This document provides information about Myasthenia Gravis from Harvard Medical School and Massachusetts General Hospital. It details the history, clinical classification, presentation, differential diagnosis, treatment, and pathophysiology of MG. Key points include that MG is caused by loss of acetylcholine receptors at the neuromuscular junction preventing signal transmission, most patients initially present with ocular or bulbar symptoms, treatment involves cholinesterase inhibitors and corticosteroids like prednisone, and acetylcholine receptor antibodies are present in many cases but their level does not correlate with severity.
This presentation will give a brief idea on proximal myopathy, causes, clinical presentation, history and physical examination, investigations to diagnose the disease easily.
It will be more helpful to medical students.
This presentation will give a brief idea on proximal myopathy, causes, clinical presentation, history and physical examination, investigations to diagnose the disease easily.
It will be more helpful to medical students.
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.
Multiple sclerosis (MS) is a demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged.This damage disrupts the ability of parts of the nervous system to communicate, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems
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 (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.
Multiple sclerosis (MS) is a demyelinating disease in which the insulating covers of nerve cells in the brain and spinal cord are damaged.This damage disrupts the ability of parts of the nervous system to communicate, resulting in a range of signs and symptoms, including physical, mental, and sometimes psychiatric problems
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 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.
Comprehensive review of Ophthalmic Manifestations of Systemic Disorders for undergraduate medical students and general practionaers. Lecture was taken by Associate Professor Dr. Zia ul Mazhry at Central Park Medical College Lahore Pakistan.
A case of Neuromyelitis optica as a presenting manifestation of Systemic Lupu...Apollo Hospitals
Neuromyelitis optica (NMO) is a well characterised, autoimmune, clinicopathological syndrome, which is uncommon and occurs as an isolated entity. Unlike multiple sclerosis, in NMO, the autoimmunity is humorally mediated and the recent availability of Antiaquaporin antibody testing has increased the positive diagnosis of this condition. NMO can also occur in patients with established Systemic Lupus Erythematosis (SLE) who have multiple autoantibodies. The presence of Antiaquaporin antibody is specific for NMO and is seen in patients with SLE who develop inflammatory CNS disease. However, Neuromyelitis optica occurring as a presenting manifestation of SLE is extremely rare and we report one such case.
Acquired autoimmune disorder. Clinically characterized by weakness of skeletal muscles, fatigability on exertion. First clinical description in 1672 by Thomas Willis
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
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
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
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comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
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Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Are There Any Natural Remedies To Treat Syphilis.pdf
Myasthenia gravis guest_lecture[1]
1. HARVARD MEDICAL SCHOOL
DEPARTMENT OF NEUROLOGY
MASSACHUSETTS GENERAL HOSPITAL
Myasthenia Gravis
Shirley H. Wray, M.D., Ph.D.
Professor of Neurology, Harvard Medical School
Director, Unit for Neurovisual Disorders
Massachusetts General Hospital
2. History
A detailed history often reveals evidence of
early, unrecognized myasthenic features:
Intermittent diplopia
Frequent purchases of new glasses to
correct blurry vision, difficulty focusing
and/or early onset of convergence
insufficnecy of a need for prism correction
Use of dark glasses to reduce diplopia or
hide drooping eyelids
3. History continued.
Avoidance of certain foods that become
difficult to chew and swallow
Cessation of activities that require
prolonged use of muscle activity
4. Myasthenia Gravis
Clinical Classification
I. Ocular alone
IIa. Mild generalized
IIb. Moderately severe generalized plus
usually some bulbar involvement
IV. Acute severe over weeks-months with
severe bulbar involvement
V. Late severe with marked bulbar
involvement
5. Ocular Myasthenia Gravis
Because the majority of patients with
myasthenia gravis present with ocular
manifestations, the ophthalmologist plays
an essential role in the diagnosis of this
condition and a high index of suspicion
facilitates the diagnosis
6. Muscle groups involved at onset
Analysis of 295 cases
Ocular alone 34%
Bulbar alone 8%
Extremities alone 15%
Ocular and bulbar 7%
7. Muscle group analysis
continued.
Ocular and extremities 7%
Bulbar and extremities 6%
Ocular, bulbar and extremities 21%
Simpson et al, Acta Neurol. Scand. 1966 suppl. 23 pl
9. Extraocular muscles continued
Bilateral ptosis and EOM paresis 57
Unilateral ptosis and EOM paresis 16
Unilateral ptosis and bilateral paresis 13
Simpson et al, Acta Neurol. Scand. 1966 suppl. 23 pl
10. Eyelids
The findings on examination of the lids may simulate:
Congenital ptosis
Senile ptosis
Horner’s syndrome
Levator dehiscence
Superior division 3rd nerve palsy
Nuclear 3rd nerve palsy
Mitochondrial myopathy
11. Ptosis
Unilateral (partial or complete), alternating
with or without paradoxical lid retraction,
or see-saw ptosis
Bilateral and asymmetric, variable in
severity
Lid twitch – Cogan sign
Variable levator function
12. Ptosis continued.
Weakness of the orbicularis oculi
Increased ptosis with repetitive eye
closure
Recovery of ptosis with gentle eye closure
13. To Document Ptosis
Measure the palpebral fissure before
testing EOM, giving Tensilon, or using
sympathomimetic drugs
Increase of ptosis on fatigue
Myasthenic lid twitch
Recovery of ptosis following gentle eye
closure
14. To document ptosis continued.
Range of levator function
+ Weakness orbicularis oculi
Photograph and compare with family
snapshots
Measure response to IV Tensilon
15. Ptosis
Myopathy Myasthenia
Symmetric Appearance Asymmetric
No Ptosis on fatigue Yes
No Lid twitch Yes
No Recovery w/ eye closure Yes
Constant Range lev. function Varies
Yes Weak orb. oculi Yes
Negative Tensilon test Positive
50% Family history Rare
Slowly Progressive Course Fluctuates
16. Saccades
Examination may show:
Intrasaccadic fatigue (slow in midflight)
Decrescendo from saccade to saccade
Hypermetria of small saccades
Hypometria of large saccades
Quiver movements and “hyperfast”
saccades
Fatigability of quick phases on OKN
17. Myasthenia Gravis
Myasthenia gravis is a disease of skeletal
muscle acetylcholine receptors. The
chemical transmitter, acetylcholine (ACh) is
unable to bind to the receptors (AChR) on
the postsynaptic membrane to transmit the
nerve impulse to muscle fibers to produce a
muscle contraction
18. Presentation (I)
MG occurs at any age, involves either
sex and begins insidiously
Second and third decades commonest
age of onset in women. Seventh and
eighth decades in men
Patients complain of specific muscle
weakness, not generalized fatigue
19. Presentation (II)
Ptosis or diplopia – initial symptoms in
65% of patients
Oropharyngeal muscle weakness –
difficulty in swallowing and talking
initial symptoms in 17% of patients
Limb weakness presenting symptom in
only 10% of cases
20. Presentation (III)
Characteristically, severity of weakness
fluctuates during the day, least in the
morning, worsening as the day
progresses, especially after prolonged use
of affected muscles
In the era before corticosteroid treatment,
approximately one-third of patients
improved spontaneously, one third
became worse and one third died
21. Presentation (IV)
Ocular myasthenia – if progressing to
generalized MG usually does so within the
first two years after onset
After 15 to 20 years, weakness becomes
fixed. The Burnt-Out-Stage + muscle
atrophy
22. Edrophonium Chloride Tensilon
Test (10 Mg in 1 cc)
Precautionary Steps:
List all medications being taken
History of drug allergy and previous
reaction to Tensilon
Perform the test in the ER with an ambu
bag, atropine and adrenalin available in
elderly patients and those with cardiac
disease
23. Administration Procedure
The ideal dose of Tensilon cannot be
predetermined
Give a 0.1 cc test dose and monitor pulse,
blood pressure and clinical state
Follow with 0.3 cc aliquotes examining for
a response in ptosis, EOM or Lancaster
strabismus screen test after each one
Once improvement is seen -- STOP
24. The defect in neuromuscular
transmission in Myasthenia
Gravis is due to:
The muscle end-plate membrane is
distorted
Acetylcholine receptors are lost from the
tips of the folds, and antibodies attach to
the postsynaptic membrane
Ach is released normally but absence of
receptors prevents the transmitter binding
to the muscle membrane
25. Acetylcholine Receptor
Antibodies
75% of cases generalized MG have serum
antibodies (Ab) that bind to huma AChR
54% with ocular MG have antibodies 10%
MG cases with no binding antibodies have
other antibodies
The AChR Ab tit varies widely among
patients with similar degrees of weakness.
The amount of Ab in the serum does not
predict the severity of the disease in
individual patients
26. Antibodies continued.
The Ab level may be low at onset on MG
and gradually become elevated in late
stage
Worthwhile to repeat test when initial
values normal
27. The Presence of AChR Antibody
is not diagnostic for MG, also
present in:
Systemic lupus erythematosus
Inflammatory neuropathy
Amyotrophic lateral sclerosis
Rheumatoid arthritis in patients taking D-
penicillamine
In cases of thymoma without MG
28. Association of MG with other
diseases
Hyperthyroidism 6%
Rheumatoid arthritis, less than
2%
Systemic lupus erythematosus 2%
Diabetes mellitus 7%
Non thymus neoplasm 3%
30. Factors that Aggravate MG
Emotional stress
Systemic illness e.g. viral URI
Thyroid disease, hyper or hypo
Pregnancy
Menstrual Cycle
Increase in body temperature
Drugs
31. Treatment
Treatment decisions are based on the
predicted response to a specific form of
therapy
Treatment goals must be individualized
according to the severity of the disease,
the patient’s age and sex, and the degree
of functional impairment
32. Treatment continued.
The response to any form of treatment is
difficult to access because the severity of
symptoms fluctuates. Spontaneous
improvement, even remissions, occur
without specific therapy, especially during
the early stages of the disease
33. CHE Inhibitors (I)
Mestinon (Pyridostigmine bromide) first
choice, dose 30-60 mg q 6-8 h/daily
Prostigmine (Neostigmine bromide) 7.5 –
15.0 mg q 6-8 h/daily
No fixed dosage schedle suits all aptients
34. CHE Inhibitors (II)
The need for ChE inhibitors varies from
day to day and during the same day
Different muscles respond differently with
any dose, certain muscles get stronger,
others do not change and still others
become weaker
The drug schedule should be titrated
according to the pateints work load and
muscle activity
35. ChE Inhibitors (III)
Many patients assume responsibility for
their own drug dose
The goal is to keep the dose low enough
to provide definite improvement 30 to 40
minutes later and allow theeffect to wear
off before the next dose
Advise patients re: adverse effects of ChE
inhibitors
36. Prednisone
Marked improvement or complete relief of
symptoms occurs in 75% of cases
Improvement in first 6 to 8 weeks, but
strength may increase to total remission
over months
Best responses in patients with recent
onset MG, but chronic disease may also
respond
37. Prednisone continued.
The severity of the disease does not
predict the ultimate improvement
Patients with thymoma have an excellent
response to prednisone before or after
thymectomy
38. Dose
Prednisone 60 to 80 mg/day given until
sustained improvement (usually 2 weeks)
then alternate days beginning with
100-120 mg tapered over months to
lowest dose necessary (usually less than
20 mg alternate days)