Myasthenia gravis is an autoimmune disorder that causes weakness in the voluntary muscles. It results from antibodies blocking or destroying acetylcholine receptors in the neuromuscular junction. Symptoms include drooping eyelids, double vision, difficulty speaking and swallowing. While there is no cure, treatment focuses on improving muscle strength and function through medications like cholinesterase inhibitors, corticosteroids and immunosuppressants. Glaucoma is a group of eye diseases that cause damage to the optic nerve and vision loss. Elevated intraocular pressure is a major risk factor. Topical medications to lower pressure include beta blockers, alpha agonists, prostaglandin analogs, and carbonic an
Drugs used in myasthenia gravis and galucomaAshviniGovande
This document provides information about myasthenia gravis (MG) and drugs used to treat it, as well as information about glaucoma and drugs used to treat glaucoma.
MG is an autoimmune disorder causing muscle weakness due to antibodies blocking acetylcholine receptors at the neuromuscular junction. Drugs used to treat MG include acetylcholinesterase inhibitors like pyridostigmine to increase acetylcholine levels, immunosuppressants to reduce antibody production, and thymectomy to remove the thymus gland source of antibodies.
Glaucoma involves increased fluid pressure in the eye damaging the optic nerve. The most common type is primary open-angle glaucoma. Drugs
Sedative hypnotics are central nervous system depressants that can produce sedation, hypnosis, and general anesthesia depending on dosage. Major classes include barbiturates, benzodiazepines, and newer non-benzodiazepine hypnotics. Barbiturates were widely used as sedatives and hypnotics until benzodiazepines were discovered in the 1960s due to their safer profile. Benzodiazepines are now the most commonly used sedative hypnotics due to their high therapeutic index and fewer drug interactions compared to barbiturates. Common sedative hypnotics include diazepam, alprazolam, nitrazepam
This document provides information about sympathomimetic agents. It discusses direct-acting, indirect-acting, and mixed-acting agents and how they work. Specific agents are described, including their properties, mechanisms of action, uses, and storage requirements. Sympathomimetic drugs act on adrenergic receptors to increase heart rate and blood pressure. Structure-activity relationships are also covered, explaining how chemical modifications impact receptor selectivity and duration of action.
1. Alcohol is produced by fermentation of sugars and its pharmacological actions include local irritation, effects on cardiovascular and respiratory systems, hypoglycemia, impacts on temperature regulation and more.
2. Chronic alcoholism can lead to complications like cirrhosis of the liver, hypertension, cardiomyopathy and more. Treatments include naltrexone, acamprosate, topiramate and disulfiram.
3. Methanol poisoning results in symptoms like vomiting, headache and can cause blindness or death if not treated. Treatments include gastric lavage, ethanol administration, fomepizole, hemodialysis and folate therapy.
This ppt covers the classification, structures and IUPAC names, Mechanism of action and uses of individual drugs...under anticonvulsants topic..Side effects/metabolism are also given for few
This document discusses the classification, structure-activity relationships, and mechanisms of action of sympathomimetic and adrenergic drugs. It categorizes these drugs based on their chemical nature, mode of action, receptor selectivity, and therapeutic effects. Key points include:
1) Sympathomimetics are classified as catecholamines which contain a catechol nucleus, or non-catecholamines which do not.
2) They can act directly on receptors, indirectly by releasing norepinephrine, or by both mechanisms.
3) Drugs show selectivity for alpha-1, alpha-2, beta-1, or beta-2 adrenergic receptors.
4) Ther
Drugs used in myasthenia gravis and galucomaAshviniGovande
This document provides information about myasthenia gravis (MG) and drugs used to treat it, as well as information about glaucoma and drugs used to treat glaucoma.
MG is an autoimmune disorder causing muscle weakness due to antibodies blocking acetylcholine receptors at the neuromuscular junction. Drugs used to treat MG include acetylcholinesterase inhibitors like pyridostigmine to increase acetylcholine levels, immunosuppressants to reduce antibody production, and thymectomy to remove the thymus gland source of antibodies.
Glaucoma involves increased fluid pressure in the eye damaging the optic nerve. The most common type is primary open-angle glaucoma. Drugs
Sedative hypnotics are central nervous system depressants that can produce sedation, hypnosis, and general anesthesia depending on dosage. Major classes include barbiturates, benzodiazepines, and newer non-benzodiazepine hypnotics. Barbiturates were widely used as sedatives and hypnotics until benzodiazepines were discovered in the 1960s due to their safer profile. Benzodiazepines are now the most commonly used sedative hypnotics due to their high therapeutic index and fewer drug interactions compared to barbiturates. Common sedative hypnotics include diazepam, alprazolam, nitrazepam
This document provides information about sympathomimetic agents. It discusses direct-acting, indirect-acting, and mixed-acting agents and how they work. Specific agents are described, including their properties, mechanisms of action, uses, and storage requirements. Sympathomimetic drugs act on adrenergic receptors to increase heart rate and blood pressure. Structure-activity relationships are also covered, explaining how chemical modifications impact receptor selectivity and duration of action.
1. Alcohol is produced by fermentation of sugars and its pharmacological actions include local irritation, effects on cardiovascular and respiratory systems, hypoglycemia, impacts on temperature regulation and more.
2. Chronic alcoholism can lead to complications like cirrhosis of the liver, hypertension, cardiomyopathy and more. Treatments include naltrexone, acamprosate, topiramate and disulfiram.
3. Methanol poisoning results in symptoms like vomiting, headache and can cause blindness or death if not treated. Treatments include gastric lavage, ethanol administration, fomepizole, hemodialysis and folate therapy.
This ppt covers the classification, structures and IUPAC names, Mechanism of action and uses of individual drugs...under anticonvulsants topic..Side effects/metabolism are also given for few
This document discusses the classification, structure-activity relationships, and mechanisms of action of sympathomimetic and adrenergic drugs. It categorizes these drugs based on their chemical nature, mode of action, receptor selectivity, and therapeutic effects. Key points include:
1) Sympathomimetics are classified as catecholamines which contain a catechol nucleus, or non-catecholamines which do not.
2) They can act directly on receptors, indirectly by releasing norepinephrine, or by both mechanisms.
3) Drugs show selectivity for alpha-1, alpha-2, beta-1, or beta-2 adrenergic receptors.
4) Ther
Biosynthesis and catabolism of acetylcholine by Dheeraj gargDheeraj Aggarwal
Acetylcholine (ACh) is an organic chemical that functions in the brain and body of many types of animals (and humans) as a neurotransmitter—a chemical message released by nerve cells to send signals to other cells, such as neurons, muscle cells and gland cells.
General Anaesthesia (Medicinal Chemistry)Yogesh Tiwari
General anaesthetics are group of drugs that produces loss of consciousness, and therefore, loss of all sensations.
The absolute loss of sensation is termed as anaesthesia.
The document discusses anti-inflammatory agents known as non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes that produce prostaglandins, which are inflammatory mediators. There are two main COX isoforms, and most NSAIDs inhibit both COX-1 and COX-2 to varying degrees. Selective COX-2 inhibitors may reduce side effects associated with COX-1 inhibition like gastric irritation. NSAIDs are classified into different categories based on their chemical structure and properties. The most common NSAIDs inhibit COX through different mechanisms of action and metabolic pathways.
