Mental illness Flashcards

1
Q

What are the two major assumptions underlying Freud’s theory of psychoanalysis? According to Freud, when does mental illness occur, and what causes it?

A
  1. Much of mental life is unconscious.
  2. Past experiences, especially in childhood, shape a person’s feelings and responses throughout life.
    -Mental illness occurs when the unconscious and conscious elements of the psyche come into conflict. It is caused by unresolved conflicts related to hidden secrets of the unconscious, often tied to childhood incidents.
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2
Q

What is the key assumption of B. F. Skinner’s theory of personality?

A

The assumption that many behaviors are learned responses to the environment. –> behaviourism

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3
Q

What does behaviorism focus on in contrast to other theories of personality? According to behaviorism, what factors influence the probability of a type of behavior increasing or decreasing? How does behaviorism view mental disorders?

A

-Behaviorism focuses on observable behaviors and their control by the environment, rejecting notions of underlying conflicts and the unconscious.
-The probability of behavior increases when it satisfies a craving or produces a pleasurable sensation (positive reinforcement), and it decreases when the consequences are deemed unpleasant or unsatisfactory (negative reinforcement).
-Behaviorism views mental disorders as maladaptive behaviors that are learned

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4
Q

What does treatment for mental disorders in behaviorism involve?

A

Treatment consists of active attempts to “unlearn” through behavior modification, either by introducing new types of behavioral reinforcement or by providing an opportunity to observe and recognize appropriate behavioral responses.

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5
Q

What is psychotherapy, and how does it relate to treating mental illness? What was one of the shortcomings of psychotherapy, according to Freud?

A

-Psychotherapy is the use of verbal communication to help the patient, and it plays a role in treating mental illness by addressing variations in behavior and early childhood experiences. However, it is not suitable for all mental disorders.
-Freud recognized the shortcomings of psychotherapy and stated that these deficiencies could be resolved by replacing psychological terms with physiological or chemical ones.

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6
Q

What were the initial symptoms of general paresis of the insane? What was the ultimate cause of general paresis of the insane, and how was it traced? how is general paresis treated? What antibiotic was found to be highly effective in treating brain infections caused by Treponema pallidum?

A

-Symptoms included mania, excitement, euphoria, and grandiose delusions
-It was caused by brain infection with Treponema pallidum, the microorganism that causes syphilis. Its cause was traced through research.
-the drug arsphenamine could effectively treat general paresis of the insane
-penicillin

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7
Q

Describe the path from gene discovery to treatment development in the context of psychiatric diseases.

A

Discovering gene mutations in individuals with psychiatric diseases, reproducing these mutations in genetically engineered mice, and studying the differences in brain function can lead to insights into pathophysiology and potential drug targets. If successful, these drugs can be used for treatment.

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8
Q

What are the unique challenges in diagnosing and treating brain diseases?

A
  1. Mental disorders are diagnosed based on signs and symptoms, not underlying causes. 2. The same diagnosis may have many causes, complicating treatment approaches. 3. Not all mental illnesses have a clear genetic basis, and some result from multiple small mutations in various genes. 4. Genetic complexity makes it difficult to develop broadly useful animal models.
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9
Q

How does the complexity of genetic causes affect mental illnesses?

A

Mental illnesses can result from the inheritance of numerous small mutations in many different genes or from gene copy number variants, where duplication or deletion of a gene or gene segment can be the single cause of a diagnosis. This genetic complexity hinders the development of animal models for research.

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10
Q

What is a radical new approach for studying brain diseases in molecular medicine in psychiatry for studying pathophysiology of neurons

A

A radical approach involves studying the pathophysiology of neurons from individual patients. Skin cells can be transformed into induced pluripotent stem cells (iPSCs), which can then be differentiated into neurons for study. However, the complexity of the brain, with its various cell types and rich interconnections, presents a challenge in understanding the pathophysiology of brain diseases.

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11
Q

What is fear, and how is it expressed in the body? Are all fears innate and species-specific? Why is fear considered adaptive, and what is its adaptive value? What happens when fear is expressed inappropriately, and what does this characterize?

A

-Fear is an adaptive response to threatening situations, and it is expressed in the body through the autonomic fight-or-flight response, which is mediated by the sympathetic division of the autonomic nervous system (ANS).
-No, not all fears are innate and species-specific. While many fears are innate (such as a mouse’s fear of a cat), fear can also be learned through experiences.
-Fear is considered adaptive because it helps individuals respond to threats appropriately. Its adaptive value lies in ensuring survival and safety in dangerous situations.
-When fear is expressed inappropriately, it characterizes anxiety disorders, which are the most common of psychiatric disorders.

