Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 > Case 12 > Flashcards

Case 12 Flashcards

1
Q

What does GABA stand for?

A

Gamma-aminobutyric acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is H0?

A

The null hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is H1?

A

The alternative hypothesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does p>0.05 show?

A

Observed difference is due to chance

Accept null

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The smaller the p value the…

A

Stronger the evidence against null

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What if the confidence interval does not contain 0?

A

0 is the value of no difference

So there is a difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is CI does contain 0?

A

There’s not a difference

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which stats test is appropriate for unpaired data (2 distinct, independent samples)?

A

Student’s t test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Which stats test is appropriate for comparing 2 scores on the same set of people?

A

Paired t test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What’s phenomenology?

A

Psychiatric symptoms e.g. Hallucinations

Delusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What’s psychopathology?

A

Study of abnormal states of mind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What’s the format of the mental state exam?

A

As mat pc I

Appearance and behaviour 
Speech
Mood
Affect
Thoughts
Perceptions
Cognition 
Insight
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What’s akathisia?

A

Subjective feeling if restlessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What’s alogia?

A

Poverty of speech

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What’s the difference between mood and affect?

A

Mood -subjective

Affect - objective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What’s a mood-congruent memory?

A

A memory consistent with the patient’s mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is labile mood?

A

Marked fluctuation of mood

E.g. Anger to crying to laughter within few minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What’s a blunted affect?

A

Reduction in intensity of emotional response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is flattened affect?

A

Show no emotion

Negative symptom of schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the schneiderian first rank symptoms?

A

Thought alienation: insertion, withdrawal, broadcast
Delusional perception
Auditory hallucination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is circumstantial thinking?

A

Over-inclusive
But reaches the point eventually
- learning difficulty/ obsessional personality?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are examples of loosened association?

A

Knights move thinking/ derailment - no/ little association between one part of sentence and the next
Word salad - senseless repetition of sounds/ phrases
Neologism - new/ made up word
- suggestive of psychosis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are schneiderian first rank symptoms highly suggestive of?

A

Schizophrenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is perseveration?

A

Repetition of a particular response even in the absence/ cessation of a stimulus
- usually organic symptom of dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What’s the difference between primary and secondary delusions?

A

Primary - bizarre

Secondary - understood in the context of prevailing emotional state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What types of delusions are there?

A

Persecution
Grandiosity
Guilt
Nihilism - nonexistence of self/ parts of self/ others/ world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What feeling is important in assessing risk of suicide?

A

Hopelessness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the difference between an illusion and a hallucination?

A

Illusion - real stimulus, misinterpretation of actual stimulus
Hallucination - no stimulus, perception in absence of stimulus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the difference between true auditory hallucination and pseudohallucination?

A

True auditory hallucination - spoken aloud

Pseudohallucination - heard within mind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are 2nd/ 3rd person auditory hallucinations?

A

2nd person - voice talks directly to patient

3rd person - running commentary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is confabulation and possible cause?

A

Fabricated/ distorted/ misinterpreted memories about oneself/ the world
Can be due to Wernicke-korsakoff’s (brain disorder from thiamine B1 deficiency)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are 4 things the patient may lack insight of?

A

Insight of abnormal symptoms
Insight of attribution of symptoms to mental disorder
Insight of appraisal of negative consequences of symptoms
Insight of acceptance of need for treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is agoraphobia?

A

Extreme/ irrational fear of open/ public places

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the positive symptoms of psychosis?

A

(something added to normality)
Delusion
Hallucinations
Catatonic symptoms - abnormal movements and behaviour
Formal thought disorder - abnormal thought processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the negative symptoms of psychosis?

A

(something taken away from normality - the 5 A’s)
Avolition - no motivation
Anhedonia - unable to feel pleasure
Affective flattening - no expression of emotion
Alogia - poverty of speech
Ascociality - social disinterest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is psychosis?

A

Loss of contact with reality
Inability to differentiate salient information
Changes in the way someone thinks/ behaves/ perceives the world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is euthymia?

A

Normal, non-deppressed, reasonably positive mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the 3 core symptoms of depression?

A

Low mood
Anhedonia - inability to feel pleasure/ loss of interest
Anergia - loss of energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How can unipolar depression be diagnosed?