A condition in which the heart is unable to pump sufficient blood
to meet the metabolic demand of the body and also unable to receive it back because every time after a systole.
ANTI ALZHEIMER'S AGENTS / DRUGS USED IN THE TREATMENT OF ALZHEIMER'S DISEASEKameshwaran Sugavanam
This document discusses drugs used to treat Alzheimer's disease. It focuses on cholinergic activators like rivastigmine and donepezil, which work by inhibiting the breakdown of acetylcholine in the brain to increase levels of this neurotransmitter that is deficient in Alzheimer's patients. It also discusses memantine, an NMDA receptor antagonist that blocks glutamate receptors and protects nerve cells from damage. Common side effects of these drugs include nausea, diarrhea, vomiting and headaches. The document provides details on the mechanisms and effects of rivastigmine and memantine as two major drug classes used to treat symptoms of Alzheimer's disease.
Neurohumoral transmission in CNS-
The term neurohumoral transmission designates the transfer of a nerve impulse from a presynaptic to a postsynaptic neuron by means of a humoral agent e.g. a biogenic amine, an amino acid or a peptide.
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.
Drug addiction, tolerance and depandanceAMANKUMAR1483
This document provides information on drug addiction, intolerance, dependence, and idiosyncrasy. It discusses what causes addiction, the stages of addiction, top abused drugs and their side effects and health consequences. It defines intolerance as experiencing toxic effects from therapeutic doses of a drug. Idiosyncrasy is an abnormal genetic reaction to a chemical producing an unusual response. Dependence occurs when drug use is prioritized over basic needs despite health risks. Tachyphylaxis is rapid tolerance development from repeated high doses. Spare receptors are those not occupied to produce maximum drug response.
This document discusses different types of natural allergens:
- Inhalant allergens include pollen, pets, dust mites, and molds which cause respiratory issues like hay fever and asthma.
- Ingestant or food allergens are present in foods and cause gastrointestinal and other symptoms when digested. Common food allergens include milk, eggs, peanuts, and wheat.
- Injectant allergens come from insect stings or injections and can cause itching, rashes, and swelling.
- Contact allergens like cosmetic ingredients or plant oils cause skin irritation and dermatitis upon contact.
- Infectant allergens are caused by bacterial or
Tragacanth is a dried gummy exudation obtained from incisions made on the stems and branches of Astragalus gummifer. It occurs in thin, flattened, ribbon-like flakes that are white or pale yellowish-white in color. Tragacanth contains two fractions - the water-soluble portion called tragacanthin and the water-insoluble portion called bassorin. It is used as a demulcent, emollient, and thickening, suspending, and emulsifying agent in pharmaceutical and food products.
1. The document discusses the structural activity relationships of various anticonvulsant drug classes including hydantoins, barbiturates, benzodiazepines, valproic acid, and succinimides. Certain aromatic or alkyl substitutions are required for optimal activity within each class.
2. New anticonvulsant compounds currently in clinical trials are discussed, such as AWD 131-138, retigabine, rufinamide, and others. These compounds have novel mechanisms of action such as blockade of voltage-activated calcium channels or increasing potassium conductance in neurons.
3. The structural features required for anticonvulsant activity are compared between drug classes to understand how chemical modifications
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 autonomic nervous system (ANS) innervates the heart, smooth muscles, glands and viscera and is divided into the parasympathetic and sympathetic nervous systems. The parasympathetic system participates in tissue building and the sympathetic system enables responses to stress. Both systems have efferent neurons that travel from the CNS to effector organs via a two-neuron chain, with preganglionic neurons synapsing in ganglia and postganglionic neurons innervating the organs. The sympathetic system originates in the thoracic and lumbar spinal cord and parasympathetic system originates in the cranial and sacral regions. The sympathetic system prepares the body for fight or flight while the parasympathetic
This document discusses CNS stimulants and nootropics, or cognition enhancers. It describes how CNS stimulants produce generalized stimulation of the central nervous system and lists various convulsants, analeptics, and psychostimulants. Nootropics are meant to enhance cerebral functions like memory and are used to treat conditions like Alzheimer's disease, dementia, and learning defects. Common nootropics discussed include cholinergic activators like donepezil and rivastigmine, the NMDA antagonist memantine, and various other drugs like piracetam. Rivastigmine inhibits acetylcholinesterase to increase cholinergic transmission in the brain. Memantine
Drug used in Parkinson,Alzheimer and CNS stimulantsRajkumar Kumawat
This document discusses several central nervous system (CNS) stimulants. It describes how Parkinsonism involves slowed movement and tremors, and can be treated with drugs that increase dopamine like levodopa. Alzheimer's disease causes dementia and memory loss, and is treated with cholinergic drugs. CNS stimulants temporarily improve mental and physical function and include xanthines like caffeine, amphetamines, and methylphenidate. Other stimulants discussed are pentylenetetrazol, nikethamide, strychnine, and lobeline.
The document discusses chiral molecules and their reactions. Chiral molecules have non-superimposable mirror images due to having four different groups attached to a carbon atom without symmetry. There are three major reactions for chiral molecules: retention, where the configuration of substrate and product remain the same; inversion, where the isomer converts to the other form through an SN2 mechanism; and racemization, where a second chiral center forms diastereomers.
Angina pectoris is caused by an imbalance between myocardial oxygen supply and demand. It can result from coronary atherosclerosis, vasospasm, or increased oxygen demand. Several classes of drugs are used to treat angina, including organic nitrates, calcium channel blockers, and beta-blockers. Organic nitrates like nitroglycerin are converted to nitric oxide to relax blood vessels. Calcium channel blockers like nifedipine and diltiazem block calcium channels to dilate arteries. Beta-blockers competitively inhibit beta-adrenergic receptors in the heart to reduce its workload. These drugs provide symptomatic relief for angina by increasing oxygen supply or reducing demand.
Myasthenia gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies block or destroy receptors at the neuromuscular junction, preventing signal transmission from nerves to muscles. Common symptoms include drooping eyelids, double vision, difficulty swallowing and breathing. While there is no cure, treatment aims to control symptoms through medications like cholinesterase inhibitors or immunosuppressants, plasmapheresis, intravenous immunoglobulin or thymectomy. Proper nutrition, rest and exercise are also important for management of the condition.
Myasthenia Gravis is a chronic autoimmune disease that causes muscle weakness by interfering with signal transmission between nerves and muscles. It is characterized by drooping eyelids, double vision, and fatigue that worsens with sustained physical activity. The underlying cause is antibodies produced against acetylcholine receptors at the neuromuscular junction that inhibit muscle contraction. While there is no cure, symptoms can be managed through acetylcholine esterase inhibitors and surgery to remove the thymus gland if tumors are present.
Biosynthesis and catabolism of acetylcholine by Dheeraj gargDheeraj Aggarwal
Acetylcholine (ACh) is an organic chemical that functions in the brain and body of many types of animals (and humans) as a neurotransmitter—a chemical message released by nerve cells to send signals to other cells, such as neurons, muscle cells and gland cells.
General Anaesthesia (Medicinal Chemistry)Yogesh Tiwari
General anaesthetics are group of drugs that produces loss of consciousness, and therefore, loss of all sensations.
