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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute Respiratory Failure (ARF) results in an inability to maintain gas exchange at a rate commensurate with the demands of the body and results in hypoxemia and/or hypercarbia, the mechanisms of which may be different. Hypoxemia commonly occurs due to Ventilation Perfusion (V/Q) mismatching, intrapulmonary shunt, diffusion defect or hypoventilation. Hypercarpnic respiratory failure may also be multifactorial but is usually due to inhibited central respiratory drive or inefficient respiratory muscle pump. Hypercapnia may occur in upper and lower airways obstruction, respiratory muscle fatigue and occasionally due to excess CO2 production (burns and excessive glucose administration). Issues in management centre around assessment of severity, determining the need for intervention, establishing diagnosis and etiology and institution of specific treatment. Diagnosis of respiratory failure may be made clinically and confirmed by blood gas analysis. Calculation of oxygenation indices will delineate extent of hypoxemia. When evaluating a child with respiratory failure, one should be aware that a child with prominent respiratory symptoms may have non-respiratory disease (i.e. metabolic acidosis, DKA) and conversely, advanced respiratory failure may be present in a child with no respiratory distress (central hypoventilation secondary to drugs, infection) careful assessment of history, complete physical examination and evaluation of lab parameters may clarify the diagnosis. Serial assessment of sensorium, respiratory symptoms, ABG and response to treatment will provide valuable clues to determine the need for intervention. Oxygen, like any drug, must be administered in a prescribed dose, only when indicated with the potential risks borne in mind. A variety of oxygen delivery devices are available; which ever device is used, the resulting FiO2 and devisable end points must be clearly determined. Hazards of oxygen therapy range from retinal damage in premature infants, damage to the alveolar capillary membrane with resultant hypoxemia) atelectasis and decreased mucociliary activity.
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PMID:Acute respiratory failure and oxygen therapy. 1133 23

Debonding of the stem-cement interface and damage accumulation in the cement mantle are basic events that contribute to the long-term failure of cemented hip reconstructions. In this work, a numerical study with these two processes coupled is presented. On the one hand, debonding of the stem-cement interface was simulated by means of a cohesive surface theory that was implemented into an interface finite element. This interface model includes a tensile-shear behavior law, the fatigue failure of the interface, and the friction evolution between both surfaces. On the other hand, damage accumulation in the cement was formulated through the theory of continuum damage mechanics, considering cement damage due to tension, creep under compression, crack closure effects, non-linear damage accumulation and cement residual stresses appearing during polymerisation. This methodology was applied to simulate and compare the degradation process of the cement and stem-cement interface in four different concepts of design: Exeter, Charnley, Elite Plus and ABG II stems. As the actual mechanical properties of the surface of each specific prosthesis are not known, we assumed the same for all of them, distinguishing between polished and matt surfaces. With this assumption, the predicted results showed that the debonding process is very different for each implant depending on the stem geometry. Lower cement deterioration was obtained for the Exeter and ABG II stems, while the lowest stem-cement interface debonding was produced in the Exeter and the Elite Plus stems.
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PMID:A comparative FEA of the debonding process in different concepts of cemented hip implants. 1625 53

A 28-year-old male was admitted for breathlessness, haemoptysis, fever and fatigue. The patient had occupational exposure to silica dust. Arterial blood gas test ABG revealed hypoxemic respiratory failure. Chest CT demonstrated ground glass opacities with interlobular septal thickening and small centrilobular nodules with patchy areas of consolidation in bilateral lungs. He was mechanically ventilated for refractory hypoxemia. The treatment with cyclophosphamide and methylprednisolone lead to recovery and extubation. The final diagnosis was diffuse alveolar haemorrhage due to perinuclear antineutrophil cytoplasmic antibody (ANCA)-associated microscopic polyangiitis (p-ANCA-associated MPA). In a tuberculosis endemic country, for patients presenting with diffuse alveolar haemorrhage (DAH), with history of silica exposure, differential diagnosis of ANCA associated vasculitis must be considered.
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PMID:Microscopic polyangiitis in a case of silica exposure: a rare presentation. 3150 20