Chapter 13 – Schizophrenia And Other Psychotic Disorders Flashcards

1
Q

Severe impairment in the ability to tell what is real and what is not real

A

Psychosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the origins of schizophrenia’s construct

A

The first detailed description was offered in 1810 by John Haslam. Other early accounts pointed to brain degeneration of hereditary origin.

The German psychiatrist Emil Kraeplin is best known for his careful description of what we now call schizophrenia. Used the term dementia praecox to refer her to a group of conditions that all seems to feature mental deterioration beginning early in life. Describe the patient as someone who become suspicious of those around him, sees poison in his food, is pursued by the police, feels his body is being influenced, or think that he’s going to be shot or that the neighbours are jeering at him. The disorder was characterized by hallucinations, apathy and indifference, withdrawn behavior, and an incapacity for regular work.

A Swiss psychiatrist Eugen Bleuler gave us the diagnostic term we still used today. Schizophrenia is from the Greek roots of sxizo meaning to split or crack, and phren meeting mind, because he believed that the condition was characterized primarily by disorganization of thought processes, a lack of coherence between thought and emotion, and an inward orientation away or split off from reality.

This does not reflect a split personality, instead there is a split within the intellect, between intellect and emotion, and between the intellect and external reality.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain epidemiology of schizophrenia

A

The lifetime risk of developing it is a little under 1%. Those who have a parent with schizophrenia have a statistically higher risk of developing the disorder. Other groups of people who are at high risk are people whose fathers were older, having a parent who works as a drycleaner, people of Afro-Caribbean origin living in United Kingdom.

Most cases begin in late adolescence and early childhood, with 18 to 30 years of age being the peak time. Although sometimes found in children, such cases are rare. Also rare is those beginning in middle age or later.

Tends to begin earlier in men then in women. In men, there is a peek in new cases between ages 20 and 24 and in women peak during the same age., But the peak is less marked then it is for men. After age 35, the number of men developing it falls markedly, where is the number of women does not. Instead there is a second rising new cases that begins around age 40.

Males also tend to have a more severe form of schizophrenia. The male to female sex ratio is 1.4:1. Women have a less severe form, but also have more symptoms of depression, and me either not be diagnosed at all or else be diagnosed with other disorders. One other possibility is that female sex hormones play some protective role, and then when oestrogen levels are low or are falling, psychotic symptoms in women often get worse. Declining levels of oestrogen around menopause might also explain the late onset schizophrenia in women

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

False belief about reality maintained in spite of strong evidence to the contrary

A

Delusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

False perceptions such as things seen or heard that are not real or present

A

Hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

The external manifestation of a disorder in thought form. The affected person fails to make sense, despite seeming to conform to the semantic and syntactic rules governing verbal communication.

A

Disorganized speech and behaviour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Symptoms such as bizarre behaviour or incomprehensible speech in schizophrenia

A

Disorganized symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Symptoms in schizophrenia that are characterized by something being added to normal behaviour or experience. Includes delusions, hallucinations, motor agitation, and marked emotional turmoil

A

Positive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Symptoms in schizophrenia that reflect an absence or deficit in normal functions. For example, blunted affect, social withdrawal, very little speech, the inability to initiate or persist in goal directed activities

A

Negative symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The lack of emotional expression

A

Flat affect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

A term referring to poverty of speech a symptom that often occurs in schizophrenia.

A

Alogia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Refers to a psychological state that is characterized by a general lack of drive or motivation to pursue meaningful goals

A

Avolition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the clinical picture of schizophrenia including the diagnostic signs of both positive and negative symptoms

A

Delusions: an erroneous belief that is fixed and firmly held despite clear contradictory evidence. These people believe things that others who share their social, religious, and cultural backgrounds do not believe, and therefore, involves a disturbance in the content of thought.
Common in schizophrenia, occurring in more than 90% of patients at sometime.
Prominent are beliefs that one’s thoughts, feelings, or actions are being controlled by external agents (made feelings or impulses), that one’s private thoughts are being broadcast indiscriminately to others (thought broadcasting), that thoughts are being inserted into one’s brain by some external agency (thought insertion), or that some external agency has robbed one of one’s thoughts (thought withdrawal).
Other common delusions are delusions of reference, where some neutral environmental event such as a television program or a song on the radio, is believed to have special and personal meeting intended only for the person. Other strange propositions, including delusions of bodily changes or removal of organs are also common.

