This document discusses cholinomimetic drugs and acetylcholine (ACh) signaling in the nervous system. It begins by describing the autonomic and somatic divisions of the nervous system. It then discusses how ACh acts as a neurotransmitter at cholinergic synapses in both divisions. Cholinomimetic drugs can be direct agonists that mimic ACh or indirect inhibitors of acetylcholinesterase (AChE) to prolong the actions of endogenous ACh. Examples of direct agonists include pilocarpine and nicotine. Indirect agonists like galantamine and donepezil inhibit AChE. The document provides detailed information on the mechanisms and clinical uses of various cholinomime
The document summarizes the pharmacology of muscarinic receptor blockade. It discusses how atropine and scopolamine are competitive muscarinic antagonists that do not affect nicotinic transmission. It describes the dose-dependent effects of atropine on various tissues and symptoms. Therapeutic uses of muscarinic antagonists include treating bradycardia, peptic ulcers, and bladder problems. Tertiary and quaternary antagonists have distinct properties and uses. M1, M2, and M3 receptor subtypes and their antagonists are also discussed.
This document presents information on parasympathomimetics, which are drugs that mimic the effects of parasympathetic nervous system stimulation. It discusses how parasympathomimetics can directly activate cholinergic receptors through agonists like acetylcholine, muscarine, and pilocarpine. It also describes how anticholinesterase drugs inhibit the acetylcholinesterase enzyme, increasing the availability of acetylcholine at cholinergic synapses. Specific parasympathomimetic drugs discussed include bethanechol, carbachol, pilocarpine, and echothiophate. The document provides details on the mechanisms of action and therapeutic uses of these cholinergic drugs.
The document discusses the parasympathetic nervous system and parasympathomimetic drugs. It provides details on:
- The parasympathetic nervous system originates from the brainstem and sacral region and uses acetylcholine as a neurotransmitter.
- Parasympathomimetic drugs like acetylcholine, muscarine, and anticholinesterases act to stimulate parasympathetic responses. Direct acting drugs activate cholinergic receptors while indirect drugs inhibit acetylcholinesterase.
- These drugs have therapeutic uses for conditions like glaucoma, urinary retention, and myasthenia gravis. Combinations of drugs are sometimes used to achieve optimal effects while minimizing side effects.
Parasympathomimetic or cholinergic drugs act on cholinergic receptors in the parasympathetic nervous system to produce effects similar to parasympathetic stimulation. They have two types of activities: muscarinic and nicotinic. Examples include direct-acting drugs like acetylcholine and indirect-acting anticholinesterases. Anticholinesterases inhibit the enzyme cholinesterase, leading to accumulation of acetylcholine at receptor sites. They are used to treat conditions like glaucoma, myasthenia gravis, Alzheimer's disease, and organophosphate poisoning.
Sympatholytic drugs (Adrenergic blockers) bind to the adrenergic receptors and prevent the action of adrenergic drugs.
These are drugs which block the actions of sympathetic division or catecholamines (adrenaline and noradrenaline).
They are competitive antagonists at both α and β adrenergic receptors.
Parasympatholytics are the drugs that block or inhibit the actions of acetylcholine at postganglionic nerve endings and cholinergic receptors. They are also referred to as anticholinergics or cholinergic blocking agents or antispasmodics.
Anticholinergic drugs include atropine and related drugs- atropine is the prototype. Atropine is obtained from the plant Atropa belladonna. Atropine and scopolamine (hyoscine) are the belladonna alkaloids. They compete with acetylcholine for muscarinic receptors and block this receptors-they are muscarinic antagonists.
This document discusses adrenergic drugs and their mechanisms and uses. It describes the endogenous catecholamines adrenaline, noradrenaline, and dopamine and their synthesis pathways. It explains the two types of adrenergic receptors - alpha and beta - and their subtypes and functions. The document classifies different adrenergic drugs like epinephrine, norepinephrine, isoproterenol, phenylephrine based on their receptor actions and clinical uses. It provides details on indications, mechanisms, effects and adverse reactions of various adrenergic drugs used for cardiovascular, respiratory, metabolic and central nervous system conditions.
This document provides an overview of opioids including their pharmacology, mechanisms of action, classifications, and clinical uses. It discusses how opioids bind to receptors in the central and peripheral nervous systems to produce analgesic and other effects. Opioids are classified based on their receptor activities and include pure agonists, partial agonists, mixed agonist-antagonists, and pure antagonists. The document reviews the central and peripheral effects of opioids as well as their indications, contraindications, and interactions. It also discusses opioid tolerance, dependence, overdose, and withdrawal.
The document summarizes the pharmacology of muscarinic receptor blockade. It discusses how atropine and scopolamine are competitive muscarinic antagonists that do not affect nicotinic transmission. It describes the dose-dependent effects of atropine on various tissues and symptoms. Therapeutic uses of muscarinic antagonists include treating bradycardia, peptic ulcers, and bladder problems. Tertiary and quaternary antagonists have distinct properties and uses. M1, M2, and M3 receptor subtypes and their antagonists are also discussed.
This document presents information on parasympathomimetics, which are drugs that mimic the effects of parasympathetic nervous system stimulation. It discusses how parasympathomimetics can directly activate cholinergic receptors through agonists like acetylcholine, muscarine, and pilocarpine. It also describes how anticholinesterase drugs inhibit the acetylcholinesterase enzyme, increasing the availability of acetylcholine at cholinergic synapses. Specific parasympathomimetic drugs discussed include bethanechol, carbachol, pilocarpine, and echothiophate. The document provides details on the mechanisms of action and therapeutic uses of these cholinergic drugs.
The document discusses the parasympathetic nervous system and parasympathomimetic drugs. It provides details on:
- The parasympathetic nervous system originates from the brainstem and sacral region and uses acetylcholine as a neurotransmitter.
- Parasympathomimetic drugs like acetylcholine, muscarine, and anticholinesterases act to stimulate parasympathetic responses. Direct acting drugs activate cholinergic receptors while indirect drugs inhibit acetylcholinesterase.