The absolute loss of sensation is termed as anaesthesia.
The document discusses anti-inflammatory agents known as non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs work by inhibiting the cyclooxygenase (COX) enzymes that produce prostaglandins, which are inflammatory mediators. There are two main COX isoforms, and most NSAIDs inhibit both COX-1 and COX-2 to varying degrees. Selective COX-2 inhibitors may reduce side effects associated with COX-1 inhibition like gastric irritation. NSAIDs are classified into different categories based on their chemical structure and properties. The most common NSAIDs inhibit COX through different mechanisms of action and metabolic pathways.
A condition in which the heart is unable to pump sufficient blood
to meet the metabolic demand of the body and also unable to receive it back because every time after a systole.
ANTI ALZHEIMER'S AGENTS / DRUGS USED IN THE TREATMENT OF ALZHEIMER'S DISEASEKameshwaran Sugavanam
This document discusses drugs used to treat Alzheimer's disease. It focuses on cholinergic activators like rivastigmine and donepezil, which work by inhibiting the breakdown of acetylcholine in the brain to increase levels of this neurotransmitter that is deficient in Alzheimer's patients. It also discusses memantine, an NMDA receptor antagonist that blocks glutamate receptors and protects nerve cells from damage. Common side effects of these drugs include nausea, diarrhea, vomiting and headaches. The document provides details on the mechanisms and effects of rivastigmine and memantine as two major drug classes used to treat symptoms of Alzheimer's disease.
Neurohumoral transmission in CNS-
The term neurohumoral transmission designates the transfer of a nerve impulse from a presynaptic to a postsynaptic neuron by means of a humoral agent e.g. a biogenic amine, an amino acid or a peptide.
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.
Drug addiction, tolerance and depandanceAMANKUMAR1483
This document provides information on drug addiction, intolerance, dependence, and idiosyncrasy. It discusses what causes addiction, the stages of addiction, top abused drugs and their side effects and health consequences. It defines intolerance as experiencing toxic effects from therapeutic doses of a drug. Idiosyncrasy is an abnormal genetic reaction to a chemical producing an unusual response. Dependence occurs when drug use is prioritized over basic needs despite health risks. Tachyphylaxis is rapid tolerance development from repeated high doses. Spare receptors are those not occupied to produce maximum drug response.
This document discusses different types of natural allergens:
- Inhalant allergens include pollen, pets, dust mites, and molds which cause respiratory issues like hay fever and asthma.
- Ingestant or food allergens are present in foods and cause gastrointestinal and other symptoms when digested. Common food allergens include milk, eggs, peanuts, and wheat.
- Injectant allergens come from insect stings or injections and can cause itching, rashes, and swelling.
- Contact allergens like cosmetic ingredients or plant oils cause skin irritation and dermatitis upon contact.
- Infectant allergens are caused by bacterial or
Tragacanth is a dried gummy exudation obtained from incisions made on the stems and branches of Astragalus gummifer. It occurs in thin, flattened, ribbon-like flakes that are white or pale yellowish-white in color. Tragacanth contains two fractions - the water-soluble portion called tragacanthin and the water-insoluble portion called bassorin. It is used as a demulcent, emollient, and thickening, suspending, and emulsifying agent in pharmaceutical and food products.
1. The document discusses the structural activity relationships of various anticonvulsant drug classes including hydantoins, barbiturates, benzodiazepines, valproic acid, and succinimides. Certain aromatic or alkyl substitutions are required for optimal activity within each class.
2. New anticonvulsant compounds currently in clinical trials are discussed, such as AWD 131-138, retigabine, rufinamide, and others. These compounds have novel mechanisms of action such as blockade of voltage-activated calcium channels or increasing potassium conductance in neurons.
3. The structural features required for anticonvulsant activity are compared between drug classes to understand how chemical modifications
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 autonomic nervous system (ANS) innervates the heart, smooth muscles, glands and viscera and is divided into the parasympathetic and sympathetic nervous systems. The parasympathetic system participates in tissue building and the sympathetic system enables responses to stress. Both systems have efferent neurons that travel from the CNS to effector organs via a two-neuron chain, with preganglionic neurons synapsing in ganglia and postganglionic neurons innervating the organs. The sympathetic system originates in the thoracic and lumbar spinal cord and parasympathetic system originates in the cranial and sacral regions. The sympathetic system prepares the body for fight or flight while the parasympathetic
This document discusses CNS stimulants and nootropics, or cognition enhancers. It describes how CNS stimulants produce generalized stimulation of the central nervous system and lists various convulsants, analeptics, and psychostimulants. Nootropics are meant to enhance cerebral functions like memory and are used to treat conditions like Alzheimer's disease, dementia, and learning defects. Common nootropics discussed include cholinergic activators like donepezil and rivastigmine, the NMDA antagonist memantine, and various other drugs like piracetam. Rivastigmine inhibits acetylcholinesterase to increase cholinergic transmission in the brain. Memantine
Drug used in Parkinson,Alzheimer and CNS stimulantsRajkumar Kumawat
This document discusses several central nervous system (CNS) stimulants. It describes how Parkinsonism involves slowed movement and tremors, and can be treated with drugs that increase dopamine like levodopa. Alzheimer's disease causes dementia and memory loss, and is treated with cholinergic drugs. CNS stimulants temporarily improve mental and physical function and include xanthines like caffeine, amphetamines, and methylphenidate. Other stimulants discussed are pentylenetetrazol, nikethamide, strychnine, and lobeline.
The document discusses chiral molecules and their reactions. Chiral molecules have non-superimposable mirror images due to having four different groups attached to a carbon atom without symmetry. There are three major reactions for chiral molecules: retention, where the configuration of substrate and product remain the same; inversion, where the isomer converts to the other form through an SN2 mechanism; and racemization, where a second chiral center forms diastereomers.
Angina pectoris is caused by an imbalance between myocardial oxygen supply and demand. It can result from coronary atherosclerosis, vasospasm, or increased oxygen demand. Several classes of drugs are used to treat angina, including organic nitrates, calcium channel blockers, and beta-blockers. Organic nitrates like nitroglycerin are converted to nitric oxide to relax blood vessels. Calcium channel blockers like nifedipine and diltiazem block calcium channels to dilate arteries. Beta-blockers competitively inhibit beta-adrenergic receptors in the heart to reduce its workload. These drugs provide symptomatic relief for angina by increasing oxygen supply or reducing demand.
Myasthenia gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies block or destroy receptors at the neuromuscular junction, preventing signal transmission from nerves to muscles. Common symptoms include drooping eyelids, double vision, difficulty swallowing and breathing. While there is no cure, treatment aims to control symptoms through medications like cholinesterase inhibitors or immunosuppressants, plasmapheresis, intravenous immunoglobulin or thymectomy. Proper nutrition, rest and exercise are also important for management of the condition.
Myasthenia Gravis is a chronic autoimmune disease that causes muscle weakness by interfering with signal transmission between nerves and muscles. It is characterized by drooping eyelids, double vision, and fatigue that worsens with sustained physical activity. The underlying cause is antibodies produced against acetylcholine receptors at the neuromuscular junction that inhibit muscle contraction. While there is no cure, symptoms can be managed through acetylcholine esterase inhibitors and surgery to remove the thymus gland if tumors are present.
