so in a patient with cholinergic crisis, the ach which is increased, it only effects the NMJ nicotinic receptors? or does it affect the entire bodies nicotinic receptors?
so in a patient with cholinergic crisis, the ach which is increased, it only effects the NMJ nicotinic receptors? or does it affect the entire bodies nicotinic receptors?
right, so does that also affect the sympathetic nervous system? as the SANS also uses nicotinic receptors at their ganglia
Entire body. That's why you see a myriad of symptoms, the "DUMBBLSS" symptoms that are due to activation of the parasympathetic NS
D-diarrhea (parasympathetic activity increases gastric motility and gastric secretion)
U-Urination (contract the trigone/bladder muscles + relax the sphincter)
M-Miosis - due to contraction of the pupillary (constrictor) sphincter muscle
B-Bradycardia (parasympathetic action on the M2 receptors of the heart)
B-Bronchoconstriction (M3)
L-Lacrimation
S-Salivation
S-Sweating
It does, but all ganglia get desensitised soon after the initial hyperactivity. Thus all that remains active is the set of postganglionic Ach receptors which are mostly parasympathetic, and thus you see signs of parasympathetic overactivity.
At the nicotinic receptors in ganglia and at the myoneural junction the accumulation of acetylcholine at first leads to an intensification of cholinergic transmission, but with continued accumulation over time, the nicotinic receptors become desensitized. There follows a failure of nicotinic, cholinergic transmission, despite the continued presence of excess transmitter. This results in flaccid paralysis of skeletal muscle and a fall off of sympathetic autonomic function. Parasympathetic autonomic function, however, remains intensified even though the parasympathetic ganglia may have been desensitized. The cholinesterase inhibitor continues to act downstream from the ganglia at the muscarinic site. Thus, at nicotinic synapses, the effects of cholinesterase inhibitors resemble those of nicotine, whereas at muscarinic synapses their effects resemble those of muscarine. Thus, nicotine poisoning resembles anticholinesterase poisoning, but lacks the signs and symptoms referable to stimulation of muscarinic receptors. At both muscarinic and nicotinic sites the effects of cholinesterase inhibitors are, in fact, mediated through acetylcholine leading to the designation of inhibitors as indirectly acting, cholinergic agonists.
Entire body. That's why you see a myriad of symptoms, the "DUMBBLSS" symptoms that are due to activation of the parasympathetic NS
D-diarrhea (parasympathetic activity increases gastric motility and gastric secretion)
U-Urination (contract the trigone/bladder muscles + relax the sphincter)
M-Miosis - due to contraction of the pupillary (constrictor) sphincter muscle
B-Bradycardia (parasympathetic action on the M2 receptors of the heart)
B-Bronchoconstriction (M3)
L-Lacrimation
S-Salivation
S-Sweating