Psychiatric Disorders, Diseases, and Disorders 1

Psychiatric Disorders, Diseases, and

Drugs











By: Tammy Poe
PSY 240
Axia University of Phoenix
June 12, 2010







Psychiatric Disorders, Diseases, and Disorders 2

Schizophrenia is a disease associated with madness. It affects 1% of the population of all
races and cultural groups, beginning in adolescence or early adulthood. Some common
symptoms of schizophrenia are: Bizarre delusions: delusions of being controlled, delusions of
persecution, and delusions of grandeur. Inappropriate affect: not reacting with appropriate levels
of emotionality to positive or negative events (Keltner, Kring, & Bonanno, 1999, Kring, 1999).
Hallucinations: Imaginary voices telling the person what to do or commenting negatively on
the persons behavior. Incoherent thought: illogical thinking, peculiar associations among ideas,
or belief in supernatural forces. Odd behavior: going long periods of time with no movement
(catatonia), a lack of personal hygiene, talking in rhymes, avoiding social interaction, and
echolalia. Schizophrenia is connected to genetics, and occurs in families with a history of
schizophrenia. Different events in a persons life can contribute to the schizophrenia, and has
multiple causes.
Areas on several different chromosomes have been involved in the vulnerability to
schizophrenia (Cowan, Kopnisky, & Hyman, 2002; Kennedy et al., 2003; Torrey & Yoken,
2000), along with a variety of early experiential factors which have been included in the
development of schizophrenia. Early infections, autoimmune reactions, toxins, traumatic injury,
and stress are early experiences thought to alter the normal course of neurodevelopment, leading
to schizophrenia in a person with genetic susceptibility ( Conklin & Iacono, 2002; Lewis &
Levitt, 2002). The discovery of the first antischizophrenic drugs was an accident during the early
1950s, which was called chlorpromazine developed by a French drug company as an
antihistamine.
Psychiatric Disorders, Diseases, and Disorders 3

Chlorpromazine which counteracts swelling had a calming effect on difficult-to-handle
psychotic patients, which was proven false. The research actually set in action the discovery that
chlorpromazine alleviates schizophrenic symptoms enough to allow institutionalized patients to
be discharged. Reserpines active ingredient snakeroot was used to treat mental illness, but it
produces a dangerous decline in blood pressure at the doses needed for an individuals treatment.
Chlorpromazine and reserpine both have two major aspects; the first is the antischizophrenic
effect of both drugs only takes affect after being medicated for 2 or 3 weeks. The second is the
onset of the antischizophrenic effect of the medication is usually associated with motor effects
which are like the symptoms of Parkinsons disease: tremors at rest, muscular rigidity, and
general decrease in voluntary movement.
There were two definite facts of the dopamine theory of schizophrenia during the 1960s; first
was the antischizophrenic drug reserpine was known to reduce the brain of dopamine and other
monoamines by breaking down the synaptic vesicles stored, which protected them from debase
enzymes. Secondly, amphetamine and cocaine can trigger schizophrenic episodes in normal
people were known to increase the extracellular levels of dopamine and other monoamines in the
brain. In 1963, Carlsson and Lindqvist researched the effects of chlorpromazine on extracellular
levels of dopamine and its metabolites (the molecule created when one is broken down) Carlsson
and Lindqvist thought that chlorpromazine and reserpine both antagonize transmission at
dopamine synapses but in different ways. Reserpine depleted the brain of dopamine and
chlorpromazine by binding to dopamine receptors. They both argued that chlorpromazine binds
to dopamine receptors without activating them.
Carlsson and Lindqvist after reexamining the dopamine theory of schizophrenia found that
high dopamine levels led to the main factor in schizophrenia, caused by high levels of activity at
Psychiatric Disorders, Diseases, and Disorders 4

