This document discusses cholinomimetics and cholinoblockers. It begins by describing the autonomic nervous system and its cholinergic and adrenergic components. It then discusses the mechanisms of acetylcholine and its interaction with nicotinic and muscarinic receptors. Specific drugs are discussed, including nicotine, cytisine, and various anticholinesterases. Ganglionic blockers and neuromuscular blockers are also covered. The document provides detailed information on the classifications, mechanisms of action, effects, uses, and side effects of these drug classes.
3 ANS PHARMACOLOGY FOR PHARMACY 01 Midwife 2015(1).pptxwakogeleta
This document discusses autonomic drugs and their classification. It begins by outlining the objectives of understanding different classes of autonomic drugs and their effects. It then provides details on the autonomic nervous system, including its divisions and neurotransmitters. The main classes of autonomic drugs discussed are cholinergic agents, anticholinergic agents, adrenergic agents, and ganglionic blockers. Specific drugs within each class are defined along with their mechanisms of action, therapeutic uses, side effects, and contraindications. Neuromuscular blocking agents are also briefly covered.
The document discusses synapses and the autonomic nervous system. It describes two types of synapses - chemical and electrical. The autonomic nervous system consists of the sympathetic and parasympathetic systems which regulate organs through the release of neurotransmitters like acetylcholine and norepinephrine. The effects of these systems are described for various organs. Drugs can act as agonists or antagonists at cholinergic and adrenergic receptors to influence the autonomic nervous system.
1. Nicotinic cholinoceptors are located in ganglia and muscles. Drugs can act as nicotinic cholinoceptor agonists or antagonists.
2. Nicotinic cholinoceptor agonists like lobeline and cytisine stimulate respiration by activating carotid body receptors. They are sometimes used to aid smoking cessation.
3. Ganglion blockers like benzohexonium and azamethonium antagonize nicotinic cholinoceptors in ganglia. They cause hypotension by blocking sympathetic ganglia and are used to treat hypertension. Side effects include dry mouth and orthostatic hypotension.
Drugs that affect the autonomic nervous systemSelf
The document discusses drugs that affect the autonomic nervous system. It describes how the autonomic nervous system regulates involuntary body functions and is divided into the sympathetic and parasympathetic divisions. It then summarizes different types of drugs that act on these divisions, including cholinergic drugs that stimulate the parasympathetic nervous system, anticholinergic drugs that block the parasympathetic nervous system, adrenergic drugs that activate the sympathetic nervous system, and adrenergic blockers that inhibit the sympathetic nervous system. Clinical uses are provided for several of these drug classes.
The document discusses the autonomic nervous system (ANS) and acetylcholine (Ach) neurotransmission. The ANS controls involuntary functions and is divided into the parasympathetic (PSN) and sympathetic (SNS) systems. Ach is the main neurotransmitter of the PSN and SNS. It binds to muscarinic and nicotinic receptors. Cholinergic drugs like anticholinesterases inhibit Ach breakdown, increasing its effects. They are used to treat conditions like myasthenia gravis but have side effects like excessive secretions. The document covers the synthesis, storage, release and effects of Ach in detail.
This document discusses the autonomic nervous system and drugs that affect it. It begins by describing the organization of the nervous system and autonomic nervous system. It then discusses exceptions in the sympathetic nervous system related to sweat glands, kidneys, and adrenal glands. The document goes on to classify drugs that can mimic or block neurotransmitters in the autonomic nervous system like acetylcholine and adrenaline. It also discusses indirect-acting drugs and different receptor types like muscarinic, nicotinic, alpha, and beta receptors. The locations and functions of these receptors are explained. Finally, examples of drugs are provided that can act as agonists or antagonists at these different receptor types.
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.
