Mental Illness Flashcards

1
Q

Explain and discuss the nature of anxiety disorders including

A

• Fear = leads to anxiety. It is a response to threat. Anxiety disorder arises when fear is experienced when it is not needed. • Panic Disorder o All of a sudden, onset of fear o Symptoms: beating of heart very fast, out of breath, pain in the chest ~30 mins o 2% suffer, mainly women (twice as much compared to men) o Can have depression concurrently • Agoraphobia o Sense of being trapped, inability to escape (fear when in elevator, outside of home etc) o 5%, women 2x more common in women than men o Negative consequence of panic disorder • Obsessive Compulsive D/O: o Repeated fear of impurity. View strongly on avoiding contamination, violence or sex. o 2% o Symptoms variable depending on stress experienced

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2
Q

Explain and discuss the nature of Affective disorders

A

Mood Disorders

  • Major Depression
    • Most common mood disorder
    • 5%
    • Symptoms: abnormal appetite, poor sleeping patterns (insomnia/ hypersomnia), tiredness, worthlessness or guilt, bad concentration
  • Depression= Dysthmia
    • 2%
    • More mild than major depression

Bipolar Disorder: recurrence of mania: feel very good about oneself (high horse/ high self esteem), alert (little sleep), talks a lot, very distracted, lots of motivation, might have poor spending habits

  • Type I: 1%, can happen with or in concurrence with depression
  • Type II: 0.6% have hypomania (more mild mania, not that crazy)
    • Productive creativity + accomplishment
    • Can be linked with major depression
    • Hypomania= you will have bouts of depression too which isn’t major (cyclothymia= swing in mood)
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3
Q

Understand and explain the biological basis of both anxiety disorders

A

Anxiety Biological Basis:

  • Humoral response to stress is caused by the Hypothalamic Pituitary Adrenal Axis (Pathway for how stress is responded to in your body)
    • Stress stimuli- > CRH (Corticotropin hormone @ hypothalamus) will tell the pituitary gland to ACTH (Adrenocorticotropic hormone) -> High BP -> tell the adrenal cortex to release CORTISOL= Stress response leads to activation of sympathetic ANS + avoidance behaviour and increased vigilance
  • The stress response pathway (HPA) is regulated
  • Regulation of CRH by
    • On = Amygdala (has bunch of nucleus called stria terminalis)
    • Off= hippocampus (glucocorticoid receptors), if high cortisol due to constant stress, hippocampus neurons weaken -> more stress response -> more damage to the hippocampus

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4
Q

Affective disorders & their biological Basis

A
  • Monoamine theory (monoamine= umbrella term for feel good nt - serotonin and norepinephrine)
    • Reduction in feel good nt
    • Depression = decrease in systems that regulate monoamine levels (so lowered feel good nt)
      • MAO enzyme= breaksdown feel good enzymes
      • Reserpine: lowers monoamines, increases BP and can cause depression
    • Imipramine (Antidepressant) stopes uptake of feel good nt, to make mood feel better
  • Diathesis (genetic predisposition based on dna or environment to disease) Stress Hypothesis:
    • Some people have diathesis for depression and as they age and experience more environmental pressure, the predisposition reaches threshold -> condition
    • Genetic component= HPA axis affected
    • Glucocorticoid receptors @ hippocampus which react to cortisol are messed up and can’t respond in appropriate manner
    • Sensory experience when younger can affect how much glucocorticoid gene is produced
    • Abuse, neglect, genes also affect mood + anxiety disorders
  • Probably both (genetic/environment-> changes monoamine thesis)
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5
Q

Anxiety Disorder Tx

A
  • Psychotherapy: keep exposing you to the stimuli in safe environment (exposing myself to rejection constantly)
  • Anxiolytic (meds that relieve anxiety) Tx:
    • BDZ (diazepam- valium)= Activate GABA channels
    • Serotonin Selective reuptake inhibitors (fluoxetine) lengthens the use of serotonin in receptors by stopping them from being taken back again.
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6
Q

