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Neuromuscular blockers can be classified as either competitive antagonists that bind reversibly to nicotinic receptors (e.g. vecuronium) or depolarizing blockers that cause sustained depolarization of the motor end plate (e.g. succinylcholine). Competitive blockers have a longer duration of action and are not antagonized by cholinesterase inhibitors, while depolarizing blockers have a very short duration due to hydrolysis by plasma cholinesterase and their effects can be reversed. Neuromuscular blockers are used adjuvantly in surgical anesthesia to facilitate procedures by providing muscle relaxation.
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Interesting case
- The patient is a 25-year-old Thai woman who presented to the emergency room after ingesting an unknown medication belonging to her sister about 1 hour prior due to a severe headache. She experienced nausea, vomiting, and drowsiness.
- On examination, she appeared drowsy with normal vital signs. ECG showed no abnormalities. Laboratory tests revealed no abnormalities except mild anemia. Drug screening of blood and gastric content was negative.
- The leading diagnosis was toxicity from a sodium channel blocking agent. Management included activated charcoal, sodium bicarbonate, and supportive care. The patient's condition improved with treatment.
Periphral acting muscle relaxant & nm blocking agents
Neuromuscular blocking agents act at the neuromuscular junction to cause paralysis or reduce muscle tone. They are classified as depolarizing or nondepolarizing. Nondepolarizing agents are further classified as long, intermediate, or short acting depending on their duration of action and route of elimination from the body. They work by competitively blocking nicotinic acetylcholine receptors. Succinylcholine is the only clinically used depolarizing agent and causes initial depolarization followed by desensitization of the neuromuscular junction. Anesthetics potentiate the effects of neuromuscular blockers. Their administration must be closely monitored to avoid respiratory paralysis or other adverse effects.
Muscle relaxant and reversal agents
This document discusses skeletal muscle relaxants and their reversal. It begins by defining neuromuscular blocking drugs as those that act at the neuromuscular junction to block neuromuscular transmission, in order to facilitate muscle relaxation for surgery. It then covers the history, classification, and mechanisms of action of both depolarizing drugs like succinylcholine and non-depolarizing drugs. It discusses the pharmacology, clinical uses, and side effects of various muscle relaxants. It concludes by addressing the reversal of neuromuscular blockade using anticholinesterase drugs like neostigmine and strategies to minimize their muscarinic side effects.
Smr-Skeletal Muscle Relaxants MOA, PK,PD,ADR
1) Skeletal muscle relaxants can be classified based on their site and mechanism of action into peripherally-acting agents like neuromuscular blockers that act at the neuromuscular junction, and centrally-acting agents like baclofen, diazepam, and dantroline that act in the central nervous system.
2) Non-depolarizing agents act by competitively blocking acetylcholine receptors at low doses and blocking ion channels at high doses, while depolarizing agents like succinylcholine act as agonists at acetylcholine receptors.
3) Baclofen acts through GABA-B receptors in the brain and spinal cord to reduce excitability
SKELETAL MUSCLE RELAXANTS
Skeletal muscle relaxants work by either depolarizing or competitively blocking nicotinic acetylcholine receptors in the neuromuscular junction. Succinylcholine is a depolarizing agent that causes initial muscle fasciculation and prolonged depolarization before hydrolysis by plasma cholinesterase. Non-depolarizing agents like atracurium and vecuronium are competitive antagonists that bind nicotinic receptors without activating them. They vary in onset, duration and route of elimination depending on whether they are short, intermediate or long acting. Pancuronium and pipecuronium have longer durations due to renal elimination while mivacurium and rapacuronium are shorter acting due to
Antiarrhythmicdrug therapy Dr Vinay Verma
This document discusses antiarrhythmic drug therapy. It describes the normal cardiac conduction pathway and how arrhythmias disrupt normal rhythm. There are several classes of antiarrhythmic drugs that work by different mechanisms, such as blocking sodium, potassium, calcium channels or beta receptors. The drugs have various uses for treating supraventricular and ventricular arrhythmias. Adverse effects and drug interactions are also reviewed for specific antiarrhythmic medications.
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
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.
