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Multiple sclerosis and mysthenia gravis

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multiple sclerosis and mysthenia gravis presentation

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Multiple sclerosis and mysthenia gravis

  1. 1. Presented By : Ms. Dorjee Dolkar Multiple Sclerosis
  2. 2. Multiple Sclerosis  Chronic, progressive, degenerative disorder of the CNS characterized by disseminated demyelination of nerve fibers of the brain and spinal cord
  3. 3. INCIDENCE Usually affects young to middle- aged adults, with onset between 15 and 50 years of age Women affected more than men
  4. 4. Etiology  Unknown cause  Related to infectious, immunologic, and genetic factors
  5. 5. Etiology  Possible precipitating factors include Infection  Environmental factor-Vitamin D  Immunologic reaction  Sex hormone  Genetic factor Poor state of health
  6. 6. PATHOPHYSIOLOGY
  7. 7. AN AUTOIMMUNE PROCESS TRIGGERED BY GENETIC AND ENVIRONMENTAL FACTORS. INFLAMMATION OF VENULES IN THE CNS AND CAUSE DISRUPTION OF BLOOD-BRAIN BARRIER ALLOWING LYMPHOCYTES TO ENTER CNS TISSUE. THESE LYMPHOCYTES PROLIFERATE AND PRODUCE IgG WHICH RELEASE INFLAMMATORY CHEMICALS CAUSE EDEMA ACUTE ATTACK PATHOPHYSIOLOGY
  8. 8. REPEATED INFLAMMATORY ATTACK MYELIN IS DEMAGED AND SEGMENT OF AXON BECOME TOTALLY DEMYELINATED AND DEGENRATED ASTROCYTE PROLIFERATES IN DEMAGE REGION OF CNS ( A PROCESS CALLED GLIOSIS). PLAGUE ( GREY AND PINKISH LESION IN THE CNS). CHRONIC LESION
  9. 9. WHEN NERVE IMPULSE TRAVEL DOWN AN AXON DEMAGED BY MS. SLOW AND WEAK AS THEY PASS ACROSS THE DEMYLENATED AREAS. IMPULSE BLOCKED ENTIRELY WHEN AXON DEGENRATED. EXTREMITY WEAK, PARESTHESIA, VISUAL DISTURBANCES, ETC. ABNORMAL NERVE IMPULSE TRANSMISSION
  10. 10. Pathophysiology
  11. 11. Pathogenesis of MS Fig. 57-1
  12. 12. Multiple Sclerosis Clinical Manifestations  Vague symptoms occur intermittently over months and years  MS may not be diagnosed until long after the onset of the first symptom
  13. 13. Multiple Sclerosis Clinical Manifestations  Common signs and symptoms include Visual, motor, sensory, cerebellar, and emotional problems
  14. 14. Multiple Sclerosis Clinical Manifestations  Motor manifestations ◦ Weakness or paralysis of limbs, trunk, and head. ◦ Diplopia (double vision) ◦ Scanning speech ◦ Spasticity of muscles
  15. 15. Multiple Sclerosis Clinical Manifestations Sensory manifestations ◦Numbness and tingling ◦Blurred vision ◦Vertigo and tinnitus ◦Decreased hearing ◦Chronic neuropathic pain
  16. 16. Multiple Sclerosis Clinical Manifestations  Cerebellar manifestations ◦ Nystagmus Involuntary eye movements ◦ Ataxia ◦ Dysarthria Lack of coordination in articulating speech ◦ Dysphagia Difficulty swallowing
  17. 17. Multiple Sclerosis Clinical Manifestations Emotional manifestations ◦Anger ◦Depression ◦Euphoria
  18. 18. Multiple Sclerosis Other Clinical Manifestations Bowel and bladder functions ◦Constipation ◦Spastic bladder: small capacity for urine results in incontinenceFlaccid bladder: large capacity for urine and no sensation to urinate
  19. 19. Multiple Sclerosis Other Clinical Manifestations Sexual dysfunction Erectile dysfunction Decreased libido Difficulty with orgasmic response Painful intercourse Decreased lubrication
  20. 20. Clinical Courses Of MS  Relapsing- Remitting MS  Primary Progressive MS  Secondary Progressive MS  Progressive Relapsing MS
  21. 21. Multiple Sclerosis Diagnostic Studies  Based primarily on history, clinical manifestations, and physical examination.  Certain laboratory tests are used as adjuncts to clinical exam
  22. 22. Multiple Sclerosis Diagnostic Studies  MRI – demonstrates presence of plaques  Spinal Tap / Lumbar Puncture: tested for infection.  Evoked Potential Test: Monitor brain wave respond to what you see and hear.
