NR 507 PATHOPHYSIOLOGY WEEK 7 TD1 Behavioral, Neurologic, and Digestive Disorders Discussion Part One (NR507)

Exam (elaborations) NR 507 PATHOPHYSIOLOGY WEEK 7 TD1 Behavioral, Neurologic, and Digestive Disorders Discussion Part One (NR507) Week 7: Behavioral, Neurologic, and Digestive Disorders One - Discussion Part Loading... 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 1, 7) 4 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 Discussion Part One (graded) • What is your differential diagnosis? • What tests do you order? • An MRI comes back and there seems to be a lesion in the temporal lobe does this change your differential? The EEG also comes back with unusual excitatory activity. What is your definitive diagnosis? In retrospect did anything bias your first differential? Responses 6/Rechel DelAntar 12/2016 12:44:25 PM Differential Diagnosis Hello professor and Class, Differential Diagnosis This is a case of a patient who was previously seen in the mall looking homeless in physical appearance who exhibits repetitive movement such as “walking to a table, sitting up, walking to a tree and urinating” oblivious to the people around him and his surroundings. Upon initial exam he has no recollections of previous events. Based on this history, we may consider: Seizures = specifically Complex Focal seizure (temporal or psychomotor seizure)with a simple partial onset followed by impairment of consciousness. In this type of seizure, the patient is able to interact with the environment with a purposeful, although inappropriate movement. Most characteristic event of this type of seizure is the automatism; common examples of automatisms are lip smacking, chewing, facial grimacing, swallowing movements, and patting, picking, or rubbing oneself or one’s clothing. The body may stiffen but the patient will continue to perform complex activities of which they are involved in such as driving. Witnesses may not recognize that anything is wrong. Temporal lobe seizures generally last 11 seconds to 8 minutes (average 2 minutes) and are followed by several minutes of postictal confusion (McCance, K.L., 2013). Diagnostic testing = Laboratory studies have to be done to rule out potential causes or triggers to seizures. MRI of the brain can be performed to check if structural lesions are causing the seizure event and is helpful in assessing temporal seizures. Temporal lobe seizures commonly result from damage to specific areas in that part of the brain. This can be due to a head injury, infection, or damage to a portion of the temporal lobe due to lack of oxygen, brain tumors, genetic syndromes, or lesions of any sort. Many of these problems also produce brain-tissue scarring called mesial temporal sclerosis. EEG within 24 hours is more sensitive for diagnosing epileptiform abnormalities as it is able to localize seizure focus. Brain cells communicate with each other and produce our consciousness, thoughts, and actions by electrochemical processes. Certain patterns of electrical activity disrupt this normal function of the brain and spread in abnormal patterns within the brain. This process can be seen on an EEG (Walter, B., 2013). With the patient’s MRI results coming back with temporal lobe lesion and an EEG reading of unusual excitatory activity, my differential diagnosis remains the same. The results support the diagnosis. In retrospect, the patient’s inability to recollect his actions made me think that he was not in control of his actions and also reminded me of post ictal stage of seizure when patients were unable to recall the seizure event is what gave bias to my differential diagnosis. References: McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby. Walter, B. (2013). Bradley’s neurology in clinical practice (6 ed.). Philadelphia, PA: Elsevier, Saunders. th Instructor Brown reply to Rechel DelAntar 6/14/2016 2:23:24 PM RE: Differential Diagnosis What symptoms are possible with right vs. left side lesion? 6/Rechel DelAntar reply to Instructor Brown 14/2016 10:20:29 PM RE: Differential Diagnosis Hello Professor and Class, Right side vs. Left side lesion The brain is the control center for all human activity, including vital processes (breathing and moving) as well as thinking, judgment, and emotional reactions. Brain lesions can be caused by injury, infection, exposure to certain chemicals, problems with the immune system, and more. Typically, their cause is unknown. Symptoms experienced by the patient vary depending on the location, type and size of the lesion. The brain is divided into two halves (hemispheres). The left half controls movement and sensation in the right side of the body, and the right half controls movement