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Questions and Answers
Which of the following statements about carbachol is true?
Which of the following statements about carbachol is true?
- It is primarily used in the treatment of glaucoma.
- It has a short duration of action.
- It provides miosis for eye surgery. (correct)
- It is commonly used due to its receptor selectivity.
Why is pilocarpine considered less potent compared to ACh and its derivatives?
Why is pilocarpine considered less potent compared to ACh and its derivatives?
- It can penetrate the CNS at therapeutic doses. (correct)
- It is not stable to hydrolysis by AChE.
- It has a quicker onset of action.
- It is a quaternary amine.
What effect does pilocarpine have when applied topically to the eye?
What effect does pilocarpine have when applied topically to the eye?
- Increased intraocular pressure
- Rapid miosis (correct)
- Relaxation of the ciliary muscle
- Dilation of the pupil
Why has the use of pilocarpine for stimulating secretions been limited?
Why has the use of pilocarpine for stimulating secretions been limited?
In which condition is pilocarpine the drug of choice for emergency lowering of intraocular pressure?
In which condition is pilocarpine the drug of choice for emergency lowering of intraocular pressure?
Why is carbachol rarely used despite its high potency?
Why is carbachol rarely used despite its high potency?
What are the two classes of postsynaptic cholinergic receptors?
What are the two classes of postsynaptic cholinergic receptors?
What enzyme is responsible for cleaving acetylcholine in the synaptic cleft?
What enzyme is responsible for cleaving acetylcholine in the synaptic cleft?
What happens when acetylcholine binds to a receptor on a cell?
What happens when acetylcholine binds to a receptor on a cell?
What is the main function of cholinergic receptors on effector organs?
What is the main function of cholinergic receptors on effector organs?
How is choline recycled in the cholinergic neuron?
How is choline recycled in the cholinergic neuron?
Which molecules mediate the activation of specific enzymes in effector cells after binding of ACh to a receptor?
Which molecules mediate the activation of specific enzymes in effector cells after binding of ACh to a receptor?
Which enzyme specifically cleaves acetylcholine into acetate and choline?
Which enzyme specifically cleaves acetylcholine into acetate and choline?
What is the mechanism of action of reversible anticholinesterase agents?
What is the mechanism of action of reversible anticholinesterase agents?
Which reversible AChE inhibitor has a short duration of action due to rapid renal elimination?
Which reversible AChE inhibitor has a short duration of action due to rapid renal elimination?
Where does acetylcholinesterase (AChE) act within the nerve terminal?
Where does acetylcholinesterase (AChE) act within the nerve terminal?
What is the main function of reversible anticholinesterase agents?
What is the main function of reversible anticholinesterase agents?
Which type of receptors can be affected by reversible AChE inhibitors?
Which type of receptors can be affected by reversible AChE inhibitors?
What is the rate-limiting step in acetylcholine synthesis at cholinergic neurons?
What is the rate-limiting step in acetylcholine synthesis at cholinergic neurons?
Which enzyme catalyzes the reaction of choline with acetyl coenzyme A to form acetylcholine in the cytosol?
Which enzyme catalyzes the reaction of choline with acetyl coenzyme A to form acetylcholine in the cytosol?
What is the role of choline in acetylcholine synthesis at cholinergic neurons?
What is the role of choline in acetylcholine synthesis at cholinergic neurons?
Which drug can inhibit the carrier system responsible for transporting choline into the cytoplasm of cholinergic neurons?
Which drug can inhibit the carrier system responsible for transporting choline into the cytoplasm of cholinergic neurons?
What is the fate of acetylcholine after it binds to the receptor at cholinergic neurons?
What is the fate of acetylcholine after it binds to the receptor at cholinergic neurons?
Apart from sweat glands, where else does the postganglionic sympathetic division of sweat glands use ACh?
Apart from sweat glands, where else does the postganglionic sympathetic division of sweat glands use ACh?
