1
Q
According to UK statistics, which group is more likely to suffer from Affective disorders?
A
black and mixed race Woman
2
Q
What is bipolar disorder (BD)?
A
disorder in which a person’s mood can switch constantly between mania (period of excitment, highperactivity and talking fast) to depression (low mood, loss of pleasure in daily activities and fatigue).
3
Q
What is mania?
A
feeling energetic, excited, talking fast
4
Q
What are the two main types of Bipolar disorder?
A
Bipolar I Disorder and Bipolar II Disorder.
5
Q
Explain Bipolar I disorder
A
This is when a person has had at least 1 maniac episode and periods of Great Depression each lasting for extended period of time.
6
Q
Explain Bipolar II Disorder
A
This is when a person has had no maniac episodes but 1 hypomania episode and at least 1 period of depression.
7
Q
Which bipolar disorder is caused by genetics and can be diagnosed in late teens?
A
Both
8
Q
What is cyclothymia?
A
mild form of bipolar disorder
9
Q
What is euthymia?
A
periods without mania and depression
10
Q
How is BD treated?
A
using lithium stabiliser
11
Q
Why is lithium a good treatment option for BD patients?
A
works quickly
safe to use (no overdose)
12
Q
What is the MOA for lithium (mood stabiliser)?
A
in the brain, lithium blocks excitatory neurotransmission (to inhibit the release of glutamate because they are too high) and stimulates the inhibitory neurotransmission (to promote release of GABA because these are low) this is to keep neurotransmitters including dopamine all at a steady level. lithium can also block IP3 and CAMp inside cells to inhibit further cell signalling in brain cells.
13
Q
What are some side effects of lithium?
A
nausea, thirst, tremor and mental confusion
14
Q
What is Major Depressive Disorder (MDD)?
A
It is a psychiatric disorder that causes low mood and loss of interest in most activities
15
Q
What are three key symptoms of Major Depressive Disorder (MDD)?
A
- Persistent low mood
- Loss of interest or pleasure in most activities
- Low energy levels
16
Q
What are some associative symptoms of MDD?
A
trouble sleeping, experiencing suicidal thoughts, experiencing low self confidence, change in appetite.
17
Q
What helps determine the severity of the depression?
A
Total number of symptoms that a person is experiencing
<4 symptoms means not depressed, 4 symptoms means mild depression, 5/6 symptoms means moderate depression and > 7 symptoms indicates severe
18
Q
What are the requirements for a diagnosis to be made for MDD?
A
symptoms must be present for at least 2 weeks and each symptom should be severe enough to be noticeable for most of the day, nearly everyday.
19
Q
What are the two main diagnostic systems that are used to classify depression?
A
- International classifications of disease (ICD) 10 & 11
- Diagnostic and statistical manual of mental health disorder, 5th edition (DSM)
20
Q
What is monoamine hypothesis?
A
hypothesis that suggests that depression results from low levels of monoamine neurotransmitters in the brain.
21
Q
What are the three key monoamines highlighted in the monoamine hypothesis of depression?
A
dopamine, serotonin and noradrenaline
22
Q
How was the monoamine hypothesis discovered?
A
when a drug (monoamine oxidase inhibitors) used to treat tuberculosis was found to have an affect on mood.
23
Q
what is the problem with monoamine hypothesis?
A
antidepressants work quickly (hours), however relief of symptoms usually takes weeks.
24
Q
What are the theories related to pathophysiology of depression
A
Glucocorticoid hypothesis of depression
Glutamate hypothesis of depression
Monoamine hypothesis of depression
Neurogenesis hypothesis of depression
GABAergic deficit hypothesis of depression
25
Which neuronal pathway in the brain is responsible for the symptoms of depression?
The dopaminergic pathways which has the reward circuitry
26
How does the reward circuitry if the brain relate to symptoms of depression?
the reward circuitry is the part of the brain that helps us feel pleasure, motivation or excitement when we do something we love. This could be eat a cake, engage in sexual intercourse, achieve a goal. A specific part of the midbrain called the ventral tegmental area (VTA) releases dopamine when we engage in something we love, the dopamine travels to various parts of the brain. To name a few hippocampus, amygdala, prefrontal cortex, nucleus accumbens. This is how we get pleasure, motivation, excitement and energy to do things. In depression this part of the brain the VTA becomes impaired and doesn’t work this reduces the dopamine levels to certain brain areas like the nucleus accumbens and the prefrontal cortex so now a person that used to find joy in life doesn’t anymore.
27
What is neuromodulation?
They way neurons in the brain talk to each other
28
What types of neurotransmitters take part in neuromodulation?
Dopamine, noradrenaline, serotonin, acetylcholine, histamine
29
What is synaptic neurotransmission
Process by which neuron's communicate with each other across the synapse
30
What happens in synaptic neurotransmission?