Myasthenia gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies block or destroy receptor sites in the muscles, interfering with nerve impulses that trigger muscle contraction. Common symptoms include drooping eyelids, double vision, difficulty chewing or swallowing, and limb weakness. While there is no cure, treatment focuses on medications to improve nerve-muscle communication and prevent respiratory complications. The condition is managed long-term through a combination of drug therapies and monitoring for potential worsening of symptoms.
This document discusses myasthenia gravis (MG), an autoimmune disorder that causes muscle weakness. There are three main types of MG that affect children - congenital MG, transient neonatal MG, and juvenile MG. Symptoms vary depending on the type but can include generalized weakness, difficulty feeding, and drooping eyelids. Treatment aims to control symptoms and prevent respiratory problems through medications, plasmapheresis, intravenous immunoglobulin, and sometimes surgery to remove the thymus gland. A study at NIMH in India found that juvenile MG has some distinctive characteristics compared to adult-onset MG, such as a higher rate of ocular symptoms and generally more benign course.
Myasthenia gravis is an autoimmune disorder that causes muscle weakness. It occurs when antibodies destroy connections between nerves and muscles. Symptoms vary but can include drooping eyelids, blurred or double vision, difficulty swallowing and speaking, and weakness in arms or legs. While there is no cure, treatment aims to control symptoms through medications that enhance nerve-muscle communication or suppress the immune system.
Myasthenia gravis is an autoimmune disorder characterized by weakness and fatigability of skeletal muscles. It is caused by antibodies that block or destroy acetylcholine receptor sites in muscles, impairing nerve signal transmission and causing weakness. Symptoms often first affect ocular muscles and may progress to other areas. Treatment focuses on immunosuppression and thymectomy in some cases. Complications can include myasthenic crisis if respiratory muscles are affected.
Myasthenia gravis is an autoimmune disease that causes muscle weakness. It is caused by antibodies that block or destroy acetylcholine receptors in the muscles. This presentation defines myasthenia gravis, lists predisposing factors like genetics and antibodies produced by the thymus gland, and explains the pathophysiology involving acetylcholine receptor blockade. It also classifies myasthenia gravis by age, lists investigations like tensilon tests, and describes the prognosis, management including immunosuppression, and homoeopathic approaches using remedies like Gelsemium and Cocculus that address muscle weakness.
Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness in the skeletal muscles. It is caused by antibodies that block or destroy acetylcholine receptors in the neuromuscular junction, preventing signal transmission from nerves to muscles. Common symptoms include drooping eyelids, double vision, difficulty speaking, swallowing and breathing. While there is no cure, treatment aims to relieve symptoms through acetylcholinesterase inhibitors, corticosteroids, immunosuppressants and managing triggers. A diagnosis involves neurological exams, blood tests to detect antibodies, and response to medication challenges.
Myasthenia gravis is a neuromuscular disorder that causes weakness in the skeletal muscles, which are the muscles your body uses for movement.
It occurs when communication between nerve cells and muscles become impaired.
This impairment prevents crucial muscle contractions from occurring, resulting in muscle weakness.
Most common primary disorder of neuromuscular transmission.
This document discusses ocular myasthenia gravis through an interview with the presenter's mother who has lived with the condition for over 30 years. The mother describes her initial symptoms of double vision and drooping eyelids. She discusses receiving a diagnosis of generalized myasthenia gravis initially and then ocular myasthenia gravis. The mother also shares details of her symptoms at their worst and best, as well as how the condition has impacted her personal and professional life. She provides advice for others living with the disease to stay positive and informed.
Myasthenia gravis is a neuromuscular junction disorder characterized by skeletal muscle weakness and fatigability caused by a decrease in acetylcholine receptors at the neuromuscular junction due to an antibody-mediated autoimmune attack. It affects individuals of all ages, with peak incidence in women in their 20s-30s and men in their 50s-60s. Symptoms include drooping eyelids, double vision, difficulty speaking and swallowing, and generalized weakness in arms and legs.
Myasthenia gravis is an autoimmune disease that causes muscle weakness. It occurs when antibodies block or change signals from nerves to muscles, weakening muscles. Common symptoms include drooping eyelids, double vision, difficulty swallowing and speaking. Diagnosis involves tests of blood, nerves and muscles. While there is no cure, treatment aims to reduce antibodies and symptoms through medications, plasmapheresis, IVIG or thymectomy. Patients require long-term management of symptoms and immunosuppression therapy.
Myasthenia gravis (MG) is a neuromuscular disorder characterized by weakness and fatigability of skeletal muscles.
The underlying defect is a decrease in the number of available acetylcholine receptors (AChRs) at neuromuscular junctions due to an antibody-mediated autoimmune attack
Myasthenia gravis is an autoimmune disorder causing muscle weakness that worsens with activity. It results from antibodies attacking acetylcholine receptors at the neuromuscular junction, impairing muscle contraction. Common symptoms include drooping eyelids, double vision, difficulty swallowing and speaking. Diagnosis involves physical exams, blood tests to detect antibodies, repetitive nerve stimulation tests, and imaging. Treatment aims to maximize acetylcholine activity and limit immunological attacks, using anticholinesterase drugs, thymectomy, plasma exchange, immunosuppressants, and behavioral modifications like rest periods.
Myasthenia gravis is an autoimmune disorder that causes muscle weakness. It occurs in approximately 2 out of every 100,000 people and can affect people of any age, sex, or race. The hallmark symptoms include muscle weakness that increases with activity and improves with rest, often affecting muscles around the eyes, face, neck, and throat. It is caused by antibodies blocking or destroying acetylcholine receptors in the neuromuscular junction, interrupting communication between nerves and muscles. While there is no cure, treatment options can help strengthen muscles and suppress antibody production.
Neuromuscular disorders affect the peripheral nervous system and cause progressive muscle weakness. While individually rare, as a group they are not uncommon. Some neuromuscular conditions can affect dental treatment for elderly patients who may have difficulty with oral hygiene. Myasthenia gravis is the most common neuromuscular disease, where antibodies prevent nerve impulse transmission to muscles causing weakness. Dental care requires awareness of medications and increased risk of secretions for patients with these disorders.
Myasthenia Gravis was first described by Thomas Willis in 1672.
“Myasthenia Gravis” literally means “muscle weakness”.
MG is often called the “snowflake disease” because it differs so much from person to person.
Definition
Myasthenia gravis (MG) is an autoimmune disease that causes chronic, progressive damage of the neuromuscular junction.
The underlying defect is a decrease in the number of available acetylcholine receptor (AChRs) at neuromuscular junctions due to an antibody-mediated autoimmune attack.
Clinical Features
Eye muscles
Drooping of one or both eyelid (Ptosis)
Double vision (diplopia)
Face and throat muscles
Dysarthria
Dysphasia
Problem in chewing
Limited facial expression
Snarling expression
Respiratory symptoms
Weakness of intercostal muscle and diaphragm.
Weakness of pharyngeal muscles
Palate muscle weakness
Nasal voice
Nasal regurgitation
Swallowing may be difficult and regurgitation of food can occur.
