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This document discusses neuromuscular blocking drugs, which prevent interaction between acetylcholine and nicotinic receptors in skeletal muscles, resulting in temporary paralysis. It classifies these drugs as depolarizing or non-depolarizing, and describes examples of each type like succinylcholine and tubocurarine. Side effects of these drugs include respiratory arrest, changes in heart rate and blood pressure, and malignant hyperthermia in the case of succinylcholine.
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BScN NMB.pptx
This document discusses neuromuscular blocking drugs, which prevent the interaction between acetylcholine and nicotinic receptors in skeletal muscles, resulting in muscle relaxation. These drugs are classified as either depolarizing or non-depolarizing agents. Depolarizing agents like succinylcholine act as agonists by depolarizing the nicotinic receptor, while non-depolarizing agents like tubocurarine competitively block acetylcholine at the nicotinic receptors. The document outlines the mechanisms, therapeutic uses, and adverse effects of various neuromuscular blocking drugs.
SKELETAL_MUSCLE_RELAXANTS.ppt
This document discusses skeletal muscle relaxants and their uses and mechanisms of action. It begins by outlining how muscle relaxants are used adjunctively in surgery to relax muscles and facilitate procedures. It then classifies muscle relaxants based on their site and mechanism of action into peripherally acting, centrally acting, and directly acting drugs. The majority of the document focuses on describing the mechanisms of action, pharmacokinetics, effects, and side effects of various peripherally acting non-depolarizing and depolarizing muscle relaxants. It also provides a brief overview of centrally acting muscle relaxants that work in the central nervous system to reduce muscle tone and spasticity.
Smooth muscle relaxants
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
Neuromuscular blocking
- Residual block
- Prolonged action of relaxant
- Organ dysfunction (liver, kidney)
- Atypical pseudocholinesterase
- Drug interactions
- Hypothermia
- Neuromuscular disease
Consider sugammadex in these cases.
Sugammadex
- Cyclodextrin that encapsulates Rocuronium and
Vecuronium molecules
- Removes them from the neuromuscular junction
- Rapid reversal of even profound block
- No side effects of anticholinesterases
- Dose dependent reversal
- 2 mg/kg reverses moderate block
- 4 mg/kg reverses profound block
- 16 mg/kg reverses
SKELETAL_MUSCLE_RELAXANTS final.pptx
This document discusses skeletal muscle relaxants, including their uses, classifications, and mechanisms of action. It covers both peripherally-acting and centrally-acting muscle relaxants. Peripherally-acting drugs include non-depolarizing neuromuscular blockers that competitively block acetylcholine receptors, and the depolarizing drug succinylcholine. Centrally-acting drugs like baclofen, tizanidine, and dantrolene act in the central nervous system or directly on muscle to reduce spasticity. The document provides details on the pharmacokinetics, effects, interactions, and side effects of various muscle relaxant drugs.
Skeletal muscle relaxants, Neuromuscular blocking agents, Neuromuscular blockers
This document discusses neuromuscular blocking agents. It begins by defining neuromuscular blocking drugs as agents that act at the neuromuscular junction to block neuromuscular transmission, facilitating muscle relaxation for surgery or ventilation. It then categorizes these drugs as either depolarizing or non-depolarizing. Succinylcholine is discussed as the primary depolarizing agent, causing initial muscle fasciculations before paralysis through prolonged depolarization. Non-depolarizing agents like pancuronium and vecuronium are competitive antagonists that block acetylcholine receptors. The document covers the mechanisms, uses, and side effects of various neuromuscular blocking drugs.
skeletalmusclerelaxants.pdf
This document discusses neuromuscular blocking agents (NMBAs), which act at the neuromuscular junction to cause muscle relaxation. It describes the two main types - depolarizing agents like succinylcholine that cause sustained depolarization, and non-depolarizing competitive antagonists that prevent acetylcholine binding. The document outlines the mechanisms, pharmacokinetics, uses for intubation and surgery, and side effects like hyperkalemia of these important drugs used during general anesthesia.