Hallucinations: a sensory experience that seems real to the person having it, but ochres in the absence of any external perceptual stimulus.
Can occur in any sensory modalities such as auditory, visual, olfactory, tactile, or gustatory, however, auditory hallucinations such as hearing voices are by far the most common.
Often have relevance for the patient at some effective, conceptual, or behaviour level and often incorporate them into their delusions. May even act on their hallucinations and do what the voices tell them to do.
Studies have shown that hallucinating patients show increased activity in Broca’s area – an area of the temporal lobe that is involved in speech production. This suggests that auditory hallucinations ochre when patients miss interpret their own self generated and verbally mediated thoughts as coming from another source.

Disorganized speech and behavior: the external manifestation of a disorder in thought form. The affected person fails to make sense, despite seeming to conform to the semantic and syntactic rules governing verbal communication. The failure is not attributable to low intelligence, poor education, or cultural deprivation.
The words and word combinations sound communicative, but the Lissner is left with little or no understanding of the point the speaker is trying to make. In some cases, completely new, made up words known as neologisms, appear in the patients speech.
Disorganized behaviour shows itself in a variety of ways such as the disruption of goal-directed activity. The impairment occurs in areas of routine daily functioning, such as work, social relations, and self-care to the extent that observers know that the person is not himself or herself anymore. May no longer maintain minimal standards of personal hygiene or me exhibit a profound disregard of personal safety and health. Sometimes appears as silliness or unusual dress.
Catatonia – patient may show a virtual absence of all movement and speech and be in what is called a catatonic stupor. May hold and an usual posture for an extended period of time without any seeming discomfort.

Positive and negative symptoms:
Positive symptoms are those that reflect and exes or distortion in a normal repertoire of behaviour and experience, such as delusions and hallucinations.
Negative symptoms reflect an absence or deficit of behaviours that are normally present. May include flat affect, alogia, avolition.
Although most patients exhibit both positive and negative symptoms during the course of their disorders, a preponderance of negative symptoms in the clinical picture is not a good sign for the patients future outcome. And although sometimes may not look very emotionally expressive, they are nonetheless experiencing plenty of emotion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

When a patient shows a virtual absence of all movement and speech.

A

Catatonia

May also be called a catatonic stupor. At other times the patient may hold an unusual posture for an extended period of time without any seeming discomfort.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Form of psychotic disorder in which the symptoms of schizophrenia co-occur with symptoms of a mood disorder.

The person has psychotic symptoms that meets criteria for schizophrenia but also has marked changes in mood for a substantial amount of time.

A

Schizoaffective disorder

Reliability is quite poor, and clinicians often do not agree.
Prognosis is somewhere between that of patients with schizophrenia and that of patients with mood disorders.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Because mood disorders can be unipolar or bipolar in type, there are also two types of schizoaffective disorder:

A

Bipolar and unipolar subtype

17
Q

Category of schizophrenic-like psychosis less than six months in duration.

Last at least a month but do not last for six months and so do not warrant a diagnosis of schizophrenia.

A

Schizophreniform disorder

Because of the possibility of an early and lasting remission after a first psychotic breakdown, the prognosis is better than that for established forms of schizophrenia

18
Q

Nurturing, giving voice too, and sometimes taking action on beliefs that are considered completely false by others; formally called paranoia.

A subtype of schizophrenia, however unlike individuals with schizophrenia, me otherwise behave quite normally. Their behaviour does not show the gross disorganization and performance deficiencies characteristic of schizophrenia, and general behavioural deterioration is rarely observed in this disorder.

A

Delusional disorder

19
Q

A subtype of delusional disorder which involves great love for a person, usually of higher status

A

Erotomania

20
Q

Brief episodes (lasting a month or less) of otherwise uncomplicated delusional thinking.

A subtype of schizophrenia that involves the sudden onset of psychotic symptoms were grossly disorganized or catatonic behavior. Even though there is often great emotional turmoil, the episode usually lasts only a matter of days, too short to warrant a diagnosis of schizophreniform disorder her. After this, the person returns to his or her former level of functioning and may never have another episode again.

A

Brief psychotic disorder

21
Q

Psychosis in which two or more people develop persistent, interlocking delusional ideas. Also known as folie à deux.