Coughing and chocking while drinking
Limb muscle weakness in MG is often proximal and may be asymmetric.
In ~85% o patients, the weakness becomes generalized, affecting the limb muscles as well.
If weakness remains restricted to the extra ocular muscles for 3 years, it is likely that it will not become generalized, and these patients are said to have ocular MG.
1. Myasthenia gravis is an autoimmune disease causing muscle weakness and fatigability due to antibodies blocking acetylcholine receptors at the neuromuscular junction.
2. Diagnosis involves eliciting a history of fluctuating weakness and physical exam findings of rapidly fatigable weakness, as well as repetitive stimulation tests and tensilon tests.
3. Treatment includes acetylcholinesterase inhibitors, immunosuppressive drugs, thymectomy, and management of myasthenic crisis with IV immunoglobulin or plasma exchange. Long-term management requires balancing medication side effects in children.
mysthenia gravis & DRUGS USED IN MYSTHENIA GRAVISsrinupappu
This document provides information about diagnosing and treating myasthenia gravis. Diagnosis involves neurological exams, blood tests, nerve stimulation tests, imaging, and pulmonary function tests. Treatments include cholinesterase inhibitors and corticosteroids to manage symptoms, immunosuppressants for long-term control, plasmapheresis or IVIg for acute episodes, and surgery to remove the thymus gland which may improve symptoms. Side effects of treatments can include infections, digestive issues, and immune system suppression.
This document provides information about orbital myositis, including:
1. Orbital myositis is an inflammatory process that primarily involves the extraocular muscles. It is characterized by acute onset unilateral periorbital pain and diplopia.
2. It most commonly affects young adults in their third decade of life and females more than males. Common symptoms include diplopia, proptosis, conjunctival hyperemia.
3. Treatment involves oral corticosteroids as the first line treatment. Methotrexate and azathioprine can be used as steroid-sparing agents for patients who cannot tolerate steroids or fail to taper off.
Similar to Dugs used in Myasthenia gravis and Glaucoma.pptx (20)
Asthma is a chronic inflammatory lung disease that causes narrowing of the airways. It affects over 300 million people worldwide. The hallmark symptoms of asthma include wheezing, coughing, chest tightness, and shortness of breath. Asthma is caused by a combination of genetic and environmental factors that lead to airway inflammation and constriction. Common triggers include allergens, viruses, exercise, and air pollution. Diagnosis involves lung function tests to measure airflow limitation and its improvement with bronchodilator medication. Treatment focuses on reducing symptoms with bronchodilators and preventing exacerbations with anti-inflammatory drugs like corticosteroids.
Asthma is a chronic disease characterized by inflammation of the airways causing coughing, wheezing, chest tightness, and difficulty breathing. It is usually caused by allergic triggers like pollen, dust mites, or animal dander that lead to bronchospasms and airway obstruction. Diagnosis involves patient history, physical exam, pulmonary function tests, and allergy testing. Treatment includes bronchodilators, corticosteroids, leukotriene modifiers, and monoclonal antibodies to reduce inflammation and prevent symptoms.
Ischaemic heart disease is caused by an imbalance between the heart's supply and demand for oxygenated blood, usually due to atherosclerosis narrowing the coronary arteries. The main symptoms are chest pain or discomfort known as angina. There are different types of angina that vary based on their triggers and patterns. Diagnosis involves tests like ECG, echocardiogram, stress tests and angiography. Treatment options include medications to reduce demands on the heart like nitrates, beta-blockers, and calcium channel blockers, as well as interventions like angioplasty, stents and bypass surgery.
Atherosclerosis is a disease where plaque builds up in the arteries. Over time, the plaque hardens and narrows the arteries, limiting blood flow. Risk factors include age, family history, smoking, high blood pressure, high cholesterol, diabetes, and obesity. Complications arise when blood flow is reduced to organs like the heart, brain, kidneys, and limbs, potentially causing heart attacks, strokes, chronic kidney disease, or poor circulation. Treatment focuses on lifestyle changes and medications to control risk factors and symptoms.
This document provides an outline for a lecture on hypertension. It begins with objectives to understand hypertension's etiology, risk factors, and complications. It then covers definitions of hypertension, classifications based on cause and clinical features, risk factors, pathogenesis, regulation of blood pressure, vascular changes in hypertension, and complications affecting the heart, blood vessels, kidneys, eyes, and brain. The lecture topics include primary and secondary causes, benign vs malignant hypertension, endocrine factors influencing blood pressure, and target organ damage.
Hypertension and its pathophysiology.pptxImtiyaz60
The document discusses hypertension and the heart. It provides details on:
- The structure and layers of the heart, including the myocardium and pericardium.
- The path of blood through the heart, from the vena cava and atria to the ventricles, valves, and out the aorta to the body.
- Additional details are given on heart size, location in the thoracic cavity, and the double-walled pericardium surrounding and protecting the heart.
This document discusses various appetite stimulants, digestants, and carminatives. It describes how appetite is influenced by several factors in the hypothalamus and gut-brain pathways. Common appetite stimulants mentioned include lemon pickles, bitter orange peel, and soups containing aromatic oils. Some medications can increase appetite but also have side effects. The document also discusses various digestive enzymes and bile acids that may aid digestion, though evidence for their efficacy is limited. Finally, it outlines several common carminative herbs and spices that can relieve gas and bloating.
Anti Ulcer drugs pharmacology and classificationImtiyaz60
This document summarizes drugs used to treat peptic ulcers. It discusses the anatomy and physiology of gastric acid secretion regulated by histamine, acetylcholine, and gastrin. It describes prostaglandins' protective role in the stomach and how H2 receptor blockers and proton pump inhibitors work to suppress acid secretion. H2 blockers competitively inhibit histamine receptors, while PPIs irreversibly inactivate the proton pump. Common medications discussed include cimetidine, ranitidine, famotidine, omeprazole, and lansoprazole. The goals of anti-ulcer therapy are relieving pain, promoting healing, and preventing complications and relapse.
Ginger and asafoetida are plants with medicinal properties. Ginger is native to Southeast Asia and cultivated in many tropical regions. It has buff-colored rhizomes with an aromatic odor and taste. Chemical constituents include volatile oils and phenolic compounds that give ginger its flavor and pharmacological effects. Asafoetida is an oleo-gum-resin obtained from Ferula plants. It occurs in tear or mass forms, has an intense odor, and chemical tests detect umbelliferone. Both ginger and asafoetida have traditional uses as carminatives, expectorants, and to treat conditions like nausea, flatulence, and asthma. They can be subject to adulteration
Leprosy is caused by Mycobacterium leprae. It primarily affects the skin and peripheral nerves, causing hypopigmented patches and thickening of nerves. There are two main forms - tuberculoid leprosy, which causes localized lesions, and lepromatous leprosy, which involves multiple organs. Diagnosis involves skin smears and biopsies to identify acid-fast bacilli. Treatment involves multidrug chemotherapy regimens containing dapsone, rifampicin, and clofazimine. Prevention focuses on contact tracing, chemoprophylaxis, isolation during reactions, and rehabilitation.
