Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In man, high doses of the "group 1" inhalation anesthetics (diethylether, cyclopropane, and fluroxene) produce relatively minor depression of ventricular function, although it is possible to depress the heart if the dose is great enough. The "group 2" drugs (halothane, methoxyflurane, etc.) produce dose-related depression in cardiac function, but reasonable caridac outputs and blood pressure can be maintained at light anethetic levels. Much the same can also be said for the intravenous barbiturates and other hypnotics. If ventilation is supported and hypovolemia avoided, large doses of the narcotic analgesics appear to produce minimal cardiac effects. The only intravenous drug which stimulates the heart is the dissociative anesthetic ketamine, and this is probably an autonomic, reflex phenomenon (as with group 1 inhalation anesthetics). Regional anesthesia and the neuromuscular blocking drugs appear to have relatively little effect on ventricular function. Most of the work in man on the effect of anesthetics has been in healthy patients or volunteers. The effects on patients with severe heart or other systemic disease may well be different. In fact, low concentrations of fluroxene have been shown to produce significant depression of stroke volume in patients with aortic vavular disease in contrast to the effects on healthy volunteers. All potent central nervous system depressant drugs possess the potential for significant cardiac depression. If such depression is undersirable in a particular patient, the only safe way to administer anesthesia is by careful titration of the dose against the best measurement of cardiac function which is available. At the present time, this would mean measuring at least direct arterial pressure, central venous pressure, and a continuous electrocardiogram. The optimal management would prpbably include recording systolic time intervals, pulmonary capillary wedge pressure, and some measure of cardiac output as well. All the skill and pharmacologic knowledge available connot substitute for vigilant monitoring and carful tiration of drug dose in the clinical situation.
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PMID:Effect of anesthetics on the heart. 24 Nov 24

Pruritus is usually caused by a primary disorder of the skin, but can also be caused by a systemic disease (Table 1). Some dermatologic conditions that cause pruritus can be inconspicuous or nonspecific (Table 2), while others are usually apparent on physical examination (Table 3). Classification of pruritus as localized (Fig. 1) vs. generalized (Fig. 3) can be helpful in arriving at a correct diagnosis. The history and physical examination are the most important diagnostic tools, though laboratory testing for systemic disease may be necessary. In refractory cases, one should consider occult systemic disease (such as malignancy), psychiatric disease (especially depression), and HIV infection. Subsequent referral to a dermatologist may be indicted. When treatment of the underlying cause of pruritus is not possible, antihistamines and topical agents (menthol, phenol, and/or pramoxine) can be helpful.
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PMID:Pruritus: a practical approach. 135 41

Thirty-three cases of infective endocarditis presenting during a 6.5 year period to a district general hospital were analysed retrospectively. The annual incidence was 22 cases per million population. Twenty-two cases had pre-existing cardiac disease, mainly valvular disease-usually rheumatic (nine cases) and prosthetic valves (10 cases). Recognizable precipitants such as recent surgery were uncommon. Two cases presented after deliberate drug overdose possibly due to depression exacerbated by systemic disease. Symptoms were usually non-specific. All but two cases had murmurs and most were pyrexial. Splinter haemorrhages and clubbing were seen in about 20% of cases. Viridans-type streptococci were the commonest infecting organisms (14 cases). Staphylococcal infection (six cases) was confined to intravenous drug abusers and patients with prosthetic valves. Five cases were culture negative. Cardiac failure was present in 13 cases at presentation and developed in seven others during treatment. Acute valve replacement was necessary in eight cases, and late replacement in three. Renal impairment (plasma urea > 8 mmol/l and/or plasma creatinine > 120 mumol/l) occurred in 19 cases during the course of their illness. Embolic phenomena occurred in 12 patients and mostly involved the central nervous system. In the 8 fatal cases, the cause of death was cardiac failure in six, cerebrovascular accident in one, and myocardial infarction in one. Four of the six patients who subsequently died of cardiac failure had been referred for surgery. Both those who were not referred had coexisting medical problems. Factors associated with increased mortality were age, male sex, cardiac failure (P < 0.01), renal impairment (P < 0.05), and embolic phenomena (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Infective endocarditis in a district general hospital. 143 86