A subtype of schizophrenia in which a delusion develops in someone who has a very close relationship with another person who is delusional. Over time, this second individual comes to believe in the delusions of the other person. In some cases, the contagion of thought may spread even further, and whole families may adopt the same delusional beliefs

A

Shared psychotic disorder

22
Q

Describe the biological causes influences in schizophrenia

A

Genetic factors:
Tends to run in families. There is overwhelming evidence for higher-than-expected rates among biological relatives of index cases, that is, the diagnosed group of people who provide the starting point for inquiry, also called probands. There is a strong association between the closeness of the blood relationship and the risk for developing the disorder.

Twin studies have shown a higher concordance for schizophrenia among identical, or monozygotic twins that among people related in any other way. Concordance rate is 28% in MZ twins and 6% in DZ twins.
Studies of the offspring of the twins without schizophrenia in discordant pairs showed that schizophrenia is just as likely in the offspring of the twins without schizophrenia than in the offspring of the twins with schizophrenia.

To attempt to overcome the shortcomings of monozygotic twin studies, where it can be expected that monozygotic twins are identical and their environments will be more similar than the environment of dizygotic twins, adoption studies have helped to achieve a true separation of hereditary from environmental influences. If concordance is greater among the patients biological been adopted relatives, a hereditary influence is strongly suggested. In one study, 16.6% of 47 adopted children whose mothers had schizophrenia were later diagnosed with schizophrenia. In contrast, none of the 50 control children developed schizophrenia. Other adoption studies have shown similar findings.

Studies that also examined the quality of the adoptive family found that communication deviance, which is a measure of how understandable and easy to follow the speech of a family member is, when combined with genetic risk for schizophrenia, was problematic. Children who were at genetic risk and who lived in families where there was high communication deviance showed high levels of thought disorder. In contrast, the control adoptees who had no genetic risk showed no thought disorder regardless of whether they were raised in a high or low communication-deviance family. Hi-risk children who were raised by adopted families low in communication deviance were healthier at follow up than any of the other three groups. If they are raised in a benign environment, even children who are at a genetic risk for schizophrenia appear to do very well. Other studies comparing dysfunctional adopted families to healthy ones have shown the same results. These findings suggest that our genetic make up may control how sensitive we are to aspects of our environments. These findings indicate a strong interaction between genetic vulnerability and an unfavourable family environment in the causal pathway leading to schizophrenia.

Molecular genetics exploring linkage analysis and candidate genes for schizophrenia are also being conducted. For instance, children who have a genetic syndrome called velocardiofacial syndrome that involves a deletion of genetic material on chromosome 22 are at high risk for developing schizophrenia. The COMT Gene located on chromosomes 22 is involved in dopamine metabolism may be involved in schizophrenia. People with a particular variant of this gene are much more likely to become psychotic as adults if they use cannabis during adolescence.

Researchers are now focussing on less complex and more homogenous phenotypes such a specific symptom clusters, that may potentially be under the control of a smaller number of genes. They are also exploring endophenotypes – discrete, stable, and measurable traits that are thought to be under genetic control. By studying these, researchers hope to get closer to specific genes that might be important in schizophrenia. Researchers are interested in people who score high on certain tests or measures that are thought to reflect a predisposition to schizophrenia.

Prenatal exposures:

Viral infection – when there was a major epidemic of influenza in Finland in 1957, there were elevated rates of schizophrenia in children born to mothers who had been in their second trimester of pregnancy at the time of the influenza epidemic. Risk of schizophrenia seems to be greatest when the mother gets the flu in the 4th to 7th month of gestation. Although the size of the effect is small and influenza clearly does not account for very many cases of schizophrenia, the fact that this association exists is very provocative. One possibility is that the mothers antibodies to the virus cross the placenta and somehow disrupt the neurodevelopment of the fetus. Other maternal infections such as rubella and toxoplasmosis have also been linked.

Rhesus incompatibility: occurs when an Rh-negative mother carries an Rh-positive fetus. Incompatibility is a major cause of blood disease in newborns, and also seems to be associated with increased risk for schizophrenia. One possibility is that the mechanism involves oxygen deprivation, or hypoxia.

Pregnancy and birth complications- much more likely to have been born following a pregnancy or delivery that was complicated in someway.

Early nutritional deficiency – schizophrenia might be caused or triggered by environmental events that interfere with normal brain development. For example, a famine at the end of World War II affecting people in Amsterdam caused the population to be severely malnourished, and fertility levels fell and the birth rate dropped. Children who were born had a twofold increase in the risk of layer developing schizophrenia. Early prenatal nutritional deficiency appears to have been the cause.

