Autoimmune Disorders

Autoimmune Disorders

Doctor Frances Angelique A. Tequillo

Cebu Doctors' University

Meanings:

* band of > 70 serious, persistent illnesses

2. underlying issue is the samefor all

2. immune system is definitely misdirected

2. body assaulting its own do it yourself

* 4th largest reason behind disability (Europe & the US)

*

Demo of:

2. immunoglobulins

* autoantibodies

2. cytotoxic To

* cells

* home antigens

* auto-antigens

1 ) persistent service of immunologic effector mechanisms

2 . that change the function and ethics of skin cells and internal organs 3. sites of appendage / tissue damage depend on the place of the resistant reaction

Good examples:

ClinicalDiagnosis| Autoantigen

Addison's Disease| p-450

Crohn's Disease| p-ANCA, pancreatic acinar cells

Ovarian Failure as well as Infertility| p-450

Pernicious Anemia| Parietal skin cells

Ulcerative Colitis| p-ANCA

Effective chronic hepatitis

Addison's disease

Autoimmune atrophic gastritis

AIHA

Dermatomyositis

Discoid lupus erythematosus

Goodpasture's syndrome

Hashimoto's thyroiditis

ITP

IDDM

MS

Myasthenia gravis

Pemphigus vulgaris

Pestilent anemia

Principal biliary cirrhosis

Primary myxedema

RA

Scleroderma

SLE

Thyrotoxicosis

Classification

Organ-specific

* both lesions & autoAb's confined to 1 organ

Midspectrum

2. localized lesions in an body organ

Organ non-specific

* autoAb's organ non-specific both lesions & autoAb's NOT limited to 1 body organ

Organ-specific disorders

• Thyroid gland

• Hashimoto's thyroiditis

• Primary myxedema

• Thyrotoxicosis

• Abdomen

• Pernicious anemia

• Adrenal

• Addison's disease

• Pancreatic

• Child diabetes

Organ-nonspecific disorders

• Muscle

• Dermatomyositis

• Kidney

• SLE

• Skin

• Scleroderma

• Joints

• Rheumatoid arthritis

Particular vs . nonspecific (Similarities)

1 . Circulating autoantibodies react with normal body constituents. installment payments on your Increased Ig concentration in serum typically found.

a few. Antibodies might appear in each one of the main Ig class.

5. Disease might not exactly always be intensifying; exacerbations & remissions happen. 5. Autoantibody tests of diagnostic benefit.

Organ-specific| Organ Nonspecific

• Antibodies & lesions are organ-specific. • Clinical & serologic overlap. • Antigens limited to lymphoid system in low concentrations. • Antigens evoke organ-specific antibodies in normal animals with complete Freund's adjunct. • Family tendency to formulate organ-specific autoimmunity. • Lymphoid invasion, parenchymal destruction by simply questionable cell-mediated hypersensitivity orautoantibodies. • Tendency to develop malignancy in the appendage. | • Antibodies & lesions will be organ non-specific. • Overlap of SLE, RA & other CTDs. • Antigens accessible in higher concentrations. • Simply no antibodies produced in animals with compatible activation. • Family tendency to develop CTDs. • Questionable malocclusions in Ig synthesis in relatives. • Lesions brought on by deposition of immune things. • Propensity to develop lymphoreticularneoplasia.

Other Things to Consider:

* abnormal interaction of T & W lymphocytes with autoantigens 2. no single theory or device known

2. potential for autoimmunity is constantly present

* lymphocytes that are potentially reactive with " self” antigens exist in the body Risk Factors:

5. Genetic elements

* Affected person age

* Exogenous factors

Genetic Factors

* Familial aggregates

2. Person may have > 1 A/I disorder

5. women > men

5. HLA & A/Idisorders

Individual age

5. Peaks by 60-70

5. Steady maximize with age group

Exogenous factors

* may alter antigens perceived as nonself

* AS WELL AS

* light

* medications

* malware

* long-term infections

5. breakdown of the immune anatomy's ability to discriminate " self” from" non-self”

Proposed mechanism:

1 . Ag-Ab complex

2 . activation of complement

several. release of inflammatory mediators

4. Elevated...

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