In this prospective study of 35 patients hospitalized for depression, TSH levels were measured before and after stimulation by TRH. The type of depression was determined and its intensity was evaluated by means of the HARD scale. Subjects with systemic disease or receiving treatments known as being likely to influence TSH levels had been excluded. In none of these 35 patients was the TSH level below the lower limit of normal values, nor was there any blunting of response to TRH. These results suggest that depression is not a cause of TSH fall and that a low TSH level with normal hormonaemia must call for scintiscanning, even in depressed subjects.
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PMID:[Ultrasensitive TSH and thyroliberin test in patients hospitalized for depression]. 190 59

In AIDS, as previously found in pernicious anemia (PA), the earliest serum marker of subnormal vitamin B12 (cobalamin) absorption, and therefore of negative B12 balance, is low serum holotranscobalamin II (holo-TC II; B12-TC II) despite normal total serum B12 level, normal serum homocysteine, and normal classic (oral free radio-B12) Schilling test. This may be accompanied by subtle and insidious damage to hematopoietic, immunologic, neuropsychiatric, nutritional and alimentary systems, confirmed by correction on therapeutic trial with B12 therapy. Our studies suggest such selective B12 deficiency occurs in about half of the HIV-1 infected, in part due to frequent depression of B12 absorption by HIV-1 attack on the gastric mucosa and/or opportunistic infection attack on the small bowel, and in part due to a telescoping of the continuum of the stages of negative B12 balance in relation to damage to B12 delivery by the infective and/or systemic disease process. In AIDS, when total serum B12 is normal despite tissue depletion of B12, if the classic Schilling test does not reveal subnormal food B12 absorption, the food Schilling test does. We hypothesize that DNA-synthesizing cells of the hematopoietic, immunologic, neurologic and other systems which have surface receptors solely for holo-TC II, and which have low B12 stores, rapidly become dysfunctional due to B12 deficiency when holo-TC II is low, while cells (such as liver cells) which also have surface receptors for holohaptocorrin (B12-haptocorrin) remain B12-replete. We believe this to be another example of the concept of selective nutrient deficiency in one cell line but not another.
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PMID:Low holotranscobalamin II is the earliest serum marker for subnormal vitamin B12 (cobalamin) absorption in patients with AIDS. 233 79

Between 10 and 30% of depressed patients, mostly bipolar, develop a therapy-resistant illness. The known causes of such chronic evolutions are discussed: misdiagnosis (underlying schizophrenia, personality disorder or dementia), drug-induced depression (neuroleptics), systemic disease (hypothyroidism, multiple sclerosis, cardiovascular or neoplastic disease etc.), or lack of efficacy (drug compliance, insufficient dosage). Remedies are suggested: adequate dosage, drug combination (Newcastle cocktail. tricyclic antidepressant + MAOI, imipramine + T3), carbamazepine in lithium-resistant cases, alprazolam, reduction in vanadium intake, sleep deprivation, psychosurgery.
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PMID:The management of resistant depression. 308 16

Family physicians and general practitioners see the majority of patients with uncomplicated rheumatic disease, yet information on database collection and clinical judgment in such practices is limited. Trained patients with uncomplicated rheumatic disease (standardized patients) were used to evaluate these abilities in 26 family physicians at the University of Arizona College of Medicine in blinded, but previously consented to, brief new encounters. Ability to formulate an assessment and to plan was evaluated as well as ability to collect diagnostic information. Few physicians explored the psychosocial impact of the illness (4 percent) or the role of depression (0 percent). In the brief encounter with a localized complaint, little inquiry was directed to systemic disease (46 percent). Physicians more uniformly asked about the chief complaint (96 percent) and time of onset (88 percent). Physical examination items most commonly omitted were evaluation of systemic joint involvement (69 percent) and muscle wasting in the involved area (59 percent). Referral occurred on 15 percent of encounters and patient education occurred in 62 percent. Three quarters of physicians developed an adequate assessment and virtually all developed an adequate patient care plan.
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PMID:Assessing clinical judgment with standardized patients. 387 26

