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BAB > L19: Anxiety And Depression > Flashcards

L19: Anxiety And Depression Flashcards

1
Q

What is the definition of anxiety disorder

A

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

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2
Q

What is the difference between normal fear and anxiety

A

Anxiety can occur without the stressor being present

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3
Q

What is the responses involved in anxiety

A

Defensive behaviour
Corticosteroid secretions
Negative emotions
Autonomic reflexes

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4
Q

What are the types of anxiety disorders

A

General anxiety disorder
Phobia anxiety
Panic disorders

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5
Q

Which type of anxiety disorder is the most common

A

General anxiety disorders

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6
Q

In normal anxiety what system is involved

A

ANS
Corticosteroid production
I.e the HPA axis

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7
Q

Describe what occurs in the HPA axis in a normal response

A

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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8
Q

Describe what happens to the HPA axis in a anxiety disorder

A

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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9
Q

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

A

Amygdala stimulates the hypothalamus

Hippocampus inhibits the hypothalamus

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10
Q

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

A

Changes within it such as neuroplasticity

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11
Q

What are the treatment methods for anxiety disorders

A

Self help
Psychological
Pharmacological

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12
Q

What does the choice of pharmacological agents depend on

A

Nature of predominant symptoms

Duration of treatment

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13
Q

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

A

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

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14
Q

How does beta adrenoceptor antagonist work

A

Reduce the somatic symptoms when the ANS system becomes elevated

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15
Q

What is the mechanism of action of benzodiazepines

A

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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16
Q

Where are particularly in the brain do benzodiazepines work at

A

Limbic system: pre-frontal cortex, amygdala

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17
Q

What are the side effects of benzodiazepines

A

Sedation

In acute overdose with alcohol it can cause respiratory depression

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18
Q

Why do we get side effects of benzodiazepines

A

There are GABAa receptors in all parts of the brain

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19
Q

What can occur if benzodiazepine is used long term

A
  • Tissue tolerance so activity of neurones becomes altered

- dependence when the individual stop taking it

20
Q

Up to how many weeks can benzodiazepines be used for

A

4 weeks

21
Q

Name examples of benzodiazepines

A

Diazepam
Nitrazepam
Midazolam

22
Q

What is the mechanism of action of monoaminergic drugs

A

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

23
Q

Name an example of a monoaminergic drug

A

Buspiraone

24
Q

What are the symptoms for major depressive disorder

A 
Misery 
Despair 
Loss of motivation 
Suicidal thoughts 
Appetite changes
25
Q

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

A

Monoamine theory

26
Q

What does the monoamine theory state

A

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

27
Q

What are the treatment methods for major depressive disorders

A

Psychotherapy
Antidepressant drugs
Electroconvulsive therapy

28
Q

What are the 4 classes of antidepressant drugs

A

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

29
Q

Describe the normal processes that occur in the monoaminergic synapses

A

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

30
Q

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

A

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

31
Q

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

A

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

32
Q

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

A

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

33
Q

What are the side effects of monoamine oxidase inhibitors

A

Cheese reaction

Antimuscarinic effects

34
Q

What is the cheese reaction

A

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

35
Q

Why do we get an anti-muscarinic effect

A

Monoamine oxidase inhibitors can bind to alpha 1 receptors

36
Q

What is the mechanism of action of tricyclic anti-depressants

A

Re-uptake inhibition of 5-HT

37
Q

What are the side effects of tri-cyclic antidepressants

A

Anti muscarinic effect

Sedative

38
Q

How do newer drugs work

A
  • mediate uptake of 5HT, NA, dopamine

- melatonin receptor agonism

39
Q

Do anti depressant drugs work

A

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

40
Q

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

A

The monoamine theory is incomplete

41
Q

What is the new theory for depression called

A

Network hypothesis

42
Q

What is the network hypothesis about

A

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

43
Q

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

A

Hippocampus

44
Q

What can happen within the hippocampus

A
  • Decrease in glucocorticoid receptors and decrease in BDNF (maintains healthy neurones)
  • Decrease in neurogenesis and neuroplasticity
45
Q

With anti-depressant drugs how does it affect the hippocampus

A

Monoamine input tot he hippocampus results in increased neurogensis and neuroplasticity

BAB (21 decks)

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