- These drugs have therapeutic uses for conditions like glaucoma, urinary retention, and myasthenia gravis. Combinations of drugs are sometimes used to achieve optimal effects while minimizing side effects.
Parasympathomimetic or cholinergic drugs act on cholinergic receptors in the parasympathetic nervous system to produce effects similar to parasympathetic stimulation. They have two types of activities: muscarinic and nicotinic. Examples include direct-acting drugs like acetylcholine and indirect-acting anticholinesterases. Anticholinesterases inhibit the enzyme cholinesterase, leading to accumulation of acetylcholine at receptor sites. They are used to treat conditions like glaucoma, myasthenia gravis, Alzheimer's disease, and organophosphate poisoning.
Sympatholytic drugs (Adrenergic blockers) bind to the adrenergic receptors and prevent the action of adrenergic drugs.
These are drugs which block the actions of sympathetic division or catecholamines (adrenaline and noradrenaline).
They are competitive antagonists at both α and β adrenergic receptors.
Parasympatholytics are the drugs that block or inhibit the actions of acetylcholine at postganglionic nerve endings and cholinergic receptors. They are also referred to as anticholinergics or cholinergic blocking agents or antispasmodics.
Anticholinergic drugs include atropine and related drugs- atropine is the prototype. Atropine is obtained from the plant Atropa belladonna. Atropine and scopolamine (hyoscine) are the belladonna alkaloids. They compete with acetylcholine for muscarinic receptors and block this receptors-they are muscarinic antagonists.
This document discusses adrenergic drugs and their mechanisms and uses. It describes the endogenous catecholamines adrenaline, noradrenaline, and dopamine and their synthesis pathways. It explains the two types of adrenergic receptors - alpha and beta - and their subtypes and functions. The document classifies different adrenergic drugs like epinephrine, norepinephrine, isoproterenol, phenylephrine based on their receptor actions and clinical uses. It provides details on indications, mechanisms, effects and adverse reactions of various adrenergic drugs used for cardiovascular, respiratory, metabolic and central nervous system conditions.
This document provides an overview of opioids including their pharmacology, mechanisms of action, classifications, and clinical uses. It discusses how opioids bind to receptors in the central and peripheral nervous systems to produce analgesic and other effects. Opioids are classified based on their receptor activities and include pure agonists, partial agonists, mixed agonist-antagonists, and pure antagonists. The document reviews the central and peripheral effects of opioids as well as their indications, contraindications, and interactions. It also discusses opioid tolerance, dependence, overdose, and withdrawal.
Adrenergic blocking agents, also known as adrenergic antagonists, block alpha and/or beta receptor sites and have the opposite effect of adrenergic agents. They are classified based on the type of adrenergic receptor they block, including alpha1, alpha2, beta1, beta2, and beta3 receptors. Common uses include treatment of hypertension, heart failure, and benign prostatic hyperplasia. Side effects may include hypotension, tachycardia, and bronchospasm.
This document summarizes cholinergic transmission and the actions of acetylcholine (ACh) as a neurotransmitter. It discusses ACh synthesis, storage, release and metabolism by acetylcholinesterase. It describes the two classes of cholinergic receptors - muscarinic and nicotinic receptors. The document outlines the pharmacological actions and uses of parasympathomimetic drugs like pilocarpine, muscarine, and anticholinesterases. It also discusses the treatment of myasthenia gravis and organophosphate poisoning using anticholinesterases.
This document discusses cholinergic agonists and their mechanisms of action. It describes how acetylcholine is synthesized and metabolized by cholinesterase. It outlines the two main types of cholinergic receptors - muscarinic and nicotinic receptors. Muscarinic receptors have subtypes that mediate various effects in the heart, blood vessels, smooth muscles and exocrine glands. Nicotinic receptors are located at autonomic ganglia and the neuromuscular junction. Some cholinergic drugs like pilocarpine are used clinically for their effects on muscarinic receptors in the eye.
This document summarizes a seminar on sympathomimetic drugs presented by Mohd Fahad and guided by Mohd. Khushtar. It discusses different types of adrenergic drugs including direct, indirect, and mixed acting sympathomimetics. It describes the actions of adrenergic drugs on various organs mediated by alpha and beta receptors. Important drugs are discussed in detail including their uses, doses, preparations, and adverse effects. The document provides an overview of adrenergic pharmacology and the therapeutic uses of sympathomimetic drugs.
The document discusses drugs that affect the autonomic nervous system, including adrenergic agents and adrenergic-blocking agents. It describes how adrenergic agents stimulate the sympathetic nervous system by mimicking norepinephrine and epinephrine. It also discusses the different types of adrenergic receptors, their locations, and their responses to stimulation. Finally, it covers the therapeutic uses, side effects, and interactions of both adrenergic agents and adrenergic-blocking agents.
