Neuropharmacology at University Of Leeds | Flashcards & Summaries

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Lernmaterialien für Neuropharmacology an der University of Leeds

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How is depression diagnosed?
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5 of the symptoms persistent for 2 weeks. Symptoms including low mood and energy, thoughts of death, 
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What is the monoamine hypothesis of depression?
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Found through patients with tuberculosis taking iproniazid which improved their mood. medications were inhibitors of monoamine oxidase so monoamInes such as dopamine, noradrenaline and serotonin wernt broken down. Increasing availability 
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Which monoamine oxidase breaks down monoamines?
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Mao-a breaks down noradrenaline and serotonin
mao-b breaks down dopamine 
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What is the issue with the monoamine theory of depression?
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Some people have no response to antidepressants that target monoamines . Some even develop depression from them. 
Non enough evidence for changes to monoamine systems 
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What is the HPA axis hypothesis for depression?
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Some patients with depression have high cortisol levels. Cortisol is released from hypothalamic pituatry adrenal axis and has a negative effect in mood 
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What is the circadian rhythm hypothesis for depression? 
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Circadian rhythms disturbed and cortisol is usually released early in the morning but depression patients see a peak later in the day. Excess cortisol decreases neurogenesis. Growth factor levels that are involved in neurogenesis also lower in those with depression  
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Monoamine oxidase inhibitors as antidepressants 
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Can increase the pool of available dopamine serotonin and norepinephrine 
can be non selective- target both A and B monoamine oxidases or selective, either A OR B  
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TESTE DEIN WISSEN
What are the issues with non selective MAOIs?
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TESTE DEIN WISSEN
Both A and B are blocked.
excess norepinephrine can bind to  adrenergic receptors on blood vessels causing vasoconstriction, raising blood pressure.
They prevent the breakdown of tyrosine so restrictions in cheese and wine intake. Tyrosine with displace noradrenaline in neurones so noradrenaline will move into blood having the effects above 
Serotonin syndrome
hypertensive crisis 
can overdose 
Lösung ausblenden
TESTE DEIN WISSEN
What are the benefits of MAO-a inhibitors?
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They can be reversible or irreversible 
they don’t prevent breakdown of tyrosine 
they are less toxic and have a higher acceptability than non-selective antidepressants   
 
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What are tricyclic antidepressants?
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They have 3 rings and block serotonin and norepinephrine transporters to prevent reuptake and elevate levels in the synaptic cleft.
They have anticholinergic side effects such as dry mouth and interact with drugs and alcohol.
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What are SSRIs?
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Serotonin reuptake inhibitors. They inhibit SERT and don’t cause tyrosine build up. They aren’t toxic in overdose and usually the first line of treatment in depression 
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What are the 6 neurocognative domains?
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Language, learning and memory, complex attention, social cognition, executive function, perceptual motor function  
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Q:
How is depression diagnosed?
A:
5 of the symptoms persistent for 2 weeks. Symptoms including low mood and energy, thoughts of death, 
Q:
What is the monoamine hypothesis of depression?
A:
Found through patients with tuberculosis taking iproniazid which improved their mood. medications were inhibitors of monoamine oxidase so monoamInes such as dopamine, noradrenaline and serotonin wernt broken down. Increasing availability 
Q:
Which monoamine oxidase breaks down monoamines?
A:
Mao-a breaks down noradrenaline and serotonin
mao-b breaks down dopamine 
Q:
What is the issue with the monoamine theory of depression?
A:
Some people have no response to antidepressants that target monoamines . Some even develop depression from them. 
Non enough evidence for changes to monoamine systems 
Q:
What is the HPA axis hypothesis for depression?
A:
Some patients with depression have high cortisol levels. Cortisol is released from hypothalamic pituatry adrenal axis and has a negative effect in mood 
Mehr Karteikarten anzeigen
Q:
What is the circadian rhythm hypothesis for depression? 
A:
Circadian rhythms disturbed and cortisol is usually released early in the morning but depression patients see a peak later in the day. Excess cortisol decreases neurogenesis. Growth factor levels that are involved in neurogenesis also lower in those with depression  
Q:
Monoamine oxidase inhibitors as antidepressants 
A:
Can increase the pool of available dopamine serotonin and norepinephrine 
can be non selective- target both A and B monoamine oxidases or selective, either A OR B  
Q:
What are the issues with non selective MAOIs?
A:
Both A and B are blocked.
excess norepinephrine can bind to  adrenergic receptors on blood vessels causing vasoconstriction, raising blood pressure.
They prevent the breakdown of tyrosine so restrictions in cheese and wine intake. Tyrosine with displace noradrenaline in neurones so noradrenaline will move into blood having the effects above 
Serotonin syndrome
hypertensive crisis 
can overdose 
Q:
What are the benefits of MAO-a inhibitors?
A:
They can be reversible or irreversible 
they don’t prevent breakdown of tyrosine 
they are less toxic and have a higher acceptability than non-selective antidepressants   
 
Q:
What are tricyclic antidepressants?
A:
They have 3 rings and block serotonin and norepinephrine transporters to prevent reuptake and elevate levels in the synaptic cleft.
They have anticholinergic side effects such as dry mouth and interact with drugs and alcohol.
Q:
What are SSRIs?
A:
Serotonin reuptake inhibitors. They inhibit SERT and don’t cause tyrosine build up. They aren’t toxic in overdose and usually the first line of treatment in depression 
Q:
What are the 6 neurocognative domains?
A:
Language, learning and memory, complex attention, social cognition, executive function, perceptual motor function  
Neuropharmacology

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