A

Core symptoms everyday for at least 2 weeks

Plus non-core symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the non-core symptoms of depression?

A 
Reduced conc
Reduced self esteem/ confidence 
Guilt, worthlessness
Pessimistic outlook 
Self harm/ suicidal idealisation   
Disturbed sleep 
Reduced appetite
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How is unipolar depression ranked in severity?

A

Mild: 2 core, 2 associated symptoms
Moderate: 2 core, 3 associated symptoms
Severe: 3 core, 4 associated symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which type of bipolar disorder has worse recovery?

A

Type 2 as more depressed days, more suicidal act

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is type 1 bipolar disorder?

A

Mania

Plus depression/ hypomania/ mixed affective state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What is type 2 bipolar disorder?

A

Hypomania

Plus depression or another episode of hypomania

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What does not occur in type 2 bipolar disorder?

A

Mania

Mixed affective state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Example of an ultradian rhythm

A

Less than a day - Sleep cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Example of an infradian rhythm

A

More than a dat - Menstrual cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How often does a circannual cycle occur?

A

Yearly/ annually

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How long is a cycle of a circadian rhythm?

A

Approximately a day (Diem)

It is thought that our internal clock is a 25 hour cycle but zeitgebers reset the clock to our usual 24 hour day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What type of sleep is slow wave sleep (SWS) and what occurs during the stage?

A

Deep - stage 3 and 4

Motor memory consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which stages of sleep are shallow?

A

1 and 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What sort of consolidation occurs in REM sleep?

A

Emotional memory consolidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

As the length of sleep goes on, what happens to slow wave sleep (SWS)?

A

SWS becomes shorter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

As the length of sleep goes on, what happens to REM?

A

REM becomes longer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How long does a sleep cycle last approximately?

A

Infant - 60mins

Adolescent - 90mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What sort of wave is seen in stage 1 of the sleep cycle?

A

Alpha waves - low amplitude, moderate frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What EEG features are seen in stage 2 of the sleep cycle?

A

K complexes
Sleep spindles
Slower frequency, higher amplitude compared to stage 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What sort of wave is seen in stage 3 of the sleep cycle?

A

Delta waves - slowest wave, large amplitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What sort of wave is seen in stage 4 of the sleep cycle?

A

Delta waves - slowest wave, large amplitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What sort of wave is seen in REM sleep?

A

Alpha waves - looks similar to stage 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which stage are the vitals (breathing, heart rate, body temp) at their lowest?

A

Stage 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is a person like in REM sleep?

A

Vitals increase
Dreaming
Paralysed apart from resp. muscles and eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

When would a patient not be paralysed during REM sleep?

A

REM sleep behavioural disorder - often precedes Parkinson’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How many hours a day do babies sleep?

A

16 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How much sleep do adults typically require?

A

7-8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What underlies seasonal affective disorder (SAD)?

A

Darker in winter months so more melatonin secreted from pineal gland
Melatonin makes you sleep and affects your biological clock and mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

When would administration of melatonin be best to reduce the effects of jet lag and shift work?

A

Just before going to bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How is sleep deprivation compensated for on subsequent nights?

A

Slow wave, non REM sleep is increased

Stage 3 and 4 almost completely restores (increased)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the photopigment in retinal ganglion cells that are sensitive to light?

A

Melanopsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the main pacemaker for endogenous rhythms and where’s it located?

A

Suprachiasmatic nucleus

Small group of cells in hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

How can the amount of light entering the eye re-set the rhythm?

A

Suprachiasmatic nucles - lies above optic chiasm

Receives info directly from eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What relevance does sleep have in regards to epilepsy?

A

Some seizures are exclusively from sleep or only on waking

Sleep deprivation provokes most seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What are the symptoms of narcolepsy?

A

Irresistible sleep
Cataplexy
Sleep paralysis
Hypnagogic hallucinations

74
Q

What is narcolepsy and what causes it?

A

Relatively rare sleep disorder
Appears to be hereditary autoimmune cause
Influenced by unknown environmental factors
Associated with HLA (human leucocyte antigen) DR2 and DQ1 genes
Low hypocretin/ orexin levels in CSF

75
Q

What is a sleep attack?

