Lecture 5: Pain Flashcards

1
Q

What is pain?

A

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

Pain is whatever the experiencing person says it is.

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2
Q

Is pain directly proportional to amount of tissue injury?

A

Not always

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3
Q

Why is pain underrated?

A

It is highly subjective

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4
Q

What does pain cause?

A

Amplifies the body’s stress response to traumatic injury (through SNS and glucocorticoids)

Causes endocrine and metabolic abnormalities

Impedes a patient’s recovery from trauma and surgery

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5
Q

What is acute pain?

A

lasts less than 6 months, subsides once the healing process is accomplished.

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6
Q

What is chronic pain?

A

involves complex processes and pathology.

Usually involves altered anatomy and neural pathways.

It is constant and prolonged, lasting longer than 6 months, and sometimes, for life.

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7
Q

Why treat pain?

A

Tissue damage has the potential to elicit mechanisms that can create disabling, refractory, chronic situations that may prolong and even
outlast the period of healing.

If you don’t treat the initial pain, it may lead to chronic pain

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8
Q

What is pain theory?

A

Severe, unrelieved acute pain results in abnormally enhanced physiological responses that lead to pronounced and progressively increasing pathophysiology

Increased pathophysiology -> increased morbidity and mortality

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9
Q

Harmful effects of pain

A

Cardiovascular and respiratory systems are significantly affected

Adrenergic stimulation

Hypercoagulation

Increased heart rate, cardiac output and myocardial oxygen consumption

Decreased pulmonary vital capacity, alveolar ventilation, functional residual capacity

Arterial hypoxemia

Supression of immune functions -> wound infections and sepsis

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10
Q

What happens to person’s social life during chronic pain syndrome

A

Pain becomes focus of life

Relationships become altered

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11
Q

Causes of chronic pain syndrome

A

Can be the result of acute, unrelieved pain (multiple trauma, phantom limb pain after amputation, repeated back surgeries)

Sometimes set,s from near-muscular disorders (fibromyalgia, rheumatoid arthritis, multiple sclerosis)

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12
Q

Pain pathways (receptors, stimulation, neurons, processes)

A

Specialized receptors = free nerve endings

Stimulation: Mechanical damage, extreme temperature, chemical irritation

2 types of neurons: A-delta and C

Four processes: transduction, transmission, modulation, perception

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13
Q

Four processes to pain

A

Transduction: Local biochemical changes in nerve endings that generate a signal

Transmission: Movement of that signal from the site of pain to the spinal cord and brain

Perception: Synthesis and analysis in the brain

Modulation: Endogenous systems in place that can inhibit pain at any point along the pathway

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14
Q

Which receptors send pain signals?

A

All receptors can

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15
Q

What are nocireceptors?

A

Involved in transduction of pain

Free nerve endings

Capacity to distinguish between noxious and innocuous stimuli

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16
Q

What happens when person is exposed to mechanical, thermal or chemical stimuli

A

Involved in transduction

Tissue damage occurs

Substances are released by the damaged tissue which facilitates the movement of pain impulse to the spinal cord.

17
Q

Substances released during transduction? What do they cause?

A

Released from traumatized tissue

Bradykinin

serotonin

substance P

histamine prostaglandin

Cell depolarization by sodium influx

18
Q

What drugs act on transduction process of pain?

A

Non-steroidal anti-inflammatories (ex: ibuprofen) - minimize the effects of substances released during transduction, especially prostaglandins.

Corticosteroids (ex: dexamethasone) - used for cancer pain, interferes with the production of prostaglandins.

19
Q

Transmission process of pain

A

Initial damage/stimulation -> nerve -> spinal cord -> brain stem -> thalamus -> central structures of brain -> pain is processed

20
Q

What is required to continue pain impulse from spinal cord to brain? What drugs targeted this step?

A

Transmission

Neurotransmitters

Opioids (narcotics) are analgesics, block release of neurotransmitters

21
Q

Two different types of peripheral that transmit pain signals from pain receptors to spinal cord

A

Transmission

A delta: “fast pain”, protective pain

C-fibers: “slow pain” nerve fibres, learning and behavioural modification

22
Q

Fast pain vs slow pain

A

See table

23
Q

Where does perception of pain occur?

A

Somatosensory cortex, cingulate cortex - sensory discrimination, emotional response (fear, anxiety, panic, subjective)

Reticular formation (increased arousal, emotional response, somatic and autonomic motor reflexes)

24
Q

Therapeutic strategies that target perception of pain

A

Behavioural strategies

Therapy

Brain can accommodate a
limited number of signals, so distraction, imagery and relaxation signals may get through the gate, leaving limited signals (such as pain) to be transmitted to the higher structures.

25
Q

How do higher vertebrates handle pain vs primitive vertebrates

A

Higher vertebrates: have anatomical components for perception of pain

Primitive vertebrates (Fish, reptiles, amphibians): avoidance or escape behaviour, poorly developed cerebral cortex

26
Q

Where does modulation process occur?

A

Descending tract (brain -> spinal cord)

Changing or inhibiting pain impulses

27
Q

What occurs during modulation

A

Descending fibres release substances (endogenous opioids or endorphins) which have capability of inhibiting transmission of pain

28
Q

Why are anti-depressants used to treat cancer pain?

A

Antidepressants interfere with reuptake of serotonin and norepinephrine, which increases their availability to inhibit noxious stimuli

29
Q

What activates descending pain modulation system?

A

STRESS!

fear

hunger

thirst

fatigue

prolonged motor activity

hypnosis

30
Q

Pain processes and possible medications

A

Perception: parenteral opioids, a2 agonists, general anaesthetics

Transmission: Local anaesthetics

Modulation: spinal opioids, a2 agonists, NMDA receptor antagonists, Ach esterases, NSAIDS, CCK antagonists, NO inhibitors, potassium channel openers

Transduction: NSAIDS, Antihistamines, Membrane stabilizing agents, local anesthetic cream, opioids, bradykinin and serotonin antagonists

See figure

31
Q

Categories of pain

A

Nociceptic: injury, trauma, infection

Neuropathic: damage or dysfunction of the peripheral or central nervous system

Visceral: Arising from internal organ (MI, appendicitis, bowel obstruction)

32
Q

Nociceptive vs neuropathic pain

A

See figure

33
Q

What does neuropathic pain feel like

A

Fire

Electricity

Typically in feet, legs and hands

34
Q

Types of neuropathic pain

A

Hyperalgesia: intense pain in response to mildly painful stimulus (pinprick)

Allodynia: pain in response to completely innocuous stimulus (touch)

35
Q

What can neuropathic pain be caused by?

A

injury (amputation and subsequent phantom limb pain)

scar tissue from surgery (back surgery high risk)

nerve entrapment (carpal tunnel)

damaged nerves (diabetic neuropathy)