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Stage 3 - Case 1 (Pain) > Lecture 5, 6 & 7: Pain Mechanisms 1&2 & Pharmaceutics/Pharmacokinetics Of Pain > Flashcards

Lecture 5, 6 & 7: Pain Mechanisms 1&2 & Pharmaceutics/Pharmacokinetics Of Pain Flashcards

1
Q

What is pain?

A
  • Complex unpleasant phenomenon and experience originating in real or potential damaged tissue
  • Uniquely experienced and can’t be defined, identified or measured
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2
Q

What are the 3 systems that interact to produce pain?

A
  • Sensory: Discriminative system processes info about the strength, intensity, spatial aspects
  • Motivational: Affective system determines approach avoidance behaviours
  • Cognitive: Evaluative. Block, modulate or enhance perception of pain. Individuals learnt behaviour concerning pain experience
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3
Q

What are the categories of pain?

A
  • Somatogenic: Pain with a known cause and localised in the body tissue. 2 types: nociceptive (harmful stimuli being detected by nociceptors on the body) and neuropathic (nerve pain when nervous system malfunctions or damaged)
  • Psychogenic: Pain with no known cause but processing of sensitive info in the CNS is disturbed. Pain is related to mental/ emotional problems
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4
Q

What is acute pain?

A
  • Protective mechanism that alerts of an experience immediately harmful to the body mobilises individual to act fast
  • Onset: Sudden
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5
Q

What are some of the body’s responses to acute pain?

A
  • Stimulation of autonomic nervous system can be observed.
  • Mydriasis (dilation of pupil), tachycardia, sweating, incr HR, RR, BP, blood sugar
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6
Q

What is chronic pain?

A
  • Is persistent or intermittent and lasts at least 3-6 months
  • Cause is often unknown and depression often results
  • Disease/ condition and not protective and extends beyond healing period
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7
Q

How can pain tolerance be decreased?

A
  • Repeated exposure to pain
  • Fatigue, anger, boredom, apprehension
  • Sleep deprivation
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8
Q

How can pain tolerance be increased?

A
  • Alcohol consumption
  • Medication
  • Warmth/ distraction
  • Strong beliefs or faith
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9
Q

What are some of the ages that can percieve pain differently?

A
  • Children and elderly
  • Infants: First 1/2 days are less sensitive to pain. Full behavioual response is seen at 3-12 months
  • Older children: 15-18yrs have lower threshold
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10
Q

How is pain percieved using the gate theory?

A
  • Tissue damage is detected by receptors
  • 2 types of nerves: small fibres which if activated send signal to spinal cord and if large fibres activated the gate is closed (no signal)
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11
Q

What are the different portions of the nervous system responsible for sensation and perception of pain?

A
  • Afferent pathways
  • CNS
  • Efferent pathways
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12
Q

What are nociceptors?

A
  • Exist as free nerve endings
  • Subclasses are mechanical, thermal and polymodal (Chemoreceptors) nociceptors
  • Localised to muscle, skin and viscera. More in skin than internal structures
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13
Q

What are the different types of mammalian cutaneous fibre types?

A
  • A beta fibres most myelinated and the fastest conducting fibres. Associated with low threshold mechanoreceptors
  • A delta fibres are myelinated (not as thick as A beta and as fast). Crucial for fast signalling of injury
  • C fibres small fibres not myelianated and conduction is slow
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14
Q

How can different classes of primary afferent nociceptors be classified?

A
  • Histochemical markers e.g. lectins (IB4) or neurofilament proteins
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15
Q

How can nociceptors be divided into subsets and which do menthol and capsaicin activate?

A
  • Nociceptors localize specific classes of receptors or ion channels sensitive to thermal or mechanical stimuli
  • TRP channels - thermal sensitivity
  • TREK - co expressed with TRPs, K+ channel, activity reduced by heat
  • ASICS and DRASICS - detect H+. cation selective. DRASICs detect mechanical stimuli
    MDEG - amiloride sensitive sodium channel
  • Menthol: Trpm8, Capsaicin: Trpv1
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16
Q

How is the pain signal perceived in the brain?

A
  • Noxious stimuli is detected by the subclasses of nociceptors which then reaches threshold and generated AP. Attached to nerve fibres A beta (low threshold), A delta (high pain and C fibres even more) and terminate in dorsal horn (in spinal cord). Transmit info via neurotransmitter glutamate
  • Travels across axon and dorsal root ganglion (cell bodies)
  • Relayed up spinal cord through spinothalmic tract –> thalamus (brain)
  • Neurotransmitters are released in the pre synapse which are detected by receptors on the spinal cord (post synapse). Synapse in the dorsal horn
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17
Q

What happens in the level of the spinal cord?

A
  • Superficial laminae 1 and 2 (substantia gelatinosa) receive nociceptive inputs
  • Nociceptor afferents distribute to laminae 1 and 2 and low threshold mechanoreceptor afferents distribute to 3-6
18
Q

What are the 3 major neuronal types in the superficial dorsal horn

A
  • Projection neurons
  • Excitatory interneurones
  • Inhibitory interneurons
  • Each can receive inputs from A and/or C fibers. Descending and propiospinal axons connect to these neurons and extensive synaptic connections.
19
Q

How does excitation occur in nociceptive transduction?

A
  • Via Glutamate (via AMPA channels) and SP (NK1R) receptors
20
Q

What are the 2 divisions of the spinothalmic tract?

A
  • The neospinothalamic tract - Carries info to the mid brain, thalamus and post central gyrus (where pain is percieved)
    The Paleospinothalmic tract- Carries info to the reticular formation, pons, limbic system, and mid brain
21
Q

What do the different parts of the brain do with sensation of pain?