Neurotransmitters are released from one neuron, they travel across the synapse and bind onto the receptors locate on the other neuron to pass signals.
31
What is volumetric neurotransmission?
Process by which neurons communicate to far away neurons instead of the ones closer to the neurotransmitter release site.
32
What happens on volumetric neurotransmission?
Neurotransmitters are released from the neuron and instead of binding to the receptors on the post synaptic neuron it sends the neurotransmitters which it has released into the extracellular fluid to bind onto far away neurons.
33
Name the neurotransmitters that take part in both?
Synaptic neurotransmission - glutamate
Volumetric neurotransmission - Monoamine neurotransmitters
34
Which area of the brain is noradrenaline released from?
Locus coeruleus
35
Which area of the brain is serotonin released from?
Raphe nucleus
36
Which area of the brain is dopamine released from?
Ventral tegmental area (VTA)
37
What are some non-pharmacological treatments used for depression?
Cognitive behavioural therapy (CBT)
38
How will CBT help depression patients?
it can help them identify and manage their triggers
39
What medications are commonly used by depression patients?
Antidepressants
40
What are the different classes of antidepressants?
Selective serotonin reuptake inhibitors (SSRIs)
Serotonin - noradrenaline reuptake inhibitors (SNRIs)
Monoamine Oxidase Inhibitors (MOI)
Tricyclic antidepressants (TCAs)
41
What are some other psychotherapies?
Behavioural therapy
Interpersonal therapy
Group therapy
Mindfulness based cognitive therapy
42
What are some brain stimulation methods that can be used In MDD?
Electroconvulsive therapy (ECT)
Vagus nerve stimulation (VNS)
Transcranial magnetic stimulation (TMS)
Deep brain stimulation (DBS)
43
What are some examples of SSRIs?
Fluoxetine, sertraline, citalopram, escitalopram, paroxetine, fluvoxamine
(friendly students can eat perfect food)
44
How do SSRIs work for depression?
Block the serotonin reuptake transporter on the presynaptic neuron to allow more serotonin to remain in the synapse and bind onto the receptors of the post synaptic neuron elevating mood.
45
What is a common side effects associated with SSRIS?
Increased risk of bleeding in older patients or those talking anticoagulants
46
What are the pros to using SSRIs compared to other antidepressants? (4)
- Better tolerated by most patients
- Reduced risk of overdose
- Less sedating effects
- Fewer muscarinic and cardiotoxic side effects than TCAs
47
Which SSRI should not be used to manage depression as 1st line in patients that have cardiovascular issues?
Citalopram
48
Which three SSRIS have a higher drug interaction than other SSRIS?
Fluoxetine, fluvoxamine and paroxetine
49
What are some examples of Tricyclic antidepressants?
Amitriptyline and clomipramine
50
How do TCAs work?
Similar MOA to SSRIS but not used much for depression as it can cause adverse side effects
51
What are some Adverse side effects that TCAs such as amitriptyline can cause?
Antimuscarinic side effects such as dry mouth and urinary retention, blurred vision, sedation, weight gain
52
What are some risks of taking TCA?
Overdose can occur
Can impact the heart
Increased risk of coma/seizure
53
What are some examples of MAOIs?
tranylcypromine, phenelzine
54
How do Monoamine oxidase inhibitors work (MOIs ?
Monoamine Oxidases are enzymes that are found in the brain that break up the monoamine neurotransmitters (serotonin, dopamine and noradrenaline) these antidepressants bind and block these enzymes from degrading the NTs so that they can bind to post synaptic neuron receptors and initiate firing - increasing mood.
55
What can MAOIs lead to?
Liver damage (hepatoxicity)
Headaches or even intracranial haemorrhage
56
What type of foods can MAOIs not be taken with?
Cheese - can lead to hypertension
57
What is electroconvulsive shock treatment (ECT)?
A psychiatric treatment where an electric current is passed through the brain to promote a short controlled seizure.
The aim is to release NT in the brain helping with mood.
58
What is the 1st line of treatment for less severe depression?
Cognitive behavioural therapy (CBT) offered first but if the patient wants medication as 1st line then prescribe sertraline.
59
What is NMDAIs and provide some examples ?
N - methyl D-aspartate receptor inhibitors
- Ketamine
- Esketamine
60
How should you navigate prescribing Antidepressants for depression?
1. Start antidepressant
2. Assess efficacy after 1-4 weeks
3. If not effects then switch to a different antidepressant and continue this for 6-9 months
4. If effect is seen in symptoms then keep and monitor for 6-9 months
5. If not tolerated then switch to a different antidepressant.
61
How do these NMDA inhibiters work?
They block NMDA receptors on inhibitory neurons, inhibiting GABA from being released, this promotes the release of Glutamate NT from the excitatory neuron onto post synaptic receptors initiating firing of the neuron.
