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In mild retardation special attention in schools or ideally special school can of value 3 buy amaryl 4mg otc. It is a term used for all permanent purchase amaryl 4 mg with mastercard, no-progressive, generalized brain damage in children irrespective of the cause. Usually some degree of spasticity symptoms are combined with mental retardation, but sometimes the mental retardation is minimal or even abscent. Prenatal: acquired disease such as congenital infection Perinatal: (shortly before or after delivery) : asphyxia, cerebral hemorrhage, b. After the first week of life: meningitis, encephalitis, cerebral malaria can also cause cerebral palsy 183 Pediatric Nursing and child health care Clinical Features: 1. Spastic paralysis if the lesion unilateral or spastic paraplegia if the lesion bilateral 2. Regular exercise under the guidance of physiotherapist help in preventing deformity and contracture 2. Parents of such children support and reassurance Prevention: • Proper antenatal and perinatal care, • early recognition of meningitis etc 13. Down’s Syndrome: Down’s syndrome is a chromosomal abnormality involving an extra chromosome (number 21) characterized by a typical physical appearance and mental handicap. Abnormal attachment of chrosomes inherited from parents 184 Pediatric Nursing and child health care Clinical Manifestations: 1. If diagnosed within the first month of life and substitution with thyroid hormone continued regularly the child will have a normal life 3. With late diagnosis and inadequate treatment the child will be severely retarded and handicapped 13. Polyuria, and polydipsia in young children are symptoms to make you think of diabetes mellitus which is not uncommon and is often overlooked Findings of sugar in urine, and an increased blood sugar prove the diagnosis. Addele Pilliteri (1987), Child health Nursing, care of the growing child, Little, Brown and Company. Addele Pilliteri (1992), Maternal and child health Nursing, care of the child bearing and child rearing family, J. A Tiu (1991), Essential Paediatric Nursing, Chelmstord, Kampala 189 Pediatric Nursing and child health care 12. Katharyn May, Laura Mahlmeister (1990), Comprehensive Maternity Nursing, nursing Process and the child bearing family, J. Maurice King, Felicity king (1978), Primary Child Care, a manual for health workers, Oxford University Press. Patricia Wiel and Cadewing, essentials of maternal and Newborn Nursing 2nd edition. Produced in collaboration with the Ethiopia Public Health Training Initiative, The Carter Center, the Ethiopia Ministry of Health, and the Ethiopia Ministry of Education. Important Guidelines for Printing and Photocopying Limited permission is granted free of charge to print or photocopy all pages of this publication for educational, not-for-profit use by health care workers, students or faculty. All copies must retain all author credits and copyright notices included in the original document. Under no circumstances is it permissible to sell or distribute on a commercial basis, or to claim authorship of, copies of material reproduced from this publication. Except as expressly provided above, no part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without written permission of the author or authors. This material is intended for educational use only by practicing health care workers or students and faculty in a health care field. We hope that it will be a good introduction to eye diseases for health science students working in Ethiopia. There are so many books about eye diseases available but hardly any, which are written from the perspective of Ethiopia, where more blind are live. The lecture note is basically focused on the community as well as clinical ophthalmology to introduce the students on the common causes and burden of blindness and their preventive aspect. So it is written for students who are intended to see patients and need to recognize each disease and recommend possible treatment. When looking at a patient with eye disease, the most important skill is to be able to recognize the appearance of each particular disease. In the management of diseases which are beyond their scope are recommended to refer as early as possible. Their main role is to pick problems early and to have an active role in the prevention of blindness. Selected pictures are used to illustrate some anatomical parts and common eye diseases to make note easier and understandable. There are several encouraging signs that there is an increasing awareness of the challenge of treatable and preventable blindness throughout the world. Our country is forming prevention of blindness to try to look realistically at the problem locally. In spite of all this, the number of avoidably blind people in Ethiopia continues to increase faster than the population. We would like to express our appreciation to The Carter Center, Atlanta Georgia for funding the activities in the development of this lecture note all the way through.