3 ANS PHARMACOLOGY FOR PHARMACY 01 Midwife 2015(1).pptxwakogeleta
This document discusses autonomic drugs and their classification. It begins by outlining the objectives of understanding different classes of autonomic drugs and their effects. It then provides details on the autonomic nervous system, including its divisions and neurotransmitters. The main classes of autonomic drugs discussed are cholinergic agents, anticholinergic agents, adrenergic agents, and ganglionic blockers. Specific drugs within each class are defined along with their mechanisms of action, therapeutic uses, side effects, and contraindications. Neuromuscular blocking agents are also briefly covered.
The document discusses synapses and the autonomic nervous system. It describes two types of synapses - chemical and electrical. The autonomic nervous system consists of the sympathetic and parasympathetic systems which regulate organs through the release of neurotransmitters like acetylcholine and norepinephrine. The effects of these systems are described for various organs. Drugs can act as agonists or antagonists at cholinergic and adrenergic receptors to influence the autonomic nervous system.
1. Nicotinic cholinoceptors are located in ganglia and muscles. Drugs can act as nicotinic cholinoceptor agonists or antagonists.
2. Nicotinic cholinoceptor agonists like lobeline and cytisine stimulate respiration by activating carotid body receptors. They are sometimes used to aid smoking cessation.
3. Ganglion blockers like benzohexonium and azamethonium antagonize nicotinic cholinoceptors in ganglia. They cause hypotension by blocking sympathetic ganglia and are used to treat hypertension. Side effects include dry mouth and orthostatic hypotension.
Drugs that affect the autonomic nervous systemSelf
The document discusses drugs that affect the autonomic nervous system. It describes how the autonomic nervous system regulates involuntary body functions and is divided into the sympathetic and parasympathetic divisions. It then summarizes different types of drugs that act on these divisions, including cholinergic drugs that stimulate the parasympathetic nervous system, anticholinergic drugs that block the parasympathetic nervous system, adrenergic drugs that activate the sympathetic nervous system, and adrenergic blockers that inhibit the sympathetic nervous system. Clinical uses are provided for several of these drug classes.
The document discusses the autonomic nervous system (ANS) and acetylcholine (Ach) neurotransmission. The ANS controls involuntary functions and is divided into the parasympathetic (PSN) and sympathetic (SNS) systems. Ach is the main neurotransmitter of the PSN and SNS. It binds to muscarinic and nicotinic receptors. Cholinergic drugs like anticholinesterases inhibit Ach breakdown, increasing its effects. They are used to treat conditions like myasthenia gravis but have side effects like excessive secretions. The document covers the synthesis, storage, release and effects of Ach in detail.
This document discusses the autonomic nervous system and drugs that affect it. It begins by describing the organization of the nervous system and autonomic nervous system. It then discusses exceptions in the sympathetic nervous system related to sweat glands, kidneys, and adrenal glands. The document goes on to classify drugs that can mimic or block neurotransmitters in the autonomic nervous system like acetylcholine and adrenaline. It also discusses indirect-acting drugs and different receptor types like muscarinic, nicotinic, alpha, and beta receptors. The locations and functions of these receptors are explained. Finally, examples of drugs are provided that can act as agonists or antagonists at these different receptor types.
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.
This document discusses cholinergic agonists, which are drugs that act on receptors activated by acetylcholine in the autonomic nervous system. It describes the synthesis and mechanisms of acetylcholine as a neurotransmitter. It then discusses various direct-acting cholinergic agonists like bethanechol, carbachol, and pilocarpine and their actions and uses. Pilocarpine is used topically to treat glaucoma by contracting the iris and ciliary muscles. The document also covers indirect agonists known as anticholinesterases, which inhibit the enzyme acetylcholinesterase and thereby increase acetylcholine levels. Physostigmine is an example of a reversible anticholinesterase
This document discusses skeletal muscle relaxants (SMRs), which are drugs that reduce muscle tone by acting at the neuromuscular junction or in the central nervous system. It classifies SMRs as peripherally or centrally acting. Peripherally acting SMRs include neuromuscular blockers like tubocurarine, which bind to nicotinic receptors and block the action of acetylcholine, causing paralysis. Succinylcholine is a depolarizing blocker that stimulates nicotinic receptors, causing depolarization and paralysis. Centrally acting SMRs like diazepam and baclofen decrease muscle tone by depressing polysynaptic reflexes in the spinal cord. SMR
1.Legal bases of medical errors and malpractice. List of medical mistakes, kinds of punishments.Write official documents.
