True/False: Somatosensation and the perception of pain
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| Pain information is transmitted to the brain in the dorsal column. | False, pain information is transmitted to the brain in the spinothalamic tracts.
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| Primary hyperalgesia occurs in undamaged tissue surrounding the originally damaged area. | False, primary hyperalgesia occurs within the damaged area. Secondary hyperalgesia occurs in the surrounding undamaged tissues.
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| The co-transmitter substance P causes a very long-lasting excitatory post-synaptic potential, thereby helping to sustain the effect of noxious stimuli. | True, the co-transmitter substance P causes a very long-lasting excitatory post-synaptic potential, thereby helping to sustain the effect of noxious stimuli.
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| The central nervous system is able to accurately distinguish between superficial pain from cutaneous structures and pain from the viscera. | False, nociceptor fibres from viscera and cutaneous structures converge on the same pathway hence there is an inability to distinguish between deep and superficial pain.
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| Inflammation affecting the diaphragm is felt in the tip of the shoulder. | True, phrenic nerve roots C3 and C5 are involved.
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| Morphine is a u-receptor agonist. | True, endogenous enkephalins are also active at u-receptors (as well as delta-receptors).
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| Naloxone is a u-receptor antagonist. | True, hence its use in the management of opiate overdose.
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| Opioid analgesics act by reducing the production of inflammatory mediators. | False, non-steroidal anti-inflammatory drugs (NSAID's) reduce the production of inflammatory mediators.
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| Opioids cause pupillary dilation. | False, opioids cause miosis (pupillary constriction) by stimulation of the parasympathetic component of cranial nerve III.
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| Co-codamol is a combination of codeine and paracetamol. | True, this is a common first-line prescription analgesic.
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| Naloxone is a long-acting u-receptor antagonist. | False, naloxone is short acting.
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| Naloxone acts more rapidly than naltrexone. | True, naloxone is rapid acting with a short duration of action whereas naltrexone is slower acting but has a longer duration of action.
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| Opioid overdose causes hyperventilation. | False, opioid overdose causes respiratory depression.
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| With repeated administration of opioids and consequent tolerance, pin-point pupils (characteristic of overdose) become less obvious. | False, there is no tolerance to pupillary constriction with repeated opioid administration.
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| Opioid overdose causes increased PaO2. | False, opioid overdose causes respiratory depression with increased PaCO2 and decreased PaO2.
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| Morphine is effective when given orally. | False, when given orally, a high rate of first pass metabolism results in poor bioavailability.
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| Morphine has a half-life of of approximately 12 hours. | False, morphine has a half-life of approximately 3 hours.
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| Codeine exhibits high oral bioavailability. | True, hence its use in oral analgesics such as co-codamol.
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| Pethidine does not cause miosis. | True, pethidine does not cause miosis.
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| Methadone has a half life exceeding 24 hours. | True, hence its usefulness as a maintenance drug in those addicted to opiates.
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| Cyclo-oxygenase metabolises arachidonic acid to leukotrienes. | False, cyclo-oxygenase metabolises arachidonic acid to prostaglandins.
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| NSAIDs upregulate cyclo-oxygenase. | False, NSAIDs inhibit cyclo-oxygenase.
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| Gastric ulceration is an important side effect of NSAID use. | True, potentially fatal bleeding may occur.
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| Reye's syndrome is associated with aspirin use in children. | True, Reye's syndrome causes liver damage and encephalopathy.
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| Tranexamic acid is an NSAID. | False, tranexamic acid is an anti-fibrinolytic and is not to be confused with mefenamic acid - which is an NSAID.
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| Local anaesthetics block the ability of axons to conduct action potentials. | True, local anaesthetics block the ability of axons to conduct action potentials.
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| Local anaesthetics block K+ channels in the axonal membrane. | False, local anaesthetics block Na+ channels in the axonal membrane.
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| Local anaesthetics are weak acids. | False, local anaesthetics are weak bases.
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| Local anaesthetics can pass straight through the lipid membrane of the axon when in the hydrophilic state. | False, in the hydrophilic state they may only enter through the open Na+ channel.
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| At low concentrations, local anaesthetics only affect small-diameter myelinated and non-myelinated fibres. | True, hence administration of local anaesthetic agents can be used to produce a differential nerve block affecting only A-delta and C fibres.
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| The sensory homunculus is organised so that a given area of the body has a proportionate area of cortex responsible for its processing, regardless of the density of sensory receptors in that area. | False, areas used for exploration which have the greatest receptor density have a disproportionately large area of corresponding sensory cortex.
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| The sensory cortex is located in the frontal lobe. | False, sensory cortex is located in the parietal lobe.
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| C type sensory afferent fibres are unmyelinated. | True, these fibres transmit information from nociceptors and thermoreceptors.
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| Fibres signalling thermal information travel in the dorsal column of the spinal cord. | False, fibres signalling thermal information travel in the spinothalamic tract of the spinal cord.
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| Slowly adapting receptors are particularly adept at signalling the rate of change and duration of a stimulus. | False, slowly adapting fibres typically signal magnitude or location whereas rapidly adapting fibres signal rate of change and duration.
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