Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Supravesical urinary diversion using a jejunal conduit may be associated with hyponatremia, hypochloremic-acidosis, hyperkalemia, azotemia, and a clinical picture of nausea, vomiting, dehydration, muscular weakness, elevated temperature, and lethargy. This syndrome is secondary to the loss of sodium chloride into the urine passing through the conduit and absorption of potassium and urea from it. Treatment and prevention of this syndrome consist of adequate supplements of sodium chloride and hydration. Intravenous hyperalimentation as the precipitating factor of a severe form of this syndrome and its successful management are described. The pathophysiology of the jejunal conduit syndrome is also discussed. Great selectivity and extreme caution are recommended with respect to the use of intravenous hyperalimentation in patients with jejunal conduits.
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PMID:The pathophysiology of the jejunal conduit syndrome and its exacerbation by parenteral hyperalimentation. 642 49

Perfusion of 2-deoxy-D-glucose (2-DG) into the IIIrd ventricle (i.c.v.) or intraperitoneal (i.p.) injections produced changes in feeding and other overt behavior, as well as indicative changes in electroencephalograms (EEG). Applications of 2-DG, either i.p. or i.c.v., induced hyperphagia within 4 hr which was then followed by hypophagia for at least 96 hr. EEGs evinced low frequency patterns during the lethargy and ataxia symptoms which were present after i.p. injection. After i.c.v. injections, the low frequency EEG during the lethargy and ataxia were not evident. Present results in connection with prior reports indicate that 2-DG has a long term bimodal effect on feeding which may be mediated through central neurons. Hypophagia after peripheral application of 2-DG appeared to be caused at least as much by concomitant traumatism as by effects on neural control of feeding.
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PMID:Bimodal effect of 2-deoxy-D-glucose on feeding. 689 Nov 21

Terfenadine (5 mg/kg body weight, q12h) and placebo (0.5 grain/dog q12h) were both administered orally as individual agents to 18 dogs with atopy in a double-blinded study. No dog improved. Hyperactivity, polyphagia, lethargy, anorexia, increased pruritus, or ocular discharge were seen in three dogs treated with terfenadine. Under the conditions of the study, terfenadine was not a useful antipruritic agent for the atopic dog.
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PMID:Failure of terfenadine as an antipruritic agent in atopic dogs: results of a double-blinded, placebo-controlled study. 805 74

A four-year-old, male neutered domestic shorthaired cat was presented with a two-week history of nasal and ocular discharge, generalised exfoliative dermatitis, intense pruritus, polydipsia, polyphagia, weight loss, intermittent hindlimb ataxia and lethargy. Cutaneous populations of Malassezia pachydermatis yeast organisms were found to be elevated. The generalised nature of the disease prompted survey radiography which revealed the presence of a cranial mediastinal mass which was subsequently resected and found to be a thymoma. Within six months of surgery, systemic and cutaneous signs had resolved and yeast counts had returned to normal, suggesting a causal relationship between the thymoma and the skin disease.
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PMID:Resolution of exfoliative dermatitis and Malassezia pachydermatis overgrowth in a cat after surgical thymoma resection. 935 5

Equine and canine Cushing's syndrome, both of which are the result of elevated cortisol levels, show some different pathogenetical and clinical features and require different therapeutical approaches. In older horses the equine Cushing's syndrome (ECS) is not uncommon. Nearly all cases result from excessive hormone production in cells of the pars intermedia of the pituitary. Besides elevated levels of adrenocorticotrope hormone (ACTH), high peripheral levels of pro-opiomelanocortin, beta-endorphines and alpha-melanocyte-stimulating hormone can be measured. In middle-aged and geriatric dogs, Cushing's syndrome is the most frequently diagnosed endocrinologic abnormality. 80-85% of cases are pituitary-dependent and 15-20% are caused by cortisol producing tumors of the adrenals. 90% of pituitary lesions can be identified as adenomas, which are localised in most cases in the pars distalis of the gland, but may occur rarely in the pars intermedia, too. Clinical symptoms in both species are characterised by wasting despite good appetite or polyphagia, reduction of muscle mass with altered fat deposition and lethargy. Whereas polydipsia/polyuria is a very common feature in dogs with Cushing's syndrome, in horses it is almost invariably a sign of concurrent secondary diabetes mellitus. A typical symptom in ECS is a continuously growing haircoat (hirsutism), whereas in canine Cushing's syndrome generalised alopecia may bring the owner to consult a veterinarian. The symptoms and diagnostic procedures in a 33-year-old mare are described. Useful diagnostic tests are reviewed with special attention to species differences in reacting to them. The therapeutic approach with dopamine-agonists such as bromocriptine and pergolide as well as cyproheptadine to ECS is reviewed.
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PMID:[Equine Cushing syndrome (ECS). Case report, review of its diagnosis and therapy and substantial differences from Cushing syndrome in dogs]. 962 47

