Quiz
NMS Semester 2 Set 2 Quiz - Anti-depressants, anti-psychotics, anxiolytics and control of pain.
Fragen in diesem Quiz (51)
1What are the three ways in which a signal is terminated at a synapse?
- AReuptake
- BEnzymatic breakdown
- CNegative feedback via autoreceptors on the presynaptic membrane
- DPositive feedback via autoreceptors on the presynaptic membrane
- EDepolarisation
- FHyperpolarisation
2What are some examples of anxiolytics?
- ABenzodiazepines
- BBarbiturates
- CAlcohol
- DMonoamine oxidase inhibitors
- ESSRI's
3What are some examples of anti-depressants?
- AMonoamine oxidase inhibitors
- BTricyclic
- CSelective serotonin reuptake inhibitors
- DBarbiturates
- EBenzodiazepines
4What are some examples of anti-psychotics?
- ATypical neuroleptics
- BAtypical neuroleptics
- CSelective serotonin reuptake inhibitors
- DBenzodiazepines
- EAlcohol
5How do anxiolytics work?
- AThey 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.
- BThey inhibit the neurotransmission at a synaptic junction which creates fewer excitatory signals in the post-synaptic membrane.
6Novel anxiolytics that block peripheral receptors instead of central ones relieve sedative symptoms.
- ARichtig
- BFalsch
7Depression is thought to be caused by monoaminergic synaptic hyperactivity.
- ARichtig
- BFalsch
8What do MAOI's do?
- AInhibit the reuptake of serotonin and noradrenaline into the pre-synaptic knob.
- BInhibit the monoamine oxidase enzyme that breaks down serotonin and noradrenaline neurotransmitters.
9What do TCA and SSRI's do?
- AThey inhibit the re-uptake of serotonin and noradrenaline from the synaptic cleft.
- BThey inhibit monoamine oxidase which breaks serotonin and noradrenaline down.
10TCA's are much more selective than SSRI's at blocking serotonin rather than noradrenaline at monoaminergic synapses.
- ARichtig
- BFalsch
11Typical neuroleptics are more selective at blocking dopamine receptors.
- ARichtig
- BFalsch
12Psychosis is thought to be caused by dopaminergic hyperactivity.
- ARichtig
- BFalsch
13Why can anti-psychotics sometimes cause parkinsonian?
- AAnti-psychotics reduce the activity at dopaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
- BAnti-psychotics increase the activity at dopaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
- CAnti-psychotics reduce the activity at monoaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
- DAnti-psychotics increase the activity at monoaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
14As well as parkinsonian, what other motor symptoms can anti-psychotics produce? (CLOZAPINE DOES NOT PRODUCE THIS)
- ATardive dyskinesia
- BDuchene muscular dystrophy
- CAtaxia
15Which three areas of the brain are affected by anti-psychotics?
- AMesolimbal
- BMesocortical
- CNigrostriatal
- DLateral hypothalamic area
- EPrimary gustatory cortex
16What do mechanical nociceptors respond to? What is an example?
- AA-delta fibres
- BC fibres
- CSharp cuts or Blunt force
- DDamaging heat
17What do polymodal nociceptors respond to? What is an example?
- AA-delta fibres
- BC fibres
- CMany modalities
- DOnly a few modalities
18Myelination tends to reflect upon what property of a primary sensory neurone?
- AThat is transmits a fast, sharp pain.
- BThat it transmits a slow, dull pain.
19Frequency coding states what?
- AThe greater the pain stimulus is, the higher the frequency of action potentials fired from the periphery to the CNS.
- BThe lower the pain stimulus is, the higher the frequency of action potentials fired from the periphery to the CNS.
20The 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)
- ARichtig
- BFalsch
21When 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?
- AExcitatory neurotransmitters are released from the a-delta/c fibre and this causes pain signals to be carried to the brain.
- BExcitatory 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.
22Rubbing 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.
- ARichtig
- BFalsch
23The GATEKEEPER sends out excitatory signals to aid pain signals passing up to the brain.
- ARichtig
- BFalsch
24Where is pain perceived?
- ASubcortically (before the cortex)
- BAt the cortex
25Where is pain localised?
- AThe cortex
- BSubcortically (before the cortex)
26The 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.
- ARichtig
- BFalsch
27Descending pathways that release endogenous opioids act where?
- AThe GATEKEEPER to enhance inhibition of pain signals ascending to the brain.
