Reply DB 1: 200 words without references including. 2 references and apa format-5 years
of publication peer-reviewed article
Neuroanatomy is the study of the relationship between structure and function in the nervous
system. The brain consists of macroscopic (larger structures like the folds of the brain) and
microscopic structures (those at the cellular and molecular level), like the interaction between
neurons and glia. (Kennedy, M., et al 2014)
Three components form the foundation of the nervous system: neurons (or nerve cells), neuroglia
(glial cells) and extracellular constituents. Neurons process information by sensing the
environment, communicating through neurotransmitters and originating our thoughts and
memories. (Kennedy, M., et al 2014). Neurons have a cell body and two types of extensions, or
processes. One is called a dendrite, and the other is the axon. Dendrites receive signals which
then send towards the cell body. The axon also transmits signal but over long distances.
In the above diagram, the neurons are communicating with another part of the brain by sending
messages through the dendrites to other parts in the brain. All neurons have a cell body known as
the soma, which is the command center of the nerves and contains the nucleus of the cell.
(Stahl's, S., 2013)
References
Kennedy-Malone, L., Fletcher, K. R., & Martin-Plank, L. (2014). Advanced Practice Nursing in
the Care of Older Adults. Philadelphia, PA: F.A. Davis.
Stahl, S. M. (2013). Stahl's Essential Psychopharmacology: Neuroscientific Basis and Practical
Applications. Cambridge, England: Cambridge University Press.
Reply DB 2: 200 words without references including. 2 references and apa format-5 years
of publication peer-reviewed articles
According to Stahl, understanding psychopharmacology begins with becoming knowledgeable of
neuroanatomy, specifically with the principles of chemical neurotransmission (2013).
Competent prescribing of psychiatric medicines requires consideration of how diseases affect the
central nervous system, how drugs act on the brain, and how psychiatric medicines affect
behavior (Stahl, 2013). A good example of why this understanding is important is that many
neurotransmitters are affected by antidepressant medications, causing serious side effects
(Edmunds & Mayhew, 2013).
The slide presented for discussion helps demonstrate the process of neurotransmission.
Anatomically, this slide depicts neurons. These interconnected nerve cells are responsible for
carrying information throughout the body, using electrical and chemical signals to coordinate
bodily functions. Simply put, neurons receive information, integrate the information to determine
whether or not to pass it on, and communicate the information to target cells of other neurons.
The anatomy of the neuron includes a cell body, or soma, branching processes of dendrites with
dendritic spines forming the dendritic tree, and a more protracted process known as the axon.
Dendrites receive information from other neurons and carry the information to the soma, the
soma receives the information, and axons carry information from the soma to other neurons. The
slide shows neuron-to-neuron connections. The connections are known as synapses. Information
is carried from the first (presynaptic) neuron to the target (postsynaptic) neuron. The axon sends
information as the axon passes by (en passant) or as the axon ends (presynaptic axon terminals)
(Stahl, 2013). The box in the slide is demonstrating the transmission of information by chemical
messengers called neurotransmitters from the presynaptic neuron to the postsynaptic neuron at
the synaptic cleft. Receptors are present on both sides of the cleft and are essential components
of chemical neurotransmission (Stahl, 2013).
While this is a fundamental analysis of the concept depicted in the slide, the process of chemical
neurotransmission is quite complicated. A thorough understanding of the principals of
neurotransmission is needed by clinicians who evaluate, diagnose, and treat psychiatric patients
because every part of chemical transmission can be targeted and influenced by psychiatric
medications (Stahl, 2013).
References
Edmunds, M. W., & Mayhew, M. S. (2013). Pharmacology for the primary care provider, 4th
edition. Elsevier.
Stahl, S. M. (2013). Stahl's essential psychopharmacology: neuroscientific basis and practical
applications, 4th edition. Cambridge University Press.
Reply DB 3: 200 words without references including. 2 references and apa format-5 years
of publication peer-reviewed articles
-Differentiate between generalized anxiety disorder and panic disorder - from an assessment
standpoint, please tell me how you can determine the clinical differences.
Panic disorders represent more isolated acute events where the patient is overwhelmed by
feelings of dread (Morrison, 2014). The patient may experience physical symptoms along with
these events. The attacks can be triggered by something or not triggered and be spontaneous, can
occur during sleep or when awake. It is more common with women and onset of the disorder
typically occurs when people are in their 20s (Morrison, 2014). These individuals also continue
to worry about additional attacks (Morrison, 2014).