A

Fall asleep usually when bored/ in relaxing surroundings
Lasts 2-5mins
Wakes feeling refreshed

76
Q

What is Sleep paralysis?

A

Inability to move just before onset of sleep/ upon waking

Can be snapped out of it by touching/ calling their name

77
Q

What is a hypnagogic hallucination?

A

Dream whilst awake and paralysed
Often terrifying
Occurs in transition from awake to asleep (agos - sleep is near)

78
Q

What is cataplexy?

A

Temporary involuntary muscle weakness or even paralysis (but still conscious) lasting few seconds - minutes
In response to emotions/ anticipation of emotion/ sudden physical effort
e.g. laughter, anger, effort to catch suddenly thrown object

79
Q

How is cataplexy treated?

A

Sodium oxybate
Antidepressants
GHB - gamma-Hydroxybutyric acid

80
Q

What are melatonin and tryptophan?

A

Weakly hypnotic
Induce natural sleep patterns
Tryptophan is a precursor of melatonin

81
Q

What are the problems with using morphine, barbiturates and benzodiazepines to help with sleep?

A

They decrease REM sleep

Increase drowsiness during waking

82
Q

What happens in Cotard’s syndrome?

A

Seen in psychotic depression and dementias

Person believes that they are already dead, no blood/ insides

83
Q

What does p

A

Reject null

There’s a statistically significant difference at 5% level

84
Q

Which pathway is primarily affected in Parkinson’s?

A

Nigrostriatal pathway (not extrapyramidal system)

85
Q

How Parkinson’s patients get bradykinesia?

A

Loss of dopaminergic neurons in substantia nigra

Leads to deregulation of extrapyramidal system that regulates posture and skeletal muscle tone

86
Q

Which disease is high dopamine seen in?

A

Schizophrenia

87
Q

Which disease is low dopamine seen in?

A

Parkinson’s

88
Q

Which part of the brain is the limbic system?

A

Subcortical areas (below cortex)

89
Q

What is the limbic system involved in?

A 
Basic emotions - fear/ pleasure/ anger
Drives - hunger/ dominance/ care of offspring 
Mood 
Tone 
Memory
90
Q

What is the prefrontal cortex involved in?

A

Planning

Executing actions

91
Q

What can lesions in the PFC cause?

A 
Dramatic changes in:
Personality 
Inability to plan 
Loss of spontaneity 
Problems with initiating speech/ movement
92
Q

What happens to the limbic system and PFC in depression?

A

Loss of connection between limbic system and PFC involving serotonin - affects normal function of PFC

93
Q

Which areas are thought to be hypoactive in depression?

A

Anterior cingulate cortex (ACC)

Dorsolateral prefrontal cortex (DLPFC)

94
Q

Which areas of the brain are thought to be hyperactive in depression?

A

Amygdala
Thalamus
Subgenual cingulate

95
Q

What are all catecholamines derived from?

A

Catecholamines - DA/ NA/ A

From tyrosine

96
Q

How is adrenaline synthesised?

A 
Tyrosine 
to L-DOPA (L-3,4-DehydrOxyPhenylAlanine) - rate limiting step 
to dopamine 
to NA
to A
97
Q

What converts tyrosine to L-DOPA?

A

Tyrosine hydroxylase

Fe2+, O2 and tetrahydrobiopterin also required

98
Q

What converts L-DOPA to dopamine?

A

L-aromatic amino acid decarboxylase (AADC)

Co-factor from vitamin B6 also required

99
Q

What converts dopamine to noradrenaline?

A

Dopamine-beta-hydroxylase (DBH)

Copper and vitamin C also required

100
Q

What converts noradrenaline to adrenaline?

A

Phenylethanolamine-N-methyltransferase (PNMT)

101
Q

How is melatonin synthesised?

A

Tryptophan
to 5-HTP (hydroxytryptophan) - rate limiting step
to serotonin (5-HT/ hydroxytryptamine)
to melatonin

102
Q

What converts tryptophan to 5-HTP (hydroxytryptophan)?

A

Tryptophan hydroxylase

103
Q

What converts 5-HTP (hydroxytryptophan) to serotonin?

A

L-aromatic amino acid decarboxylase (AADC)

104
Q

Where is serotonin converted to melatonin?

A

Pineal gland

105
Q

What effect does Ghrelin have?

