deck_4825178 Flashcards
(44 cards)
What is Microscopic polyangiitis?
Similar condition granulomatosis with polyangiitis, but the trigger that initiates this condition is not known.
What symptoms are associated with Microscopic polyangiitis?
fever, anorexia, weight loss, fatigue, and renal failure (rapidly progressing glomerulonephritis is possible)
Clinical findings with Microscopic polyangiitis?
p-ANCA with specificity for myeloperoxidase or MPO-ANCA (a granule component of neutrophils)
Diagnosis of Microscopic polyangiitis?
renal function tests; measurement of MPO-ANCA titers
Treatment of Microscopic polyangiitis?
plasma exchange, anti-inflammatory drugs
What is Bullous pemphigoid?
an acute or chronic autoimmune skin disease, involving the formation of blisters, more appropriately known as bullae, at the space between the skin layers epidermis and dermis
Cause of Bullous pemphigoid?
autoimmune condition mediated by IgG specific for 2 proteins Dystonin (also called bullous pemphigoid Antigen 1) and/or type XVII collagen (also called bullous pemphigoid Antigen 2)
Symptoms of Bullous pemphigoid?
bullae (deep blisters) erupt, most commonly at the inner thighs and upper arms, but the trunk and extremities are frequently both involved. Any part of the skin surface can be involved. Oral lesions are present in a minority of cases
Diagnosis of Bullous pemphigoid?
based on two biopsies of the skin, one submitted for routine H&E staining and one for immunofluorescence studies
Treatment of Bullous pemphigoid?
topical steroids and other anti-inflammatory drugs
What is Hashimoto’s thyroidosis?
autoimmune condition that typically results in hypothyroidism (although some patients experience periods of hyperthyroidism. Can be mediated by CD4 and-or CD8 T cells or antibodies, and ADCC appears to play an important role in some patients (Ab-mediated, of course).
What are the symptoms of Hashimoto’s?
weight gain, depression, mania, sensitivity to heat and cold, paresthesia, chronic fatigue, panic, bradycardia, tachycardia, congestive heart failure, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, joint stiffness, menorrhagia, myxedematous psychosis, cramps, memory loss, vision problems, infertility and hair loss
What is the cause of Hashimoto’s?
T cell infiltrates result in destruction of thyroid cells (mediated by CD8 and/or CD4 T cells); antibodies specific for thyroid peroxidase (TPO) and/or thyroglobulin can cause gradual destruction of follicles in the thyroid gland
Diagnosis of Hashimoto’s?
detecting elevated levels of auto antibodies specific for thyroid microsomes (antimicrosomal Ab), thyroglobulin (antithyroglobulin Ab), and thyroid peroxidase (anti-TPO Ab) in the serum; Testing for thyroid-stimulating hormone (TSH), Free T3, Free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti- microsomal antibodies can help obtain an accurate diagnosis
Treatment of Hashimoto’s?
thyroid hormone replacement therapy
What is Polymyositis?
an autoimmune disease mediated by CD4 and CD8 T cells (type 4 hypersensitivity)
What are the symptoms of Polymyositis?
pain, marked weakness and/or loss of muscle mass in the proximal musculature, particularly in the shoulder andpelvic girdle. The hip extensors are often severely affected, leading to particular difficulty in ascending stairs and rising from a seated position. Thickening of the skin on the fingers and hands (sclerodactyly) is a frequent feature, although this is non- specific and occurs in other autoimmune connective tissue disorders
Cause of Polymyositis?
It is hypothesized that an initial injury causes release of muscle auto antigen, which is subsequently taken up by macrophages and presented to CD4+ T helper cells. Activated TH cells synthesize IFN-γ that stimulate further macrophages and further inflammatory mediator release like IL-1 and TNF-α. Another important event in the pathogenesis of polymyositis is the increased expression of MHC proteins by m/s cells. Auto-Ag is presented in association with MHC-I molecules on the surface of myocytes and is recognized by CD8 cytotoxic T cells that subsequently initiate cell destruction
Diagnosis of Polymyositis?
is fourfold, including elevation of creatine kinase, history and physical examination, electromyograph (EMG) alteration, and a positive muscle biopsy
Lab findings of Polymyositis?
antibodies: anti Jo-1 antibodies (in >65% of patients); anti-SRP (signal recognition particle) antibodies; anti-Mi- 2 antibodies (Mi-2 antigen is a component of the nuclesome remodeling-deacetylase complex involved in transcriptional regulation.o elevated serum creatine kinase is characteristic, but not specific to polymyositis.o treatment: line treatment for polymyositis is corticosteroids; other anti-inflammatory agents used in non-responsivepatients• Dermatomyositis: similar to polymyositis except that both muscles and skin are involved
What is Celiac disease?
(also called Coeliac disease or celiac sprue): autoimmune condition of the small intestine that is caused by hypersensitivity to gluten; autoimmune response causes damage to intestinal villi, diminishing intestinal absorption
Symptoms of Celiac disease?
pain and discomfort in the digestive tract, chronic constipation and diarrhea, failure to thrive (in children), anemia and fatigue
Genetic pre-disposition to Celiac disease?
Almost all people with coeliac disease have either the variant HLA-DQ2 allele or (less commonly) the HLA-DQ8 allele
Causes of Celiac disease?
It is unclear whether this disease is mediated by auto-antibodies alone, CD4 or CD8 T cells alone, or some combination of those three immune responses. It is likely a combination of all three.