What is the intermediate duration of action for neostigmine?
What is the intermediate duration of action for neostigmine?
Which of the following is a therapeutic use of neostigmine?
Which of the following is a therapeutic use of neostigmine?
What adverse effect is NOT associated with neostigmine use?
What adverse effect is NOT associated with neostigmine use?
Why is neostigmine contraindicated when intestinal or urinary bladder obstruction is present?
Why is neostigmine contraindicated when intestinal or urinary bladder obstruction is present?
Which cholinesterase inhibitor has a duration of action longer than neostigmine but still intermediate?
Which cholinesterase inhibitor has a duration of action longer than neostigmine but still intermediate?
What is the main deficiency in patients with Alzheimer's disease that leads to the use of cholinesterase inhibitors like tacrine, donepezil, rivastigmine, and galantamine?
What is the main deficiency in patients with Alzheimer's disease that leads to the use of cholinesterase inhibitors like tacrine, donepezil, rivastigmine, and galantamine?
What is the primary adverse effect associated with reversible anticholinesterase agents such as donepezil, rivastigmine, and galantamine?
What is the primary adverse effect associated with reversible anticholinesterase agents such as donepezil, rivastigmine, and galantamine?
What is the mechanism of action of irreversible anticholinesterase agents like organophosphates?
What is the mechanism of action of irreversible anticholinesterase agents like organophosphates?
Which compound is an irreversible anticholinesterase agent that forms a covalent bond at the active site of AChE?
Which compound is an irreversible anticholinesterase agent that forms a covalent bond at the active site of AChE?
What is required for the restoration of acetylcholinesterase (AChE) activity after irreversible inhibition by organophosphates?
What is required for the restoration of acetylcholinesterase (AChE) activity after irreversible inhibition by organophosphates?
Which of the following is a true statement about the mechanism of action of echothiophate?
Which of the following is a true statement about the mechanism of action of echothiophate?
Which organophosphate compound is used as an insecticide and can bind covalently to AChE?
Which organophosphate compound is used as an insecticide and can bind covalently to AChE?
What is the major disadvantage of tacrine compared to other anticholinesterases?
What is the major disadvantage of tacrine compared to other anticholinesterases?
Which anticholinesterase agent permanently inactivates AChE by forming a covalent bond at its active site?
Which anticholinesterase agent permanently inactivates AChE by forming a covalent bond at its active site?
Why were many irreversible organophosphate anticholinesterases initially developed by the military?
Why were many irreversible organophosphate anticholinesterases initially developed by the military?
What happens to the AChE enzyme after it is covalently modified by echothiophate?
What happens to the AChE enzyme after it is covalently modified by echothiophate?
What is the primary toxic manifestation of toxicity with irreversible AChE inhibitors like organophosphates?
What is the primary toxic manifestation of toxicity with irreversible AChE inhibitors like organophosphates?
Why is pralidoxime (2-PAM) ineffective in treating the central nervous system (CNS) effects of organophosphates?
Why is pralidoxime (2-PAM) ineffective in treating the central nervous system (CNS) effects of organophosphates?
What effect can pralidoxime have on peripheral effects of organophosphates if administered before aging of the alkylated enzyme occurs?
What effect can pralidoxime have on peripheral effects of organophosphates if administered before aging of the alkylated enzyme occurs?
Why is pralidoxime less effective with newer nerve agents that lead to aging of the enzyme complex within seconds?
Why is pralidoxime less effective with newer nerve agents that lead to aging of the enzyme complex within seconds?
In the context of anticholinesterase agents, what does pralidoxime essentially displace on the enzyme?
In the context of anticholinesterase agents, what does pralidoxime essentially displace on the enzyme?
What is the limitation of pralidoxime in reversing the effects of organophosphates if aging of the alkylated enzyme has already occurred?
What is the limitation of pralidoxime in reversing the effects of organophosphates if aging of the alkylated enzyme has already occurred?
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