Pathology Help!!!!!!!!!!!!!!!!!!!!!!!!!?

One Response for "Pathology Help!!!!!!!!!!!!!!!!!!!!!!!!!?"

1. shelley_ December 22nd, 2009 at 5:29 pm

   Whoa some of them could stump Einstein! however I can answer some of the questions from life experience. My mother had Parkinson’s Disease.
   2. Answer the following about Parkinson’s disease:
   A. Describe the etiology of Parkinson’s.
   Pathophysiology
   Although the etiology of Parkinson’s disease is not completely understood, the condition probably results from a confluence of several factors. The first is an age-related attrition and death of the approximately 450,000 dopamine-producing neurons in the pars compacta of the substantia nigra. 1 For every decade of life there is estimated to be a 9% to 13% loss of these dopamine-producing neurons. If carried to its logical extreme, those patients achieving very great age are destined to lose approximately 70% to 80% of these critical neurons before the first signs and symptoms of the disease appear. This age-related attrition may also be the explanation for the subtle extrapyramidal findings that are often found in the octogenarian patient.
   Since the early 1980s and the discovery of a potent neurotoxin (MPTP-MPP+), a by-product of illicit drug synthesis, the environment has figured prominently in proposed etiologies for Parkinson’s disease. 2,3 After the original description of this environmental “insultâ€� to the dopamine-producing cells of the substantia nigra, a number of other environmental neurotoxins have been described that have led to the parkinsonian state. These discoveries have led to the suggestion that Parkinson’s disease may arise as a combined consequence of the ongoing aging process coupled with environmental exposure(s) that accelerate the process of nigral cell death. The unusual clustering of individuals who later developed Parkinson’s disease (including the actor Michael J. Fox), in a Canadian recording studio, emphasizes the possible relation of environment to disease development.
   The third component of the puzzle is the possibility that some individuals may have a predetermined genetic susceptibility to these environmental insults. Although Parkinson’s disease has been observed to occur throughout the world and in virtually all ethnic groups, there is a low incidence among Asians and African patients as opposed to white patients. This observation suggests that genetic factors may have an important role in disease production. Other evidence involves twin studies, which initially failed to show a high concordance rate among monozygotic twins but is now being reconsidered in light of new evidence. 4 In addition, family history appears to be a strong predictor, after age, for development of the disease. Recently, a number of families in Greece and Italy with a high penetrance of Parkinson’s disease were shown to have a mutation on chromosome 4 for the alpha-synuclein gene. 5 This is a presynaptic protein of unknown function but with the potential, on further study of this mutated gene, to provide insights into the pathogenesis of this form of autosomal dominant Parkinson’s disease. Another gene abnormality on the long arm of chromosome 6 has been identified in patients with a peculiar autosomal recessive form of young-onset disease. The protein product of this gene is named Parkin and seems to promote the degradation of certain neuronal proteins. It is closely related to the ubiquitin family of proteins involved in several neurodegenerative disease states. 6 Research continues at a very high level to identify susceptibility genes and to shed additional light on the genetics of Parkinson’s disease.
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   Signs, Symptoms, and Diagnosis
   The diagnosis of Parkinson’s disease is a clinical exercise. A useful starting point begins by identifying parkinsonism at definite, probable, and possible levels. Using several clinical extrapyramidal features (resting tremor, rigidity, bradykinesia, postural instability, and freezing) one can confidently say a patient has definite Parkinsonism if he or she has any two of those five features, with one of the two being tremor or bradykinesia.
   Once a diagnosis of parkinsonism is made, it is imperative for the physician to exclude pharmacologic causation. Since the recognition, decades ago, that reserpine can produce extrapyramidal side effects, the list of medications that can cause parkinsonism continues to increase each year (Box 1). In addition, unexplained extrapyramidal disease in a young person should always prompt exclusion of Wilson’s disease, a metabolic disorder of copper metabolism leading to degenerative changes in the brain.
   Box 1: Medications That May Produce Parkinsonism
   Phenothiazines
   Butyrophenones
   Selective serotonin reuptake inhibitors
   Amiodarone
   Diltiazem
   Metoclopramide
   Valproic acid
   The asymmetrical and unilateral onset of resting tremor is probably the single best clinical clue that one is dealing with true Parkinson’s disease, although some of the parkinsonisms can manifest in a similar fashion. A robust response to levodopa is also considered a strong