Maternal stress – if a mother experiences an extremely stressful event late in her first trimester or early in the second, the risk of schizophrenia is increased. It is thought that the increase in stress hormones that pass to the foetus via the placenta might have negative effects on the developing brain.

Genes and environment in schizophrenia – a synthesis: genetic risk for schizophrenia emerges in one of two ways. The first is from a large number of common jeans of which the individual contribution is likely very small but when interacting together, they set the stage for the development of the illness. The other way is through very rare genetic mutations which could be highly specific to certain people or to certain families.

Neurodevelopmental perspective: schizophrenia is a disorder in which the development of the brain is disturbed very early on. Risk may start with the presence of certain genes that, if turned on, have the potential to disrupt the normal development of the nervous system. This means that the stage for schizophrenia, in the form of abnormal brain development, maybe set very early on in life, but problems may not be apparent until other triggering events take place or until the normal maturation of the brain reveals them. Home videos of the facial and emotional expressions of pre-schizophrenia children as compared to healthy-outcome children showed more motor abnormalities for the pre-schizophrenia children including unusual hand movements and less positive facial emotion and more negative facial emotion. Sometimes apparent by age 2. The most consistent findings from hi-risk research is that children with a genetic risk for schizophrenia are more deviant then control children on research tasks that measure attention, and adolescents are also rated lower in social competence. Early motor abnormalities might also be an especially strong predictor such as a facial tics, blinking, and tongue thrusts.

Structural and functional brain abnormalities:

Neural cognition – schizophrenia patients experience many problems with their narrow cognitive functioning. For example, they perform much worse than healthy controls on a broad range of neuropsychological tests and newly diagnosed patients perform about the same as patients who have been ill for many years. When asked to respond to a stimulus as quickly and appropriately as possible, a measure of reaction time, patients do poorly compared with controls, show deficits on the continuous performance task which requires the subject to attend to a series of letters or numbers and then to detect an intermittently presented target stimulus that appears on the screen along with the letters or numbers. They’re also problems with working memory, they show less pre-frontal brain activity on memory tasks. Between 54 and 86% of people also show I-tracking disfunction and are deficient in their ability to track a moving target such as a pendulum. Only about 6 to 8% of the general population shows problems with eye tracking. 50% of first-degree relatives of schizophrenia patients also show eye tracking problems even though they do not have the disorder themselves. The strongest finding concerns a psychological measure called P 50. When two clicks are heard in close succession, the brain produces a positive electrical response to each click about 50 ms after the click. In normal subjects, the response to the second click is less marked then the response to the first click because the normal brain dampens, or gates, responses to repeated sensory events. If this didn’t happen, habituation to a stimulus would never ocher. Patients with schizophrenia respond almost to strongly to the second click as to the first. This is referred to as poor P 50 suppression and is also more likely to be found in degree relatives of the person with schizophrenia. May be the result of problems with specific receptors in the hippocampus of the medial temporal lobe.
This evidence suggests that patients with schizophrenia have problems with the active, functional allocation of attentional resources and that they are unable to attend well on demand.

Loss of brain volume – compared with controls, patients with schizophrenia have enlarged brain ventricles, with males possibly be more affected than females. However this only appears in a significant minority of patients. Enlarge the brain ventricles are important because they are an indicator of a reduction in the amount of brain tissue and implies that the brain areas that border the ventricles have somehow shrunk or decrease in volume, the ventricular space becoming larger as a result. MRIs show about a 3% reduction in whole brain volume relative to that in controls.
This suggests that in addition to being a neurodevelopmental disorder, it is also a neuroprogressive disorder characterized by a loss of brain tissue over time.

Affected brain areas – there is evidence of reductions in the volume of regions in the frontal and temporal lobe’s which play critical roles in memory, decision-making, and in the processing of auditory information.

White matter problems – involves problems with white matter, nerve fibres that are covered in a myelin sheath where myelin acts as an insulator and increases the speed and efficiency of conduction between nerve cells. White matter is crucially important for the connectivity of the brain. Schizophrenia have reductions in white matter volume as well as structural abnormalities in the white matter itself. At the clinical level, white matter abnormalities have been shown to be correlated with cognitive impairments and also predict later social functioning.

Brain functioning – examples are low frontal lobe activation of patients when they are involved in mentally challenging tasks. This brain area does not seem able to kick into action when patient perform complex tasks. Others show hyper activation, suggesting that they are having to work harder to be successful on the task. In both cases, the brain is not functioning in an optimal and efficient way.

