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Neuroscience Y2S2 > Neurobiology of Disease 2 > Flashcards

Neurobiology of Disease 2 Flashcards

1
Q

Is ADHD a neurodevelopmental or a neurodegenerative condition? (1)

A

Neurodevelopmental

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2
Q

In what year was ADHD defined as a condition? (1)

a) 2007
b) 1968
c) 1824
d) 1921

A

b) 1968

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3
Q

Give two possible reasons why 20% of prison inmates are thought to suffer with ADHD. (2)

A
  • Impulsiveness
  • Inability to see future consequences of an event or decision
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4
Q

Name the criteria used to diagnose ADHD. (1)

A

DSM-V

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5
Q

Complete the sentence relating to ADHD. (2)

According to the DSM-V, the prevalence of ADHD is thought to be …………………….., with the …………….. gender being twice as likely to have the condition.

A

3-5%

males

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6
Q

What is hyperkinetic disorder, and how does it relate to ADHD? (2)

A

WHO previously defined a hyperkinetic disorder as a similar condition to ADHD

however it had more stringent criteria and a lower prevalence than ADHD.

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7
Q

Name two symptom categories which are applicable to ADHD. (2)

A
  • Inattentive symptoms
  • Hyperactivity/Impulsivity symptoms
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8
Q

Give nine possible inattentive symptoms of ADHD. (9)

A
  • Lack of attention to detail
  • Difficulty to sustain attention
  • Avoid sustained attention
  • Not listening
  • Cannot follow through instructions
  • Difficulty organising tasks
  • Lose or misplace objects
  • Easily distracted
  • Forgetful
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9
Q

Give 8 possible hyperactivity/impulsivity symptoms of ADHD. (8)

A
  • Fidgeting
  • Restless during activities
  • Running about
  • Excessively loud
  • Always ‘on the go’
  • Talks excessively
  • Blurts out answers
  • Interrupts or intrudes on others
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10
Q

Give three criteria, regarding the symptoms of ADHD in children, which must be fulfilled before a diagnosis can be made. (3)

A
  • 6 or more symptoms, for at least 6 months, before age 12
  • Symptoms present in at least 2 life areas (school, home, social setting)
  • Behaviours must be developmentally inappropriate for the age of the child
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11
Q

How many symptoms of ADHD must adults show to get a diagnosis? (1)

A

5

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12
Q

Name the term that is applied to ADHD in adults, when they currently no longer have enough symptoms to meet the criteria but have had in the past. (1)

A

Partial remission

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13
Q

When ADHD is diagnosed, it can be put into one of three categories. Name the three categories. (3)

A
  • Combined
  • Predominantly inattentive
  • Predominantly hyperactive/impulsive
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14
Q

What is the heritability of ADHD between identical twins? (1)

A

70-90%

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15
Q

Complete the sentence relating to ADHD. (1)

Having a first degree relative with ADHD increases risk by ……………..

A

5%

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16
Q

True or false? Explain your answer if applicable.

ADHD is among the most heritable of psychological disorders.

A

True

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17
Q

What is meant by ‘heritability’? (1)

A

A measure of how well differences in people’s genes account for differences in traits.

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18
Q

Name six possible genes which are thought to be associated with ADHD. (6)

For an extra six marks, state (in brackets) what type of protein each gene encodes. (6)

A

SLC6A3 (DAT)

DRD4 (D4 receptor)

DRD5 (D5 receptor)

SLC6A4 (5HT reuptake transporter)

HTR1B (5HT1B receptor)

SNAP25 (SNAP25 vesicle protein)

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19
Q

Which of the following statements best applies to gene polymorphisms associated with ADHD? (1)

a) A polymorphism in a single gene, inherited from a parent, is enough to cause ADHD in the offspring

b) There are multiple gene polymorphisms possible, each conferring a small risk - no single gene is sufficient or causal on its own

A

b) There are multiple gene polymorphisms possible, each conferring a small risk - no single gene is sufficient or causal on its own

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20
Q

An odds ratio of what number means that there is no association between an exposure and an outcome? (1)

A

1

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21
Q

Regarding the genes thought to be associated with ADHD, which of the following ranges would you expect the odds ratios to be? (1)

a) 0-1
b) 1-2
c) 2-3
d) 3-4

A

b) 1-2

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22
Q

In ADHD, give two phenotypic traits which may be associated with D4 receptor polymorphisms. (2)

