By K. Gembak. Salem International University. 2018.

    They may derive from an age-related alteration of the microfilamentous actin system generic forzest 20 mg with amex. Age related volume loss of the brain involves the white matter more than the gray matter buy forzest 20 mg on line. Extensive loss of the cerebral white matter with subsequent dementia may be caused by vasculopathies. Hypertensive vascular changes (fibrosis of the walls of the vessels) cause hypoperfusion of the centrum semi-ovale. A gradual loss of oligodendrocytes, myelin and neuronal processes occurs with a reactive gliosis and widening of the perivascular spaces. Prominent involvement of the subcortical white matter is termed Binswanger disease. Dementing illnesses with a destructive or demyelinating process include progressive multifocal leukoencephalopathy, the encephalopathy of the acquired immune deficiency syndrome, and multiple sclerosis. Formalin fixed, coronal slice of the right cerebral hemisphere of a 93-year-old, demented woman. The dorsal, elongated framed area includes part of the nucleus basalis of Meynert or substantia innominata. Among other areas, the substantia innominata including the nucleus basalis of Meynert, and the amygdala degenerate in Alzheimer disease, Alzheimer disease Lewy body variant, diffuse Lewy body disease, and in Parkinson disease. The rostral half of the thalamus may be atrophic (usually medial > lateral) in Pick disease. Formalin fixed, coronal slice of the left cerebral hemisphere of a 83-year-old demented man. The dorsomedian nucleus and the anterior nucleus of the thalamus, which are the limbic nuclei, are severely atrophic. The lateral ventricle is widened, as is the sylvian fissure reflecting the loss of parenchyma. Medial aspect of the hemi brainstem including the lower edge of the mesencephalon, which contains a portion of the substantia nigra, especially the pars compacta. The short (blue) bar within the fourth ventricle indicates the site of the locus coeruleus. Resting on the ventral aspect of the pons is the longitudinally sectioned, normal basilar artery. In summary, the areas that are vulnerable to degeneration causing dementing illnesses with or without movement disorders are amygdala; allocortex: entorhinal and pyriform cortices, hippocampal formation; mammillary bodies, anterior and dorsomedian nuclei of thalamus; neocortex (homotypical > heterotypical); neostriatum, nucleus coeruleus, and raphe nuclei. The growing awareness of the early signs of mental decline caused by neurodegeneration has increased the 7 8 incidence of the diagnosis of dementia. Likewise, the increasing life expectancy with the 9 growing number of elderly individuals raises the prevalance of dementing illnesses since dementia or neurodegeneration occurs primarily late in life. On external examination of the brain the hallmarks of atrophy are the narrowing of the gyri and widening of the sulci (Fig. The atrophy is diffuse with a predilection for the prefrontal, parietal, and temporal regions. On examination of the cut sections, the brunt of the atrophy involves the white matter and cortex notably in the areas mentioned above; the amygdaloid nucleus, hippocampal formation, and the anterior part of the thalamus. The ventricular system is widened proportionally to the volume loss of the parenchyma. The nucleus coeruleus is pale in contrast to the usually well-pigmented pars compacta of the substantia nigra. The microscopic changes are found almost throughout the brain; however, their severity varies according to the regions. Especially involved are the areas exhibiting the most prominent atrophy including the amygdaloid nucleus, hippocampal formation, and the following regions of the cerebral cortex: temporal, prefrontal, and parietal. The pathologic changes include: 1) A decrease of neuronal density the severity of which varies according to region 2) Neurofibrillary tangles of Alzheimer (Figure 8). In advanced stages of the disease they may be found within the motor or visual cortices or both. Neuronal tangles occur within the amygdaloid nucleus, hippocampus, substantia innominata (nucleus of Meynert), hypothalamus, thalamus, raphe nuclei, nucleus coeruleus, and reticular formation.