62
How does psilocybin work?
When Psilocybin enters the body it converts into its active form psilocin. The psilocin then acts like serotonin and binds to 5-HT2A serotonin receptors on the causing intracellular signalling to occur which leads to series of intracellular processes and eventually increased excitability.
63
What is anxiety?
Feeling of fear, worry, unease about something that might happen in the future
64
Which response of the body is anxiety feeling being compared to?
Fight or flight response
65
What are some common symptoms of anxiety?
Shortness of breath, Palpitations, Chest pains
Flushes, Sweating, dry mouth, dizziness
66
Explain the Yerkes Dodson curve?
Law which states the relationship between arousal (stress/alertness) and performance
When arousal is low performance is low, when arousal is moderate the performance is at optimum levels when the arousal is high so is the performance of an individual
67
What are the two types of anxiety?
Healthy anxiety
pathological anxiety
68
What is healthy anxiety?
anxiety experienced under stress
E.g. exams, competition
69
What is pathological anxiety?
Anxiety experienced even when there is no real reason to be anxious, fearful
E.g. fear of elevators, fear of spiders
70
How many people are affected by mental health problems in a year?
1 in 4 people
71
What gender suffers from 2 or more symptoms of depression ?
Males - 12%
72
What gender suffers from 2 or more symptoms of anxiety ?
Females -14%
73
Which ethnicities are found to have anxiety disorders?
Chinese
Mixed
Arab
74
What is generalised anxiety disorder?
Mental health disorder where person lives in constant fear or worries about simple things in everyday life
75
How long does someone need to experience worry for to be diagnosed with GAD?
6 months
76
What other mental health disorders is GAD associated with?
Depression, alcohol & substance misuse
77
Can you list some symptoms that GAD patient in primary care present with?
Headaches, muscle tension, GI symptoms, back pain and insomnia - all physical
78
What screening tool is used to measure the severity of generalised anxiety disorder and its response to treatment?
Generalised anxiety disorder 7 (GAD-7)
79
What is the main difference between generalised anxiety disorder vs major depressive disorder?
Patients with GAD are described as being helpless and patients with MDD feel hopeless
80
What are the two main classifications of anxiety?
Specific phobia
Generalised anxiety disorder (GAD)
81
What is specific phobia?
Strong fear about one specific thing
82
What are some common symptoms of specific phobia?
Fear of animal, blood, injections, injury
83
Which region of the brain plays a central role in anxiety disorders?
Limbic system
84
Which neurotransmitters are involved in anxiety disorders?
GABA and serotonin
85
Describe how the neural circuits control or promote anxiety?
The amygdala in the brain detects a threat and generates anxiety and fear signals that travel to the BNST (Bed nucleus stria terminals) here the BNST keeps the anxiety signals going which causes the hypothalamus and the brainstem to bring about symptoms of anxiety. The prefrontal cortex all tries to stop it.
86
What class of drugs are used to treat anxiety?
Anxiolytics
87
What are some examples of anxiolytics?
Benzodiazepines, SSRIs, TCAs, 5-HT agonists
88
What are benzodiazepines ?
These are anti-epileptic drugs used to stop seizures but can also be used for anxiety.
89
What are some examples of benzodiazepines?
These are all drugs ending in "zam" e.g. diazepam, lorazepam, temazepam.
90
How do benzodiazepines work?
They act as allosteric modulators at GABA A channels on the post synaptic neuron and increase the opening of GABA A channels.
91
What can cause the receptor shape to become altered?
Mutation of the a2 subunit of the receptor
92
What happens if the shape of the receptor becomes altered?
BZD cannot bind properly and won’t be able to ignite effect causing less GABA in synapse and no therapeutic effect.
93
Name the benzodiazepines that have a fast, slow, intermediate half-life?
Fast – midazolam < 5 hours
Slow - temazepam and lorazepam 5-20 hours
Intermediate – nitrazepam
94
Which BZD has a half-life of > 40 hours in the blood before elimination?
Diazepam and chlorodiazpoxide
95
What are some of the most common side effects of benzodiazepines?
Can cause overdose, patient might develop tolerance to drug (increased dose needed), patient can develop drug dependence.
96
What is the main purpose of SSRIs?
To increase serotonin levels in the brain boosting mood, energy in patients with affective disorders
97
Serotonin Is also implicated in what disorder?
Panic
98
What are the different types of serotonin receptors and briefly list what they could be involved in?
5-HT1a - anxiety, sexual function
5-HT1c - anxiety, migraine pain
5-HT1D - migraine pain
5-HT2 - anxiety, depression,
5-HT3 - migraine pain, emesis
5-HT4 - anxiety
99
How is the SSRI dosing for anxiety vs SSRI dosing for depression?