Sympatholytics, also known as adrenergic antagonists or blocking agents, work in opposition to adrenergic agents by blocking alpha and beta receptor sites. They are classified based on the type of adrenergic receptor they block, including alpha1, alpha2, beta1, beta2, and beta3 receptors. Common alpha blockers include phenoxybenzamine, ergot alkaloids, phentolamine, tolazoline, prazosin, terazosin, doxazosin, and tamsulosin. Common beta blockers mentioned include propanolol, acetabutolol, atenolol, betaxolol, carvedilol, metoprol
cholinergic receptors definetion and classifcation to 1-nicotinic and 2-muscarinic ...and their subtybes ..... then the sites and the mechanism ... and last the drugs effect
This document summarizes a presentation about ganglions and ganglion stimulants and blockers. It defines a ganglion as a cluster of nerve cell bodies in the autonomic nervous system. It describes how ganglion stimulants like nicotine activate nicotinic receptors on postganglionic neurons. These stimulants are used to help people quit smoking by reducing nicotine cravings and withdrawal symptoms. Ganglion blockers inhibit transmission between preganglionic and postganglionic neurons by antagonizing nicotinic receptors. They were previously used to treat hypertension but caused intolerable side effects. The document outlines the mechanisms, effects, uses and side effects of both ganglion stimulants and blockers
Ganglionic stimulants like nicotine can activate nicotinic receptors in autonomic ganglia, resulting in the stimulation of both sympathetic and parasympathetic responses. Although they have limited medical use, nicotine has been used experimentally to help identify nerve fibers. Ganglionic blockers are competitive antagonists at nicotinic receptors that reduce autonomic tone, and were once used to treat hypertension and peptic ulcers but caused intolerable side effects. Trimethaphan is a short-acting ganglionic blocker occasionally used for controlled hypotension. Mecamylamine has been studied for smoking cessation by blocking nicotine's rewarding effects but also causes constipation. Currently there is no significant
cholingeric and Anticholinesterase drug in detail .this ppt contains introduction ,mechanism of action ,pharmacological action ,uses and adverse effect of the drug
Adrenergic agonists and antagonists act on adrenergic receptors. Agonists like epinephrine and norepinephrine directly stimulate receptors, whereas antagonists like prazosin competitively block receptor activation. These drugs have widespread effects throughout the body due to the sympathetic nervous system's role in functions like heart rate, blood pressure, bronchodilation and uterine contraction. Care must be taken with certain drugs that can cause severe side effects like hypotension or bronchospasm.
Adrenergic antagonists are drugs that inhibit the function of adrenergic receptors. There are two main groups - alpha adrenergic blockers and beta adrenergic blockers. Alpha blockers relax smooth muscles in blood vessels and the prostate gland, and are used to treat high blood pressure, BPH, and other conditions. Beta blockers are used to treat high blood pressure, angina, arrhythmias, heart failure, and migraine by blocking the effects of epinephrine and slowing the heart rate. Common alpha blockers discussed are prazosin, tamsulosin, and terazosin, while common beta blockers include propranolol, metoprolol, and aten
This document provides an overview of parasympathomimetic agents or cholinergic drugs. It discusses the organization of the nervous system and types of cholinergic receptors. Cholinergic drugs are classified as directly acting or indirectly acting. Directly acting drugs like choline esters and pilocarpine directly bind to muscarinic and nicotinic receptors. Indirectly acting drugs like physostigmine and neostigmine inhibit acetylcholinesterase and prolong the action of acetylcholine. These drugs have therapeutic uses in conditions like myasthenia gravis and glaucoma. Organophosphate poisoning is also discussed which occurs due to inhibition of acetylcholinesterase.
Anti-adrenergic drugs antagonize the action of adrenaline and related drugs by competitively blocking alpha and/or beta receptors. Alpha blockers such as prazosin are used to treat hypertension and benign prostatic hyperplasia by dilating arteries and reducing prostate tone. Beta blockers like propranolol non-selectively block both beta 1 and 2 receptors and are used for hypertension, angina, arrhythmias and migraine. Drugs for glaucoma work by reducing intraocular pressure through various mechanisms such as decreasing aqueous humor production or increasing outflow.
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine by binding to adrenergic receptors. They can be classified as direct-acting agonists like epinephrine, indirect-acting agonists like amphetamines, or mixed-action agonists like ephedrine. Common uses include pressor agents, cardiac stimulants, bronchodilators, nasal decongestants, CNS stimulants, and anorectics. Examples discussed in more detail include epinephrine, norepinephrine, dopamine, dobutamine, ephedrine, amphetamines, phenylephrine, and pseudophedrine.
Adrenoceptors are membrane bound receptors located throughout the body on neuronal and non-neuronal tissues where they mediate a diverse range of responses to the endogenous catecholamines- noradrenaline and adrenaline.
They are G protein coupled receptors.
Binding of catecholamine to the receptor is responsible for fight or flight response.
Parasympathomimetic or cholinergic drugs mimic the action of the stimulated parasympathetic nervous system. They are classified as direct-acting cholinergic agonists that directly bind to cholinergic receptors, or indirect-acting agonists that inhibit acetylcholinesterase to prolong the action of acetylcholine. Direct agonists like bethanechol are used to treat atonic bladder while indirect agonists like physostigmine and neostigmine are used to treat myasthenia gravis by blocking the antibodies that inhibit acetylcholine receptors. Myasthenia gravis is an autoimmune disorder where antibodies block acetylcholine receptors at the neuromuscular junction, weakening muscles.
This document provides an overview of nitric oxide (NO) including its chemistry, synthesis via nitric oxide synthase (NOS) enzymes, mechanisms of action, roles in various organ systems, and therapeutic applications. Key points discussed include the 3 isoforms of NOS (eNOS, nNOS, iNOS), NO's vasodilatory effects via soluble guanylate cyclase activation, roles in inflammation and the cardiovascular, nervous, and reproductive systems, and use of NO donors and NOS inhibitors for conditions like pulmonary hypertension and erectile dysfunction.
Muscarine is an alkaloid found in the Amanita muscaria mushroom that causes only muscarinic effects. It can cause profuse salivation, lacrimation, sweating, blood vessel dilation and hypotension, miosis, and spasm of accommodation in the eyes. Mushroom poisoning may occur due to ingestion of poisonous mushrooms containing toxins like muscarine, amatoxins, or gyromitrins. Early onset poisoning features muscarinic symptoms like excessive sweating and salivation within 1-2 hours.
Adrenergic blocking agents, also known as adrenergic antagonists, block alpha and/or beta receptor sites and have the opposite effect of adrenergic agents. They are classified based on the type of adrenergic receptor they block, including alpha1, alpha2, beta1, beta2, and beta3 receptors. Common uses include treatment of hypertension, heart failure, and benign prostatic hyperplasia. Side effects may include hypotension, tachycardia, and bronchospasm.
