NR 507
PATHOPHYSIOLOGY WEEK
7 TD3 Behavioral,
Neurologic, and Digestive
Disorders Discussion Part
Three
,Week 7: Behavioral, Neurologic, and Digestive Disorders -
Discussion Part Three
Loading...
Discussion
This week's graded topics relate to the following Course Outcomes (COs).
1 Analyze pathophysiologic mechanisms associated with
selected disease states. (PO 1)
2
Differentiate the epidemiology, etiology, developmental
considerations, pathogenesis, and clinical and laboratory
manifestations of specific disease processes. (PO 1)
3
Examine the way in which homeostatic, adaptive, and
compensatory physiological mechanisms can be supported
and/or altered through specific therapeutic interventions. (PO
4
1, 7)
Distinguish risk factors associated with selected disease
states. (PO 1)
5 Describe outcomes of disruptive or alterations in specific
physiologic processes. (PO 1)
6 Distinguish risk factors associated with selected disease
states. (PO 1)
7 Explore age-specific and developmental alterations in
physiologic and disease states. (PO 1, 4)
,Discussion Part Three (graded)
A 19-year-old freshman in college has been brought to your office by campus
security. The patient had been standing on top of the school chapel proclaiming that
he was the prophet of God and that God was speaking to him. In fact he claimed to
actually hear God’s voice. When he is in your office you notice that he is speaking
very fast, can’t seem to sit still and his sentences at times don’t seem to make
sense. He states, “I saw the professor sit on the ham sandwich and eat the raw
calculus in his mind”
• What is your differential diagnosis, how does it fit how might it not fit?
• Based on the top of your differential what is the epidemiology of that disorder?
Responses
Lorna Durfee 6/14/2016 7:13:47 PM
Discussion Part Three
A 19-year-old freshman in college has been brought to your office by campus security.
The patient had been standing on top of the school chapel proclaiming that he was the
prophet of God and that God was speaking to him. In fact, he claimed to actually
hear God’s voice. When he is in your office you notice that he is speaking very fast,
can’t seem to sit still and his sentences at times don’t seem to make sense. He states,
“I saw the professor sit on the ham sandwich and eat the raw calculus in his mind”
What is your differential diagnosis, how does it fit how might it not fit?
Based on the top of your differential what is the epidemiology of that disorder?
Doctor Brown:
My chosen differential is Differential #1: Schizophrenia.
McCance, Huether & Brashers (2014) explain that schizophrenia is a severe emotional
disorder that manifests itself with delusions, hallucinations, and a break from reality.
This disorder results in bizarre, withdrawn, and inappropriate behavior (McCance et.
al., 2014, p. 179). The authors relate that recent studies have shown associations
between schizophrenia and genes that have products that interact with glutamate
receptors (McCance et. al, 2014, pp. 179-180). The receptors are dysbindin,
neuregulin 1, and D-amino acid oxidase activator. Another susceptibility is gene
DISC1. Each of these has been seen in multiple populations and replicated. The
exact mechanisms which mutations in the genes contribute to schizophrenia are not
known at this time (McCance et. al, 2014, p. 180).
Also, Tohyama, Miyata, Hattori, Shimizu, and Matsuzaki (2015) report that several
susceptibility genes have been found in schizophrenia and major depression. They are
disrupted-in-schizophrenia 1 (DISC1), dysbindin and pituitary adenylate cyclase-
activating polypeptide (PACAP). The findings in DISC1 is related to neural
development directly via the adhesion molecules or the partners of DISC1. They are
elongation protein 1 (FEZ1), DISC1-binding zinc-finger protein (DBZ) and kendrin.
PACAP regulates neural development. Dysbindin is involved with the neural
development and regulates the centrosomal microtubule network and formation.
, The molecules that have been reviewed are involved in neural development and
several neuropsychiatric disorders. Both DISC and DBZ are found in
oligodendrocytes and thus in regulating oligodendrocyte and differentiation. There is
also evidence that suggest that disturbance in oligodendrocyte development and major
depression (Tohyama et. al., 2015, p. 137).