Affective D/O Tx

A
  • Electroconvulsive Therapy (ETC): electrical stimulation of temporal lobes (@ hippocampus) after patients are numbed up.
    • Good relief, but can lead to memory loss (~ 6 months worth) and ability to store memories.
  • Psychotherapy: help change views, good if depression not severe (mild- moderate)
  • Antidepressants to increase feel good nt:
    • Stop uptake both of feel good nt: Impiprimine tricyclic cpmpounds
    • Stimulate serotonin termincal: SSRI (fluxetine)
    • Inhibit reuptake of noreadrenaline: reboxetine
    • Stop breakdown of feel good nt: MAO inhibitor (phenelzine)
  • Lithium= Stabilise mood/ stop repeated bout of mania/ depression. Flattens your behaviour
  • Cognitive behavioural Tx:
    • Brain neuroplasticity= help identify negative patterns of thinking with practical self help tools
  • New research
    • Antidepressants emphasise HPA system ~ increases amount glucocorticoid receptors @ hippocampus leading to more serotonin
    • If using SSRI for long periods -> neuronal damage in hippocampus
    • ETC should be last option if other tx fails for severe depression. Works to lower activity of where stress is always active. Immediate relief if suffering from depression
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7
Q

1) Discuss some associations of two anxiety disorders: Panic disorder and agoraphobia.

A

Panic disorder - incidence in 2% of the population - recurrent attacks of intense terror that appear without warning - last a few minutes but terrifying experience - sudden activation of the sympathetic nervous system, leading to sweating, wildly beating heart and trembling - victim continuously dreads another attack (though occasional) Agoraphobia - affects 5% of the population - many people with panic disorders also experience agoraphobia, a fear of public places or situations in which help might not be available - being in a situation where escape might be difficult

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8
Q

2) What do brain imaging studies reveal about brain structures involved in anxiety disorders?

A

Imaging studies of people with anxiety disorders show increased activity in the cingulated cortex and parahippocampal gyrus and enhanced response to anxietyprovoking stimuli in the amygdala and prefrontal cortex. This could be due to excessive neurotransmission in the anterior cingulated cortex, prefrontal cortex, amygdala and parahippocampal regio

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9
Q

Y is a 36 year old man, educated and has 2 college degrees. Y is generally calm outwardly but had been a prodemocracy activist in communist Poland, a dangerous position, so his family had to eventually escape from Poland. He began to experience severe spells that were initially diagnosed as some sort of heart condition. He would breathe heavily, sweat, experience heart palpitations, chest pain. During the attacks he was unable to communicate coherently and would be taken away by ambulance to emergency. Cardiac problems were overruled. Which mental illness is Y most likely to be suffering from and what could be the cause?

A

Generalised Anxiety disorder- described as persistently high levels of anxiety often accompanied by maladaptive behaviour to reduce anxiety; thought to be caused by chronic stress. Y may have had continuing worries (and stress) about repercussions of his political activities and this eventually found expression in generalized anxiety attacks.

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10
Q

4) Discuss the transmitters involved in the neural mechanism of anxiety.

A

Many transmitters are involved but evidence in strong for GABA (gamma aminobutyric acid) and 5-HT (5-hydroxytryptamine).

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11
Q

5) List some anxiolytic drugs used to treat anxiety disorders.

A

Anxiolytic drugs: Benzodiazepines (diazepam)- produce their effects by enhancing GABA-mediated inhibition in many brain areas involved in anxiety, including the raphe nucleus. Refer to figure below. Tricyclic antidepressants (amitriptyline) have anxiolytic activity- mechanism unknown. Β-adrenoceptor antagonists have a limited use in treatment of situational anxiety (e.g. in musicians) where palpitations and tremor are the main symptoms. Serotonin reuptake inhibitor (SSRI) (Prozac) – (mainly used for treatment of mood disorders- discussed below) is also used to treat anxiety disorders. SSRI act to prolong the actions of released serotonin at their receptors by inhibiting reuptake. One adaptive response to SSRIs is an increase in the glucocorticoid receptors in the hippocampus. SSRIs may act to dampen anxiety by feedback regulation of cortico-tropin-releasing hormone (CRH) neurons in the hypothalamus.