A
  • Novelty seeking behaviour
  • Inattention
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23
Q

In relation to ADHD, give the precise location of the DRD4 receptor gene on the chromosome. (1)

Use the structure of 00A00.0

A

11p15.3

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24
Q

In what brain network is the DRD4 receptor gene particularly prevalent? (1)

A

Frontal-cortical network

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25
Q

Describe the specific polymorphism of the DRD4 receptor gene which confers high risk (OR1.9) for ADHD. (1)

A

48 base pair repeat

7 repeat allele confers high risk

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26
Q

Describe the molecular/cellular result of a mutation in the DRD4 receptor gene in ADHD. (2)

A
  • Attenuated/reduced AC coupling of the dopamine receptor
  • Reduced cAMP response
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27
Q

In relation to ADHD, give the precise location of the DAT1 gene on the chromosome. (1)

Use the structure of 00A00.0

A

5p15.3

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28
Q

In ADHD, if there is a mutation in the DAT1 gene, in which brain region is DAT expression likely to be affected? (1)

A

Striatum

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29
Q

Describe the specific polymorphism of the DAT1 gene which confers high risk (OR1.16) for ADHD. (1)

A

480 base pair repeat

10x repeats

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30
Q

Describe the molecular/cellular result of a mutation in the DAT1 gene in ADHD. (2)

A

Elevated DAT expression

Less synaptic dopamine

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31
Q

Give eight environmental risk factors for ADHD. (8)

Also give one which has been suggested, but for which there is currently not enough evidence. (1)

A
  • Extreme prematurity and low birth weight
  • Maternal smoking/toxins/alcohol
  • Neonatal hypoxia
  • Low social class / social depravation
  • Learning disability
  • Institutional rearing
  • Lead exposure
  • Other neurological disorders such as epilepsy, encephalitis, brain trauma

Food allergies have been suggested but not enough evidence

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32
Q

Do individual environmental risk factors or genetic risk factors have larger odds ratiosin ADHD? (1)

Which category has the larger impact when combined? (1)

A

Environmental

Genetics have larger impact when combined

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33
Q

Complete the passage related to ADHD. (4)

Environmental and genetic risk factors interact to result in fronto-striatal ………………………….. dysfunction.

This results in developmentally inappropriate …………………, …………………., and ……………….. behaviour.

A

monoamine

hyperactive

impulsive

inattentive

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34
Q

Briefly describe three volumetric changes in the brain seen in ADHD. (3)

A
  • Smaller brain (particularly right frontal lobe)
  • Smaller basal ganglia
  • Smaller cerebellum
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35
Q

Match the percentage reduction in brain size, to the brain region, as seen in ADHD. (4)

4%
12%
6%
8%

Right frontal lobe
Basal ganglia
Whole brain
Cerebellum

A

4% - whole brain
12% - cerebellum
6% - basal ganglia
8% - right frontal lobe

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36
Q

In ADHD, a reduction in the size of the right frontal lobe is seen.

Give nine functions of the right frontal lobe. (9)

A
  • Motor function
  • Problem solving
  • Spontaneity
  • Memory
  • Language
  • Initiation
  • Judgement
  • Impulse control
  • Social behaviour
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37
Q

Describe how you would expect the volumetric change in the basal ganglia to develop throughout the childhood/adolesence of someone with ADHD. (1)

A

Transient change which usually normalises by about 18yrs of age

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38
Q

Describe how you would expect the volumetric change in the cerebellum to develop throughout the childhood/adolesence of someone with ADHD. (1)

A

Still pronounced at 18yrs, does not usually normalise

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39
Q

At what age do the volumetric changes in the brain seen in ADHD manifest? (1)

A

About 6yrs

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40
Q

True or false? Explain your answer if appropriate. (1)

In ADHD, the volumetric changes seen in the brain correlate with severity.

A

True

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41
Q

True or false? Explain your answer if appropriate. (1)

In ADHD, the volumetric changes in the brain are seen irrespective of medication status and co-morbidities.

A

True

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42
Q

Name six areas of the brain where functional changes are seen in ADHD. (6)

All of these brain areas are related to what two functions? (2)

A
  • Dorsolateral prefrontal cortex
  • Ventrolateral prefrontal cortex
  • Parietal cortex
  • Dorsal anterior midcingulate cortex
  • Striatum
  • Cerebellum

All these areas are related to cognitive and attentive functions.

