L19: Anxiety And Depression Flashcards
What is the definition of anxiety disorder
An inappropriate or excessive manifestation of the fear response often to a stressor
What is the difference between normal fear and anxiety
Anxiety can occur without the stressor being present
What is the responses involved in anxiety
Defensive behaviour
Corticosteroid secretions
Negative emotions
Autonomic reflexes
What are the types of anxiety disorders
General anxiety disorder
Phobia anxiety
Panic disorders
Which type of anxiety disorder is the most common
General anxiety disorders
In normal anxiety what system is involved
ANS
Corticosteroid production
I.e the HPA axis
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
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
If there isn’t a stressor that is stimulating the hypothalamus in anxiety disorder, what is
Amygdala stimulates the hypothalamus
Hippocampus inhibits the hypothalamus
What happens to the limbic system that causes to drive the hypothalamus
Changes within it such as neuroplasticity
What are the treatment methods for anxiety disorders
Self help
Psychological
Pharmacological
What does the choice of pharmacological agents depend on
Nature of predominant symptoms
Duration of treatment
What are the 3 main classes of drugs used in anxiety disorders
1) beta adrenoceptors antagonist
2) benzodiazepines
3) monoaminergic drugs
How does beta adrenoceptor antagonist work
Reduce the somatic symptoms when the ANS system becomes elevated
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
Where are particularly in the brain do benzodiazepines work at
Limbic system: pre-frontal cortex, amygdala
What are the side effects of benzodiazepines
Sedation
In acute overdose with alcohol it can cause respiratory depression
Why do we get side effects of benzodiazepines
There are GABAa receptors in all parts of the brain
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
