This document discusses various types of myopathies and dystrophies. It describes how myopathy is a muscle defect that is not neurological in nature, and can be genetic, congenital, metabolic, or drug-induced. It then focuses on different muscular dystrophies such as Duchenne muscular dystrophy, which affects boys and causes progressive weakness. Other dystrophies discussed include Becker, Emery-Dreifuss, limb girdle, and facioscapulohumeral dystrophy. Various metabolic myopathies are also summarized, including those involving glucose and glycogen metabolism.
In this slideshow, we covered most of neuromuscular disorders which might face you in medicine in general and in pediatrics in particular.
We hope if you find this slideshow helpful for your seeking of this subject.
Cheers,
In this slideshow, we covered most of neuromuscular disorders which might face you in medicine in general and in pediatrics in particular.
We hope if you find this slideshow helpful for your seeking of this subject.
Cheers,
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 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.
Dr Abdullah Ansari
PG-2 (Medicine)
AMU ALIGARH
A general approach to periodic paralysis....
(including hypokalemic periodic paralysis and thyrotoxic periodic paralysis, and other “Channelopathies” or “Membranopathies)
Pathophysiology
Epidemiology
Primary or familial periodic paralysis
Secondary periodic paralysis
Conventional classification of periodic paralysis
Classification of primary periodic paralysis based on ion-channel abnormalities
Clinical approach to a case of periodic paralysis
History of muscle weakness
Age of onset
Family history
Timing
Intensity
History of administration of certain drugs
Clinical examination
Differential Diagnosis
Laboratory investigations
Serum K+
CPK and serum myoglobin
ECG
EMG
Nerve conduction studies
Provocative Testing
Muscle biopsy
Treatment
Prognosis
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.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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
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.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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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).
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 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
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
3. MYOPATHY AND DYSTROPHY
• Myopathy is a term applied to an acquired or developmental
defect in certain muscles. It is not a neurological disease, and
should be distinguished from neuropathic conditions such as
MOTOR NEURONE DISEASE (MND), which tend to affect the
distal limb muscles. The main subdivisions are:
1. genetically determined
2. Congenital
3. Metabolic
4. drug-induced
5. and myopathy (often inflammatory) secondary to a distant
carcinoma.
3
MYOPATHY &DYSTROPHY
4. • Progressive muscular dystrophy is characterized by
symmetrical wasting and weakness, the muscle fibers
being largely replaced by fatty and fibrous tissue, with no
sensory loss. Inheritance may take several forms, thus
affecting the sex and age of victims.
• The commonest type is DUCHENNE MUSCULAR
DYSTROPHY, which is inherited as a sex-linked disorder. It
nearly always occurs in boys.
4
MYOPATHY &DYSTROPHY
11. MUSCULAR DYSTROPHY
• are inherited myopathy characterized by progressive
muscles weakness °eneration &subsequent
replacement by fibrous & fatty connective tissue
• Historically were categorized by their:
• Age onset /distribution of weakness& pattern of
inheritance
• The genetic mutation &abnormal gene product were
defined for many of them
MUSCULARDYSTROPHY
11
13. DUCHENNE MD
• Incidence: 1/3500 male birth
• 1/3 new mutation
• Age of onset: as early as 2-3y with delay milestones
• Progressive limb girdle pattern
• Fall 5-6y/difficult climb stair 8y, confined to wheelchair 12y
MUSCULARDYSTROPHY
13
14. • Joint contractures 6-10y
• Calf hypertrophy is early
• Muscles atrophy late
• Progressive kyphoscliosis due to Paraspinal muscles weakness
• Reflex: biceps/knee/lost by age 10y
• ankle preserved late in disease
• Respiratory distress after age 10
MUSCULARDYSTROPHY
14
15. • Cardiac: generally asymptomatic
• CHF, arrhythmia late
• 90% abnormal ECG :tall R wave,deep Q wave
• Echo: hypokinesia ,dilatation of ventricular wall
• GI: intestinal pseudo obstruction
• IQ: one SD below N
MUSCULARDYSTROPHY
15
16. LAB
• A dystrophin gene deletion can be detected by:
• DNA analyses from leukocytes by PCR in 2/3 patient or DNA
muscles
• The other 1/3 diagnosed by… muscles biopsy( dystrophin
defferentiade by stain, typical features of MD)
• EMG:myopathic &fibrillation
• Note :if DNA study +ve no need for EMG &muscles biopsy
MUSCULARDYSTROPHY
16
17. BECKERS MD
• Is milder form
• 5/100,000
• Age :5-15y
• Wheelchair at 30y
• Cardiac similar to duchenne
• Death by age 40
• Dx: DNA, muscle biopsy decrease in dystrophin
• CK:moderatly elevated
17
18. TREATMENT
• No treatment prevent the progression
corticosteroid :controlled trial with predinsone 0,75mg/kg
demonstrate moderate improvement in strength &delay
progression to wheel chair& respiratory compromise
18
20. • CK :normal to or only moderate elevated