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43
Q

Functional abnormalities are particularly seen in the dorsolateral prefrontal cortex in ADHD.

Give three cognitive processes that this area of the brain is associated with. (3)

A

Decision making

Mood regulation

Conflict management

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44
Q

Functional abnormalities are particularly seen in the striatum in ADHD.

Give two cognitive processes that this area of the brain is associated with (related to ADHD). (2)

A
  • Cognition
  • Social behaviour
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45
Q

In three words, describe the main neurotransmitter pathology in ADHD. (1)

A

Fronto-striatal dopaminergic hypofunction

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46
Q

Give two findings that you would expect to see on an fMRI in ADHD, regarding the fronto-striatal complex. (2)

A
  • Smaller
  • Less active
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47
Q

Give a PET finding in ADHD related to the striatum. (1)

A

Reduced metabolism

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48
Q

Describe the striatal density of DAT that you would expect to see in ADHD. (1)

A

Higher density

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49
Q

How might the sensory cortex be changed in ADHD, and what effect/symptom might this have? (2)

A

Hyperactive sensory cortex

which results in enhanced perception.

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50
Q

Briefly describe the double hit mechanism of hypodopaminergic dysfunction seen in ADHD, in terms of the molecular changes in the brain. (2)

Why do these molecular changes happen? (1)

A
  • Increased DAT uptake
  • Reduced D4 activation

The molecular changes happen due to genetic polymorphisms.

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51
Q

Name a developmental impact of ADHD which may happen at pre-school age. (1)

A

Behavioural disturbance

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52
Q

Name 4 developmental impacts of ADHD which may happen at school age. (4)

A
  • Behavioural disturbance
  • Academic impairment
  • Poor social interaction
  • Peer acceptance
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53
Q

Name 5 developmental impacts of ADHD which may happen in adolescence. (5)

A
  • Academic impairment
  • Poor social interaction
  • Lower self-esteem
  • Smoking/drugs
  • Criminality
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54
Q

Name 5 developmental impacts of ADHD which may happen at college age. (5)

A
  • Academic failure
  • Occupational difficulties
  • Low self-esteem
  • Alcohol and substance abuse
  • Injury/accidents
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55
Q

Name 6 developmental impacts of ADHD which may happen in adulthood. (6)

A
  • Unemployment
  • Low self-esteem
  • Relationship problems
  • Motor accidents
  • Marital discord
  • Alcohol and substance abuse
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56
Q

Name five disorders that often co-occur with ADHD. (5)

A
  • Conduct disorder
  • Tics
  • Mood disorders
  • Anxiety disorder
  • Oppositional defiant disorder
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57
Q

Complete the sentence relating to ADHD. (1)

Only …………….. percent of all people diagnosed with ADHD are diagnosed with ADHD alone.

A

31

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58
Q

Match the conditions up with the percentage of people diagnosed with ADHD who also have that condition. (5)

Conduct disorder
Oppositional defiant disorder
Tics
Anxiety disorder
Mood disorders

14%
11%
4%
34%
40%

A

Conduct disorder - 14%

Oppositional defiant disorder - 40%

Tics - 11%

Anxiety disorder - 34%

Mood disorders - 4%

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59
Q

Apart from dopamine, name another neurotransmitter which is thought to be involved in the pathophysiology of ADHD. (1)

A

Glutamate

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60
Q

In regards to ADHD, name two areas of the brain where dopaminergic and glutamatergic neurotransmission are able to interact with each other. (2)

A

Striatum

Prefrontal cortex

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61
Q

Several polymorphisms in the genes encoding which glutamate receptors (inotropic or metabotropic) are thought to be associated with ADHD? (1)

A

Both

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62
Q

Complete the sentence relating to ADHD. (1)

Alterations to glutamatergic signalling caused by inotropic receptor changes may result in …………………. symptoms.

A

Attention deficit

63
Q

Complete the sentence relating to ADHD. (1)

Alterations to glutamatergic signalling caused by metabotropic receptor changes may result in …………………. symptoms.