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12
Q

What are panic attacks, and how do they manifest? How long do panic attacks typically last?

A

-Panic attacks are sudden episodes of intense terror that occur without warning. They manifest with symptoms such as palpitations, sweating, trembling, shortness of breath, chest pain, nausea, dizziness, tingling sensations, and chills or blushing. People often report an overwhelming fear of dying or going crazy during a panic attack.
-Panic attacks are usually short-lived, lasting less than 30 minutes.

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13
Q

Can panic attacks be triggered by specific stimuli?

A

Yes, panic attacks can occur in response to specific stimuli, but they can also happen spontaneously.

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14
Q

What is panic disorder, and how is it characterized? What percentage of the population suffers from panic disorder, and is there a gender difference in its prevalence? When is the onset of panic disorder most common? What are some common comorbidities associated with panic disorder?

A

-Panic disorder is characterized by recurring, seemingly unprovoked panic attacks and persistent worry about having further attacks.
-About 2% of the population suffers from panic disorder, which is twice as common in women as in men.
-The onset of panic disorder is most common after adolescence but before the age of 50 years.
-Half of the individuals with panic disorder will also suffer from major depression, and 25% of them will develop alcoholism or substance-abuse problems. and may lead to agoraphobia

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15
Q

What is agoraphobia, and what are some of its characteristics?

A

Agoraphobia is characterized by severe anxiety in situations where escape might be difficult or embarrassing, leading to avoidance of situations such as being alone outside the home, in crowds, cars, airplanes, or on bridges or elevators. It often occurs as an adverse outcome of panic disorder and affects about 5% of the population, with a higher incidence among women than men.

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16
Q

What is the long-lasting consequence of trauma, and what are its symptoms? What percentage of the adult population in the United States is affected by PTSD?

A

-The long-lasting consequence of trauma can be post-traumatic stress disorder (PTSD), which includes symptoms such as increased anxiety, intrusive memories, dreams or flashbacks of traumatic experiences, irritability, and emotional numbness.
-PTSD affects 3.5% of the adult population in the United States.

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17
Q

What are obsessions in obsessive-compulsive disorder (OCD), and how are they characterized? What are compulsions in OCD, and why are they performed? What percentage of the population is affected by OCD, and when does it usually appear?

A

-Obsessions in OCD are recurrent, intrusive thoughts, images, ideas, or impulses that the individual perceives as inappropriate, grotesque, or forbidden.
-Compulsions in OCD are repetitive behaviors or mental acts performed to reduce the anxiety associated with obsessions. Examples include repeated hand-washing, counting, and checking.
-OCD affects over 2% of the population, with an equal incidence among men and women. It typically appears in young adulthood, and symptoms can fluctuate in response to stress levels.

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18
Q

What is the stress response? How does a healthy person regulate the stress response?

A

-The stress response is the coordinated reaction to threatening stimuli, characterized by avoidance behavior, increased vigilance and arousal, activation of the sympathetic division of the ANS (autonomic nervous system), and the release of cortisol from the adrenal glands.
-A healthy person regulates the stress response through learning, which allows them to appropriately respond to threatening stimuli.

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19
Q

What is the hallmark of anxiety disorders?

A

The hallmark of anxiety disorders is the occurrence of an inappropriate stress response, either when a stressor is not present or when it is not immediately threatening.

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20
Q

What part of the brain is centrally involved in orchestrating the stress response?

A

the hypothalamus is centrally involved in orchestrating appropriate humoral, visceromotor, and somatic motor responses related to the stress response.

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21
Q

What is the role of the hypothalamic-pituitary-adrenal (HPA) axis in the stress response?

A

The HPA axis plays a significant role in regulating the humoral response of the stress response, involving the hypothalamus, pituitary gland, and adrenal glands in releasing cortisol to respond to stress.

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22
Q

What is the hormonal response to stress, specifically involving cortisol (glucocorticoid)?

