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Neuro > Neuromodulation > Flashcards

Neuromodulation Flashcards

1
Q

What is the function of dopamine?

A

A neuromodulator related to motor control, reward mechanisms, and overall cerebral cortex function

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2
Q

When do dopamine neurons release their transmitters?

A

When an unexpected reward is received or in response to stimuli that are predictive of reward

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3
Q

What are the main effects of the neurotransmitters norepinephrine and epinephrine?

A

Brain arousal, sympathetic nervous system (ex. fight or flight responses)

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4
Q

What is the main function of serotonin?

A

Mood regulation with some functions in autonomic roles and promotion of wakefullness

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5
Q

What is the function of histamine as a neurotransmitter?

A

It is part of anxiety and stress-hormone release system

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6
Q

Where is histamine found in the brain?

A

Within the hypothalamus in neurons of the tuberomammillary nucleus

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7
Q

Which peptide neuromodulators enhance and suppress pain?

A

Enhance: substance P

Suppress: endorphins and enkephalin

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8
Q

What are the three major sources of dopamine?

A

substantia nigra pars compacta (in the basal ganglia nucleus of the midbrain)

ventral tegmental area (adjacent to substantia nigra in midbrain)

hypothalamus (provides dopamine to sympathetic branch of ANS and pituitary)

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9
Q

Where is norepinephrine and epinephrine produced?

A

Locus ceruleus in the dorsal pons

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10
Q

Where is serotonin produced?

A

Raphe nuclei (extends up through brainstem)

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11
Q

What are the major centers of acetylcholine production?

A

basal forebrain nuclei

brainstem nuclei (pedunculopontine and laterodorsal tegmental nuclei of the pons)

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12
Q

What is the function of hypocretin?

A

It stimulates appetite and is involved in metabolism, energy management, and sleep-wake cycles

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13
Q

Where is hypocretin produced?

A

Lateral hypothalamus

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14
Q

What is the general effect of NE on GPCR signaling?

A

Often stimulating (beta) but can cause inhibition (alpha2). Terminated by norepinephrine transporters and MAOs

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15
Q

What is the mechanism of termination of serotonin action?

A

serotonin transporter (SERT) and MAOs

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16
Q

What are the two major receptor types for dopamine? What do they do?

A

D1 class - activate adenylate cyclase and are generally stimulating

D2 class - inhibit adenylate cyclase and are generally inhibitory

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17
Q

What is the most prominent location of D1 class receptors?

A

Basal ganglia neurons of the striatum and links the “direct pathway” for initiation of movement

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18
Q

What is the most prominent location of D2 class receptors?

A

Basal ganglia neurons of the striatum that provide a link to the “indirect pathway” for inhibition of movement

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19
Q

Which neurotransmitters are involved in staying awake?

A

Norepinephrine, serotonin, acetylcholine, histamine, hypocretin

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20
Q

Which neurotransmitters are involved in non-REM sleep?

A

GABA

Galanin

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21
Q

Which neurotransmitters are involved in REM sleep?

A

Acetylcholine (most)

GABA

Galanin

Glycine

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22
Q

Which correctly matches a neuromodulator with its principal nucleus of origin?

a) histamine, raphe nuclei
b) acetylcholine, hypothalamus
c) serotonin, hypothalamus
d) norepinephrine, locus ceruleus
e) dopamine, hypothalamus

A

d) norepinephrine, locus ceruleus

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23
Q

Which neuromodulator has a major source of origin (cell bodies) in the telencephalon?

a) acetylcholine
b) norepinephrine
c) serotonin
d) histamine
e) 5-HTP

A

a) acetylcholine

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24
Q

Which is a common feature of the initial synthetic step for Dopamine and Serotonin?

a) hydroxylase enzyme
b) tyrosine amino acid
c) tryptophan amino acid
d) monoamine oxidase
e) 5-HTP

A

a) hydroxylase enzyme

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25
Q

Which is not a feature of the signaling mediated by neuromodulators?

a) amplification of effects by enzymes that convert multiple molecules
b) rapid and discrete action
c) wide variety of potential ultimate effects
d) phosphorylation of membrane proteins
e) control of overall neuronal excitability

A

b) rapid and discrete action

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26
Q

Cocaine and amphetamines share which action?

a) reduction of the duration and spatial extent of dopamine action
b) increase the duration and spatial extent of dopamine action
c) increasing the activity of the dopamine transporter
d) increasing the action of the serotonin transporter
e) reduction of the symptoms of schizophrenia

A

b) increase the duration and spatial extent of dopamine action

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27
Q

What is the mechanism of levodopa?

