Questão 1
Questão
What are the three ways in which a signal is terminated at a synapse?
Questão 2
Questão
What are some examples of anxiolytics?
Questão 3
Questão
What are some examples of anti-depressants?
Questão 4
Questão
What are some examples of anti-psychotics?
Questão 5
Questão
How do anxiolytics work?
Responda
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They bind to a different site to GABA and increase the affinity of the receptor for GABA, causing increased inhibition and the user to feel drowsy.
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They inhibit the neurotransmission at a synaptic junction which creates fewer excitatory signals in the post-synaptic membrane.
Questão 6
Questão
Novel anxiolytics that block peripheral receptors instead of central ones relieve sedative symptoms.
Questão 7
Questão
Depression is thought to be caused by monoaminergic synaptic hyperactivity.
Questão 8
Questão
What do MAOI's do?
Questão 9
Questão
What do TCA and SSRI's do?
Questão 10
Questão
TCA's are much more selective than SSRI's at blocking serotonin rather than noradrenaline at monoaminergic synapses.
Questão 11
Questão
Typical neuroleptics are more selective at blocking dopamine receptors.
Questão 12
Questão
Psychosis is thought to be caused by dopaminergic hyperactivity.
Questão 13
Questão
Why can anti-psychotics sometimes cause parkinsonian?
Responda
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Anti-psychotics reduce the activity at dopaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
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Anti-psychotics increase the activity at dopaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
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Anti-psychotics reduce the activity at monoaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
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Anti-psychotics increase the activity at monoaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
Questão 14
Questão
As well as parkinsonian, what other motor symptoms can anti-psychotics produce? (CLOZAPINE DOES NOT PRODUCE THIS)
Questão 15
Questão
Which three areas of the brain are affected by anti-psychotics?
Questão 16
Questão
What do mechanical nociceptors respond to? What is an example?
Questão 17
Questão
What do polymodal nociceptors respond to? What is an example?
Responda
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A-delta fibres
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C fibres
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Many modalities
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Only a few modalities
Questão 18
Questão
Myelination tends to reflect upon what property of a primary sensory neurone?
Responda
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That is transmits a fast, sharp pain.
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That it transmits a slow, dull pain.
Questão 19
Questão
Frequency coding states what?
Responda
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The greater the pain stimulus is, the higher the frequency of action potentials fired from the periphery to the CNS.
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The lower the pain stimulus is, the higher the frequency of action potentials fired from the periphery to the CNS.
Questão 20
Questão
The laminar order in which primary sensory neurones synapse in the spinal cord means that each "sheet" in the spinal cord receives input from a particular part of the body (somatotopic)
Questão 21
Questão
When a painful stimulus is detected and an action potential is propagated to the spinal cord, how is the pain then transmitted up to the brain?
Responda
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Excitatory neurotransmitters are released from the a-delta/c fibre and this causes pain signals to be carried to the brain.
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Excitatory neurotransmitter are released from the a-delta/c fibre which stimulate an inhibitory interneurone to inhibit the GATEKEEPER. This inhibits the inhibitory GATEKEEPER and weakens the inhibition that the GATEKEEPER provides to the ascending pain signal. This allows pain signals to carry up to the brain.
Questão 22
Questão
Rubbing your knee activates a-beta mechanoreceptor fibres which cause excitatory neurotransmitter release to the GATEKEEPER which then releases more inhibitory signals to block pain signals going to the brain.
Questão 23
Questão
The GATEKEEPER sends out excitatory signals to aid pain signals passing up to the brain.
Questão 24
Questão
Where is pain perceived?
Questão 25
Questão
Where is pain localised?
Questão 26
Questão
The emotional (psychogenic) element of pain means that it is not just a single part of the brain that takes part in pain signal processing, but many different regions that co-ordinate together.
Questão 27
Questão
Descending pathways that release endogenous opioids act where?
Questão 28
Questão
Primary hyperalgesia occurs where?
Questão 29
Questão
Secondary hyperalgesia occurs where?
Questão 30
Questão
Primary hyperalgesia occurs due to what process?
