Systemic lupus Erytromatosis and Graves’ Disease K R.pptx

1. 1.SYSTEMICLUPUS ERYTROMATOSIS
2.GRAVES’ DISEASE
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2. INTRODUCTION
Systemic lupus Erytromatosis:-
 Its a chronic Multisystem Inflammatory Autoimmune Diseases
 Associated with abnormalities of immune system
 Causes :- interactions among Genetic, Hormonal, Environmental and immunologic factor.
Effects:-
 Skin
 Joints
 Serous member
 Renal system
 Hematological system
 Neurological system
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3. EPIDEMIOLOGY
 SlE affects 2 to 8 persons per 100,000 in United States
 Most cases occurs in women of child bearing years
 African, Asian, Hispanic, and Native Americans 3 times more likely to develop than
white
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4. ETIOLOGY ANDPATHOPHYSIOLOGY
 Etiology is unknown
Most probable causes are
• Genetic influence
• Hormones
• Environmental factors
• Certain medications
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5. CLINICALMANIFESTATION
 Ranging from a relatively mild disorders to rapidly progressing,
affecting many body system.
 Most commonly affects the skin, muscles lining of lungs, heart,
nervous tissue, and kidneys.
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6. DERMATOLOGIC
Dermatologic
 Cutaneous vascularlesions
 Butterfly rash
 Oral/ nasopharyngeal ulcer
 Alopecia
Malar rash
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7. MUSCULOSKELETAL
 Polyarthralgia with morning stiffness
 Arthritis
 Swan neck
 Ulnar deviation
 Subluxation with hyperlaxity of joint
 Swan neck deformity
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8. HEMATOLOGICAL
 Formation of antibodies against blood clles
 Anemia ( lack of red blood cells or dysfunctional red blood cells)
 Thrombocytopenia ( low blood platelets count)
 Leukopenia ( low white blood cell count)
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9. RENAL
 Lupus nephritis ( inflammation of the kidney)
* Ranging from mild proteinuria to glomerulonephritis.
* Primary goal in treatment is slowing the progression.
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10. DIAGNOSTIC STUDIES
 No specific test .
 SLE is diagnosed primarily on criteria related to patient history, physical examination
and laboratory findings.
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11. LABORATORY TEST
 Complete blood count
 Erythrocyte sedimentation Rate
 Kidney and liver assessment
 Urinalysis
 Antinuclear antibodies
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12. IMAGINGTESTS
 Chest x – ray
 Echocardiogram
 Biopsy
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13. TREATMENT
 There is no cure for SLE. The goal of treatment is to control symptoms. Severe symptoms
that involve the
Heart, lungs, kidneys, and other organs often need treatment by specialists.
 Mild forms of the disease may be treated with:
 Nonsteroidal anti-inflammatory drugs (NSAIDs) for joint symptoms and pleurisy. Talk to
your provider before taking these medicines.
 Low doses of corticosteroids, such as prednisone, for skin and arthritis symptoms.
 Corticosteroid creams for skin rashes.
 Hydroxychloroquine, a medicine also used to treat malaria.
 Methotrexate may be used to reduce the dose of corticosteroids
 Belimumab, a biologic medicine, may be helpful in some people.
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14. TREATMENT
 Treatments for more severe SLE may include:
 High-dose corticosteroids.
 Immunosuppressive medicines (these medicines suppress the immune system). These
medicines are used if you have severe lupus that is affecting the nervous system, kidney
or other organs. They may also be used if you do not get better with corticosteroids, or
if your symptoms get worse when you stop taking corticosteroids .
 Medicines most commonly used include mycophenolate, azathioprine and
cyclophosphamide. Because of its toxicity, cyclophosphamide is limited to a short course
of 3 to 6 months. Rituximab (Rituxan) is used in some cases as well.
 Blood thinners, such as warfarin (Coumadin), for clotting disorders such as
antiphospholipid syndrome.
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15. GRAVES DISEASE
THYRIOD GLAND
 The thyriod gland is a butterfly shaped endocrine gland that is normally located
in the lower front of the neck
 The thyroids job is to make thyroid hormones which are secreted into the blood
and then carried to every tissue in the body
 Thyriod hormone helps the body use energy, stay warm and keep the brain,
heart, and muscles, and organ working as they should.
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16. GRAVES DISEASE
 It’s an auto immune disease in which the patients own immune system attacks the thyriod gland
causing it to produce too much thyroxine.
 Thyroxine ( T4) is a hormone produced by the thyroid gland that has four iodine molecules
attached to it’s molecular structure.
 T4 as well as other thyroid hormone help regulate growth and control metabolism in the body.
 Although graves disease may develop at any age in both men and women, it’s more commonly
effects women aged 20 yes or more
 Currently, there are no medications or treatment to stop the patients immune system from
attacking their thyriod gland
 How ever, treatment can exist which can ease the symptoms and bring down the production of
thyroxine
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17. GRAVES DISEASE
 The syndrome typically includes two major categories of phenomena: -
 Those specific to graves disease and caused by the autoimmunity includes the
exopthalmos thyriod enlargement and thyriod stimulation and dermal changes.
 The second set of problem is caused by the excess thyriod hormone This
thyrotoxicocis or hyperthyroidism Doesn’t differ from that induced by any other
causes excess of thyriod hormone
 Its an autoimmune conditions that effects thyriod function Causing enlargement and
overacting of the thyriod.
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18. EPIDEMIOLOGY
 100- 200 cases per 100,000 every year , internationally
 Significantly higher incidence in women, 7.1ratio.,
 Most common amongst young women, But can occur at any age of 20-40
 No definitive genetic linkage.
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19. SIGNS ANDSYMPTOMS
 Most distinct sign ( bulging eye)
exophthalamos.
 Enlargment of the thyriod ( goitre)
 Increased appitite coupled with weight
loss
 Heat intolerance and diaphoresis
 Hyperactivity and fatigability.
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20. IMAGESOF EXOPHTHALOMOS AND HYPERTHYROIDISM
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21. GRAVES DISEASE
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22. PATHOPHYSIOLOGY
 Autoantibodies( TSI, TBII TG1) target and binds to TSH Rceptors
 Autoantibodies acts like ( TSH), thyrotropin causes excessive release of T3 and T4 into the blood
 This spike in thyriod hormone release, causes TSH level to decrease ( negative feedback)
pathophysiology.
 Exophthalmos is caused by antibodies attackIng eye muscle Fibroblast, Forcing a changes into adipose
tissue
 The resulting adipose tissue builds up, exerting a pressure behind the eyes “ Pressure builds up
constrict draining veins resulting oedema
 The increase in the appetite and weight loss, the heat intolerance and daiphooedema are caused by
the thyriod hormone increasing the basal metabolic rate
 Hyperactivity and Fatigability Occurs as thyroxine over stimulates motor end plate of the
neuromuscular junction.
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23. DIAGNOSIS
 Blood test is carried out, to checking for
increase free thyroxine and
Triiodothyronine
levels in the blood.
 Exophthalamos and non pitting pretibial
Myxoedema are unique features of Graves
Diesase when coupled with hyperthyroidism
Confirmatory.
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24. PROGNOSIS WITH TREATMENT
 The prognosis is normally very positive, without any major
complications barring any that may arise from thyroidectomy
 Without treatment there are long term health problems, excessively
dry eyes, blindness, continued muscle degradation etc.
Treatment
 Antithyroid drugs ( methimazole), Radioiodine, Thyriodectomy.
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25. REFERENCES
 Immunology by Gupta
 www.slideshare.com
 https://www.ncbi.nlm.nih.gov.book
 www.wikipedia.com
 www.microbiology.note.com
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