A

increases dopamine availablity (used for Parkinson’s disease)

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28
Q

What is a symptom of excess serotonin? Insufficiency?

A

Excess: mania

Insufficiency: depression

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29
Q

What is the mechanism of cocaine?

A

It blocks DAT and increases the duration and spatial extent of dopamine

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30
Q

How is the action of dopamine terminated?

A

DAT and MAO

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31
Q

What is the difference between pain and nociception?

A

nociception = physical transmission of electrical signals triggered by tissue damage from tissues to the brain

pain = conscious determination by the individual of an unpleasant sensation often accompanied by tissue damage

32
Q

What is pain transduction?

A

conversion of energy from a noxious thermal, mechanical, or chemical stimulus into electrical energy (nerve impulses) by sensory receptors

33
Q

What is pain transmission?

A

transmission of transduced pain signals from the site of transduction to the spinal cord and brain

34
Q

What is pain perception?

A

appreciation of signals arriving in higher structures as pain

35
Q

What is pain modulation?

A

the descending inhibitory and facilitory input from the brain that influences nociceptive transmission at the level of the spinal cord in the dorsal horn

36
Q

Name some drugs/interventions that influence each of the following pain processes: transduction, transmission, perception, and modulation.

A

Transduction: local anaesthetics and NSAIDs

Transmission: local anaesthetics, application of cold, antiepileptics, opioids

Perception: opioids

Modulation: opioids, antidepressants

37
Q

What are the functions of the A-delta and C vibers?

A

Both are painfibers involved in transmitting pain from the periphery to the dorsal horn of the spinal cord

A-delta = “fast” pain

C = “slow” pain

38
Q

What is pain sensitization?

A

a number of mechanisms work together to increase the intensity of transmitted nociception and to recruit non-nociceptive fibers (A-beta) into transmitting pain

makes pain difficult to treat because blocking A-beta fibers cause patients to lose touch functions

39
Q

What types of pain are NSAIDs useful for?

A

they reduce nociceptor sensitizationin the periphery, but can also reduce the sensitization in the CNS

40
Q

What are antiepileptic drugs used for in the context of pain?

A

effective at treating pain states resulting from nervous tissue damage (aka neuropathic pain)

41
Q

What are antidepressants used for in the context of pain management?

A

treating chronic pain by facilitating the descending inhibitory modulation of pain transmissionin the dorsal horn of the spinal cord

42
Q

What is the difference in treatment goals between chronic and acute pain?

A

acute pain = addressed aggressively, goal is to eliminate pain

chronic pain = goal is to manage the pain to maximize daily function and minimize pain but not eliminate it

43
Q

What is a multimodal approach of pain management?

A

the use of a variety of different analgesic methods that work by different mechanisms

44
Q

Nociception and pain are related in that:

a) nociception cannot occur without pain
b) pain cannot occur without nociception
c) nociception is purely subjective
d) nociception is more easily assessed than pain
e) pain can be assessed in cognitively functioning patients while nociception cannot be

A

e) pain can be assessed in cognitively functioning patients while nociception cannot be

45
Q

In central sensitization of pain, the term “wind up” refers to:

a) the release of acetylcholine from non-nociceptive fibers
b) the sprouting of non-nociceptive fibers onto nociceptive synapses
c) the increased electrical activity following C fiber stimulation in the dorsal horn
d) the release of prostaglandins to enhance nociception
e) all of the above

A

c) the increased electrical activity following C fiber stimulation in the dorsal horn

46
Q

Most oral skeletal muscle relaxants primarily work by:

a) direct inhibition of acetylcholine release
b) nonspecific suppression of CNS polysynaptic pathways
c) suppression of calciumrelease in peripheral skeletal muscle fibers
d) blockade of nicotinic acetylcholine receptors
e) blockade of calcium channels in peripheral skeletal muscle fibers

A

b) nonspecific suppression of CNS polysynaptic pathways

47
Q

The role of antidepressants in pain includes:

a) treating neuropathic pain by affecting descending inhibitory pathways
b) use of SSRIs in treating inflammatory pain
c) treatment of depression which is likely causingthe pain
d) treatment of acute postoperative pain
e) enhancing binding of endorphins to opioid receptors

A

a) treating neuropathic pain by affecting descending inhibitory pathways

48
Q

What is “wind up” in pain?