2.Medical errors and malpractice in your national legislation. List of medical mistakes, kinds of punishments. Write official documents.
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.
Unit 3 Drugs Affecting PNS (As per PCI syllabus)Mirza Anwar Baig
This document provides an overview of a lecture on drugs acting on the autonomic nervous system. It discusses the autonomic neurotransmission and classification of drugs into parasympathomimetics, parasympatholytics, sympathomimetics, and sympatholytics. Specific drugs discussed in detail include direct-acting cholinergic agonists like acetylcholine and indirect-acting cholinergic agonists like anticholinesterase agents. Anticholinergic drugs like atropine are also summarized in terms of their mechanisms and therapeutic uses.
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
1. The document discusses the autonomic nervous system and drugs that act on it. It covers the classification of the nervous system, the actions of the sympathetic and parasympathetic systems, and neurotransmitters.
2. Drugs are classified as agonists that mimic neurotransmitters or antagonists that block neurotransmitter actions. Cholinergic drugs act at acetylcholine receptors and adrenergic drugs act at norepinephrine receptors.
3. The main cholinergic drugs discussed are acetylcholine, nicotine, and muscarine agonists as well as acetylcholinesterase inhibitor antagonists like neostigmine and organophosphates. Anticholinergic antagonists like atrop
drugs that affect the autonomic nervous system.ppt [autosaved] [autosaved]Sujit Karpe
This document provides an overview of the autonomic nervous system and discusses various adrenergic and cholinergic drugs. It defines the sympathetic and parasympathetic nervous systems and describes how adrenergic drugs stimulate the sympathetic system while cholinergic drugs stimulate the parasympathetic system. It then discusses the classification, mechanisms of action, effects and uses of various adrenergic and cholinergic drugs including catecholamines, alpha and beta receptor agonists and antagonists, anticholinesterases and direct acting cholinergic drugs. It also touches on myasthenia gravis and organophosphorus poisoning.
Here are the answers to your questions:
1. Neostigmine should not be used in ophthalmology due to its muscarinic side effects like miosis. Atropine is preferred.
2. Antidotes for different poisonings:
- Irreversible AcHe-inhibitors: Pralidoxime
- Atropine poisoning: Physostigmine
- Pilocarpine poisoning: Atropine
3. Complete the table:
poison Antidotes
Irreversible AcHe-inhibitors Pralidoxime
Atropine Physostigmine
Pilocarpine Atropine
Physostigmine None needed
Tub
This document provides an introduction to autonomic pharmacology and discusses cholinergic and anticholinergic drugs. It describes the autonomic nervous system, including its sympathetic and parasympathetic divisions. Cholinergic transmission is mediated by acetylcholine and hydrolyzed by cholinesterase. Cholinergic drugs such as acetylcholine act on muscarinic and nicotinic receptors to affect various organs. Anticholinesterases inhibit cholinesterase and amplify the effects of endogenous acetylcholine. They are used to treat conditions like glaucoma, myasthenia gravis, and postoperative ileus. Their overdose requires supportive care and antidotes like atropine.
The document discusses the autonomic nervous system and cholinergic drugs. It describes the parasympathetic and sympathetic nervous systems. Cholinergic drugs act as parasympathomimetics by stimulating muscarinic and nicotinic cholinergic receptors. They can be direct-acting agonists like acetylcholine or indirect-acting inhibitors of acetylcholinesterase. Common cholinergic drugs are discussed along with their mechanisms of action, uses, and side effects.