Tuberculosis (TB) is a chronic bacterial infection caused by Mycobacterium tuberculosis that typically forms granulomas in the lungs. It is treatable with a combination of anti-TB drugs over a 6-12 month period to kill both actively replicating and dormant bacilli. Diagnosis involves physical exam, chest x-ray, tuberculin skin test, and sputum culture. Risk factors include HIV infection, poverty, and crowded living conditions.
Stroke is the 5th leading cause of death in the US. There are three main types of stroke: ischemic, hemorrhagic, and transient ischemic attacks (TIAs). Ischemic strokes, which account for 85% of cases, occur when a blood clot blocks an artery supplying blood to the brain. Hemorrhagic strokes occur when a brain artery ruptures due to conditions like hypertension. TIAs are temporary and cause no permanent damage but indicate risk for future strokes. Symptoms of stroke appear suddenly and include face drooping, arm weakness, speech difficulties, and severe headache. Diagnostic tests help determine the type and location of stroke. Lifestyle changes and medical treatment can help prevent strokes.
The thyroid gland is located in the neck below the larynx. It produces thyroid hormones including thyroxine (T4) and triiodothyronine (T3) which increase metabolism in nearly every organ system. Iodine is necessary for thyroid hormone production. Disorders include hypothyroidism, where thyroid hormone production is inadequate, and hyperthyroidism, where production is excessive. Graves' disease is an autoimmune cause of hyperthyroidism. Cretinism results from untreated congenital hypothyroidism and causes severe physical and mental impairment.
Inflammatory bowel disease (IBD) represents a group of chronic disorders that cause prolonged inflammation of the digestive tract. The two main types are ulcerative colitis, which causes inflammation and ulcers in the lining of the large intestine, and Crohn's disease, which is a chronic inflammatory disease that can affect any part of the gastrointestinal tract from mouth to anus. IBD is treated through a combination of medications, dietary changes, and sometimes surgery, with the goals of inducing and maintaining remission of symptoms, preventing complications, and avoiding surgery if possible. Treatments include aminosalicylates, corticosteroids, immunosuppressants, biologics that target tumor necrosis factor, and antimicrobial agents.
Tannins are polyphenolic compounds found in many plants. They are classified as hydrolysable tannins, condensed tannins, or pseudo-tannins. Hydrolysable tannins are hydrolyzed by acids into gallic acid or ellagic acid, while condensed tannins are more resistant to hydrolysis. Tannins are extracted using mixtures of polar and non-polar solvents due to their high molecular weight. Identification tests for tannins include the gelatin test, Goldbeater's skin test, and reactions with ferrous sulfate or ferric chloride that produce colors. Pterocarpus marsupium, or Bijasal, is a plant source of k
This document discusses various drug classes used in the treatment of heart failure, including their mechanisms and effects. Diuretics reduce preload on the heart by reducing extracellular fluid volume through natriuresis. Vasodilators such as nitroglycerin and ACE inhibitors reduce preload and afterload by dilating blood vessels. Nesiritide is a natriuretic peptide that causes vasodilation and natriuresis. β-blockers improve outcomes in heart failure by inhibiting the deleterious effects of sympathetic activation on the heart.
Tuberculosis (TB) is a bacterial infection caused by Mycobacterium tuberculosis that most commonly infects the lungs. It can be treated with antibiotics. TB is spread through airborne droplets when an infected person coughs or sneezes. While latent TB means the immune system has contained the infection and the person is not infectious, active TB means the person is sick and can spread the disease. Standard TB treatment involves a combination of antibiotics like isoniazid, rifampin and ethambutol over a period of 6-9 months.
The document discusses infectious diseases and infectious agents. It covers host barriers to infection like the skin, respiratory system, gastrointestinal tract, and urogenital tract. It describes how these barriers can fail and allow infection. It also discusses the different classes of infectious agents including bacteria, viruses, fungi and parasites. The document outlines the different types of inflammatory responses infections can cause like suppurative inflammation, granulomatous inflammation, and cytopathic responses. It covers how microbes can evade the immune system and the various ways infections can be transmitted.
The document defines key terms related to the electrophysiology of the heart such as action potential, membrane potential, refractory period, and threshold potential. It then describes the four phases of the cardiac action potential: Phase 0 involves stimulation and sodium/calcium influx causing depolarization; Phase 1 involves partial repolarization through ion efflux; Phase 2 involves a plateau phase through continued ion fluxes; Phase 3 involves full repolarization through ion efflux slower than depolarization. Phase 4 is the interval between repolarizations. The cardiac action potential triggers mechanical contraction. An electrocardiogram detects and records the summed action potentials to analyze patterns like the P, QRS, and T waves related to atrial depolarization, ventricular depolarization
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
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.
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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This presentation was provided by Steph Pollock of The American Psychological Association’s Journals Program, and Damita Snow, of The American Society of Civil Engineers (ASCE), for the initial session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session One: 'Setting Expectations: a DEIA Primer,' was held June 6, 2024.
Strategies for Effective Upskilling is a presentation by Chinwendu Peace in a Your Skill Boost Masterclass organisation by the Excellence Foundation for South Sudan on 08th and 09th June 2024 from 1 PM to 3 PM on each day.
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
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
How to Add Chatter in the odoo 17 ERP ModuleCeline George
In Odoo, the chatter is like a chat tool that helps you work together on records. You can leave notes and track things, making it easier to talk with your team and partners. Inside chatter, all communication history, activity, and changes will be displayed.
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This presentation includes basic of PCOS their pathology and treatment and also Ayurveda correlation of PCOS and Ayurvedic line of treatment mentioned in classics.
3. INTRODUCTION
• Myasthenia gravis (MG) is a complex, autoimmune disorder in which
antibodies destroy neuromuscular connections.
• Causes problems with the nerves that communicate with muscles.
• Affects the voluntary muscles of the body, especially the eyes, mouth, throat,
and limbs.
4. • Characterized by weakness and rapid fatigue of any of the muscles under the
voluntary control.
• The cause of myasthenia gravis is a breakdown in the normal
communication between nerves and muscles.
• No cure for myasthenia gravis, but treatment can help relieve signs and
symptoms – such as weakness of arm or leg muscles, double vision,
drooping eyelids, and difficulties with speech, chewing, swallowing and
breathing.
5.
6.
7. TYPES OF MYASTHENIA GRAVIS
Three types of MG in children:
• Congenital MG - Very rare non-immune form of MG that is inherited as an autosomal
recessive disease.
• Symptoms of congenital MG usually begin in the baby's first year and are life-long.
• Transient neonatal MG - Between 10 and 20 percent of babies born to mothers with MG
may have a temporary form of MG.
• Neonatal MG usually lasts only a few weeks, and babies are not at greater risk for
developing MG later in life.
• Juvenile MG - This auto-immune disorder develops typically in female adolescents.
• It is a life-long condition that may go in and out of remission. About 10 percent of MG
cases are juvenile-onset.
8. SYMPTOMS
• Congenital MG symptoms may begin in the first year, with generalized weakness in the
arms and legs, and delays in motor skills such as crawling, sitting, and walking
• Babies with neonatal MG may be weak, with a poor suck, and may have respiratory
difficulty.
• A few babies may need the help of a mechanical breathing machine if their respiratory
muscles are too weak to breathe on their own.
• Juvenile MG symptoms may begin gradually over weeks or months.
