week 20 - psychopathology part 2 Flashcards

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1
Q

Describe the diagnostic criteria for mood disorders.

mde

A

the criteria for an MDE require five or more of the following nine symptoms, including one or both of the first two symptoms, for most of the day, nearly every day:
depressed mood
diminished interest or pleasure in almost all activities
significant weight loss or gain or an increase or decrease in appetite
insomnia or hypersomnia
psychomotor agitation or retardation
fatigue or loss of energy
feeling worthless or excessive or inappropriate guilt
diminished ability to concentrate or indecisiveness
recurrent thoughts of death, suicidal ideation, or a suicide attempt
These symptoms cannot be caused by physiological effects of a substance or a general medical condition (e.g., hypothyroidism).
Everyone experiences brief periods of sadness, irritability, or euphoria. This is different than having a mood disorder, such as MDD or BD, which are characterised by a constellation of symptoms that causes people significant distress or impairs their everyday functioning.

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2
Q

Describe the diagnostic criteria for mood disorders.

manic hypomanic

A

The core criterion for a manic or hypomanic episode is a distinct period of abnormally and persistently euphoric, expansive, or irritable mood and persistently increased goal-directed activity or energy.

The mood disturbance must be present for one week or longer in mania (unless hospitalisation is required) or four days or longer in hypomania.

Concurrently, at least three of the following symptoms must be present in the context of euphoric mood (or at least four in the context of irritable mood):

Manic episodes are distinguished from hypomanic episodes by their duration and associated impairment; whereas manic episodes must last one week and are defined by a significant impairment in functioning, hypomanic episodes are shorter and not necessarily accompanied by impairment in functioning.

inflated self-esteem or grandiosity
increased goal-directed activity or psychomotor agitation
reduced need for sleep
racing thoughts or flight of ideas
distractibility
increased talkativeness
excessive involvement in risky behaviours

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3
Q

Describe the diagnostic criteria for mood disorders.

unipolar

A

​​MDD is defined by one or more MDEs, but no history of manic or hypomanic episodes.

Criteria for PDD are feeling depressed most of the day for more days than not, for at least two years. At least two of the following symptoms are also required to meet criteria for PDD:
poor appetite or overeating
insomnia or hypersomnia
low energy or fatigue
low self-esteem
poor concentration or difficulty making decisions
feelings of hopelessness

Like MDD, these symptoms need to cause significant distress or impairment and cannot be due to the effects of a substance or a general medical condition. To meet criteria for PDD, a person cannot be without symptoms for more than two months at a time.

PDD has overlapping symptoms with MDD. If someone meets criteria for an MDE during a PDD episode, the person will receive diagnoses of PDD and MDD.

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4
Q

Describe the diagnostic criteria for mood disorders.

bipolar

A

Three major types of BDs are described by the DSM-5 (APA, 2013). Bipolar I Disorder (BD I), which was previously known as manic-depression, is characterised by a single (or recurrent) manic episode.

A depressive episode is not necessary but commonly present for the diagnosis of BD I. Bipolar II Disorder is characterised by single (or recurrent) hypomanic episodes and depressive episodes. Another type of BD is cyclothymic disorder, characterised by numerous and alternating periods of hypomania and depression, lasting at least two years.

To qualify for cyclothymic disorder, the periods of depression cannot meet full diagnostic criteria for an MDE; the person must experience symptoms at least half the time with no more than two consecutive symptom-free months; and the symptoms must cause significant distress or impairment.

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5
Q

Understand age, gender, and ethnic differences in prevalence rates of mood disorders. And risk factors too.
\MDD

A

MDD
⅕ Americans will meet the criteria for MDD at one point in their lifetime
The average age for someone to develop a disorder is mid 20s
The age of onset is decreasing rapidly
59% of people experience anxiety disorder
32% experience an impulse control disorder
24% produce a substance use disorder
Women experience 2x-3x higher rates of MDD
This gender difference emerges during puberty
MDD is inversely correlated with SES
Higher rates of MDD are associated with lower SES
European Americans are more likely to have MDD than African and Hispanic Americans
MDD is taken less seriously in Black people
Their MDD is often more severe and taken less seriously
Depression is not limited to western countries - it is found in all cultures

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6
Q

Understand age, gender, and ethnic differences in prevalence rates of mood disorders. And risk factors too.