Introduction to ANS (autonomous nervous system) & cholinergic drugsManoj Kumar
This document provides an overview of the autonomic nervous system (ANS) and cholinergic system. It defines key terms like neurons, the central and peripheral nervous systems. It describes the sympathetic and parasympathetic divisions of the ANS. The document outlines the cholinergic neurotransmitter acetylcholine, its synthesis and receptors. It discusses cholinergic drugs that act as agonists or antagonists at muscarinic and nicotinic receptors. Conditions like glaucoma and myasthenia gravis are summarized. Adverse effects of cholinergic drugs and treatment of organophosphate poisoning are also covered.
Anticholinergics Kampala international university.pptxYIKIISAAC
This document discusses anticholinergic agents, which are drugs that inhibit the action of acetylcholine at cholinergic receptors in the central and peripheral nervous system. It describes the different types of cholinergic receptors, including muscarinic (M1-M5) and nicotinic (N1, N2) receptors. It provides examples of anticholinergic drugs that act as antagonists at these receptors, such as atropine, scopolamine, ipratropium, and ganglionic blockers. The document also discusses the clinical uses of anticholinergic agents for conditions like bradycardia, gastrointestinal disorders, and as pre-operative medications to reduce secretions. The main
RDS occurs in premature babies whose lungs are not fully developed due to a lack of surfactant. Surfactant coats the air sacs in the lungs and keeps them open for gas exchange. A baby with RDS may experience fast breathing, grunting, changes in skin color or chest retractions. Doctors diagnose RDS through physical exams, chest x-rays, echocardiograms or blood tests. Treatment focuses on replacing surfactant or providing breathing support through nasal CPAP, ventilation or nutrition. While some infants recover, RDS can cause complications like bronchopulmonary dysplasia or brain and lung damage, especially in very premature babies.
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This document discusses cholinergic agonists, which are drugs that act on receptors activated by acetylcholine in the autonomic nervous system. It describes the synthesis and mechanisms of acetylcholine as a neurotransmitter. It then discusses various direct-acting cholinergic agonists like bethanechol, carbachol, and pilocarpine and their actions and uses. Pilocarpine is used topically to treat glaucoma by contracting the iris and ciliary muscles. The document also covers indirect agonists known as anticholinesterases, which inhibit the enzyme acetylcholinesterase and thereby increase acetylcholine levels. Physostigmine is an example of a reversible anticholinesterase
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1.Legal bases of medical errors and malpractice. List of medical mistakes, kinds of punishments.Write official documents.
2.Medical errors and malpractice in your national legislation. List of medical mistakes, kinds of punishments. Write official documents.
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.
Unit 3 Drugs Affecting PNS (As per PCI syllabus)Mirza Anwar Baig
This document provides an overview of a lecture on drugs acting on the autonomic nervous system. It discusses the autonomic neurotransmission and classification of drugs into parasympathomimetics, parasympatholytics, sympathomimetics, and sympatholytics. Specific drugs discussed in detail include direct-acting cholinergic agonists like acetylcholine and indirect-acting cholinergic agonists like anticholinesterase agents. Anticholinergic drugs like atropine are also summarized in terms of their mechanisms and therapeutic uses.
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
1. The document discusses the autonomic nervous system and drugs that act on it. It covers the classification of the nervous system, the actions of the sympathetic and parasympathetic systems, and neurotransmitters.
2. Drugs are classified as agonists that mimic neurotransmitters or antagonists that block neurotransmitter actions. Cholinergic drugs act at acetylcholine receptors and adrenergic drugs act at norepinephrine receptors.
3. The main cholinergic drugs discussed are acetylcholine, nicotine, and muscarine agonists as well as acetylcholinesterase inhibitor antagonists like neostigmine and organophosphates. Anticholinergic antagonists like atrop
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This document provides an overview of the autonomic nervous system and discusses various adrenergic and cholinergic drugs. It defines the sympathetic and parasympathetic nervous systems and describes how adrenergic drugs stimulate the sympathetic system while cholinergic drugs stimulate the parasympathetic system. It then discusses the classification, mechanisms of action, effects and uses of various adrenergic and cholinergic drugs including catecholamines, alpha and beta receptor agonists and antagonists, anticholinesterases and direct acting cholinergic drugs. It also touches on myasthenia gravis and organophosphorus poisoning.
