NMS Semester 2 Set 2 Quiz - Anti-depressants, anti-psychotics, anxiolytics and control of pain.

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Question 1

Question
What are the three ways in which a signal is terminated at a synapse?
Answer
  • Reuptake
  • Enzymatic breakdown
  • Negative feedback via autoreceptors on the presynaptic membrane
  • Positive feedback via autoreceptors on the presynaptic membrane
  • Depolarisation
  • Hyperpolarisation

Question 2

Question
What are some examples of anxiolytics?
Answer
  • Benzodiazepines
  • Barbiturates
  • Alcohol
  • Monoamine oxidase inhibitors
  • SSRI's

Question 3

Question
What are some examples of anti-depressants?
Answer
  • Monoamine oxidase inhibitors
  • Tricyclic
  • Selective serotonin reuptake inhibitors
  • Barbiturates
  • Benzodiazepines

Question 4

Question
What are some examples of anti-psychotics?
Answer
  • Typical neuroleptics
  • Atypical neuroleptics
  • Selective serotonin reuptake inhibitors
  • Benzodiazepines
  • Alcohol

Question 5

Question
How do anxiolytics work?
Answer
  • 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.
  • 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.
Answer
  • True
  • False

Question 7

Question
Depression is thought to be caused by monoaminergic synaptic hyperactivity.
Answer
  • True
  • False

Question 8

Question
What do MAOI's do?
Answer
  • Inhibit the reuptake of serotonin and noradrenaline into the pre-synaptic knob.
  • Inhibit the monoamine oxidase enzyme that breaks down serotonin and noradrenaline neurotransmitters.

Question 9

Question
What do TCA and SSRI's do?
Answer
  • They inhibit the re-uptake of serotonin and noradrenaline from the synaptic cleft.
  • They inhibit monoamine oxidase which breaks serotonin and noradrenaline down.

Question 10

Question
TCA's are much more selective than SSRI's at blocking serotonin rather than noradrenaline at monoaminergic synapses.
Answer
  • True
  • False

Question 11

Question
Typical neuroleptics are more selective at blocking dopamine receptors.
Answer
  • True
  • False

Question 12

Question
Psychosis is thought to be caused by dopaminergic hyperactivity.
Answer
  • True
  • False

Question 13

Question
Why can anti-psychotics sometimes cause parkinsonian?
Answer
  • Anti-psychotics reduce the activity at dopaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
  • Anti-psychotics increase the activity at dopaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
  • Anti-psychotics reduce the activity at monoaminergic synapses. This can be so extreme that motor function is impaired and parkinson like symptoms are experienced.
  • 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)
Answer
  • Tardive dyskinesia
  • Duchene muscular dystrophy
  • Ataxia

Question 15

Question
Which three areas of the brain are affected by anti-psychotics?
Answer
  • Mesolimbal
  • Mesocortical
  • Nigrostriatal
  • Lateral hypothalamic area
  • Primary gustatory cortex

Question 16

Question
What do mechanical nociceptors respond to? What is an example?
Answer
  • A-delta fibres
  • C fibres
  • Sharp cuts or Blunt force
  • Damaging heat

Question 17

Question
What do polymodal nociceptors respond to? What is an example?
Answer
  • A-delta fibres
  • C fibres
  • Many modalities
  • Only a few modalities

Question 18

Question
Myelination tends to reflect upon what property of a primary sensory neurone?
Answer
  • That is transmits a fast, sharp pain.
  • That it transmits a slow, dull pain.

Question 19

Question
Frequency coding states what?
Answer
  • The greater the pain stimulus is, the higher the frequency of action potentials fired from the periphery to the CNS.
  • 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)
Answer
  • True
  • False

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
  • Excitatory neurotransmitters are released from the a-delta/c fibre and this causes pain signals to be carried to the brain.
  • 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.
Answer
  • True
  • False

Question 23

Question
The GATEKEEPER sends out excitatory signals to aid pain signals passing up to the brain.
Answer
  • True
  • False

Question 24

Question
Where is pain perceived?
Answer
  • Subcortically (before the cortex)
  • At the cortex

Question 25

Question
Where is pain localised?
Answer
  • The cortex
  • Subcortically (before the cortex)

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.
Answer
  • True
  • False

Question 27

Question
Descending pathways that release endogenous opioids act where?
Answer
  • The GATEKEEPER to enhance inhibition of pain signals ascending to the brain.
  • The GATEKEEPER to enhance pain signals ascending to the brain.