• The child may become excessively tired after very little activity, and begin to have problems
chewing and swallowing.
• Drooping eyelids may be so severe that the child cannot see.
9. Eye muscles
In more than half the people who develop MG, their first signs and
symptoms involve eye problems:
• Drooping of one or both eyelids (ptosis)
• Double vision (diplopia), which may be horizontal or vertical
• Blurred vision, which may come and go
10. Face and throat muscles
• In about 15 percent of people with myasthenia gravis, the first symptoms involve face
and throat muscles, which can cause difficulties with:
• Speaking. The speech may be very soft or sound nasal, depending upon which
muscles have been affected.
• Swallowing. May choke very easily, which makes it difficult to eat, drink or take
pills. In some cases, liquids may come out of the nose.
• Chewing. The muscles used for chewing may wear out halfway through a meal,
particularly if eating
• something hard to chew, such as sugarcane.
• Facial expressions. Family members may note "lost smile" if the
muscles that control facial expressions are affected.
11. Arm and leg muscles
▪ Myasthenia gravis can cause weakness in arms and legs, but this usually
happens in conjunction with muscle weakness in other parts of the body –
such as eyes, face or throat.
▪ The disorder usually affects arms more often than legs.
▪ If it affects legs, may waddle when walking.
Normal dumbbell Weakness dumbbell
12. When to see a doctor
• If having trouble with:
• Breathing
• Seeing
• Swallowing
• Chewing
• Walking
13. CAUSES
• Myasthenia gravis may be inherited, genetic disease, acquired by
babies born to mothers with MG
• Nerves communicate with the muscles by releasing chemicals, called
neurotransmitters, which fit precisely into receptor sites on the muscle
cells.
• In myasthenia gravis, immune system produces antibodies that block or
destroy many of the muscles receptor sites for a neurotransmitter called
acetylcholine.
• With fewer receptor sites available, muscles receive fewer nerve
signals, resulting in weakness.
14. Chemicals messengers, called neurotransmitters, fit precisely into receptor
sites on your muscle cells. In myasthenia gravis, certain receptor sites are
blocked or destroyed, causing muscle weakness.
16. • It's believed that the thymus gland, a part of the
immune system located in the upper chest
beneath the breastbone, may trigger or maintain
the production of these antibodies.
• Large in infancy, the thymus is small in healthy
adults. But, in some adults with myasthenia
gravis, the thymus is abnormally large.
• Some people also have tumors of the thymus.
• Usually, thymus gland tumors are
noncancerous.
17. COMPLICATIONS
• Myasthenic crisis: A life-threatening condition, which occurs when the
muscles that control breathing become too weak to do their jobs.
Emergency treatment is needed to provide mechanical assistance with
breathing.
• Thymus tumors: About 15 percent of the people who have myasthenia
gravis have a tumor in their thymus, a gland under the breastbone that is
involved with the immune system. Most of these tumors are
noncancerous.
18. Other disorders
• Underactive or overactive thyroid. The thyroid gland, located in the
neck, secretes hormones that regulate metabolism. If thyroid is
underactive, body uses energy more slowly. An overactive thyroid makes
body use energy too quickly.
• Lupus. Disease of immune system. Common symptoms include painful
or swollen joints, hair loss, extreme fatigue and a red rash on the face.
• Rheumatoid arthritis. Caused by problems with immune system. It is
most conspicuous in the wrists and fingers, and can result in joint
deformities that make it difficult to use hands.
19. Diagnostic tests
• Blood tests
• Genetic tests - diagnostic tests that evaluate for conditions that
have a tendency to run in families.
• Electromyogram (EMG) - a test that measures the electrical activity
of a muscle or a group of muscles.
• An EMG can detect abnormal electrical muscle activity due to
diseases and neuromuscular conditions.
• Muscle biopsy - a small sample of the muscle is removed and
examined to determine and confirm a diagnosis or condition.
20. TREATMENTS & DRUGS
• Specific treatment to age, overall health, and medical history and extent
of the condition
• No cure for MG, but the symptoms can be controlled.
• MG is a life-long medical condition and the key to medically managing
MG is early detection.
• The goal of treatment is to prevent respiratory problems and provide
adequate nutritional care to the child since the swallowing and
breathing muscles are affected by this condition.
21. Medications
• Cholinesterase inhibitors. Drugs like pyridostigmine (Mestinon)
enhance communication between nerves and muscles.
• These drugs don't cure, but improves muscle contraction and strength.
• Corticosteroids. These types of drugs inhibit the immune system,
limiting antibody production.
• Prolonged use of corticosteroids, can lead to serious side effects, like
bone thinning, weight gain, diabetes, increased risk of some infections,
and increase and redistribution of body fat.
• Immunosuppressants.
• Doctor may also prescribe other medications that alter immune system,
like azathioprine (Imuran), cyclosporine (Sandimmune, Neoral) or
mycophenolate (CellCept).
22. Therapy
• Plasmapheresis. This procedure uses a filtering process similar to
dialysis.
• Blood is routed through a machine that removes the antibodies that
are blocking transmission of signals from nerve endings to muscles
receptor sites. However, the beneficial effects usually last only a few
weeks.
• Intravenous immune globulin. This therapy provides body with
normal antibodies, which alters immune system response.
• It has a lower risk of side effects than do plasmapheresis and
immune- suppressing therapy, but it can take a week or two to start
working and the benefits usually last less than a month or two.
23. • Thymectomy - surgical removal of the thymus gland. The role of the thymus
gland in MG is not fully understood, and the thymectomy may or may not improve
a child's symptoms.
• About 15 percent of the people who have MG have a tumor in their thymus
• For people with MG who don't have a tumor in the thymus, it's unclear whether the
potential benefit of removing the thymus outweighs the risks of surgery.
• This is an individualized decision between patient and the doctor, but most doctors
don't recommend surgery if:
• Symptoms are mild
• Symptoms involve only the eyes
• Patients over 60 years old
Surgery
24. • Plasmapheresis - a procedure that removes abnormal antibodies from the
blood and replaces the child's blood with normal antibodies through
donated blood.
• Extent of the problems is dependent on the severity of the condition and the
presence of other problems that could affect the child.
• In severe cases, a breathing machine may be required to help the child
breathe easier.
• It is important to allow the child as machine dependent function and self
care, especially with juvenile MG, as possible and to promote age-
appropriate activities to ensure a sense of normalcy.
26. What is glaucoma ?
• Glaucoma – ancient meaning (Greek) clouded or
blue- green hue
• Glaucoma – blindness coming from advancing years
(!)
• Second leading cause of blindness
• Glaucoma is a group of disorders characterized
by a progressive optic neuropathy resulting in a
characteristic appearance of optic disc &
specific pattern of irreversible visual field
defects that are associated frequently but not
invariably with ↑IOP (>21 mm Hg)
• All types of glaucoma – progressive optic
neuropathy due to the death of retinal ganglion
cells (RGCs)
27. Aqueous humor dynamics
• Aqueous is continuously produced by the ciliary
body (2-3 µl/minute)
• Aqueous flows from the posterior chamber
through the pupil into the anterior chamber
• Aqueous filters largely through the trabecular
meshwork (90%) and canal of Schlemm→
episcleral venous plexus and into systemic
circulation.