A

Bipolar disorders
Lifetime rate expected to be at 4.4%
Commonly occurs with other disorders
65% of people with BD have another psychiatric disorder
This is associated with poorer illness course
Prevalence of BD varies by country
US highest at 4.4%, India lowest with 0.7%
BD in Black people is similar to white people
Hispanic Americans and African Americans with a mood disorder were more likely to remain persistently ill than European Americans
Compared with European Americans with BD, African Americans tend to be underdiagnosed for BD
Hispanic Americans with BD have been shown to receive fewer psychiatric medication prescriptions and specialty treatment visits. Misdiagnosis of BD can result in the underutilization of treatment or the utilisation of inappropriate treatment, and thus profoundly impact the course of illness.
As with MDD, adolescence is known to be a significant risk period for BD; mood symptoms start by adolescence in roughly half of BD cases
Longitudinal studies show that those diagnosed with BD prior to adulthood experience a more pernicious course of illness relative to those with adult onset, including more episode recurrence, higher rates of suicidality, and profound social, occupational, and economic repercussions.

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7
Q

Know effective treatments of mood disorders.

Depressive disorders

A
Depressive disorders
There are many treatment options available for people with MDD. First, a number of antidepressant medications are available, all of which target one or more of the neurotransmitters implicated in depression.The earliest antidepressant medications were monoamine oxidase inhibitors (MAOIs). MAOIs inhibit monoamine oxidase, an enzyme involved in deactivating dopamine, norepinephrine, and serotonin. Although effective in treating depression, MAOIs can have serious side effects. Patients taking MAOIs may develop dangerously high blood pressure if they take certain drugs (e.g., antihistamines) or eat foods containing tyramine, an amino acid commonly found in foods such as aged cheeses, wine, and soy sauce. 
Tricyclics, the second-oldest class of antidepressant medications, block the reabsorption of norepinephrine, serotonin, or dopamine at synapses, resulting in their increased availability. Tricyclics are most effective for treating vegetative and somatic symptoms of depression. Like MAOIs, they have serious side effects, the most concerning of which is being cardiotoxic.
Selective serotonin reuptake inhibitors (SSRIs; e.g., Fluoxetine) and serotonin and norepinephrine reuptake inhibitors (SNRIs; e.g., Duloxetine) are the most recently introduced antidepressant medications. SSRIs, the most commonly prescribed antidepressant medication, block the reabsorption of serotonin, whereas SNRIs block the reabsorption of serotonin and norepinephrine. SSRIs and SNRIs have fewer serious side effects than do MAOIs and tricyclics. In particular, they are less cardiotoxic, less lethal in overdose, and produce fewer cognitive impairments. They are not, however, without their own side effects, which include but are not limited to difficulty having orgasms, gastrointestinal issues, and insomnia
Other biological treatments for people with depression include electroconvulsive therapy (ECT), transcranial magnetic stimulation (TMS), and deep brain stimulation. ECT involves inducing a seizure after a patient takes muscle relaxants and is under general anaesthesia. ECT is a viable treatment for patients with severe depression or who show resistance to antidepressants although the mechanisms through which it works remain unknown. A common side effect is confusion and memory loss, usually short-term. Repetitive TMS is a noninvasive technique administered while a patient is awake. Brief pulsating magnetic fields are delivered to the cortex, inducing electrical activity. TMS has fewer side effects than ECT, and while outcome studies are mixed, there is evidence that TMS is a promising treatment for patients with MDD who have shown resistance to other treatments. Most recently, deep brain stimulation is being examined as a treatment option for patients who did not respond to more traditional treatments like those already described. Deep brain stimulation involves implanting an electrode in the brain. The electrode is connected to an implanted neurostimulator, which electrically stimulates that particular brain region. Although there is some evidence of its effectiveness, additional research is needed.
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8
Q

Know effective treatments of mood disorders.

bd

A

Patients with BD are typically treated with pharmacotherapy. Antidepressants such as SSRIs and SNRIs are the primary choice of treatment for depression, whereas for BD, lithium is the first line treatment choice. This is because SSRIs and SNRIs have the potential to induce mania or hypomania in patients with BD.

Lithium acts on several neurotransmitter systems in the brain through complex mechanisms, including reduction of excitatory (dopamine and glutamate) neurotransmission, and increasing of inhibitory (GABA) neurotransmission. Lithium has strong efficacy for the treatment of BD.

However, a number of side effects can make lithium treatment difficult for patients to tolerate. Side effects include impaired cognitive function, as well as physical symptoms such as nausea, tremor, weight gain, and fatigue.

Some of these side effects can improve with continued use; however, medication noncompliance remains an ongoing concern in the treatment of patients with BD. Anticonvulsant medications (e.g., carbamazepine, valproate) are also commonly used to treat patients with BD, either alone or in conjunction with lithium.
There are several adjunctive treatment options for people with BD. Interpersonal and social rhythm therapy is a psychosocial intervention focused on addressing the mechanism of action posited in social zeitgeber theory to predispose patients who have BD to relapse, namely sleep disruption.