Skeletal muscle relaxants (or) Neuromuscular blockers
Skeletal muscle relaxants (or) Neuromuscular blockers
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BScN NMB.pptx
This document discusses neuromuscular blocking drugs, which prevent the interaction between acetylcholine and nicotinic receptors in skeletal muscles, resulting in muscle relaxation. These drugs are classified as either depolarizing or non-depolarizing agents. Depolarizing agents like succinylcholine act as agonists by depolarizing the nicotinic receptor, while non-depolarizing agents like tubocurarine competitively block acetylcholine at the nicotinic receptors. The document outlines the mechanisms, therapeutic uses, and adverse effects of various neuromuscular blocking drugs.
SKELETAL_MUSCLE_RELAXANTS.ppt
This document discusses skeletal muscle relaxants and their uses and mechanisms of action. It begins by outlining how muscle relaxants are used adjunctively in surgery to relax muscles and facilitate procedures. It then classifies muscle relaxants based on their site and mechanism of action into peripherally acting, centrally acting, and directly acting drugs. The majority of the document focuses on describing the mechanisms of action, pharmacokinetics, effects, and side effects of various peripherally acting non-depolarizing and depolarizing muscle relaxants. It also provides a brief overview of centrally acting muscle relaxants that work in the central nervous system to reduce muscle tone and spasticity.
Smooth muscle relaxants
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
Neuromuscular blocking
- Residual block
- Prolonged action of relaxant
- Organ dysfunction (liver, kidney)
- Atypical pseudocholinesterase
- Drug interactions
- Hypothermia
- Neuromuscular disease
Consider sugammadex in these cases.
Sugammadex
- Cyclodextrin that encapsulates Rocuronium and
Vecuronium molecules
- Removes them from the neuromuscular junction
- Rapid reversal of even profound block
- No side effects of anticholinesterases
- Dose dependent reversal
- 2 mg/kg reverses moderate block
- 4 mg/kg reverses profound block
- 16 mg/kg reverses
SKELETAL_MUSCLE_RELAXANTS final.pptx
This document discusses skeletal muscle relaxants, including their uses, classifications, and mechanisms of action. It covers both peripherally-acting and centrally-acting muscle relaxants. Peripherally-acting drugs include non-depolarizing neuromuscular blockers that competitively block acetylcholine receptors, and the depolarizing drug succinylcholine. Centrally-acting drugs like baclofen, tizanidine, and dantrolene act in the central nervous system or directly on muscle to reduce spasticity. The document provides details on the pharmacokinetics, effects, interactions, and side effects of various muscle relaxant drugs.
Skeletal muscle relaxants, Neuromuscular blocking agents, Neuromuscular blockers
This document discusses neuromuscular blocking agents. It begins by defining neuromuscular blocking drugs as agents that act at the neuromuscular junction to block neuromuscular transmission, facilitating muscle relaxation for surgery or ventilation. It then categorizes these drugs as either depolarizing or non-depolarizing. Succinylcholine is discussed as the primary depolarizing agent, causing initial muscle fasciculations before paralysis through prolonged depolarization. Non-depolarizing agents like pancuronium and vecuronium are competitive antagonists that block acetylcholine receptors. The document covers the mechanisms, uses, and side effects of various neuromuscular blocking drugs.
skeletalmusclerelaxants.pdf
This document discusses neuromuscular blocking agents (NMBAs), which act at the neuromuscular junction to cause muscle relaxation. It describes the two main types - depolarizing agents like succinylcholine that cause sustained depolarization, and non-depolarizing competitive antagonists that prevent acetylcholine binding. The document outlines the mechanisms, pharmacokinetics, uses for intubation and surgery, and side effects like hyperkalemia of these important drugs used during general anesthesia.
Skeletal muscle relaxants (or) Neuromuscular blockers
Skeletal muscle relaxants (or) Neuromuscular blockers
Classification and Mechanism of action of drugs.
