By C. Kaffu. Defiance College.
Vertex Presentation (cephalic presentation) where the fetus head is the presenting part purchase levitra plus 400mg mastercard erectile dysfunction 18, most common and safest birth position buy levitra plus 400 mg mastercard erectile dysfunction diabetes causes. Each topic summary is designed for use in conjunction with the relevant didactic lecture given during the rotation. Original and Review Articles – Original, and review articles are provided for residents who seek a more comprehensive understanding of a topic. We recognize that residency is a busy time, but we hope that you will take the time to read articles relevant to the management of your patients. In order to facilitate learning at many levels, several other educational opportunities are available. Tutorials – These are 20-30 minute sessions offered during the rotation that will provide the resident with hands on experience (e. The goal of morning rounds is to develop treatment plans that can be defended by the best available scientific evidence. In addition, morning rounds are an opportunity for residents to test their knowledge, gauge their progress in critical care education, and recognize the limits of the current medical practice. The faculty and fellows of Boston University Pulmonary and Critical Care section hope that you enjoy your rotation in the medical intensive care unit. Management and Optimal Timing of Tracheostomy / Literature Chapters on Cardiopulmonary Critical Care G. During respiration air is humidified reducing atmospheric pressure by 47mmHg to 713mmHg so the maximal inspired partial pressure of oxygen is 149mmHg. Hemoglobin has 4 binding sites for oxygen, and if all are occupied then the oxygen capacity would be saturated. With a normal cardiac output of 5 l/min, the delivery of oxygen to the tissues at rest is approximately 1000 ml/min: a huge physiologic reserve. Dissolved in blood - Dissolved oxygen follows Henry’s law – the amount of oxygen dissolved is proportional to the partial pressure. If this was the only source of oxygen, then with a normal cardiac output of 5L/min, oxygen delivery would only be 15 ml/min. Fick equation: This is computed by determining the amount of oxygen that has been lost between the arterial side and the venous side and multiplying by the cardiac output. Only marginal increases in oxygen content occur with saturations above 88-90% so this should be your goal. Remember: short-term risk of low oxygen is greater than short-term risk of administering too much oxygen. Oxygen Toxicity: Initial concern for oxygen toxicity came from the discovery that therapeutic oxygen causes blindness in premature babies with respiratory distress syndrome. The performance of a particular device depends: 1) flow rate of gas out of the device, and 2) inspiratory flow rate created by the patient. In the ideal device, gas flow exceeds the patient’s peak inspiratory flow so as not to entrain air from the atmosphere. Nasal cannula: The premise behind nasal cannula is to use the dead space of the nasopharynx as a reservoir for oxygen. There are a couple of problems with nasal cannula: 1) they need to be positioned at the nares, 2) effectiveness is influenced by the pattern of breathing - there appears to be little difference whether the patient is a mouth or a nose breather, but it is important that the patient exhale through their mouth. Initiating Mechanical ventilation Aim: Provide adequate ventilation and oxygenation without inducing barotrauma/volutrauma. Unstable hemodynamics: Hypotension is common after intubation–probably multi- factorial including pre–intubation hypovolemia which is increased by peri-intubation 8 analgesia and anesthesia, immediate effects of positive pressure ventilation on venous return; acidosis (hyperventilate pre-intubation). Agitation: Don’t forget that if paralytic agent has been use ensure patient also receives an anxiolytic/anmesic agent like benzodiazepine. Pressure Control Ventilation (see below) Uses Square Pressure wave form-hypothetically allows for recruitment of alveolar gas exchange units by maintaining inspiratory pressures for longer periods. Turning patient to prone position results in recruitment of previously collapsed alveoli- The majority of patients respond within 30 minutes. Protein-rich fluid escapes into the alveolar space and interstitium leading to impaired lung compliance and gas exchange.
