- Joined
- Oct 7, 2014
- Messages
- 524
- Reaction score
- 810
Not sure if this is the right place to post Step 1 questions, but this has been bugging me for a long time now.
Backstory to question:
There are two types of Cholinomimetic agents: 1) Direct agonists 2) Indirect agonists
From what I understand, Direct agonists affect mainly muscarinic receptors.
Indirect agonists (anticholinesterases) affect both muscarinic and nicotinic receptors.
Cholinesterase inhibitor poisoning results in the symptoms known as DUMBBELSS:
Diarrhea,
Urination,
Miosis,
Bronchospasm,
Bradycardia,
Excitation of skeletal muscle and CNS,
Lacrimation,
Sweating, and
Salivation).
Where Excitation of Skeletal muscle and CNS are d/t extra stimulation of Nicotinic receptors.
This is where my question is:
Nicotinic Receptors are found in these areas:
1) Between pre and post synaptic nerves of BOTH sympathetic and parasympathetic NS.
2) NMJ of skeletal muscle in somatic NS
3) Brain
4) Adrenal medulla
Overstimulation of nicotinic receptors at site 1 would cancel out since it's both sympathetic and parasympathetic- so no effect there. At site 2 and 3 it would cause the excitation of skeletal muscle and CNS seen in cholinesterase inhibitor poisoning.
QUESTION: Why is there no stimulation of the adrenal medulla to release Epi & Norepi ??!??! Why wouldn't ACh levels rise here as well?
One hypothesis: This drug works by inhibiting ACh degradation, for there to be ACh at the adrenal medulla in the first place, there would need to be sympathetic stimulation. So theoretically it will only OVER-stimulate medulla if the person's sympathetic system is active at the moment?
Sorry for the long post and my spelling/grammar, any replies appreciated!
Backstory to question:
There are two types of Cholinomimetic agents: 1) Direct agonists 2) Indirect agonists
From what I understand, Direct agonists affect mainly muscarinic receptors.
Indirect agonists (anticholinesterases) affect both muscarinic and nicotinic receptors.
Cholinesterase inhibitor poisoning results in the symptoms known as DUMBBELSS:
Diarrhea,
Urination,
Miosis,
Bronchospasm,
Bradycardia,
Excitation of skeletal muscle and CNS,
Lacrimation,
Sweating, and
Salivation).
Where Excitation of Skeletal muscle and CNS are d/t extra stimulation of Nicotinic receptors.
This is where my question is:
Nicotinic Receptors are found in these areas:
1) Between pre and post synaptic nerves of BOTH sympathetic and parasympathetic NS.
2) NMJ of skeletal muscle in somatic NS
3) Brain
4) Adrenal medulla
Overstimulation of nicotinic receptors at site 1 would cancel out since it's both sympathetic and parasympathetic- so no effect there. At site 2 and 3 it would cause the excitation of skeletal muscle and CNS seen in cholinesterase inhibitor poisoning.
QUESTION: Why is there no stimulation of the adrenal medulla to release Epi & Norepi ??!??! Why wouldn't ACh levels rise here as well?
One hypothesis: This drug works by inhibiting ACh degradation, for there to be ACh at the adrenal medulla in the first place, there would need to be sympathetic stimulation. So theoretically it will only OVER-stimulate medulla if the person's sympathetic system is active at the moment?
Sorry for the long post and my spelling/grammar, any replies appreciated!