Neuromuscular junction pharmacology, drugs used
The document discusses the neuromuscular junction, which allows motor neurons to transmit signals to muscle fibers and cause contraction. It consists of a presynaptic motor neuron, synaptic cleft, and postsynaptic muscle fiber. Acetylcholine is released from the motor neuron, binds to nicotinic receptors on the muscle fiber, and triggers an action potential for contraction. Neuromuscular blocking agents used in surgery work by competitively blocking acetylcholine receptors. They can be depolarizing like succinylcholine or non-depolarizing like tubocurarine. Centrally-acting muscle relaxants reduce muscle tone by affecting the central nervous system. Disorders of the neuromuscular junction include myast
Skeletal muscle relaxants
Skeletal muscle relaxants act either peripherally at the neuromuscular junction or centrally in the central nervous system to reduce muscle tone and cause paralysis. Peripherally acting drugs include non-depolarizing neuromuscular blockers like atracurium and vecuronium which competitively block acetylcholine receptors, and depolarizing drugs like succinylcholine which continuously stimulate nicotinic receptors. Centrally acting drugs like baclofen, diazepam and tizanidine reduce muscle tone by depressing polysynaptic reflexes in the spinal cord without affecting consciousness. These drugs are used to reduce muscle spasms, spasticity and provide muscle relaxation during surgery or ventilation.
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skeletalmusclerelaxants-151101095949-lva1-app6891 (1).pptx
This document provides information on neuromuscular blocking agents (NMBAs). It discusses the types of NMBAs, including depolarizing agents like succinylcholine and non-depolarizing agents. Succinylcholine acts like acetylcholine at the neuromuscular junction, causing initial fasciculations before paralysis. Non-depolarizers are competitive antagonists that block nicotinic receptors. The document outlines the mechanisms, pharmacokinetics, uses and side effects of various NMBAs. It also covers topics like reversal agents, malignant hyperthermia, and factors affecting succinylcholine metabolism.
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Skeletal muscle relaxants consist of both antispasticity and antispasmodic agents, a distinction prescribers often overlook. The antispasticity agents-baclofen, tizanidine, dantrolene, and diazepam-aid in improving muscle hypertonicity and involuntary jerks.
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This document discusses skeletal muscle relaxants. It classifies them as centrally-acting or peripherally-acting drugs. Peripherally-acting drugs are further divided into depolarizing and non-depolarizing blockers. Non-depolarizing blockers are competitive antagonists that bind to nicotinic receptors at the neuromuscular junction, preventing the opening of sodium channels and muscle contraction. They include long, intermediate, and short-acting drugs eliminated through the kidneys or liver. Dantrolene is a directly-acting muscle relaxant that decreases calcium release and excitation-contraction coupling in skeletal muscle. Centrally-acting relaxants like diazepam and midazolam facilitate GABA,
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This document discusses neuromuscular blocking agents (NMBAs) and muscle relaxants. It begins by outlining the history of neuromuscular blocking, then describes the two main types - depolarizing agents like succinylcholine and non-depolarizing agents. It explains how each type works in the body and their uses in anesthesia. Potential adverse effects and drug interactions are also reviewed. The document provides an in-depth overview of the classes of NMBAs and muscle relaxants, their mechanisms of action, and considerations for use.
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This document provides information about cholinergic antagonists (also known as anticholinergic or parasympatholytic drugs). It discusses two main classes - muscarinic receptor antagonists and nicotinic receptor antagonists. Muscarinic receptor antagonists like atropine block muscarinic receptors and have various therapeutic effects. Nicotinic receptor antagonists are further divided into neuromuscular junction blocking agents and ganglionic blocking agents. Neuromuscular junction blocking agents are used as muscle relaxants during anesthesia while ganglionic blockers inhibit transmission in both parasympathetic and sympathetic ganglia. The document outlines the mechanisms, sites of action, uses and adverse effects of various cholinergic antagonists.
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This document discusses the pharmacology of nicotinic and muscarinic agonists and antagonists. It describes how nicotine preferentially stimulates ganglionic nicotinic receptors and the complex effects this has on the cardiovascular, gastrointestinal, and urinary systems. It also discusses ganglionic blockers that reduce transmission in both the sympathetic and parasympathetic ganglia. Finally, it covers nicotinic antagonists that act as skeletal muscle relaxants, including non-depolarizing drugs like tubocurarine and depolarizing drugs like succinylcholine.
