3-Types and description of necrosis

There are six distinctive morphological patterns of necrosis:

1. Coagulative necrosis is characterized by the formation of a gelatinous (gel-like)

substance in dead tissues in which the architecture of the tissue is maintained. Coagulation
occurs as a result of protein denaturation, causing albumin to transform into a firm and opaque
state. This pattern of necrosis is typically seen in hypoxic (low-oxygen) environments, such
as infarction. Coagulative necrosis occurs primarily in tissues such as the kidney, heart and
adrenal glands. Severe ischemia most commonly causes necrosis of this form.

This type of necrosis occurs when the structure and enzymic protein undergo primary
denaturation leading to increase in the intracellular acidosis of the cell.

2. Liquefactive necrosis (or colliquative necrosis), in contrast to coagulative

necrosis, is characterized by the digestion of dead cells to form a viscous liquid mass. This is
typical of bacterial, or sometimes fungal, infections because of their ability to stimulate an
inflammatory response. The necrotic liquid mass is frequently creamy yellow due to the
presence of dead leukocytes and is commonly known as pus. Hypoxic infarcts in the brain
presents as this type of necrosis, because the brain contains little connective tissue but high
amounts of digestive enzymes and lipids, and cells therefore can be readily digested by their
own enzymes.This type of necrosis is caused by highly powerful catalytic enzymes which
undergo autolysis or heterolysis.
3. Gangrenous necrosis can be considered a type of coagulative necrosis that resembles
mummified tissue. It is characteristic of ischemia of lower limb and the gastrointestinal tracts.
If superimposed infection of dead tissues occurs, then liquefactive necrosis ensues. Here the
tissues are affected by the necrosis condition and the condition gets elevated due to bacterial
super addition.
4. Caseous necrosis can be considered a combination of coagulative and liquefactive
necrosis, typically caused by mycobacteria (e.g. tuberculosis), fungi and some foreign
substances. The necrotic tissue appears as white and friable, like clumped cheese. Dead cells
disintegrate but are not completely digested, leaving granular particles. It most prominently
occurs in the tubercle which is considered a granuloma. In this type of condition, the cell
architecture is completely destroyed and lysis of macrophages occurs leading to caseating
granulomas.
 5. Fat necrosis is specialized necrosis of fat tissue, resulting from the action of
activated lipases on fatty tissues such as the pancreas. In the pancreas it leads to
acute pancreatitis, a condition where the pancreatic enzymes leak out into the peritoneal cavity,
and liquefy the membrane by splitting the triglyceride esters into fatty acids through
fat saponification. Calcium, magnesium or sodium may bind to these lesions to produce a
chalky-white substance.
6. Fibrinoid necrosis is a special form of necrosis usually caused by immune-mediated
vascular damage. It is marked by complexes of antigen and antibodies, sometimes referred to
as “immune complexes” deposited within arterial walls together with fibrin. In this type
of necrosis fibrocytes are affected by collagen necrosis and the fibers start degenerating leading
to fragmentation of collagen fibers

C.Calcification: process, types and description

Calcification is the accumulation of calcium salts in a body tissue. Calcifications may be
classified on whether there is mineral balance or not, and the location of the calcification.
Calcifications can form in many places throughout your body: small and large arteries, heart
valves, brain, where it is known as cranial calcification, joints and tendons, such as knee joints,
soft tissues like breasts and muscles, kidney, bladder, and gallbladder. Some calcium buildup
is harmless. These deposits are believed to be the body’s response to inflammation, injury, or
certain biological processes. However, some calcifications can disrupt organ function and affect
blood vessels.

1-Types and description

Calcification implies the abnormal deposition of calcium salts, together with smaller amounts
of iron, magnesium, and other minerals. When the deposition occurs in dead or dying tissues,
it is called dystrophic calcification; it occurs in the absence of calcium metabolic derangements
(i.e., with normal serum levels of calcium). In contrast, the deposition of calcium salts in normal
tissues is known as metastatic calcification and almost always reflects some irregularities in
calcium metabolism (hypercalcemia).
ii-Dystrophic Calcification. Dystrophic calcification is encountered in areas of necrosis of any
type. It is virtually inevitable in the atheromas of advanced atherosclerosis, associated with
injury in the aorta and large arteries and characterized by accumulation of lipids. Although
dystrophic calcification may be an incidental finding indicating insignificant past cell injury, it
may also be a cause of organ dysfunction. For example, calcification can develop in aging or
damaged heart valves, resulting in severely compromised valve motion. The pathogenesis of
dystrophic calcification involves initiation (or nucleation) and propagation, both of which may
be either intracellular or extracellular; the ultimate end product is the formation of crystalline
calcium phosphate. Initiation in extracellular sites occurs in membrane-bound vesicles; in
normal cartilage and bone they are known as matrix vesicles, and in pathologic calcification
they derive from degenerating cells. It is thought that calcium is initially concentrated in these
vesicles by its affinity for membrane phospholipids, while phosphates accumulate as a result of
the action of membrane-bound phosphatases. Initiation of intracellular calcification occurs in
the mitochondria of dead or dying cells that have lost their ability to regulate intracellular
calcium. After initiation in either location, propagation of crystal formation occurs. This is
dependent on the concentration of Ca2+ and PO4 − in the extracellular spaces, the presence of
mineral inhibitors, and the degree of collagenization, which enhances the rate of crystal growth.

ii-Metastatic Calcification. Metastatic calcification can occur in normal tissues whenever there
is hypercalcemia. The four major causes of hypercalcemia are (1) increased secretion of
parathyroid hormone, due to either primary parathyroid tumors or production of parathyroid
hormone-related protein by other malignant tumors; (2) destruction of bone due to the effects
of accelerated turnover, immobilization, or tumors; (3) vitamin D–related disorders including
vitamin D intoxication and sarcoidosis; and (4) renal failure, in which phosphate retention leads
to secondary hyperparathyroidism