  23. 23. Multiple Sclerosis Pharmacological Management Drug Therapy ◦ Corticosteroids Treat acute exacerbations by reducing edema and inflammation at the site of demyelination Do not affect the ultimate outcome or degree of residual neurologic impairment from
  24. 24. Cont…. ◦ Immunosuppressive Therapy  Azathioprine (Imuran)  Cyclophosphamide ( cytoxan) Because MS is considered an autoimmune disease Potential benefits counterbalanced against potentially serious side effects
  25. 25. Cont…..  Antispasmotics (muscle relaxants)  Baclofen (Lioresal)  Dantrolene ( Dantrium)  Diazepam (Valium) To relieve muscle spasm.
  26. 26. Multiple Sclerosis Collaborative Care  Physical therapy helps  Relieve spasticity  Increase coordination  Train the patient to substitute unaffected muscles for impaired ones
  27. 27. Multiple Sclerosis Collaborative Care  Nutritional therapy includes megavitamins and diets consisting of low- fat, gluten-free food, and raw vegetables  High-protein diet with supplementary vitamins is often prescribed
  28. 28. PLASMAPHERESIS:  This therapy is to remove inflammatory agents such as T- lymphocytes through exchange plasma while suppressing immune response and inflammation.
  29. 29. Surgical Management:  ACHILLES TENOTOMY: Indicated to severe spasticity and deformity. Relieve foot drop from sever plantar flexion by transected the achilles tendon.
  30. 30. Multiple Sclerosis Nursing Assessment  Health History Risk factors Precipitation factors Clinical manifestations
  31. 31. Multiple Sclerosis Nursing Diagnoses  Ineffective airway clearance r/t decreased cough mechanism.  Risk for injury r/t blurred vision as evidenced by unable to see clearily.  Altered nutrition less than body requirement r/t dysphagia as evidenced by inability to control spasticity.  Activity intolerence r/t fatigue as evidenced by unable to perform ADLs.
  32. 32. Myasthenia Gravis “Grave Muscle Weakness”
  33. 33. Myasthenia Gravis Autoimmune disease affecting the neuromuscular junction Not a brain disorder – brain functions normally Characterized by fluctuating muscle weakness and fatigability Disease may be generalized or ocular specific
  34. 34. INCIDENCE Occurs in all races MG affects 14 per 100,000 people in the United States Can affect any age group Women – peak incidence 20's to 30's Men – peak incidence 50's to 60's Three times more common in women than men More common in asian race than other
  35. 35. CAUSES No single cause has been identified Abnormal thymus tissue found in most patients with MG Thymic tumors found in 15% of patients Virus infections have been found in some cases and are a suspected cause  Antibodies blocking Acetylcholine.
  36. 36. Genetic Factors Myasthenia Gravis is not a genetically inherited disease Some families appear to carry a gene that increases the risk for developing the disease No specific gene has been identified and there are no tests for genetic screening
  37. 37. Exacerbation Trigger Factors Infection Stress Fatigue Cathartics (laxatives) Heat (sauna, hot tubs, sunbathing)
  38. 38. Pathophysiology
  39. 39. Signs and Symptoms  Affects any of the muscles that you control voluntarily, certain muscle groups are more commonly affected than others  OCULAR AND FACIAL MUSCLE:  Difficulty speaking (dysarthria)  Difficulty swallowing (dysphagia),  Drooping eyelids (ptosis)  Double vision (diplopia)  Nasal-sounding speech and weak neck muscles that give the head a tendency to fall forward or backward.