Responda
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Noxious stimulus occurs after initial injury -> AXON REFLEX -> SP and CGRP release -> vasodilatation + immune cell activation -> Bradykinin, PG etc "inflammatory soup"
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Noxious stimulus occurs after initial injury -> AXON REFLEX -> Bradykinin and CGRP release -> vasodilatation + immune cell activation -> SP, PG etc "inflammatory soup"
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Noxious stimulus occurs after initial injury -> AXON REFLEX -> SP and Bradykinin release -> vasodilatation + immune cell activation -> CGRP, PG etc "inflammatory soup"
Questão 31
Questão
Which receptor does substance P act?
Questão 32
Questão
Which receptor does Glutamate act at?
Questão 33
Questão
Glutamate is usually released during normal, acute pain, rather than Substance P.
Questão 34
Questão
Why does binding of Substance P and Glutamate cause secondary hyperalgesia?
Responda
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Binding of Substance P and Glutamate activate the NK-1 and AMPA receptors respectively. This causes sufficient depolarisation in order to repel the magnesium dependent block out of the VG Ca2+ channel. Calcium entry causes 2ndry messenger activation and increased neurone responsiveness. This increases the rate of AP firing and explains why pain is more intense in secondary hyperalgesia.
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Binding of Substance P and Glutamate activate the AMPA and NK-1 receptors respectively. This causes sufficient depolarisation in order to repel the magnesium dependent block out of the VG Ca2+ channel. Calcium entry causes 2ndry messenger activation and increased neurone responsiveness. This increases the rate of AP firing and explains why pain is more intense in secondary hyperalgesia.
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Binding of Substance P and Glutamate activate the NK-1 and AMPA receptors respectively. This causes sufficient depolarisation in order to repel the calcium dependent block out of the VG Ca2+ channel. Calcium entry causes 2ndry messenger activation and increased neurone responsiveness. This increases the rate of AP firing and explains why pain is more intense in secondary hyperalgesia.
Questão 35
Questão
Neuropathic pain is the overall sensation of pain; the physiological factor and the psychogenic factor.
Questão 36
Questão
Name two types of endogenous opioids
Responda
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Enkephalins
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Beta-endorphins
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Naloxone
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Pethidine
Questão 37
Questão
Name two types of therapeutic agent opioids
Responda
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Heroin
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Codeine
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Methadone
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Fentanyl
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Beta-endorphins
Questão 38
Questão
Name four types of synthetic agent opioids
Questão 39
Questão
Opioids are usually administered parenterally as the GIT does not absorb opioids well.
Questão 40
Questão
What are the three sites of action for opioids?
Responda
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Inhibition of primary sensory neurones synapsing to second order neurones in the spinal cord
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Excitation of the nucleus raphe magnus which causes inhibition of pain signals at the spinal cord level
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Excitation of the nucleus reticularis which causes inhibition of pain signals at the spinal cord level
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Decreased excitability of peripheral nociceptor neurones
Questão 41
Questão
What does label 2 show?
Responda
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Activation of the G-protein
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Less opening of Ca2+ channels - less neurotransmitter release
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More opening of K+ channels - leading to hyperpolarisation
Questão 42
Questão
What does label 3 show?
Questão 43
Questão
What does label 4 show?
Responda
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Activation of the G-protein
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Less opening of Ca2+ channels - less neurotransmitter release
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More opening of K+ channels - leading to hyperpolarisation
Questão 44
Questão
Opioids inhibit adenylyl cyclase which leads to increased cAMP levels.
Questão 45
Questão
What effects occur due to opioid action?
Questão 46
Questão
What are two problems with prolonged opioid use?
Questão 47
Questão
NSAIDS are cyclo-oxygenase inhibitors.
Questão 48
Questão
Aspirin is a competitive inhibitor of COX.
Questão 49
Questão
COX enzymes catalyse the reaction that turns arachidonic acid into prostaglandins. Inhibition of COX therefore reduces prostaglandin production and thus inflammation.
Questão 50
Questão
As a result of the action of NSAIDs, what effects are produced?
Responda
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Anti-pyretic - decreases the temp set point in the hypothalamus
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Anti-inflammatory - dec PG = dec vasodilation
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Analgesia - dec PG = decrease sensitivity of nerves to inflammatory pain
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Anti-inflammatory - dec PG = inc vasodilation
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Anti-pyretic - decreases the temp set point in the basal ganglia
Questão 51
Questão
Prostaglandins help to produce the mucus lining of the stomach, therefore NSAIDs can cause increased risk of peptic ulcers.