Nerve Agents


This is a video to explain how nerve agents function and why they are so deadly. Nerve agents originated from insecticides. They are highly potent and have been misused in the past for assassinations, terrorist attacks and during warfare. For example, Tabun and sarin gas were first used In the Iran- Iraq War between 1980 and 1988. Thousands of people were killed and even more were injured. In 1995 homemade sarin gas was used in a terrorist attack on the Tokyo subway, 13
people were killed and over 5,000 were injured. Most recently the nerve agent Novichok was used in an assassination attempt on
Sergei and Yulia Skripal. The police officer first to arrive to the scene was also in a life threatening condition, but all three have now managed to recover. Unfortunately a couple of months later, a person unknowingly picked up the perfume bottle used to transport the nerve agent and died due to the exposure. All the victims from these events showed similar symptoms. A person who has been poisoned by a nerve agent may present a few or all of the following: They may have seizures, they may lose consciousness, they can stop breathing (also known as
apnoea), The Pupils may constrict known as “pin-point pupils” Hypersecretion of the lacrimal glands in the eye, salivary glands, sweat glands and bronchial glands in the airways can occur: This causes tears, frothing at
the mouth, profuse sweating and the airways being blocked with mucus. The airways can also constrict and narrow Episodes of fast heart rate (known as
tachycardia) and episodes of slow heart rate (known as bradycardia) may occur separately or periodically after one and other which leads to heart dysrhythmias. Convulsions may start and smaller localised muscle spasms can occur The victim may also feel nauseous or start to vomit And they may face urinary and fecal
incontinence So why do these symptoms present? Well to understand that first of all you have to understand how a normal nerve synapse works. For nervous impulses to travel around the body they have to pass over gaps between neurons called synapses. At these synapses, The arriving nervous impulse triggers the release of neurotransmitters such as acetylcholine into the synaptic cleft. Acetylcholine binds to two types of receptors on the post-synaptic terminal on the other side of the cleft, These two types are: muscarinic receptors which, for example, trigger involuntary muscle contractions for
smooth muscle And nicotinic receptors which can trigger
voluntary muscle contractions for skeletal
muscle. Acetylcholine is then quickly broken down by the enzyme acetylcholinesterase into two parts: choline and acetic acid. This stops the impulse. The choline is then reabsorbed into the pre-synaptic terminal and recycled. So how do nerve agents affect this? Well, typically, there are 3 ways a nerve agent can enter the body – inhalation, ocular absorption or skin contact and ingestion. Different nerve agents have differing severity of symptoms depending on the dose administered. When the nerve agent reaches the synapses in the body its active component, an organophosphate, covalently bonds to the binding sites of
acetylcholinesterase. This bond is permanent until reversed by an antidote. Acetylcholine can’t be broken down and so accumulates in the synaptic cleft. With more Acetylcholine building up, the
receptors on the post-synaptic terminal become overstimulated and the neuron
continuously sends on nervous impulses. Muscarinic, nicotinic or a combination of both receptors can be overstimulated, producing the different symptoms in the victim. How should we treat these life-threatening symptoms? FIRST OF ALL: only trained personnel should approach the contaminated site and attempt to treat the patient! When it comes to treating the symptoms the severity of the symptoms depends on the route of exposure and dose of the nerve agent. Immediate treatment options are split into two categories: Combatting the nerve agent directly to reduce its impact on the patient And stabilising and supporting the patient To combat the nerve agent directly you must: Remove the patient from the contaminated area and remove all contaminated material. Knowing the route of exposure is important as this will inform you if the patient is still in
contact with the source. Atropine is a competitive inhibitor of the nerve agent and will prevent it binding to the Acetylcholinesterase. It must be administered quickly in order to be effective as it will not inhibit organophosphates that have already bonded with
Acetylcholinesterase Pralidoxime chloride is the antidote for nerve agent poisoning. It will allow for regeneration of
Acetylcholinesterase by binding with the
organophosphate and removing it. To stabilise and support the patient you must consider the most life-threatening symptoms: If the patient is struggling to breathe, dry the airways and move the patient so that any saliva or mucus blocking the airways can drain away. If in respiratory arrest the patient will need an artificial respirator and oxygen Salbutamol can also be administered to relax the smooth muscle and widen the
airways A patient suffering from convulsive seizures may be at risk of hurting themselves. You can try and protect them by padding out their surroundings. Diazepam can be administered to stop seizures and convulsions We hope you’ve been able to learn something new about nerve agents today!
Thank you for watching!

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