and sensation in the left side. Therefore, damage to the right side of the brain may cause movement problems or weakness on the body's left side. For majority of the population, the left half of the brain is responsible for verbal and logical functions including language (listening, reading, speaking, and writing), thought and memory involving words. Patients with this type of lesion will exhibit right side weakness, aphasia, slow speech and decreased attention span. The right half is responsible for nonverbal and intuitive functions such as putting bits of information together to make up an entire picture, recognizing oral and visual patterns and designs (music and art), and expressing and understanding emotions. Patients with this type of lesion will exhibit left sided weakness, will have difficulty with complex communication such as difficulty identifying relevant information, inability to interpret body language and relevant information. They tend to be very literal in their interpretation of things and situations. Left hemispheric damage may produce a right hemianopsia or quadranopsia. They have flat affect and at times are impulsive (Novack, T., n.d.). Right Hemispheric damage may not only produce a left homonymous hemianopsia or quadranopsia, but it may also produce a severe attention disorder to the left side called left hemispatial inattention or visual neglect. Spatial orientation, body position and nonverbal communications may become impaired in some individuals. Emotional and behavioral problems may occur. Thinking skills may be effected. Meanwhile, many patients will be unaware of the full extent of their impairment. They may even deny they have a problem (Manasco, H., 2014). References: Manasco, H. (2014). Introduction to neurogenic Communication Disorders. Burlington, MA: Jones and Bartlett Learning. Novack, T. (n.d.). Understanding TRI part 2: Brain Injury Impact on Individual Functioning. Retrieved from Understanding-TBI/Brain-Injury-Impact-On- Individuals-Functioning. Brittany Heller 6/12/2016 1:51:25 PM AD "Alzheimer disease is a neurodegenerative disorder of uncertain cause and pathogenesis that primarily affects older adults and is the most common cause of dementia" ( Wolk & Dickerson, 2016, p. 1). AD typically affects patients older than 60 years and is rarely occurs in less than 60 (Wolk & Dickerson, 2016, p. 1). Some have suggested that there is a mutation in genes that alter beta-amyloid protein production and metabolism (Wolk & Dickerson, 2016, p. 1). Genes that are mutated include APP, PSEN1, and PSEN2 (Wolk & Dickerson, 2016, p. 1). AD also had three common areas of cortical thinning patterns that were observed which are the medial temporal, diffuse, and patietal dominant atrophy subtypes (Hwang, Kim, Jeon, Lee, HOne, Roh, Lee, Koh, & Noh, 2016, p. 1). The thinning of the cortical areas may suggest a predictive pattern in the pathophysiology of AD. Memory impairment is the most common symptom of AD. "Executive dysfunction and visuospatial impairment are often present relatively early, while deficits in language and behavioral symptoms often manifest late in the disease course" (Wolk & Dickerson, 2016, p. 2). Other symptoms can include executive function and judgement/problem solving, behavioral and psychological symptoms, apraxia, olfactory dysfunction, sleep disturbances, and seizures ( Wolk & Dickerson, 2016, p. 5). After completing a standardized mental status scale, the first test I would order would be an MRI. "Brain MRI can document potential alternative or additional diagnoses of cerebrovascular disease, other structural disease, and regional brain atrophy suggesting frontotemporal dementia or other types of neurodegenerative disease" ( Wolk & Dickerson, 2016, p. 6). If the MRI came back with a lesion in the temporal lobe, this would not change my diagnosis. "The most characteristic focal finding in AD is reduced hippocampal volume and medial temporal lobe atrophy" (Wolk & Dickerson, 2016, p. 6). Seizures are one of the clinical manifestations that can be present in AD. "Temporal lobe epilepsy is the most common form of partial or localization related to epilepsy" (Holmes, Sirven, & Fisher, 2013, p. 1). For temporal lobe seizures, an EEG would be essential for diagnosing purposes. On an EEG, sharp waves or spikes would be seen showing unusual activity (Holmes et al., 2013, p. 4). After thinking about this diagnosis, the memory loss was a key factor in deciding on the AD diagnosis. Due to his repetitive actions, I thought he could possibly have OCD as well. Not having the age of the patient also made this difficult to diagnosis this. Not recognizing the police also had a judgement impairment