Here are the answers to your questions:
1. Neostigmine should not be used in ophthalmology due to its muscarinic side effects like miosis. Atropine is preferred.
2. Antidotes for different poisonings:
- Irreversible AcHe-inhibitors: Pralidoxime
- Atropine poisoning: Physostigmine
- Pilocarpine poisoning: Atropine
3. Complete the table:
poison Antidotes
Irreversible AcHe-inhibitors Pralidoxime
Atropine Physostigmine
Pilocarpine Atropine
Physostigmine None needed
Tub
This document provides an introduction to autonomic pharmacology and discusses cholinergic and anticholinergic drugs. It describes the autonomic nervous system, including its sympathetic and parasympathetic divisions. Cholinergic transmission is mediated by acetylcholine and hydrolyzed by cholinesterase. Cholinergic drugs such as acetylcholine act on muscarinic and nicotinic receptors to affect various organs. Anticholinesterases inhibit cholinesterase and amplify the effects of endogenous acetylcholine. They are used to treat conditions like glaucoma, myasthenia gravis, and postoperative ileus. Their overdose requires supportive care and antidotes like atropine.
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I would do the following:
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2. Taper and discontinue the ropinirole and alprazolam which can worsen hallucinations.
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Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
Certified as an ISO/IEC 27001: Information Security Management Systems (ISMS) Lead Implementer, Data Protection Officer, and Cyber Risks Analyst, Denis brings a heightened focus on data security, privacy, and cyber resilience to every endeavor.
His expertise extends across a diverse spectrum of reporting, database, and web development applications, underpinned by an exceptional grasp of data storage and virtualization technologies. His proficiency in application testing, database administration, and data cleansing ensures seamless execution of complex projects.
What sets Denis apart is his comprehensive understanding of Business and Systems Analysis technologies, honed through involvement in all phases of the Software Development Lifecycle (SDLC). From meticulous requirements gathering to precise analysis, innovative design, rigorous development, thorough testing, and successful implementation, he has consistently delivered exceptional results.
Throughout his career, he has taken on multifaceted roles, from leading technical project management teams to owning solutions that drive operational excellence. His conscientious and proactive approach is unwavering, whether he is working independently or collaboratively within a team. His ability to connect with colleagues on a personal level underscores his commitment to fostering a harmonious and productive workplace environment.
Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
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Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
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"Learn about all the ways Walmart supports nonprofit organizations.
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The webinar may also give some examples on how nonprofits can best leverage Walmart Business+.
The event will cover the following::
Walmart Business + (https://business.walmart.com/plus) is a new shopping experience for nonprofits, schools, and local business customers that connects an exclusive online shopping experience to stores. Benefits include free delivery and shipping, a 'Spend Analytics” feature, special discounts, deals and tax-exempt shopping.
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Answers about how you can do more with Walmart!"
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3. Efferent innervation of the body occurs
via autonomic nerves (innervating visceral
organs, blood vessels and glands) and
motor nerves of skeletal muscles.
Autonomic innervation is subdivided into
cholinergic (parasympathetic) and
adrenergic (sympathetic).
There are two main mediators:
acetylcholine and norepinephrine).
4. •The efferent pathway of the autonomic nerves
consists of two neurons: preganglionic and
ganglionic (postganglionic).
•The bodies of preganglionic neurons in the
cholinergic system have craniosacral localization.
Cranial nuclei are located in the midbrain and
medulla oblongata. Cholinergic fibers are inside the
pairs of cranial nerves (III, VII, IX, X).
•In the sacral part preganglionic neurons originate
from the lateral horns of the spinal cord gray
substance.
5.
6. •In the adrenergic system, the bodies of
preganglionic neurons are mainly located in the
lateral horns of the thoracolumbar part of the
spinal cord.
