Increase in the size of an organ due to an increase in the size of cells

Also often see increased protein synthesis, increased size or number of intracellular organelles

Increase in the size of an organ or tissue caused by an increase in the number of cells

ex: glandular proliferation in breasts during pregnancy

Failure of cell production

In fetus = agenesis

In adults = permanent loss of precursor cells in proliferative tissues (ex: bone marrow)

Decrease in cell production that is less extreme than aplasia.

ex: Turner syndrome and Klinefelter syndrome

Decrease in size of an organ or tissue resulting from a decrease in the mass of preexisting cells.

Caused by disuse, nutritional/oxyten deprivation, deminished endocrine stimulation, aging, denervation.

Feature autophagic granules.

Replacement of one benign differentiated tissue by another

Squamous, osseous, myeloid

Es: replacement of columnar epithelium by squamous at the squamocolumnar junction of cervix.

Can occur in resp. epithelium of bronchus, in endometrium, and in pancreatic ducts.

Associated with chronic irritations.

Often reversible.

Formation of new bone at sites of tissue injury.

Cartilaginous metaplasia may also occur.

Proliferation of hematopoietic tissue at sites other than bone marrow.

ex: liver or spleen

Obsrtution of arterial blood flow.

Most common cause of anoxia/hypoxia.

cellular swwelling due to decreased ATP availability.

Characterized by presence of large vacuoles in cytoplasm

Whorl-like structures originating from damaged membranes.

Seen in reversible membrane damage in late stage hypoxia.

Cell surface deformity caused by disorderly function of cellular cytoskeleton.

Seen in reversible membrane damage in late stage hypoxia

Caused by irreversible damage to cell membranes.

Massive calcium influx.

Extensive calcification of mitochondria.

Aspartate aminotransferase (AST)

Lactate dehydrogenase (LDH)

Creatine kinase (CK or CPK)

3-5 min for neurons

1-2 hours for myocardial cells and hepatocytes

Many hours for skeletal muscles

Have single unpaired electron in outer orbital.

ex: superoxide and hydroxyl

Intracellular enzymes (glutathione peroxidase, catalase, superoxide dismutase).

Exogenous and endogenous antioxidants (vit A, C, E, cystein, glutathione, selenium, ceruoplasmin,transferrin).

Spontaneous decay

Tissue death that is the sum of degradative and inflammatory reactions occuring after tissue death caused by injury.

Occurs within living organisms

Degradative reaction in cells caused by intracellular enzymes indigenous to the cell.

Can occur after death

Cellular degradation by enzymes derived from sources extrinsic to the cell.

ex: bacteria, leukocytes

Results from a sudden cutoff of blood supply to an organ - particularly heart and kidney.

General architecture is well preserved, nuclear changes, increased cytoplasmic binding of acidophilic dyes.

Enzymatic liquification of necrotic tissue (often CNS) caused by loss of blood supply.

Also occurs in areas of bacterial infection.

Necrotic tissue is soft and liquified

Shares features of both coagulation and liquefactive necrosis.

Most commonly seen in TB granulomas.

Architecture not preserved but tissue not liquefied.

Gross appearance is soft and cheese-like. Histological appearance is amorphous with increased affinity for acidophilic dyes.

Most often results from interruption of blood supply to a lower extremity or the bowel.

Changes depend on tissue involved and whether it is wet or dry.

Characterized by deposition of fibrin-like proteinaceous material in walls of afteries.

Often observed as pasrt of immune-mediated vasculitis.

Smudgy pink appearance in vascular walls.

Actual necrosis may or may not be present.

Liberation of pancreatic enzymes with autodigestion of pancreatic parenchyma.

Trauma to fat cells.

Necrotic fat cells, acute inflammation, hemorrhage, calcium soap formation, clustering of lipid-laden macrophages in pancreas

Programmed cell death.

Regulated by BCL-2 gene.

Does not elicit inflammatory response.

Fatty change/fatty metamorphosis.

Accumulation of intracellular parenchymal triglycerides.

Often in liver, heart, kidney.

Caused by: increased transport of triglycerides to affected cells; decreased mobilization of fat from cells; decreased use of fat by cells; overproduction of fat in cells.

characteristic homogenous, glassy, eosinophilic appearance.

Caused by nonspecific accumulations of proteinaceous material.

Pulmonary accumulation of carbon, silica, and iron dust.

Plubism - lead poisoning.

Argyria - silver poisoning.

Iron-containing pigment consisting of aggregates of ferritin.

Golden brown amorphous aggregates recognised by Prussian blue staining.

Normally in small amounts as physiologic iron stres in tissue macrophages of bone marrow, liver, and spleen.

Caused by mutation of Hfe gene on chromosome 6.

Damage to liver, pancreas, myocardium, and multiple endocrine glands and melatin deposition in skin.

Causes bronze diabetes = micronodular cirrhosis, diabetes mellitus, skin pigmentation.

Serum shows increased iron and decreased total iron-binding capacity.

Yellowish fat soluble pigment that is an end product of membrane lipid peroxidation.

Commonly accumulates in elderly patients = "wear and tear" pigment

Most often found in hepatocytes and at poles of nuclei of myocardial cells.

Calcification caused by hypercalcemia.

Hypercalcemia caused by: hyperparathyroidism, osteolytic tumors, hyperviatminosis D, exessive Ca intake

Calcification in previously damaged tissue (ex: areas of old trauma, TB lesions, scarred heart valves, atherosclerotic lesions).

Not caused by hypercalcemia.

Serum Ca concentrations normal.