A

-Cortisol is released from the adrenal cortex in response to an elevation in the blood level of adrenocorticotropic hormone (ACTH), which is released by the anterior pituitary gland in response to corticotropin-releasing hormone (CRH). CRH is released into the blood by parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus
-The hippocampus contains numerous glucocorticoid receptors that respond to the cortisol released from the adrenal gland in response to HPA system activation
-Overexpression of CRH in genetically engineered mice leads to increased anxiety-like behaviors, while genetically eliminating CRH receptors in mice results in reduced anxiety-like behavior compared to normal mice.

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23
Q

What brain structures regulate the HPA axis and the stress response? What is the role of the amygdala in the stress response?

A

-The amygdala and the hippocampus regulate the HPA axis and the stress response.
-The amygdala processes sensory information related to fear and activates the stress response when the central nucleus of the amygdala becomes active.

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24
Q

How does the bed nucleus of the stria terminalis contribute to the stress response?

A

The bed nucleus neurons activate the HPA axis and the stress response downstream from the amygdala.

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25
Q

How does the hippocampus regulate the HPA axis?

A

Hippocampal activation suppresses CRH release, participating in the feedback regulation of the HPA axis by inhibiting CRH release when cortisol levels are high. hippocampus deactivates the HPA axis

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26
Q

What can continuous exposure to cortisol, as seen in chronic stress, lead to?

A

Continuous exposure to cortisol can cause hippocampal neurons to degenerate, potentially setting off a vicious cycle of increased stress response and more hippocampal damage.

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27
Q

What has been observed in the hippocampus of some people with PTSD?

A

Human brain imaging studies have shown a decrease in the volume of the hippocampus in some people suffering from PTSD.

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28
Q

How do the amygdala and hippocampus receive information from the neocortex- related to anxiety?

A

Both the amygdala and hippocampus receive highly processed information from the neocortex, and elevated activity of the prefrontal cortex is a consistent finding in humans with anxiety disorders.

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29
Q

How do the amygdala and hippocampus regulate the HPA axis and the stress response?

A

The amygdala and hippocampus regulate the HPA axis and the stress response in a push-pull fashion, with the amygdala promoting stress responses, and the hippocampus inhibiting excessive stress responses.

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30
Q

What are the available treatments for anxiety disorders?

A

Psychotherapy and anxiolytic medications are available treatments for anxiety disorders.

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31
Q

How does psychotherapy typically treat anxiety disorders?

A

Psychotherapy involves gradually increasing exposure to anxiety-inducing stimuli while reinforcing the idea that these stimuli are not dangerous. It aims to alter brain connections so that stress responses are reduced.

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32
Q

What are anxiolytic medications, and how do they work?

A

Anxiolytic medications are drugs that reduce anxiety. They work by altering chemical synaptic transmission in the brain. Two major classes of these drugs are benzodiazepines and serotonin-selective reuptake inhibitors.

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33
Q

How do benzodiazepines affect GABA receptors?

A

Benzodiazepines bind to specific sites on GABA receptors, making GABA more effective in opening chloride channels and producing inhibition in the brain.

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34
Q

What is the role of GABA in the brain, and why is its proper function important?

A

GABA is a crucial inhibitory neurotransmitter in the brain. Its proper function is essential for maintaining brain stability. Too much inhibition can lead to coma, while too little can result in seizures.

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35
Q

What is the site on GABAA receptors that benzodiazepines bind to, and what effect does this binding have?

A

Benzodiazepines bind to a specific site on GABAA receptors, enhancing the effectiveness of GABA in opening chloride channels and facilitating inhibition in the brain.

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36
Q

What are benzodiazepines, and why are they commonly used?

A

Benzodiazepines, including Valium (diazepam), are highly effective treatments for acute anxiety. They are often used to reduce anxiety symptoms.

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37
Q

How does alcohol relate to anxiety and benzodiazepines?

A

Ethanol, the active ingredient in alcoholic beverages, has anxiolytic effects, which can explain the social use of alcohol to reduce anxiety. However, it’s also a reason for the co-occurrence of anxiety disorders and alcohol abuse.

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38
Q

Why might benzodiazepine treatment be necessary for some individuals with anxiety disorders?

A

The calming actions of benzodiazepines may result from suppressing activity in brain circuits associated with the stress response. In some cases, benzodiazepine treatment might be needed to restore normal function to these circuits.

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39
Q

What did a study using positron emission tomography (PET) imaging reveal about benzodiazepine binding sites in patients with panic disorder?

A

PET imaging showed a reduction in benzodiazepine binding sites in regions of the frontal cortex that exhibit hyperactive responsiveness during anxiety. This suggests that alterations in GABA receptor regulation could be a cause of anxiety disorders.