A growing body of literature provides support for the central role of sleep dysregulation in BD. Consistent with this literature, IPSRT aims to increase rhythmicity of patients’ lives and encourage vigilance in maintaining a stable rhythm.

The therapist and patient work to develop and maintain a healthy balance of activity and stimulation such that the patient does not become overly active (e.g., by taking on too many projects) or inactive (e.g., by avoiding social contact). The efficacy of IPSRT has been demonstrated in that patients who received this treatment show reduced risk of episode recurrence and are more likely to remain well

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9
Q

anhedonia

A

Loss of interest or pleasure in activities one previously found enjoyable or rewarding.

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10
Q

attributional style

A

The tendency by which a person infers the cause or meaning of behaviours or events.

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11
Q

early adversity

A

Early adversity - Single or multiple acute or chronic stressful events, which may be biological or psychological in nature (e.g., poverty, abuse, childhood illness or injury), occurring during childhood and resulting in a biological and/or psychological stress response.

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12
Q

grandiosity

A

Inflated self-esteem or an exaggerated sense of self-importance and self-worth (e.g., believing one has special powers or superior abilities).

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13
Q

hypersomnia

A

Excessive daytime sleepiness, including difficulty staying awake or napping, or prolonged sleep episodes.

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14
Q

psychomotor agitation

A

Increased motor activity associated with restlessness, including physical actions (e.g., fidgeting, pacing, feet tapping, handwringing).

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15
Q

psychomotor retardation

A

A slowing of physical activities in which routine activities (e.g., eating, brushing teeth) are performed in an unusually slow manner.

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16
Q

social zeitgeber

A

Zeitgeber is German for “time giver.” Social zeitgebers are environmental cues, such as meal times and interactions with other people, that entrain biological rhythms and thus sleep-wake cycle regularity.

17
Q

Describe the signs and symptoms of schizophrenia and related psychotic disorders.

A

Someone acting oddly. They may have been dressed in an unusual way, perhaps dishevelled or wearing an unusual collection of clothes, makeup, or jewellery that did not seem to fit any particular group or subculture.

They may have been talking to themselves or yelling at someone you could not see. If you tried to speak to them, they may have been difficult to follow or understand, or they may have acted paranoid or started telling a bizarre story about the people who were plotting against them.

Psychotic disorders involve many different types of symptoms, including delusions, hallucinations, disorganised speech and behaviour, abnormal motor behaviour (including catatonia), and negative symptoms such anhedonia/amotivation and blunted affect/reduced speech.

Delusions are false beliefs that are often fixed, hard to change even when the person is presented with conflicting information, and are often culturally influenced in their content

Hallucinations - perceptual experiences that occur even when there is no stimulus in the outside world generating the experiences. They can be auditory, visual, olfactory (smell), gustatory (taste), or somatic (touch).

The most common hallucinations in psychosis (at least in adults) are auditory, and can involve one or more voices talking about the person, commenting on the person’s behaviour, or giving them orders. The content of the hallucinations is frequently negative (“you are a loser,” “that drawing is stupid,” “you should go kill yourself”) and can be the voice of someone the person knows or a complete stranger. Sometimes the voices sound as if they are coming from outside the person’s head. Other times the voices seem to be coming from inside the person’s head, but are not experienced the same as the person’s inner thoughts or inner speech.
Talking to someone with schizophrenia is sometimes difficult, as their speech may be difficult to follow, either because their answers do not clearly flow from your questions, or because one sentence does not logically follow from another. This is referred to as disorganised speech, and it can be present even when the person is writing. Disorganised behaviour can include odd dress, odd makeup (e.g., lipstick outlining a mouth for 1 inch), or unusual rituals (e.g., repetitive hand gestures).

Abnormal motor behaviour can include catatonia, which refers to a variety of behaviours that seem to reflect a reduction in responsiveness to the external environment. This can include holding unusual postures for long periods of time, failing to respond to verbal or motor prompts from another person, or excessive and seemingly purposeless motor activity.

18
Q

Describe the most well-replicated cognitive and neurobiological changes associated with schizophrenia.

A

This emphasis on cognition in schizophrenia is in part due to the growing body of research suggesting that cognitive problems in schizophrenia are a major source of disability and loss of functional capacity. The cognitive deficits that are present in schizophrenia are widespread and can include problems with episodic memory, working memory, and other tasks that require one to “control” or regulate one’s behaviour.