Cytoarchitecture- The organization of cells in the brain. In patients with schizophrenia this structure is thought to be compromised due to the disruption of the migration of neurons in the brain prenatally.

Brain development in adolescence

Synthesis – it has been proposed that genetic risk for schizophrenia may be associated with reduced brain development early in life. This is why it healthy twins who had a co-twin with schizophrenia had smaller brain volumes than healthy controls. It is unlikely that schizophrenia is the result of anyone problem in any one specific region of the brain. If there is a problem at any point in the functional circuits or regions that are linked to other regions by network of interconnections, the circuit will not function properly.

Neurochemistry – The most important neurotransmitter implicated in schizophrenia is dopamine. The dopamine hypothesis dates back to the 1960s and it was derived from three important observations. The first is the pharmacological action of the drug chlorpromazine or Thorazine , Which can block dopamine receptors and had been shown to be helpful for patients with schizophrenia. Second, amphetamines which produce a functional excess of dopamine, had lead in some cases to a form of psychosis that involve paranoia and auditory hallucinations. This provided clinical evidence that a drug that gave rise to a functional excess of dopamine also gave rise to a psychotic state that looked a lot like schizophrenia. Thirdly, clinical studies that actually treated patients by giving them drugs that increase the availability of dopamine in the brain, such as Parkinson’s treated by L-DOPA, can result in significant complications such as psychotic symptoms. This pointed to the role of dopamine in inducing psychosis. Dopamine may have this effect by determining how much salience we give to internal and external stimuli. Dysregulated dopamine transmission may actually make us pay more attention to and give more significance to stimuli that are not especially relevant or important, this is called aberrant salience. Postmortem studies show that there are about 1.4 times more D2 receptors in the brains of deceased patients with schizophrenia, and early PET studies also found evidence for more than a two fold increase in D2 receptors in living patients compared to controls. D2 is a dopamine receptor. These receptors are also elevated in the healthy cotwins of patients with schizophrenia. Current thinking is that people with schizophrenia are supersensitive to dopamine arising because they have greater numbers of a form of D2 receptor that has a very high affinity for dopamine.
Another neurotransmitter implicated in schizophrenia is the excitatory neurotransmitter glutamate. Reasons that researchers believe glutamate might be involved in schizophrenia are because PCP or angel dust blocks glutamate receptors, and also induces symptoms that are very similar to those of schizophrenia. When people with schizophrenia take PCP, it exacerbates their symptoms. Second, editions had to stop using ketamine, which is an anesthetic, because when it is given intravenously to normal subjects, it produces schizophrenia like positive and negative symptoms and when given to patients who schizophrenia is stable and well-controlled, it exacerbates hallucinations, delusions, and thought disorder. Does not have these effects when administered to children whose brains are not mature enough yet maybe. Ketamine also blocks glutamate receptors. Concentrations of glutamate in postmortem brains of patients with schizophrenia have been found to be lower in both the prefrontal cortex and the hippocampus compared with the levels in control subjects. Glutamate levels are also low in the brains of living patience.

23
Q

Describe psychosocial and cultural factors as causal influences in schizophrenia

A

Bad families: series that were popular many decades ago that schizophrenia was caused by destructive parental interactions, have foundered for lack of empirical support. Another idea that has not stood the test of time is the double-bind hypothesis, which occurs when the parent present the child with ideas, feelings, and demands that are mutually incompatible, but no solid support for these ideas has ever been reported.
However, families who show unusual communication patterns known as communication deviants may actually reflect genetic susceptibility to schizophrenia on the part of the relative.

Families and relapse: the kind of living situation patients have after leaving the hospital has been shown to predict how well they would fare clinically. Patient to return home to live with parents or with a spouse were at a higher risk of relapse then patients who left the hospital to live alone or with siblings. Highly emotional family environments might be stressful to patients. The construct of expressed emotion is a measure of the family environment that is based on how a family member speaks about the patient during a private interview with a researcher. Has three main elements: criticism, hostility, and emotional over involvement, which is the most important of these is criticism, which reflects dislike or disapproval of the patient. Expressed emotion has been repeatedly shown to predict relapse in patients with schizophrenia and research shows that when EE levels in families are lowered, patient’s relapse rates also decrease. EE made trigger relapse because patients are highly sensitive to stress, they have pre-existing biological vulnerabilities to increase the probability of relapse.

