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Depression documentation

In view of the well-documented inhibition of dihydrofolate reductase by aminopterin (325), methotrexate (326) and related compounds it is generally accepted that this inhibitory effect constitutes the primary metabolic action of folate analogues and results in a block in the conversion of folate and dihydrofolate (DHF) to THF and its derivatives. As a consequence of this block, tissues become deficient in the THF derivatives, and this deficiency has many consequences similar to those resulting from nutritional folate deficiency. The crucial effect, however, is a depression of thymidylate synthesis with a consequent failure in DNA synthesis and arrest of cell division that has lethal results in rapidly proliferating tissues such as intestinal mucosa and bone marrow (B-69MI21604, B-69MI21605). [Pg.326]

The section was perforated in several locations due to severe, localized wastage on internal surfaces (Fig. 6.23A and B). The cooling water had a history of low-pH excursions, with documented depressions to a pH below 5. The system also had been plagued with high sulfate-reducing bacteria counts. [Pg.150]

The symptoms of hypothyroidism maybe confused with symptoms associated with aging, such as depression, cold intolerance, weight gain, confusion, or unsteady gait. The presence of these symptoms should be thoroughly evaluated and documented in the preadministration assessment and periodically throughout therapy. [Pg.533]

The anxiety disorders are common and surprisingly disabling conditions. Studies on the health economics of generalized anxiety disorder, panic disorder, social anxiety disorders and obsessive compulsive disorder document the cost to the individual and to society. Attention has focused on the major psychiatric disorders such as depression, schizophrenia and the dementias. Studies suggest that many anxiety disorders are of early onset and too often chronic they are quite common and impose a heavy burden on society. More studies will be needed to discern the fine grain in the survey material and to identify more precisely the location and type of societal costs. These factors will vary from country to country, from district to district, between men and women and between various age groups. [Pg.65]

Differentiating between depression and dementia can be difficult, so symptoms of depression should be documented for several weeks prior to initiating therapy for the treatment of depression with AD. Citalopram and sertraline are recommended as first-line agents because of their efficacy in placebo-controlled trials.49 Indications for the use of antidepressants include depression characterized by poor appetite, insomnia, hopelessness, anhedonia, withdrawal, suicidal thoughts, and agitation. [Pg.521]

Interpersonal therapy and cognitive behavioral therapy are types of psychotherapy that have well-documented efficacy for the treatment of MDD. Psychotherapy alone is an initial treatment option for mild to moderate cases of depression, and it may be useful when combined with pharmacotherapy in the treatment of more severe cases of depression. In fact, the combination of psychotherapy and pharmacotherapy can be more effective than either treatment modality alone in cases of severe or recurrent MDD. Psychotherapy can be especially helpful for patients with significant psychosocial stressors, interpersonal difficulties, or comorbid personality disorders.16... [Pg.572]

Androgens are important for general sexual function and libido, but testosterone supplementation is only effective in patients with documented low serum testosterone levels. In patients with hypogonadism, testosterone replacement is the initial treatment of choice, as it corrects decreased libido, fatigue, muscle loss, sleep disturbances, and depressed mood. Improvements in ED may occur, but they should not be expected to occur in all patients.23 The initial trial should be for 3 months. At that time, re-evaluation and the addition of another ED therapy is warranted. Routes of administration include oral, intramuscular, topical patches or gel, and a buccal tablet. [Pg.787]

The equivalence of high and low doses of antidepressants is well known, yet doctors often increase the dose of the antidepressant when their patients do not improve. Why do they do this The official Summary of Product Characteristics for Prozac provides a clue. It notes that in the fixed dose studies of patients with major depression there is a flat dose response curve, providing no suggestion of advantage in terms of efficacy for using higher than the recommended doses . Nevertheless, despite the absence of evidence that higher doses produce better effects, the very same document advises physicians as follows ... [Pg.36]

Treatment Effect in Randomized Clinical Trials A Meta-Analytic Evaluation, Depression and Anxiety 19 (2004) 10-19 Leo, Jonathan, Academic Freedom and Controversy over the Publication of Factually Correct, Publicly Available Information (2009) http //online.wsj.com/public/resources/documents/leo statement for WSJ.htm[25/o4/2009 17 56 46]... [Pg.209]

Both genetic and nongenetic factors play roles in the transmission of mood disorders. The familial nature of mood disorders is well established. Studies over the past 20 years have consistently documented higher rates of mood disorder in the relatives of individuals with major depression and bipolar disorder than in relatives of healthy controls [6,7], The familial aggregation of mood disorders is the outcome of both genetic and environmental factors. [Pg.888]

