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THE OXFORD COLLEGE OF SCIENCE

DEPARTMENT OF MICROBIOLOGY.

Seminar report on : AUTOIMMUNE DISEASES.

Submitted By, Under Guidance


DEEPTHI M VIENNA FERNANDEZ Ma’am
2ND Year ,3RD MSc Microbiology ASSISTANT PROFESSOR
Reg No. – P03MS21S0244 Department of Microbiology.
CONTENT :-
 INTRODUCTION OF AUTOIMMUNE DISEASES.
 SYSTEMIC LUPUS ERYTHEMATOSUS.

 MULTIPLE SCLEROSIS .

 RHEUMATOID ARTHRITIS.

 GRAVE’S DISEASE.

 MYASTHENIA GRAVIS.

 REFERENCE .

 PREVIOUS YEAR QUESTIONS.

 CONCLUSOIN.
INTRODUCTION :-
 Autoimmune diseases is a group of disorders in which tissue injury is
caused by humoral [by auto-antibodies] or cell mediated immune
response [by auto-reactive T cells] to self antigens.
 The immune system attack self-cells.
 The attack can be either very specific tissue or to a large no. of tissues.
 Once started ,it is hard to stop.
SYSTEMIC LUPUS ERYTHEMATOSUS –
ATTACKS MANY TISSUES.
 SLE is a chronic disease that causes inflammation in connective
tissue, such as cartilage and the lining of blood vessels, which
provides strength and flexibility to structures throughout the body.
 Best example of a Systemic Autoimmune disease is SLE.
 Women’s aged from 20-40 years.
 The ratio is 10:1.
Symptoms :-
 Fever ,weakness , arthritis ,fatigue ,malaise ,
skin rashes, pleurisy and kidney dysfunction.
Epidemiology :-
 Lupus is more frequent in African-American
and Hispanic women than in Caucasians.
Pathogenesis :-
 Affected individuals may produce auto-antibodies to a vast array of
tissues, antigens such as DNA, histones , RBC s , platelets, leukocytes
and clotting factors .
 Auto-antibody specific for RBC and platelets can lead to complement-
mediated lysis , resulting in hemolytic anemia and thromobocytopenia.
 Auto-antibodies with various nuclear antigens are deposited along the
walls of small blood vessels, a type III hypersensitive reaction
develops.
•It activates complement system and generate membrane-attacks
complexes and complement split products damage the wall of the blood
vessel , resulting in vasculitis and glomerulonephritis.
•Excessive complement SLE produces complement split products C3a
and C5a which is 3 or 4 times higher than normal which leads to tissue
damage .

LABORATORY DIAGNOSIS :-
•Complete Blood Count and ESR
•Kidney and liver assessment
•Urinalysis
•SLE focuses on the antinuclear antibodies[ANA] which are directed
against double stranded or single stranded DNA, nucleoprotein,
histones and nucleolar RNA.
•Indirect immunofluorescent staining with serum from SLE patients
produces various characteristic nucleus-staining patterns.
SYSTEMIC LUPUS ERYTHEMATOSUS

TREATMENT :-

•Anti-inflammatory medications
•Steroids creams for rashes
•Corticosteroids
•Antimalarial
MULTIPLE SCLEROSIS – ATTACKS THE CENTRAL
NERVOUS SYSTEM.
 MS is a demyelinating disease,in which
insulating covers of nerve cells in the brain
and spinal cord are damaged.
 Age group - 20 to 40 years.

Symptoms :-
 Numbness in limbs or severe like paralysis
 loss of vision, fatigue

 tingling and lack of coordination .

 A breakdown in myelin sheath leads to

numerous neurologic dysfunctions.


Epidemiology :-
 Neurologic disability - western countries
 And also common in hemisphere and in United states .
Pathogenesis :-
 Individual produce auto-reactive T-cells that causes inflammatory
lesions along the myelin sheath of nerve fibers.
 The cerebrospinal fluid with active MS contains T-lymphocytes ,which
infiltrate the brain tissue and causes inflammation lesions ,destryoing
the myelin.
Laboratory Diagnosis :-
There are no specific tests for MS
•BLOOD TEST
•SPINAL TAP[LUMBAR PUNCTURE]
•MRI
•Evoked potential tests

Treatment :-
•Corticosteroids
•Plasma exchange [plasmapheresis]

•Injectable treatments : Interferons beta medications,Glatiramer acetate


and Monaclonal antibodies .