dopamine receptors. The drug haloperidol a potent antischizophrenic drug had a low affinity for
dopamine receptors. Dopamine binds to more than one receptor; in fact five have been noticed.
Chlorpromazine and other antischizophrenic drugs are in the same chemical class (the
phenothiazines) all bind to D, and D2 receptors, and other antischizophrenic drugs in its
chemical class (the butyrophenones) all bind to D2 receptors but not to D1 receptors. The
binding of butyrophenones to D2 receptors had also led to another examination in the dopamine
theory of schizophrenia.
Schizophrenia was said to be caused by hyperactivity specifically at D2 receptors, and not at
dopamine receptors (Snyder, 1978). Snyder and other colleagues had confirmed that the degree
to which neuroleptics (antischizophrenic drugs) bind to D2 receptors is related to the
effectiveness in suppressing schizophrenic symptoms. Schizophrenia is also associated with
brain damage, and abnormally small cerebral cortex and abnormally large cerebral ventricles
(Frith & Dolan, 1998). Even though brain damage is known to be widespread, it is not evenly
distributed. The cortical damage is seen more in the prefrontal, cingulate, and medial temporal
areas of the cortex.
There are two patterns of brain damage observed in schizophrenics that are a problem for the
dopamine theory that provides no rational for the diffuse pattern of brain damage that is
observed. The question behind brain pathology of schizophrenics is whether or not it is
developmental. An important finding suggests that schizophrenia is a result of disordered early
brain development. Brain pathology tends to be extensive when the disorder is first diagnosed
and little evidence of damage (Wong, Buckle, & Van Tol, 2000). Therefore, the dopamine theory
has no explanation for this effect.
Psychiatric Disorders, Diseases, and Disorders 5

Depression is something all of us have experienced at least once in our lives. Its a normal
reaction death, financial devastation, or serious health issues. There are those people who get
depressed are out of proportion, these people fall deeply in despair and lose the ability to
experience pleasure, and for no reason at all. Their depression could become so extreme that it is
almost impossible for them to meet essential requirements such as keeping a job, maintain social
contacts, or maintain their own personal hygiene, and these people suffer from clinical
depression. Depression is not the only affective disorder (psychotic disorder of emotion).
Mania is another major type of depression, and mania is the opposite of depression. Mania is
characterized by overconfidence, impulsivity, distractibility, and high energy. During mild
mania, people become talkative, energetic, impulsive, positive, and very confident. At this time,
they can be effective at tasks, and fun to be around. However, when mania becomes extreme, it
is a serious problem. The florid manic often wake to unbridled enthusiasm, with an outflow of
incessant chatter that continues nonstop from topic to topic. In other words, no task is too
difficult, and no goal is unattainable.
This type of confidence and grandiodity along with high energy, distractibility, and a leap-
before-you-look impulsiveness can result in continuous disasters or unpaid bills, and broken
relationships. Bipolar affective disorders are those who suffer depression and experience periods
of mania. Those who do not experience periods of mania suffer from unipolar affective disorder.
Depression triggered by a negative experience is called reactive depression, and becoming
depressed for no cause or reason is called endogenous depression. Genetic differences among
people in the development of affective disorders and twins suffer from the same disorder
unipolar or bipolar.
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Many have researched the casual role of experience in affective disorders has put their
attention towards the role of stress in the etiology of depression. Research has proven that
stressful experiences can trigger attacks of depression in people who are already stressed
(Brown, 1993). The discovery of antidepressant drugs was marketed in 1957, and there were four
major classes of drugs used in treatments of affective disorders. Monoamine oxidase inhibitors;
Iproniazid was the first antidepressant drug that was developed for treating tuberculosis.
Iproniazid increases the levels of monoamines (norepinephrine and serotonin) by inhibiting the
activity of monoamine oxidase (MAO).
There are several side effects the MAO inhibitors have: the most dangerous is the cheese
effect because cheese, wine, and pickles contain an amine called tryamine, which elevates blood
pressure. Usually these foods rarely have an effect on blood pressure because the tryamine is
broken down in the liver by MAO. Although, people who take MAO inhibitors and eat or drink
tryamine-rich foods do have the risk of strokes caused by rising blood pressure. Tricyclic
antidepressants; got its name because of their antidepressant action, and their chemical structures
include three rings of atoms. Imipramine, the first trycyclic antidepressant was first thought of as
an antischizophrenic drug. Trycyclic antidepressants block the reuptake of both serotonin and
norepinephrine, increasing their levels in the brain, and a safe alternative to MAO inhibitors.
Lithium; a metallic ion, was used to block mania, and it was made by accident by John Cade.
He mixed urine of a manic patient with lithium to form a soluble salt. He injected guinea pigs to
see if it would induce mania, and the urine solution seem to have a calming effect. Cade realized
it wasnt the uric acid that caused the calming effect, it was. His theory was considered foolish
because the lithium salt caused nausea. Cades view were that the guinea pigs appear calm, but
they were actually sick.
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Lithium is a mood stabilizer, a drug that blocks the movement between depression and mania,
instead of treating depression. The selective monoamine-reuptake inhibitors, introduced in the
late 1980s as the selective serotonin-reuptake inhibitors (SSRIs) used for treating depression.
SSRI inhibitors bring agonistic effects on serotonergic transmission by blocking the reuptake of
serotonin from synapses. Prozac (fluoxetine), the first SSRI developed for depression is not
effective in treating depression, but it was taken in by the psychiatric community and prescribed
to millions of people today. Prozac and other SSRIs are accountable to two things: the first, there
were reports that had few side effects, and secondly, they can help a wide range of psychological
disorders as well as depression.
SSRIs were considered effective against disorders, and they were considered the function of
psychotherapy, and had had a remarkable impact on psychiatry and clinical psychology. The
monoamine theory is associated with underactivity at the serotonergic and noradrenergic
synapses. This theory is supported by the results of autopsy studies (Nemeroff, 1998). However,
the monoamine theory does not stand strong because it is based on the fact that monoamine
agonists are used to treat depression, although 25% of patients agree with these treatments.
According to the diathesis-stress model of depression, the second theory of depression, some
people inherit a diathesis which is incapable of initiating the disorder by itself.
When a person is faced with stress early in life, their symptoms become permanently
sensitized, overreacting to mild stressors for the rest of their lives. This theory is based on the
finding that depressed people will release more stress hormones (Brown, Rush, & McEwen,
1999; Holsboer, 2000; Young et al., 2000). There are five classes of anxiety disorders.
Generalized anxiety disorder; characterized by stress responses and extreme feelings of anxiety
that occur in the absence of any abvious precipitating stimulus (Pinel, 2007). Phobic anxiety
Psychiatric Disorders, Diseases, and Disorders 8