The cardinal clinical manifestations of major depression with melancholic features include sustained anxiety and dread for the future as well as evidence of physiological hyperarousal (e.g., sustained hyperactivity of the two principal effectors of the stress response, the corticotropin-releasing-hormone, or CRH, system, and the locus ceruleus-norepinephrine, or LC-NE, system). Sustained stress system activation in melancholic depression is thought to confer both behavioral arousal as well as the hypercortisolism, sympathetic nervous system activation, and inhibition of programs for growth and reproduction that consistently occur in this disorder. Data also suggest that activation of the CRH and LC systems in melancholia are involved in the long-term medical consequences of depression such as premature coronary artery disease and osteoporosis, the two-three-fold preponderance of females in the incidence of major depression, and the mechanism of action of antidepressant drugs. In addition, recent data reveal important bidirectional interactions between stress-system hormonal factors in depression and neural substrates implicated in many discrete behavioral alterations in depression (e.g., the medial prefrontal cortex, important in shifting affect based on internal and external cues, the mesolimbic dopaminergic reward system, and the amygdala fear system). We have also advanced data indicating that the hypersomnia, hyperphagia, lethargy, fatigue, and relative apathy of the syndrome of atypical depression are associated with concomitant hypofunctioning of the CRH and LC-NE systems. These data indicate the need for an entirely different therapeutic strategy than that used in melancholia for the treatment of atypical depression, and they suggest that this subtype of major depression will be associated with its own unique repertoire of long-term medical consequences.
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PMID:The endocrinology of melancholic and atypical depression: relation to neurocircuitry and somatic consequences. 989 54

Medical records of 10 cats with transient clinical diabetes mellitus were reviewed. At the time diabetes was diagnosed, clinical signs included polyuria and polydipsia (10 cats), weight loss (8 cats), polyphagia (3 cats), lethargy (2 cats), and inappetence (1 cat). Mean (+/- SD) fasting blood glucose concentration was 454 +/- 121 mg/dL, mean blood glucose concentration during an 8-hour period (MBG/8 hours) was 378 +/- 72 mg/dL, and glycosuria and trace ketonuria were identified in 10 and 5 cats, respectively. Baseline serum insulin concentration was undetectable (6 cats) or within the reference range (4 cats) and serum insulin concentration did not increase after i.v. glucagon administration in any cat. Insulin-antagonistic drugs were being administered to 5 cats and concurrent disorders were identified in all cats. Management of diabetes included administration of glipizide (6 cats), insulin (3 cats), or both (1 cat), discontinuation of insulin-antagonistic drugs, and treatment of concurrent disorders. Insulin and glipizide treatment was discontinued 4-16 weeks (mean, 7 weeks) after the initial diagnosis of diabetes was confirmed. At the time treatment for diabetes was discontinued, clinical signs had resolved, mean fasting blood glucose concentration was 102 +/- 48 mg/dL, MBG/ 8 hours was 96 +/- 32 mg/dL, glycosuria and ketonuria were not identified in any cat, and concurrent disorders (except mild renal insufficiency in 1 cat) had resolved. Significant (P < .05) increases occurred in postglucagon serum insulin concentrations, insulin peak response, and total insulin secretion, compared with values obtained when clinical diabetes was diagnosed. Histologic abnormalities were identified in pancreatic islets of 5 cats in which pancreatic biopsies were obtained and included decreased number of islets (4 cats), islet amyloidosis (3 cats), and vacuolar degeneration of islet cells (3 cats). Mean beta cell density was significantly (P < .001) decreased in diabetic cats compared with control cats (1.4 +/- 0.7 versus 2.6 +/- 0.5%, respectively). Cells within islets stained positive for insulin, however, the number of insulin-staining cells per islet and the intensity of insulin staining were decreased in 5 and 2 cats, respectively. Clinical diabetes had not recurred in 1 cat after 6 years, in 4 cats lost to follow-up after 1.5, 1.5, 2.0, and 2.5 years, and in 2 cats that died 6 months and 5.5 years after clinical diabetes resolved. Clinical diabetes recurred in 3 cats after 6 months, 14 months, and 3.4 years, respectively. These findings suggest that cats with transient clinical diabetes have pancreatic islet pathology, including decreased beta cell density, and that treatment of diabetes and concurrent disorders results in improved beta cell function, reestablishment of euglycemia, and a transition from a clinical to subclinical diabetic state.
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PMID:Transient clinical diabetes mellitus in cats: 10 cases (1989-1991). 1005 60