A

Signals to brain that stomach is empty

106
Q

What effect does Leptin have?

A

Stimulates brain to want to stop eating

107
Q

What signs do babies with prader-willi syndrome show?

A

Hypotonia

Failure to suckle

108
Q

What is hyperphagia and when do prader-willi syndrome patients develop it?

A

Pathological overeating
Failed satiety response from failure in homeostatic regulation
Age 2-6

109
Q

Which hormone level is increased in prader-willi syndrome?

A

Orexigenic ghrelin

110
Q

What is the main excitatory neurotransmitter of the CNS?

A

Glutamate

111
Q

What is the main inhibitory neurotransmitter of the CNS?

A

GABA

112
Q

What do inhibitory neurotransmitters cause?

A

They cause Cl- to enter the membrane making it more negative inside
So action potential is less likely
As membrane hyperpolarised

113
Q

What do inhibitory neurotransmitters cause?

A

Cause Na+ to enter the membrane making it more positive inside towards threshold
Making action potential more likely

114
Q

What triggers vesicles to migrate to terminal?

A

Ca2+ influx into the membrane

115
Q

What’s required for vesicle fusion?

A

SNARE proteins

116
Q

What are the monoamine neurotransmitters?

A

Dopamine, noradrenaline, adrenaline and serotonin

117
Q

What does the chemical/ molecular hypothesis of depression propose?

A

Depression is caused by a chemical imbalance in the brain

Antidepressants work by counteracting the molecular changes

118
Q

What does the monoamine hypothesis of depression propose?

A

Depression is caused by a deficiency in serotonin or noradrenaline at functionally important receptor sites in the brain
Antidepressants work by increasing extracellular monoamine concentration

119
Q

What does the network hypothesis of depression propose?

A

Depression is caused by problems in information processing within neural networks
Antidepressants work by gradually improving information precessing within these networks - enhance connectivity then activity-dependent pruning of synapses selects out and stabilises the active synapses

120
Q

What would the most recent combination of the chemical and network hypothesis predict?

A

Antidepressants initiate a self repair process
Plasticity in neural networks and chemical neurotransmission indivisibly cooperate and gradually bring about mood elevation

121
Q

What are the 2 elements of the neuroendocrine mechanism in depression?

A

Corticotrophin releasing hormone is elevated in brain and CSF in depression
And also
Reduced grey matter volume in PFC and hippocampus
Most of the grey matter is taken up by neuronal processes and synapses so this may mean that there’s reduced neuronal complexity and connectivity in depression

122
Q

How do antidepressants fit into/ support the neuroendocrine mechanism?

A

Antidepressants increase neurone production in rodent hippocampus
The delayed onset of clinical effect of antidepressants correlates with the time it takes newly generated neurone to differentiate and mature enough to participate in information processing several weeks after birth

123
Q

What do antidepressants increase levels of?

A

Serotonin, NA and dopamine

124
Q

What are the 2 principle mechanisms of antidepressants?

A
  • Molecular transporter (re-uptake) inhibition - more monoamines remain in synapse
  • Monoamine oxidase inhibition - DA, NA and adrenaline remain in synapse
125
Q

What is the most effective treatment for depression?

A

Electroconvulsive shock treatment

126
Q

How long do antidepressants take to show clinical improvement?

A

Several weeks

127
Q

What is neurotransmitter is reduced in anxiety and how do anxiolytics tackle this?

A

Less GABA in cortex
Benzos activate GABAa receptors - positive allosteric modulators
(GABA is an inhibitory neurotransmitter so neuronal excitability is therefore decreased)

128
Q

What are the 2 neurotransmitters thought to be involved in schizophrenia?

A

Glutamate

Dopamine

129
Q

What’s the dopamine theory of psychosis and what evidence is there to support it?

A

Psychosis is caused by EXCESSIVE DOPAMINE
Cocaine and amphetamine increase DA and can produce psychotic symptoms
Most antipsychotic drugs act via dopamine-related mechanisms

130
Q

What’s the glutamate theory of psychosis and what evidence is there to support it?

A

Psychosis is caused by LOW GLUTAMATE

Glutamate NMD receptor antagonists produce psychotic symptoms

131
Q

What causes the positive symptoms of schizophrenia?