Generalized anxiety disorders do not include panic episodes but patients with this disorder worry
about a variety of things in their life and have feelings of nervousness or anxiety, and tend to feel
this way often (Morrison, 2014).
In the clinical setting it would be important to ask questions around frequency of events since
panic disorder involves acute episodes, this should be able to be identified. If patient states they
have always been a worrier or feel nervous in majority of situations, they more than likely would
have generalized anxiety.
3. How do you determine the difference between depressive disorders and anxious disorders?
Can they present with the same or similar symptoms?
People with major depressive disorder can feel down for long periods of time. People with
anxiety can also have depressive episodes but anxiety should be able to be identified through
interview with the patient. Patients with anxiety would probably talk about worry or nervousness
while depression is more feeling down or fatigued and not being able to be successful in
completing tasks (Keltner & Steels, 2019). Patient with depression may have a flat affect and
have issues with appetite change and weight changes (Generalized Anxiety Disorder vs Major,
2017). The patient with anxiety may experience physical symptoms like irritable bowel, racing
heart, chest pressure, or shaky (Generalized Anxiety Disorder vs Major, 2017).
Reply DB 4: 200 words without references including. 2 references and apa format-5 years
of publication peer-reviewed articles
General Anxiety Disorder (GAD) is a chronic debilitating disorder where patients experience
“excessive or unreasonable worry or apprehension” (Keltner and Steele, 2018). GAD is typically
associated with MDD with a median onset of 30 years old. Symptoms must be present for 6
months, most days of the week. Patients experience restlessness, fatigue, difficulty concentrating,
irritability, and sleep disturbances. They have great difficulty coping and develop chronic issues
with functioning.
On the other hand, panic disorders tend to be sudden onset and situational, accompanied with
fight-or-flight symptoms. They typically present to the ED with CP, SOA, hyperventilation,
choking sensation, and fear of dying. Patient with panic disorder are excessively worried about
having another panic attack sometimes leading to avoidance behavior and isolation. Typical
onset are patients their 20s. Symptoms must be present for 1 month (Morrison, 2014).
Both GAD and panic disorder can manifest physical symptoms, as mentioned above; however,
the symptoms tend to be different. Both are treated with SSRIs and SNRIs, along with CBT.
Panic disorder may require benzodiazepines for short term/immediate relief; however, should be
titrated off quickly due to addiction and dependency issues (Keltner and Steele, 2018).
DB 5: 200 words without references including. 2 references and apa format-5 years of
publication peer-reviewed articles
On intake, Mary Lou would be assessed initially with the ABC's to ensure no life threatening
event was occurring and then, for an immediate assessment for a stroke due to her symptoms of
flaccidity of her left and left leg despite no pulling of the face due to the varying symptoms that
can occur through the different regions of the brain. In addition , she has risk factors of birth
control and smoking that can contribute to a stroke. Assessment of disability is determined with
the National Institutes of Health Stroke Scale which will allow staff to score the severity of
possible stroke from a TIA to a severe life threatening situation. History (family history, social
history past medical history), HPI, ROS (which will need to include the timing of symptoms and
onset, back or cervical neck injury or discomfort, loss of sensation, loss of bowel or bladder
function), physical exam (including neurological and reflex testing) and medication review will
contribute to differential. Non-contrast/ contrast CT will be ordered immediately to R/O stroke or
tumor. If symptoms continue and indicated with a CT that is negative, MRI may be considered
due to its sensitivity with minor ischemic and TIA strokes. Determination if an ischemic stroke
has occurred, needs to be determined within 4.5 of initial symptoms for treatment with
recombinant tissue plasminogen activators. Vital signs, lab work such as CBC, CMP, TSH,
cholesterol, glucose testing, CBC, PT, PTT and CPK (rule out muscle damage) all should be
ordered immediately with CT scan. (Musuka, Wilton, Traboulsi &Hill, 2015) Personally, I
would also add CRP and sed rate to assist with ruling out inflammation and infectious processes.
Additional testing, that maybe required ECG, EEG, and MRI of spine or CT with myelography if
MRI is unavailable to R/O nerve roots or spinal cord process, CSF to R/o Guillen-Barre’
syndrome, myelitis, or demyelinating peripheral neuropathy if suspected. Testing to support
differential diagnosis of denervation injuries (e.g., stroke, spinal cord injury, denervation
diseases e.g., guillan Barre’ syndrome, CNS infection and myasthenia crisis. (Asimos, 2018)
Asimos, A. W. (2018, September 4). Evaluation of the patient with acute weakness in the
emergency department. Retrieved from https://www.uptodate.com/contents/evaluation-of-theadult-with-acute-weakness-in-the-emergency-department (Links to an external site.)
