Liver deficiency

L The answer is a. (Hardman, p 922) Lactulose is a synthetic disaccharide (galactose-fructose) that is not absorbed. In moderate doses, it acts as a laxative. In higher doses, it is capable of binding ammonia and other toxins that form in the intestine in severe liver deficiency and that are believed to cause the encephalopathy. Loperamide is an antidiarrheal opioid lorazepam is a CNS depressant loxapine is a heterocyclic antipsychotic. 

Individuals with a glucose-6-phosphatase (G-6-P —> Glucose, in the liver) deficiency develop a glycogen storage disease. This condition results in hypoglycemia, low blood sugar, accumulation of lactic acid and ketones. Distal kidney tubule excretion of uric acid is inhibited and hyperuricemia (XS uric acid) and gout results. 

Dietaiy sources cereals, pulses, yeast, liver Deficient diseases... 

Iodine occurs to a minute extent (less than 0.001 %) in sea water, but is found in greater concentration, combined in organic form, in certain seaweeds, in oysters and in cod livers. Crude Chile saltpetre, or caliche contains small amounts of sodium iodate, NalOj. from which iodine can be obtained (see below). Some insoluble iodides, for example liiose of silver and mercury(II), occur in Mexico. Iodine is found in the human body in the compound thyroxin in the thyroid gland deficiency of iodine in diet causes enlargement of this gland (goitre). 

Insight from the PPARa Knockout Mouse. PPARa-deficient adult mice are viable, fertile, and healthy, indicating that PPARa is not essential for embryonic development. When adult PPARa-7- mice are treated with fibrates, the characteristic response to PP is abolished, with no liver weight increase, no increase in... 

Cyano- and hydroxocobalamin - both can be converted to the physiologically relevant coenzymes methyl- and 5 -deoxyadenosylcobalamin in the liver -are used for therapeutical applications. When pernicious anemia caused by chronic atrophic gastritis has been diagnosed, it is treated as follows During the first 7 days of treatment, 1000 pg of hydroxocobalamin/d are administered parenterally, usually intramuscularly. Then, the same dose is given once weekly for 4-6 weeks. The aim is to alleviate the deficiency symptoms and at the same time to replenish the stores. Afterwards, 1000 pg hydroxocobalamin should be given parenterally every 2 months lifelong to avoid relapse [1, 2]. 

Glycogenosis type VI (liver myophosphorylase deficiency) gives rise to hepatomegaly and hypoglycemia in childhood. The enzyme involved is under separate genetic control from the muscle isoform and has been assigned to chromosome 14. 

Glycogenosis type VIII (phosphorylase b kinase deficiency) gives rise to myopathy and liver disease, either singly or in combination. Phosphorylase b kinase (PBK) converts the inactive b form of both muscle and liver phosphorylases to the active a forms of the enzymes. The ischemic lactate test sometimes shows a flat result as in McArdle s disease, but is more likely to be normal. Histochemical demonstration of myophosphorylase activity in tissue sections shows a near-normal reaction due to the presence of phosphorylase a. Accumulation of glycogen is modest and found mainly in type 2 (fast-twitch glycolytic) muscle fibers. 

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