• The muscle biopsy :myopathic &fewer dystrophic
• DNA:mutation gene in Xq28 code for protien emerin
20
21. LIMB GIRDLE DYSTROPHY
• AR majority
• Onset: adolescence or late
childhood: sever child recessive muscular dystrophy
21
22. • AR: defect in sacroglycan component of the DGC(
sacroglycanopathy(
• Alpha sacrglycan adhelin is account for 20%
• Onset:childhood& variable
• No intellectual impairment or cardiac
• Muscle biopsy :immune stain absent or diminished for
sacroglycan 22
23. • AD: onset: second and third decades
• Protein defect:caveolin-3
• There are multiple subtypes
• AD type 1:1A,1B …
• AR type 2:
23
24. CONGENITAL MUSCULAR DYSTROPHY
• AR
Perinatal onset
• c/p:hypotonia &proximal weakness,arthrogryposis
• Two types
• CNS involvement: sever mental retardation ,visual, seizure
..cerebrocular dysplasia, progressive death by age 10-12
• No CNS :classic type MRI (hypomyelination), benign outcome,
non progressive
• Muscle biopsy :dystrophy…
24
25. FSH
• Inheritance: AD
• Variable expression within the families
• Age: childhood or adult life
• C/P: weakness early facial then descending
to scapula stabilizer muscles &muscles of the upper limb& distal weakness ..peroneal ,the rate
of progression to forearm &pelvic girdle
• Asymmetrical/ deltoid preserved / joint contracture are uncommon
• Popeye hand/ winging scapula/ no muscle hypertrophy
• Early onset worse prognosis
• 20% require wheelchair
25
26. WORK UP
• CK:N or mild elevation
• Muscles biopsy: myopathic dystrophic& occasionally prominent
mononuclear infiltrate
• Gene: ch 4q35 gene deletion
26
27. MYOTONIC DYSTROPHY
• AD, CTG repeat
• Affect : skeletal,cardiac,
smooth muscles, eye,endocrine &brain
• Onset :at any age ,usually at late 2nd decade
• Some individual can be symptoms free their entire
life
• Sever form :congenital myotonic dystrophy
27
28. • C/P:weakness: (facial,temporalis wasting,ptosis,neck
flexor,distal weakness progress to involve limb girdle)
• Weakness >myotonia
• May be areflexic
28
29. SYSTEMIC
• Posterior sub scapular cataract
• Testicular atrophy& impotence
• Intellectual impairment
• Hypersomnia (central & obstructive)
• Respiratory failure
• Elevation of serum glu, rarely frank DM
• GI: dysphagea, pseudo obstruction
• Cardiac conduction defect sudden death
• Fetal loss in female
29
30. PROMM
• AD
• Proximal weakness, no distal weakness
• Myotonia &myalgia
• Less cardiac &other organ involvement except cataract
30
31. WORK UP
• CK:N or mild elevation
• EMG: myopathic & myotonia
• Muscle biopsy: atrophic, non specific
• Gene :CTG repeat >50 in ch19q13.2
31
32. TTT
• Myotonia rarely sever to require tt: phenytoin is the only safe
drug
• Annual ECG ..pacemaker may required
• Positive pressure ventilation support
• High risk in surgery (cardiac &respiratory)
• Sedation & opiod use with caution
32
33. DISTAL DYSTROPHY
• Types
• AD:4th &6th decade
• AR:in early adult onset/late second or early 3rd
• CK :elevated 200xN AR
33
34. OCULOPHARENGEAL
• AD
• Onset:5th &6th decade
• Ptosis &dysphagea later all extra ocular muscles
&extremities affected (limb girdle) but distal can be
significant in some variant
• Slow progressive ,death from aspiration pneumonia or
starvation
• Ck:n or mild elevated
• Muscle biopsy :rim vacuoles
• Genetic GCG repeat in ch14 34
36. CONGENITAL MYOPATHY
• Are distinguished from dystrophy in three respect:
• Characteristic morphologic alteration
• At birth
• Non progressive
• However there are exception to all these generalization
• Inheritance: are variable
36
37. • c/p: hypotonia with subsequent developmental delay
• Reduce muscles bulk, slender body build &long narrow face
• Skeletal abnormalities: high arched palate ,pectus exacavitum, kyphscliosis,
dislocated hip, pes cavus)
• Absent or reduced muscle stretch reflex
• Weakness: limb girdle mostly, but distal weakness exist
• CK &EMG may be normal
• Muscle biopsy: the diagnostic method
37
38. CENTRAL CORE MYOPATHY
• Characterized by discrete zones of myofibrillar disruption in
the center of muscles fiber
• AD but can be sporadic
• Mutation ch 19,similar to malignant hyperthermia patient
• So anesthesia precaution are necessary
38
39. NEMALINE MYOPATHY
• Pathology: the presence of rods or melamine bodies within
muscles fiber
• AD or AR
• c/p:
• Sever neonatal form which is fatal in the first year of life
• Mild static
• Slowly progressive from birth or early childhood
• Note :rods can present in HIV related myopathy ,some
inflammatory
39
40. CENTRO NUCLEAR (MYOTUBULAR)
• Pathology: large central nuclei in the muscle fiber
• X linked/AD/AR
• sever neonatal/static or slowly progressive
• c/p: ptosis & opthalmoparesis
• Genetic defect: mutation in myotubularin gene Xp28
40
43. METABOLIC MYOPATHY
• Clues to hereditary metabolic myopathy
• Excersize induce weakness &myoglobinuria…glycogen &lipid
• Part of diffuse neurological syndrome…mitochondrial
43
44. GLUCOSE/GLYCOGEN
• Glucose &its storage is essential for the short term anaerobic energy
(glycogensis)
• Two clinical presentation:
• 1-dynamic:type V/V11/V111/1X//XX1
• 2-static:fix weakness
1/111/1V
• Inheritance:AR except for phosphoglycerate kinase
44
45. GLYCOGENSIS WITH EXERCISE INTOLERANCE
• C/P: exercise intolerance in the childhood followed by
excertional induced muscle pain &myoglobinurea in sec or 3rd
decade..