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    For an avian virus to be easily transmitted between humans buy 20 mg forzest, it is fundamental that it acquires the ability to bind cells that display the 2-6 receptors so that it can enter the cell and replicate in them order 20mg forzest with visa. While single amino acid substitutions can significantly alter re- ceptor specificity of avian H5N1 viruses (Gambaryan 2006), it is presently un- known which specific mutations are needed to make the H5N1 virus easily and sustainably transmissible among humans, but potential routes whereby H5N1 might mutate and acquire human specificity do exist (Stevens 2006). Apart from H5N1, human infection generally resulted in mild symptoms and rarely in severe illness (Du Ry van Beest Holle 2003, Koopmans 2004). H5N1: Making Progress At the moment, H5N1 infection in humans is relatively rare, although there must have been widespread exposure to the virus through infected poultry. This in an indicator that the species barrier to the acquisition of this avian virus is still quite high for H5N1 – despite having been in circulation for nearly 10 years. However, over the past years, H5N1 strains seem to have become more pathogenic and to have expanded their range of action: Individual Management 29 • The H5N1 influenza strain continues to evolve (Li 2004), and some clones have broader binding properties which may reflect a certain degree of adapta- tion in human hosts (Le 2005). H5N1 has expanded its host range not only in avian species (Perkins 2002), but also in mammals, naturally infecting humans, tigers, leopards, domestic cats and a stone marten (Keawcharoen 2004, Thanawongnuwech 2005, Amonsin 2006). However, when fed with H5N1 virus-infected chickens, cats developed severe disease and trans- mitted the virus to other cats (Kuiken 2004). Cats may excrete virus not only via the respiratory tract but also via the digestive tract (Rimmelzwaan 2006), suggesting that spread by potentially novel routes within and between mam- malian hosts might be possible. In influenza manage- ment, this one-line medical wisdom theoretically translates as: 1) three prophylaxis defence lines (exposure prophylaxis, vaccination, prophylactic use of antiviral drugs); and 2) one treatment defence line (antiviral drugs). Due to the very nature of influenza infection – infected individuals may be infectious for as long as 24– 48 hours before the onset of symptoms – exposure prophylaxis is virtually impossible during an ongoing epidemic or pandemic, especially in our highly 30 Influenza 2006 during an ongoing epidemic or pandemic, especially in our highly mobile and densely populated world. Epidemic Prophylaxis Exposure Prophylaxis Basic personal hygiene measures, invented more than a century ago, are still the cornerstones of prophylaxis. Vaccination Vaccination against influenza viruses is the second cornerstone in preventing influ- enza. Recommendations regarding the composition of the vaccine are issued yearly on the basis of detailed investigations of circulating strains. The rate of influenza vaccination depends on a number of variables, including explicit physician recommendation and media coverage (Ma 2006). In healthy primed adults, the efficacy after one dose may be as high as 80-100 %, while in unprimed adults (those receiving their first influenza immunisation), effi- cacy is in this range after two doses. The evidence of efficacy and effectiveness of influenza vaccines in individuals aged 65 years or older has recently been reviewed. Well matched vaccines prevented hospital admission, pneumonia, respiratory diseases, cardiac disease, and death. The effectiveness is better in people living in homes for the elderly than in elderly indi- viduals living in the community (Jefferson 2005). Inactivated vaccine reduces exac- erbations in patients with chronic obstructive pulmonary disease (Poole 2006). In- fluenza vaccines are efficacious in children older than two years but little evidence is available for children under two (Smith 2006). Nasal spray of live vaccines seemed to be better at preventing influenza illness than inactivated vaccines. Antiviral Drugs In selected populations, antiviral drugs may be a useful option in those not covered or inadequately protected by vaccination. It should be emphasised, though, that the prophylactic use of available antiviral drugs is by no means a substitute for the yearly vaccination recommended by national health services. Individual Management 31 Candidates for short-term prophylactic use of antiviral drugs are high-risk patients who are vaccinated only after an epidemic has already begun, as well as unvacci- nated high-risk contacts of an individual with influenza. In some cases, prophylaxis could be indicated when a current epidemic is caused by a strain which is not repre- sented in the vaccine. Of the two available drug classes, the adamantanes (amantadine, rimantadine) re- cently came under pressure when the global prevalence of adamantane-resistant influenza viruses was found to have significantly increased from 0. During this period, oseltamivir or zanamivir should be selected if an antiviral medication is used for the treatment and prophylaxis of influenza. Epidemic Treatment In uncomplicated cases, bed rest with adequate hydration is the treatment of choice for most adolescents and young adult patients (Hoffmann 2006b). If rimantadine and amantadine are used, it is important to reduce the emergence of antiviral drug-resistant viruses.