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40
Q

What are SSRIs, and how are they used in the treatment of mood disorders? How do SSRIs work in the brain to affect serotonin levels? Apart from mood disorders, what other psychiatric condition can SSRIs effectively treat?

A

-SSRIs are serotonin-selective reuptake inhibitors, and they are commonly used to treat mood disorders such as depression.
-SSRIs inhibit the reuptake of serotonin in the brain, which prolongs the actions of serotonin at its receptors.
-SSRIs are highly effective in treating obsessive-compulsive disorder (OCD) and have been found to be beneficial in other psychiatric disorders.

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41
Q

How do SSRIs differ from benzodiazepines in terms of the onset of their anxiolytic (anxiety-reducing) effects?

A

Unlike benzodiazepines, the anxiolytic effects of SSRIs are not immediate and develop slowly over several weeks of regular dosing.

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42
Q

What is one proposed mechanism for the anxiolytic effect of SSRIs related to the hippocampus?

A

One adaptive response to SSRIs is an increase in glucocorticoid receptors in the hippocampus, which may dampen anxiety by enhancing the feedback regulation of CRH neurons in the hypothalamus.

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43
Q

What novel drug targets are being explored for the treatment of anxiety disorders?

A

Researchers are exploring CRH receptors as potential drug targets for the treatment of anxiety disorders, as CRH plays a role in the central circuits involved in the stress response and anxiety.

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44
Q

What is the most common mood disorder?

A

Major depression is the most common mood disorder, affecting 6% of the population every year.

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45
Q

What are the cardinal symptoms of major depression?

A

The cardinal symptoms of major depression are lowered mood and decreased interest or pleasure in all activities.

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46
Q

How long must the cardinal symptoms of major depression be present for a diagnosis? What are some other symptoms of major depression?

A

-For a diagnosis of major depression, the cardinal symptoms must be present every day for a period of at least 2 weeks and not be obviously related to bereavement.
-Other symptoms of major depression include loss of appetite (or increased appetite), insomnia (or hypersomnia), fatigue, feelings of worthlessness and guilt, a diminished ability to concentrate, and recurrent thoughts of death.

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47
Q

How long do episodes of major depression usually last?

A

Episodes of major depression usually don’t last longer than 2 years, although the disease has a chronic, unremitting course in about 17% of patients.

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48
Q

What is dysthymia, and how does it differ from major depression?

A

Dysthymia is another expression of depression, afflicting 2% of the adult population. It is milder than major depression but has a chronic, “smoldering” course, and it seldom disappears spontaneously.

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49
Q

Is there a gender difference in the prevalence of major depression and dysthymia?

A

Yes, major depression and dysthymia are twice as common in women as in men.

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50
Q

What is bipolar disorder?

A

Bipolar disorder is a recurrent mood disorder characterized by episodes of mania or mixed episodes of mania and depression, also known as manic-depressive disorder.

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51
Q

What is mania in the context of bipolar disorder?

A

Mania is a distinct period of abnormally elevated, expansive, or irritable mood experienced during bipolar disorder.

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52
Q

What are some common symptoms of mania?

A

Common symptoms of mania include inflated self-esteem, decreased need for sleep, increased talkativeness, flight of ideas, distractibility, and increased goal-directed activity.

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53
Q

How can mania affect judgment in individuals with bipolar disorder?

A

Mania can lead to impaired judgment, resulting in behaviors like spending sprees, promiscuity, or reckless actions.

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54
Q

How many main types of bipolar disorder are there, and what are they?

A

There are two main types of bipolar disorder: Type I, characterized by full-blown manic episodes, and Type II, characterized by hypomania, a milder form of mania.

55
Q

What is the prevalence of Type I bipolar disorder in the population?

A

Type I bipolar disorder affects approximately 1% of the population, and it occurs equally among men and women.

56
Q

What is hypomania, and in which type of bipolar disorder is it typically seen?

A

Hypomania is a milder form of mania and is typically seen in Type II bipolar disorder. It may lead to increased efficiency, accomplishment, or creativity

57
Q

What is cyclothymia, and when is it used to describe a condition?

A

Cyclothymia is a condition in which hypomania alternates with periods of less severe depression. It is used to describe a condition when hypomania alternates with periods of depression that are not severe enough to be labeled as “major” depression.

58
Q

What is the monoamine hypothesis of mood disorders?

