Which of the following symptoms of the patient are most likely due to the activation of nicotinic Nm receptors only? A 35-year-old farmer is brought to the emergency room with severe abdominal cramps and vomiting. He refers that he was working in the field with an organophosphate pesticide and presents with all typical symptoms of acetylcholine excess.
A. Salivation, decreased blood pressure B. Difficulty in breathing, miosis C. Diarrhea, sweating D. Bradycardia, urinary urgency E. Diplopia, difficulty in swallowing
Nicotinic poisoning describes the symptoms of the toxic consequences of inhaling or ingesting too much acetylcholine. Nicotinic poisoning can be potentially deadly, although severe or fatal overdoses are quite rare. Some of the most common symptoms of the toxic effect of nicotine include cramps, vomiting, increased salivation, diarrhea, low blood pressure, muscular weakness, and constant tearing of the eyes.
Acetylcholine is a chemical that operates in the brain and bodies of humans and animals. It is the principal neurotransmitter of the parasympathetic nervous system. Too much acetylcholine is linked to depression and many other negative symptoms.
The correct answer to this question is E, Diplopia, difficulty in swallowing. ENM receptors are found in only the motor endplate. The symptoms in this question must be referring to the skeletal muscles because of the location of the ENM receptors. When these receptors are activated, it opens the ion channel up.
When this happens, the endplate becomes depolarized, which is an act called endplate potential. Eventually, this leads to depolarization blockage, which is a block in the skeletal muscles. The muscles of the pharynx become striated, which makes it difficult for the person to swallow. The rest of the answers are caused by muscarinic receptors activation.
Diplopia, difficulty in swallowing-answer: enm receptors are found only in the motor endplate and therefore the symptoms must refer toskeletal muscles. when nm receptor are activated by acetylcholine the ion channel opens soallowing na+ to enter the cell. the endplate membrane become depolarized and thisdepolarization is called endplate potential. if its amplitude reaches the threshold for excitationvoltage-gated na+ channels open, so generating an action potential that propagates thedepolarization and causes the contraction of the skeletal muscle. the endplate depolarizationis short-lasting, since acetylcholine is rapidly metabolized. however when an excessive amountof acetylcholine causes a persistent activation of nm receptors, a loss of electrical excitabilityof the muscle cell occurs. the main reason for this loss is that, even if the membrane is stilldepolarized because of the activation of nm receptors, voltage-sensitive sodium channelsbecome inactivated and therefore not able to open in response to a brief depolarizing stimulus.this loss of electrical excitability in the presence of a depolarized membrane is calleddepolarization blockade. the main consequence of this block in skeletal muscle cells is theparalysis of the muscle. it should be noted that this paralysis is not due to the blockade of nmreceptors but to the persistent activation of those receptors. when the paralysis involves theextrinsic muscles of the eye, diplopia results. the paralysis of the striated muscles of thepharynx causes difficulty in swallowing.a, b, c, d) all these effects are due to the activation of muscarinic receptors.