Intramyelinic edema is recognized as a splitting of the myelin sheath at the interperiod line purchase 400mg levitra plus free shipping erectile dysfunction treatment los angeles. More detailed descriptions of these and other diseases of myelin can be found in the supplementary reading levitra plus 400mg generic erectile dysfunction prescription medications. It is the prototypic and most frequently encountered demyelinating disease in humans. The prevalence varies with genetic background and latitude and usually affects young people (20-40 years of age), particularly women. Such attacks are followed by complete or partial remission and subsequent relapses ("chronic relapsing" multiple sclerosis). Attacks appear to be precipitated by infection, trauma, pregnancy or excessive heat; however controlled studies often fail to confirm these observations. The earliest presentation may be that of a young woman who complains of paresthesias or visual difficulties and yet, when tested, does not show any objective abnormalities (signs). There is no completely reliable laboratory test available at the present time to diagnose these patients at their initial presentation, however several types of tests are helpful in supporting this diagnosis. Evoked potentials (visual, auditory, and somatosensory) can also help demonstrate clinically silent lesions. Analysis of cerebrospinal fluid frequently shows evidence of inflammation (mild mononuclear pleocytosis, elevated IgG levels or oligoclonal IgG bands on electrophoresis) or myelin breakdown (elevated myelin basic protein levels). Sites of predilection include the pial surface of the optic nerves and chiasm, spinal cord and basis pontis and the periventricular white matter of the cerebrum, cerebellum and brainstem - that is, regions in proximity to cerebrospinal fluid and to deep cerebral veins. The gross and microscopic appearances of demyelinative plaques vary with their age. Whether oligodendrocytes are lost at this early stage is still a matter of debate, but most evidence indicates that the loss of oligodendrocytes follows damage to myelin. The perivenular myelinated axons appear to be affected first (perivenous demyelination) and are in immediate physical contact with macrophages, which are presumed to cause separation and thinning of myelin lamellae. Reactive astrocytosis is also prominent at this stage, but lipid-laden macrophages appear later. The risk of the disease is highest in monozygotic twins and increased in first degree relatives compared to nonrelated individuals. This association is believed to confer an immune responsiveness to whatever the etiologic antigen may be. People living in northerly latitudes (colder climates) have a higher prevalence (northern U. Some argue that this is related to similar genetic backgrounds of people living in the northern latitudes of Europe and North 117 America. A second environmental factor appears to be an infectious agent that is contracted before the age of 15 years. Measles virus remains the most persistent contender, but a retrovirus may be the culprit. This autoreactivityis thought to be precipitated by exposure to an infectious agent early in life. Acute Disseminated Encephalomyelitis In contrast to multiple sclerosis, this disease is uncommon, affects children more than adults and is usually seen following a viral infection or vaccination. The onset is acute and typically there is diffuse involvement of the brain, spinal cord and meninges. Postinfectious encephalomyelitis most commonly follows measles (rubeola) infection. The majority of patients with postinfectious encephalomyelitis completely recover, if appropriately treated with steroids, while approximately 10% die and approximately 10% demonstrate persistent deficits. Historically, the most important causes of postvaccinal encephalomyelitis are rabies vaccines produced in brain tissue (no longer done in this country) and smallpox vaccine (no longer administered). The prognosis in these patients is similar to those with postinfectious encephalomyelitis. However, inflammatory cells are largely lymphocytes and discrete perivenous lesions are the rule rather than the exception. This pathogenesis of acute disseminated encephalomyelitis appears to represent an immune destruction of myelin, which is not dependent upon direct invasion of the brain by virus. Experimental allergic encephalomyelitis, an autoimmune, inflammatory demyelinating disease, 118 appears to be an excellent model for this human disease. Acute hemorrhagic leukoencephalitis Acute hemorrhagic leukoencephalitis (Weston Hurst disease) is thought to be an hyperacute form of acute disseminated encephalomyelitis.
Active demyelinative lesion (acute plaque) with perivascular collections of mononuclear cells (mostly small lymphocytes) discount 400 mg levitra plus with mastercard erectile dysfunction newsletter. This distinguishes these lesions from infarctions in which both axons and myelin are similarly destroyed buy levitra plus 400mg fast delivery erectile dysfunction pump how do they work. Chronic Plaque with loss of myelin staining, loss of oligodendrocytes and isomorphic gliosis. Isomorphic gliosis usually reflects loss of myelin within myelinated fiber tracts where the astrocytes are believed to be physically forced into this parallel arrangement. Small perivenous foci of complete demyelination with sparse mononuclear cells The perivenular localization is the hallmark of this monophasic disease following vaccinations or viral infections. The pathogenesis is not believed to be direct infection of the nervous system by the virus but an allergic cross-reaction between myelin proteins and homologous viral proteins. Frequent sparing of arcuate or "U" fibers This gross appearance is characteristic of many leukodystrophies; they differ from each other in their microscopic and ultrastructural features. Abnormal myelin breakdown products staining metachromatically (reddish brown) and decrease of myelinated nerve fibers This leukodystrophy in particular also affects the peripheral nerve severely. Clusters of multinucleated and uninucleated globose or globoid cells (top center and bottom left) Instead of metachromasia or inflammation, this leukodystrophy is characterized by the accumulation of globoid cells. The galactocerebrosidase deficiency results in the accumulation of psychosine rather than the expected galactocerebroside. Demyelination in mid-central basis pontis This lesion is most commonly seen after too rapid correction of hyponatremia. It entered our world of medicine when parenteral administration of solutions became available. The lesion is largely one of intramyelinic edema and thus appears