Could ACh increase at synapses in the body (in somesynaptic clefts) due to organ
ID: 3509680 • Letter: C
Question
Could ACh increase at synapses in the body (in somesynaptic clefts) due to organophosphate poisoning? Could ACh increase in thecentral nervous system (CNS) due to organophosphate poisoning? Could ACh increase in autonomic ganglia due to organophosphate poisoning? A) yes, yes, yes B) no, no, no C) yes, no, yes D) yes, no, no
Would ACh increase at the neuromuscular junction in skeletal muscledue to organophosphate poisoning? A) yes B) no –there is no ACh at the neuromuscular junction
Should atropine have an effect at neuromuscular junction receptors in skeletal muscle? A) yes, it should (does) block receptors there B) no, it should not (does not) block receptors there
Jeremy’s lower than normal heart rate when he first comes to the emergency department is due to stimulation of ___________________ receptors on heart muscle cell membranes. A) alpha-1 B) beta-1 C) nicotinic D) muscarinic E) B and D
Explanation / Answer
Pathophysiology of Organophosphate Poisoning
ACh is a simple molecule synthesized from choline and acetyl-CoA through the action of choline acetyl-transferase. Neurons that synthesize and release ACh are termed cholinergic neurons. When an action potential reaches the terminal button of a presynaptic neuron a voltage-gated calcium channel is opened. The influx of calcium ions, Ca2+, stimulates the exocytosis of presynaptic vesicles containing ACh, which is thereby released into the synaptic cleft. Once released, ACh must be removed rapidly in order to allow repolarization to take place; this step, hydrolysis, is carried out by the enzyme, AchE. The AchE found at nerve endings is anchored to the plasma membrane through a glycolipid.
ACh receptors are ligand-gated cation channels composed of four different polypeptide. Two main classes of ACh receptors have been identified on the basis of their responsiveness. These are the muscarinic and nicotinic receptors. Both receptor classes are abundant in the human brain. Nicotinic receptors are further divided into those found at neuromuscular junctions and those found at neuronal synapses. The activation of ACh receptors by the binding of ACh leads to an influx of Na+ into the cell and an efflux of K+, resulting in a depolarisation of the postsynaptic neuron and the initiation of a new action potential. When AchE is inhibited ACh accumulates at the synapses, and cholinergic ‘overdrive’ occurs with resulting signs and symptoms characteritistics of the stimulation of the parasympathetic nervous system
Answers:
Answer of 01 st question : A) yes, yes, yes
2nd question: Yes
3rd question: A
Should atropine have an effect at neuromuscular junction receptors in skeletal muscle? A) yes, it should (does) block receptors there B) no, it should not (does not) block receptors there
Jeremy’s lower than normal heart rate when he first comes to the emergency department is due to stimulation of __D_muscarinic________________ receptors on heart muscle cell membranes. A) alpha-1 B) beta-1 C) nicotinic D) muscarinic E) B and D