Cholinergic neurotransmision
This document discusses cholinergic neurotransmission. It defines acetylcholine as a neurotransmitter that transmits signals across chemical synapses. It describes the properties of neurotransmitters in general and lists acetylcholine as one that acts at both excitatory nicotinic and inhibitory muscarinic receptors. It then focuses on the muscarinic receptor system, outlining the subtypes, locations, and functions. It also discusses cholinergic transmission sites, synthesis and storage of acetylcholine, and the actions of cholinergic agonists and antagonists.
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.
L 4: Cholinergic antagonists
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.
Anti-arrhythmic evaluation
This document provides information on the evaluation of anti-arrhythmic agents. It discusses various in vitro, in vivo, and clinical models used to evaluate these drugs. In vitro techniques include studying isolated cardiac myocytes and using isolated guinea pig papillary muscle preparations. In vivo models described are the Langendorff technique, aconitine-induced arrhythmias in rats, digoxin-induced arrhythmias, and mechanically-induced arrhythmias like coronary ligation models. Clinical evaluation methods and the Vaughan-Williams classification of anti-arrhythmic drugs are also summarized.
anti-arrhythmics
This document summarizes antiarrhythmic drug therapy for pediatric patients. It discusses empiric diagnosis of arrhythmias and the Vaughn-Williams classification of antiarrhythmic drugs. Specific drug classes and agents are described including their mechanisms of action, uses, dosages, and side effects for treating arrhythmias like supraventricular tachycardia, atrial flutter, ventricular tachycardia, and ventricular fibrillation. Emphasis is placed on selecting the appropriate antiarrhythmic based on the specific arrhythmia and consulting with a cardiologist for long-term or complex cases.
Skeletal Muscle Relaxants
Skeletal muscle relaxants work by blocking acetylcholine receptors at the neuromuscular junction, relaxing muscles. There are two main types - depolarizing and non-depolarizing. Succinylcholine is the only depolarizing drug used clinically. It causes initial fasciculations before prolonged muscle relaxation. Non-depolarizing drugs like tubocurarine and vecuronium are competitive antagonists that do not activate acetylcholine receptors, preventing muscle contraction. They have short, intermediate, or long durations of action and differ in side effects and metabolism. Dantrolene works via a different mechanism by preventing calcium release in muscles.
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Periphral acting muscle relaxant & nm blocking agents
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Skeletal muscle relaxants, Neuromuscular blocking agents, Neuromuscular blockers
Skeletal muscle relaxants, Neuromuscular blocking agents, Neuromuscular blockers
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This document discusses the classification and cellular mechanisms of opioid receptors. There are four main types of opioid receptors: mu, delta, kappa, and ORL-1. Each receptor type is activated by different endogenous peptides and exogenous drugs. When activated, the receptors modulate various central and physiological processes like pain, locomotion, stress, and reward/addiction pathways. The document provides an overview of the endogenous and exogenous agonists and antagonists that act on each receptor subtype.
Pk2
This document discusses clinical pharmacokinetics and pharmacodynamics. It defines pharmacokinetics as how the body affects a drug through absorption, distribution, metabolism and elimination. Factors like age can impact these processes in pediatric patients. It also discusses pharmacodynamics, how drugs act on the body, and how pharmacokinetics and pharmacodynamics together can help individualize drug therapy and decrease adverse effects.
Kinetika En 2002
- Pharmacokinetics is the study of the absorption, distribution, metabolism, and excretion of drugs in the body over time. It aims to quantitatively account for the amount of drug in the body and the rate it is cleared.
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This document provides an overview of pharmacokinetic concepts including the four main processes of absorption, distribution, metabolism, excretion, and various pharmacokinetic models. It discusses how drugs move through the body, factors that affect drug concentrations over time, and complexity of drug interactions within the body. Examples are provided to illustrate key pharmacokinetic principles such as the effect of dosage form on absorption rate and how organ function influences drug elimination rates.
Kinetika En 2002
Pharmacokinetics is the study of drug absorption, distribution, metabolism, and excretion in the body. The key pharmacokinetic parameters include volume of distribution (Vd), clearance (CL), and elimination half-life (t1/2). Vd represents the apparent volume needed to contain the total amount of drug at the observed plasma concentration. CL is the volume of plasma cleared of drug per unit time, determined by metabolism and excretion. t1/2 is the time for drug concentration to reduce by half, dependent on Vd and CL. These parameters allow quantification of drug behavior in the body over time.