This document summarizes cholinergic transmission and the actions of acetylcholine (ACh) as a neurotransmitter. It discusses ACh synthesis, storage, release and metabolism by acetylcholinesterase. It describes the two classes of cholinergic receptors - muscarinic and nicotinic receptors. The document outlines the pharmacological actions and uses of parasympathomimetic drugs like pilocarpine, muscarine, and anticholinesterases. It also discusses the treatment of myasthenia gravis and organophosphate poisoning using anticholinesterases.
This document discusses cholinergic agonists and their mechanisms of action. It describes how acetylcholine is synthesized and metabolized by cholinesterase. It outlines the two main types of cholinergic receptors - muscarinic and nicotinic receptors. Muscarinic receptors have subtypes that mediate various effects in the heart, blood vessels, smooth muscles and exocrine glands. Nicotinic receptors are located at autonomic ganglia and the neuromuscular junction. Some cholinergic drugs like pilocarpine are used clinically for their effects on muscarinic receptors in the eye.
This document summarizes a seminar on sympathomimetic drugs presented by Mohd Fahad and guided by Mohd. Khushtar. It discusses different types of adrenergic drugs including direct, indirect, and mixed acting sympathomimetics. It describes the actions of adrenergic drugs on various organs mediated by alpha and beta receptors. Important drugs are discussed in detail including their uses, doses, preparations, and adverse effects. The document provides an overview of adrenergic pharmacology and the therapeutic uses of sympathomimetic drugs.
The document discusses drugs that affect the autonomic nervous system, including adrenergic agents and adrenergic-blocking agents. It describes how adrenergic agents stimulate the sympathetic nervous system by mimicking norepinephrine and epinephrine. It also discusses the different types of adrenergic receptors, their locations, and their responses to stimulation. Finally, it covers the therapeutic uses, side effects, and interactions of both adrenergic agents and adrenergic-blocking agents.
Sympatholytics, also known as adrenergic antagonists or blocking agents, work in opposition to adrenergic agents by blocking alpha and beta receptor sites. They are classified based on the type of adrenergic receptor they block, including alpha1, alpha2, beta1, beta2, and beta3 receptors. Common alpha blockers include phenoxybenzamine, ergot alkaloids, phentolamine, tolazoline, prazosin, terazosin, doxazosin, and tamsulosin. Common beta blockers mentioned include propanolol, acetabutolol, atenolol, betaxolol, carvedilol, metoprol
cholinergic receptors definetion and classifcation to 1-nicotinic and 2-muscarinic ...and their subtybes ..... then the sites and the mechanism ... and last the drugs effect
This document summarizes a presentation about ganglions and ganglion stimulants and blockers. It defines a ganglion as a cluster of nerve cell bodies in the autonomic nervous system. It describes how ganglion stimulants like nicotine activate nicotinic receptors on postganglionic neurons. These stimulants are used to help people quit smoking by reducing nicotine cravings and withdrawal symptoms. Ganglion blockers inhibit transmission between preganglionic and postganglionic neurons by antagonizing nicotinic receptors. They were previously used to treat hypertension but caused intolerable side effects. The document outlines the mechanisms, effects, uses and side effects of both ganglion stimulants and blockers
Ganglionic stimulants like nicotine can activate nicotinic receptors in autonomic ganglia, resulting in the stimulation of both sympathetic and parasympathetic responses. Although they have limited medical use, nicotine has been used experimentally to help identify nerve fibers. Ganglionic blockers are competitive antagonists at nicotinic receptors that reduce autonomic tone, and were once used to treat hypertension and peptic ulcers but caused intolerable side effects. Trimethaphan is a short-acting ganglionic blocker occasionally used for controlled hypotension. Mecamylamine has been studied for smoking cessation by blocking nicotine's rewarding effects but also causes constipation. Currently there is no significant
cholingeric and Anticholinesterase drug in detail .this ppt contains introduction ,mechanism of action ,pharmacological action ,uses and adverse effect of the drug
Adrenergic agonists and antagonists act on adrenergic receptors. Agonists like epinephrine and norepinephrine directly stimulate receptors, whereas antagonists like prazosin competitively block receptor activation. These drugs have widespread effects throughout the body due to the sympathetic nervous system's role in functions like heart rate, blood pressure, bronchodilation and uterine contraction. Care must be taken with certain drugs that can cause severe side effects like hypotension or bronchospasm.
Adrenergic antagonists are drugs that inhibit the function of adrenergic receptors. There are two main groups - alpha adrenergic blockers and beta adrenergic blockers. Alpha blockers relax smooth muscles in blood vessels and the prostate gland, and are used to treat high blood pressure, BPH, and other conditions. Beta blockers are used to treat high blood pressure, angina, arrhythmias, heart failure, and migraine by blocking the effects of epinephrine and slowing the heart rate. Common alpha blockers discussed are prazosin, tamsulosin, and terazosin, while common beta blockers include propranolol, metoprolol, and aten
This document provides an overview of parasympathomimetic agents or cholinergic drugs. It discusses the organization of the nervous system and types of cholinergic receptors. Cholinergic drugs are classified as directly acting or indirectly acting. Directly acting drugs like choline esters and pilocarpine directly bind to muscarinic and nicotinic receptors. Indirectly acting drugs like physostigmine and neostigmine inhibit acetylcholinesterase and prolong the action of acetylcholine. These drugs have therapeutic uses in conditions like myasthenia gravis and glaucoma. Organophosphate poisoning is also discussed which occurs due to inhibition of acetylcholinesterase.
Anti-adrenergic drugs antagonize the action of adrenaline and related drugs by competitively blocking alpha and/or beta receptors. Alpha blockers such as prazosin are used to treat hypertension and benign prostatic hyperplasia by dilating arteries and reducing prostate tone. Beta blockers like propranolol non-selectively block both beta 1 and 2 receptors and are used for hypertension, angina, arrhythmias and migraine. Drugs for glaucoma work by reducing intraocular pressure through various mechanisms such as decreasing aqueous humor production or increasing outflow.
