Ahmed Cannot Run

Ahmed Cannot Run

1. Anatomy of the foot

2. muscle weakness

   • causes
     • 1- infection: poliomyelitis, lyme disease. 2-neurological: Demyelinating disorders: Guillain-Barré syndrome. 3-Medications Statin> atorvastatin (Lipitor) ,Amiodarone (oral route). 4-Electrolyte: Hyperkalemia. 5- Genetics 6-Metabolic: Glycogenoses> Acid maltase deficiency
   • nutrients required for muscle development
     • Calcium ,Iron, Vitamin D, Vitamin B12, Magnesium, Zinc,OMEGA 3, VITAMN C ,VITAMIN B12, PROTEINS
   • History Taking
     • Introduction: Greeting the patient, insure privacy - Duration &Location- progression Radiation -Quality (Pain Scales /questionnaire) & Quantity -Aggravating factors &Alleviating factors
     • -family history -medication history -previous infection or trauma. -Growth parameters"Milestones" -Vaccination schedule
   • Examination
     • Physical Examination
       • Introduction & Consent "HEPA" -Inspection "SSSP" -Palpation: Skin Temperature, Joints ,Tendons ,Ligaments
         • Move: -Dorsiflexion -Plantar Flexion -Inversion -Eversion -Flexion of great toe
           • Special Test: Inversion and Eversion stress test: for ligaments medial and lateral -Thompson’s test for tendoachillies rupture -Tests for Morton’s metatarsalgia
             • Closure: -Test Gait -Inspect the footwear- Drapes the patient
     • Neurological
       • The motor system: -Fasciculations and muscle wasting -Tone Clonus Power at hip, knee, ankle, and tarsal joints Coordination -Heel–shin test -Toe–finger test
       • The sensory system:- Dermatomes -The superficial or cutaneous reflexes
       • Gait

3. Duchene Muscular Dystrophy

   • sever progressive X-linked inherited disease characterized by progressive degeneration of the skeletal muscle especially those of the shoulder and pelvic griddle
     • A mutation in the gene encoding for dystrophin protein, which is Xp21 gene.
   • Pathogenesis:due to loss of dystrophin
     • 1-fragile sarcolemma 2-loss of interaction between the sarcolemma and extracellular matrix. 3-separation of the sarcolemma from the basal lamina.
       • Leading to:1-increased osmotic fragility of dystrophic muscles. 2-exceesive influx of calcium ions. 3-release of soluble muscle enzymes such as Creatine kinase. 4-Necrosis of the muscle cell.
   • Clinical Progression
     • characteristic clinical features are: –Progressive weakness –Intellectual impairment –Hypertrophy of the calves –Proliferation of connective tissue in muscle
   • Complications
     • Cardiac: -Arrhythmias -Cardiomyopathy
     • Orthopaedic problems :-Joint contractures -Osteopenia –because of immobility but also secondary to steroid treatment -Scoliosis
     • Infectious -Pulmonary infections Pulmonary -Respiratory insufficiency with decreased total lung capacity, decreased residual lung volume
   • Investigations
     • Serum Creatine Kinase
       • Used to:- detect myositis -detect muscle damage due to myopathies such as muscular dystrophy.
         • Normal Range: 40-300U/L
     • Electromyography
       • is a diagnostic procedure to assess the health of muscles and the nerve cells that control them (motor neurons).
         • EMG results can reveal nerve dysfunction, muscle dysfunction or problems with nerve-to-muscle signal transmission.
     • Thyroid Function Test
       • Are blood tests that determine the function of the thyroid gland -Helps in the diagnosis of two conditions: Hypothyroidism Hyperthyroidism
     • Western Blot
       • method to detect and analyze proteins
         • In DMD case to detect dystrophin abscent
     • muscle biopsy
       • Shows myopathic changes such as; connective tissue proliferation, scattered degenerating and regenerating myofibres
   • Epidemiology: one in 5,000 boys, which are 200 per million births> globally . graph present 2012
   • Management & treatment
     • Physical and occupational therapy
       • Exercise -Braces, standing frames and wheelchairs -Diet
     • stem cell & gene therapy
     • Medications:
       • Corticosteroids such as prednisone, can help improve muscle strength
         • Heart medications, such as angiotensin-converting enzyme (ACE) inhibitors or beta blockers, if muscular dystrophy damages the heart.
   • Prognosis
     • death occurs usually at about 18-20yrs of age.
       • The causes of death are: –Respiratory failure –Heart failure –Pneumonia –Aspiration –Airway obstruction.

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