A

hyperactivity/impulsivity

64
Q

Very briefly describe the effect that hypodopaminergic neurotransmission in ADHD may have on glutamatergic neurotransmission. (2)

A
  • Decreased dopamine causes more active NMDARs/AMPARs
  • Increase in glutamate activity
65
Q

What would be the usual effect of D2 stimulation on glutamatergic neurotransmission? (1)

A

NMDAR inhibition

66
Q

What would be the usual effects of D4 stimulation on glutamatergic neurotransmission? (2)

A

Depression of AMPAR-mediated excitation of PFC neurones

Decreased AMPAR expression at synapse

67
Q

In ADHD, what is the effect of striatal glutamate release on dopaminergic neurotransmission? (1)

A

Facilitates DA release by acting on NMDARs

68
Q

In ADHD, AMPA KO mice display what change to their striatal DA concentration? (1)

A

Elevated

69
Q

Name three possible psychostimulants which can be used to treat ADHD. (3)

A
  • Methylphenidate
  • Dexamphetamine
  • Lis-dexamphetamine
70
Q

Complete the sentence relating to psychostimulants in ADHD. (2)

Psychostimulants bind to ………………….., and may also inhibit ……………

A

DAT

NET

71
Q

What is the difference between dexamphetamine and lis-dexamphetamine to treat ADHD? (1)

A

Lis-dexamphetamine is a prodrug and has to be converted in the body.

72
Q

Name a common form of methylphenidate used to treat ADHD. (1)

A

Ritalin

73
Q

Name a common form of dexamphetamine used to treat ADHD. (1)

A

Adderall

74
Q

Stimulants (such as methylphenidate and amphetamine) tend to have mixed effects on dopamine and norepinephrine neurotransmission in ADHD.

Name a medication that acts solely on dopaminergic neurotransmission. (1)

A

Bupropion

75
Q

Stimulants (such as methylphenidate and amphetamine) tend to have mixed effects on dopamine and norepinephrine neurotransmission in ADHD.

Name two medications that act solely on noradrenergic neurotransmission. (2)

A

Guanfacine

Atomoxetine

76
Q

What type of medication is atomoxetine, as used in ADHD? (1)

A

Noradrenaline reuptake inhibitor

77
Q

Give an advantage of using non-stimulant medications to treat ADHD. (1)

A

Potentially less addiction

78
Q

What type of medication is guanfacine, as used in ADHD? (1)

A

Alpha2 adrenoreceptor agonist

79
Q

Give two more recently licenced treatments (and their general effects on NTs) for ADHD. (2)

A
  • Alpha2 adrenoreceptor agonists (increase NA)
  • Tricyclic antidepressants (inhibit NET)
80
Q

How might the levels of noradrenaline be different in people with ADHD? (1)

A

Too low

81
Q

Name two types of medications used in ADHD which affect glutamatergic neurotransmission. (2)

Give an example of each of these. (2)

A

NMDA antagonist (memantine)

mGluR agonist (fasoracetam)

82
Q

Give five beneficial effects of increasing dopamine and NE in ADHD. (5)

A
  • Increased cognitive function
  • Increased attentiveness
  • Decreased distractibility
  • Decreased hyperactivity
  • Decreased behavioural disruption
83
Q

Give eight potential effects of medications used to treat ADHD. (8)

A
  • Insomnia
  • Increased HR/BP
  • Nausea/vomiting
  • Abdominal pain
  • Tics
  • Decreased appetite
  • Decreased bodyweight
  • Decreased growth rate
84
Q

What would you expect to see in a DAT radiolabelled binding study in ADHD? (1)

How would this be different after four weeks of methylphenidate treatment? (1)

How would this be different after 12 months of methylphenidate treatment? (1)

A

Increased DAT binding (so increased DAT levels)

After 4 weeks methylphenidate this binding would be reduced

After 12 months methylphenidate this binding would be increased

85
Q

What are the effects on DAT expression of long-term methylphenidate use? (1)

What effect might this have on the efficacy of the treatment? (1)

A

Compensatory increase in DAT

Treatment efficacy reduced

86
Q

Describe the mechanism of how methylphenidate is able to enhance dopaminergic neurotransmission in ADHD. (3)

A
  • Block DAT transporter
  • Less DA taken up into presynaptic terminal
  • More DA in synaptic cleft to bind to postsynaptic receptors
87
Q

Describe the mechanism of how amphetamine is able to enhance dopaminergic neurotransmission in ADHD. (6)

A
  • Inhibits DAT by binding to alternative site
  • Amphetamine also taken up by DAT into presynaptic neurone
  • Blocks VMAT2 on vesicles
  • Less DA loaded into vesicles
  • More DA in cytoplasm
  • DA released from neurone via reverse DAT transport
88
Q

With regards to stimulant pharmacology in ADHD, is methylphenidate firing rate dependent or independent? (1)

A

Firing rate dependent

89
Q

With regards to stimulant pharmacology in ADHD, is amphetamine firing rate dependent or independent? (1)

A

Firing rate independent

90
Q

11C-Raclopride is used in PET scans and binds to D2 receptors in the striatum. This technique is commonly used in ADHD research.

