage?

A

(gray matter-type lesion)

  • Medial
  • Apathy
  • Emotional emptiness
  • False well-being
  • Akinetic mutism
44
Q

Irritative, inflammatory, or electrophysiological damage causes _____ symptoms

A

“positive”

45
Q

Insomnia criteria?

A
  • > 30min to fall asleep OR

- 6h or less per night on 3 or more nights per week

46
Q

Insomnia risk factors?

A

Females, increasing age, unemployment, divorced, widowed, separated, or lower socioeconomic status

47
Q

Most common cause of excessive daytime sleepiness?

A

Sleep deprivation - Volitional sleep loss

48
Q

Insomnia dDx?

A
  • Short duration sleep
  • – No impaired daytime function
  • Sleep deprivation (volitional sleep loss)
  • – most common cause of excessive daytime sleepiness
49
Q

Insomnia Tx?

A
  • Nonpharmacologic (Sleep hygiene and stimulus control, Cognitive behavioral therapy)
  • Pharmacologic (6-8 weeks) benzodiazepine, nonbenzodiazepine and melatonin agonists
  • – Short- versus long-acting medication
50
Q

Sleep Apnea Sx?

A
  • Loud snoring, gasping, snorting or choking
  • Excessive daytime sleepiness
  • Attention, concentration and memory problems
  • Low mood, depression, irritability
  • Morning headache, nausea
51
Q

Sleep Apnea health risks?

A

Hypertension, cardiac arrhythmias, stroke, seizure, risk of accidents or injuries due to fatigue

52
Q

Define “Apnea”

A

The cessation, or near cessation, of airflow <10% baseline for at least 10 seconds

53
Q

Obstructive vs. Central sleep apnea?

A

Obstructive — airflow is absent but ventilatory effort persists

Central — absence of airflow AND ventilatory effort

54
Q

Obstructive sleep apnea Tx?

A
  • Weight loss
  • CPAP/BiPAP
  • Surgery
  • Somnoplasty
  • Uvulopalatopharyngoplasty (UPPP) and laser-assisted uvulopalatoplasty (LAUP)
  • Genioglossus advancement, bimaxillary advancement
  • Bariatric surgery
  • Oral appliances
55
Q

Narcolepsy

A
  • Disorder of sleep-wake control
  • Elements of sleep intrude into wakefulness and elements of wakefulness intrude into sleep

1) chronic daytime sleepiness
2) cataplexy
3) hypnagogic hallucinations
4) sleep paralysis

56
Q

Cataplexy

A

Emotionally-triggered transient weakness w/ preserved consciousness

– 60% of narcoleptics develop cataplexy within 3-5 years

57
Q

Hypnagogic hallucinations

A

Vivid, often frightening visual, tactile or auditory hallucinations that occur as patient is falling asleep

Hypnapompic = upon awakening, less common

58
Q

Sleep paralysis

A

Complete inability to move for 1-2 minutes immediately after awakening.

(+/-) hypnopompic hallucinations or a sensation of suffocation.

59
Q

Narcolepsy w/ cataplexy usually begins when?

A

Usually begins in teens and early twenties

60
Q

Narcolepsy w/ cataplexy etiology?

A

Loss of orexin signaling

  • Genetic factors
  • – DQB1*0602 haplotype
  • Rare brain lesions
  • – Posterior thalamus, midbrain
  • – Secondary narcolepsy
61
Q

Narcolepsy: Multiple Sleep Latency test?

A

Performed day after nocturnal polysomnography

  • nap for up to 20 minutes at 2-hour intervals,
  • for each nap
  • – time to the onset of sleep (sleep latency)
  • – time from sleep onset to the onset REM sleep (REM-sleep latency)
  • Mean sleep latency (<8 min) ~ severity of sleepiness
  • Occurrence of REM sleep in 2 or more naps
62
Q

Narcolepsy Tx?