Individuals with schizophrenia also have difficulty with what is referred to as “processing speed” and are frequently slower than healthy individuals on almost all tasks. Importantly, these cognitive deficits are present prior to the onset of the illness and are also present, albeit in a milder form, in the first-degree relatives of people with schizophrenia.

This suggests that cognitive impairments in schizophrenia reflect part of the risk for the development of psychosis, rather than being an outcome of developing psychosis. Further, people with schizophrenia who have more severe cognitive problems also tend to have more severe negative symptoms and more disorganised speech and behaviour.

In addition, people with more cognitive problems have worse function in everyday life
Some people with schizophrenia also show deficits in what is referred to as social cognition, though it is not clear whether such problems are separate from the cognitive problems described above or the result of them. This includes problems with the recognition of emotional expressions on the faces of other individuals. Individuals with schizophrenia who have more problems with social cognition also tend to have more negative and disorganised symptoms, as well as worse community function.

The advent of neuroimaging techniques such as structural and functional magnetic resonance imaging and positron emission tomography opened up the ability to try to understand the brain mechanisms of the symptoms of schizophrenia as well as the cognitive impairments found in psychosis. For example, a number of studies have suggested that delusions in psychosis may be associated with problems in “salience” detection mechanisms supported by the ventral striatum. These are regions of the brain that normally increase their activity when something important (aka “salient”) happens in the environment. If these brain regions misfire, it may lead individuals with psychosis to mistakenly attribute importance to irrelevant or unconnected events. Further, there is good evidence that problems in working memory and cognitive control in schizophrenia are related to problems in the function of a region of the brain called the dorsolateral prefrontal cortex (DLPFC). These problems include changes in how the DLPFC works when people are doing working-memory or cognitive-control tasks, and problems with how this brain region is connected to other brain regions important for working memory and cognitive control, including the posterior parietal cortex, the anterior cingulate and temporal cortex. In terms of understanding episodic memory problems in schizophrenia, many researchers have focused on medial temporal lobe deficits, with a specific focus on the hippocampus. This is because there is much data from humans and animals showing that the hippocampus is important for the creation of new memories. However, it has become increasingly clear that problems with the DLPFC also make important contributions to episodic memory deficits in schizophrenia, probably because this part of the brain is important for controlling our use of memory.
Magnitude resonance neuroimaging studies have also identified changes in cellular architecture, white matter connectivity, and grey matter volume in a variety of regions that include the prefrontal and temporal cortices. People with schizophrenia also show reduced overall brain volume, and reductions in brain volume as people get older may be larger in those with schizophrenia than in healthy people. Taking antipsychotic medications or taking drugs such as marijuana, alcohol, and tobacco may cause some of these structural changes. However, these structural changes are not completely explained by medications or substance use alone. Further, both functional and structural brain changes are seen, again to a milder degree, in the first-degree relatives of people with schizophrenia. This again suggests that neural changes associated with schizophrenia are related to a genetic risk for this illness.

19
Q

Describe the potential risk factors for the development of schizophrenia.

A

There is no schizophrenia gene. The genetic risk for schizophrenia reflects the summation of many different genes that each contribute something to the likelihood of developing psychosis

It is challenging to identify specific genes associated with risk for psychosis.

Many studies suggest that at least some of the genes potentially associated with schizophrenia are also associated with other mental health conditions, including bipolar disorder, depression, and autism

problems during pregnancy such as increased stress, infection, malnutrition, and/or diabetes have been associated with increased risk of schizophrenia.

Complications that occur at the time of birth and which cause hypoxia (lack of oxygen) are also associated with an increased risk for developing schizophrenia

Children born to older fathers are also at a somewhat increased risk of developing schizophrenia. Further, using cannabis increases risk for developing psychosis, especially if you have other risk factors

The likelihood of developing schizophrenia is also higher for kids who grow up in urban settings and for some minority ethnic groups.

20
Q

Describe the controversies associated with “clinical high risk” approaches to identifying individuals at risk for the development of schizophrenia.

A

An important research area on risk for psychosis has been work with individuals who may be at “clinical high risk.” These are individuals who are showing attenuated (milder) symptoms of psychosis that have developed recently and who are experiencing some distress or disability associated with these symptoms.

When people with these types of symptoms are followed over time, about 35% of them develop a psychotic disorder, most frequently schizophrenia. In order to identify these individuals, a new category of diagnosis, called “Attenuated Psychotic Syndrome,” was added to Section III (the section for disorders in need of further study) of the DSM-5 (see Table 1 for symptoms).