•Oral treaments : Teriflunomide, Dimethyl fumarate and Monomethyl


fumarate.
RHEUMATOID ARTHRITIS- ATTACKS JOINTS.
 Chronic systemic disease of the joints it can damage body
systems,including the skin,eyes,lungs ,heart and blood vessels.
 Affecting women from 40-60 years old .
Symptoms :-
 Chronic inflammation of the joints
 hemotologic

 cardiovascular and respiratory systems

are affected.
Pathogenesis :-
They produce a group of auto-antibodies
called Rheumatoid factors[RA Factor]
are reactive with determinants in the Fc region of IgG antibody.
 The classical RF is an IgM antibody such auto-antibodies bind to
normal circulating IgG forming IgM-igG complexes that are deposited
in the joints.
 These immune complex can activate the complement cascade,
resulting type III hypersensitivity ,which leads to chronic
inflammation of the joints .
 The synovial fluid of these patients contain increased no. of T cells
and macrophages.
LABORATORY DIAGNOSIS :-
 BLOOD TESTS :-
 Rheumatoid factor and anti-cyclic citrullinated peptide[anti-
CCP]antibodies .
 IMAGING TESTS :-X-rays , MRI , Ultrasound tests.
TREATMENT :-
NO cure . Early stage treatment begins with medications known as
disease-modifying antirheumatic drugs [DMARDs].
MEDICATIONS :-
 NSAIDs[nonsteroidal anti-inflammatory drugs]
 Steroids
 Conventional DMARDs
 Biological agents
 Targeted synthetic DMARDs
GRAVE’S DISEASES.
 Basedow’s disease.
 Disorder of the bufferfly shaped gland in the throat [thyroid].
 It is an autoimmune disease in which the our own immune system
attacks the thyroid gland,causing it to produce thyroxine.
 T4 and others thyroid hormones - regulation of growth and control
metabolism .
 It can affect both men and women , common in women aged 20 years
or more.
 Causes :- Exophthalmos , thyroid enlargement ,affects thyroid
stimulation and dermal changes.
 Excess thyroid hormone production leads to hyperthyroidism.
 Ratio is 7:1
SIGNS AND SYMPTOMS : -
 Bulging eyes
 Enlargement of thyroid gland
 Increased appetite ,coupled with
weight loss
 Heat intolerance and diaphoresis
 Hyperactivity and fatigability

Pathogenesis :-
They produces auto-antibodies that bind the receptor for TSH and
mimic the normal action ,activating adenylate-cyclase and resulting
in production of thyroid hormones which are over-stimulated. Hence
called as long-acting thyroid-stimulating antibodies[LATS].
DIAGNOSIS :-
 Blood test checking for increased free Thyroxine and
Triiodothyronine levels.
 Exophthalmos and non-pitting tribial myxoedema are unique
features when it is coupled with hyperthyroidism.

Treatment :-
 Antithyroid drugs [ methimazole ]
 Radioiodine
 Thyroidectomy.
MYASTHENIA GRAVIS
 The protype autoimmune disease mediated by blocking antibodies.
 Affects the myoneural junction.
 3 times more common in women .
Pathogenesis :-
They produces auto-antibodies that bind the acetylcholine receptors
on the motor-end plates of muscles ,blocks normal reaction and
induce complement mediated lysis of cells.
Symptoms :-
•Visual problems- drooping eyelids and double vision.
•Muscle weakness and fatigue .
•Facial muscle causing mask-like appearance.
•Trouble swallowing or pronouncing words
•Weakness of neck or limbs.

Diagnosis :-
•Blood test
•Genetic tests
•Nerve conduction studies
•Electromyogram.

Treatment :-
•Medicine : Anti-cholinesterase medicines ,steroids,
or immunosuppressive
•Thymectomy
•Plasmapheresis
•Immunoglobulin.
CONCLUSION :-

 Autoimmune disease is a over active immune reaction in


which the body attacks it’s own tissue and cells as if they are
foreign invaders.
 Women makeup 78% of all cases.
 Medical science is striving to design therapies that prevent
autoimmune disease.
REFERENCE :-

 Kuby , Janis etat[2003],Immunology ,5th edition ,W.H Freeman


and company, Chapter – 20:Autoimmunity
Page number : 465- 467.
 https://www.slideshare.net/MMASSY/auto-immune-diseases

 https://www.mayaclinic.org/diseases-condition/multiple-scleros
is/diagnosis-treatment-diseases
 https://www.mayoclinic.org/diseases-condition/rheumatoid-arth
ritis/diagnosis-treatment/drc-20353653
 https://www.mayoclinic.org/diseases-conditions/lupus/diagnosi
s-treatment/drc-20365790
 https://www.hopkinsmedicine.org/health/conditions-and-diseas
es/myasthenia-gravis
PREVIOUS YEAR QUESTIONS :-

1. Multiple Sclerosis - 3 and 5 Marks


2. Explain the pathogenesis , symptoms , diagnosis and
management of Rheumotoid arthritis and SLE - 15 Marks
3. Autoimmunity - 3 Marks
Thank You ……

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