to be another example of cytotoxic edema. Vacuolar appearance of intramyelinic edema involving deep cortex and arcuate fibers (bottom) with a barely perceptible increase in cortical astrocytes. This fatal disease of infancy (Canavan’s disease) is usually seen in a localized population (Ashkenazi Jews) and is now known to be due to deficiency of aspartoacylase. In contrast to most leukodystrophies, the cortical arcuate fibers are preferentially involved in this disease. Top: Nodes of Ranvier demarcate normal internodes, each with a single Schwann cell nucleus. Bottom: Remyelinated internodes shorter than normal, and thinner (not shown) Conduction block of action potentials appears early with subsequent breakdown of internodal myelin. Macrophages recruited from the blood stream are the chief removers of myelin sheath. Conduction reappears at reduced velocity as Schwann cell forms new thinner myelin sheaths. Bottom: Short and thin remyelinated internodes flanked by residual internodes of normal length and caliber The combined length of the three new internodes equals the length of the normal internode on the left. This implies that the original internode was replaced by three internodes (and three Schwann cells). Thinly-myelinated nerve fiber surrounded by concentric processes of Schwann cell cytoplasm, resembling a sliced onion (bottom). Longitudinal section of an onion bulb next to normal internodes (top) Onion bulb formation reflects repeated episodes of demyelination and remyelination over a period of months or years, each round producing Schwann cells and redundant cell processes. Some bulbs without a visible myelin sheath, presumably containing a naked axon with insufficient remyelination. The neuropathy in this disease is thought to be caused by T cells and/or autoantibodies acting on the surface membrane of Schwann cells, but target antigens have not been identified in most instances. The diagnostic features of a chronic demyelinative neuropathy are: 1) Segmental demyelination of teased nerve myelinated fibers. Next: Axons and myelin breaking down and blood- borne macrophages appearing to remove debris. Myelin breakdown into a linear train of myelin ovoids (debris) secondary to axonal degeneration. All myelin sheaths distal to the point of transection of the axon have broken down simultaneously to form a series of globules of phagocytosed myelin debris within macrophages, known as myelin ovoids. In the ventral nerve roots, loss of fibers mostly reflects loss of lower motor neurons in the ventral horn, but peripherally motor nerves demonstrate a minor distal axonopathy that may antedate death of the nerve cell.
The cardiovascular system is composed of the heart and a continuous system of blood vessels including arteries proven 400 mg levitra plus impotence beavis and butthead, arterioles purchase 400mg levitra plus fast delivery erectile dysfunction pump nhs, capillaries, venules, and veins. The innermost layer is the tunica intima, which includes a single layer of cells lining the lumen called the endothelium. There are important histological differences in the composition of these layers within each component of this system, which will be explored later in this lab. Valve Ventricle Atrium #17 Heart, Monkey, Sagittal Section (Mallory-Azan) The epicardium includes a layer of simple squamous epithelium called the mesothelium and underlying supportive connective tissue. The epicardium is the outermost layer surrounding the heart, and is comparable to the tunica adventitia of vessels. In the region of the atrium the epicardium contains fatty connective tissue and vessels of the coronary circulation. The distribution of blue-staining collagen fibers reveals the fascicle organization of the myocardium, which is comparable to the tunica media. In areas where muscle 47 fascicles are longitudinally sectioned, note the intercalated discs which appear as red-staining step-like lines perpendicular to the long axis of the fiber. The endocardium contains an endothelium on the free surface and underlying supportive connective tissue. Conduction continues through the atrioventricular bundle of His and into Purkinje fibers of the ventricles. Purkinje fibers are hypertrophied cardiac muscle fibers that are specialized for conducting an impulse rather than for contraction. They contain one or two nuclei, centrally situated in a pale staining mass of sarcoplasm that is rich in mitochondria and glycogen. Major branches of the bundle of His lie outside the myocardium in the subendocardium, as seen on the right side of this slide. Purkinje fibers traverse the myocardium where the terminal From left to right: muscle fiber, connective tissue, branches merge into muscle fascicles. This purkinje fibers, connective tissue, muscle fiber is seen in favorable longitudinal sections as a point where the Purkinje fibers become smaller, more densely stained, and indistinguishable from fascicles of muscle fibers. Individual muscle fibers are grouped in fascicles that are seen in both cross and longitudinal section on this slide. The fascicles are bounded by connective tissue containing blood vessels of the coronary circulation and nerve fibers. Remember that red blood cells are often visible in the lumen of blood vessels, however they will not be present in every lumen due to preparation of the slides. Larger vessels have a common structural plan in that they are composed of three concentric coats or tunics. This consists of the endothelial lining and its basement membrane, and a delicate layer of loose subendothelial connective tissue. The nuclei of the simple squamous epithelial cells of the endothelium protrude into the lumen of the vessel. In arteries and arterioles, an internal elastic membrane delimits the outer margin of the tunica intima. This coat consists predominantly of fibroelastic connective tissue whose fibers generally occur in a longitudinal array. In larger muscular arteries, there is frequently an external elastic membrane separating the tunica adventitia from the tunica media. Arteries have an internal elastic membrane (although it is less distinctive in large elastic arteries). It is predominantly muscular in arterioles and most arteries, but is predominantly elastic in the largest arteries (the so-called elastic arteries) such as the aorta and the common carotid. A useful generalization is that arteries have a relatively thick wall with a small lumen, whereas veins have a relatively thin wall and a broad lumen. Arterioles and small arteries exhibit a distinctive Artery top, vein bottom arrangement of endothelial cells and smooth muscle fibers in their walls.
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