Uric acid is a purine derivative, increased by purine salvage reactions that convert purines, purine ribonucleosides, and purine deoxyribonucleoside to mononucleotides (incorrect answer 4).
 
Such salvage reactions require much less energy than de novo synthesis (incorrect answers 1, 2). The liver is the major site of purine nucleotide biosynthesis and provides excess purines for other tissues that cannot synthesize purines. 

A defect in hypoxanthine-guanine phosphoribosyl transferase, one of the enzymes of purine salvage, is responsible for purine overproduction and subsequent hyperuricemia observed in Lesch-Nyhan syndrome.

Acetylcholinesterase receptor opens an ion channel, undergoes irreversible conformational changes when exposed to carbamates , it is inactivated in myasthenia gravis

Prothrombin production in the liver is dependent upon Vitamin K intake

The synthesis of urea takes place in the liver by the process called ''Ornithine cycle'' or "Urea cycle"
This cycle was discovered by Hans Krebs and Kurt Henseleit in the year 1932.
The Ornithine cycle is completed in 5 steps:
1. Conversion of ammonia into carbamoyl phosphate
2.The transfer of carbamoyl group from carbamoyl phosphate to ornithine
3. Releasing of the formed citrulline into the cytosol
4. Cleavage of argininosuccinate
5. Hydrolysis of Arginine: The final step involves the hydrolysis of Arginine into urea and ornithine

The enzyme phosphatidate phosphatase converts phosphatidic acid to diacylglycerol during synthesis of triacylglycerides.

The function of adipose tissue is the storage of fatty acids as triacylglycerols in times of plenty and the release of fatty acids during times of fasting or starvation.

Fatty acids taken in by adipocytes are stored by esterification to glycerol-3-phosphate. Glycerol-3-phosphate is derived almost entirely from the glycolytic intermediate dihydroxyacetone phosphate through the action of glycerol-3-phosphate dehydrogenase. Glycolytic enzymes are active in adipocytes during triglyceride synthesis, but those of glycogen degradation (low levels in adipocytes) and gluconeogenesis (ie, glucose-6-phosphatase) are not.

Glycerol kinase is not present to any great extent in adipocytes, so that glycerol freed during lipolysis is not used to reesterify the fatty acids being released.

The enzyme triacylglyceride lipase is turned on by phosphorylation by a cyclic AMP-dependent protein kinase following epinephrine stimulation.