Sympathomimetic drugs mimic the actions of norepinephrine and epinephrine by binding to adrenergic receptors. They can be classified as direct-acting agonists like epinephrine, indirect-acting agonists like amphetamines, or mixed-action agonists like ephedrine. Common uses include pressor agents, cardiac stimulants, bronchodilators, nasal decongestants, CNS stimulants, and anorectics. Examples discussed in more detail include epinephrine, norepinephrine, dopamine, dobutamine, ephedrine, amphetamines, phenylephrine, and pseudophedrine.
Adrenoceptors are membrane bound receptors located throughout the body on neuronal and non-neuronal tissues where they mediate a diverse range of responses to the endogenous catecholamines- noradrenaline and adrenaline.
They are G protein coupled receptors.
Binding of catecholamine to the receptor is responsible for fight or flight response.
Parasympathomimetic or cholinergic drugs mimic the action of the stimulated parasympathetic nervous system. They are classified as direct-acting cholinergic agonists that directly bind to cholinergic receptors, or indirect-acting agonists that inhibit acetylcholinesterase to prolong the action of acetylcholine. Direct agonists like bethanechol are used to treat atonic bladder while indirect agonists like physostigmine and neostigmine are used to treat myasthenia gravis by blocking the antibodies that inhibit acetylcholine receptors. Myasthenia gravis is an autoimmune disorder where antibodies block acetylcholine receptors at the neuromuscular junction, weakening muscles.
This document provides an overview of nitric oxide (NO) including its chemistry, synthesis via nitric oxide synthase (NOS) enzymes, mechanisms of action, roles in various organ systems, and therapeutic applications. Key points discussed include the 3 isoforms of NOS (eNOS, nNOS, iNOS), NO's vasodilatory effects via soluble guanylate cyclase activation, roles in inflammation and the cardiovascular, nervous, and reproductive systems, and use of NO donors and NOS inhibitors for conditions like pulmonary hypertension and erectile dysfunction.
Muscarine is an alkaloid found in the Amanita muscaria mushroom that causes only muscarinic effects. It can cause profuse salivation, lacrimation, sweating, blood vessel dilation and hypotension, miosis, and spasm of accommodation in the eyes. Mushroom poisoning may occur due to ingestion of poisonous mushrooms containing toxins like muscarine, amatoxins, or gyromitrins. Early onset poisoning features muscarinic symptoms like excessive sweating and salivation within 1-2 hours.
This document provides an overview of cholinergic drugs, which act on the parasympathetic nervous system. It begins with an introduction to cholinergic transmission and the discovery of acetylcholine. It describes the different types of cholinoceptors and their locations. The document then discusses the pharmacological actions of direct and indirect cholinergic drugs. It provides examples of therapeutic uses for various drugs in conditions like glaucoma and myasthenia gravis. Screening methods for cholinergic drugs are also summarized. The document concludes by stating that cholinergic pharmacology is an established field but further research is still needed for cognitive enhancing drugs.
I had made a comprehensive presentation that covers the types of burns,causes,method to calculate the percentage of burns,symptoms&signs and management of burns.Hope it will be very much useful for medical students and emergency care physicians.
This document discusses cholinergic drugs and receptors. It describes two main types of cholinergic receptors - muscarinic and nicotinic receptors. It also classifies cholinergic drugs into direct-acting drugs like choline esters and alkaloids, and indirect-acting drugs that inhibit cholinesterase enzymes. Finally, it provides details on the properties and uses of some choline ester drugs like acetylcholine, bethanechol, carbachol, and methacholine.
Cholinomimetic drugs act by mimicking or blocking the actions of the neurotransmitter acetylcholine. These drugs are useful in modifying autonomic functions and are used to treat various clinical conditions. There are two main types of cholinomimetic drugs - direct-acting drugs that stimulate muscarinic or nicotinic receptors, and indirect-acting drugs called anticholinesterases that inhibit the enzyme acetylcholinesterase and prolong the actions of acetylcholine. Examples of direct-acting drugs include pilocarpine and nicotine, while common anticholinesterases include donepezil, galantamine, and neostigmine.
The document discusses muscle relaxants and the neuromuscular junction. It describes how skeletal muscle relaxants act either peripherally at the neuromuscular junction or centrally in the spinal cord to reduce muscle tone. Neuromuscular blocking agents are used during anesthesia and ventilation to provide muscle relaxation. The document then goes into detail about the motor neuron, acetylcholine synthesis and receptors, and classification of different muscle relaxants.
This document discusses parasympathomimetic drugs, which mimic the effects of the parasympathetic nervous system. It describes how these drugs activate parasympathetic receptors, especially muscarinic and nicotinic acetylcholine receptors. It provides details on the mechanisms of different parasympathomimetic drugs, including how they stimulate receptors to produce various effects in the body. Specific drugs discussed include acetylcholine, carbachol, and their therapeutic uses and side effects.
Acetylcholine -
Acetylcholine is an organic chemical that functions in the brain and body of many types of animals as a neurotransmitter—a chemical message released by nerve cells to send signals to other cells, such as neurons, muscle cells and gland cells.
This document discusses acetylcholine (ACh), a neurotransmitter that functions in the brain and body. It defines ACh, describes its synthesis and release, mechanisms of action, sites of function in the body, including the neuromuscular junction and autonomic nervous system. It also discusses the pharmacology of ACh, including agonists like pilocarpine and neostigmine, and antagonists like atropine. ACh exerts its effects by binding to nicotinic and muscarinic receptors.
The document discusses the cholinergic system and neuromuscular blocking drugs. It begins by outlining the objectives and intended learning outcomes, which are to understand the locations of acetylcholine receptors, the synthesis and fate of acetylcholine, and the classifications and effects of various cholinergic drugs. It then describes the autonomic nervous system, including its parts, locations of ganglia, innervations of organs, and neurotransmitters. Next, it explains the synthesis, storage, release, binding, termination and recycling of acetylcholine. It also classifies cholinergic receptors and their locations and mechanisms. Finally, it discusses the classifications, actions, uses and effects of cholinergic drugs that directly activate receptors
pharmacology,clinical pharmacology,clinical,injections,pharmacological,what is pharmacology,lethal injection drugs,pharmacology definition,Plus review of anatomy of the ANS
The document discusses muscle relaxants and neuromuscular blocking agents. It covers their classification, mechanisms of action, administration, and side effects. Specifically, it describes how succinylcholine causes initial muscle stimulation followed by paralysis through prolonged depolarization of motor end plates. It also notes that residual paralysis can occur in 42% of patients even after administration of reversal agents, and that a train-of-four ratio above 0.7 correlates with clinical recovery.