What would you expect to see in terms of the PET signal given off if methylphenidate is added? Explain your answer. (2)

A

Reduced signal

Because methylphenidate increases DA, which competes with raclopride and displaces it from the receptor.

91
Q

True or false? Explain your answer if appropriate. (1)

In addition to medications, it has been found that rewards (either physical or psychological) also have a positive effect in ADHD.

A

True

92
Q

Complete the sentence relating to rewards as a way of improving ADHD symptoms. (3)

Rewards (either physical or psychological) have been shown to increase dopaminergic function in the ………………….. and …………………………, as well as increasing both DA and NA in the ……………………..

A

Striatum

Nucleus accumbens

Frontal cortex

93
Q

Give six positive effects of reward on behaviour and functioning in ADHD. (6)

A
  • Increased motivation
  • Enhanced executive function
  • Increased focus
  • Increased attention
  • Increased effort
  • More on-task behaviour
94
Q

Give five medical conditions which can present with anxiety. (5)

A
  • Generalised anxiety disorder (GAD)
  • Panic disorder
  • Obsessive compulsive disorder (OCD)
  • Post-traumatic stress disorder (PTSD)
  • Phobias
95
Q

Briefly describe the diagnostic criteria for GAD. (6)

A
  • Excessive anxiety or worry
  • Which is difficult to control
  • About a number of events or situations
  • Associated with a number of other psychological or physical symptoms
  • Which causes significant distress or impairment of functioning
  • And not better explained by substance use or another medical condition
96
Q

Give seven potential symptoms, along with anxiety, which form part of the diagnostic criteria for GAD. (6)

A
  • Restlessness (or feeling on edge)
  • Fatigue
  • Difficulty concentrating
  • Irritability
  • Muscle tension
  • Sleep disturbance
97
Q

Name two physical symptoms that can often be experienced in GAD, however do not form part of the diagnostic criteria. (2)

HINT: these symptoms can often be controlled using beta blockers

A

Dizziness

Heart palpitations

98
Q

How does panic disorder differ from GAD? (1)

A

Panic disorder features regular panic attacks

99
Q

Describe the onset and duration of a panic attack. (2)

A

Come on quickly

Lasts for about 5-20 minutes

100
Q

Describe two general aspects of the diagnostic criteria for panic disorder. (2)

A
  • Recurrent, unexpected panic attacks
  • Followed by persistent worry about having another, or a maladaptive behaviour to avoid having attacks
101
Q

Define a panic attack. (1)

A

Abrupt surge of intense fear or intense discomfort that reaches a peak within minutes, and features a range (4 or more) of symptoms.

102
Q

Give 13 potential symptoms of a panic attack. (13)

A
  • Palpitations, pounding heart, or accelerated heart rate
  • Sweating
  • Trembling or shaking
  • Sensations of shortness of breath or smothering
  • Feelings of choking
  • Chest pain or discomfort
  • Nausea or abdominal distress
  • Dizziness, unsteady, light-headed, faint
  • Chills or heat sensations
  • Paresthesias (numbness or tingling)
  • Derealisation or depersonalisation
  • Fear of losing control or going crazy
  • Fear of dying
103
Q

Define ‘obsessive compulsive disorder’. (3)

A

A combination of obsessive thoughts and compulsive activity

which are time consuming

and impact on day-to-day functioning.

104
Q

What is an obsession, in terms of OCD? (1)

A

Unwanted/unpleasant thoughts that cause anxiety

105
Q

What is an compulsion, in terms of OCD? (1)

A

Repetitive behaviour undertaken to supress negative thoughts.

106
Q

What proportion of people exposed to trauma will be affected by PTSD? (1)

A

1 in 3

107
Q

Briefly describe what is meant by PTSD. (3)

A

An anxiety disorder caused by traumatic events

which are relived through nightmares or flashbacks

with sufferers also showing avoidance of linked memories.

