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.
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.
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: Introduction, Risk Factors, Diagnosis and TreatmentEnriqueAlvarez93
Introduction about Multiple Sclerosis.
Risk factors affect to Multiple Sclerosis.
When to Suspect Multiple Sclerosis.
Evaluation and Diagnosis of Multiple Sclerosis.
How to treatment of Multiple Sclerosis.
Treatment of Multiple Sclerosis with Monoclonal Antibody.
Myasthenia Gravis is a neuromuscular disorder primarily characterized by muscle weakness and muscle fatigue. Although the disorder usually becomes apparent during adulthood, symptom onset may occur at any age.
Multiple sclerosis (MS) is a demyelinating disease of central nervous system which includes brain and spinal cord.
it affect the myelin and by damaging the the myelin producing cell -Oligodendrocytes, which leads to sensory, motor and cognitive problems.
Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system). In MS , the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body.
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.
Multiple sclerosis: Introduction, Risk Factors, Diagnosis and TreatmentEnriqueAlvarez93
Introduction about Multiple Sclerosis.
Risk factors affect to Multiple Sclerosis.
When to Suspect Multiple Sclerosis.
Evaluation and Diagnosis of Multiple Sclerosis.
How to treatment of Multiple Sclerosis.
Treatment of Multiple Sclerosis with Monoclonal Antibody.
Myasthenia Gravis is a neuromuscular disorder primarily characterized by muscle weakness and muscle fatigue. Although the disorder usually becomes apparent during adulthood, symptom onset may occur at any age.
Multiple sclerosis (MS) is a demyelinating disease of central nervous system which includes brain and spinal cord.
it affect the myelin and by damaging the the myelin producing cell -Oligodendrocytes, which leads to sensory, motor and cognitive problems.
Multiple sclerosis (MS) is a potentially disabling disease of the brain and spinal cord (central nervous system). In MS , the immune system attacks the protective sheath (myelin) that covers nerve fibers and causes communication problems between your brain and the rest of your body.
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.
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.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
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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
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
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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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
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Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
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- 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
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
2. 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.
3. The hallmark of myasthenia gravis is muscle weakness
that worsen after period of activity and improves after
period of rest.
As a clinical entity, myasthenia gravis was not
recognized until Samuel Wilks in 1877 described bulbar
and peripheral muscular weakness. In the Lancet of June
2, 1934, the remarkable discovery of physostigmine
treatment by Dr. Mary Walker was published, which was
to become the mainstay of symptomatic treatment.
4. Certain muscles such as those that control eye and
eyelid movement, facial expression, chewing, talking,
and swallowing are often (but not always) involved in
the disorder. The muscle that control breathing and
neck and limb movements may also be affected.
There is no known cure but available treatments can
control the symptoms and often allow people to have
a relatively high quality of life.
5. In MG, the receptors at the muscle surface are destroyed
or deformed by antibodies that prevent a normal muscular
reaction from occurring.
The causative factor is unknown, but the disorder may
have a genetic link.
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.
Those affected often have a large thymus gland or develop
a thymoma.
6.
7. Factors that can worsen myasthenia
gravis
Fatigue
Illness
Stress
Extreme heat
Some medications — such as beta
blockers, calcium channel blockers,
quinine and some antibiotics
8. MG is rare, having a prevalence of 2–7 in 10,000.
Myasthenia Gravis is most common in the people at the
age of 40 and above.
This mainly affects the older people and the middle
aged people.
There are more women than men and the age of the
participants ranged from 40to 82.
The prevalence of this disease is found to be more in
China (64,942) followed by India (53,253) and is found
to be least in Bhutan (109).
9. The following table attempts to extrapolate the prevalence rate for
Myasthenia Gravis to the populations of various countries and regions
in Asia:
10. In MG, antibodies are directed toward the acetylcholine receptor
at the neuromuscular junction of the skeletal muscle
Resulting in:
Decreased number of acetylcholine receptors at the post synaptic muscle membrane
postsynaptic folds are simplified or flattened
Decreased neuromuscular transmission
Weakness of muscle contraction
Therefore, although Ach is released normally, it produces small end-plate potentials
that may fail to trigger muscle action potentials.
11. Failure of transmission at many
neuromuscular junctions results in
weakness of muscle contraction.
The amount of Ach released per impulse
normally declines on repeated activity
(termed presynaptic rundown).
14. An immune response to muscle-specific kinase
(musk), a protein involved in achR clustering at
neuromuscular junctions, can also result in
myasthenia gravis, with reduction of achRs
demonstrated experimentally.
