AUTO IMMUNE DISEASE

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AUTO IMMUNE DISEASE

• Dr Hari hara iyer

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• Auto Immunity is a condition in which structural
  or functional damage is produced by the action of
  immunologically competent cells or antibodies
  against normal components of body.

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CLASSIFICATION

• Organ Specific
• Endocrine
• Alimentary
• Blood
• Others Myasthenia gravis (Muscles

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MYASTHENIA GRAVIS

• Other names Gold flam disease
• Hoppe Gold flam disease
• Asthenic bulbar
• Bulbo spiral paralysis
• Termenology meaning mys muscle
• asthenia weakness (no atrophy)
• gravis - Serious
• serious muscle weakness

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Definition

• MG is a serious auto immune disorder affecting
  the neuromuscular junction causing chronic
  progressive muscular weakness beginning usually
  in the extra ocular muscles and lids.
• Women Male
• 3 2
• at
• 20 30 years 50 60 years

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Pathogenisis

• Neuro muscular
• 1 nerve---ant horn eg spinal muscular
  atropy
• ----UMN amylotropic lateral
  sclerosis
• ----Peripheral nerve Diabetic
  neuropathy
• 2Junction MG
• 3Muscleduchennes muscular dystrophy

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• Site
• Neuro muscular Junction
• Normal Pathology
• Acetyl choline when binds with Ach receptor (in
  muscles) a depolarization occours an action
  potential is created, which initiates muscle
  contraction
• M. G.
• Damaged due to endolysis
• Ach. Receptors reduced is No
• Blocked due to attached antibodies
• ? So decreased transmission ? failure of action
  potential ? weakened muscle contraction
• M. G. is related thymic hyperplacia

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• Examination of neuromuscular function by immuno
  chemical technique has demonstrated Ig G C3
  C9 protein.
• Chance of muscle weakness is babies to born to MG
  mothers, as Ig G can cross placenta.
• Clinical Features
• Weakness and faliguability of muscle.
• Weakness increased by use improved by rest and
  sleep

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• Characteristic distribution
• Cranial muscles esp. Lids extra ocular muscles
  are involved
• first ? symptom /sign
• ? Diplopia or ptosis
• Sharking expression when attempt to smile
• Facial Weakness
• Weakness is chewing
• Speech Nasal timbre
• Weakness of palate dys arthria
• Weakness of tonue mushy quality
• difficulty in swallowing

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• ? Limb weakness Proximal first a symmetric
• Last Stage
• First weakness with no wasting. But later
  weakness, wasting, involvement of respiratory
  muscle and it can lead to crisis.
• Diagnosis
• Symptoms Anti Ach Receptor Radioimmuno assay
• Definite if it is ve

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• DD
• Congenital myasthenic syndrome
• Drug induced myasthenia
• Lambert Eaton myasthenic Syndrome
• Neurasthenia, Hyper thyroidism, thymoma
• Rx
• Anticholinestrase medications
• Thymectomy
• Immuno suppression

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• Miasm
• In the initial stages when the pathology is
  reversible the miasmatic expression is psora.
  Later there is reduction in Ach receptor sites
  due destruction of it by endolysis. So the
  syphilitic miasm comes into play.
• Medicines
• Curar
• Gelsemium
• Nat.mur
• Pic.acid
• Sulphur

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AUTO IMMUNE DISEASE OF EYES

• Two types of auto immune disease
• Cataract surgery sometimes leads to intra ocular
  inflammation caused by auto immune response to
  lens protein. This is known as phacoanaphylaxis.
• Usually lens protein is kept inside the capsule
  and it is not leaked outside. But a frank
  rupture due to surgery or trauma may leak it out
  of lens capsule and lead to a sensitive reaction
  and anaphylaxis. There occurs lymphocytic and
  plasma cell useful tration to ant chamber and
  manifest as allergic reaction

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• One eye may be injured. The other eye also
  develops inflammation later.
• Here the uveal antigen or pigment is responsible
  for the inflammation of the other eye. The
  studies are showing that complement fixing
  antibodies in the uveal pigment are shown to
  occur in the blood after ocular injury

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• Clinical Features
• Irritability and low grade indolent crisis is
  present in the inflamed eye after a penetrating
  injury. The cris has koppe nodules later it
  become thickened. After two weeks to two months
  the inflammation begins insidiously in the
  sympathizing eye also. Often the first symptom
  is photophobia and blurring of vision due to lack
  of accommodation. The disease progresses until
  it demonstrates as thickened cris Keratic
  precipitates in the second eye similar to those
  of the existing eye.

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• DD
• Phacoanaphylaxis
• In this lesion starts as bilateral and lens
  extraction controls phacoanaphilaxiz. But it
  does not control sympathetic ophthalmia (Pan
  uveites)
• Treatment
• Prophylactic Enucleation of hopeless eye with in
  7-8 days saves the other eye. Once signs of
  inflammation starts in the sympathizing eye,
  enucleation of the existing eye is useless

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• Miasm
• Syphilitic
• Medicine
• Uveitis Arn, Aur, Bry, Gel, Hep, Kalibich,
  Kali-i, Merc. Rh- tox, Sil