108
Q

Give eight criteria that must be met for a diagnosis of PTSD. (8)

A
  • Exposure to traumatic stressor
  • Reexperiencing symptoms
  • Avoidance behaviours
  • Cognitive distortions
  • Increased arousal
  • Symptoms for more than 1 month
  • Symptoms create distress or functional impairment
  • Symptoms not caused by medication, substance use, or illness
109
Q

Define ‘phobia’. (1)

A

Overwhelming and debilitating fear of something that is often of little or no actual danger.

110
Q

Give four examples of specific phobias. (4)

And two examples of complex phobias. (2)

A
  • Spiders
  • Heights
  • Flying
  • Injections
  • Agoraphobia
  • Social phobia
111
Q

Give four possible techniques or ways of gaining evidence that can be used to determine the neurobiology of GAD. (4)

A
  • Neuroimaging
  • Genetic studies
  • Neurotransmitters and responses to treatment
  • Neuroendocrine studies
112
Q

What is the normal, physiological role of the prefrontal cortex in anxiety? (1)

A

Controls rational, logical thought to reduce anxiety.

113
Q

What is the normal, physiological role of the anterior cingulate cortex in anxiety? (1)

A

Amplifies negative information (from the amygdala) which increases anxiety.

114
Q

What is the normal, physiological role of the amygdala in anxiety? (1)

A

Inhibits the prefrontal cortex and initiates fight-or-flight response

115
Q

Describe a hypothesis of anxiety disorders relating to the prefrontal cortex, ACC, and amygdala. (3)

A
  • Amygdala function disrupted (and amygdala increased in size)
  • PFC-amygdala connectivity disrupted
  • Imbalance between ACC amplifying anxiety and PFC dampening anxiety (ACC may hyperactivate amygdala)
116
Q

What is a possible technique that could be used to investigate connectivity between the prefrontal cortex and amygdala in GAD? (1)

A

resting state fMRI

117
Q

Patients with GAD and healthy controls underwent resting state fMRI scans.

What would you expect to see in these two groups, in relation to the functional connectivity between the PFC and amygdala? (1)

A

Patients with GAD showing weaker functional connectivity.

118
Q

Family studies show how much heritability in GAD? (1)

A

About 30%

119
Q

In general, give two brain processes that are controlled by the risk genes for GAD. (2)

A
  • Monoamine neurotransmission
  • Neurotrophic signalling
120
Q

Name four risk genes for GAD. (4)

A
  • 5HT reuptake transporter (SERT)
  • 5HT-1A receptor
  • Monoamine oxidase A
  • BDNF gene
121
Q

Describe the change in the SERT gene which may confer greater risk of GAD. (1)

A

Short allele

122
Q

Describe the change in the 5HT1A gene which may confer greater risk of GAD. (1)

What is the functional consequence of this gene mutation? (1)

A

C1019G polymorphism

Results in increased negative feedback and decreased serotonergic signalling

123
Q

Describe two changes in the monoamine oxidase A gene which may confer greater risk of GAD. (2)

What is the functional consequence of these gene mutations? (1)

A

T941G polymorphism

Long allele

Result in increased monoamine metabolism and decreased monoamine signalling.

124
Q

Describe the change in the BDNF gene which may confer greater risk of GAD. (1)

What is the functional consequence of this gene mutation? (1)

A

Val66Met polymorphism

Decreased BDNF activity

125
Q

Give three environmental risk factors for GAD. (3)

A
  • Childhood trauma
  • Stressful family circumstances
  • Natural disasters
126
Q

Gene-environment interactions are thought to play a role in the development of GAD.

Which gene changes are thought to interact with childhood trauma to increased risk of GAD? (3)

A

5HT Transporter (SERT)

COMT

MAOA

127
Q

Gene-environment interactions are thought to play a role in the development of GAD.

Which gene changes are thought to interact with hurricane victims to increased risk of GAD? (1)

A

Neuropeptide Y variants

128
Q

Gene-environment interactions are thought to play a role in the development of GAD.

Which gene changes are thought to interact with daily life stress to increase risk of GAD? (1)

A

5HT transporter variants

129
Q

Gene-environment interactions are thought to play a role in the development of GAD.

