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NRNP 6635 Study Guide(Final-Exam), NRNP 6635 - Psychopathology and Diagnostic Reasoning, Walden University. £15.13
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NRNP 6635 Study Guide(Final-Exam), NRNP 6635 - Psychopathology and Diagnostic Reasoning, Walden University.

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NRNP 6635 Study Guide(Final-Exam), NRNP 6635 - Psychopathology and Diagnostic Reasoning, Walden University.

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  • January 9, 2024
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  • 2023/2024
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lOMoARcPSD|20734855




Final Exam study Guide
NRNP: 6635 Psychopathology and Diagnostic
Reasoning

, lOMoARcPSD|20734855




Chapter 7 Schizophrenia Spectrum and Other Psychotic Disorders
Schizophrenia-symptoms are variable and include changes in perception, emotion, cognition,
thinking, & behavior. The effects of these manifestations vary by person and can change over
time, but the illness is always severe and is usually long-lasting. Onset is typically before age
25. Affects people of all socioeconomic backgrounds. Patients and families tend to suffer poor
care due to lack of knowledge of schizophrenia. It is one of the most common of the serious
mental disorders but its essential nature remains unclear. Sometimes it is referred to as a
syndrome, the schizophrenias or the schizophrenia spectrum. There is no lab testing for
schizophrenia.
History-Symptoms of schizophrenia have been documented throughout history. Early Greek
physicians noted patients with delusions of grandeur, paranoia, and deterioration in cognitive
function and personality. It wasn’t until the 19th Century that schizophrenia became a
medical condition worthy of being studied.
Benedict Morel (1809-1873)-coined the term demence precoce- to identify deterioration
in patients who illness began in adolescence
Emil Kraepelin (1856-1939)-Identified dementia precox (from demece precoce)-a condition
that identified an early onset change in cognition identified with hallucinations and
delusions. He also distinguished manic and depressive episodes as well as paranoia
Eugene Bleuler coined the term schizophrenia (replacing dementia precox). He chose the term
for the schisms in the thoughts, behaviors, and emotions of the patients. He chose phrenia
because he did not believe the disorder was associated with dementia. Schizophrenia is often
misconstrued by lay people as multiple personality disorder, which is a separate disorder
(schism-can mean split or division, but it can also mean differences in which he was
describing the differences). 4As: Associations, Affect, Autism, Ambivalences. Secondary
(Accessory): hallucinations, delusions
Ernst Kretschmer (1888-1926)- compiled data to support the idea that people with
schizophrenia were more slender, athletic, and dysplastic body types rather than those with short,
stocky physiques.
Kurt Schneider (1887-1967)- contributed a description of first-rank symptoms, which he
stressed should not be rigidly applied. He stated that diagnoses should not be based solely
on first-rank symptoms but if a patient presented with no first-rank symptoms, second-rank
symptoms and clinical appearance should be observed.
Karl Jaspers (1883-1969)-psychiatrist and philosopher played a major role in developing
existential psychoanalysis. His work paved the way to understand the psychological meaning of
schizophrenic signs and symptoms of delusions and hallucinations.
Adolf Meyer (1866-1950)- founder of psychobiology saw schizophrenia as a reaction to life
stresses. It was a maladaptation that was understandable in terms of the patient’s life experiences.
Meyer’s view was represented in the nomenclature of 1950s, which was referred to the
schizophrenic reaction. In later editions of DSM the term reaction was dropped.

Epidemiology-The presence of Schizophrenia in the US is 1/100 or 1%. NIH reports the US
lifetime percent is 0.6-1.9%. Total population lifetime percent is 0.5% in a single year. Only
about half of those with schizophrenia will obtain treatment, despite the severity.

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Gender and Age-Schizophrenia affects men and women equally. However, onset usually occurs
earlier in men. Peak ages are 10-25 for men and 25-35 for women. Nearly 1/3 of all female
schizophrenia patients are first diagnosed with hospitalizations. 3-10% of women onset after age
40. 90% of patients onset between 10-55 years of age. It is very rare to present before age 10
or after age 60, regardless of gender. In general, females typically have a better outcome than
males.

Reproductive Factors-first-degree relatives have a 10x greater risk of developing schizophrenia
than the general population.

Medical Illness- people will schizophrenia have a higher mortality rate from accidents and
natural causes than the general population. Studies show that up to 80% of schizophrenia
patients have concurrent medical illnesses and up to 50% of these conditions may be
undiagnosed.