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12
Q

Summary of drugs used for anxiety

A

Acute anxiety

  • Benzodiazepines (e.g. diazepam) - rapid onset - sedative - dependence - use 2-4 weeks only
  • Drugs acting on 5-HT receptors - 5-HT1A agonists - buspirone

Chronic anxiety

  • Antidepressants - Venlafaxine (generalised anxiety disorder) - selective serotonin uptake inhibitors - fluvoxamine (obsessive compulsive disorder) - citlopram (panic disorder) - MAO inhibitors - moclobemide (social phobia)

Reduction of autonomic symptoms - -

  • Bblockers - propranolol
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13
Q

Affective disorders (also known as mood disorders). Describe characteristic of each disorder:

A
  • Depression and mania are affective disorders or disorders of mood. When the mood fluctuates between depression and mania it is known as bipolar disorder.
  • Some characteristics of depression are: - sadness - apathy - low self esteem - withdrawal from others - anorexia - early morning waking Some characteristics of mania are: - euphoria - delusions of grandeur - mental overactivity
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14
Q

List some of the main symptoms of depression.

A

prolonged feelings of worthlessness and guilt - disruption of normal eating habits - sleep disturbance - general slowing of behaviour

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15
Q

2) Describe mania and its relationship to bipolar disorder.

A

Mania: the opposite extreme form of depression, characterized by excessive euphoria: - grandiose plans - hyperactive behaviour

Bipolar disorder: periods of mania often change. Sometimes abruptly, into states of depression and back again to mania.

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16
Q

3) A significant factor in understanding depression is reactivity to stress. Explain.

A

When we are stressed, the hypothalamic-pituitary adrenal system (HPA) is stimulated to produce stress hormones- steroids such as cortisol (hydrocortisone). Monoamines modulate secretion of hormones by the HPA axis. Abnormality in HPA-axis modulation is oversecretion of cortisol form adrenal glands. When you are stressed the hypothalamus secretes corticotropin-releasing hormone, which stimulates the pituitary to produce adrenocortocotropic hormone (ACTH). ACTH stimulates adrenal medulla to produce cortisol. The hypothalamic neurons that start this are regulated by norepinephrine neurons in the locus coerulus. If cortisol release is too high, the norepinephrine neurons fail to regulate the cortisol. High levels of cortisol are harmful to neurons and chronic increases lead to destruction of neurons in the hippocampus.

17
Q

4) (i) Discuss Prozac, a major drug for treating depression and its advantage and disadvantage.

A

Flouxetine (Prozac) is a serotonin reuptake inhibitor (SSRI) that effectively increases serotonin in the cortex. This drug does not have the autonomic side effects of tricyclics (e.g. imipramine, amitriptyline: antidepressants). But may cause nausea and gastrointestinal problems

18
Q

treatments for depression besides prozac:

A

Most of the drugs in the treatment of depression inhibit the reuptake of norepinephrine and/or serotonin (5-HT). Less commonly used drugs are inhibitors of monoamine oxidase (MAOIs) Because both uptake inhibitors and MAOIs increase the amount of norepinephrine and/or 5-HT in the synaptic cleft and so enhance the action of these transmitters, it has been argued that depression results form an ‘underactivity’ of these monoaminergic systems. This is the monoamine theory of depression.

  • Amine uptake inhibitors
  • Tricyclic antidepressants (e.g. imipramin, amitriptyline) have proven antidepressant actions. Some have sedative actions (amitryptyline) and are more useful for agitated and anxious patients.
  • Monoamine uptake inhibitors
  • The MOAIs (e.g. phenelzine) are irreversible non-selective inhibitors of MAO. Efficacy is similar to the tricyclics but unwanted side effects (e.g postural hypotension) and potentially serious interaction with foods containing tyramine have limited their use. Moclobemide is a newer drug that selectively inhibits MAOA phenelzine.
19
Q

Describe Lithium’s mechanism and it’s uses

A

Inside the neuron Lithium prevents the normal turnover of phosphatidyl inositol (PIP2), a precursor for 2nd messenger molecules generated in reponse to activation of some Gcoupled neurotransmitter receptors. Lithium also interferes with adenylyl cyclase, essential for generating 2nd messenger cAMP, and glycogen synthase kinase (important for cellular metabolism). Why Lithium is a effective treatment of bipolar disorder is still not completely known.