L19: Anxiety And Depression Flashcards by selcan icli

What is the definition of anxiety disorder

An inappropriate or excessive manifestation of the fear response often to a stressor

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What is the difference between normal fear and anxiety

Anxiety can occur without the stressor being present

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What is the responses involved in anxiety

Defensive behaviour
Corticosteroid secretions
Negative emotions
Autonomic reflexes

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What are the types of anxiety disorders

General anxiety disorder
Phobia anxiety
Panic disorders

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Which type of anxiety disorder is the most common

General anxiety disorders

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In normal anxiety what system is involved

ANS
Corticosteroid production
I.e the HPA axis

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Describe what occurs in the HPA axis in a normal response

1) hypothalamus is activated at the paraventricular nucleus due to a stressor
2) hypothalamus releases CRF to the anterior pituitary gland
3) anterior pituitary gland releases ACTH to the adrenal gland
4) the adrenal gland releases cortisol which negatively feedbacks to the hypothalamus

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Describe what happens to the HPA axis in a anxiety disorder

1) the hypothalamus is activated without a stress at the paraventricular nucles
2) hypothalamus releases CRF to the anterior pituitary gland
3) anterior pituitary gland releases ACTH to the adrenal gland
4) adrenal gland releases cortisol
5) the negative feedback system by cortisol is impaired so the hypothalamus continues to stimulate the HPA axis

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If there isn’t a stressor that is stimulating the hypothalamus in anxiety disorder, what is

Amygdala stimulates the hypothalamus

Hippocampus inhibits the hypothalamus

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What happens to the limbic system that causes to drive the hypothalamus

Changes within it such as neuroplasticity

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What are the treatment methods for anxiety disorders

Self help
Psychological
Pharmacological

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What does the choice of pharmacological agents depend on

Nature of predominant symptoms

Duration of treatment

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What are the 3 main classes of drugs used in anxiety disorders

1) beta adrenoceptors antagonist
2) benzodiazepines
3) monoaminergic drugs

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How does beta adrenoceptor antagonist work

Reduce the somatic symptoms when the ANS system becomes elevated

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What is the mechanism of action of benzodiazepines

1) Benzodiazepines binds to the allosteric site of GABAa receptors
2) GABAa is an inhibitory neurotransmitter in the brain
3) benzodiazepines increase the activity of GABAa receptors
4) this results in calcium influx to cause hyper polarisation of the neurones so it is less active

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Where are particularly in the brain do benzodiazepines work at

Limbic system: pre-frontal cortex, amygdala

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What are the side effects of benzodiazepines

Sedation

In acute overdose with alcohol it can cause respiratory depression

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Why do we get side effects of benzodiazepines

There are GABAa receptors in all parts of the brain

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What can occur if benzodiazepine is used long term

Tissue tolerance so activity of neurones becomes altered

- dependence when the individual stop taking it

Up to how many weeks can benzodiazepines be used for

4 weeks

Name examples of benzodiazepines

Diazepam
Nitrazepam
Midazolam

What is the mechanism of action of monoaminergic drugs

Affect the monoamine levels in the brain by affecting 5-HT and serotonin

Name an example of a monoaminergic drug

Buspiraone

What are the symptoms for major depressive disorder

Misery 
Despair 
Loss of motivation 
Suicidal thoughts 
Appetite changes

What is the theory that causes a suggestion to how depression occurs

Monoamine theory

What does the monoamine theory state

Depression is due to hypoactivity of monoaminergic (5HT, NA) synapses in the brain

What are the treatment methods for major depressive disorders

Psychotherapy Antidepressant drugs Electroconvulsive therapy

What are the 4 classes of antidepressant drugs

1) Selective serotonin re-uptake inhibitors 2) tricyclics antidepressants 3) monoamine oxidase inhibitors 4) newer antidepressants

Describe the normal processes that occur in the monoaminergic synapses

1) 5-HT is released from the vesicles 2) 5-ht is then taken back up by the pre-synaptic terminal 3) 5HT is either degenerated by monoamine oxidase or becomes packaged into vesicles

What is the mechanism of action of selective serotonin re-uptake inhibitors

Inhibit the re-uptake of 5HT by the pre-synaptic terminal so 5HT increases in the intra synaptic gap

What are the side effects of selective serotonin re-uptake inhibitors

GI: Nausea and vomiting Wright changes - due to action of 5-HT on the hypothalamus Suicidal thoughts Serotonin syndrome- too much serotonin in the body

What is the mechanism of action of mono-amine oxidase inhibitors

1) Inhibit the enzyme monoamine oxidase in the pre-synoptic terminal 2) more 5-HT is packaged into vesicles and is released 3) this increases the intra-synaptic terminal level of 5-ht

What are the side effects of monoamine oxidase inhibitors

Cheese reaction | Antimuscarinic effects

What is the cheese reaction

Food that contain tyramine displaces the NA from the SNS so there is more NA released which causes an increase in BP as NA cannot be Brocken down by mono amine oxidase

Why do we get an anti-muscarinic effect

Monoamine oxidase inhibitors can bind to alpha 1 receptors

What is the mechanism of action of tricyclic anti-depressants

Re-uptake inhibition of 5-HT

What are the side effects of tri-cyclic antidepressants

Anti muscarinic effect | Sedative

How do newer drugs work

- mediate uptake of 5HT, NA, dopamine | - melatonin receptor agonism

Do anti depressant drugs work

Not all as 30% of patients do not respond to it

If the anti depressant drugs are not working what does this suggest

The monoamine theory is incomplete

What is the new theory for depression called

Network hypothesis

What is the network hypothesis about

1) in depression there is an increase in CRF from the hypothalamus and cortisol from the adrenal gland 2) a continous hyperacitity of the HPA axis can lead to depression i.e ongoing anxiety can lead to depression

What does the increasing levels of cortisol from the adrenal glands effect that causes depression

Hippocampus

What can happen within the hippocampus

- Decrease in glucocorticoid receptors and decrease in BDNF (maintains healthy neurones) - Decrease in neurogenesis and neuroplasticity

With anti-depressant drugs how does it affect the hippocampus

Monoamine input tot he hippocampus results in increased neurogensis and neuroplasticity