• (Second wind phenomena)
• work up: CK/EMG normal
between the attack in early stage but after attack( myopathic
&fibrillation)
• Forearm exercise test
• Enzyme assay
• Muscle biopsy
• Genetic for mutation 45
46. GLYCOGENSIS WITH FIXED WEAKNESS
• Acid maltase deficiency:
• Enzyme convert glycogen to glucose
• Three clinical variant:
• Infantile: pompes: progressive weakness ,enlargement of
heart, tongue &liver death by age 2
• Juvenile type: proximal weakness, may calf hypertrophy
death by age 20 from respiratory failure
• Adult type:2&7th progressive limb girdle or
scapuloperoneal .no liver ,no heart involvement
46
47. WORK UP
• CK :moderately increased
• EMG: myopathic changes &myotonic discharge in paraspinus
• Enzyme assay:
• Muscle biopsy: a vacuolar myopathy with high glycogen content
• Genetic: mutation in ch 17
47
49. CPT
• Type 1:infancy &child hood with hepatic dysfunction
• Type 2:exertional myalgia &myoglobinurea,
it is the most frequently definable metabolic defect presenting
with myoglobinurea
• AR ,gene 1p32
• The attacks occur after prolonged exercise, fasting, febrile
illness
• Unlike mecardle disease the patient can tolerate brief exercise
,no second wind phenomena
• Muscle strength are normal at rest 49
50. LAB
• CK:n at rest
• Forearm exercise test :N
• EMG: n at rest ,&myopathic during the attack
• Muscle biopsy: usually N ,except of myopathic changes after
rhabdomylsis
• Enzyme assay
• ttt &meal frequency: increase CHO intake
&education about fasting &exercise
50
52. CHANNELOPATHY
• Non dystrophic myotonia
• Periodic paralysis
• It due to mutation in different channels gene leading to :
• Hyper excitability :myotonia
• In excitability: paralysis
52
53. CHLORIDE CHANNELOPATHY
• Mutation in CL channel..hyperexcitability after depolarization
• Myotonia congenita:
• AD..thomsen /AR:becker
• C/P: muscle hypertrophy,
myotonia/becker type has fluctuating limb girdle weakness
53
57. PARAMYTONIA CONGENITA
• AD
• Onset :1st decade
• Paradoxical myotonia (Aggravated by warm as well cold)
• Face ,neck,forearm
• After several attempt of eye closure the patient can not open
the eye
• ttt: Na channels blocker mexiletine
57
58. HYPERKALAMIC PERIODIC PARALYSIS
• K sensitive periodic paralysis
• Onset :1st decade
• Attack last:1-2 h
• During attack: areflexic with no ocular or respiratory muscles
weakness
• Strength is n between the attack, but some patient has
interictal limb girdle weakness
• Some families have myotonia ¶myotonia
• Aggravated: fasting/cold, shortly after exercise, K load, early
AM
58
59. • Episodes are rarely serous enough to require acute ttt
• ttt:
• oral CHO
• Prevention: thiazide,B agonist, low K,high CHO
• Avoid fasting, strenuous exercise/
59
61. HYPOKALEMIA
• AD:
• It is the most frequent form of periodic paralysis
• Common in male
• Age: adolescence
• The attacks 3-24h/vague prodorme of stiffness
&heaviness& rarely ocular, bulbar, respiratory involved
• Early Myotonia of eyelid & late interictal proximal
weakness
61
62. • Aggravated: CHO meal, cold,hrs post exercise, sleep
• Work up:K level q 30min /TFT/
• R/O 2nd causes of hypokalemia
• Tttt:
• Acute: oral K Q30min ,if symptoms sever iv K
• Prevention:
• Low CHO, low sodium diet ,spirnolactone,
trimetrine
62