Autonomic nervous system introduction and cholinergic systemDr. Siddhartha Dutta
This document discusses the autonomic nervous system (ANS) and cholinergic drugs. It begins by describing the ANS and its role in regulating vital functions. Acetylcholine is the primary neurotransmitter of the parasympathetic nervous system. Cholinergic drugs such as acetylcholine esters and anticholinesterases work by increasing acetylcholine levels in the body. Anticholinesterases inhibit the acetylcholinesterase enzyme, preventing the breakdown of acetylcholine. These drugs have applications in conditions like glaucoma, Alzheimer's disease, and myasthenia gravis.
The neurotransmission in cholinergic synapses involves the release of acetylcholine from nerve fibers and its action on cholinoceptors on target cells. Acetylcholine is synthesized from acetyl-CoA and choline and packaged into vesicles for storage and release. When an action potential arrives, voltage-gated calcium channels open, calcium enters the presynaptic terminal, triggering vesicle fusion and acetylcholine release. Acetylcholine can bind muscarinic or nicotinic cholinoceptors, eliciting various responses. Acetylcholinesterase terminates the action of acetylcholine by hydrolyzing it. Cholinergic drugs include cholinomimetics that directly activate receptors
The document discusses the autonomic nervous system and cholinergic agents. It describes how the autonomic nervous system is divided into the parasympathetic and sympathetic systems. The parasympathetic system uses acetylcholine as its neurotransmitter and causes effects such as decreasing heart rate and dilation of blood vessels. The sympathetic system uses norepinephrine as its neurotransmitter and causes effects like increasing heart rate and constriction of blood vessels. The document then focuses on the biosynthesis, storage, release and breakdown of acetylcholine, as well as the different types of acetylcholine receptors.
clinical pharmacology,clinical,injections,pharmacological,what is pharmacology,lethal injection drugs,pharmacology definition,Plus review of anatomy of the ANS
The document discusses the pharmacology of the autonomic nervous system. It describes how the sympathetic and parasympathetic divisions typically function in opposition to prepare the body for fight or flight responses versus rest and digestion. Acetylcholine is the neurotransmitter for preganglionic and parasympathetic fibers, while norepinephrine is released by postganglionic sympathetic fibers. Muscarinic and nicotinic receptors mediate the effects of acetylcholine. Cholinergic drugs can either directly activate these receptors or indirectly inhibit acetylcholinesterase to increase endogenous acetylcholine levels.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise boosts blood flow, releases endorphins, and promotes changes in the brain which help enhance one's emotional well-being and mental clarity.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help boost feelings of calmness, happiness and focus.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like anxiety and depression.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document provides information about the Post Graduate Common Entrance Test to be held on July 1st, 2017 from 2:30 pm to 4:30 pm for various Masters programs. It lists instructions for candidates regarding filling the answer sheet correctly and details about the structure of the test, which will consist of 75 multiple choice questions worth 100 marks to be completed within 120 minutes. Candidates are advised to carefully read and follow the guidelines for appearing in the exam.
Civil Service 2019 Prelims Previous Question Paper - 2Eneutron
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Civil Service 2019 Prelims Previous Question Paper - 1Eneutron
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Civil Service 2018 Prelims Previous Question Paper - 2Eneutron
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Civil Service 2018 Prelims Previous Question Paper - 1Eneutron
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Civil Service 2017 Prelims Previous Question Paper - 2Eneutron
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms for those who already suffer from conditions like depression and anxiety.
Civil Service 2017 Prelims Previous Question Paper - 1Eneutron
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise stimulates the production of endorphins in the brain which elevate mood and reduce stress levels.
This document contains the question paper for SNAP 2013 along with the answers to the 150 multiple choice questions. It directs test takers to an online site to attempt previous SNAP papers and provides information about exam preparation resources available on the site such as daily practice questions, preparation strategies, coaching classes, and current affairs.
This document contains the question paper for SNAP 2014 along with the answers to the 150 multiple choice questions. It provides a link to attempt similar past year papers online and lists exam preparation resources for SNAP like daily practice questions, preparation strategies, coaching class recommendations, and current affairs.
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
These lecture slides, by Dr Sidra Arshad, offer a simplified look into the mechanisms involved in the regulation of respiration:
Learning objectives:
1. Describe the organisation of respiratory center
2. Describe the nervous control of inspiration and respiratory rhythm
3. Describe the functions of the dorsal and respiratory groups of neurons
4. Describe the influences of the Pneumotaxic and Apneustic centers
5. Explain the role of Hering-Breur inflation reflex in regulation of inspiration
6. Explain the role of central chemoreceptors in regulation of respiration
7. Explain the role of peripheral chemoreceptors in regulation of respiration
8. Explain the regulation of respiration during exercise
9. Integrate the respiratory regulatory mechanisms
10. Describe the Cheyne-Stokes breathing
Study Resources:
1. Chapter 42, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 36, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 13, Human Physiology by Lauralee Sherwood, 9th edition
Our backs are like superheroes, holding us up and helping us move around. But sometimes, even superheroes can get hurt. That’s where slip discs come in.
