This document discusses myasthenia gravis (MG), an autoimmune disorder causing muscle weakness. It begins with background on MG and outlines the anatomy of the neuromuscular junction which is affected. The pathology of MG involves antibodies blocking acetylcholine receptors, impairing muscle contraction. Clinical presentation includes fluctuating weakness worsened by exertion, especially in extraocular muscles. Diagnosis involves testing for acetylcholine receptor antibodies, with treatment including acetylcholinesterase inhibitors and immunomodulators.
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
Disorders of the neuromuscular junction include Myasthenia gravis, Lambert-Eaton myasthenic syndrome, Botulism, Tetanus, Strychnine intoxication, Organophosphates poisoning and neuromyotonia. Pharmacology of the NMJ is also reviewed in brief.
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing. It can result in double vision, drooping eyelids, trouble talking, and trouble walking.
Myasthenia gravis (MG) is a long-term neuromuscular disease that leads to varying degrees of skeletal muscle weakness. The most commonly affected muscles are those of the eyes, face, and swallowing. It can result in double vision, drooping eyelids, trouble talking, and trouble walking.
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Myasthenia gravis is an either autoimmune or congenital neuromuscular disease that leads to fluctuating muscle weakness and fatigue. In the most common cases, muscle weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the excitatory effects of the neurotransmitter acetylcholine on nicotinic receptors at neuromuscular junctions. Alternatively, in a much rarer form, muscle weakness is caused by a genetic defect in some portion of the neuromuscular junction, that is inherited at birth as opposed to developing it through autoimmunity later in life or through passive transmission by the mother's immune system at birth.
Acquired autoimmune disorder. Clinically characterized by weakness of skeletal muscles, fatigability on exertion. First clinical description in 1672 by Thomas Willis
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Best Ayurvedic medicine for Gas and IndigestionSwastikAyurveda
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
3. Background
Acquired autoimmune disorder
Clinically characterized by:
Weakness of skeletal muscles
Fatigability on exertion.
First clinical description in 1672 by Thomas
Willis
4.
5. Postsynaptic surface
Ach + AChR
Opening AChR ion channel
End-plate potential generation
Opening VGSC at the bottom of
synaptic fold
Muscle action potential and
contraction
6. Anatomy
Neuromuscular Junction (NMJ)
Components:
Presynaptic membrane
Postsynaptic membrane
Synaptic cleft
Presynaptic membrane contains vesicles with
Acetylcholine (ACh) which are released into
synaptic cleft in a calcium dependent manner
ACh attaches to ACh receptors (AChR) on
postsynaptic membrane
7. Anatomy
Neuromuscular Junction (NMJ)
The Acetylcholine receptor (AChR) is a sodium
channel that opens when bound by ACh
There is a partial depolarization of the postsynaptic
membrane and this causes an excitatory postsynaptic
potential (EPSP)
If enough sodium channels open and a threshold
potential is reached, a muscle action potential is
generated in the postsynaptic membrane
8. Pathology
A chronic Autoimmune
Disease
Affects the
Neuromuscular junction
Postsynaptic
acetylcholine receptors
on muscle cells plasma
membrane are no
longer recognized as
‘self’ and elicit the
generation of auto
antibodies.
9. Pathology
IgG antibody is produced against the acetylcholine
receptors and fixes to receptor sites, blocking the
binding of acetylcholine.
Diminished transmission and lack of muscular
depolarization results.
10. Pathology
Several Types of Myasthenia Gravis
Neonatal Myasthenia Gravis: A transient condition in
10% to 15% of infants born to mothers with MG.
Congenital Myasthenia
Juvenile Myasthenia: Onset is around 10 years of
age.
Ocular Myasthenia
Generalized Autoimmune Myasthenia
11. Immunopathogenesis
bind to AChR and alter function
promote endocytosis and accelerate
degradation of AChR (cross-linking)
complement-mediated damage to AChR Ab +
epitopes α subunit in “main immunogenic
region” (MIR) (molecular mimicry)
12. Pathophysiology
In MG, antibodies are directed toward the
acetylcholine receptor at the neuromuscular
junction of skeletal muscles
Results in:
Decreased number of nicotinic acetylcholine
receptors at the motor end-plate
Reduced postsynaptic membrane folds
Widened synaptic cleft
13. Induction of a myasthenic-like syndrome in
mice by injecting a large quantitiy of
immunoglobulin G from MG patients
14. Pathophysiology
Anti-AChR antibody is found in 80-
90% of patients with MG
Proven with passive transfer
experiments
MG may be considered a B cell-
mediated disease
Antibodies
Top photo shows a rabbit with "floppy" ears
after an injection of receptor antigens.