A 16-year-old male was admitted for repeated episodes of hypersomnia, hyperphagia, and abnormal behavior, the first of which was preceded by alcohol and marijuana use. He was started on lithium therapy and lethargy and hyperphagia gradually improved, although he remained oppositional and irritable. After careful evaluation, his symptoms were concluded to meet Critchley's criteria for the diagnosis of Klein-Levin syndrome, which was supported by his response to prophylactic use of lithium.
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PMID:A Sleepy, Hungry Teenager. 1035 85

Menstruation is a biological phenomenon that has been subject of myths and taboos within and among various cultures. These myths distort the reality surrounding menstruation and create ambivalent feelings about the value and usefulness of this function outside of its necessity as mean of reproduction. Thus studies concerning menstruation need to take into account cultural and psychosocial factors that define the meaning, values and behavior associated with this biological phenomenon. According to several studies, 70% of women experience psychological faintness during this menstrual phase, 40% of them have these symptoms at each menstruation and between 3 to 8% of them suffer severely reacquiring medical support. This entity called premenstrual dysphoric disorder is defined by the presence of several symptoms (distress, tension, irritability, moodiness.) with a significant impairment in work or social functioning beginning during the week before and ending within a few days after the onset of menses. Several studies conducted over the past few years suggested that selective serotonin reuptake inhibitors (SSRIs) and serotoninergic tricyclic drugs may be more effective than other types of antidepressants in treating PMS symptoms. Two protocols are proposed; a continuous treatment or intermittent use during few days during pre-menstrual and menstrual phase for several cycles. The objective of the current study was to evaluate the prevalence of a potential premenstrual dysphoric disorder (PMDD) during one menstrual cycle, in a representative sample of general population of Casablanca, according the DSM IV criteria. On the other hand, a questionnaire, available from the authors, was used to explore socio-demographic data. Among 618 women interviewed, 310 met the criteria of a potential PMDD (50.2%). The mean age of the population with PMDD was 32.2 8 years ranging from 20 to 50 years; 54.8% of them were married, 33.9% of them were single and 66.5% of them had between 1 to 4 children. Two third of them were without a professional activity. During this premenstrual phase the following symptoms were found among the whole sample: marked depressive mood, feeling of hopelessness, or self-depreciation thoughts (77.7%, n=241%); difficulty of concentration (65%, n=201); marked change in appetite, overeating or specific food craving (82.8%, n=256); marked affective lability, with sadness tearful and increased sensitivity to rejection (65.8%, n=204); hypersomnia or insomnia (59.7%, n=185); subjective sense of being overwhelmed or out of control (55.7%, n=172); lethargy, excessive fatigability (91.6%, n=283); physical symptoms including breast tenderness, swelling, headache, joint or muscular pain, and a sensation of bloating and weight gain (81.9%, n=253). The most severe symptoms were fatigue and irritability. On the other hand, 73.9% of the sample had a disturbance in their socio-professional lives as a consequence to the psychological disturbances. Half of these women consulted a physician, mostly a general practitioner. These data are in accordance with the literature, confirming that this disorder is common and has a bad impact on mental health and on quality of life of the women suffering from PMDD.
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PMID:[Assessment of premenstrual dysphoric disorder symptoms: population of women in Casablanca]. 1250 65

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.
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PMID:Canine hyperadrenocorticism. 1603 96


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