Adhd Medication Shortage Uk - trinexpharmacy.comreignlana06
The UK is currently facing a Adhd Medication Shortage Uk, which has left many patients and their families grappling with uncertainty and frustration. ADHD, or Attention Deficit Hyperactivity Disorder, is a chronic condition that requires consistent medication to manage effectively. This shortage has highlighted the critical role these medications play in the daily lives of those affected by ADHD. Contact : +1 (747) 209 – 3649 E-mail : sales@trinexpharmacy.com
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd...Donc Test
TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version TEST BANK For Community and Public Health Nursing: Evidence for Practice, 3rd Edition by DeMarco, Walsh, Verified Chapters 1 - 25, Complete Newest Version Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Study Guide Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Stuvia Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Test Bank For Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Pdf Download Course Hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Answers Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Ebook Download Course hero Community and Public Health Nursing: Evidence for Practice 3rd Edition Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Chapters Download Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Pdf Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Study Guide Questions and Answers Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Ebook Download Stuvia Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Questions Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Studocu Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Quizlet Community and Public Health Nursing: Evidence for Practice 3rd Edition Test Bank Stuvia
2. The motor (efferent) portion of the nervous system can be divided
into two major subdivisions: autonomic and somatic.
The autonomic nervous system (ANS) is largely independent
in that its activities are not under direct conscious control.
It is concerned primarily with visceral functions such as
cardiac output, blood flow to various organs, and digestion,
which are necessary for life.
The somatic division is largely concerned with consciously
controlled functions such as movement, respiration, and posture.
Nerve impulses elicit responses in smooth, cardiac,
and skeletal muscles, exocrine glands, and
postsynaptic neurons by liberating specific
chemical neurotransmitters.
3. By using drugs that mimic or block the actions of chemical
transmitters, we can selectively modify many autonomic
functions. These functions involve a variety of effector
tissues, including cardiac muscle, smooth muscle,
vascular endothelium, exocrine glands, and
presynaptic nerve terminals.
Autonomic drugs are useful in many clinical conditions.
4. The ANS has two major portions:
the sympathetic (thoracolumbar) division and
the parasympathetic (craniosacral) division.
Both divisions originate in nuclei within the CNS
and give rise to preganglionic efferent fibers that
exit from the brain stem or spinal cord and
terminate in motor ganglia.
The sympathetic preganglionic fibers leave the
CNS through the thoracic and lumbar spinal nerves.
The parasympathetic preganglionic fibers leave the
CNS through the cranial nerves (especially the third,
seventh, ninth, and tenth) and the third and fourth
sacral spinal roots.
7. Parasympathetic nerves regulate processes
connected with energy assimilation (food intake,
digestion, absorption) and storage.
These processes operate when the body
is at rest, allowing increased bronchomotor tone
and decreased cardiac activity. Secretion of saliva
and intestinal fluids promotes the digestion of
foodstuffs; transport of intestinal contents is
speeded up because of enhanced peristaltic activity
and lowered tone of sphincter muscles.
To empty the urinary bladder (micturition),
wall tension is increased by detrusor activation
with a concurrent relaxation of sphincter tonus.
8. Activation of ocular
parasympathetic
fibers results in nar-
rowing of the pupil
and increased curva-
ture of the lens,
enabling near
objects to be
brought into focus
(accommodation).
9. ACh serves as mediator at terminals
of all postganglionic parasympathetic
fibers, in addition to fulfilling its trans-
mitter role at ganglionic synapses with-
in both the sympathetic and parasym-
pathetic divisions and the motor end-
plates on striated muscle. However, dif-
ferent types of receptors are present at
these synaptic junctions.
11. ACh is highly concentrated in
synaptic storage vesicles present in
the axoplasm of the terminal. ACh
is formed from choline and
activated acetate acetylcoenzyme
A, a reaction catalyzed by the
enzyme choline acetyltransferase.
The highly polar choline is actively
transported into the axoplasm. The
specific choline transporter is
localized exclusively to membranes
of cholinergic axons and terminals.
12.
13. During activation of the nerve
membrane, Ca2+
enters into the
axoplasm through voltage-gated
channels to activate protein kinases. As
a result, vesicles close to the presynaptic
membrane and fuse with this membrane.
During fusion, vesicles discharge their
contents into the synaptic gap. ACh
quickly diffuses through the synaptic gap.
The molecule of ACh is a little longer
than 0.5 nm. The synaptic gap is as
narrow as 30–40 nm.
14. At the postsynaptic effector cell membrane, ACh
reacts with its receptors. Because these receptors
can also be activated by the alkaloid muscarine,
they are referred to as muscarinic (M-)
cholinoceptors. In contrast, at ganglionic and motor
endplate cholinoceptors, the action of ACh is
mimicked by nicotine and they are,
therefore, said to be nicotinic (N-) cholinoceptors.
Released ACh is rapidly hydrolyzed and
inactivated by a specific acetylcholine esterase,
present on pre- and postjunctional membranes, or
by a less specific serum choline esterase (butyryl
choline esterase), a soluble enzyme present in
serum and interstitial fluid.
15.
16. M-cholinoceptors can be classified
into subtypes according to their molec-
ular structure, signal transduction, and
ligand affinity in the M1, M2, M3 subtypes, etc.
M1-receptors are present on nerve cells, e.g.,
in ganglia, where they mediate a facilitation of
impulse transmission from preganglionic axon
terminals to ganglion cells.
M2-receptors mediate acetylcholine effects on
the heart. Opening of K+
channels leads to
slowing of diastolic depolarization in sinoatrial
pacemaker cells and a decrease in heart rate.
17. M3-receptors are found in the glandular
epithelia (which respond with activation of
phospholipase C and increases secretory
activity) and in smooth muscle.
In smooth vessels, the relaxant action
of ACh on muscle tone is indirect,
because it involves stimulation of
M3-cholinoceptors on endothelial cells
that respond by liberating NO.
In the CNS, where all subtypes are present,
cholinoceptors serve diverse
functions, including regulation of cortical
excitability, memory, learning, pain processing,
and brain stem motor control.
20. Characteristic of Nicotinic receptors
NM-cholinoceptors
Location: neuromuscular junction
Function: depolarization of muscle end
plate and contraction of skeletal muscle
NN-cholinoceptors
Location: autonomic ganglia
Function: depolarization
postganglonic membrane
(in adrenal medula –
catecholamine release)
21. The NM-receptor
is a macroprotein with
5 subunits, which are
arranged like a rosette
surrounding the Na+
channel. The two alpha
subunits carry two ACh
binding sites with nega-
tively charged groups
which combine with the
cationic group of ACh
and open Na+
channel.
