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Inhaled dysfunction

Still technique for treating rib somatic dysfunctions generally relates to the positional finding, anterior or posterior, of the involved rib. A simple relationship between an anterior rib and an inhalation dysfunction and a posterior rib and an exhalation dysfunction is drawn, which also contributes to the initial placement into the freedom of motion followed by engagement of the barriers. Some modification can also be included for pump or bucket handle components as well. [Pg.385]

Glassification of Substance-Related Disorders. The DSM-IV classification system (1) divides substance-related disorders into two categories (/) substance use disorders, ie, abuse and dependence and (2) substance-induced disorders, intoxication, withdrawal, delirium, persisting dementia, persisting amnestic disorder, psychotic disorder, mood disorder, anxiety disorder, sexual dysfunction, and sleep disorder. The different classes of substances addressed herein are alcohol, amphetamines, caffeine, caimabis, cocaine, hallucinogens, inhalants, nicotine, opioids, phencyclidine, sedatives, hypnotics or anxiolytics, polysubstance, and others. On the basis of their significant socioeconomic impact, alcohol, nicotine, cocaine, and opioids have been selected for discussion herein. [Pg.237]

It is not clear if the effects on cranial nerve dysfunction from inhalation exposure are attributable to trichloroethylene or its decomposition products. For example, while a number of limited animal studies report neuropathies associated with exposure to trichloroethylene (Bardodej and Vyskocil 1956 Barret et al. 1987 Lawrence and Partyka 1981 McCunney 1988), there are some animal studies which report that these effects resulted from exposure to the trichloroethylene decomposition product, dichloroacetylene (Barret et al. 1992 Buxton and Hayward 1967 Cavanagh and Buxton 1989 Feldman 1970 Humphrey and McClelland 1944). [Pg.152]

REVIEW OF INHALANTS EUPHORIA TO DYSFUNCTION. Charles Wtn. Sharp,... [Pg.275]

Renal Effects. The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, and few or no nuclear inclusion bodies, reduction in glomerular filtration rate, and azotemia. These effects are irreversible. The acute form is reported in lead-intoxicated children, whose primary exposure is via the oral route, and sometimes in lead workers. The chronic form is reported mainly in lead workers, whose primary exposure is via inhalation. Animal studies provide evidence of nephropathy similar to that which occurs in humans, particularly the acute form (see Section 2.2.3.2). [Pg.64]

Recently, it has been shown that inhalation of MWNTs caused suppression of the systemic immunity without resulting in significant lung inflammation or tissue damage [82,83]. Inhaled MWNTs in fact modified the functionality of spleen cells in exposed mice [82]. Notably, the activity of cyclooxygenase (COX) enzymes in spleen was affected as a response to a cytokine (TGF(5) released from the lungs. This cytokine activated the COX pathway in the spleen, triggering T-cell dysfunction and systemic immunosuppression [83]. [Pg.192]

Botulism. Clinical features include symmetric cranial neuropathies (i.e., drooping eyelids, weakened jaw clench, and difficulty swallowing or speaking), blurred vision or diplopia, symmetric descending weakness in a proximal to distal pattern, and respiratory dysfunction from respiratory muscle paralysis or upper airway obstruction without sensory deficits. Inhalational botulism would have a similar clinical presentation as food-borne botulism however, the gastrointestinal symptoms that accompany foodborne botulism may be absent. [Pg.372]

Histamine also occurs naturally in plant tissues. It arises from the decomposition of histidine, but its function has not been elucidated. Histamine levels in some plants are surprisingly high - 1,340 pg/g in the blossoms of the spinach plant ( ). It is the exposure of man and animal to this botanical histamine with a possible physiological action that makes histamine of agricultural importance. The inhalation of cotton dust, for instance, has been related to byssinosis, a respiratory disease involving a lung dysfunction. [Pg.302]

In humans, the most important effect associated with inhalation exposure to 2-hexanone is neurological dysfunction, most commonly observed as peripheral neuropathy. Widespread attention was brought to this phenomenon after a 1973 outbreak of distal neuropathy in an Ohio fabric... [Pg.21]

Prockop L, Couri D. 1977. Nervous system damage from mixed organic solvents. In Sharp CW, ed. Review of inhalants Euphoria to dysfunction. Washington, DC U.S. Government Printing Office,... [Pg.83]

HPA suppression In responsive patients, inhaled corticosteroids may permit control of asthmatic symptoms with less HPA suppression. Because these agents are absorbed and can be systemically active, the beneficial effects in minimizing or preventing HPA dysfunction may be expected only when recommended dosages are not exceeded. Take particular care in observing patients postoperatively or during periods of stress for evidence of a decrease in adrenal function. [Pg.753]

DPIs do not utilize Freon propellants, but use either with or without lactose as vehiculum. These devices have a clinical efficacy similar to standard metered-dose inhalers, but may be easier to use in selected patients, since a minimal inspiratory flow rate is necessary to inhale from a DPI. Therefore, the DPI may be difficult for patients with an insufficient inspiratory flow rate, which occurs in children, the elderly, people with severe COPD shared with diaphragm dysfunction, and during an exacerbation. The inspiratory flow rate is associated with the internal resistance of the device used. For instance the turbuhalor has a significant internal resistance and its delivered dose is dependent from the inspiratory flow rate. [Pg.640]

Yohimbine (4.43) is an antagonist. Yohimbine, an indole alkaloid closely related to reserpine—an a antagonist—has been evaluated as a potential treatment for male erectile dysfunction. Naphazoline (4.46) and other a-agonist imidazoline compounds are nasal decongestants, used by inhalation to decrease swelling of the nasal mucosa. Overdependence on and overuse of these drugs can lead to rebound swelling. [Pg.230]

Most drugs used in anaesthesia are metabolised in the liver by phase I reactions, mediated by cytochrome P-450 enzymes. These are susceptible to destruction by cirrhosis, so that the biotransformation of drugs, such as opioids (except morphine), benzodiazepines, barbiturates, and inhalational agents, may be markedly altered in severe liver disease. These enzymes are found in the centrilobular areas, which are more prone to hypoxia. In contrast, the enzymes responsible for phase II reactions, found predominantly in the peripheral areas, often function normally even in advanced disease. The disposition of benzodiazepines that are eliminated primarily by glucuronidation, e.g. lorazepam and oxazepam, are unaffected by chronic liver disease. For drugs with low hepatic extraction, advanced hepatocytic dysfunction decreases phase I and II biotransformation with a reduced clearance and prolongation of the elimination half-life. This is often partially offset by an increased free fraction due to decreased protein binding. [Pg.286]

Deaths due to ingestion or inhalation of 1,2-dichloroethane have been attributed to circulatory and respiratory failure repeated exposures in the occupational environment have been associated with anorexia, nausea, abdominal pain, irritation of the mucous membranes, dysfunction of liver and kidney and neurological disorders (lARC, 1979). [Pg.513]


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See also in sourсe #XX -- [ Pg.486 , Pg.487 , Pg.488 ]




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