Abnormal plasma reactions

Abnormal plasma reactions often damage the quality of polymer films. Other than the deviation of the reaction conditions from the standard, there are some factors which affect the quality of product significantly. 

The plasma Hp level rises in disease, like the concentration of fibrinogen and orosomucoid (J8, N5), and this is most likely the result of increased synthesis. The degree of abnormality seems largely to follow the activity of the inflammatory reaction of the disease (infections, tumors, aseptic necrosis). Treatment with cortisol will normalize all three of the above-mentioned plasma proteins. We do not yet know the link between inflammatory reaction and the changed synthesis of Hp and the other plasma proteins. A deeper knowledge of Hp synthesis and the pathophysiology of the inflammatory reaction is necessary for proper utilization in clinical work of the individual Hp values found in diseased subjects. 

Neuroleptics increase the toxicity of the sunlight to human skin, causing discolorations and other adverse dermal reactions. Researchers noted this phenomenon, called phototoxicity, and set out to study its effects on cells loaded with the neuroleptics fluphenazine, perphenazine, or thioridazine (Bastianon et al., 2005). They found that exposure of these cells to light caused abnormalities in both the plasma membrane and mitochondria. 

Rates of hepatic synthesis of many plasma proteins are affected by a patient s endocrine status. The effects of some steroid hormones on individual plasma protein levels are given in Table 20-5. The plasma protein levels characteristic of a specific disease may therefore be complicated by the steroid status of a patient and by an inflammatory acute phase reaction. The abnormal steroid status may be the result of an intrinsic hormonal disorder or of treatment with steroid hormones, as in inflammation. 

Behavioral disorders such as anorexia, sleep disturbances, and pain insensitivity associated with hyperammonemia have been attributed to increased tryptophan transport across the blood-brain barrier and the accumulation of its metabolites. Two of the tryptophan-derived metabolites are serotonin and quinolinic acid (discussed later). The latter is an excitotoxin at the N-methyl-D-aspartate (NMDA) glutamate receptors. Thus, the mechanism of the ammonium-induced neurological abnormalities is multifactorial. Normally only small amounts of NH3 (i.e., NH4 ) are present in plasma, since NH3 is rapidly removed by reactions in tissues of glutamate dehydrogenase, glutamine synthase, and urea formation. 

Z3. Zsigmond, E. K., and Eilderton, T. E., Abnormal reaction to procaine and suc-cinylcholine in a patient with inherited atypical plasma cholinesterase Case report. Can. Anaesth. Soc. J. 15, 498-500 (1968). 

In acute infective hepatitis, there is almost invariably a decreased rate of removal of BSP (B37, D7, M21, N5, W31, Z5), rose bengal (K6, S41), and indocyanine green (L5, L8, H27). The BSP plasma disappearance curve shows a reduced slope in the first phase and a flat second phase (D7, II). Abnormal dye handling is one of the most consistent biochemical flndings in acute hepatitis it occurs, as a rule, before bilirubin can be detected in the urine, before the serum bilirubin is elevated or the flocculation reactions become abnormal (N5). 

Though many of these tissue abnormalities remain to be explained, the totality of the abnormalities seen in familial LCAT deficiency provides striking evidence for the importance of the LCAT reaction in plasma lipoprotein metabolism, emd shows how failure to form CE in the plasma can influence the composition and function of tissues. The possibihty that renal glomeruli are particularly sensitive to the composition of plasma lipoproteins clearly deserves to be explored. 

ADVERSE EFFECTS Dronabinol has complex effects on the CNS, including a prominent central sympathomimetic activity that can lead to palpitations, tachycardia, vasodilation, hypotension, and conjunctival injection (bloodshot eyes). Patient supervision is necessary because marijuana-hke highs e.g., euphoria, somnolence, detachment, dizziness, anxiety, nervousness, panic, etc.) can occur, as can more disturbing effects such as paranoid reactions and thinking abnormalities. After abrupt withdrawal of dronabinol, an abstinence syndrome manifest by irritability, insomnia, and restlessness can occur. Because of its high affinity for plasma proteins, dronabinol can displace other plasma protein-bound drugs, whose doses may have to be adjusted as a consequence. Dronabinol should be prescribed with great caution to persons with a history of substance abuse because it also may be abused by these patients. 

Adverse reactions of idoxuridine include such local reactions as pain, pruritus, edema, burning, and hypersensitivity. Systemic administration of idoxuridine by IV injection may be given in an emergency, but this leads to bone marrow toxicities, such as leukopenia, thrombocytopenia, and anemia. It also may induce stomatitis, nausea, vomiting, abnormalities of liver functions, and alopecia. Idoxuridine has a plasma half-life of 30 minutes and is rapidly metabolized in the blood to idoxuracil and uracil. 

---