Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Viral myocarditis is the result of a viral infection that produces myocardial necrosis and triggers an immune response to eliminate the viral agent. Many pathogenic mechanisms may contribute to myocardial cell loss including the following: cytokine production contributing to disease severity; viral persistence, which may produce an autoimmune response to cardiac myosin; and viral invasion of vascular endothelium causing vascular spasm with reperfusion injury. The compensatory response of the myocardium to these mechanisms of cell loss is hypertrophy, which results in fibrosis, scarring, and dilation. The myocardial cell loss and physiological response produces a child with fever, lethargy, symptoms of congestive heart failure, cardiogenic shock, or new onset arrhythmias. The initial presentation may be subtle, but if left untreated will go on to produce severe symptoms. The focus of diagnostic studies is to evaluate cardiac function, identify the viral agent, and eliminate other causes of global cardiac dysfunction. Treatment must provide for support of cardiac function through inotropic and afterload-producing agents while providing rest for the stressed cardiac muscle. The nursing care of children with viral myocarditis must focus on continual assessment of the cardiovascular system while supporting the recovery of myocardial function.
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PMID:Viral myocarditis in children. 885 48

A 18-year-old Dutch Warmblood mare was referred for colic. Upon arrival, lethargy, blindness, head pressing, ataxia, and circling were the main clinical signs. On rectal examination a hard mass and oedema around the cranial mesenteric artery were palpated. Plasma liver enzyme activities and the ammonia level were elevated. Atrial fibrillation with a pulse frequency of 36-52 beats per minute was noticed. On both sides a holosystolic murmer with the maximum intensity on the right side could be auscultated. Postmortem examination revealed eccentric hypertrophy of the right atrium and a pale spotted myocardium, most prominently of the right ventricle, with secondary venous congestion of the azygos and mesenteric veins. The liver changes were indicative of chronic congestion. Despite the normal pulse rate, it appeared that congestive heart failure due to cardiomyopathy, was responsible for the presenting symptoms of this patient.
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PMID:Atrial fibrillation associated with central nervous symptoms and colic in a horse: a case of equine cardiomyopathy. 956 65

Chronic severe subclinical systemic hypertension was diagnosed in a 28-yr-old male western lowland gorilla (Gorilla gorilla gorilla). Thoracic radiography, electrocardiography, and echocardiography revealed an enlarged heart with a hypertrophied left ventricle, mitral regurgitation, and a persistent left bundle branch block. Enalapril, later combined with nifedipine, was of some value in reducing the hypertension, with partial reversal of cardiac enlargement and resolution of the bundle branch block. Two years after initiation of treatment, the gorilla developed lethargy and dyspnea. The diagnosis of heart failure was confirmed under anesthesia; the gorilla did not recover and was euthanized. Postmortem examination confirmed congestive heart failure with chronic, fibrosing cardiomyopathy similar to that in other gorillas.
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PMID:Chronic hypertension with subsequent congestive heart failure in a western lowland gorilla (Gorilla gorilla gorilla). 1048 43

A 17-year-old, 1-kg, colony-housed, male squirrel monkey (Samiri sciureus) developed clinical signs of congestive heart failure. The monkey presented with lethargy, increased heart and respiratory rates, and mild abdominal distention. The clinical history, laboratory analysis, and radiographic findings were consistent with heart failure due to dilative cardiomyopathy. Gross and microscopic examination of the heart confirmed a dilative cardiomyopathy. This is the first report describing congestive heart failure caused by dilative cardiomyopathy in a squirrel monkey. Spontaneous dilative cardiomyopathy may be infrequently observed in the squirrel monkeys because they are not routinely housed in the research environment during their advancing years.
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PMID:Dilative cardiomyopathy leading to congestive heart failure in a male squirrel monkey (Saimiri sciureus). 1151 76

Ateleia glazioviana is an important poisonous plant from southern Brazil. Heavy losses in cattle from this region occur each year due to ingestion of the plant. The epidemiological, clinical, gross and histopathological features of A. glazioviana poisoning in cattle are described here from a 5-year field survey in southern Brazil. A. glazioviana poisoning in cattle induces 3 clinical presentations: abortions, disease characterized by lethargy, and cardiac failure. The latter is associated with marked necrosis and fibrosis of the myocardium and can cause sudden death or congestive heart failure.
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PMID:Field observations of Ateleia glazioviana poisoning in cattle in Southern Brazil. 1120 77