The SSRI dosing for anxiety is higher
100
List some advantages of SSRIS compared to other antidepressants?
No overdose, no tolerance, no withdrawal symptoms unless patient stops suddenly, provides no weight gain.
101
What are some disadvantages of SSRIS?
4-6 weeks to see effect
Full benefit develops after 12 weeks
Symptoms get worse temporarily before getting better
102
What are some common side effects of SSRIS?
Sexual dysfunction, insomnia, headaches, nausea
103
What is buspirone and what receptor does it bind to?
It is a partial agonist that binds and inhibits the serotonin (5-HT1A) receptor to manage anxiety
104
What conditions can buspirone be used to treat?
Generalised anxiety disorder (GAD)
Social phobias
105
What are the 4 benefits of buspirone?
Provides no sedation, no impact on Benzodiazepines when used tother, no tolerance developed or withdrawal, no misuse
106
What are some of the disadvantages of using buspirone?
Nausea, headache, insomnia, restless, dizziness
107
What is the management of GAD?
1. Assess GAD patients and educate them
2. Monitor symptoms over time
3. If symptoms don’t improve offer psychosocial interventions e.g. talking therapies
4. If not helped, then prescribe medication
108
How many different serotonin receptors are there?
7 (5HT1- 5HT7)
Each have subtypes
109
What do all these serotonin receptors have in common?
Similar 3D structure of active site where ligands bind
110
What is 5 hydroxy tryptamine?
Another name for serotonin
It shows hydroxyl group attached to 5th carbon on the tryptamine (naturally occurring chemical compound found in the body)
111
Which class of compounds does LSD belong to?
Ergoline
112
What % of similarities are found in the structure of subgroups of 5-HT2?
70-80%
113
What are some drugs that bind/block serotonin receptors (5-HT) on dopamine neurons?
Atypical Antipsychotics – olanzapine, risperidone, clozapine, aripiprazole.
114
Which Atypical antipsychotic are tricyclic (contain 3 fused rings)?
Olanzapine and clozapine, risperidone
115
Which Atypical Antipsychotics bind to 5-HT2A/ 5-HT2C receptors?
Clozapine and olanzapine
116
What is the role of 5-HT2A receptors and what happens when they are blocked?
5-HT2A receptors help regulate body temperature, sleep, appetite, learning, heart function, and muscle movement. Blocking them (as with clozapine or olanzapine) can cause weight gain and affects mood and sleep.
117
What can block 5-HT2C receptors help with?
Blocking 5-HT2C receptors may help treat anxiety, mood, and sleep disorders.
118
What is the major difference between both olanzapine and clozapine?
They have different aryl group
119
Which enzyme is both olanzapine and clozapine metabolised by?
CYP 1A2
120
What is the dopamine hypothesis in schizophrenia?
Schizophrenia results when we get too much dopamine signalling taking place in the brain.
121
What is the main role of antipsychotics in schizophrenia?
Reduce dopaminergic neurotransmission in the brain to alleviate symptoms by binding onto 5-HT receptors on dopamine signalling neurons.
122
Why are Atypical Antipsychotics considered more effective than Typical Antipsychotics?
Because Atypical Antipsychotics alleviate both positive symptoms such as hallucinations, delusions and disordered thinking (D2 + 5-HT) and now negative symptoms of schizophrenia (5-HT strongly and D2 weakly) to like anhedonia – the inability to feel joy, avolition – not care.
123
What condition is methylphenidate, dexfetamine used to treat?
ADHD
124
Describe the chemical composition of methylphenidate?
Contains 2 chiral centres C1, C2
4 isomers
R, R and S, S
125
Which stereoisomer of dexfetamine is more potent?
S – steroisomer
126
What is the R stereoisomer of dexamphetamine called?
Levoamphetamine
127
What is SAR for dexfetamine
128
What is serotonin hypothesis of depression?
Depression occurs due to low serotonin
129
How can we use SSRIs to improve symptoms?
blocking reuptake of serotonin to presynaptic neuron, increase serotonin levels in synapse.
130
What are the goals of the SSRIS?
Bind selectively to only SERT
Has to inhibit SERT on binding
Should not bind to other neurotransmitter receptors like TCAs causing side effects like that of the heart.
131
Where is citalopram mostly metabolised and with what enzymes?
Liver – CYP 2C19, CYP 3A4, CYP2D6
132
What is the name of the S form of citalopram
escitalopram
133
Which part of the SSRI molecule is necessary for its selectivity to SERT only?
Halogen and the substituents that are attached onto them
134
What is the most potent SSRI?
Paroxetine
135
What is the difference between the structure of fluoxetine and paroxetine?
difference is fluoxetine linear structure is folded into a ring forming paroxetine
MP324 2025
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