Which gene changes are thought to interact with family relationship stress to increase risk of GAD? (1)

A

Neuropeptide S receptor 1 variants

130
Q

Give three neurotransmitters which may be implicated in GAD. (3)

A
  • GABA
  • 5HT
  • Neuropeptides
131
Q

Give two ways in which GABA may be implicated in GAD. (2)

Give a piece of evidence that supports this. (1)

A
  • Dysregulated inhibitory neurotransmission
  • GABAa receptor downregulated

Symptoms may be treated with GABAa agonists, which supports the theory of GABA being involved.

132
Q

Briefly describe how 5HT may be associated with GAD, and give a piece of evidence that supports this. (2)

A

Decreased 5HT may be associated with GAD

given that symptoms can be treated with SSRIs (which increase 5HT).

133
Q

Briefly describe a piece of evidence suggesting why neuropeptides are thought to play a role in GAD. (1)

What are current clinical trials showing surrounding this relationship? (1)

A

Patients are hypersensitive to cholecystokinin agonists

However trials investigating CCK antagonists have been unsuccessful.

134
Q

Name a neuroendocrine pathway which may be altered in GAD. (1)

A

HPA axis

135
Q

How is the HPA axis thought to be altered in GAD? (1)

A

Negative feedback may be lost leading to increased cortisol.

136
Q

Give five considerations during the assessment and treatment of GAD. (5)

A
  • Mental health history
  • Environmental stressors
  • Medical and drug history
  • Degree of distress and functional impairment
  • Risk of suicide
137
Q

Give three general aims of GAD treatment. (3)

A
  • Relieve symptoms
  • Improve quality of life
  • Prevent relapse
138
Q

Name two possible treatment routes that can be taken for GAD. (2)

A
  • Pharmacological management
  • Non-pharmacological management
139
Q

Suggest five possible non-pharmacological treatment options for GAD. (5)

A
  • Self help
  • Meditation/relaxation/mindfulness
  • Exercise
  • Lifestyle changes
  • Psychotherapy
140
Q

Suggest a pharmacological way of treating autonomic symptoms in GAD. (1)

Give an example. (1)

A

Beta-adrenoreceptor antagonists

Propranolol

141
Q

Suggest four possible pharmacological ways of treating anxiety symptoms in GAD. (4)

A

SSRIs

SNRIs

Atypical antidepressants

Benzodiazepines

142
Q

What target are atypical antidepressants thought to work on in the brain? (1)

A

5HT receptors

143
Q

In what situation would benzodiazepines be useful to treat GAD? (1)

A

In a crisis (short-term use)

144
Q

Apart from GAD, give three uses for benzodiazepines. (3)

A
  • Insomnia
  • Epilepsy
  • Pre-surgical medication
145
Q

(Using four words), give a very brief description of how benzodiazepines work. (1)

A

Enhance effects of GABA

146
Q

Describe the structure of a GABAa receptor. (1)

A

5 SUBUNITS:
2x alpha
2x beta
1x gamma

Going in a circle,
y, a, b, a, b, y, a, b, a, b, y

147
Q

Where on a GABAa receptor does GABA usually bind? (1)

A

Between a and b subunits

148
Q

Where on a GABAa receptor does a benzodiazepine usually bind? (1)

A

Between a and y subunits

149
Q

What is the effect of a benzodiazepine molecule binding to a GABAa receptor? (5)

A
  • Confirmational change
  • Enhanced GABA binding
  • More channel opening
  • More Cl- influx (hyperpolarisation)
  • Reduced neuronal activity
150
Q

Benzodiazepines do not directly activate GABAa receptors, but enhance GABA binding.

What is the name given to benzodiazepines (and other molecules) that act in this way? (1)

A

Positive allosteric modulators (PAMs)

151
Q

Give three general issues that are faced with current treatments for GAD. (3)

A
  • Non-responsive patients
  • Relapse
  • Side effects
152
Q

Give three particularly troubling side effects that patients experience with GAD treatments. (3)

A
  • Sexual dysfunction
  • Drowsiness
  • Weight gain
153
Q

Ketamine, riluzole, and xenon may be next generation, novel treatments for GAD.

Briefly describe how these drugs are thought to work. (1)

A

Tend to decrease glutamatergic signalling

154
Q

Apart from glutamatergic drugs, give four other potential next generation, novel treatments for GAD. (4)

A
  • Neurosteroids
  • Cannabinoids
  • MDMA
  • L-DOPA

Neuroscience Y2S2 (15 decks)

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