A

The hypothesis that mood disorders, particularly depression, result from a deficit in central diffuse modulatory systems, specifically a decrease in monoamine neurotransmitters like norepinephrine and serotonin

59
Q

How did the drug reserpine contribute to the understanding of depression?

A

Reserpine, a drug used to control high blood pressure, caused severe depression in some cases by depleting central catecholamines and serotonin, suggesting a link between these neurotransmitters and depression.

60
Q

What is the role of monoamine oxidase (MAO) inhibitors in mood elevation?

A

MAO inhibitors, initially introduced to treat tuberculosis, led to mood elevation by inhibiting the enzyme MAO, which is responsible for breaking down catecholamines and serotonin in the brain.

61
Q

How does imipramine function as an antidepressant?

A

Imipramine, an antidepressant, inhibits the reuptake of released serotonin and norepinephrine, enhancing their action in the synaptic cleft and supporting the monoamine hypothesis of mood disorders.

62
Q

What is the key concept of the monoamine hypothesis of mood disorders?

A

The key concept is that mood disorders, especially depression, are associated with a deficiency in monoamine neurotransmitters (norepinephrine and serotonin) in the brain, and many modern antidepressant treatments aim to boost neurotransmission at these synapses.

63
Q

Why is there a discrepancy between the immediate effects of antidepressant drugs on synaptic transmission and the delay in their antidepressant action?

A

Antidepressant drugs have rapid effects on synaptic transmission, but their antidepressant action takes several weeks to develop, suggesting that other factors are involved

64
Q

that issue arises from the fact that drugs raising norepinephrine (NE) levels, like cocaine, are not effective as antidepressants?

A

The ineffectiveness of drugs like cocaine as antidepressants challenges the idea that simply increasing NE levels in the synaptic cleft is sufficient for treating depression

65
Q

What is the new hypothesis regarding the mechanism of action for effective antidepressant drugs?

A

The new hypothesis suggests that effective antidepressant drugs promote long-term adaptive changes in the brain, including alterations in gene expression, to alleviate depression.

66
Q

How does the new hypothesis explain the delay in the antidepressant action of drugs?

A

The delay in antidepressant action is attributed to the time needed for these drugs to induce adaptive changes in the brain, rather than just their immediate effects on neurotransmission.

67
Q

What is one area of the brain that has been implicated in mood disorders and may undergo adaptive changes in response to antidepressant treatment?

A

The HPA (hypothalamic-pituitary-adrenal) axis is one such brain area that has been implicated in mood disorders and may undergo adaptive changes in response to antidepressant treatment.

68
Q

What is the medical term for a predisposition for a certain disease, including mood disorders?

A

Diathesis.

69
Q

What factors contribute to mood disorders, according to the diathesis–stress hypothesis?

A

Mood disorders result from a combination of genetic predisposition (diathesis) and environmental stressors

70
Q

What is the key site where genetic and environmental influences converge to cause mood disorders?

A

The HPA (Hypothalamic-Pituitary-Adrenal) axis is the primary site where genetic and environmental factors intersect to lead to mood disorders.

71
Q

How is the HPA axis activity affected in severely depressed patients?

A

Severely depressed patients exhibit hyperactivity of the HPA axis, characterized by elevated blood cortisol levels and increased concentrations of CRH (Corticotropin-Releasing Hormone) in the cerebrospinal fluid.

72
Q

What are some behavioral effects produced by injecting CRH into the brains of animals, resembling major depression symptoms?

A

Injection of CRH leads to symptoms such as insomnia, decreased appetite, reduced interest in sexual activity, and increased expression of anxiety-like behaviors.

73
Q

In a healthy brain, what normally occurs when cortisol activates hippocampal glucocorticoid receptors?

A

Activation of hippocampal glucocorticoid receptors by cortisol triggers a feedback mechanism that inhibits the HPA axis, regulating stress responses.

74
Q

How does early sensory experience influence glucocorticoid receptor gene expression in rats, and what are the consequences for their adult behavior?

A

Rats receiving ample maternal care as pups express more glucocorticoid receptors in the hippocampus. This leads to reduced anxiety and better stress response regulation in adulthood.

75
Q

Can the positive effects of maternal care be replicated in adult rats through increased tactile stimulation?

A

No, increasing tactile stimulation in adult rats does not have the same positive effect on glucocorticoid receptor expression and anxiety reduction as maternal care during the critical early postnatal period.

