Some of the pharmacology regarding the NMJ had been previously mentioned in the pathophysiology section. The rest will be covered here. There are some chemicals that cause irreversible inhibition of the ACh esterase, the enzyme responsible for degrading ACh into choline and acetic acid in the synaptic cleft. This results in the accumulation of ACh throughout the nervous system, resulting in overstimulation of muscarinic and nicotinic receptors. Irreversible inhibitors of ACh esterase include the They are commonly used as an insecticide, such as malathion and parathion. The effects of organophosphates are reversed using a competitive inhibitor such as atropine and/or pralidoxime, which regenerates ACh esterase if given early enough before enzyme aging occurs via hydrolysis of the R group.[8]

Pathophysiological processes related to GAGs are very broad in range due to the ubiquitous nature of GAGs in the body. This section will describe how GAGs are involved in the pathophysiology of various infectious processes as well as a group of rare genetic diseases known as Mucopolysaccharidoses (MPS) related to the metabolism of GAGs.

Firdous Physiology Fulll

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