The National Institutes of Health (2016) relate that past genome analyses have found
more than 100 genetic regions related to schizophrenia risk. The specific genes that
put a patient at risk are still unknown. Dr. Steve McCarroll, from the Broad Institute
and Harvard Medical School, and his team have examined the region with the
strongest link. They have found that there are associations near the C4 gene which
encodes for complement component 4. The C4 gene is part of the complement
cascade where the immune system has a pathway that eliminates pathogens and
cellular debris. The scientists found that the more strongly a variation correlation with
expression of C4A, the stronger the correlation with schizophrenia. When examining
brain tissue and neurons from human brains they found C4 production in the neurons,
especially at synapses. It is possible that C4 may be working with other components
of the complement cascade to promote synaptic pruning. With testing, they found that
C4 tags the synapse for pruning with another protein called C3. The higher the level
of C4 in mice the greater the pruning. Dr. Thomas Lehner of the NIH relates that
pruning gets rid of the excess connections we do not need so that the brain performs at
an optimum level. However, with too much pruning it can impair mental function.
Dr. Lehner feels this could help explain the delayed age of onset and the shrinkage of
the brain’s working tissue. Perhaps stopping this process could help be the
transformation needed to identify the problem behind schizophrenia (The National
Institutes of Health, 2016).
How does it fit, or not fit?
Using the DSM-5, we know that two of Criterion A symptoms are necessary for any
diagnosis of schizophrenia. The second change is that additionally, in Criterion A, an
individual must have one of three of the positive symptoms: including delusions,
hallucinations, and disorganized speech. There must be one of the positive symptoms
to sustain a reliable diagnosis of schizophrenia. This patient exhibits three of the
criteria listed in the DSM-5 for the diagnosis of schizophrenia as positive indicators
for the disorder. The determination of a diagnosis is based on provided information.
In this particular case, we do not have all the required information such as past
medical history, physical examination, tests and procedures that could help delineate
more clearly and more precisely an accurate diagnosis. I would want to investigate the
use of drugs. I would also like to determine if there is another medical condition.
However, given the information provided, I am certain that this patient is exhibiting
the criteria for schizophrenia.
What is the epidemiology of that disorder?
Although the question did not include the etiology, I found that it was important to
include. Holder and Wayhs (2014), explain that genetics have an important role in the
etiology of schizophrenia. However, most patients do not have any background or
family history of psychosis. The variations in genetics for this disease have not been
completely identified. What is possible is that environmental factors could have a
role. Other contributing factors for the development of schizophrenia include growing
up in an urban area, the use of marijuana, infections, complications in obstetrics, and
central nervous system infection in childhood (Holder & Wayhs, 2014, p. 775).
PATHOPHYSIOLOGY WEEK
7 TD3 Behavioral,
Neurologic, and Digestive
Disorders Discussion Part
Three
,Week 7: Behavioral, Neurologic, and Digestive Disorders -
Discussion Part Three
Loading...
Discussion
This week's graded topics relate to the following Course Outcomes (COs).
1 Analyze pathophysiologic mechanisms associated with
selected disease states. (PO 1)
2
Differentiate the epidemiology, etiology, developmental
considerations, pathogenesis, and clinical and laboratory
manifestations of specific disease processes. (PO 1)
3
Examine the way in which homeostatic, adaptive, and
compensatory physiological mechanisms can be supported
and/or altered through specific therapeutic interventions. (PO
4
1, 7)
Distinguish risk factors associated with selected disease
states. (PO 1)
5 Describe outcomes of disruptive or alterations in specific
physiologic processes. (PO 1)
6 Distinguish risk factors associated with selected disease
states. (PO 1)
7 Explore age-specific and developmental alterations in
physiologic and disease states. (PO 1, 4)
,Discussion Part Three (graded)
A 19-year-old freshman in college has been brought to your office by campus
security. The patient had been standing on top of the school chapel proclaiming that
he was the prophet of God and that God was speaking to him. In fact he claimed to
actually hear God’s voice. When he is in your office you notice that he is speaking
very fast, can’t seem to sit still and his sentences at times don’t seem to make
sense. He states, “I saw the professor sit on the ham sandwich and eat the raw
calculus in his mind”
• What is your differential diagnosis, how does it fit how might it not fit?
• Based on the top of your differential what is the epidemiology of that disorder?
Responses
Lorna Durfee 6/14/2016 7:13:47 PM
Discussion Part Three
A 19-year-old freshman in college has been brought to your office by campus security.
The patient had been standing on top of the school chapel proclaiming that he was the
prophet of God and that God was speaking to him. In fact, he claimed to actually
hear God’s voice. When he is in your office you notice that he is speaking very fast,
can’t seem to sit still and his sentences at times don’t seem to make sense. He states,
“I saw the professor sit on the ham sandwich and eat the raw calculus in his mind”
What is your differential diagnosis, how does it fit how might it not fit?