23. Acetylcholine receptor stimulants
and cholinesterase inhibitors
together comprise a large group of drugs
that mimic ACh (cholinomimetic agents)
Cholinoceptor stimulants are classified by their
spectrum of action depending on the type
of receptor – muscarinic or nicotinic, that is activated.
They are also classified by their mechanism of
action because some cholinomimetic drugs bind
directly to (and activate) cholinoceptors, while
others act indirectly by inhibiting the hydrolysis
of endogenous ACh.
24. I. DIRECT-ACTING CHOLINERGIC DRUGS
(1) Choline ester
(stimulants of M- and N-receptors):
Acetylcholine, Carbachol, etc.
(2) Alkaloids
a) stimulants of M-receptors:
Pilocarpine, Cevimeline (dry mouth),
Bethanechole, Musacarine, Phalloidin
b) stimulants of N-receptors:
Nicotine, Cytisine (Tabex®
), Lobeline
26. 50
100
150
200
A B C D1 min
M- и N-effects of ACh
Bloodpressure[mmHg]
ACh
2 mcg i.v.
ACh
50 mcg
ACh
50 mcg
ACh
5 mg
M-
effect
M-
effect
N-
effect
Atropine
2 mg i.v.
29. Pilocarpine Hydrochloride
eye drops (Pilocar®
)
- sol. 1%, 2%, 4%
- in open angle glаucoma
Applied to the eye, it
penetrates cornea and
promptly causes
miosis, ciliary muscle contra-
ction, and fall in intraoccular
tension (< 22 mm) lasting 4-8 h.
Side effect: painful spasm of
accommodation for near vision.
Systemic effects:
sweating, salivation
Cardiovascular effects: in small doses – fall in BP, but in high
doses elicits rise in BP and tachycardia, probably due to
ganglionic stimulation (through muscarinic receptors)
30. Development of
angle closure
glaucoma and
its reversal
by miotics
A. Mydriasis occurs in an eye with narrow iridocorneal angle
and the iris makes contact with the lens blocking passage of
theaqueous from the posterior to the anterior chamber.
B. Possibly builds up behind the iris which bulges forward and
closes the iridocorneal angle thus blocking aqueous outflow.
C. Miotic makes the iris thin and pushes it away from the lens
removing the pupillary block and restoring aqueous drainage.
36. II. INDIRECT-ACTING CHOLINERGIC DRUGS
(anticholinesterase drugs: antiChEs)
(1) Reversible drugs (most are carbamates)
a) With N3+
(cross BBB)
Alkaloids: Galantamine, Physostigmine
Synthetic drugs:
Donepezil, Rivastigmine, Tacrine
b) With N4+
(do not cross BBB)
Demecarium, Edrophonium (Tensilon®
)
Neostigmine, Pyridostigmine
37. (2) Irreversible anticholinesterase agents
(most of them are organophosphates)
a) Thiophosphate insecticides
Parathion
Malathion (Pedilin®
– used in pediculosis)
b) Nerve paralytic gases
for chemical warfare:
Tabun
Sarin
Soman
cockroachcockroach
40. AntiChEs inhibit ChE and protect ACh from
hydrolysis. They produce cholinergic effects
and potentiates ACh both in vivo and in vitro.
Lipid soluble agents (physostigmine and
organophosphates) have more marked
muscarinic and CNS effects, stimulates
ganglia but action on skeletal muscles is less
prominent (NB: the action of Galantamine
on skeletal muscles is much stronger in
comparison with neostigmine).
41. Lipid insoluble antiChEs (neostigmine and
other quaternary ammonium compounds)
produce more marked effect on the skeletal
muscles (direct action on muscle end-plate
NN-cholinoceptors as well).
Stimulate ganglia but muscarinic effects
are less prominent.
They do not penetrate in CNS and
have no central effects.
42. Prof. D. Paskov
(1914–1986)
Galantamine
(Nivalin®
)
Galantamine is antiChEs
with direct N-action used in:
•Myastenia gravis
•Alzheimer’s disease
•Poliomyelitis
•Postoperative paresis of GIT and bladder
•As antagonist of competitive
myorelaxants with less
side effects than neostigmine
43. Myasthenia gravis (MG) is a disease affecting skeletal muscle
neuromuscular junctions. An autoimmune process causes
production of antibodies that bind to the a subunits of the
nicotinic receptor. This effect causes accelerated degradation
of the receptor and blockade of ACh binding to receptors on
muscle end plates. Frequent findings are ptosis, diplopia,
difficulty in speaking and swallowing, and extremity weakness.
Severe disease may affect all the muscles, including those
necessary for respiration.
The disease resembles the neuromuscular paralysis produced
by tubocurarine and similar nondepolarizing neuromuscular
blocking drugs. Patients with myasthenia are
sensitive to the action of curariform drugs and other drugs that
interfere with neuromuscular transmission e.g., aminoglycoside
antibiotics. Anti-ChEs are extremely valuable as therapy
for myasthenia. Almost all patients are also treated with
immunosuppressant drugs and some with thymectomy.
Edrophonium is used as a diagnostic test in myasthenia gravis.
44. Diagrams of (A) normal and (B) myasthenic
neuromuscular junctions. The MG junction
has a normal nerve terminal; a reduced number
of AChRs and a widened synaptic space.
45. • In the Alzheimer’s disease in the brain
tissue there are amyloid plaques and
neurofibrillarly tangles, as well as loss
of cholinergic neurons.
• Cholinacetyl trasferase activity
in the cortex and hippocampus
is reduced from 30% to 70%.
• Loss of cholinergic neurons contributes
for to much of the learning and memory deficit.
• The number of M-cholinoceptors is not
affected, but the number of N-receptors
is reduced.