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Cephalosporins are a class of beta-lactam antibiotics that share a beta-lactam ring structure with penicillins and other beta-lactams. They work by binding to penicillin-binding proteins in bacterial cell walls to inhibit cell wall synthesis. First generation cephalosporins are mainly active against gram-positive cocci, while later generations have increased gram-negative coverage. Each generation also has distinct and expanded clinical uses depending on their antimicrobial spectrum.
AUPDATE
This document discusses various antibiotics, their uses, and emerging issues with antibiotic resistance. It provides guidance on empiric treatment for common infections like community-acquired pneumonia and skin/soft tissue infections.
For a case of community-acquired pneumonia, the patient was initially treated empirically with Augmentin and clarithromycin per guidelines. Testing later found penicillin-resistant Streptococcus pneumoniae, requiring a change to higher dose beta-lactams, vancomycin, or fluoroquinolones.
A case of cellulitis grew methicillin-resistant Staphylococcus aureus despite initial Augmentin treatment. The drug of choice for MRSA is vancomycin,
05052008OvarianTelehealth
The document discusses ovarian cancer treatment and management. It covers symptoms, risk factors, diagnosis methods, surgical staging and debulking, chemotherapy options including the gold standard of intravenous carboplatin and paclitaxel as well as emerging intraperitoneal chemotherapy showing increased survival. It emphasizes the importance of complete surgical staging and aggressive cytoreductive surgery for optimal outcomes and challenges of ensuring all patients receive standard of care treatment by gynecologic oncologists.
mati
- Ovarian cancer is the 4th leading cause of cancer death in women in the US, with a 5-year survival rate of only 35% for advanced cases. Most cases are diagnosed at an advanced stage due to non-specific early symptoms.
- There is no consensus on screening guidelines due to a lack of evidence that screening reduces mortality. Current screening methods like ultrasound and CA-125 lack sensitivity and specificity.
- Several large trials are underway to evaluate new screening strategies using ultrasound, tumor markers, and genetic testing to enable earlier detection when treatment is most effective. Improved screening methods are needed to reduce ovarian cancer mortality rates.
DrTerespolsky
This document discusses hereditary breast and ovarian cancer and the role of genetics in cancer risk. It provides an overview of BRCA1 and BRCA2 genes which are known to increase the risk of breast and ovarian cancers when mutated. Individuals with mutations in these genes have a high lifetime risk, up to 85%, of developing breast cancer and 16-44% risk for ovarian cancer. Referral to a cancer genetics clinic is recommended for those with a strong family history or personal history of related cancers to determine risk and recommend screening and management options.
15
1. Ovarian cancer is the most common type of ovarian tumor and the 7th most common cancer in women.
2. Early stages of ovarian cancer are often asymptomatic but later stages can cause pressure symptoms like abdominal pain or bloating.
3. Ovarian cancer commonly spreads directly to nearby structures in the abdomen or through the lymphatic system to distant lymph nodes.
gopalan031607
Ovarian cancer is the 8th most common cancer in women and the 5th leading cause of cancer death. It has a median age of diagnosis of 60 years old and 68% of cases are metastatic at diagnosis. Risk factors include family history, personal history of breast cancer, infertility, and lack of pregnancy. Genetic mutations like BRCA1/2 account for 10-15% of cases. Symptoms are often vague. Treatment involves surgical staging and debulking followed by platinum-based chemotherapy, with the goal of optimal cytoreduction to ≤1cm residual disease.
IncidentalomaTalk
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Nikiforov
This document summarizes genetic alterations involved in the progression of well-differentiated thyroid carcinomas to poorly differentiated and anaplastic carcinomas. It discusses mutations in genes such as BRAF, RAS, RET/PTC, and PAX8-PPARγ that are involved in early-stage well-differentiated and follicular carcinomas. Additional mutations in p53 and β-catenin are thought to direct dedifferentiation and progression to later stages. Studies of mutations and loss of heterozygosity support a model where well-differentiated tumors progress through poorly differentiated to anaplastic carcinomas through the accumulation of these genetic alterations.
Thpt
1. The patient has a history of thyroid cancer with metastases to the lungs and skull, and underwent total thyroidectomy and parathyroidectomy.
2. Treatment options for recurrent or metastatic thyroid cancer include radioactive iodine treatment, surgery, external beam radiation, and molecularly targeted therapies.
3. Molecular targeted therapies that show promise for thyroid cancer work by inhibiting pathways involved in cell signaling and angiogenesis, such as the MAPK and PI3K pathways, or by restoring radioiodine uptake.
