Basement Membrane Abnormalities

Health & Medicine Technology

Renal pathology tutorial for nephrologists

Glomerular Basement Membrane abnormalities

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Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of renal function,[4][5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months)[5] with glomerular crescent formation seen in at least 50%[5] or 75%[4] of glomeruli seen on kidney biopsies. If left untreated, it rapidly progresses into acute renal failure[6] and death within months. In 50% of cases, RPGN is associated with an underlying disease such as Goodpasture syndrome, systemic lupus erythematosus or granulomatosis with polyangiitis; the remaining cases are idiopathic. Regardless of the underlying cause, RPGN involves severe injury to the kidneys' glomeruli, with many of the glomeruli containing characteristic glomerular crescents (crescent-shaped scars)

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AML:ACUTE MYELOID LEUKAEMIA for medical colleges teaching faculty and students as well. it includes AML causes , histopathological slides of subclasses of Acute myeloid leukemia, classification , diagnosis, management modalities, complications .Acute leukemias are stem cell disorders characterized by malignant neoplastic proliferation and accumulation of immature and non functional hematopoietic cells in the bone marrow. The neoplastic cells show increased proliferation and/or decreased apoptosis. If the defect primarily affects the common myeloid progenitor (CMP) then it is called Acute myeloid leukemia. Acute myeloid leukemia (AML) is a neoplastic disease characterized by infiltration of the blood, bone marrow, and other tissues by proliferative, clonal undifferentiated cells of the hematopoietic system. AML is the result of a sequence of somatic mutations in a multipotential primitive hematopoietic cell or, in some cases, a more differentiated progenitor cell. It can be slow growing or rapidly fatal. AML is the predominant form of leukemia during the neonatal period Incidence : 1.5/100,000/year in infants decreases to approximately 0.4 per 100,000 children ages 5 to 9 years, increases gradually to 1.0 persons per 100,000 until age 25 years, and thereafter increases exponentially until the rate reaches approximately 25/100,000 persons. AML accounts for 15 to 20 percent of the acute leukemias in children and 80 percent of the acute leukemias in adults. Men > Women (4.5 : 3) HEREDITY 1) Chromosomal aneuploidy like Trisomy 21 noted in Down syndrome 2) Defective DNA repair, e.g., Fanconi anemia, Bloom syndrome, and Ataxia telangiectasia 3) Congenital neutropenia ie Kostmann syndrome 4) Germline mutations of CCAAT/enhancer-binding protein α (CEBPA), runt-related transcription factor 1 (RUNX1), and tumor protein p53 (TP53) have also been associated with a higher predisposition to AML RADIATION Peaks after 5 to 7 yrs of exposure. Therapeutic radiation alone seems to add little risk of AML but can increase the risk in people also exposed to alkylating agents. CHEMICAL AND OTHER EXPOSURES Exposure to benzene, plastic, rubber, petroleum products, paint, ethylene oxide, herbicides and pesticides can increase the risk. Smoking can also increase the risk DRUGS Anticancer drugs are the leading cause of therapy-associated AML. Alkylating agent–associated leukemias occur on average 4–6 years after exposure, and affected individuals have aberrations in chromosomes 5 and 7. Topoisomerase II inhibitor–associated leukemias occur 1–3 years after exposure, and affected individuals often have aberrations involving chromosome 11q23. Other agents like Chloramphenicol, phenylbutazone, and, less commonly, chloroquine and methoxypsoralen. SYMPTOMS : Present with nonspecific symptoms initially. Fatigue is the first symptom Fever with or without infection will be present in approximately 10% patients Bleeding, easy bruising occasional

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