A

Overactivity of D2 receptors (positive +, overactivity +)

Changes in mesolimbic pathway from VTA to nucleus accumbens, amygdala and hippocampus

132
Q

What causes the negative symptoms of schizophrenia?

A

Under-activity of D1 receptors in mesocortical pathway (negative -, under activity -)
(Negative and one both contain letter N)

133
Q

Is the nigrostriatal dopaminergic pathway affected in schizophrenics?
Which structures does the nigrostriatal dopaminergic pathway connect?

A

No

Connects substantia nigra to dorsal striatum (caudate nucleus and putamen)

134
Q

How does hypofunction of NMDA (type of glutamate receptor) contribute to schizophrenia?

A

Decreases activity of mesocortical dopaminergic neurons - negative symptoms
Increases activity of mesolimbic dopaminergic neurons - positive symptoms

135
Q

Where do serotonin projections from the nucleus raphê magnus project to?

A

Cerebellum and spinal cord

136
Q

Where do ascending serotonin projections from the raphê nuclei project to?

A

Thalamus, hypothalamus, striatum, amygdala, hippocampus and cerebral cortex

137
Q

What are behavioural traits seen in depression with too little serotonin?

A

Trouble sleeping
Problems with anger control
Increase in appetite for starchy foods

138
Q

Can serotonin cross the blood brain barrier?

A

No

139
Q

What effect do
a) hallucinogenic drugs
b) antipsychotic drugs
have on serotonin receptors?

A

a) hallucinogenic drugs - many are agonists of serotonin receptors
b) antipsychotic drugs - many are antagonists of serotonin receptors

140
Q

Which enzyme converts glutamic acid into GABA (gamma amino butyric acid)?

A

Glutamic acid decarboxylase (GAD)

141
Q

What do guvacine, nipecotic acid and tiagabine do?

A

Inhibit GABA transport

142
Q

What converts GABA into succinic semialdehyde and where does this reaction mainly occur?

A

Gamma-amino butyric acid transaminase (GABAT)

Mainly in astrocytes

143
Q

What type of GABA receptors are there and where’re they located?

A

GABAa receptors: ligand-gated ion channels mainly on postsynaptic membrane
GABAb receptors: G protein-coupled on pre and postsynaptic membranes

144
Q

What do GABAb receptors do?

A

Gi/Go coupled
Inhibit voltage-gated Ca2+ channels
Open K+ channels
Inhibits adenylyl cyclase

145
Q

Which regions of the brain is GABA involved with?

A

Dopaminergic neurons in nigrostriatal system synapse onto GABAergic neurons
Lower concentration of GABA in grey matter
GABA abundant in nucleus accumbens

146
Q

Where is the largest cluster of noradrenergic neurons and where else are they found?

A

Largest cluster - locus coeruleus in rostral pons

Smaller clusters in medulla

147
Q

What does alcohol and nicotine do to dopamine levels?

A

Increase DA levels

If it feels good - DA neurons probably involved except enjoyment of food by endorphins

148
Q

What can be given as Parkinson’s treatment and why?

A

L-DOPA
Can cross blood-brain-barrier
Can be converted to dopamine
Avoids rate-limiting step of converting tyrosine to L-DOPA

149
Q

What’s the adverse drug effect of L-DOPA as Parkinson’s treatment?

A

Hallucination

150
Q

What does the mesocortical pathway connect?

A

Ventral tegumental area

to cortical areas of frontal lobes

151
Q

What does the mesolimbic pathway connect?

A

Cell bodies in midbrain ventral tegumental area
Medial forebrain bundle projects to parts of limbic system
Especially the nucleus accumbens and amygdaloid nucleus

152
Q

Where is the VTA and what is it involved in?

A

Brain stem

Involved in pleasure system/ reward circuit

153
Q

Which pathway contains most of the dopamine?

A

Nigrostriatal pathway - substantia nigra to dorsal striatum (caudate nucleus and putamen)

154
Q

What does the corpus striatum consist of?

A

Caudate nucleus
Lentiform nucleus: Putamen and Globus pallidus
Nucleus accumbens

155
Q

Which areas contain a lot of dopamine?

A

VTA
Corpus striatum
Substantia nigra
Frontal cortex, limbic system and hypothalamus

156
Q

What causes the adrenarche?

