Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During recent years, research in critical care medicine has focused on the role of the gastrointestinal tract in the pathogenesis of multiple organ failure and nosocomial infection, and on preventive measures. Gram-negative bacterial overgrowth of the oropharynx and stomach has been proved to be a cause of nosocomial pneumonia. Topical application of antibiotics into the oropharynx and stomach, and preservation of gastric acidity have been shown to be effective prophylaxis in ventilated patients. Recent studies have demonstrated that gastric alkalinisation is no longer necessary for the prevention of stress ulcer bleeding in critically ill patients. Tissue hypoxaemia, not gastric acidity, is the underlying pathomechanism of stress ulcer bleeding. In experimental investigations, pirenzepine and sucralfate improved gastric mucosal oxygen supply. Both compounds effectively prevent bleeding without increasing gastric pH. In mechanically ventilated patients, significantly lower rates of pneumonia occur with both of these drugs compared with antacids or histamine H2-receptor antagonists. Topical antibiotics (selective digestive decontamination) are most effective in patients with alkaline gastric juice, but of only marginal clinical relevance in those with acidic gastric contents. Isoflurane, propofol and clonidine have been recently investigated for sedation of ventilated patients. Isoflurane may lead to fluoride accumulation after more than 1 day. Propofol dosage has to be increased more often after 4 to 7 days, leading to fat overload and significantly increased costs. Clonidine was highly effective in patients with 'sympathetic overshoot', e.g. those experiencing alcohol or opioid withdrawal. Wound infections are an important problem in burn patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Critical care pharmacotherapy. A review. 768 5

The normal indigenous flora of the human gastrointestinal tract comprises a remarkably complex yet stable colony of more than 400 separate species, living in a symbiotic relationship with the human host. Stability of that flora is accomplished by multiple mechanisms including gastric acidity, gut motility, bile, products of immune cells in the gut epithelium, and competition between microorganisms for nutrients and intestinal binding sites. The indigenous flora influences multiple aspects of physiologic homeostasis and forms a key component of normal host defenses against infection by exogenous pathogens. Critical illness is associated with striking changes in patterns of microbial colonization, best described in the oropharynx and upper gastrointestinal tract. Pathological colonization occurs with the same species that is predominate in nosocomial infections, and descriptive studies suggest that such colonization is a risk factor for infection. Moreover, prophylactic measures that prevent pathological gut colonization in experimental circumstances reduce rates of nosocomial infection in critically ill patients and, in the case of selective decontamination of the digestive tract, reduce mortality risk. Conventional approaches to infectious diseases have conceptualized microorganisms as inimical and focused on eradicating them as rapidly and fully as possible. Insights from the study of critically ill patients suggest that that relationship is better understood as a symbiotic one and that preservation, rather than elimination, of the indigenous flora provides the greatest promise of clinical benefit to this vulnerable population.
 ...
PMID:Gastrointestinal flora and its alterations in critical illness. 1058 83