A

Nonpharmacologic (regular and adequate sleep schedule, scheduled daytime naps, avoidance of drugs that produce daytime sleepiness or insomnia, psychosocial support group)

Pharmacologic

  • Daytime sleepiness
  • – Modafinil, methylphenidate, amphetamines
  • – Epworth Sleepiness Score to assess for residual sleepiness
  • Cataplexy
  • – REM sleep-suppressing medication (eg, venlafaxine ER, fluoxetine, atomoxetine)
  • – GHB Gamma hydroxybutyrate
63
Q

Parasomnias

A

Episodic behaviors that intrude onto sleep

  • Sleep quality generally remains unaffected
  • Occur at sleep onset or assoc with REM or NREM sleep
  • NREM - arousal parasomnias
  • – Confusional arousals, sleep terrors, sleepwalking
  • REM - nightmares, REM behavior disorder
64
Q

What is the difference in prevalence of psychiatric disorders between developed & developing nations?

A

No consistent differences in prevalence between

developed and developing countries

65
Q

3 most frequently encountered psychiatric disorders?

A

Depression, anxiety, & substance abuse

66
Q

What is “positive psychology”?

A

The study of what enables

i.e. happiness, interest, contentment, calm, optimism, love, humor, hope, etc.

67
Q

Dimensional vs. Categorical

A
  • Dimensional: On a continuum (no clear line btwn normal & illness)
  • Categorical: Discrete, clear boundaries (clear line btwn normal & illness)

*Most medical diagnoses are dimensional

68
Q

T or F? ALL psychiatric diagnoses are dimensional

A

True

69
Q

All psychiatric diagnoses involve disturbance in _____

A

function.

  • Disturbance may be GLOBAL, eg self-care
  • Or SPECIFIC, eg an eating disorder
  • It may be self-perceived as a disorder by the individual, eg depression
  • Or may be perceived primarily by others, e.g. consequences of paranoia
70
Q

Freudian Theory: Conscious? Preconscious? Unconscious?

A

Conscious = contact w/ outside world

Preconscious = Material just beneath the surface of awareness

Unconscious = Well below surface of awareness; difficult to retrieve

71
Q

Freudian Theory: what levels of consciousness does Ego include?

A

Conscious, Preconscious, & Unconscious

72
Q

Freudian Theory: what levels of consciousness does Superego include?

A

Conscious, Preconscious, & Unconscious

conscience

73
Q

Freudian Theory: what levels of consciousness does ID include?

A

Unconscious only

primitive drives

74
Q

Maslow’s 4 components of hierarchy?

A

Physiological > Security > Belonging > Self-actualization

75
Q

Defenses are _____ conscious awareness

A

OUTSIDE

76
Q

In non-human animals _____ plays a key role in mating, pair bonding and parenting

A

Oxytocin

77
Q

Both owner’s and dog’s _____ rise when human pets animal

A

Both owner and dog oxytocin rise when human

pets animal

78
Q

What neurotransmitter?

  • Involved in regulation of feeding, grooming, & responses to stress
  • Released during sexual response in humans
A

Oxytocin

79
Q

Developing awareness of others’ emotional states helps ______

A

affiliation

80
Q

What is “Theory of Mind”?

A

The ability to recognize that someone else has a different mind from ones own, infer their mental state, predict behavior based on what THEY might be thinking or feeling

81
Q

Human tendency to demonize those who are “out-group” is an example of _____

A

stigma

82
Q

What are the 4 major aspects of etiology used in psychiatry?

A

Biologic
Psychologic
Social
Behavioral

83
Q

Typical Mixed Cutaneous Nerve contains 3 primary afferent nerve fiber types (peripheral), what are these?

A
A-ß = large-diameter myelinated fibers
A‐δ = small-diameter myelinated fibers
C-fibers = unmyelinated fibers
84
Q

If using Opioids, always use what other drug(s)?

A

Stool softeners