76
Q

What are some known risk factors for developing mood and anxiety disorders in humans, as suggested by animal findings?

A

Genetic factors, early childhood abuse or neglect, and other life stresses are risk factors for mood and anxiety disorders in humans.

77
Q

What brain region consistently shows increased resting-state metabolic activity in depressed patients?

A

The anterior cingulate cortex.

78
Q

What does the anterior cingulate cortex connect to in the brain in relation to depression?

A

It connects to other regions of the frontal cortex, hippocampus, amygdala, hypothalamus, and brain stem.

79
Q

How is the anterior cingulate cortex activity affected by autobiographical recall of a sad event?

A

Activity in the anterior cingulate cortex increases during autobiographical recall of a sad event.

80
Q

What role does the anterior cingulate cortex play in relation to depression symptoms?

A

It is considered an important link between an internally generated emotional state and the HPA (hypothalamic-pituitary-adrenal) axis.

81
Q

What is one of the most effective treatments for depression and mania that involves inducing seizure activity in the temporal lobes?

A

Electroconvulsive Therapy (ECT)

82
Q

How is ECT administered in terms of the placement of electrodes?

A

Electrical currents are passed between two electrodes placed on the scalp.

83
Q

What is significant about the speed of relief provided by ECT, especially in some cases?

A

ECT can provide relief quickly, sometimes after the first session, which is crucial in cases where suicide risk is high.

84
Q

What is one of the adverse effects associated with ECT, particularly regarding memory? How does ECT affect the storage of new information? Although the exact mechanism remains unknown, what is one of the temporal lobe structures affected by ECT?

A

Memory loss, including memories of events that occurred before treatment, which can extend back up to 6 months. ECT can temporarily impair the storage of new information. The hippocampus, which plays a role in regulating CRH and the HPA axis.

85
Q

What is the primary goal of psychotherapy when treating depressed patients? Has the neurobiological basis of psychotherapy for depression been firmly established?

A

The main goal of psychotherapy is to help depressed patients overcome negative views of themselves and their future. No, the neurobiological basis of psychotherapy for depression has not been firmly established.

86
Q

What are the four major classes of antidepressant drugs mentioned in the paragraph?

A

-Tricyclic compounds (e.g., imipramine)
-SSRIs (Selective Serotonin Reuptake Inhibitors, e.g., fluoxetine)
-NE- and 5-HT-selective reuptake inhibitors (e.g., venlafaxine)
-MAO inhibitors (Monoamine Oxidase Inhibitors, e.g., phenelzine)

87
Q

What is the common mechanism of action among all antidepressant drugs mentioned in the paragraph?

A

They all elevate the levels of monoamine neurotransmitters in the brain.

88
Q

How long does it typically take for the therapeutic actions of antidepressant drugs to develop?

A

The therapeutic actions of these drugs take weeks to develop.

89
Q

What adaptive responses in the brain are associated with the clinical effectiveness of antidepressant treatment,

A

-Dampening of the hyperactivity of the HPA (Hypothalamic-Pituitary-Adrenal) system.
-Changes in glucocorticoid receptor expression in the hippocampus.
-Increased neurogenesis (proliferation of new neurons) in the hippocampus.

90
Q

What is the clinical challenge associated with the delayed onset of antidepressant effects?

A

patients can feel discouraged when their expectations for improvement are not met, and this can temporarily exacerbate the depression.

91
Q

What is the potential significance of ketamine in the context of rapidly acting antidepressants?

A

A single intravenous dose of ketamine can rapidly alleviate symptoms of depression for several days, suggesting the possibility of rapidly acting antidepressant medications. However, ketamine itself is not a practical long-term treatment for depression due to its side effects.

92
Q

Why is ketamine not a practical long-term treatment for depression, despite its rapid antidepressant effects?

A

Ketamine can cause severe psychotic episodes that require hospitalization. Its antidepressant effects are observed only after the drug is eliminated from the body and psychotic symptoms diminish.

93
Q

what unexpected effect did lithium have on guinea pigs, contrary to Cade’s initial prediction? What is the primary effect of lithium treatment on patients with bipolar disorder? How does lithium affect neurons?