A

Activation of hypothalamic-pituitary-adrenal axis

Causing increase in adrenal androgens

157
Q

What does the increase in adrenal androgens during adrenarche cause?

A

Development of secondary sexual characteristics

Changes in sweat glands

158
Q

What happens in gonadarche?

A

Gonadotropin-releasing hormone pulsatile secretion from hypothalamus during sleep (initiated by activation of hypothalamic-pituitary-gonadal axis)
Stimulates anterior pituitary production of LH and FSH
Leading to gonadal maturational changes
Leading to secretion of gonadal steroid oestrogen and testosterone

159
Q

When do girls/ boys have linear growth spurts and why?

A

Girls - 12 years
Boys - 14 years
GH secreted from anterior pituitary during sleep
Prolonged HPA axis activation thought to suppress GH secretion

160
Q

What are the 3 main effects of sex steroids on behaviour and via which structures does it have its effect?

A

Facilitation of reproductive behaviours - hypothalamus
Reorganisation of sensory and association regions - visual cortex, amygdala, hippocampus
Motivation and reward-related behaviour - nucleus accumbens, dopaminergic pathways to prefrontal cortex

161
Q

What is grey matter made of?

A

Neuron cell bodies, dendrites, glial cells

162
Q

What is white matter made of?

A

Axons

163
Q

What happens to the volume of grey and white matter in adolescence?

A

Linear increase in white matter volume

Grey matter volume has pre-pubertal increase, post-pubertal loss

164
Q

Why are adolescents more likely to encage in risky behaviour?

A

Prefrontal cognitive-control network not fully developed
Subcortical motivational drive network is being rapidly remodelled - sensitive to social and emotional stimuli
Decision to engage not influenced by cognitive processes alone - still participate when aware of risks

165
Q

What are the risk factors for metabolic syndrome?

A 
Large waistline 
High triglyceride level
Low HDL level 
High blood pressure
High blood sugar
166
Q

What is metabolic syndrome?

A

A combination of diabetes, high bp and obesity

That puts you at greater risk of heart disease, stroke and other conditions affecting blood vessels

167
Q

Weight gain can be induced by several antipsychotic drugs, most notably…?

A

Olanzapine and clozapine

168
Q

How do olanzapine and clozapine cause weight gain?

A

By inhibition of histamine H1 and serotonin 2c receptors

169
Q

Name 2 adverse side effects of Clozapine apart from weight gain

A

Hyperlipidaemia

Hypertension

170
Q

What is an adverse drug effect of long term Risperidone use?

A

Hyperprolactinaemia

171
Q

What is effective in reducing Clozapine-induced adverse drug effects?

A

Aripiprazole

172
Q

Which type of antipsychotics pose the greatest risk of weight gain and metabolic syndrome?

A

2nd generation antipsychotics

173
Q

What can be given for weight gain from antipsychotic medication?

A

Metformin

174
Q

Why are psychosis patients at greater risk of metabolic syndrome?

A

Antipsychotic medication can cause weight gain
Negative symptoms of psychosis - abolition and anhedonia may lead to lack of exercise and poor diet
Other lifestyle factors: substance use, smoking, stress

175
Q

What’s activated in psychological stress?

A

Sympathetic adrenomedullary system

Limbic-hypothalamic-pituitary-adrenal axis

176
Q

What is the 1st line of treatment for depression?

A

Cognitive behavioural therapy

177
Q

What are the disadvantages of MAOI compared to SSRIs and SNRIs?

A

More side effects

Number of dietary restrictions

178
Q

What is dysthymic disorder?

A

Persistent and long standing depressed mood that is not severe enough to be a depressive disorder

179
Q

What is the average age of psychosis in men/ women?

A

Men: 18-25
Women: 25-35

180
Q

How is life-expectancy affected in schizophrenia?

A

15-20 years less than national average

Main causes of death: suicide and comorbid somatic conditions

181
Q

What is the possible danger to a patient who takes a 2nd generation antipsychotic of quitting/ reducing smoking?

A

Clozapine and olanzapine and nicotine are metabolised by the same enzyme
Smoking cessation leads to enzyme activity reduction over several days, less medication is metabolised and plasma levels increase
Toxic levels of medication can accumulate in a matter of days

Year 2 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions