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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A review of three recent cases of death due to childhood asthma revealed consistent themes of depression, emotional precipitation of attacks, unsupportive families, and a tendency to deny asthma symptoms. Possible psychosomatic mechanisms are identified as potentially important for the interaction of emotions and asthma.
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PMID:Psychological factors in fatal childhood asthma. 359 9

There is evidence from pediatric tertiary care centers in the United States that childhood deaths from asthma in hospitalized patients are becoming increasingly rare, while asthma mortality outside the hospital appears to be on the rise. When a young outpatient with asthma dies, the event is apt to be sudden and unanticipated and the victim is likely to be a preadolescent or adolescent who has suffered from asthma most of his or her life and who, despite ongoing bronchodilator therapy, requires hospitalizations for treatment of status asthmaticus. Patients in this age cohort have a strong tendency to underuse, overuse, or neglect to use prescribed medications, possibly as a gesture of emerging independence or because of the depression engendered by a chronic illness. In some instances serious psychosocial pathology accounts for noncompliance. For a patient with chronic asthma with a high-risk profile, any departure from an ongoing treatment regimen may result in respiratory failure. Pathologic complications of asthma may also act to upset the precarious physiologic equilibrium these patients have established. Unsuspected chronic pneumonia may lead to further increases in a chronically high degree of oxygen desaturation. Hypoxic seizures during an asthma attack may precipitate pulmonary edema. Tension pneumothorax has an even greater fatality potential for high-risk patients with asthma than it has for other patients with asthma, and pulmonary hypertension with cor pulmonale may develop because of chronic hypoxia. Some sudden deaths in children with chronic, severe asthma are unassociated with any of the above, making it necessary to entertain still other hypotheses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An analysis of fifteen childhood asthma fatalities. 362

Patients with severe air-flow obstruction receiving mechanical ventilation are at risk of inadvertent pulmonary hyperinflation with morbidity and mortality caused by pneumothorax and circulatory depression. Nine patients with severe air-flow obstruction (5 asthma, 4 chronic air-flow obstruction) requiring mechanical ventilation were studied while sedated and therapeutically paralyzed. Pulmonary hyperinflation during steady-state ventilation was quantified by measuring total exhaled volume during 20- to 40-s apnea (end-inspiratory lung volume, VEI). Patients were studied at 3 levels of minute ventilation (VE) (10, 16, and 26 L/min) and at each VE, 3 levels of tidal volume (VT) (0.6, 1.0, and 1.6 L) and 3 levels of inspiratory flow (VI) (40, 70, and 100 L/min for VT = 1.0 L). There were progressive increases in VEI when VT was increased or when expiratory time (TE) was decreased either by an increase in rate (and hence VE) or by a decrease in VI (at a constant VE) reaching lung volumes as high as 3.6 +/- 0.4 L above FRC. Alveolar, central venous, and esophageal pressure rose in parallel with lung volumes, and hypotension was seen in most patients at highest lung volumes. Peak airway pressure (Ppk) was predominantly related to inspiratory flow and did not reflect changes in lung volume. Levels of ventilation required for normocapnia prior to paralysis (15.7 +/- 2.3 L/min) were associated with hypotension in 7 patients and probable hyperinflation in excess of 1.96 +/- 0.17 L above FRC. VEI is a simple, reproducible measurement of pulmonary hyperinflation and may be more important than Ppk in the causation of barotrauma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of ventilatory pattern on hyperinflation, airway pressures, and circulation in mechanical ventilation of patients with severe air-flow obstruction. 366 41

Right ventricular function was investigated in seven asthmatic patients during an acute attack, using simultaneous bedside right heart catheterization and two-dimensional echocardiography (2DE). Hemodynamic and echocardiographic data were compared during four successive periods of the respiratory cycle: inspiration, early expiration, mid-expiration, and late expiration. During inspiration, 2DE showed a significant increase in right ventricular area at both end-systole and end-diastole. This inspiratory right ventricular enlargement coexisted with a significant reduction in 2DE stroke area and pulmonary artery pulse pressure suggesting an inspiratory reduction in right ventricular stroke output. A transient depression of right ventricular function during deep inspiratory effort in asthma was thus strongly suggested. The negative pressure surrounding the right ventricle at inspiration is advocated as the causative factor enabling reduction in the hydraulic force effecting right ventricular ejection. The highly negative pleural pressure probably holds the right ventricular free wall and restrains its systolic inward motion, as suggested by the finding of a concomitant inspiratory reduction in right ventricular developed pressure and 2DE fractional area contraction.
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PMID:Inspiratory impairment in right ventricular performance during acute asthma. 366 92