Thyroid Disease
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- A 45-year-old female presented with a thyroid nodule that was found to be papillary carcinoma on biopsy. Near-total or total thyroidectomy is the recommended treatment.
- Her prognosis is favorable at ~90% 10-year survival given her diagnosis of papillary carcinoma and surgery. Ongoing monitoring is still recommended.
THYCER
1. Thyroid cancer is the most common endocrine malignancy, with papillary thyroid cancer being the most common type.
2. Treatment involves surgical removal of part or all of the thyroid gland followed by radioactive iodine ablation and thyroid hormone suppression.
3. Follow up care involves monitoring of thyroid levels and imaging tests to check for recurrence or spread of cancer. Outcomes depend on cancer type, stage, and individual risk factors.
DrRobertFoxUtahSSF
1. New diagnostic criteria have been developed to clarify the diagnosis of Sjogren's syndrome and diminish confusion in clinical practice and research.
2. The diagnosis of Sjogren's syndrome can be challenging as minor salivary gland biopsies and ANA blood tests sometimes have variable or non-specific results.
3. While Sjogren's syndrome and SLE share some similarities, Sjogren's syndrome has distinct clinical manifestations and treatment considerations compared to SLE.
Sjögren's_syndrome~_Role_for_Cevimeline
1) The document discusses Sjogren's Syndrome, an autoimmune disease characterized by dry eyes and mouth, and evolving concepts for treating it based on pathogenesis involving lymphocytic infiltrates impairing salivary and lacrimal gland function rather than full destruction.
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n-mBloc
- 4. D-tubocurarine pancuronium Vecuronium Decamethonium Succinylcholine Depolarizing Blockers Competitive Blockers
- 6. Classification of Blockers Renal and liver 1-2 1-2 Intermediate duration; competitive Rocuronium Renal and liver 4-6 4-6 Long duration; Competitive Pancuronium Plasma cholinesterase 12-18 2-4 Short duration; Competitive Mivacurium Plasma cholinesterase 30-40 2-4 Intermediate duration; Competitive Atracurium Renal and liver 80-120 4-6 Long duration; Competitive D-tubocurarine Plasma cholinesterase 6-8 1-1.5 Ultrashort acting; Depolarizing Succinylcholine Elimination Duration (min) Onset time (min) Pharmacological Properties Agent
- 7. Muscle AP Nerve AP Left Leg Muscle Stimulation Right Leg Nerve Stimulation Right Leg Muscle Stimulation Site of Action of d-Tubocurarine
- 8. G: gallamine; TC: tubocurarine; NEO: neostigmine; S: succinylcholine. Non-depolarizing Block
- 9. Depolarizing Block C10: decamethonium TC: tubocurarine NEO: neostigmine S: succinylcholine
- 10. Comparison of Competitive and Depolarizing Blocking Agents No antagonism Transient reversal Effect of KCl or tetatnus on block Transient fasciculations None Initial excitatory effect Partial, persisting depolarization Elevated threshold to Ach; no depolarization Effect on motor end plate No antagonism Reverse Efect of cholinesterase inhibitors May be additive None/antagonistic Effect of previous decamethonium Antagonistic Additive Effect of previous d-tubocurarine Depolarizing Competitive
- 11. Dual Block by Depolarizing Agents C10: decamethonium; NEO: neostigmine; TC: tubocurarine NEO reversed the blockade by C10.
- 12. Depolarizing Blocker Competitive Blockade Competitive Blocker Noncompetitive Blockade (desensitization) (electrogenic Na pump) (direct channel block) Changing Nature of Neuromuscular Blockade
- 13. Sequence of Paralysis Fingers, orbit (small muscles) limbs Trunk neck Intercostals Diaphragm Recovery in Reverse
- 16. Systolic BP Systolic BP % Change in Systolic BP with d-Tubocurarine as a Function of Dose and Depth of Anesthesia Increasing Dose of d-tubocurarine Increasing Depth (% Halothane) 0.25% 0.5% 0.75% 6 mg/m 2 12 mg/m 2 18 mg/m 2
- 17. Influence of Type of Anesthetic on Enhancement of Neuromuscular Blockade By d-Tubocurarine
- 18. HR CO SVR MAP Hemodynamic Effects of d-Tubocurarine and Pancuronium