The characteristic pathologic abnormality in this disease is numerous Rosenthal fibers that are present in astrocyte processes that line the pial surface buy amaryl 1 mg with mastercard, blood vessels and ependyma cheap 4 mg amaryl overnight delivery. Rosenthal fibers contain large quantities of alpha B-crystallin, which is a small heat shock protein. The role that these inclusions play in the pathogenesis of this disease is unknown. The splitting of myelin disrupts the interperiod line, suggesting that the fluid accumulation, while within the myelin sheath, is extracellular. Generally, areas in which there is close admixture of gray matter with its rich capillary network and white matter with its susceptible myelin sheaths are characteristically at risk. Patients who demonstrate central pontine myelinolysis at autopsy may have been asymptomatic or have shown severe problems such as coma and quadriplegia, depending on the extent of the lesion. Many patients with this disorder are initially hyponatremic and then undergo rapid correction of serum sodium. It is believed that a too rapid correction of the hyponatremia results in extravascular hypernatremia in the affected areas and intramyelinic edema. The recent recognition of this lesion seems to coincide with the advent of intravenous lines, which has allowed clinicians to infuse large quantities of fluids and electrolytes rapidly. Subacute combined degeneration of the spinal cord is due to vitamin B12 deficiency. Vacuolization of the posterior and lateral columns of the spinal cord is seen by light microscopy, and electron microscopy shows intramyelinic edema. N-acetyl- aspartic acid is normally a very abundant amino acid in the mammalian nervous system however its function is completely unknown. Aspartoacylase deficiency is an autosomal recessive disease, primarily affecting those of Ashkenazi Jewish ancestry. It usually presents at 2-6 months of age with psychomotor retardation and hypotonic flaccidity and progresses to spastic quadriparesis, decerebration and seizures. The vacuoles in white matter primarily correspond to the intramyelinic accumulation of fluid. In addition to this, the astrocytes in deep cortex and white matter also become vacuolated. At the 124 ultrastructural level, both protoplasmic and fibrous astrocytes demonstrate elongated mitochondria with abnormal cristae and matrices. The ultrastructural observations suggest that the astrocyte may play a significant role in the pathogenesis of this disease. Diagnosis is made by detecting elevated levels of N-acetyl-aspartic acid in urine. Weakness is the chief symptom, but peripheral neuropathies can also produce sensory and autonomic symptoms with or without motor dysfunction. The clinical findings can help classify patients with neuromuscular disorders (Table I), but they overlap. Therefore, diagnosis often requires serum creatine kinase activity, electrodiagnostic studies and biopsy of muscle or nerve (or both). The two different fiber types can be distinguished and visualized in tissue sections by histochemical stains. Their major functions include maintenance of posture and prolonged, low- intensity motor activity as in jogging. These fibers are recruited for use during vigorous motor activity such as sprinting or lifting heavy weights with maximal exertion. The muscle fibers of a single motor unit are not grouped together but normally are distributed widely over a large area of muscle. All of the fibers of the unit have the same histochemical type, an expression of the capacity of motor neurons to determine muscle fiber type. Two different forms of regeneration occur in the axons: 1) The well-known regenerative response of axons proximal to the site of axotomy. These axonal sprouts can grow and supply adjacent denervated muscle fibers, a phenomenon known as collateral reinnervation. Schwann cells and muscle satellite cells act as the cellular basis of regeneration of myelin sheaths and muscle fibers. As a result, classification of these disorders is based largely on which populations of cells are affected morphologically and clinically. Neuromuscular disorders have been separated into five general categories: myelinopathies, neuronopathies, axonopathies, disorders of neuromuscular transmission, and myopathies. The disorders discussed in this lecture have been selected to illustrate basic pathologic principles of disease in four of these major categories. Disorders of neuromuscular transmission, myasthenic syndromes, will not be discussed. The distinction between motor neuron diseases and peripheral neuropathies is artificial, however, and overlap exists in the functional and structural features of both classes. Symptoms and signs of peripheral neuropathy often begin distally in the extremities and later involve proximal regions of limbs if the disease progresses. The cause of the distal distribution is not understood in detail, but there is presumably more than one mechanism.
