Ahmed Cannot Run - created from Mind Map

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Anatomy of the foot

muscle weakness

Duchene Muscular Dystrophy

causes

nutrients required for muscle development

History Taking

Examination

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

Calcium ,Iron, Vitamin D, Vitamin B12, Magnesium, Zinc,OMEGA 3, VITAMN C ,VITAMIN B12, PROTEINS

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

Physical Examination

Neurological

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

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

sever progressive X-linked inherited disease characterized by progressive degeneration of the skeletal muscle especially those of the shoulder and pelvic griddle

Pathogenesis:due to loss of dystrophin

Clinical Progression

Complications

Investigations

Epidemiology: one in 5,000 boys, which are 200 per million births> globally . graph present 2012

Management & treatment

Prognosis

A mutation in the gene encoding for dystrophin protein, which is Xp21 gene.

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.

characteristic clinical features are: –Progressive weakness –Intellectual impairment –Hypertrophy of the calves –Proliferation of connective tissue in muscle

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

Serum Creatine Kinase

Electromyography

Thyroid Function Test

Western Blot

muscle biopsy

Used to:- detect myositis -detect muscle damage due to myopathies such as muscular dystrophy.

Normal Range: 40-300U/L

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.

Are blood tests that determine the function of the thyroid gland -Helps in the diagnosis of two conditions: Hypothyroidism Hyperthyroidism

method to detect and analyze proteins

In DMD case to detect dystrophin abscent

Shows myopathic changes such as; connective tissue proliferation, scattered degenerating and regenerating myofibres

Physical and occupational therapy

stem cell & gene therapy

Medications:

Exercise -Braces, standing frames and wheelchairs -Diet

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.

death occurs usually at about 18-20yrs of age.

The causes of death are: –Respiratory failure –Heart failure –Pneumonia –Aspiration –Airway obstruction.