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    Fat emboli and gaseous emboli tend to produce global cerebral dysfunction rather than typical stroke because they are copious purchase forzest 20mg without prescription; and numerous small intraparenchymal blood vessels become occluded order 20mg forzest amex. Fat emboli arise from the marrow of fractured long bones, enter the venous system, and filter through the lung into the systemic circulation. Vasculitis An inflammatory process in blood vessel walls can produce infarction by swelling the wall and narrowing the lumen, by damaging the endothelial lining and inducing thrombosis, or by destroying the vessel wall (necrotizing vasculitis) giving rise to hemorrhage. Among the fungi that invade the central nervous system opportunistically, Aspergillus, Phycomyces and Candida commonly infiltrate the blood vessels; Cryptococcus does not. Hematologic Hematologic disorders affecting the coagulability, viscosity, or oxygen-carrying capacity of blood can cause, or more likely contribute to, infarction in the brain - among them the leukemias, sickle cell disease, thrombotic thrombocytopenic purpura, polycythemia, disseminated intravascular coagulation, and anticoagulant therapy. Spontaneous hemorrhages in the brain parenchyma and subarachnoid space are often a result of underlying cerebrovascular disease, although trauma can also result in hemorrhages in these sites. The most common site of rupture is one of the sizable arteries that run deep in the basal ganglia as the lenticulostriate branches of the middle cerebral artery. Less common sites of hypertensive hemorrhages are the corpus medullaris of the cerebellum and the brain stem, almost always the pons. Massive hemorrhage in the basal ganglia is attended by immediate loss of consciousness - which would be unusual in the more common stroke on the basis of infarction. The mass effect is immediate and surrounding brain swelling and pressure are more marked than with infarction. Even with optimal medical management, the most important prognostic factor remains the size of the hemorrhage. Dissection of the hemorrhage into the ventricle is incompatible with life for more than a few hours. With hypertensive hemorrhage in the cerebellum, secondary compression of vital centers in the brain stem is the main threat to survival and timely removal of the hematoma may prove effective. Pathologically, the damage from intracerebral hemorrhage is compounded by foci of hemorrhagic infarction surrounding the hematoma. Slowly the blood is resorbed and survivors end up with a cavity outlined by ragged walls stained by blood pigments. The initial symptoms are head pain, typically explosive, promptly followed by depression of consciousness of variable degree. It is a delayed effect, not usually seen during the first 48 hours after rupture, and it persists for days before it resolves spontaneously. The behavior of arterial spasm is unpredictable, a second bleed in short order at the site of rupture is frequent, and the ideal time at which the defect should be repaired is not an easy surgical judgment. The mechanism for the arterial spasm remains unknown and the search for pharmacologic measures that will prevent or correct it continues. Saccular aneurysms are called congenital, but they rarely occur in young children. Whether an embryologic maldevelopment underlies their appearance in later life is moot. They are located at or near arterial junctions, particularly between the posterior communicating artery and the internal carotid or the posterior cerebral artery, at the short anterior communicating artery, and at the first branching of the middle cerebral artery in the Sylvian fissure. They usually rupture near the dome, where the wall of the aneurysm is likely to be thinnest. Giant aneurysms are probably saccular aneurysms that enlarge slowly by repeated internal thrombosis and repair without hemorrhaging. Their wall becomes fairly thick, although not uniformly so, they attain a diameter of a few centimeters, and they become symptomatic as a tumor mass compressing adjacent structures. Fusiform aneurysms are segmental distensions of severely atherosclerotic arteries, notably the basilar or a vertebral artery, and are also called atherosclerotic aneurysms. Arteriovenous malformation The second major cause of spontaneous subarachnoid hemorrhage is rupture of a congenital vascular malformation of the arteriovenous type. These vessels are interconnected and shunt arterial blood directly into venous channels. The vessel walls are of uneven thickness and composition, often of ambiguous denomination, and not proportional to the caliber of the lumen. They are located mainly in the subarachnoid space, but they always extend into the cortex and sometimes into the white matter also. Blood flow through the malformation is hemodynamically abnormal, they thrombose, they leak or hemorrhage, and neuronal degeneration, foci of encephalomalacia, and astroglial reaction and fibrosis in the intervening parenchyma are the rule.