The disorders discussed in this lecture have been selected to illustrate basic pathologic principles of disease in four of these major categories cheap amaryl 1mg with visa. Disorders of neuromuscular transmission cheap amaryl 2 mg overnight delivery, myasthenic syndromes, will not be discussed. The distinction between motor neuron diseases and peripheral neuropathies is artificial, however, and overlap exists in the functional and structural features of both classes. Symptoms and signs of peripheral neuropathy often begin distally in the extremities and later involve proximal regions of limbs if the disease progresses. The cause of the distal distribution is not understood in detail, but there is presumably more than one mechanism. If multifocal lesions of nerves are random, then the longer nerve fibers, which serve the distal region of limbs, have a greater probability of being affected than shorter fibers. Examples include the axonopathy of vasculitic neuropathy and the myelinopathy of Guillain-Barre syndrome. In distal axonopathies (dying back neuropathy), interference with axoplasmic flow may account for the greater dysfunction of the longest nerve fibers. Two-thirds of patients suffer an acute infectious illness, often with influenza-like symptoms or diarrhea, one to six weeks prior to the onset of symptoms. In 1976, a large number of people in United States received swine influenza virus vaccine and developed a slightly increased risk of Guillain-Barré syndrome. This was widely publicized and created concern about subsequent 130 vaccination, but other flu vaccines have not been associated with this risk. The symptom spreads over hours and days to involve symmetrically the arms, trunk, face, and, occasionally, the extraocular and pharyngeal muscles. Weakness becomes the most important manifestation and requires ventilatory assistance in about one third of patients. Clinical signs of weakness are associated with depressed or absent deep tendon reflexes. Clinical recovery usually begins two to four weeks after onset of symptoms and continues over the ensuing weeks or months. About 10% of patients die of their disease and another 15% have severe residual disability. Laboratory: Cerebrospinal fluid shows elevation of protein in most patients at maximal weakness but may be normal during the first few days of illness. Deposits of C3d (a fragment of the C3 component of complement) and membrane attack complex (C5b-9) have been observed on the outer (abaxonal) surface Schwann cell membrane of myelin sheaths during the early stage of the disease. Axons are spared relative to demyelination, but nerves often show Wallerian degeneration of mild degree. The cause of this axonal degeneration is not known, but possible mechanisms include a secondary or bystander effect of the inflammatory response or a direct antibody attack of axons as well as myelin sheaths (see below). The loss of axons is thought to be responsible for the residual weakness in 15% of patients who do not recover strength. The earliest pathological event is the migration of lymphocytes across the walls of venules into the endoneurium, where they become "activated" and attract blood- borne monocytes. The monocytes, rather than lymphocytes, attack the myelin sheaths based on electron microscopic examination. The myelin sheath is stripped away and the myelin fragments are phagocytosed by the monocytes, acquiring the 131 morphological features of macrophages. After about one week, the Schwann cells begin to form new myelin sheaths along the denuded segments of axons based on studies of experimental animals. The conduction of action potentials in these nerve fibers is slower than normal but does not produce detectable weakness. Rather, weakness correlates with conduction block and axonal degeneration in this disorder. Peripheral nerves in these patients show axonal degeneration with little or no pathological signs of segmental demyelination. Deposits of C3d, C5b-9 and IgG have been observed on the axolemma, most pronounced at the nodes of Ranvier, in the initial phase of the disease. The monocytes first appear at the nodes and periaxonal space between the axon and the myelin sheath and are later associated with degeneration with subsequent removal of cellular debris. High titer circulating autoantibodies to myelin are found in patients during the active stage of disease. These findings suggest molecular mimicry acting through an immune response to the bacterium. The antibodies to the bacterium could then crossreact and attack carbohydrate epitopes of peripheral nerve myelin and axolemma. The disorder responds to plasmapheresis and intravenous gamma globulin, but treatment with glucocorticoids is often recommended for long-term treatment because it is less expensive. Onion bulbs are produced by repeated cycles of segmental demyelination and remyelination occurring over a period of months or years. The characteristic clinical features include an often childhood onset of weakness in distal leg muscles, very slow progression, atrophy of leg muscles (stork leg or inverted champagne bottle appearance) and foot deformity (pes cavus and hammer toes).