Bottom shows the same rabbit after
receiving edrophonium.
15. Pathophysiology
T-cell mediated immunity has some influence
Thymic hyperplasia and thymomas are
recognized in myasthenic patients*
17. Epidemiology
Frequency
Annual incidence in US- 2/1,000,000 (E)
Worldwide prevalence 1/10,000 (D)
Mortality/morbidity
Recent decrease in mortality rate due to advances in treatment
3-4% (as high as 30-40%)
Risk factors
Age > 40
Short history of disease
Thymoma
Sex
F-M (6:4)
Mean age of onset (M-42, F-28)
Incidence peaks- M- 6-7th decade F- 3rd decade
18. Clinical presentation
Ocular and generalized MG
Modified osserman classification
Burnt-out stage : after 15-20 years, untreated
weakness becomes fixed, and atrophic
19. Clinical Manifestations
Insidious onset
May first appear during pregnancy, during the postpartum
period, or in combination with the administration of
anesthetic agents.
Complaints
Most individuals complain of fatigue and
progressive weakness.
The person usually has a history of frequent respiratory
tract infections.
20. Clinical Manifestations
Muscles affected
First muscles affected
Muscles of the eyes, mouth, face, throat and neck.
The most affected muscles are the extra ocular (eye) muscles
and levator muscles.
Second most affected muscles
Muscles of mastication, swallowing, facial expression, and
speech.
Less frequently affected muscles
Neck, shoulder girdle, and hip flexors
All muscles are weak in the advanced stage of the disease.
21. Clinical Manifestations
Other occurrences
Myasthenic Crisis happens when extreme muscle
weakness causes quadriparesis or quadriplegia, difficulty
swallowing, and shortness of breath. A person in this state
is in danger of respiratory arrest.
Cholinergic Crisis occurs from anticholinesterase drug
toxicity. This is similar to Myasthenic Crisis, but also
includes increased intestinal motility with diarrhea and
complaints of cramping, fasciculation, bradycardia,
constriction of the pupils, increased salvation, and
sweating. A person in this state may also be in danger of
respiratory arrest.
22. Clinical Presentation
Fluctuating weakness increased by exertion
Weakness increases during the day and improves
with rest
Extraocular muscle weakness
Ptosis is present initially in 50% of patients and
during the course of disease in 90% of patients
Head extension and flexion weakness
Weakness may be worse in proximal muscles
23. Clinical presentation
Progression of disease
Mild to more severe over weeks to months
Usually spreads from ocular to facial to bulbar to truncal
and limb muscles
Often, symptoms may remain limited to EOM and eyelid
muscles for years
The disease remains ocular in 16% of patients
Remissions
Spontaneous remissions rare
Most remissions with treatment occur within the first three
years
24. Clinical presentation
Basic physical exam findings
Muscle strength testing
Recognize patients who may develop respiratory
failure (i.e. difficult breathing)
Sensory examination and DTR’s are normal
Onset from mild to maximal weakness is
less than 36 months in 83% of patients
26. Clinical presentation
Facial muscle weakness is almost
always present
Ptosis and bilateral facial muscle
weakness
Sclera below limbus may be exposed due
to weak lower lids
27. Clinical presentation
Bulbar muscle weakness
Palatal muscles
“Nasal voice”, nasal regurgitation
Chewing may become difficult
Severe jaw weakness may cause jaw to hang open
Swallowing may be difficult and aspiration may
occur with fluids—coughing and choking while
drinking
Neck muscles
Neck flexors affected more than extensors
28. Clinical presentation
Limb muscle weakness
Upper limbs more common than lower limbs
Upper Extremities
Deltoids
Wrist extensors
Finger extensors
Triceps > Biceps
Lower Extremities
Hip flexors (most common)
Quadriceps
Hamstrings
Foot dorsiflexors
Plantar flexors
29. Clinical presentation
Respiratory muscle weakness
Weakness of the intercostal muscles and the diaghram
may result in CO2 retention due to hypoventilation
May cause a neuromuscular emergency
Weakness of pharyngeal muscles may collapse the upper
airway
Monitor negative inspiratory force, vital capacity and tidal
volume
Do NOT rely on pulse oximetry
Arterial blood oxygenation may be normal while CO2 is retained
30. Clinical presentation
Occular muscle weakness
Asymmetric
Usually affects more than one extraocular muscle and
is not limited to muscles innervated by one cranial
nerve
Weakness of lateral and medial recti may produce a
pseudointernuclear opthalmoplegia
Limited adduction of one eye with nystagmus of the
abducting eye on attempted lateral gaze
Ptosis caused by eyelid weakness
Diplopia is very common
31. Clinical presentation
Co-existing autoimmune diseases
Hyperthyroidism
Occurs in 10-15% MG patients
Exopthalamos and tachycardia point to hyperthyroidism
Weakness may not improve with treatment of MG alone in
patients with co-existing hyperthyroidism
Rheumatoid arthritis
Scleroderma
Lupus
32. Clinical presentation
Causes
Idiopathic
Penicillamine
AChR antibodies are found in 90% of patients
developing MG secondary to penicillamine exposure
Drugs
35. Lambert-Eaton myasthenic syndrome (LEMS)
is a rare condition in which weakness results
from an abnormality of acetylcholine (ACh)
release at the neuromuscular junction. Recent
work demonstrates that LEMS results from an
autoimmune attack against voltage-gated
calcium channels (VGCC) on the presynaptic
motor nerve terminal.