Infection and Birth Season- People who develop schizophrenia are more likely to be born
during the winter or early spring and less likely to be born during late spring or summer.
Northern Hemisphere people with schizophrenia are more likely to be born January to April.
Southern Hemisphere people with schizophrenia are more likely to be born July-September.
Season-specific changes, such as infections, influenza, viral infections, epidemics, diet
changes, maternal starvation during pregnancy, rhesus factor incompatibility, and genetic
predisposition.

Substance Abuse- Substance abuse occurs commonly in schizophrenia. Tobacco use occurs in
greater than 50%, alcohol abuse in 40%, cannabis over 50%. Nicotine dependency occurs in up
to 90% of schizophrenic patients.

Population Density- The incidence of schizophrenia in children with 1-2 parents with
schizophrenia is twice as high in cities as it is in rural areas. This suggests the social stressors in
urban settings may influence the development of schizophrenia in at-risk persons.

Socioeconomic & Cultural Factors- Schizophrenia is a life-long illness. Patients with
schizophrenia account for 15%-45% of the homeless population in America. Development of
effective antipsychotic medication, treatment, and better rights for persons with mental illness
since the mid 1950s has improved the view of mental illness. Patients with schizophrenia
occupy 50% of mental health hospital beds and 16% of psychiatric patients receiving treatment.

Etiology- genetic contribution accounts for some, if not all, of cases. Some studies suggest the
age of the father correlates with development of schizophrenia citing those born to fathers
over age 60 were at a greater risk for developing schizophrenia.

Biochemical Factors
Dopamine Hypothesis- hypothesizes that schizophrenia results from too much dopaminergic
energy. Excessive dopamine in patients with schizophrenia has been linked to more severe
psychotic symptoms. There have been reports of increased dopamine in the amygdala, decreased
density of dopamine transporter, and increased numbers of dopamine type 4 receptors in the
entorhinal cortex.

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Serotonin-current hypothesis suggest excess serotonin causes positive and negative
schizophrenia symptoms. Clozapine and other 2nd gen antipsychotics coupled with the
effectiveness of clozapine to decrease positive sx in chronically ill patients, contributing to the
validity of this proposition.

Norepinephrine-anhedonia (the inability to feel emotion or pleasure) is a noted feature of
schizophrenia. A neuronal degeneration of norepinephrine has been linked to this.
Pharmacological & biochemical data to support this theory is inconclusive.

GABA- has been implicated. GABA in the hippocampus leads to hyperactivity of dopaminergic
neurons.

Neuropeptides- (substance P & neurotensin) in the catecholamine & indolamine
neurotransmitters influence the actions of these neurotransmitters.

Glutamate- implicated bc ingestion of phencyclidine, a glutamate antagonist, produces an acute
syndrome similar to schizophrenia. The hypotheses proposed include those of hyperactivity,
hypoactivity, & glutamate-induced neurotoxicity.

Acetylcholine and Nicotine- postmortem studies indicate decreased muscarinic and nicotinic
receptors in the caudate-putamen, hippocampus, and selected regions of the prefrontal cortex.
These receptors play a role in regulation of neurotransmitter systems involved in cognition,
which is impaired in schizophrenia.

Neuropathology-In the 19th century, neuropathologists failed to identify a neuropathological
cause for schizophrenia, so they classified it as a functional disorder. By the end of the 20th
century, researchers had made significant strides in revealing a neuropathological cause-
predominantly in the limbic system & basal ganglia (in the cerebral cortex, thalamus, and
brainstem). Loss of brain volume appears to result from reduce density of the axons, dendrites,
and synapses that mediate associative functions of the brain. Synaptic density is highest at 1
year and then pares down to adult values in early adolescence.

Cerebral Ventricles- CT scans consistently show lateral and 3rd ventricular enlargement and
some reduction in cortical volume. Reduced volume of cortical gray matter has been indicated in
the early stages of the disease. Some studies indicate that lesions present on CT are present at
the onset of the illness and do not progress throughout the disease process.

Reduced Symmetry- Reduced symmetry has been noted in several areas of the brain with
schizophrenia: temporal, frontal, and occipital lobes. This is believed to have originated during
fetal life.

Limbic system- because of the role of the limbic system in emotional control, the limbic system
is indicated in the development of schizophrenia. Post-mortem studies show decrease in the size
of the region (including amygdala, hippocampus, and parahippocampal gyrus). MRI indicates the
hippocampus is also functionally abnormal with glutamate distribution disturbances noted.
Disorganized neurons are also noted in the hippocampus.

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