Depolarising and non depolarising smr
This slide gives brief and complete description about depolarising and non depolarising skeletal muscle relaxants. The font size is also big and the number of words in each slide is also optimum so that it looks good when projected.
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This document summarizes information about skeletal muscle relaxants. It discusses that these drugs are used to treat skeletal muscle spasticity and can act centrally or peripherally. Peripherally acting muscle relaxants are further divided into neuromuscular blocking agents and directly acting agents. Neuromuscular blocking agents are classified as depolarizing or non-depolarizing based on their mechanism of action at the neuromuscular junction. The key depolarizing agent discussed is succinylcholine and the key non-depolarizing agents discussed are tubocurarine and pancuronium. Dantrolene is highlighted as a directly acting agent that works by interfering with calcium release from muscle stores. Adverse
Copy of skeletal muscle relaxants / dental implant courses
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.
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This document discusses different classes of cholinergic antagonists including muscarinic antagonists, nicotinic neuromuscular junction blockers, and ganglionic blockers. It provides details on specific drugs such as atropine, scopolamine, succinylcholine, tubocurarine, and hexamethonium. The mechanisms of action, therapeutic uses, and adverse effects of these cholinergic antagonists are described. Sites of action include muscarinic receptors, nicotinic receptors at neuromuscular junctions, and nicotinic receptors in autonomic ganglia.
Skeletal muscle relaxant
Skeletal muscle relaxants can act peripherally at the neuromuscular junction, centrally in the central nervous system, or directly on muscle contractile mechanisms. Peripherally acting drugs include competitive blockers like tubocurarine and depolarizing agents like succinylcholine. Centrally acting drugs like diazepam and baclofen reduce muscle tone by depressing spinal reflexes. Dantrolene acts directly on muscle to inhibit calcium release and contraction. These drugs are used to reduce muscle spasms and tone in various neurological and orthopedic conditions as well as in anesthesia and electroconvulsive therapy.
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This document provides information on neuromuscular blocking agents (NMBAs). It discusses the types of NMBAs, including depolarizing agents like succinylcholine and non-depolarizing agents. Succinylcholine acts like acetylcholine at the neuromuscular junction, causing initial fasciculations before paralysis. Non-depolarizers are competitive antagonists that block nicotinic receptors. The document outlines the mechanisms, pharmacokinetics, uses and side effects of various NMBAs. It also covers topics like reversal agents, malignant hyperthermia, and factors affecting succinylcholine metabolism.
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This slide gives brief and complete description about depolarising and non depolarising skeletal muscle relaxants. The font size is also big and the number of words in each slide is also optimum so that it looks good when projected.
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offering a wide range of dental certified courses in different formats.
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Copy of skeletal muscle relaxants / dental implant courses
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Hypersensitivity.pdf
Hypersensitivity reactions can be subdivided into four main types:
Type 1 is an immediate hypersensitivity mediated by IgE antibodies and involves allergic reactions. Type 2 involves cytotoxic reactions mediated by IgG and IgM antibodies activating complement and destroying cells. Type 3 occurs when antigen-antibody complexes deposit in tissues, activating complement and causing inflammation. Type 4 is a delayed hypersensitivity mediated by T cells and involves reactions like tuberculosis.
BScN Corticosteroids.pptx
This document discusses corticosteroids, which are steroid hormones produced by the adrenal cortex. It describes the different types of corticosteroids based on their duration of action and includes examples of inhaled corticosteroids. The mechanism of action and pharmacological effects are explained. Clinical uses for corticosteroids include replacement therapy for adrenal insufficiency and treatment of conditions like rheumatoid arthritis. Adverse effects are also outlined such as Cushing's syndrome, weight gain, hyperglycemia, osteoporosis, and adrenal suppression.