Adverse effects of copper deficiency can be documented in terrestrial plants and invertebrates, poultry, small laboratory animals, livestock — especially ruminants — and humans. Data are scarce or missing on copper deficiency effects in aquatic plants and animals and in avian and mammalian wildlife. Copper deficiency in sheep, the most sensitive ruminant mammal, is associated with depressed growth, bone disorders, depigmentation of hair or wool, abnormal wool growth, fetal death and resorption, depressed estrous, heart failure, cardiovascular defects, gastrointestinal disturbances, swayback, pathologic lesions, and degeneration of the motor tracts of the spinal cord (NAS 1977). [Pg.171]

For variant angina, reduction in symptoms and nitroglycerin consumption as documented by a patient diary can assist the interpretation of objective data obtained from ambulatory ECG recordings. Evidence of efficacy includes the reduction of ischemic events, both ST-segment depression and elevation. Additional evidence is a reduced number of attacks of angina requiring hospitalization, and the absence of MI and sudden death. [Pg.155]

Assessments that measure changes in symptoms from one session to the next can be quite helpful in documenting progress on reducing anxiety or depression. The therapist or counselor can use those data when discussing progress with other staff, or can even share such data with the client if it is deemed to be useful for the client. I would not share those data in order to confront lack of progress, however, because that would place a client on the defensive. [Pg.172]

Neurological Effects. Neurological effects in hrnnans after acute inhalation exposure to chloroform are well documented because chloroform has been used as an anesthetic for surgery. Inhaled chloroform acts as a depressant on the central nervous system. Chronic inhalation exposure to chloroform resulted in exhaustion, lack of concentration, depression, and irritability in occupationally exposed people (Challen et al. 1958). In a case study, chloroform inhalation for 12 years resulted in psychotic episodes, hallucinations, and convulsions (Heilbmnn et al. 1945). Central nervous system toxicity was observed in humans after oral exposure to chloroform, which suggests that the effects of inhalation and oral exposure are similar. In case reports of patients who intentionally or accidentally ingested several ounces of chloroform, deep coma with abolished reflexes occurred within a few minutes (Piersol et al. 1933 Schroeder 1965 Storms 1973). [Pg.155]

Patients with depression usually do not present initially to mental health professionals. Most visit their primary care physicians, complaining not of depressed mood but of other symptoms of depression. Fatigue, insomnia, loss of appetite, loss of interest in sex, muscle tension, body aches, and poor concentration are all commonly reported. These so-called masked presentations of depression may in part explain the documented failure of primary care physicians to diagnose depression reliably. This underscores the importance of considering depression in the differential diagnosis of physical complaints that appear vague or exaggerated. [Pg.41]

Antidepressants. There are numerous reasons to expect that antidepressants may be helpful in the treatment of AN. First, depressed mood and other symptoms of depression such as anhedonia, decreased energy, poor concentration, and psychomotor retardation are common in cases of starvation from any cause. Second, AN patients and their family members have high rates of comorbid MDD and OCD, illnesses best treated with antidepressant medications. Finally, weight gain is a well-documented side effect of many antidepressants including the tricyclic antidepressants (TCAs) and mirtazapine. [Pg.214]

The excellent clinical efficacy of the TCAs has been well documented and the pharmacokinetic profiles are favourable. The most serious disadvantage of the TCAs lies in their cardiotoxicity. Thus, with the exception of lofepramine, all the tricyclic antidepressants, including maprotiline, block the fast sodium channels in the heart which can lead to heart block and death. Approximately 15% of all patients with major depression die by suicide and a high proportion of these (up to 25%) do so by taking an overdose of TCAs. Such a dose can be as low as 5-10 times the recommended daily dose. [Pg.169]


See other pages where Depression documentation is mentioned: [Pg.5]    [Pg.17]    [Pg.287]    [Pg.527]    [Pg.219]    [Pg.466]    [Pg.586]    [Pg.105]    [Pg.73]    [Pg.27]    [Pg.40]    [Pg.175]    [Pg.380]    [Pg.438]    [Pg.888]    [Pg.308]    [Pg.635]    [Pg.816]    [Pg.1073]    [Pg.1087]    [Pg.1139]    [Pg.1522]    [Pg.27]    [Pg.161]    [Pg.282]    [Pg.74]    [Pg.85]    [Pg.91]    [Pg.300]    [Pg.104]    [Pg.249]    [Pg.295]   


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Major depressive disorders documenting

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