• Aqueous also exits to a smaller extent through the
ocular venous system (10%)
– Uveoscleral outflow (ciliary body, choroid,
scleral vessels)
28. Types of glaucoma
• Congenital glaucoma
• Primary glaucoma
– Open angle
– Closed angle
• Secondary glaucoma – lens
induced, traumatic or steroid
induced
• Absolute glaucoma
29. Therapeutic goal
• Lower IOT by
– Reduction of aqueous humor secretion
– Promoting aqueous drainage
• Lowering of IOT retards the progression of optic nerve
damage even in normal/low i.o.t
30. Open angle/wide angle/chronic simple glaucoma
• Genetically predisposed degenerative disease affecting patency of
trabecular meshwork
• Meshwork becomes less efficient at draining
• IOP builds up progressively
• Damage of the optic nerve
• Has no symptoms in its early stages after middle age
• Ocular hypotensive drugs - reduce formation of AH, increase drainage or
protect optic nerve
34. β- adrenergic blocker in glaucoma - MOA
• Topical β- adrenergic blockers have been the first line of drugs - PG F2α
are preferred now
• Contrast to miotics – no effects on pupil size, tone of cilliary
muscle and outflow facility
• Lower IOP by reducing aqueous formation
– Down regulation of adenylylcyclase due to β2 receptor blockade in
cilliary epithelium
– Reduction of blood flow
• Advantages over miotics – produce less ocular side effects,
lipophillic and weak anaesthetic (corneal hyposthesia and damage)
35. β- adrenergic blockers – contd.
• Ocular side effects: mild and infrequent
– Stinging, redness, dryness
– Corneal hypoesthesia
– Blurred vision
• Systemic adverse effects: Major limitation of use
– Nasolacrima duct
– Life threatening bronchospasm – COPD and asthma
– Bradycardia, heart block and CHF – ADRs
36. Individual drugs – beta blockers
• Timolol (0.25-0.5% eye drops): Non-Selective- β1 + β2
• sympathomimetic action
• ↓ IOT by 20-35% - 1 hour to 12 hours
• Smooth and well sustained action after chronic dosing→ high level of clinical
safety – advantage
• 30% patients response
• Betaxolol (0.5 %)
• Selective β1 blocker - Less bronchopulmonary, probably less cardiac, central
and metabolic effects
• Exert protective effect on retinal neurones
• Less efficacious in ↓ IOT than timolol (β2)
• Levobunolol: Once daily dosing alt. to timolol
Ocular and systemic side effects similar to timolol
37. α – adrenergic agonists
• MOA
– α1 constrict ciliary body - reduced aqueous secretion
– α2 in ciliary epithelium reduce aqueous secretion
– Secondary role in enhancing drainage of aqueous mainly
through uveoscleral outflow and also trabecular outflow
• Dipivefrine (0.1 %)
Adrenaline – ocular smarting, reactive hyperemia
Prodrug of adrenaline→ Adr. ↓ IOT by ↑ uveoscleral
outflow,↑ trabecular outflow (β2), ↓ aqueous production (α1
+ α2 )
Not used now due to systemic effects & ocular intolerance
Maybe used as an add-on therapy
38. α – adrenergic agonists – contd.
• Apraclonidine (0.5- 1%): Clonidine congener
– No CNS penetration - acts on both α1 & α2 receptors of ciliary body→
↓ aqueous production.
– ↓ IOT by ~25%
– ADRs: itching, lid dermatitis, follicular conjunctivitis, mydriasis, eyelid
retraction, dryness of mouth and nose etc.
– Use is restricted to short term control of IOT spikes (trabeculoplasty or
iridotomy).
• Brimonidine (0.2%): Newer clonidine congener, more selective to α2
– More lipophilic than apraclonidine
– ↓ IOT by 20-27% by ↓ aq. production and ↑ uveoscleral flow.
– Uses both in short term (post surgery) and long term therapy in
glaucoma. – add on therapy
39. Prostaglandin analogues
• Low concentration of PGF2α analogues ↓ IOT by:
• Increase uveoscleral outflow (↑ciliary tissue permeability and vascular
permeability)
• Trabecular outflow less marked
• Latanoprost (0.005% eye drop)
• Topically IOT ↓ 25-35%, well sustained
• ↓ IOT in normal pressure glaucoma also
• Ocular irritation and pain
• Good efficacy, once daily application and absence of systemic
complications – first choice in open angle glaucoma
• Other ADRs: Blurring of vision, iris pigmentation, thickening and
darkening of eye lashes etc.
• Travoprost and Bimatoprost: similar efficacy with Latanoprost
40. Carbonic anhydrase inhibitors
• Carbonic anhydrase present within ciliary epithelial cells generates HCŌ3 ion
secreted into aq. humour.
• Inhibition of carbonic anhydrase - Limits generation of bicarbonate ion →
reduction of aqueous humour
• Acetazolamide:
– Orally – 0.25 gm 6-12 hourly
– Used to supplement ocular hypotensive drugs for short term indication like angle
closure, before & after surgery/laser therapy
– Long term use when IOP not controlled by topical drugs
• Side effects: Systemic s/e – paresthesia, anorexia, hypokalemia,
acidosis, malaise, depression (on long term use)
• Dorzolamide: 2% eyedrop topical – 20% efficacy
41. Miotics
• In 1970s – were standard antiglaucoma drugs
• Last option because of several drawbacks – myopia, diminution of
vision, headache
• Pilocarpine:
Causes miosis by contraction of iris sphincter muscle →
removes pupillary block and reverses obliteration of iridocorneal
angle
Contraction of ciliary muscle → pulls on scleral spur and
improves trabecular patency.
Max of 10-20% IOP reduction - 0.5%to 4% solution
42. OAG – current approach
• Monotherapy with Latanoprost or a topical β - blocker
• If not target attained – change to alternative drug or both
together
• Brimonidine/dorzolamide (or dipivefrine) used when above
two contraindicated
• Acetazolamide and Miotics – last option
43. Angle closure (narrow angle, acute congestive) Glaucoma
• Emergency situation occurring in person with narrow iridocorneal
angle and shallow anterior chamber
• IOT raised after it is being precipitated by mydriasis
• IOT rises rapidly to very high levels (40 - 60 mmHg)
• Marked congestion of eyes and severe headache
• Failure to lower IOT → loss of sight
• Definite treatment – surgery (iridotomy/laser therapy)
45. Therapy of closed angle glaucoma
1. Hypertonic mannitol (20%) 1.5-2 g/kg or Glycerol (10%):
• IV infusion – decongest eye by osmotic action
• Glycerine 50% - retention enema
2. Acetazolamide (0.5g) IV followed by oral BD started concurrently
3. Miotic: If above reduced the IOP -topical Pilocarpine 1-4 % every 10
mins initially & then at longer intervals.
4. Topical β blocker: Timolol 0.5% 12 hourly in addition.
5. Latanaprost (0.005%) / Apraclonidine (1%) may also be
added.
Chronic narrow angle: miotic/other drugs for longer period
46. Must know
• Different categories of drugs used in open angle glaucoma
• Their sites and mechanism of action
• Management of closed angle glaucoma