However, adding this diagnostic category to the DSM-5 created a good deal of controversy. Many scientists and clinicians have been worried that including “risk” states in the DSM-5 would create mental disorders where none exist, that these individuals are often already seeking treatment for other problems, and that it is not clear that we have good treatments to stop these individuals from developing psychosis.

However, the counter arguments have been that there is evidence that individuals with high-risk symptoms develop psychosis at a much higher rate than individuals with other types of psychiatric symptoms, and that the inclusion of Attenuated Psychotic Syndrome in Section III will spur important research that might have clinical benefits. Further, there is some evidence that non-invasive treatments such as omega-3 fatty acids and intensive family intervention may help reduce the development of full-blown psychosis in people who have high-risk symptoms.

21
Q

Describe the treatments that work for some of the symptoms of schizophrenia.

A

The first line of treatment for schizophrenia and other psychotic disorders is the use of antipsychotic medications.
There are two primary types of antipsychotic medications, referred to as “typical” and “atypical.”

The fact that “typical” antipsychotics helped some symptoms of schizophrenia was discovered serendipitously more than 60 years ago
These are drugs that all share a common feature of being a strong block of the D2 type dopamine receptor. Although these drugs can help reduce hallucinations, delusions, and disorganised speech, they do little to improve cognitive deficits or negative symptoms and can be associated with distressing motor side effects.

The newer generation of antipsychotics is referred to as “atypical” antipsychotics. These drugs have more mixed mechanisms of action in terms of the receptor types that they influence, though most of them also influence D2 receptors.
These newer antipsychotics are not necessarily more helpful for schizophrenia but have fewer motor side effects. However, many of the atypical antipsychotics are associated with side effects referred to as the “metabolic syndrome,” which includes weight gain and increased risk for cardiovascular illness, Type-2 diabetes, and mortality.

22
Q

alogia

A

A reduction in the amount of speech and/or increased pausing before the initiation of speech.

23
Q

anhedonia/amotivation

A

A reduction in the drive or ability to take the steps or engage in actions necessary to obtain the potentially positive outcome.

24
Q

catatonia

A

Behaviours that seem to reflect a reduction in responsiveness to the external environment. This can include holding unusual postures for long periods of time, failing to respond to verbal or motor prompts from another person, or excessive and seemingly purposeless motor activity.

25
Q

delusions

A

False beliefs that are often fixed, hard to change even in the presence of conflicting information, and often culturally influenced in their content.

26
Q

diagnostic criteria

A

The specific criteria used to determine whether an individual has a specific type of psychiatric disorder. Commonly used diagnostic criteria are included in the Diagnostic and Statistical Manual of Mental Disorder, 5th Edition (DSM-5) and the Internal Classification of Disorders, Version 9 (ICD-9).

27
Q

disorganized behaviour

A

Behaviour or dress that is outside the norm for almost all subcultures. This would include odd dress, odd makeup (e.g., lipstick outlining a mouth for 1 inch), or unusual rituals (e.g., repetitive hand gestures).

28
Q

disorganized speech

A

Speech that is difficult to follow, either because answers do not clearly follow questions or because one sentence does not logically follow from another.

29
Q

dopamine

A

A neurotransmitter in the brain that is thought to play an important role in regulating the function of other neurotransmitters.

30
Q

flat affect

A

A reduction in the display of emotions through facial expressions, gestures, and speech intonation.

31
Q

functional capacity

A

The ability to engage in self-care (cook, clean, bathe), work, attend school, and/or engage in social relationships.

32
Q

hallucinations

A

Perceptual experiences that occur even when there is no stimulus in the outside world generating the experiences. They can be auditory, visual, olfactory (smell), gustatory (taste), or somatic (touch).

33
Q

magnetic resonance imaging

A

A set of techniques that uses strong magnets to measure either the structure of the brain (e.g., grey matter and white matter) or how the brain functions when a person performs cognitive tasks (e.g., working memory or episodic memory) or other types of tasks.

34
Q

neurodevelopmental

A

Processes that influence how the brain develops either in utero or as the child is growing up.

35
Q

positron emission tomography

A

A technique that uses radio-labelled ligands to measure the distribution of different neurotransmitter receptors in the brain or to measure how much of a certain type of neurotransmitter is released when a person is given a specific type of drug or does a particularly cognitive task.

36
Q

processing speed

A

The speed with which an individual can perceive auditory or visual information and respond to it.

37
Q

psychopathology

A

Illnesses or disorders that involve psychological or psychiatric symptoms.

38
Q

working memory

A

The ability to maintain information over a short period of time, such as 30 seconds or less.