Since inhibition of cyclooxygenase precipitates asthmatic attacks in patients with aspirin idiosyncrasy, we have evaluated the effects of pharmacologic inhibition of thromboxane A2 (TXA2) synthetase, next to cyclooxygenase enzyme in arachidonic acid cascade. Sixteen patients with aspirin-induced asthma received increasing doses on 3 days (25 to 400 mg) of an imidazole derivative, OKY-046, which specifically blocks TXA2 synthetase. Twenty-three healthy control subjects received a single dose of 400 mg of OKY-046. In both patients and control subjects, the inhibitor at a dose of 400 mg produced (1) a pronounced fall in thromboxane B2 serum levels, (2) a rise in serum 6-keto-prostaglandin F1 alpha, and (3) a depression in platelet aggregability to arachidonic acid and adenosine diphosphate. The drug, however, neither precipitated attacks of asthma nor impaired pulmonary function tests throughout a 24-hour observation period. Five patients, but none of the control subjects, developed transient nasal congestion about 1 hour after taking the drug. Thus, inhibition of TXA2 synthetase, contrary to inhibition of cyclooxygenase, does not affect bronchopulmonary function in patients with asthma and aspirin intolerance.
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PMID:Effects of inhibition of thromboxane A2 synthesis in aspirin-induced asthma. 369 61

We have obtained physiologic and psychiatric evaluations on five subjects with episodic laryngeal dyskinesia (LD) and compared them with three patients with expiratory laryngeal stridor and asthma (ELS), and five with chronic asthma (CA). Laryngoscopy confirmed adduction of the vocal cords. Diminished inspiratory flow rates with an expiratory/inspiratory ratio of 1.5 to 3.3 was demonstrated by flow volume studies. Flows improved strikingly while breathing an 80 percent helium/20 percent oxygen mixture. Patients with LD showed varying degrees of depression and sought some form of secondary gain. A histrionic personality, conversion or factitious disorders are not an essential part of this syndrome. Tracheostomy may seldom be necessary in the managing of the acute crisis of LD. Reassurance, oxygen, intermittent positive pressure, and sedation may be sufficient. Mildly depressed patients decreased the frequency and severity of wheezing episodes after receiving reassurance and a clear explanation of ventilatory mechanics.
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PMID:Episodic laryngeal dyskinesia. Clinical and psychiatric characterization. 376 75

We have previously demonstrated a depression of airway, vascular, and cutaneous H2-histamine receptor function in sheep with experimental allergic asthma. In the present investigation, we wished to determine if there is a depression of gastric H2-receptor function in subjects with allergic bronchial asthma. In eight normal subjects and seven subjects with allergic bronchial asthma and bronchial reactivity to ragweed antigen, gastric H2-receptor function was assessed by measuring basal and maximal stimulated acid output following pretreatment with a placebo or the H2-antagonist, cimetidine. Maximal stimulated acid output was defined as the peak acid output (PAW mEq/hr) of hydrochloric acid following a subcutaneous injection of histalog (1.5 mg/kg), and selective H2-stimulation as delta PAO = PAOplacebo-PAOcimetidine. While basal acid output was not different between the two groups, mean (+/- SD) PAO was significantly lower in the asthmatic group (14.0 +/- 8.2 mEq/hr) than the normal group (27.9 +/- 9.4 mEq/hr) (p less than 0.01). Mean PAO expressed as percent of predicted maximum was 112 +/- 36 percent in the normal group and 61 +/- 34 percent in the asthmatic group (p less than 0.01). Mean delta PAO was significantly higher in the normal group (17.1 +/- 4.8 mEq/hr) than in the asthmatic group (7.0 +/- 5.3 mEq/hr) (p less than 0.005) indicating suppressed selective H2-receptor stimulation in the latter. We conclude that in subjects with bronchial asthma and marked bronchial hyperreactivity to ragweed antigen, there is a depression of gastric H2-histamine receptor function.
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PMID:Suppression of gastric H2-receptor mediated function in patients with bronchial asthma and ragweed allergy. 395 75