SERM.pptx
Selective estrogen receptor modulators (SERMs) are a class of drugs that act as either estrogen agonists or antagonists depending on the tissue. They have estrogenic effects on bone, liver, and protein synthesis but antiestrogenic effects on breast and uterine tissue. Common SERMs include tamoxifen for breast cancer and raloxifene for osteoporosis. While SERMs can help prevent fractures and breast cancer progression, they also increase risks of blood clots, endometrial cancer, and other side effects. Hormonal oral contraceptives contain synthetic estrogens and progestins that prevent ovulation and thickening of cervical mucus to inhibit pregnancy. They are used for contraception as
BScN ANTIDIABETICS.pptx
This document discusses anti-diabetic hormones and oral hypoglycemic agents (OHA) used to treat diabetes mellitus. It describes insulin, the main types of insulin preparations, and their clinical indications and adverse effects. It also outlines the classes of OHAs including sulfonylureas, biguanides like metformin, their mechanisms of action, clinical uses, and adverse effects. Sulfonylureas work by inhibiting ATP-sensitive potassium channels in beta cells to stimulate insulin release while metformin improves glucose control through various mechanisms in the liver and gastrointestinal tract.
PEPTIC ULCER SMDC.ppt
This document discusses drug treatment for acid peptic disease. It classifies drugs into those that reduce acid activity like proton pump inhibitors and H2 receptor blockers, mucosal protectants like sucralfate, and prostaglandin analogs like misoprostol. It describes the mechanisms, clinical uses, and adverse effects of representative drugs in each class. Regimens for H. pylori eradication involving combinations of drugs are also outlined.
ANTIEMETIC AGENTS.pptx
This document discusses various antiemetic agents used to treat vomiting. It classifies antiemetics into several categories based on their mechanism of action, including histamine 1 receptor blockers, 5HT3 receptor antagonists, prokinetics, muscarinic receptor blockers, antipsychotics, NK1 receptor antagonists, cannabinoids, and glucocorticoids. Each drug class is described in terms of its mechanism of action, common uses, and potential adverse effects.
BScN ANTIHISTAMINES.pptx
Histamine is a chemical produced in mast cells that mediates allergic and inflammatory reactions. Antihistamines work by competitively blocking the H1 receptor and are used to treat allergic conditions, motion sickness, chemotherapy-induced vomiting, and morning sickness. First generation antihistamines are more sedating and have anticholinergic effects while second generation have less sedation but can cause arrhythmias. Serotonin is a neurotransmitter with receptors 1-7 and agonists are used to treat anxiety, migraines, and irritable bowel syndrome while antagonists treat carcinoid tumors and cold-induced urticaria.
Expectorant.pptx
This document discusses antitussive drugs, which are used to suppress cough. It describes two types of antitussive drugs: centrally-acting drugs that work by inhibiting the cough center in the brain, and peripherally-acting drugs that reduce cough by acting on components of the cough reflex in the respiratory tract. Examples of commonly used centrally-acting antitussives include opioids, dextromethorphan, and antihistamines. Peripherally-acting antitussives include expectorants, bronchodilators, local anesthetics, and nasal decongestants. The document also discusses the mechanisms and side effects of various antitussive drugs.
BScN NSAIDs.pptx
This document discusses NSAIDs (non-steroidal anti-inflammatory drugs) and their classification and mechanisms of action. It focuses on aspirin and paracetamol. NSAIDs work by inhibiting the cyclooxygenase enzymes COX-1 and COX-2, which are involved in prostaglandin synthesis. Aspirin irreversibly inhibits both COX enzymes, reducing pain and inflammation. Paracetamol/acetaminophen is safer for the stomach as its mechanism is specific to the central nervous system. The document also covers the therapeutic uses and adverse effects of these NSAIDs.
BScN GENERAL ANESTHETICS.pptx
This document discusses general and local anesthetics. It describes how general anesthetics cause unconsciousness, analgesia, amnesia, muscle relaxation and loss of reflexes. Inhaled anesthetics like halothane and intravenous drugs like thiopentone and propofol are covered. Local anesthetics like lidocaine work by blocking sodium channels to prevent nerve impulses from being transmitted from the site of stimulation. The therapeutic uses and potential adverse effects of various general and local anesthetics are summarized.