Based on the top of your differential what is the epidemiology of that disorder?
Doctor Brown:
My chosen differential is Differential #1: Schizophrenia.
McCance, Huether & Brashers (2014) explain that schizophrenia is a severe emotional
disorder that manifests itself with delusions, hallucinations, and a break from reality.
This disorder results in bizarre, withdrawn, and inappropriate behavior (McCance et.
al., 2014, p. 179). The authors relate that recent studies have shown associations
between schizophrenia and genes that have products that interact with glutamate
receptors (McCance et. al, 2014, pp. 179-180). The receptors are dysbindin,
neuregulin 1, and D-amino acid oxidase activator. Another susceptibility is gene
DISC1. Each of these has been seen in multiple populations and replicated. The
exact mechanisms which mutations in the genes contribute to schizophrenia are not
known at this time (McCance et. al, 2014, p. 180).
Also, Tohyama, Miyata, Hattori, Shimizu, and Matsuzaki (2015) report that several
susceptibility genes have been found in schizophrenia and major depression. They are
disrupted-in-schizophrenia 1 (DISC1), dysbindin and pituitary adenylate cyclase-
activating polypeptide (PACAP). The findings in DISC1 is related to neural
development directly via the adhesion molecules or the partners of DISC1. They are
elongation protein 1 (FEZ1), DISC1-binding zinc-finger protein (DBZ) and kendrin.
PACAP regulates neural development. Dysbindin is involved with the neural
development and regulates the centrosomal microtubule network and formation.
, The molecules that have been reviewed are involved in neural development and
several neuropsychiatric disorders. Both DISC and DBZ are found in
oligodendrocytes and thus in regulating oligodendrocyte and differentiation. There is
also evidence that suggest that disturbance in oligodendrocyte development and major
depression (Tohyama et. al., 2015, p. 137).
The National Institutes of Health (2016) relate that past genome analyses have found
more than 100 genetic regions related to schizophrenia risk. The specific genes that
put a patient at risk are still unknown. Dr. Steve McCarroll, from the Broad Institute
and Harvard Medical School, and his team have examined the region with the
strongest link. They have found that there are associations near the C4 gene which
encodes for complement component 4. The C4 gene is part of the complement
cascade where the immune system has a pathway that eliminates pathogens and
cellular debris. The scientists found that the more strongly a variation correlation with
expression of C4A, the stronger the correlation with schizophrenia. When examining
brain tissue and neurons from human brains they found C4 production in the neurons,
especially at synapses. It is possible that C4 may be working with other components
of the complement cascade to promote synaptic pruning. With testing, they found that
C4 tags the synapse for pruning with another protein called C3. The higher the level
of C4 in mice the greater the pruning. Dr. Thomas Lehner of the NIH relates that
pruning gets rid of the excess connections we do not need so that the brain performs at
an optimum level. However, with too much pruning it can impair mental function.
Dr. Lehner feels this could help explain the delayed age of onset and the shrinkage of
the brain’s working tissue. Perhaps stopping this process could help be the
transformation needed to identify the problem behind schizophrenia (The National
Institutes of Health, 2016).
How does it fit, or not fit?
Using the DSM-5, we know that two of Criterion A symptoms are necessary for any
diagnosis of schizophrenia. The second change is that additionally, in Criterion A, an
individual must have one of three of the positive symptoms: including delusions,
hallucinations, and disorganized speech. There must be one of the positive symptoms
to sustain a reliable diagnosis of schizophrenia. This patient exhibits three of the
criteria listed in the DSM-5 for the diagnosis of schizophrenia as positive indicators
for the disorder. The determination of a diagnosis is based on provided information.
In this particular case, we do not have all the required information such as past
medical history, physical examination, tests and procedures that could help delineate
more clearly and more precisely an accurate diagnosis. I would want to investigate the
use of drugs. I would also like to determine if there is another medical condition.
However, given the information provided, I am certain that this patient is exhibiting
the criteria for schizophrenia.
What is the epidemiology of that disorder?
Although the question did not include the etiology, I found that it was important to
include. Holder and Wayhs (2014), explain that genetics have an important role in the
etiology of schizophrenia. However, most patients do not have any background or
family history of psychosis. The variations in genetics for this disease have not been
completely identified. What is possible is that environmental factors could have a
role. Other contributing factors for the development of schizophrenia include growing
up in an urban area, the use of marijuana, infections, complications in obstetrics, and
central nervous system infection in childhood (Holder & Wayhs, 2014, p. 775).
