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 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 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.
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 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 (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 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.
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 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.
www.ophthalclass.blogspot.com has the complete class and MCQs on lids and adnexa for undergraduate medical students. The third class in this series deals with blepheroptosis. The subtopics include diagnosis of ptosis, pseudoptosis, classification of ptosis into congenital and acquired ptosis and finally a brief discussion on the management of ptosis. Clinical features of congenital myogenic ptosis, Marcus jaw winking phenomenon, aponeurotic ptosis, neurogenic ptosis (III nerve palsy and Horner’s syndrome), CPEO, myasthenia gravis, traumatic and mechanical ptosis are explained.
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
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.
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
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Cardiac conduction defects can occur due to various causes.
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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
3. introduction
• Neuromuscular junction : the synapse
between motor neuron and muscle fiber is called
the neuromuscular junction.
• Motor end plate contain nicotinic receptors, and
the Ach binds to these receptors leads to
conformational changes,
the channels opens & permeability of motor end
plate to Na+ & K+ increases.
4.
5. Myasthenia gravis:
• Is an acquired autoimmune disorder.
• Is caused by autoantibodies that block the
function of postsynaptic Ach receptors at motor
end plate.
• Some 60% of cases are associated with a peculiar
reactive hyperplasia of intrathymic B cells.
• And another 20% are associated with thymoma.
7. Myasthenia gravis can involve either the external
ocular muscle selectively (ocular MG)
or the general voluntary muscle system
(generalized MG) ,the symptoms usually
fluctuate tending to be worse later in the day
(diurnal fluctuation) .
they are worsened by exertion
8. • Ocular muscle involvement is usually bilateral
and asymmetrical and typically is associated
with ptosis and diplopia.
• Ocular muscles are affected in nearly all patients
after a year of disease.
9. • weakness of other muscles innervated by cranial
nerves result in loss of facial expression.
• Abnormal fatigability of the limb muscles
difficulty in combing the hair, lifting objects
repeatedly ,climbing stares, walking, and
running.
10. • The symptoms are ocular in 40% ,
• And are generalized in 40%,
• involve only the extremities in 10%
• and involve only bulbar or bulbar and eye
muscles in another 10%.
11. • In about 10% the MG is associated with another
autoimmune disease, circulating Ach receptor
antibodies can be detected in most infants born
to myasthenic mothers, but only 12% of such
children develop transit neonatal MG,usually
during the first few hours of life.
• The disease is caused by transfer of Ach receptor
antibodies is self limited
13. Anticholinesterase tests
(tensilon test)
Edrophonium given intravenously acts within a few
seconds and lasts for a few minutes. Two milligrams of
the drug are injected intravenously over 15 seconds. If no
response occurs in 30 to 45 seconds, an additional 8 mg
is injected. The evaluation of the response requires
objective assessment of one or more signs not easily
influenced by motivation, such as degree of ptosis and
range of ocular movements.
14. Anticholinesterase tests
(tensilon test) cont.
Possible cholinergic side effects of the drug include
fasciculations, flushing, lacrimation, abdominal cramps,
nausea, vomiting, and diarrhea. The drug must be given
cautiously to patients with cardiac disease because it may
cause sinus bradycardia, atrioventricular block, and,
rarely, cardiac arrest. Atropine should be available
during the test. Edrophonium should not be given to
patients having respiratory difficulty.
15. Repetitive Nerve Stimulation
Supramaximal stimulation of a motor nerve at 2 or 3 Hz
results in a 10% or greater decrement of the amplitude of
the evoked compound muscle action potential from the
first to the fifth response. The test is positive in about
75% with generalized MG, provided that two or more
distal and two or more proximal muscles are examined.
It is less frequently abnormal (approximately 50%) in
purely ocular MG.
16. Single Fiber Electromyography
Single fiber electromyography (SFEMG) is currently the
most sensitive method for diagnosis of MG and reveals
increased jitter and blocking in 99% of patients with
generalized MG and in 97% of those with purely ocular
MG when a weak muscle is tested. SFEMG is usually
available only in specialized EMG laboratories
17. Blood Tests and Radiography
The AChR antibody test measures the binding of antibody
to AChR labeled with radioactive αbungarotoxin. The
antibody-binding test result is positive in nearly all adults
with moderately severe or severe MG, in 80% with mild
generalized MG, and in 50% with ocular MG. Some patients
without AChR have abnormal antibodies to MuSK, a
muscle-specific tyrosine kinase with a role in aggregation of
AChR and the end plate. Striated muscle antibodies also
occur in MG patients. Their role is unknown, but they are
often associated with thymoma. Because of the frequency of
thymomas, chest x-ray studies and chest computed
tomography (CT) scanning are indicated.
19. Oral anticholinesterases
Pyridostigmine (60 mg tablet) is widely used. The duration of action
is 3–4 hours, the dose (usually 4–16 tablets daily) determined by
response. Pyridostigmine prolongs acetylcholine action by inhibiting
cholinesterase. Overdose of anticholinesterases causes severe
weakness (cholinergic crisis). Muscarinic side-effects, e.g. colic and
diarrhoea, are common; oral atropine (antimuscarinic) 0.5 mg helps
to reduce this. Anticholinesterases help weakness but do not alter
the natural history of myasthenia.
20. Immunosuppressant drugs
• These drugs are used in patients who do not
respond to pyridostigmine or who relapse on
treatment. Steroids are often used. There is
improvement in 70%, although this may be
preceded by an initial relapse. Azathioprine,
mycophenolate and other immunosuppressants
are also used.
21. • Plasmapheresis and intravenous
immunoglobulin
• During exacerbations these interventions are of
value.
22. Thymectomy
• Thymectomy improves prognosis, more so in
women than men below 50 years with positive
AchR antibodies, even in patients without a
thymoma. Cases positive for anti-MuSK
antibodies tend not to improve following
thymectomy. When a thymoma is present, the
potential for malignancy also makes surgery
necessary.
23.
24. Reference
• Andreoli and Carpenter s cecil essentials of
Medicine 8th edition
by: Thomas E. Andreoli, Ivor J. Benjamin, Ropert C. Griggs, Edward J.
wing
•Robbins Basic Pathology 9th edition
Vinay Kumar, Abul K. Abbas, Jon C. Aster
8th edition
• by Parveen Kumar and Michael Clark
• published by Elsevier