Depressive disorders typically are characterized by depressed mood and lack of interest in
pleasurable activities. These patients feel worthless and are high risk for SI. These patients
typically present with depressed mood, significant weight loss or gain, insomnia or hypersomnia,
daily psychomotor agitation or retardation, fatigue, and energy loss, diminished concentration,
feelings of worthlessness, and recurrent thoughts of death. These patients may present with poor
hygiene, pacing and inability to sit still, slow speech or poverty of speech, slowing of body
movement, and drooping posture. They may also c/o abdominal pain, CP, N/V, and sexual
dysfunction (Keltner and Steele, 2018).
On the other hand, anxiety disorders are typically characterized by unreasonable worry that the
patient is unable to control. Patients experience restlessness, fatigue, difficulty concentrating,
irritability, and sleep disturbances. They have great difficulty coping and develop chronic issues
with functioning. Patients with panic disorder can develop panic attacks which create a great deal
of fear. Panic attacks are typically unexpected and situational. They manifest into physical
symptoms including CP, shortness of breath, palpitations, choking sensation, and fear of dying.
Most episodes peak within 10 minutes and slowly resolve. They patient feels if they are going
crazy and fear that they will have another one, leading to isolation and avoidance of people and
places (Keltner and Steele, 2018).
Depressive disorders and anxious disorders can present the same or very similar symptoms.
Depressive disorders and anxious disorders can both produce extensive physical symptoms
ranging from fatigue, insomnia, and restlessness, to more severe symptoms including CP,
palpitations, SOA, and sweating. Both disorders are predominantly females (2:1), and onset of
disorder is 20-30. Anxiety disorders have a high genetic correlation with depressive disorders.
Panic attacks occur in 15% of patients with MDD. Both can cause severe impairment of social,
occupational, and interpersonal functioning (Keltner and Steele, 2018).
DB 6: 200 words without references including. 2 references and apa format-5 years of
publication peer-reviewed articles
First, let’s take a minute to talk about somatoform disorders with special attention to conversion
disorders. Patients with somatic symptoms have likely been evaluated by clinician’s multiple
times for a multitude of complaints. These complaints typically require a significant medical
work up, yielding negative results. In somatic disorders the patient is manifesting their
psychological symptoms into physical symptoms. This is typically secondary to some sort of past
trauma or stressor in their life. These patients are largely undiagnosed and once diagnosed
requires CBT and psychodynamic therapy, along with possible introduction of a SSRI, SNRI, or
TCA (Keltner and Steele, 2018).
For starters, Mary Lou’s symptoms are NOT consistent with a typical neurological diagnosis;
however due to her physical complaints in the setting of smoking and current use of birth
control, I feel we must rule out an acute neurological event. This patient would need a minimum
of CT head, +/- MRI/MRA, and neurological consult (if work up had not been recently done).
However, please note, according to Morrison (2018), “the criteria don’t require patients to
undergo laboratory or imaging tests. The requirement is only that, after a careful physical and
neurological evaluation, the patient’s symptom can not be explained by a known medical or
neurological disease process” (pg 263).
If all medical results are negative and there is no reason for neurological deficients, I feel that it
is important to rule out psychological disorders at this time. With no physical explanation of
symptoms, it’s important to obtain a detailed medical history, family history, social history, a
current in depth history of present illness, along with MSE. It’s also important to speak with
family. Conversion disorder typically have a strong genetic link (Morrison, 2014). It is important
to determine if the patient is more focused on symptoms rather than fear of disease. If so, this
would rule out illness of anxiety disorder (Morrsion, 2104). Since the patient doesn’t complain of
pain this would likely rule out somatic symptoms disorder. In patients with conversion disorder it
is important to assess their concern or anxiety about the symptoms. If their concern is low for
significant debilitating symptoms this is referred to as “la belle indifference” which is a classic
sign of conversion disorder (Morrison, 2014). Lastly, it is highly important to try and find the
root cause for the somatic disorder. Why are they transferring psychological issues/pain into
physical symptoms? This will help complete the story and strengthen the diagnosis.
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