A

A form of sensitization when the NMDA receptor is switched on and sensitizes second order neurons in the dorsal horn of the spinal cord

Leads to amplification of C fiber signals postsynaptically

49
Q

What is central reorganization in pain?

A

A-beta fibers become painful, leading to allodynia

50
Q

What is the effect of prostaglandins on pain?

A

PGs sensitize pain nerve endings and sensitize CNS pain

51
Q

What is PCA in the context of pain?

A

patient controlled analgesia, dispenses pain medication (up to a certain amount) when patient pushes a button

52
Q

What are peripheral nerve blocks?

A

infused analgesia that blocks sensory and motor fibers

53
Q

How is ketamine used for pain management?

A

It is used in IV form

acts on the NMDA receptor of the secondary neuron

54
Q

How do antidepressants manage pain?

A

They block the reuptake of 5-HT and NE and enhance the descending inhibitory system for pain

55
Q

How do anti-epileptic drugs treat pain?

A

They decrease excitation and increase inhibition of pain

they block voltage sensitive Na+ channels to alter excitability

56
Q

When should opioids be used?

A

If they work (if the pain can theoretically be treated by the mechanism of opioids), if function is consistently abused, if there is no tolerance or abuse

57
Q

What two factors determine the onset and duration of action of anesthetics?

A

lipid solubility and redistribution of the drug

58
Q

What is the mechanism of barbituates?

A

activates GABA-A receptors and increases duration of chloride conductance, leading to neuronal hyperpolarization

59
Q

What are the pharmacokinetics of barbituates?

A

short acting duration due to redistribution of the drug from the brain to more slowly equilibrating tissues

60
Q

What is the relationship between half life and duration of infusion of thipental?

A

increased duration of infusion leads to increased half life

61
Q

What are the side effects of barbituates?

A

myocardial depression

hypotension

central medullary respiratory depression

decreased cerebral metabolic rate of O2 consumption (and decreased blood flow)

62
Q

What is the mechanism of action of propofol?

A

activates a GABA-A receptor and increases duration of chloride conductance, leading to neuronal hyperpolarization

63
Q

What are the advantages of propofol over thiopental?

A
  • can use for long duration
  • antiemetic effects
  • mild bronchodilating properties
64
Q

What are the side effects of propofol?

A

hypotension, loss of systemic vascular resistance and peripheral vasodilation, central medullary respiratory depression, decreased cerebral oxygen demand and blood flow

65
Q

What is the mechanism of action of etomidate?

A

activates GABA-A receptors and increases duration of chloride conductions leading to neuronal hyperpolarization

66
Q

What are the side effects of etomidate?

A

nausea, central medullary respiratory depression, decreased brain oxygen demand and blood flow

does maintain cardiovascular stability and blood pressure

67
Q

What is the mechanism of action of benzodiazepines?

A

enhancement of the inhibitory response by acting on GABA-A to increase the frequency of chloride channel opening

safer than barbituates

68
Q

What are some examples of benzodiazepines?

A

midazolam, diazepam, flumazenil

69
Q

What is the mechanism of action of ketamine?

A

ketamine inhibits the NMDA-receptor to produce anesthesia

70
Q

What are the side effects of ketamine?

A

post-operative psychic phenomena, sympathomimetic actions (increased HR and BP), bronchodilation, increased salivation, nystagmus

71
Q

How is potency measured for inhalation anaesthetics?

A

expressed in terms of the minimum alveolar concentration - concentration at which 50% of the general population would remain unresponsive to surgical incision

72
Q

What are the clinical features of nitrous oxide as an gaseous anaesthetic?

A

efficacious but weak agent

no muscular relaxation

inhibits the NMDA receptor, but has no effect on the GABA-A receptor

73
Q

What is the mechanism of action of volatile anesthetics?

A

they enhance the inhibitory response mediated by GABA-A receptors

74
Q

How are inhalation anesthetics taken up?

A

It depends on the partial pressure of the gas relative to pressure in different parts of the body

75
Q

What is the relationship between blood flow and anaesthetic uptake?

A

higher blood flow = faster uptake of anesthetic to tissue

76
Q

What are side effects of inhalational/volatile anesthetics?

A

hypotension (via myocardial depression and reduced SVR)

respiratory depression

CNS depression, increased cerebral blood flow, decreased cerebral O2 demand

77
Q
A

Neuro (12 decks)

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