A

-Contrary to his prediction, lithium had a calming effect on guinea pigs.
-Lithium is highly effective in stabilizing the mood of patients with bipolar disorder, preventing the recurrence of mania and episodes of depression.
-In solution, lithium is a monovalent cation that passes through neuronal sodium channels. Inside the neuron, it prevents the normal turnover of phosphatidyl inositol (PIP2), interferes with adenylyl cyclase and glycogen synthase kinase.

94
Q

Why is the exact reason for lithium’s effectiveness in treating bipolar disorder still unknown?

A

The exact reason for lithium’s effectiveness remains unknown, but it appears to involve adaptive changes in the central nervous system (CNS) with long-term use.

95
Q

What is the last resort treatment for severe depression when other methods fail?

A

Implanting an electrode deep in the brain.

96
Q

What brain region is targeted for electrical stimulation to treat depression?

A

The anterior cingulate cortex, specifically Brodmann’s area 25.

97
Q

How did patients describe the effect of electrical stimulation during the operation? What is the current status of using deep brain stimulation for depression?

A

-They described a “sudden calmness” or “lightness” and the “disappearance of the void.”
-It is considered preliminary, and additional studies are underway to confirm initial results.

98
Q

What is schizophrenia characterized by? When does schizophrenia typically become apparent?

A

Schizophrenia is characterized by a loss of contact with reality and a disruption of thought, perception, mood, and movement. Schizophrenia typically becomes apparent during adolescence or early adulthood and usually persists for life.

99
Q

What are the two categories of symptoms in schizophrenia, and what do they reflect?

A

The symptoms of schizophrenia fall into two categories: positive and negative. Positive symptoms reflect the presence of abnormal thoughts and behaviors, while negative symptoms reflect the absence of responses that are normally present.

100
Q

Can you name some examples of positive symptoms in schizophrenia?

A

Positive symptoms in schizophrenia include delusions, hallucinations, disorganized speech, and grossly disorganized or catatonic behavior.

101
Q

What are some examples of negative symptoms in schizophrenia?

A

Negative symptoms in schizophrenia include reduced expression of emotion, poverty of speech, difficulty in initiating goal-directed behavior, and memory impairment.

102
Q

What are some common delusions in individuals with schizophrenia?

A

Individuals affected by schizophrenia often have delusions organized around a theme, such as believing that powerful adversaries are out to get them.

103
Q

What are some examples of bizarre voluntary movements seen in schizophrenia?

A

Schizophrenia can be accompanied by peculiarities of voluntary movement, including immobility and stupor (catatonia), bizarre posturing and grimacing, and senseless, parrot-like repetition of words or phrases.

104
Q

Why is one identical twin sometimes spared from schizophrenia when the other has it?

A

The difference is likely due to environmental factors that interact with genetic vulnerability. Faulty genes can make individuals susceptible to environmental influences that trigger schizophrenia.

105
Q

When do the biological changes causing schizophrenia likely begin?

A

The biological changes associated with schizophrenia may begin early in development, possibly prenatally.

106
Q

What environmental factors have been linked to an increased risk of developing schizophrenia?

A

Viral infections during fetal and infant development, poor maternal nutrition, and environmental stresses throughout life have been implicated as contributing factors to schizophrenia.

107
Q

How does marijuana use relate to the risk of developing schizophrenia?

A

Several studies suggest that marijuana use can increase the risk of developing schizophrenia, especially in genetically vulnerable adolescents.

108
Q

What physical brain changes are associated with schizophrenia?

A

-Schizophrenia is associated with physical brain changes, including enlarged lateral ventricles, which reflect the shrinkage of brain tissue around them. The brains of individuals with schizophrenia tend to have a larger ventricle-to-brain-size ratio compared to those without the disorder.
-Structural changes in the brains of individuals with schizophrenia include defects in myelin sheaths surrounding axons, reduced cortical thickness, abnormal neuronal lamination, and changes in synapses and neurotransmitter systems.

109
Q

Are defects in myelin sheaths common in schizophrenia?

A

Yes, individuals with schizophrenia often exhibit defects in the myelin sheaths surrounding axons in their cerebral cortex, although it’s unclear whether this is a cause or consequence of the disease

110
Q

what are some common findings in the cortical structure of individuals with schizophrenia?

A

Common findings in the cortical structure of individuals with schizophrenia include reduced cortical thickness and abnormal neuronal lamination.

111
Q

Which neurotransmitters have been implicated in schizophrenia?

A

Alterations in chemical synaptic transmission mediated by dopamine and glutamate have been implicated in schizophrenia

112
Q

What neurotransmitter is associated with the mesocorticolimbic dopamine system and schizophrenia?

