Question 1
Question
What are the three ways in which a signal is terminated at a synapse?
Question 2
Question
What are some examples of anxiolytics?
Question 3
Question
What are some examples of anti-depressants?
Question 4
Question
What are some examples of anti-psychotics?
Question 5
Question
How do anxiolytics work?
Answer
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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.
Question 6
Question
Novel anxiolytics that block peripheral receptors instead of central ones relieve sedative symptoms.
Question 7
Question
Depression is thought to be caused by monoaminergic synaptic hyperactivity.
Question 8
Question
What do MAOI's do?
Question 9
Question
What do TCA and SSRI's do?
Question 10
Question
TCA's are much more selective than SSRI's at blocking serotonin rather than noradrenaline at monoaminergic synapses.
Question 11
Question
Typical neuroleptics are more selective at blocking dopamine receptors.
Question 12
Question
Psychosis is thought to be caused by dopaminergic hyperactivity.
Question 13
Question
Why can anti-psychotics sometimes cause parkinsonian?
Answer
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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.
Question 14
Question
As well as parkinsonian, what other motor symptoms can anti-psychotics produce? (CLOZAPINE DOES NOT PRODUCE THIS)
Question 15
Question
Which three areas of the brain are affected by anti-psychotics?
Question 16
Question
What do mechanical nociceptors respond to? What is an example?
Question 17
Question
What do polymodal nociceptors respond to? What is an example?
Answer
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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
Question 18
Question
Myelination tends to reflect upon what property of a primary sensory neurone?
Answer
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That is transmits a fast, sharp pain.
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That it transmits a slow, dull pain.
Question 19
Question
Frequency coding states what?
Answer
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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.
Question 20
Question
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)
Question 21
Question
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?
Answer
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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.
Question 22
Question
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.
Question 23
Question
The GATEKEEPER sends out excitatory signals to aid pain signals passing up to the brain.
Question 24
Question
Where is pain perceived?
Question 25
Question
Where is pain localised?
Question 26
Question
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.
Question 27
Question
Descending pathways that release endogenous opioids act where?
Question 28
Question
Primary hyperalgesia occurs where?
Question 29
Question
Secondary hyperalgesia occurs where?
Question 30
Question
Primary hyperalgesia occurs due to what process?
Answer
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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"
Question 31
Question
Which receptor does substance P act?
Question 32
Question
Which receptor does Glutamate act at?
Question 33
Question
Glutamate is usually released during normal, acute pain, rather than Substance P.
Question 34
Question
Why does binding of Substance P and Glutamate cause secondary hyperalgesia?
Answer
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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.
Question 35
Question
Neuropathic pain is the overall sensation of pain; the physiological factor and the psychogenic factor.
Question 36
Question
Name two types of endogenous opioids
Answer
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Enkephalins
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Beta-endorphins
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Naloxone
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Pethidine
Question 37
Question
Name two types of therapeutic agent opioids
Answer
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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
Question 38
Question
Name four types of synthetic agent opioids
Question 39
Question
Opioids are usually administered parenterally as the GIT does not absorb opioids well.
Question 40
Question
What are the three sites of action for opioids?
Answer
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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
Question 41
Question
What does label 2 show?
Answer
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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
Question 42
Question
What does label 3 show?
Question 43
Question
What does label 4 show?
Answer
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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
Question 44
Question
Opioids inhibit adenylyl cyclase which leads to increased cAMP levels.
Question 45
Question
What effects occur due to opioid action?
Question 46
Question
What are two problems with prolonged opioid use?
Question 47
Question
NSAIDS are cyclo-oxygenase inhibitors.
Question 48
Question
Aspirin is a competitive inhibitor of COX.
Question 49
Question
COX enzymes catalyse the reaction that turns arachidonic acid into prostaglandins. Inhibition of COX therefore reduces prostaglandin production and thus inflammation.
Question 50
Question
As a result of the action of NSAIDs, what effects are produced?
Answer
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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
Question 51
Question
Prostaglandins help to produce the mucus lining of the stomach, therefore NSAIDs can cause increased risk of peptic ulcers.