Question 28

Question
Primary hyperalgesia occurs where?
Answer
  • CNS
  • Peripheral nervous system

Question 29

Question
Secondary hyperalgesia occurs where?
Answer
  • CNS
  • Peripheral nervous system

Question 30

Question
Primary hyperalgesia occurs due to what process?
Answer
  • Noxious stimulus occurs after initial injury -> AXON REFLEX -> SP and CGRP release -> vasodilatation + immune cell activation -> Bradykinin, PG etc "inflammatory soup"
  • Noxious stimulus occurs after initial injury -> AXON REFLEX -> Bradykinin and CGRP release -> vasodilatation + immune cell activation -> SP, PG etc "inflammatory soup"
  • 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?
Answer
  • NK-1
  • AMPA
  • NMDA

Question 32

Question
Which receptor does Glutamate act at?
Answer
  • NK-1
  • AMPA
  • NMDA

Question 33

Question
Glutamate is usually released during normal, acute pain, rather than Substance P.
Answer
  • True
  • False

Question 34

Question
Why does binding of Substance P and Glutamate cause secondary hyperalgesia?
Answer
  • 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.
  • 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.
  • 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.
Answer
  • True
  • False

Question 36

Question
Name two types of endogenous opioids
Answer
  • Enkephalins
  • Beta-endorphins
  • Naloxone
  • Pethidine

Question 37

Question
Name two types of therapeutic agent opioids
Answer
  • Heroin
  • Codeine
  • Methadone
  • Fentanyl
  • Beta-endorphins

Question 38

Question
Name four types of synthetic agent opioids
Answer
  • Pethidine
  • Fentanyl
  • Methadone
  • Buprenorphine (partial agonist)
  • Fluoxetine
  • Enkephalins

Question 39

Question
Opioids are usually administered parenterally as the GIT does not absorb opioids well.
Answer
  • True
  • False

Question 40

Question
What are the three sites of action for opioids?
Answer
  • Inhibition of primary sensory neurones synapsing to second order neurones in the spinal cord
  • Excitation of the nucleus raphe magnus which causes inhibition of pain signals at the spinal cord level
  • Excitation of the nucleus reticularis which causes inhibition of pain signals at the spinal cord level
  • Decreased excitability of peripheral nociceptor neurones

Question 41

Question
What does label 2 show?
Answer
  • Activation of the G-protein
  • Less opening of Ca2+ channels - less neurotransmitter release
  • More opening of K+ channels - leading to hyperpolarisation

Question 42

Question
What does label 3 show?
Answer
  • Activation of G-protein
  • Less opening of Ca2+ channels - less neurotransmitter release
  • More opening of K+ channels - leading to hyperpolarisation

Question 43

Question
What does label 4 show?
Answer
  • Activation of the G-protein
  • Less opening of Ca2+ channels - less neurotransmitter release
  • More opening of K+ channels - leading to hyperpolarisation

Question 44

Question
Opioids inhibit adenylyl cyclase which leads to increased cAMP levels.
Answer
  • True
  • False

Question 45

Question
What effects occur due to opioid action?
Answer
  • Analgesia
  • Constriction of smooth muscle at all sites
  • Nausea
  • Relaxation of smooth muscle at all sites
  • Euphoria at all sites

Question 46

Question
What are two problems with prolonged opioid use?
Answer
  • Tolerance - due to increased adenylyl cyclase expression
  • Dependence - withdrawal symptoms

Question 47

Question
NSAIDS are cyclo-oxygenase inhibitors.
Answer
  • True
  • False

Question 48

Question
Aspirin is a competitive inhibitor of COX.
Answer
  • True
  • False

Question 49

Question
COX enzymes catalyse the reaction that turns arachidonic acid into prostaglandins. Inhibition of COX therefore reduces prostaglandin production and thus inflammation.
Answer
  • True
  • False

Question 50

Question
As a result of the action of NSAIDs, what effects are produced?
Answer
  • Anti-pyretic - decreases the temp set point in the hypothalamus
  • Anti-inflammatory - dec PG = dec vasodilation
  • Analgesia - dec PG = decrease sensitivity of nerves to inflammatory pain
  • Anti-inflammatory - dec PG = inc vasodilation
  • 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.
Answer
  • True
  • False
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