  40. 40. Musculoskeletal System: o Weakness and Fatigue  Immobility  Decreased function of limbs
  41. 41. Respiratory System Weakening of intercostal muscle.  Decreased diaphragm movement  Breathlessness and dyspnea  Poor gas exchange
  42. 42. Nutritional  Dysphagia  Decreased ability to move tongue  Inability to feed self  Weight loss  Dehydration  Aspiration
  43. 43. Cont….. Symptoms tend to progress over time, usually reaching their worst within a few years after the onset of the disease Worsening muscle weakness with repeat activity
  44. 44. Diagnosis test Edrophonium test (Tensilon)  Antiacetylcholine receptor antibody serum level  Pulmonary Function Test Single-fiber electromyography (EMG) Imaging scans Eg: CT or MRI
  45. 45. Tensilon Test Injection may result in a sudden, although temporary, improvement in muscle strength — an indication of myasthenia gravis. Acts to block an enzyme that breaks down acetylcholine, the chemical that transmits signals from nerve endings to muscle receptor sites.
  46. 46. Diet/Nutrition Eat small meals and snacks five to six times a day Avoid using low fat or diet products when possible Avoid eating lemons or tonic water Eat warm rather than hot food Runny or puree diet when swallowing is difficult Alternate sips of liquid to avoid food from sticking AVOID eating chewy or dry crumbly foods
  47. 47. Medications/Treatment Immunosuppressive Therapy Prednisone Azathioprine Acetylcholinesterase Inhibitors First line of therapy Neostigmine bromide (Pyridostigmine) Edrophonium chloride (Tensilon)
  48. 48. Surgical Management Thymectomy Removal of thymus gland. • Recommended to those who gets dysphagia due to thymus gland. • Thymus tumor
  49. 49. Nursing Diagnosis:  Risk for injury r/t ptosis as evidenced by loss os motor control.  Ineffective airway clearance r/t nonproductive cough as manifested by decreased rib cage movement.  Impaired swallowing r/t fatigue and dysphagia as manifested by unable to swallow food.
  50. 50. Cont.. Impaired social interaction r/t change in body image as evidenced by decreased motor function.  Fatigue r/t increased energy need for muscle movement as evidenced by unable to perform ADL’s.  Ineffective therapeutic regimen r/t insufficient knowledge as evidenced by depression and potential for complication.
  51. 51. Myasthenic Crisis VS. Cholinergic Crisis Myasthenic Crisis Under medication  Increased HR/BP/RR  Bowel and bladder incontinence  Decreased urine output  Absent cough and swallow reflex  May need mechanical ventilation  Temporary improvement of symptoms with administration of Tensilon Cholinergic Crisis Overmedication  Decreased BP  Abd cramps  N/V, Diarrhea  Blurred vision  Pallor  Facial muscle twitching  Constriction of pupils  Tensilon has no effect  Symptoms improve with administration of anticholinergics (Atropine)
  52. 52. Patient Teaching  Teach patient/family disease process, complications, and treatments  Teach patient about their medications uses dosage etc  Teach medications to use with caution d/t muscle exacerbation Beta blockers, calcium channel blockers, quinine, quinidine, procainamide, some antibiotics, neuromuscular blocking agents  Avoid certain medications D-penicillinamine, A-interferon, botulinum toxin
  53. 53. Cont…….. Teach of both Myasthenic Crisis and Cholinergic Crisis Help patient plan daily activity to coincide with energy peaks Stress need for rest periods Explain that exacerbations, remissions, and daily fluctuations are common Avoid strenuous exercise, stress, infection, exposure to hot or cold temperatures Teach patient to wear medic-alert bracelet
  54. 54. Prognosis Chronic disease with periods of exacerbation and sometimes remissions Disease course is highly variable Symptoms respond well to treatment and in most cases the patient can live a normal or nearly normal life Ocular Myasthenia has the best prognosis
  55. 55. SUMMARY

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