- BThe GATEKEEPER to enhance pain signals ascending to the brain.
28Primary hyperalgesia occurs where?
- ACNS
- BPeripheral nervous system
29Secondary hyperalgesia occurs where?
- ACNS
- BPeripheral nervous system
30Primary hyperalgesia occurs due to what process?
- ANoxious stimulus occurs after initial injury -> AXON REFLEX -> SP and CGRP release -> vasodilatation + immune cell activation -> Bradykinin, PG etc "inflammatory soup"
- BNoxious stimulus occurs after initial injury -> AXON REFLEX -> Bradykinin and CGRP release -> vasodilatation + immune cell activation -> SP, PG etc "inflammatory soup"
- CNoxious stimulus occurs after initial injury -> AXON REFLEX -> SP and Bradykinin release -> vasodilatation + immune cell activation -> CGRP, PG etc "inflammatory soup"
31Which receptor does substance P act?
- ANK-1
- BAMPA
- CNMDA
32Which receptor does Glutamate act at?
- ANK-1
- BAMPA
- CNMDA
33Glutamate is usually released during normal, acute pain, rather than Substance P.
- ARichtig
- BFalsch
34Why does binding of Substance P and Glutamate cause secondary hyperalgesia?
- ABinding 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.
- BBinding 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.
- CBinding 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.
35Neuropathic pain is the overall sensation of pain; the physiological factor and the psychogenic factor.
- ARichtig
- BFalsch
36Name two types of endogenous opioids
- AEnkephalins
- BBeta-endorphins
- CNaloxone
- DPethidine
37Name two types of therapeutic agent opioids
- AHeroin
- BCodeine
- CMethadone
- DFentanyl
- EBeta-endorphins
38Name four types of synthetic agent opioids
- APethidine
- BFentanyl
- CMethadone
- DBuprenorphine (partial agonist)
- EFluoxetine
- FEnkephalins
39Opioids are usually administered parenterally as the GIT does not absorb opioids well.
- ARichtig
- BFalsch
40What are the three sites of action for opioids?
- AInhibition of primary sensory neurones synapsing to second order neurones in the spinal cord
- BExcitation of the nucleus raphe magnus which causes inhibition of pain signals at the spinal cord level
- CExcitation of the nucleus reticularis which causes inhibition of pain signals at the spinal cord level
- DDecreased excitability of peripheral nociceptor neurones
41What does label 2 show?
- AActivation of the G-protein
- BLess opening of Ca2+ channels - less neurotransmitter release
- CMore opening of K+ channels - leading to hyperpolarisation
42What does label 3 show?
- AActivation of G-protein
- BLess opening of Ca2+ channels - less neurotransmitter release
- CMore opening of K+ channels - leading to hyperpolarisation
43What does label 4 show?
- AActivation of the G-protein
- BLess opening of Ca2+ channels - less neurotransmitter release
- CMore opening of K+ channels - leading to hyperpolarisation
44Opioids inhibit adenylyl cyclase which leads to increased cAMP levels.
- ARichtig
- BFalsch
45What effects occur due to opioid action?
- AAnalgesia
- BConstriction of smooth muscle at all sites
- CNausea
- DRelaxation of smooth muscle at all sites
- EEuphoria at all sites
46What are two problems with prolonged opioid use?
- ATolerance - due to increased adenylyl cyclase expression
- BDependence - withdrawal symptoms
47NSAIDS are cyclo-oxygenase inhibitors.
- ARichtig
- BFalsch
48Aspirin is a competitive inhibitor of COX.
- ARichtig
- BFalsch
49COX enzymes catalyse the reaction that turns arachidonic acid into prostaglandins. Inhibition of COX therefore reduces prostaglandin production and thus inflammation.
- ARichtig
- BFalsch
50As a result of the action of NSAIDs, what effects are produced?
- AAnti-pyretic - decreases the temp set point in the hypothalamus
- BAnti-inflammatory - dec PG = dec vasodilation
- CAnalgesia - dec PG = decrease sensitivity of nerves to inflammatory pain
- DAnti-inflammatory - dec PG = inc vasodilation
- EAnti-pyretic - decreases the temp set point in the basal ganglia
51Prostaglandins help to produce the mucus lining of the stomach, therefore NSAIDs can cause increased risk of peptic ulcers.
- ARichtig
- BFalsch
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