Tissue Accumulations and Deposits PDF

Tissue accumulations and deposits By Dr:Asmaa Gaber Abdou Professor of Pathology Faculty of Medicine Menoufia University  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification  Amyloidosis...

Tissue accumulations and deposits By Dr:Asmaa Gaber Abdou Professor of Pathology Faculty of Medicine Menoufia University  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification  Amyloidosis Isthe extracellular deposition of abnormal protein  Nature of amyloid material P component Fibril protein Amyloid light Amyloid associated AL protein AA  Localized Systemic Primary Secondary Amyloid light Amyloid associated Haemodialysis associated Hereditary (transthyretin( (Beta 2 microglobulin) neuropathy Familial Mediterranean fever Localized amyloidosis Pathogenesis of systemic Amyloidosis Primary secondary Multiple meyloma  Secondary Amyloidosis Rheumatoid arthritis Chronic suppurative conditions Empyema Lung abscess bronchiectasis Infective granulomas tuberculosis Malignant tumors Hodgkin lymphoma Gastric carcinoma Renal cell carcinoma  Primary (idiopathic) amyloidosis Secondary amyloidosis Causes and -Idiopathic Chronic inflammatory or malignant predisposing factors -Multiple myeloma (malignant tumor destructive disease of plasma cells affecting bone marrow)  Rheumatoid arthritis. (figure 1)  Chronic suppurative conditions -Monoclonal gammopathy (bronchiectasis, empyema, lung abscess).  Infective granulomas (tuberculosis).  Malignant tumors (Hodgkin lymphoma, gastric and renal cell carcinoma). Pathogenesis Malignant plasma cells secretes light Inflammatory conditions activate chain of immunoglobulin leading to macrophages which secrete inteleukins accumulation of amyloid light protein that stimulat liver to synthesize serum which is accumulated in tissues amyloid associated protein which then converted to amyloid associated protein Type of amyloid AL (amyloid light) AA (amyloid associated)  Amyloid Stains Gross staining Lugol’s iodine stain Iodine and sulphuric acid stain **Microscopic staining Haematoxylin and eosin stain Congo red stain Metachromatic stain Gross affection of any organ Enlarged Firm Rubbery liver Liver amyloidosis renal amyloidosis  Glomeruli proteinuria Collecting tubules Diabetes insipidus Afferent arteriols Arteriolosclerosis, ischemia, reduced kidney Focal type Diffuse type  Heart failure Stenosis or regurge of valves Addison arrythemia disease Intestinal obstruction malabsorption Diagnosis of Amyloidosis Biopsy Complications renal failure Heart failure Intestinal obstruction Addison disease Case Amyloid goiter  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification  hyalinosis Microscopic change in tissue manifested by homogenous structrureless and pinkish coloration Types of Hyalinosis Connective tissue hyalinosis Cellular hyalinosis Mallory body in alcoholic cirrhosis Russel bodies in inflammation rich in plasma cells  Benign prostatic hyperplasia Zinker degeneration  Amyloidosis Hyalinosis Gross and microscopic Microscopic change only change Extracellular deposition Cellular and Extracellular deposition Has definite It has no definite structure biochemical structure Has special stains No special stains  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigment Gout Pathological calcification  Mucin Mucoid change if deposited inside the cell as in catarrhal inflammation Myxomomatous if mucin deposited outside the cell as in umbilical cord and leiomyoma  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification Disturbance in pigment metabolism endogenous pigment Melanin pigment deficiency of melanin *albinism *leucoderma  Pigment Exogenous Endogenous Anthracosis Melanin Lead lipofuscin Parasitic Haemoglobin derived pigmentation haemosiderosis tattoing Iron pigment haemochromatosis Increase in melanin pigment exposure to sun chloasma Naevi melanoma Addison disease Lipochrome (lipofuscin) pigment Brown atrophy of heart  Haemoglobin derived pigments Bilirubin Haemosidrin hematin Localized Haemosiderosis Generalized haemosiderosis RBCs destruction Excess iron in diet Blood transfusion and iron therapy Haemochromatosis Inborn errors of iron metabolism Liver Pancreas Skin heart  Exogenous pigmentation Inhalation as anthracosis Inoculation as tattoing Ingestion as lead Parasitic pigmentation  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification  Gout Disturbance in purine metabolism leading to sodium urate crystals deposition in tissue Causes of gout Primary or hereditary (disturbabce of purine metabolism) Secondary mostly due to leukaemia Sites of deposition Joints Non articular cartilage as nose and ear Kidney leading to renal failure  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification  Pathological calcification Pathological deposition of calcium salts in sites other than bone and teeth. Types: *Dystrophic calcification Why dead tissue is liable for calcification  Metastatic calcification deposition of calcium salts in living tissue due to either increase in calcium absorption or mobilization -hypervitaminosis D -hyperparathyroidism -metastatic bone lesions **calcinosis **stone formation  Amyloidosis Hyalinosis Mucoid and myxomatous change Deposited pigments Gout Pathological calcification Thank you