•Axons of preganglionic neurons terminate at the
autonomic ganglia in the synaptic contacts with
ganglionic neurons.
•Sympathetic ganglia are located outside the
bodies organs, and parasympathetic are mostly
located inside the organs.
7. •Choline is accumulated in cholinergic
presynaptic nerve endings via an active
transport mechanism linked to a Na+ pump.
Acetylcholine is synthesized from choline
and acetyl-CoA and accumulated in synaptic
vesicles.
•Ach is released from synaptic vesicles.
•Ach interacts with its receptors, but it is
inactivated by acetylcholinesterase.
8.
9. Types of cholinergic receptors:
N are nicotine-sensitive
M are muscarine-sensitive
Nn (1) are:
in ganglia,
in the carotid
sinus,
in the adrenal
medulla.
Nm(2) are in skeletal
muscles
•M1 are located in the
Central nervous system,
enterochromaffin cells of
the stomach.
•M2 are in the heart.
•M3 are in smooth muscles
of organs, glands of
external secretion,
endothelium of vessels.
12. Nicotine is an alkaloid of tobacco leaves.
It is used in experimental pharmacology to
analyze the mechanism of drugs action.
Nicotine affects both central and peripheral
N-cholinoceptors. It has a two-phase effect
because it stimulates N-CR in low doses
but it blocks them when it is used in high
doses.
Tolerance and dependence develop to
nicotine.
13. •Nicotine interacts with N-CR of the autonomic
ganglia and changes the functions of organs.
•N. stimulates the chemoreceptors of the
sinocarotid zone and reflexively activates
respiratory and vasomotor centers. In high
doses N. causes the inhibition of these centers.
•In low doses N. stimulates N-cholinoceptors of
the chromaffin cells of the adrenal glands and
increases the release of epinephrine. In high
doses it causes the opposite effect.
14. •Nicotine has a marked effect on the
CNS. It increases the release of
dopamine into the Central nervous
system, a person experiences the
pleasure of smoking. If a person does
not smoke, dopamine levels drop and
the person feels unwell. Dependence
to nicotine develops.
15.
16.
17.
18. EFFECTS OF NICOTINE
Effects Low doses High doses
The heart rate ↓ ↑
Blood pressure ↑ ↓
Intestinal
motility
↑ ↓
The secretion of
exocrine glands
↑ ↓
19.
20. ACUTE POISONING
Abdominal pain, vomiting, nausea, diarrhea,
Raised sweating,
Headache, dizziness, visual impairment,
hearing disorders, disorientation.
In severe cases: lowering of blood pressure,
oppression of the heart, oppression of the
respiratory center.
Help: Adsorbents, gastric lavage;
Anticholinergics; artificial ventilation,
symptomatic therapy
21. • N. in low doses can be used for the treatment of tobacco dependence. It
stimulates receptors and helps stop Smoking. We can used for example:
22. •Cytisine is sometimes used in clinical
practice as respiratory stimulant of reflex
action. It stimulates receptors of carotid
sinus. It stimulates receptors of adrenal
medulla, increases the release of
epinephrine and increases arterial pressure.
•Indications: depression of breathing
(morphine poisoning, carbon monoxide,
drowning, injury), to aid “quitting”
smoking.
23. •Cytisine is an analeptic because it restores
depressed breathing and reduced pressure.
It is effective only after intravenous
administration.
24. •Anticholinergics block the cholinergic
receptors, prevents their interaction with
acetylcholine and disrupts the conduction of
nerve impulses.
N-Cholinoblockers:
N-cholinoblockers
Ganglionblockers
Neuromuscular relaxants (curare-like drugs)
25. •Ganglionic blockers block sympathetic and
parasympathetic ganglia, N-CR of the adrenal
medulla and carotid body.