which leaned more towards AD as well. Holmes, G., Sirven, J., & Fisher, R. (2013). What is temporal lobe epilepsy? Epilepsy Foundation. Retrieved at: Hwang, J., Kim, C., Jeon, S., Lee, J., Hong, Y., Roh, J., Lee, J., Koh, J., 7 Na, D. (2016) Prediction of Alzheimer's disease pathophysiology based on cortical thickness patterns. Alzheimers Dementia, 2, 58- 67. doi: 10.1016/.2015.11.008. Retrieved at: Wolk, D., & Dickerson, B. (2016). Clinical features and diagnosis of Alzheimer Disease. UpToD. Retrieved at: topickey Lanre Abawonse reply to Brittany Heller 6/14/2016 8:46:21 PM RE: AD Brittany, your narration is great. I would like to add some few points to your diagnosis and the findings on the magnetic resonance imaging MRI. Just as you selected Alzheimer’s disease as your number diagnosis, I did the same on my selection. Alzheimer’s disease is one of many conditions that are worth putting into consideration when patients have results that indicate temporal lobe lesions. The consideration of symptoms can also include alcoholism and substance abuse etc. Upon further study of temporal lobe lesions resulting effects on patients, it has been suggested that there are a behavioral changes in these patients. Gudmundsson et. al., (2015) suggested that cortical atrophy, indicating neurodegeneration, is commonly seen on imaging of the aging brain of a patient who has temporal lobe lesions on MRI. In addition, cortical atrophy may also be an expression of small vessel disease. Prospective populationbased studies using magnetic resonance imaging (MRI) report that white matter changes increase the risk of subsequent dementia. With these findings, it could suggest that this patient is going through behavioral changes and this is evidenced by the patient’s lack of insight along with memory impairment. Gudmundsson, P., Olesen, P. J., Simoni, M., Pantoni, L., Östling, S., Kern, S., & ... Skoog, I. (2015). White matter lesions and temporal lobe atrophy related to incidence of both dementia and major depression in 70-year-olds followed over 10 years. European Journal Of Neurology, 22(5), 781-e50. 6/Jonathan Bidey reply to Brittany Heller 17/2016 12:20:14 PM RE: AD Brittany, Excellent post! You did a wonderful job describing which genes are involved with Alzheimer’s disease (AD). You also did a wonderful job describing the physical changes which occur in the brain during AD. I particularly enjoyed your description of the use of MRI in diagnosing AD. You mentioned hippocampal volume and its correlation to AD. MRIs are not only used to evaluate hippocampal findings, but also to assess for other potential causes of symptoms (Li et al., 2014). Studies are suggesting that changes in hippocampal volume may soon be able to be detected before any symptoms or memory loss has occurred. By assessing for these changes early on, prior to the onset of disease, it is possible that therapies will be designed to slow the onset for those at risk (Li et al., 2014). Excellent post! -Jonathan Reference: Li, M., Oishi, K., He, X., Qin, Y., Gao, F., & Mori, S. (2014). An efficient approach for differentiating Alzheimer's disease from normal elderly based on multicenter MRI using gray-level invariant features. PLoS ONE, 9(8), 1-13. Lorna Durfee 6/13/2016 6:35:51 AM Discussion Part One Scenario: aYpopue aarrea nact eth, ea nlodc yaol um wailtln aensds tyhoeu p seeres oan p “awtieanlkt w50h ofe aept ptoe aar sta tbol eb es iht odmowelne,s sa nbdy ahfitse pr h5y sseiccaoln ds he tgoe thsi us ps uarnrdo uwnadlkins gtos. aW threeen athned puorliincaet ecso mone ,i th”e H igen roerpeesa tths etmhi sa as citfi othne 5y atirmenes’ ta tphpearere.nLtalyte or,b yliovuio guos thoi mw ohrek h aansd n soi trteincgo lilne cetxioanm o rfo hoims b3e hisa tvhioe rs abmy eth pee mrsaolnl.! Now, he is your patient, when you talk to Repetitive urination, agnosia, aphasia, apraxia, lesion in temporal lobe? What is your differential diagnosis? • What tests do you order? • An MRI comes back, and there seems to be a lesion in the temporal lobe does this change your differential? The EEG also comes back with unusual excitatory activity. What is your definitive diagnosis? In retrospect did anything bias your first differential? Doctor Brown: DIFFERENTIALS: Differential #1: Head trauma, with brain injury, traumatic brain injury with cognitive dysfunction Differential #2: Brain dysfunction. Differential #3: Excessive alcohol consumption and Wernicke-Korsakoff Syndrome Differential #4: Schizophrenia with agnosia. Differential #5: Temporal lobe epilepsy. My chosen differential diagnosis is Differential #1: Head Trauma or traumatic brain injury. 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