A
  • Thalamus, sensitive cortex: perceiving, describing, localising
  • Parts of the thalamus, brainstem and reticular formation: identify dull longer lasting and diffuse pain
  • The reticular formation and limbic system: Control the emotional and affective response to pain
22
Q

What is the role of the efferent analgesic system and what is its mechanisms?

A
  • Role: Inhibition of afferent pain signals
    1. Pain afferents stimulate the neurons in the periaqueductal gray (gray matter surrounding cerebral aqueduct in the midbrain results in activation of efferent antinociceptive pathways
    2. From there impulses are transmitted through spinal cord to dorsal horn
    3. There they inhibit or block transmission of nociceptive signals at the level of the dorsal horn
23
Q

What is congenital analgesia and erythromelagia?

A
  • Congenital analgesia: Can’t feel pain.
  • Erythromelalgia: causes redness and burning pain in different parts of the body. Hereditary and heterozygous
  • Both mutations in gene SCN9A - Na+ : channels either not transmitting AP or too often.
24
Q

How do nociceptors sensitive following injury?

A
  • Reduce threshold and in increase in response amplitude
  • Peripheral and Central sensitization - lower stimuli and build response (increased response)
  • Activation of thermal nociceptor is lowered and previously unresponsive A afferent mechanoreceptor responds
25
Q

What is primary hyperalgesia?

A
  • Condition where pain is perceived more intensely in the area injured.
  • Charactrized by increased spinal activation from in response to stimulation of A delta and C nociceptors
  • Hypersensitivity to mechanical and heat stimulus by sensitisation (respond more) of peripheral nociceptors
26
Q

What is Secondary Hyperalgesia?

A
  • That causes increased sensitivity in areas not affected by injury
  • Not accounted for by peripheral mechanisms
  • Central sensitisation (brain and spinal cord) w/ A beta fibres
27
Q

What are the main things that happen in sensitization and what mediators are released?

A
  • Damaged tissue, inflammatory and tumour cells release chemical mediators : Histamine, leukotrienes, bradykinin, norepinephrine
  • Afferent firing threshold is lowered
  • Reaponse to fixed stimulus increased
  • Spontaneous activity increased
28
Q

How is Chronic pain cause more increased pain sensations?

A
  • Tissue damage -> sensitised C afferent-> Hyperalgesia (increased pain)
  • Nerve damage -> sensitised C afferents -> Hyperalgesia and Allodynia (touch evoked pain)
    Innocuous stimulation -> Normal A beta afferents Allodynia
29
Q

What is neuropathic pain and what causes it?

A
  • Pain initiated or caused by a primary lesion or dysfunction in the nervous system
  • No obvious cause busy some common causes: alcoholism, amputation, back/leg/hip problem
30
Q

Why is Allodynia and Hyperalgesia?

A
  • Allodynia: Pain from a stimulus that doesn’t normally evoke pain. Thermal, mechanical
  • Hyperalgesia: Exaggerated response to a normally painful stimulus
31
Q

What is dysaesthesia and hyperpathia?

A
  • Dysaethesia: Unpleasant/ abnormal sensation (spontaneous or provoked)
  • Hyperpathia: Abnormally painful reaction to a stimulus. Especially repetitive stimulus
32
Q

What does accumulation of sodium channels at ectopic impulse sites mean?

A
  • One of the mechanism lowering action potential threshold and for spontaneous activity in damaged primary afferents
33
Q

What type of nociceptors are essential in secondary Hyperalgesia?

A
  • Capsaicin- insensitive A - nociceptors
34
Q

Give a summary of neuropathic pain mechanisms for peripheral nervous system?

A
  • Threshold for activation of injured primary afferents is lowered
  • Sensitization of peripheral afferents by inflammatory mediators
    Ectopic discharges may arise from the injury site or DRG. Changes to Na+ channels expression
35
Q

Give a summary for neuropathic pain mechanisms in the central nervous system

A

Central Sensitisation in the cord
– 2o to peripheral inputs
– 2o to central changes
• Reduced inhibition
• Functional (neurotransmitter) & anatomical (sprouting) changes in
Aβ fibres -> tactile allodynia (pain induced by light touch)
• Increased synaptic efficacy (increased glutamate release, co- release of glutamate and a peptide, activation of novel receptors e.g. NMDA or mGluRs
• Reduced inhibition/altered GABA receptor expression
• Up-regulation of postsynaptic receptors (e.g for substance P)
• Gene expression and altered phenotype of central neurones
• Unmasking of silent synapses
• Re-wiring of spinal or brain circuitry

36
Q

What is Fibromyalgia?

A
  • Disorder of pain processing due to abnormalities in how pain signals are processed in the CNS
  • 50% less stimulus is needed to evoke pain
  • Symptoms are: chronic widespread pain, fatigue, sleep disturbance
37
Q

How is codeine converted into morphine and how is morphine metabolised?

A
  • Codeine undergoes oxidation (Oxidative demethylation) -> morphine
  • Morphine undergoes glucuronidation to get either morphine 3-O-Glucuronide or morphine 6-O-Glucuronide
38
Q

How much codeine is converted into morphine?

A
  • 10%
  • Some patients cant convert codeine into morphine therefore no opiate effect
39
Q

What is suboxone used to treat and what is it made of?

A
  • Used to treat opioid addiction
  • Made of buprenorphine and naloxone. (Naloxone has a poor bioavailability under the tongue
40
Q

How do you increase heroin solubility?

A
  • Add acid (citric) to dissolve. Too much acid causes vein damage
  • Heat up
    Makes into a salt which is more soluble
41
Q

Name some anaesthetics

A
  • Nitrous oxide
  • Chloroform
  • Halothane
  • Isoflurane

Stage 3 - Case 1 (Pain) (13 decks)

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