Asthma is a complex and multifactorial illness. Early theories focused on the psychosomatic aspects of this disease and more work has been done through the years to explore these theories and to further elucidate the variety of psychiatric conflicts, personality traits, and stressors, and the role they play in asthma. More recently, mechanisms have been postulated whereby these conflicts can influence the pathologic process in the lungs causing symptoms of asthma. These seem to act at the level of the limbic system and hypothalamus, the autonomic nervous system, and the immunologic system. Many psychiatric factors play a strong role in maintenance of the asthma. Family interactions, anxiety, depression, panic-fear, and many others can facilitate or impede compliance with an appropriate medical regimen. Although all these variables have yet to be sorted out definitively, asthma is certainly an area where psychiatrists can have a major therapeutic impact.
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PMID:Psychiatric aspects of asthma in adults. 407 8

Asthmatic children were matched with a group of nonasthmatic children for sex and age. Scores on content analysis scales representing nine emotional elements on their reactions were compared. Lack of emotional expression was hypothesized but not observed in the asthmatics. The main pattern of reaction identified was of directly and indirectly expressed anger and statements of helplessness, yet many expressions of competence and good feelings. This pattern did not vary according to sex or grade of the children, but only according to age. Preadolescent asthmatic children showed more depression and fewer good feelings than the younger children, and their characteristic pattern was dominated by indirectly expressed anger.
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PMID:Patterns of psychological reaction to asthma in children. 407 81

Data is reviewed on premenstrual symptoms which have been related to high suicide and accident rates, employment absentee rates, poor academic performance and acute psychiatric problems. A recent study of healthy young women indicated that 39% had troublesome premenstrual symptoms, 54% passed clots in their menses, 70% had cyclical localized acneiform eruptions and only 17% failed to experience menstrual pain. Common menstrual disorders are classified as either dysmenorrhea or the premenstrual syndrome. Symptoms for the latter usually begin 2-12 days prior to menstruation and include nervous tension, irritability, anxiety, depression, bloated breasts and abdomen, swollen fingers and legs, headaches, dizziness, occasional hypersomia, excessive thirst and appetite. Some women may display an increased susceptibility to migraine, vasomotor rhinitis, asthma, urticaria and epilepsy. Symptoms are usually relieved with the onset of menses. While a definitive etiological theory remains to be substantiated, symptomatic relief has been reported with salt and water restriction and simple diuretics used 7 to 10 days premenstrually. Diazapam or chlordiazepoxide treatment is recommended before oral contraceptive therapy. The premenstrual syndrome may persist after menopause, is unaffected by parity, and sufferers score highly on neuroticism tests. Primary or spasmodic dysmenorrhea occurs in young women, tends to decline with age and parity and has no correlation with premenstrual symptoms or neuroticism. Spasmodic or colicky pain begins and is most severe on the first day of menstruation and may continue for 2-3 days. Treatment of dysmenorrhea with psychotropic drugs or narcotics is discouraged due to the risk of dependence and abuse. Temporary relief for disabling pain may be obtained with oral contraceptives containing synthetic estrogen and progestogen but the inherent risks should be acknowledged. Both disorders have been correlated to menstrual irregularity. Amenorrhea in many women may be precipitated by simple psychological events such as leaving home, while severely stressful events produce a higher incidence. Unless a physiological factor such as malnutrition is operating, menses usually recur spontaneously within a few months. Amenorrhea is a constant feature of anorexia nervosa and may precede related attitudes toward eating and body weight. This syndrome is best regarded as a chronic and often severe neurotic disorder requiring combined physiological and psychological treatment, although some evidence exists to indicate an endocrine disorder. Extensive basic research is needed on the complex relationship between the neuroendocrine system and emotion.
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PMID:Premenstrual symptoms. 473 36


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