Depression and anxiety were measured during the course of a double-blind, placebo-controlled trial of the histamine H2-receptor antagonist, ranitidine (150 mg twice daily), in patients suffering from duodenal ulcer but free of systemic disease. There were 25 patients in the ranitidine group (mean age: 33.2 years) and 28 in the placebo group (mean age: 37.2 years). In both groups there was a highly significant and progressive decrease in depression and anxiety scores over the 4 weeks of treatment. There were no instances of mental confusion. In our group of otherwise physically healthy patients, ranitidine appeared to be free of neuropsychiatric complications.
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PMID:Effect of the H2-receptor antagonist ranitidine on depression and anxiety in duodenal ulcer patients. 633 Jul 16

Inflammatory periodontal disease arises as a response to bacterial plaque. This response, however, may be modified by systemic factors such as nutritional deficiency, hormonal imbalance or severe systemic disease. One such systemic disease that may modify host response to local etiologic factors is systemic lupus erythematosus (SLE). Depression of thrombocyte production is very rarely associated with SLE. A search of the medical literature has revealed only one such reported case. The case history that follows is of a 17-year-old black female with severe gingivitis and spontaneous gingival bleeding associated with systemic lupus erythematosus and amegakaryocytic thrombocytopenia. It is believed to be the first such case reported in the dental literature. The clinical, radiographic and hematologic findings will be presented and the medical and periodontal therapy discussed.
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PMID:Periodontal disease associated with amegakaryocytic thrombocytopenia in systemic lupus erythematosus. 693 47

The normoxic ventilatory drive contributes to the normal level of ventilation, and the hypoxic ventilatory drive contributes to the maintenance of adequate gas exchange in the presence of ventilation/blood flow maldistribution and increased mechanical load to breathing. This respiratory drive arises principally from stimuli at the carotid chemoreceptors. The reflex cardiovascular responses to hypoxia also contribute to the delivery of O2 to vital organs, and their efficacy depends on the integrity of the respiratory response and the autonomic nervous system as well as the function of the vascular system. Prolonged exposure to hypoxemia from altitude, cyanotic congenital heart disease, and chronic pulmonary disease impair the ventilatory response to hypoxia. In addition, the respiratory and cardiovascular responses to hypoxemia are impaired by familial or acquired abnormalities of the autonomic effector system. There is growing evidence that impaired respiratory response to hypoxemia is a major factor in recurrent respiratory failure in obesity, obstructive pulmonary disease, idiopathic or familial "hypoventilation," and contributes to disturbances in oxygenation during sleep [152, 189, 192, 202]. Although the ventilatory response to hypoxemia was traditionally thought to be resistant to the effects of inhalational anesthetics, barbiturates, and narcotics, there is abundant evidence that in fact the ventilatory response to hypoxia is more sensitive to depression by drugs than the ventilatory response to CO2. In addition, the hemodynamic responses to hypoxia are modified by anesthesia and anesthetic techniques. The clinical implications of these observations are wide. The ventilatory and cardiovascular response to hypoxemia will be altered, and usually depressed by age, disease processes, premedicant and anesthetic drugs, and autonomic blocking drugs. The cardiovascular responses will be modified indirectly by altered ventilatory control due to neuromuscular blocking drugs and controlled ventilation. Thus, not only will the responses to hypoxemia be depressed by anesthesia but the early clinical hemodynamic signs will be modified or absent, or indeed the cardiovascular response will further impair oxygen delivery. Furthermore, it is not only anesthetic doses that impair the reflex respiratory responses, but also subanesthetic doses of inhalational anesthetics and premedicant doses of barbiturates and narcotics. Hence the patient in the perioperative period continues to have impaired respiratory response to hypoxemia. As anesthetic and surgical care extends to older patients, patients with systemic disease, and recipients of cardiovascular peripheral and central drugs, the clinical implications of the impairment of ventilatory and cardiovascular responses to hypoxia, and the maintenance of organ and system function, escalate. Only a few hesitant steps have been taken into this vast arena of clinical and experimental research.
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PMID:Respiratory and cardiovascular responses to hypoxemia and the effects of anesthesia. 702 55


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