    Try to use your patients’ cases as learning examples for large blocks of information and use downtime in the hospital to study order forzest 20mg mastercard. Make sure to plan a reading schedule starting the first week—it is really hard to cover all the material if you don’t stick to a schedule order forzest 20 mg amex. You will need to study on most of your days off, so make sure to leave some time on those days to do work. Time is an issue during the exam, so practice doing the questions quickly and efficiently (you will want to do timed sets of questions to get yourself ready). Tips for Succeeding: • Be enthusiastic and always helpful, and remember that your team will help you if you help them. You will not know everything about their medical issues, but if you know the answers to questions such as where the patient lives, his/her family history, his/her hemoglobin, etc. You have more time than anyone else on the team, and your patients are stuck in the hospital and could really use some friendly med student attention. If you have a good relationship with your patients, you will enjoy the rotation more, and you will provide an important service to the team. These presentations do not need to include PowerPoint (in fact, you will probably look like an unpleasant gunner if you even touch PowerPoint), but a one-page hand out with a pertinent article is appreciated (and gives your attending something with your name on it when s/he is doing your evaluation—attendings frequently mention your presentation in the evals). If you haven’t been asked to give a topic presentation by the end of your second week, mention it to your resident or attending to see if there is an appropriate time for you to talk to the team for 5-10 minutes. If you are asked a question that you don’t know the answer to, admit that you don’t know it and be sure to read up on it for next time. The same thing definitely goes for bringing food in—make sure you let your fellow student know if you plan to bring something in for the group (he/she may want to pitch in and bring something too). We all like to think that we are simply outstanding on our own, but the truth is that an attending is much more likely to remember how great the “med students” on a rotation were than to recall that you knew an answer that your colleague didn’t. During this rotation, you will have your own patients and will get to apply everything that you’ve been learning in the classroom for the past 10 months. Along the same lines, don’t 35 jump in and answer a question posed to someone else, even if you did just read about it and know the answer by heart. It’s fine to sit and study in a quiet area if you have some free time, but make sure your team knows where you are and that your phone is on. Family Medicine Rotation Structure: During your month of family medicine, you will be at a site with anywhere from 0-4 other medical students. Although the physicians with whom you work will have inpatients, you will be working mainly in the outpatient setting. You will be seeing patients presenting for routine check-ups and screening, well-child visits, ob/gyn concerns, sick visits, injuries, psychiatric concerns, and everything else you can think of. Depending on your site, you may have formal teaching sessions each day or on specific days during the week. Responsibilities: • Seeing Patients: In the beginning of your rotation, you may shadow a resident or an attending; however, at most sites you will quickly start to see patients on your own. You will be given their chief complaint and should focus your history on this complaint; however, remember that family medicine is all about preventive care, and so you should not forget the rest of your history either and should do a complete physical exam. This is a clinic that patients present to for acute problems, and some of these may be straightforward. This type of presentation is different from those on inpatient medicine in that it is done immediately after you see the patient. You are thus not expected to know every answer about the patient’s needs or to have expertise on their complaints. You should try to get comfortable presenting, know everything you can about your patient, and try to find time before presenting to organize your thoughts regarding possible interventions. Keep it brief and focused, and use the opportunity to practice presenting without detailed notes or planning. If you are told to write in the chart, this is all you need to do (be sure to leave some space for your attending to write).

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