Urban living: being raised in an urban environment seems to increase a persons risk for developing schizophrenia.

Immigration: recent immigrants have much higher risks of developing schizophrenia then do people who are native to the country of immigration. Urban living and immigration may cause stress or social adversity that may contribute to the disorder. It has been found that immigrants with darker skin have a much higher risk of developing schizophrenia then there was with lighter skin, which raises the possibility that experiences of being discriminated against could leave some immigrants to develop a paranoid and suspicious outlook on the world which could set the stage for development of schizophrenia. May also be related from stress that results from social disadvantage and social defeat that have an effect on dopamine release or dopamine activity in key neural circuits.

Cannabis abuse: people with schizophrenia are twice as likely as people in the general population to smoke cannabis. Compared to those who would never use cannabis, young men who are heavy cannabis users by the time they were 18 or more than six times more likely to have develop schizophrenia 27 years later. Findings suggest that using cannabis during adolescence more than doubles a persons risk of developing schizophrenia at a later stage of life. People who carry a particular form of the COMT gene are at increased risk for developing psychotic symptoms in adulthood if they used cannabis during adolescence.

24
Q

Describe the clinical outcome for people with schizophrenia

A

15 to 25 years after developing schizophrenia, around 30% have a generally favourable outcome and can be thought of as being recovered. Only 16% of patients recover to the extent that they no longer need any treatment, and for a minority of patients, long-term institutionalization is necessary. Around a third of patients show continued signs of illness, usually with prominent negative symptoms.

Schizophrenia reduce his life expectancy by 14.6 years for men. Women with schizoaffective disorder or have a reduced lifespan of 17.5 years. May be related to long-term use of antipsychotic medications, obesity, smoking, poor diet, use of illicit drugs, and lack of physical activity. There is also a risk of suicide.

25
Q

Genetic research strategy in which occurrences of a disorder in an extended family is compared with that of a genetic marker for a physical characteristic or biological process that is known to be located on a particular chromosome.

A

Linkage analysis

26
Q

Genes that are of specific interest to researchers because they are thought to be involved in processes that are known to be a aberrant in that disorder. For example, serotonin transporter genes in depression, or dopamine receptor genes in schizophrenia

A

Candidate genes

27
Q

Discrete, measurable traits that are thought to be linked to specific genes that might be important in schizophrenia or other mental disorders

A

Endophenotypes

28
Q

Neurotransmitter from the catecholamine family that is initially synthesized from tyrosine, an amino acid common in the diet. Produced from L – dopa by the enzyme dopamine decarboxylase

A

Dopamine

29
Q

And excitatory neurotransmitter that is widespread throughout the brain

A

Glutamate

30
Q

Type of negative communication involving excessive criticism and emotional overinvolvement directed at a patient by family members

A

Expressed emotion or EE

31
Q

Describe pharmacological approaches to treating schizophrenia

A

Schizophrenia is usually treated with antipsychotic drugs that usually block dopamine D2 receptors in the brain.

First generation antipsychotics: includes medications like chlorpromazine or Thorazine and haloperidol or Haldol, which were among the first to be used to treat psychotic disorders. They are also sometimes referred to as neuroleptics, and these medications revolutionized the treatment of schizophrenia when they were introduced in the 1950s. First generation antipsychotics are thought to work because they are dopamine antagonists, which means that they block the action of dopamine, primarily by blocking or occupying the D2 dopamine receptors.
Work best for the positive symptoms of schizophrenia.
Common side effects include drowsiness, dry mouth, and weight gain. Some experience what are known as extrapyramidal side effects, EPS, which are involuntary movement abnormalities such as muscle spasms, rigidity, and shaking that resemble Parkinson’s disease and African-Americans are at an increased risk. Usually controlled by taking other medications. Other side effects are tardive dyskinesia which involves marked involuntary movements of the lips and tongue that results from taking neuroleptics for long periods of time. In very rare cases there is a toxic reaction called neuroleptic malignant syndrome characterized by high fever and extreme muscle rigidity and if left untreated can be fatal.