A 56-year-old man with persistently elevated liver enzyme levels, fatigue, lethargy and a 9.0 kg weight loss over six months underwent a percutaneous liver biopsy that demonstrated multiple granulomas. Screening serologies were positive for histoplasmosis, and he was started on itraconazole treatment. He returned to hospital the same night with coffee-ground emesis and in Addisonian crisis requiring parenteral steroids and intensive care unit support. An abdominal computed tomography scan revealed bilaterally enlarged, nonenhancing adrenal glands suggestive of infarcts, presumed secondary to histoplasmosis. Treatment was initiated with amphotericin B, and Histoplasma capsulatum was cultured from his urine and cerebrospinal fluid. A serum immunodiffusion test was also positive for both H and M bands, indicating active infection with Histoplasmosis species. His serum and urine samples were also weakly positive for the antigen. Despite complications of renal failure, pneumonia and congestive heart failure, he recovered with medical therapy and was discharged home to complete a prolonged course of itraconazole therapy. While hepatic granulomas often reflect an occult disease process, the cause may remain undiscovered in 30% to 50% of patients despite exhaustive investigations. H capsulatum is an uncommon cause of granulomatous liver disease, and with its protean clinical presentation, a high index of suspicion is needed to make the diagnosis and avoid the potentially high fatality rate associated with disseminated infection.
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PMID:A case of Histoplasma capsulatum causing granulomatous liver disease and Addisonian crisis. 1169 4

Young mice tolerate myocardial loss after coronary artery ligation (CAL) without congestive heart failure (CHF) signs or mortality. We predicted a CHF phenotype after CAL in aged mice. Left coronary artery ligation produced permanent myocardial infarcts (MI). Mortality was higher in male 14-mo-old C57BL/6N mice (Older mice) than in 2-mo-old mice (Young mice) (16 of 25 Older mice died vs. 0 of 10 Young mice, P < 0.02). After 8 wk, rales, weight loss, and lethargy preceded deaths. Captopril (50 mg x kg(-1) x day(-1)) increased Older mouse survival (6 of 22 died, P < 0.02). Captopril improved systolic function (peak aortic blood velocity) from 76 +/- 6% of baseline in untreated Older mice to 93 +/- 8% (P < 0.036). At 24 h, MI comprised 28 +/- 4% of the left ventricle in Young mice, surprisingly larger than that in Older mice (18 +/- 2%, P < 0.011). Endocardial area underlying the infarct scar was significantly larger in Older mice than in Young mice. Captopril did not reduce expansion but markedly reduced septal hypertrophy. Aging reduces compensatory ability in mice despite smaller acute infarcts. Less effective myocardial repair, greater infarct expansion, and septal hypertrophy are seen with aging. Aging is a more relevant murine model of post-MI heart failure in patients.
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PMID:Heart failure and greater infarct expansion in middle-aged mice: a relevant model for postinfarction failure. 1178 10

Many patients develop confusion, lethargy, and cognitive and behavioral abnormalities during or after cardiac decompensation. Congestive heart failure and the accompanying elevation in systemic venous pressure and decrease in cardiac output can lead to changes within the cranial cavity that cause an encephalopathy. At times, excess cerebrospinal fluid accumulates within the cranium causing an apathetic state identical to that seen in patients with other causes of hydrocephalus. Awareness of the syndrome of cardiac encephalopathy and optimal management of congestive heart failure and body fluids can reverse the neurologic dysfunction. In some patients with excess cerebrospinal fluid, lumbar puncture with removal of cerebrospinal fluid can reverse the apathetic state.
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PMID:Cardiac Encephalopathy. 1509 13

A male fennec fox (Fennecus zerda) kit was examined for lethargy, inappetence, and weight loss. Clinical findings included respiratory distress, a gallop rhythm, and retinochoroiditis. Radiography indicated pleural effusion and cardiomegaly. Echocardiographic findings included left ventricular dilatation, low left ventricular ejection fraction, and atrioventricular valvular regurgitation. Necropsy findings were compatible with a diagnosis of congestive heart failure caused by myocarditis. Histopathology showed a disseminated infection with Toxoplasma gondii causing myocarditis, skeletal polymyositis, gastrointestinal myositis, and panuveitis. Toxoplasma-induced myocarditis should be included in the differential diagnosis of heart failure and retinochoroiditis in the fennec fox.
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PMID:Heart failure caused by toxoplasmosis in a fennec fox (Fennecus zerda). 1553 72

An 8-yr-old male meerkat (Suricata suricatta) presented with sudden lethargy. A globular-shaped heart associated with pleural effusion on chest thoracic radiographs was consistent with congestive heart failure, and echocardiography was performed under general anesthesia. It revealed an Ebstein anomaly, with mild pericardial effusion and marked right heart enlargement. The animal was treated with imidapril chlorydrate. After 4 mo of treatment, thoracic radiographs still showed right-sided cardiomegaly; however, the animal appeared clinically normal.
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PMID:Ebstein anomaly in a meerkat (Suricata suricatta). 1573 99


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