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NURSING MANAGEMENT OF PATIENT WITH MYASTHENIA GRAVIS, Lecture notes of Nursing

NURSING MANAGEMENT OF PATIENT WITH MYASTHENIA GRAVIS : - CAUSES, CLINICAL MANIFESTATIONS, SYMPTOMS, COMPLICATIONS, ASSESSMENT AND DIAGNOSTIC FINDINGS, MANAGEMENT

Typology: Lecture notes

2014/2015

Available from 07/25/2022

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Myasthenia Gravis
Myasthenia Gravis is a Latin term meaning Grave Muscle Weakness
Definition:-
MG is an autoimmune disorder affecting the myoneural junction (also called
neuromuscular junction) and is characterised by varying degrees of weakness of voluntary
muscles
The weakness of skeletal muscles worsens upon exertion and improves after rest
periods. Myasthenia gravis results from failure or error in transmission of impulses between
nerves and muscles. Although it is a relatively rare condition, myasthenia gravis can affect
people of all ages, and is most commonly seen in women younger than 40 years old and in
men above 60 years old.
At present, there is still no cure for myasthenia gravis, but treatment aims in
relieving signs and symptoms and improving the patient's quality of life.
Causes:-
Autoantibodies directed at acetylcholine receptors:
Muscles and nerves communicate through neurotransmitters, which are chemicals
released by the nerves and matches into the receptor sites found in the neuro-muscular
junction. When a continuous problem in this process of transmission occurs, myasthenia
gravis can develop. The immune system blocks the receptor sites for a neurotransmitter
called acetylcholine by producing antibodies. Less receptor sites cause insufficient
acetylcholine secretion and fewer nerve signals result in muscle weakness. These antibodies
also block protein function and tyrosine kinase, a protein enzyme associated in the
formation of neuro-muscular junction.
Thymus gland may trigger and maintain levels of antibodies that block acetylcholine
receptors
It is also associated with thymus tumours
There is also a type of myasthenia gravis that is antibody-negative, wherein the root
cause is the antibodies are working against Lipoprotein-related protein 4, and not by
blocking the acetylcholine.
Clinical manifestations:-
Muscle weakness with activity- hallmark sign
Ocular myasthenia - weakness of the eye muscles
Ptosis -drooping of one or both eyelids
Diplopia - double vision
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Myasthenia Gravis

Myasthenia Gravis is a Latin term meaning Grave Muscle Weakness

Definition:-

MG is an autoimmune disorder affecting the myoneural junction (also called neuromuscular junction) and is characterised by varying degrees of weakness of voluntary muscles The weakness of skeletal muscles worsens upon exertion and improves after rest periods. Myasthenia gravis results from failure or error in transmission of impulses between nerves and muscles. Although it is a relatively rare condition, myasthenia gravis can affect people of all ages, and is most commonly seen in women younger than 40 years old and in men above 60 years old. At present, there is still no cure for myasthenia gravis, but treatment aims in relieving signs and symptoms and improving the patient's quality of life.

Causes:-

 Autoantibodies directed at acetylcholine receptors: Muscles and nerves communicate through neurotransmitters, which are chemicals released by the nerves and matches into the receptor sites found in the neuro-muscular junction. When a continuous problem in this process of transmission occurs, myasthenia gravis can develop. The immune system blocks the receptor sites for a neurotransmitter called acetylcholine by producing antibodies. Less receptor sites cause insufficient acetylcholine secretion and fewer nerve signals result in muscle weakness. These antibodies also block protein function and tyrosine kinase, a protein enzyme associated in the formation of neuro-muscular junction.

  • Thymus gland may trigger and maintain levels of antibodies that block acetylcholine receptors
  • It is also associated with thymus tumours
  • There is also a type of myasthenia gravis that is antibody-negative, wherein the root cause is the antibodies are working against Lipoprotein-related protein 4, and not by blocking the acetylcholine.

Clinical manifestations:-

- Muscle weakness with activity- hallmark sign

  • Ocular myasthenia - weakness of the eye muscles
  • Ptosis - drooping of one or both eyelids
  • Diplopia - double vision
  • Speech impairment- Dysphonia
  • Difficulty in chewing and swallowing- Dysphagia
  • Change in facial expression
  • Respiratory failure-late symptom
  • Generalised weakness of arms, legs, neck

Factors that may aggravate myasthenia gravis include:

  • Fatigue
  • Pre-existing illness
  • Stress
  • Certain medications such as beta blockers, certain aesthetics, and some antibiotics
  • Pregnancy- in rare cases, mothers with myasthenia gravis have children who are born with the same condition (known as neonatal, myasthenia gravis or congenital myasthenic syndrome)
  • Menstrual period

DIAGNOSES:-

1) Anti cholinesterase Inhibitor Test It is done by iv administration of edrophonium chloride to the patient .Then assess the patient after 30 seconds , facial muscle weakness and ptosis should resolve for about 5 minutes 2) Ice Test Ice pack is placed over patient's eye for 1 minute. Ptosis should resolve temporarily. 3) Repetitive Nerve Stimulation Demonstrates a decrease in successive action potentials 4) Magnetic Resonance Imaging May demonstrate enlarged thymus gland

TREATMENT:-

1) Pharmacologic Therapy

  • Pyridostigmine bromide (anticholinesterase medication)
    • Prednisone (immunomodulating agent) suppress antibody production
    • Intravenous Immune globulin (IVIG) destroy and neutralise autoantibodies
  1. Plasmapheresis Plasmapheresis is the procedure that uses a filtration process to remove the antibiotics Repeated procedure is needed for the treatment but the benefits usually lasts for only a few weeks. Associated risks include hypotension, bleeding, cardiac problems and allergic reaction.