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)

Body fluid gas pressure and electrolytes of patients with ruptured aneurysm were continuously analyzed. Intracranial pressure (ICP) was regulated at the level of 120-100 mm H2O by cerebral ventricular drainage. There was no significant change in the pH, PCO2, HCO3-, Na+, K+, Ca++ in the cerebrospinal fluid (CSF) of patients with slight or moderate disturbance of consciousness (lethargic-drowsy state). The PcsfO2 of the patients with marked disturbances of consciousness (semicoma-coma) was significantly low. PcsfO2 of the patients with cerebral vasospasm was significantly lower than for those without vasospasms. PcsfO2/PaO2 was 0.27 +/- 0.01 in the patients with vasospasm and 0.50 +/- 0.01 in those with vasospasm. PcsfO2 tended to decrease in patients with markedly bloody CSF. When the bloody CSF was cleared by ventricular drainage, PcsfO2 increased. PcsfO2 did not return to a normal value in the patients with marked disturbances of consciousness despite sufficient arterial oxygen tension. This suggests that PcsfO2 and PcsfO2/PaO2 should provide a convenient index for the prognosis of patients with ruptured aneurysm.
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PMID:Body fluid oxygen tension and prognosis in patients with ruptured aneurysm. 4 45

Extensive water, sodium, chloride, bicarbonate, and potassium losses occur in the diarrheal calf. The water loss is entirely from the extracellular space. In severe cases, hypovolemic shock occurs with the blood volume decreased by as much as one-half. Acidosis, which results from fecal bicarbonate loss, lactic acidosis, and renal dysfunction, results in tissue buffering, which in turn causes the efflux of cellular potassium ions. Although there is a total body potassium deficit, plasma potassium concentration is increased. This, in conjunction with an intracellular deficit, causes weakness, lethargy, and potassium cardiotoxicosis resulting in death. Hypoglycemia also contributes to the weakness and lethargy seem as calves become moribund. These losses from the body and shifts in fluids and electrolytes must be understood to develop the most effective rationale for supportive therapy.
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PMID:Pathophysiologic changes due to coronavirus-induced diarrhea in the calf. 21 8

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

The pathogenesis of the rare hypernatremia, usually described in the literature as "neurogenic" or "essential" hypernatremia, consists of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. As etiology, disturbances of the neoplastic, vascular and degenerative type and malformations in the hypothalamic area are known. In patients with the hypodipsia-hypernatremia syndrome, dysfunction of the anterior pituitary lobe, obesity, abnormal regulation of body temperature, psychomotor retardation and episodic muscular weakness are frequently encountered as additional abnormalities. A 6-year-old patient is described with hypodipsia-hypernatremia syndrome manifest for 3 years. Besides hypernatremia, hypodipsia and the relative insensitivity of the osmoreceptors regulating ADH release, elevated body temperature, polyphagia and obesity, partial hypothalamic-hypophyseal dysfunction, lethargy and psychomotor retardation are the principal findings. An inflammatory lesion or one occupying an intracranial space was not demonstrable until now. Under forced water intake and hypocaloric diet the patient has progressed well with nearly complete normalization of the hypernatremia, body temperature and obesity.
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PMID:Hypodipsia-hypernatremia syndrome. 42 94

Water hemlock is a ubiquitous plant that can be mistaken for a turnip as in the case reported. Oral ingestion causes an explosive illness consisting of nausea, vomiting, abdominal cramps, and grand mal seizures that can progress to cyanosis and death. In the reported case a 30-year old man was found semi-comatose some 75 minutes after ingesting a "turnip". The history revealed profuse emesis shortly after eating lunch that changed from bile to frank blood. There was a mean orthostatic blood pressure change of 30 torr, with an increase in the heart rate of 10%. Neurologic examination revealed a lethargic patient. Following administration of 4 liters of Ringer's lactate the patient's blood pressure stabilized and with continued isotonic fluid maintenance he improved rapidly. This case indicates that appropriate management should be directed toward protecting the patient's airway from gastric aspiration, restoring the intravascular and extracellular volume deficit, and controlling cerebral edema.
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PMID:A case of water hemlock poisoning. 49 28

The effect of colchicine (1 mg/kg intraperitoneally on two successive days) on the absorption of isoniazid, quinidine and sulphafurazole (sulfisoxazole) from the rat small intestine was studied in situ and in vitro. Colchicine produced two different types of histological damage in the small intestine, one with degenerative and the other with regenerative changes predominating. The small intestinal surface area was variably reduced. The colchicine-treated rats were lethargic and hypothermic as compared to controls. Colchicine retarded the disappearance of fluid and all three drugs from the small intestinal lumen in situ 2 days after the first colchicine injection. In vitro the total amounts of fluid and drugs passed through the intestinal wall were not significantly changed by colchicine, although there was a slight tendency towards an increased absorption of quinidine. Hence, colchicine as an antimitotic drug decreases drug absorption from the rat small intestine in situ, apparently due to the decreased surface area of the small intestine, the decreased water flux through the intestinal wall, the retarded intestinal motility and hypothermia of the rats. In vitro the changes are small, which makes the in vitro tests less suitable for studying the effect of colchicine on absorption.
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PMID:Effect of colchicine on drug absorption from the rat small intestine in situ and in vitro. 71 41