disorders are triggered by exposure to particular objects such as birds, spiders, snakes, or
situations such as being around huge crowds of people, or being afraid of the dark, or afraid of
storms. Panic disorders are rapid-onset attacks of extreme fear and severe symptoms of stress
such as choking, heart palpitations, or shortness of breath.
Obsessive-compulsive disorders are recurring, and uncontrollable obsessions, impulses such
as repeatedly flipping a light switch, or washing hands over and over. Posttraumatic stress
disorders is the persistent pattern of psychological distress followed by the exposure to extreme
stress (MCNally, 2003; McNally, Bryant, & Ehlers, 2003; Newport & Nemeroff, 2000).
Agoraphobia is the fear of public places and open spaces. The Pharmacological treatment of
anxiety has two drugs that are effective against anxiety disorders. Benzodiazepines (valium or
Librium) are prescribed for treating anxiety disorders, and they are prescribed as a sleep-
inducing drug. The side-effects are: sedation, disruption of motor skills, tremors, nausea, and
withdrawal reaction which causes a person to experience a relapse of anxiety.
Tourette syndrome is a disorder of tics; involuntary, repetitive, stereotyped movements or
vocalizations) (Jankovic, 2001; Leckman et al., 2001). During childhood Tourette syndrome
affects a childs motor skills such as blinking or head movements. Overtime the symptoms
become more severe such as making lewd gestures, hitting, touching things, squatting, hopping,
and twirling. More common verbal tics includes inarticulate sounds such as barking or grunting,
uttering obscenities (coprolalia), repeating words after another person (echolalia), or repeating
ones own words over and over (palilalia). Some patients also show signs of attention-deficit/
hyperactivity disorder, obsessive-compulsive disorder, or both (Sheppard et al., 1999).
Psychiatric Disorders, Diseases, and Disorders 9

Tourette syndrome tics can be suppressed for short periods of time with concentration and
effort of an individual. Although in doing so, a discomfort or tension builds up in the body which
then releases frequent and intense tics. It is difficult to study the neural mechanisms of Tourette
syndrome because of three components; the first, there are on animals with Tourette syndrome,
controlled experiments are difficult, studies that involve direct manipulation of the brain are
impossible. Secondly, no certain gene has been found in the development of the disorder, and no
important sources of clues have been found. Thirdly, due to the involuntary movements and
brain imaging is very difficult. The treatment of Tourette syndrome begins with family, friends,
and teachers getting educated about the nature of the syndrome, then focusing on the ancillary
emotional problems such as anxiety or depression.
Once these steps have been taken, treating the symptoms is put in place by being treated with
neuroleptics (Lang, 2001; Riddle & Carlson, 2001). The treatment of Tourette syndrome is
consistent with the hypothesis that the disorder is related to an abnormality of the basal ganglia-
thalamus-cortex feedback circuit. The theory is that Tourette syndrome is a neurodevelopmental
disorder that results from excessive dopaminergic innervations of the striatum and the associated
limbic cortex (Jankovic, 2001).





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References
Pinel. , 2007. Retrieved 12, June 2010.