Second-generation antipsychotics: in the 1980s a new class of anti-psychotic medications began to appear. The first was clozapine or Clozaril which was initially reserved for use with treatment-refractory patients, those who were not helped by other medications, it is now used widely today. 
Other examples of second-generation antipsychotics are risperidone (Risperdal), olanzapine (Zyprexa), quetiapine (Seroquel), and ziprasidone (Geodon). More recent additions include aripiprazole or Abilify, and lurasidone or Latuda. 
Called second-generation antipsychotics because they cause fewer extrapyramidal symptoms then the earlier medications. Do not seem to be any more effective than earlier medications.
Side effects include drowsiness, weight gain, diabetes, and in rare cases, clozapine also causes a life-threatening drop in white blood cells known as agranulocytosis. New research is showing that antipsychotic medications may actually contribute to the progressive brain tissue loss seen in schizophrenia.
32
Q

Medications that alleviate or diminish the intensity of psychotic symptoms such as hallucinations or delusions

A

Antipsychotics or neuroleptics

33
Q

A side effect of antipsychotic medications that cause involuntary movement abnormalities such as muscle spasms, rigidity, and shaking that resemble Parkinson’s disease

A

Extrapyramidal side effects

34
Q

A side effect of long-term use of neuroleptics that involves marked involuntary movements of the lips and tongue and sometimes the hands and neck

A

Tardive dyskinesia

35
Q

A toxic reaction to antipsychotics characterized by high fever and extreme muscle rigidity, and if left untreated can be fatal

A

Neuroleptic malignant syndrome

36
Q

Training efforts designed to help patients improve their neurocognitive skills such as memory and vigilance. The hope is that this will also help improve patients overall level of functioning

A

Cognitive remediation

37
Q

Describe psychosocial treatment approaches to schizophrenia

A

Family therapy: the idea is to reduce relapse in schizophrenia by changing those aspects of the patient-relative relationship that were regarded as central to the expressed emotion construct. Generally involves working with patients and their families to educate them about schizophrenia, to help them improve their coping and problem-solving skills, and to enhance communication skills, especially the clarity of family communication.

Case management: case managers are people who help patients find the services they need in order to function in the community. Assertive community treatment programs are a specialized form that involves multidisciplinary teams with limited caseloads to ensure that discharge patients don’t get overlooked and lost in the system.

Social-skills training: aimed at improving the functional outcomes, which are how well patients do in their everyday lives, in patients with schizophrenia, who often have trouble forming relationships, finding and keeping a job, or living independently. Designed to help patients acquire the skills they need to function better on a day-to-day basis, including employment skills, relationship skills, self-care skills, and skills in managing medications for symptoms. Social routines are broken down into smaller more manageable components.

Cognitive remediation: using practice and other compensatory techniques to help patients improve some of their neurocognitive deficits, for example problems with verbal memory, vigilance, and performance on card sorting tasks. The hope is that these improvements will translate into better overall functioning. Does seem to help improve their attention, memory, and executive functioning skills and also show improvements in their social functioning.

Cognitive-behavioral therapy: only recently used as a treatment because patients were formally considered too impaired. Goal is to decrease the intensity of positive symptoms, reduce relapse, and decrease social disability. Working together, therapist and patient explore the subjective nature of the patients delusions and hallucinations, examine evidence for and against their veracity or truthfulness, and subject delusional beliefs to reality testing.

Individual treatment: personal therapy is a non-psychodynamic approach that equips patients with a broad range of coping techniques and skills. The therapy is staged, which means that it comprises different components that are administered at different points in the patient’s recovery.
Psycho education where patients are educated about the illness and its treatment is also helpful and has shown that patients are less likely to relapse or be remitted and also function better overall and are more satisfied with the treatment they receive

38
Q

Explain the difficulties associated with trying to prevent schizophrenia

A

It has been suggested that public health changes that improve obstetric care for women with schizophrenia and first-degree relatives of schizophrenia patients would result in fewer birth complications.
Another suggestion is to prevent cannabis abuse in 15-year-olds.
Current efforts, however, centre around early intervention for people who are at high clinical risk of developing the disorder. The idea is to treat patients in the prodromal stage before full-blown psychotic symptoms develop. May include prescribing antipsychotic medications. Ethical concerns are prescribing medications to someone without symptoms and the risks of doing so. These medications have side effects. Is also difficult to accurately identify these people and current strategies me cast too wide of a net. The majority of people identified as being at high-risk are not on their way to developing a psychotic disorder and routinely prescribing them antipsychotics is therefore not warranted.

39
Q

Disorder characterized by hallucinations, delusions, disorganized speech and behavior, as well as problems in self-care and general functioning.

The Hallmark of this disorder is a significant loss of contact with reality, referred to as psychosis.

A

Schizophrenia