Black-tailed prairie dogs (Cynomys ludovicianus) were deprived of food and water for several weeks during the fall and winter in a cold-room hibernaculum (Ta 5-8 degrees C), and for several days at room temperature during the summer. Body temperatures (Tb) were determined periodically in nine animals by radiotransmitters implanted in the abdomen. Animals deprived of food and water in the summer were killed when maximum urine concentration was achieved. Eight animals in the winter were active when killed after 7-35 days in the hibernaculum with Tb between 18 and 36 degrees C. Five animals that became torpid periodically in the winter were killed after 19-42 days in the hibernaculum when their Tb indicated torpor (Tb less than 13 degrees C). Active animals in the summer and winter possessed pronounced renal corticomedullary urea and sodium concentration gradients. Torpid animals lacked these gradients and had lower urine and plasma osmotic concentrations than active animals. Plasma urea values and terminal osmolal U/P ratios were lowest in torpid prairie dogs.
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PMID:Effects of cold exposure and dehydration on renal function in black-tailed prairie dogs. 83 53

In the spring of 1975, many species of waterfowl and common crows (Corvus brachyrhynchos) were found dead in Phelps County, Nebraska. About 25,000 water fowl and at least 3,000 crows died in the epornitic. Few waterfowl were seen dying, but the crows experienced a chronic illness during which they became debilitated and were lethargic and dyspneic. Gross and microscopic lesions in the waterfowl were typical for acute avian cholera. The crows had dark, firm areas within the lungs, loosely adhered yellow fibrous material in the pericardial sac and air sacs and, occasionally, liver abscesses. Microscopically, focal purulent pneumonia was present and a fibrinopurulent exudate overlaid a granulomatous reaction on the heart and lung surfaces. Isolation of Pasteurella multocida serotype 1 confirmed the diagnosis of acute and chronic avian cholera in the waterfowl and crows, respectively.
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PMID:An epornitic of avian cholera in waterfowl and common crows in Phelps County, Nebraska, in the spring, 1975. 86 53

1. An attempt was made to evaluate the pathophysiology of symptoms of hyponatremia as related to changes in brain water and electrolytes. Studies were carried out in 66 hyponatremic patients and 5 groups of experimental animals. 2. In hyponatremic patients, symptoms (depression of sensorium, seizures) correlated well with plasma Na+ (r = 0.64, p less than .001), but there was substantial overlap. In patients with acute hyponatremia, all were symptomatic and 50% died. Among patients with hyponatremia of at least 3 days duration, sympatomatic patients had plasma Na+ (115 +/- 1 mEq/L) which was significantly less (p less than .001) than that of asymptomatic patients (plasma Na+ = 122 +/- 1 mEq/L). Among symptomatic patients, mortality was 12% and 8% had seizures, while none of the asymptomatic patients died or had seizures. 3. Among 14 patients with acute (less than 12 hrs) hyponatremia, the mean plasma Na+ was 112 +/- 2 mEq/L. All such patients had some depression of sensorium and four had grand male seizures. Seven of these patients were treated with hypertonic (862 mM) NaCl, while four were treated only with fluid restriction. Of the seven patients treated with hypertonic NaCl, five survived, while three of four patients treated with fluid restriction died. There was no evidence of circulatory congestion or cerebral damage in the patients treated with hypertonic NaCl. 4. Among rabbits with acute (2-3 hours) hyponatremia (plasma Na+ = 119 +/- 1 mEq/L), all had grand mal seizures and 86% died. All such animals had cerebral edema (brain H2O content 17% above control value) but brain content of Na+, K+ and Cl- was normal. 5. Rabbits with 3 1/2 days of hyponatremia (plasma Na+ = 122 +/- 2 mEq/L) appeared to be asymptomatic, even though brain water content was 7% above normal (p less than .01). 6. Rabbits with 16 days of more severe hyponatremia (plasma Na+ = 99 +/- 3 mEq/L) were weak, anorexic, lethargic and unable to walk. Brain water content was 7% above normal, although brain osmolality (218 +/- 12 mOsm/kg H2O) was similar to plasma (215 +/- 8 mOsm/kg). Brain content of Na+, K+, Cl- and osmoles was 17 to 37% less than normal values, so that the brain established osmotic equilibrium with plasma primarily by means of a loss of electrolytes. 7. These studies suggest that in patients with hyponatremia, symptoms and morbidity are only grossly correlated with either magnitude or duration of hyponatremia. Symptoms appear to correlate best with the interplay between a net increase in brain water versus a loss oof brain electrolytes. However, even asymptomatic animals have subclinical brain edema when plasma Na+ is below 125 mEq/L, and such edema may cause permanent brain damage. Thus, many patients with similar levels of plasma Na+, particularly when they are symptomatic, should probably be treated with hypertonic NaCl infusions.
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PMID:Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. 125 11

The interrelationships between cerebral edema, intracranial pressure (ICP), and cerebral blood flow (CBF) were studied in acute and chronic triethyl tin sulfate treated rats. Prior to pentobarbital anesthesia behavioral observations were made. ICP and regional CBF were measured under steady state conditions and brain water content was determined by vacuum drying of the right cerebral hemisphere. Control and chronic animals were neurologically normal. There were two distinct acute groups: (1) acute low pressure (ALP) animals - alert but tetraperetic, and (2) acute high pressure (AHP) animals - deeply stuporous, with minimal pain response and gross EEG slowing. ICP was significantly elevated only in AHP animals. Hemispheric CBF was significantly reduced in AHP and chronic animals. The interaction of increased pressure and edema (AHP) produced the greatest decrease in CBF, although deep white flows were significantly affected in all experimental groups. Chronic animals had significantly lower flow in four of seven regions compared to ALP animals despite no significant difference in ICP. Water content was significantly increased in all experimental groups with the greatest increase in the chronic animals. In the absence of any significant increase in ICP, cerebral edema appears to cause a significant reduction in cerebral blood flow and this reduction corresponds with the magnitude and location of the edema.
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PMID:Alterations in behavior, brain electrical activity, cerebral blood flow, and intracranial pressure produced by triethyl tin sulfate induced cerebral edema. 125 1


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