The pathogenic antibodies are igG, and are t cell
dependent.
Immunotherapeutic strategies directed against either
the antibody-producing b cells or helper t cells are
effective in this antibody-mediated disease.
15. The autoimmune response is initiated and maintained in mg is not
completely understood, but the thymus appears to play a role in
this process.
The thymus is abnormal in ∼75% of patients with MG; in ∼65%
the thymus is “hyperplastic,” with the presence of active germinal
centers detected histologically, though the hyperplastic thymus is
not necessarily enlarged.
An additional 10% of patients have thymic tumors (thymomas).
Muscle-like cells within the thymus (myoid cells),
*Bear AChRs on their surface
*May serve as a source of autoantigen and trigger the
autoimmune reaction within the thymus gland.
16. Thymus gland, a part of your immune system located in the upper
chest beneath the breastbone, may trigger or maintain the production
of antibodies that result in the muscle weakness common in MG.
17. Myasthenia gravis may be inherited as a rare, genetic
disease, acquired by babies born to mothers with MG
Nerves communicate with the muscles by releasing
chemicals, called neurotransmitters.
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.
18. The main symptom of myasthenia gravis is weakness in
the voluntary skeletal muscles, which are muscles under
our control. The failure of muscles to contract normally
occurs because they can’t respond to nerve impulses.
Without proper transmission of the impulse, a blocked
communication occurs between nerve and muscle and
weakness results.
Weakness associated with myasthenia gravis typically
gets worse with more activity and improves with rest.
Some of the main symptoms to be noticed are:
19. 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)
Blurred vision, which may come and go
20. 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.
21. › Chewing. The muscles used for chewing may
wear out halfway through a meal, particularly if
eating.
› Facial expressions. Family members may note
"lost smile" if the muscles that control facial
expressions are affected
22. 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
23. If having trouble with:
Breathing
Seeing
Swallowing
Chewing
Walking
24. History Diplopia, ptosis, Weakness in characteristic
distribution, Fluctuation and fatigue: worse with
repeated activity, improved by rest Effects of previous
treatments .
Physical examination Ptosis, diplopia Motor power
survey: quantitative testing of muscle strength ,Forward
arm abduction time(5 min), Vital capacity, Absence of
other neurologic signs.
25. Edrophonium test:
Injection of the chemical edrophonium (Tensilon) may result
in a sudden, although temporary, improvement in muscle
strength — an indication that may have myasthenia gravis.
Edrophonium- acts to block an enzyme that breaks down
acetylcholine, the chemical that transmits signals from nerve
endings to muscle receptor sites.
Blood analysis: A blood test may reveal the presence of
abnormal antibodies that disrupt the receptor sites where
nerve impulses signal muscles to move.
26. Single-fiber electromyography (EMG):
EMG measures the electrical activity
traveling between brain and muscle. It
involves inserting a very fine wire electrode
through skin and into a muscle. In single-
fiber EMGs, a single muscle fiber is tested.
Imaging scans: CT scan or an MRI to
confirm a tumor or other abnormality in
thymus.
• SINGLE FIBER-EMG
• CT CHEST
27. A. THERAPEUTIC MANAGEMENT:
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)
28. 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, but it can take a
week or two to start working and the benefits usually last
less than a month or two.
29. 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.
30. Because the cause of myasthenia gravis is unknown, there is
no way to prevent it. However, once the disease has
developed, there may be ways to prevent episodes of
worsening symptoms or flare-ups:
Give yourself plenty of rest.
Avoid strenuous, exhausting activities.
Avoid excessive heat and cold.
Avoid emotional stress.
31. Whenever possible, avoid exposure to any kind of
infection, including colds and influenza (flu). You
should be vaccinated against common infections,
such as influenza.
Work with your doctor to monitor your reactions to
prescription medications. Some drugs commonly
prescribed for other problems, such as infections,
heart disease or hypertension, may make myasthenia
gravis worse. You may need to choose alternative
therapies or avoid some medications entirely.
32. Harrisons Neurology in clinical medicine
http://www.ninds.nih.gov/disorders/myasthenia_gravis/detai
l_myasthenia_gravis.htm ( for fact sheet & possible
questions asked by patient’s family )
http://www.drugs.com/health-guide/myasthenia-gravis.html
https://en.wikipedia.org/wiki/Myasthenia_gravis
Myasthenia Gravis A Manual for the Health Care
Provider, Jemes F. Haward, M. D