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NMB.pptx
- 3. NEUROMUSCULAR BLOCKING DRUGS These Drugs prevent interaction between Ach and Nicotinic receptors in the skeletal muscles. It results in temporary Paralysis of skeletal muscles and muscle relaxation. These drugs are classified according to their mechanism of action. 1- Depolarizing agents- Non competitive, agonist 2- Non depolarizing, Competitive, antagonist.
- 4. CLASSIFICATION OF NEUROMUSCULAR BLOCKERS 1- Depolarizing agents- Non competitive, agonist Succinylcholine 2- Non depolarizing, Competitive, antagonist d-Tubocurarine Metocurine Doxacurium Atracurium Mivacurium Cisatracurium
- 5. DEPOLARIZING AGENTS- NON COMPETITIVE, AGONIST Succinylcholine (Suxamethonium) : Mechanism of action: It attaches to the nicotinic receptor and acts like Ach to depolarize the junction. Phase I: Depolarization of the receptor, transient fasciculation or muscle twitching Phase II: Continuous depolarization Gradual repolarization, and flaccid paralysis
- 7. SEQUENCE OF PARALYSIS Neck, limbs Face, Jaw, eyes Pharynx trunk Respiratory RECOVERY IN REVERSE
- 8. DEPOLARIZING AGENTS- NON COMPETITIVE, AGONIST Therapeutic uses of succinylcholine 1- Endotracheal intubation for induction of anaesthesia 2- During electroconvulsive shock treatment. Adverse effects of succinylcholine Apnea Hyperkalemia Muscle pains ( myalgia)
- 9. DEPOLARIZING AGENTS- NON COMPETITIVE, AGONIST Malignant hyperthermia Persistent release of Ca from sarcoplasmic reticulum in patients with abnormal RyR1, Ryanodine receptors. 1-Severe contraction leading to rigidity 2- Rigidity 3- Heat production from skeletal muscles 4- Metabolic acidosis 5- Tachycardia Treatment: Treatment with dentrolene- it blocks the Ca release from sarcoplasmic reticulum of skeletal muscle Temperature control with cooling blankets.
- 10. NON DEPOLARIZING, COMPETITIVE, ANTAGONIST. Tubocurarine Mechanism of action: Competitively block Ach at the nicotinic receptors Prevent depolarization and inhibit muscular contraction. Their competitive action can be overcome by administration of cholinesterase inhibitors, such as Neostigmine Edrophonium
- 12. SEQUENCE OF PARALYSIS Fingers, orbit (small muscles) limbs Trunk neck Intercostals Diaphragm RECOVERY IN REVERSE
- 13. NON DEPOLARIZING, COMPETITIVE, ANTAGONIST. Therapeutic uses of Tubocurarine: 1-Maintenance of anesthesia. 2-For intubation where succinylcholine is contraindicated 3-Muscle relaxation during surgery 4-Facilitation of mechanical ventilation
- 14. NON DEPOLARIZING, COMPETITIVE, ANTAGONIST. Adverse effects of Tubocurarine: Respiratory arrest Heart rate may increase Decrease in blood pressure Bronchospasm Skin wheals
- 15. NON DEPOLARIZING, COMPETITIVE, ANTAGONIST. ATRACURIUM It is an intermediate-acting muscle relaxant.. It is inactivation in plasma by spontaneous non enzymatic degradation Its metabolite -Laudanosine-crosses BBB-may cause seizure Causes mild histamine release Duration of action : 25 -35min Stereoisomers of Atracurium Cisatracurium Gantacurium
Editor's Notes
- administration of succinylcholine to a patient who is deficient in plasma cholinesterase or who has an atypical form of the enzyme can lead to prolonged apnea due to paralysis of the diaphragm. : succinylcholine increases potassium release from intracellular stores. excessive muscle contractions
- or inability of sarcoplasmic reticulum to sequestor Ca via Ca transporter)-prolonged release of Ca- massive muscle contraction-increased body temperature