Question

Case Study Organophosphate Poisoning

John has a number of prize apple trees in his backyard. To prevent them from becoming infested with insects, he sprayed them with an organophosphate insecticide. He was in a rush to spray the trees before leaving town on vacation, and he failed to pay attention to the safety precautions on the packaging. He sprayed the trees without using any skin or respiratory protection. Soon he experienced severe stomach cramps, double vision, difficulty breathing, and was diagnosed with organophosphate poisoning. While in the emergency room, his physician administered a drug, and soon many of john’s symptoms subsided.

Organophosphate insecticides exert their effects by binding to the enzyme acetylcholinesterase within synaptic clefts, rendering it ineffective. Thus, the organophosphate poison and acetylcholine “compete” for the acetylcholinesterase as the organophosphate poison increases in concentration the enzyme is less effective in degrading acetylcholine. Organophosphate poisons affect synapses in which ACh is the neurotransmitter, including skeletal muscle synapses and some smooth muscle synapses, such as the wall of the stomach, intestines, and air passageways.

Question:
Explain the spastic contractions that occurred in John’s skeletal muscles. Include the function of this enzyme in normal muscle contractions, how increases in acetylcholine and less acetylcholinesterase affects skeletal muscle, what would happen if John did not get to the hospital and why this would happen. To answer this question fully you will write at least a paragraph.

Answer 1

Acetylcholine is the neurotransmitter in the cholinergic system

Acetylcholine is rapidly hydrolysed to choline and acrtic acid by enzymes cholinesterases

There are cholinergic receptors which is of two types muscarinic and nicotinic actions

skeletal muscle actions are mediated by the nicotinic receptors which acts on neuromuscular junctions(NMJ)

At high concentration of ACh ,it initially produces twitching,fasciculatioms followed by prolonged depolarisation of NMJ

So in this case of organ phosphate poisoning there is increase in tge concentration of acetylcholine at the sybaptic cleft causes skeletal muscle spastic contractions

If he doesn't get to the hospital there is central effects which are convulsions,coma and death are usually due to respiratory failure

DIAGNOSIS

History of exposure

characteristic signs and symptoms

Estimating the cholinesterase activity in blood,which is decreased

TREATMENT

Remove the contaminated clothes,wash skin with soap and water

Airway should be maintained

Gastric lavage should be continued till the returning fluid is clear

SPECIFIC MEASURES

1.Atropine: It is the first drug to be given in organophosphate poisoning

2.Oximes:Neuromuscular transmission can be improved by giving cholinesterase reactivators such as pralidoxime,obidoxume