Classification
Bis-Quaternary ammonium salts do not penetrate
the BBB
1. Short-acting drugs (5-20 minutes): Trepirium
iodide
2. Average duration (3-4 hours): Azametonium
bromide, Hexamethonium benzolsulfonate
3. Long-acting (tertiary amines): Pachycarpine (6-
8 hours)
26. •They dilate arterial and venous vessels,
decrease blood pressure, reduce preload
and postload of the heart, improve blood
circulation in organs (lower limbs),
improve tissue trophism .
•They reduce smooth muscle tone
(intestine, bronchi, except myometrium),
secretion of exocrine glands (salivary,
gastric). But they can increase tone of
uterine and stimulate labor.
27. Indications for the use:
Obliterating endarteritis, pulmonary edema,
arterial embolism, hypertensive crisis.
Short-acting drugs can be used for controlled
hypotension during operation. They are
administered IV drip, dilate vessels, decrease
arterial pressure and reduce hemorrhage during
thyroidectomy and mastectomy. In neurosurgery
they reduce the possibility of the development of
brain edema.
Spastic pain (colic), bronchospasm, gastric and
duodenal ulcer.
28. SIDE EFFECTS:
Orthostatic collapse develops after an
abrupt change of the body’s position in
space. Marked and rapid decrease in the
arterial pressure develops after transition
from horizontal to vertical position.
Syncope.
Constipation, urinary retention.
Accommodation disorder, mydriasis.
Dysarthria, dysphagia.
29. •DRUGS BLOCKING NEUROMUSCULAR
TRANSMISSION (NEUROMUSCULAR
RELAXANTS, PERIPHERAL MUSCLES
RELAXANTS)
•They inhibit neuromuscular transmission on the
level of postsynaptic membrane, interacting
with N-cholinoceptors of the endplates.
•Curare was the first muscle relaxant. Its extract
was obtained from plants in South America and
used as an arrow poisoning.
34. Antidepolarizing drugs block N-ChR and prevent
depolarizing effect of acetylcholine. They act
competitive. If the concentration of acetylcholine
in the area of block is increased significantly this
will lead to restoration of the neuromuscular
transmission.
Depolarizing drug excite N-ChR and causes steady
depolarization of the postsynaptic membrane. In
the beginning, depolarization development is
manifested by muscular fasciculations. Soon after
a myoparalytic effect develops.
35.
36.
37.
38. Muscles are relaxed in a certain sequence:
Muscles of the face and neck;
The lower and upper limbs;
Muscles of the trunk;
Respiratory muscles;
The diaphragm.
Myoparalytic action range: the range between doses in
which drugs paralyze more sensitive muscles, and doses
that cause respiratory arrest.
Artificial ventilation of the lungs is required when using
muscle relaxants
39. Antagonists:
Antagonists of the antidepolarizing
drugs are anticholinesterase drugs
(Neostigmine, Galanthamine).
The action of depolarizing drug
(suxamethonium) can be reversed by
the administration of fresh citrated
blood, containing plasma
cholinesterase, which hydrolyzes
suxamethonium.
40. INDICATIONS FOR THE USE
In anaesthesiology during the
performance of most operations on the
organs of the thoracic and abdominal
cavities, on the upper and lower limbs;
Tracheal intubation, bronchoscopy,
reduction and reposition of bone fracture
fragments;
The treatment of tetanus and epilepsy.
41. SIDE EFFECTS:
Tachycardia (pancuronium), fluctuations
in blood pressure,
Allergic reactions,
Arrhythmia, increase in intraocular
pressure, muscular pains, long-term
apnoea (suxamethonium).
42. Comparative characteristics
of Pipecuronium and Suxamethonium
Effects Pipecuronium Suxamethonium
Effect on the
endplate
membrane
Stabilization Depolarization
Muscle
fasciculations
Absent Observed at the
beginning of the
action
Interaction with
Neostigmine
Antagonism Sinergism
43. Anticholinesterases
The action of these drugs is directed to acetylcholinesterase
in a cholinergic synapse.
Anticholinesterase drugs bind to active centers of
acetylcholinesterase and impair hydrolysis of acetylcholine.