36. Diagnostic procedure
Pharmacological testing : Edrophonium chloride
(tensilon) test
Serological testing : Antibody against AChR
Electrophysiological testing : RNST, SFEMG
Other : ocular cooling
37. Work-up
Lab studies
Anti-acetylcholine receptor antibody
Positive in 74%
80% in generalized myasthenia
50% of patients with pure ocular myasthenia
Anti-striated muscle
Present in 84% of patients with thymoma who are
younger than 40 years
38. Work-up
Lab studies
Interleukin-2 receptors
Increased in generalized and bulbar forms of MG
Increase seems to correlate to progression of disease
39. Work-up
Imaging studies
Chest x-ray
Plain anteroposterior and lateral views may identify a
thymoma as an anterior mediastinal mass
Chest CT scan is mandatory to identify thymoma
MRI of the brain and orbits may help to rule out
other causes of cranial nerve deficits but should
not be used routinely
42. Workup
Pharmacological testing
Edrophonium (Tensilon test)
Patients with MG have low numbers of AChR at
the NMJ
Ach released from the motor nerve terminal is
metabolized by Acetylcholine esterase
Edrophonium is a short acting Acetylcholine
Esterase Inhibitor that improves muscle
weakness
Evaluate weakness (i.e. ptosis and
opthalmoplegia) before and after administration
44. Workup
Pharmacological testing
Edrophonium (Tensilon test)
Steps
0.1ml of a 10 mg/ml edrophonium solution is
administered as a test
If no unwanted effects are noted (i.e. sinus
bradychardia), the remainder of the drug is injected
Consider that Edrophonium can improve weakness in
diseases other than MG such as ALS, poliomyelitis,
and some peripheral neuropathies
45.
46. Treatment
AChE inhibitors
Immunomodulating therapies
Plasmapheresis
Thymectomy
Important in treatment, especially if thymoma is
present
47. Treatment
AChE inhibitor
Pyridostigmine bromide (Mestinon)
Starts working in 30-60 minutes and lasts 3-6 hours
Individualize dose
Adult dose:
60-960mg/d PO
2mg IV/IM q2-3h
Caution
Check for cholinergic crisis
Others: Neostigmine Bromide
48. Treatment
Immunomodulating therapies
Prednisolone
Most commonly used corticosteroid in US
Significant improvement is often seen after a
decreased antibody titer which is usually 1-4 months
No single dose regimen is accepted
Some start low and go high
Others start high dose to achieve a quicker response
Clearance may be decreased by estrogens or digoxin
Patients taking concurrent diuretics should be
monitored for hypokalemia
49. Treatment
Behavioral modifications
Diet
Patients may experience difficulty chewing and
swallowing due to oropharyngeal weakness
If dysphagia develops, liquids should be thickened
Thickened liquids decrease risk for aspiration
Activity
Patients should be advised to be as active as
possible but should rest frequently and avoid
sustained activity
Educate patients about fluctuating nature of
weakness and exercise induced fatigability
50. Complications of MG
Respiratory failure
Dysphagia
Complications secondary to drug treatment
Long term steroid use
Osteoporosis, cataracts, hyperglycemia, HTN
Gastritis, peptic ulcer disease
Pneumocystis carinii
51. Prognosis
Untreated MG carries a mortality rate of 25-
31%
Treated MG has a 4% mortalitiy rate
40% have ONLY occular symptoms
Only 16% of those with occular symptoms at
onset remain exclusively occular at the end of 2
years