A

Dopamine.

113
Q

How does amphetamine use relate to schizophrenia?

A

Amphetamine use, which increases dopamine release, can lead to psychotic episodes with positive symptoms similar to schizophrenia, suggesting a link between excessive dopamine and psychosis

114
Q

How do neuroleptic drugs like chlorpromazine work in treating schizophrenia?

A

Neuroleptic drugs, including chlorpromazine, block dopamine receptors (specifically the D2 receptor), helping to control the positive symptoms of schizophrenia.

115
Q

What is the dopamine hypothesis of schizophrenia?

A

According to the dopamine hypothesis, psychotic episodes in schizophrenia are triggered by the activation of dopamine receptors.

116
Q

Why is there a strong correlation between the effectiveness of neuroleptic drugs and their ability to bind to D2 receptors?

A

Neuroleptic drugs are effective in treating schizophrenia because they block D2 receptors, which are implicated in the disorder’s positive symptoms.

117
Q

What is the term used for newly developed antipsychotic drugs, like clozapine, that have little effect on D2 receptors?

A

Atypical neuroleptics.

118
Q

What distinguishes atypical neuroleptics from traditional neuroleptic drugs?

A

Atypical neuroleptics, like clozapine, act in a novel way and have different mechanisms of action compared to traditional neuroleptic drugs.

119
Q

Why are atypical neuroleptics called “atypical”?

A

They are called “atypical” because they do not primarily affect dopamine D2 receptors, unlike traditional neuroleptic drugs

120
Q

What neurotransmitter system is suspected to be involved in the mechanism of action of atypical neuroleptics?

A

Serotonin (5-HT) receptors are suspected to interact with atypical neuroleptics, contributing to their neuroleptic effects.

121
Q

What adverse effects are associated with PCP and ketamine use?

A

PCP and ketamine intoxication can lead to hallucinations and paranoia, which can last for days.

122
Q

What symptoms do PCP and ketamine intoxication share with schizophrenia?

A

PCP and ketamine can induce both positive and negative symptoms of schizophrenia.

123
Q

How do PCP and ketamine affect neurotransmission?

A

PCP and ketamine inhibit NMDA receptors, which use glutamate as a neurotransmitter.

124
Q

What is the glutamate hypothesis of schizophrenia?

A

The glutamate hypothesis suggests that schizophrenia results from diminished activation of NMDA receptors in the brain.

125
Q

How do researchers create animal models of schizophrenia?

A

Animal models of schizophrenia can be established by using low doses of PCP or genetically engineering mice with fewer NMDA receptors, which leads to schizophrenia-like behaviors.

126
Q

How do PCP and ketamine differ from other NMDA receptor inhibitors in terms of their mechanism of action?

A

PCP and ketamine block NMDA receptors by entering the channel and clogging the pore, but only when the receptors are active and the channels are open.

127
Q

What population of neurons is thought to be involved in the psychomimetic effects of PCP and ketamine?

A

The effects of PCP and ketamine may be mediated by cortical GABAergic neurons in the cerebral cortex with high ongoing activity and tonic NMDA receptor activation.

128
Q

What deficiency has been observed in the cortex of individuals with schizophrenia?

A

Postmortem examination of the brains of individuals with schizophrenia has revealed a deficiency in cortical interneurons

129
Q

What is the conventional drug therapy for schizophrenia?

A

Conventional neuroleptics, such as chlorpromazine and haloperidol, act at D2 receptors

130
Q

How do conventional neuroleptics affect the symptoms of schizophrenia?

A

They reduce the positive symptoms of schizophrenia in the majority of patients.

131
Q

What are some side effects of conventional neuroleptics?

A

Side effects can include symptoms resembling Parkinson’s disease, such as rigidity, tremor, and difficulty initiating movements, as well as tardive dyskinesia characterized by involuntary movements of the lips and jaw.

132
Q

How are atypical neuroleptics different from conventional ones?

A

Atypical neuroleptics, such as clozapine and risperidone, do not act directly on the dopamine receptors in the striatum and are more effective against the negative symptoms of schizophrenia.

133
Q

What is the focus of current drug research for schizophrenia treatment?

A

Current drug research is focused on the NMDA receptor, with the hope that increasing NMDA receptor responsiveness, in combination with decreasing D2 receptor activation, will further alleviate the symptoms of schizophrenia