The mediator is accumulated in synapses
and stimulates M and N – cholinoceptors.
The mechanism of acetylcholinesterase inhibition is reversible.
After inhibition, enzymatic activity of the enzyme
is restored and it continues to control
acetylcholine level in synapses.
44. Irreversible anticholinesterases (Armine, Ecothiophate,
Organophosphate and carbamate insecticids, nerve gases for
chemical war Tabun, Sarin, Soman inhibit activity of the
enzyme without its restoration.
Pharmacological effects of Anticholinesterase drugs:
44
These drugs produce:
М- cholinomimetic effects N- cholinomimetic effects
They act on eyes, smooth muscles, secretion of excretory glands
and heart work like M-cholinomimetics.
(these effects were described above)
45. 45
Influence on skeletal muscles:
Anticholinesterase drugs facilitate neuromuscular
transmission due to indirect stimulation
of postjunctional N– cholinoceptors
and increase tone of striated muscles.
Influence on the CNS:
At small doses, anticholinesterase drugs take stimulatory effect,
whereas at high doses they produce inhibitory effect on the CNS.
46. 46
However, only tertiary structure compounds pass cross
the blood-brain barrier well.
Physostigmine Galantamine
Aminostigmine Tacrine
Donepezil
Quaternary compounds badly pass cross the blood-brain barrier
and practically don’t cause effects in the CNS.
Neostigmine Pyridostigmine bromide
Distigmine bromide Ambenonium chloride
47. Therapeutic use of Anticholinesterase drugs
Anticholinesterase drugs are used for:
1. Treatment of glaucoma: Physostigmine, Armine, Echothiophate
2. Stimulation of peristalsis in postoperative atony of the intestines,
paralytic obstruction, atony of the urinary bladder and
uterine inertia (powerless labor):
Neostigmine, Distigmine, Physostigmine
3. Treatment and diagnostics of myasthenia gravis:
(chronic autoimmune disease causing muscle weakness:
autoantibodies reduce number of free Nn receptors)
Neostigmine, Pyridostigmine, Ambenonium, Edrophonium
48. 4. As pharmacological antagonists in overdoses of
nondepolarizing muscle relaxants: Neostigmine
5. Treatment of overdoses of drugs with anticholinergic action
(atropine, phenothiazines, tricyclic antidepressants):
Physostigmine, Galantamine
6. Treatment of Alzheimer’s disease:
Tacrine, Donepezil, Rivastigmine
49. Hypersalivation
Nausea, spastic stricture of muscles of the intestine and urinary bladder,
diarrhea
Bronchospasm and apnoe
Bradycardia, arrhythmia
Frequency of urination
Miosis
Twitchings of tongue and skeletal muscles
49
Adverse effects of anticholinesterase drugs:
50. Cholinesterase reactivators
50
Drugs of this group restore
acetylcholinesterase inhibited by anticholinesterases
with irreversible action (organophosphates & carbamates).
The main acetylcholinesterase reactivators are:
Isonitrozine
Trimedoxime
bromide
Alloxime Pralidoxime Obidoxime
51. Reactivators contain oxime group (=N-OH).
They attach to the anionic site of
acetylcholinesterase which remains unoccupied
in the presence of organophosphate inhibitor.
Its oxime end reacts with the phosphorous
atom attached to the esteratic site: the
oxime:phosphonate diffuses away leaving the
reactivated ChE.
51
Mechanism of acetylcholinesterase reactivator action:
52. Acetylcholinesterase reactivators are
used as specific antagonists of
organophosphorous compounds.
They are ineffective as an antidotes to
carbamate antiChEs (Physostigmine,
Neostigmine, Carbaryl, Propoxur) in
which case the anionic site of the enzyme
is not free to provide attachment to it.
52
53. Atropine as well as reactivators is the basic
pharmacological antidote in anticholinesterase
poisoning.
Atropine inhibits bronchospasm, bronchorrhea,
bradycardia and blockade of heart conductive
system.
53