1. Lecture on pathological anatomy for the 3-rd year students T.Filonenko
Cells Death
Lecture on pathological anatomy for the 3-rd year students
T.Filonenko

2. Cells Death
It is the premature death and destruction of cell in the living organism under action of factors of critical damage
Classification of Cells Death, based on the mechanism of development:
necrosis
pathogenic inducted apoptosis
immunological elimination of cells.

4. karyopicnosis
karyorrhexis
karyolysis

5. According to the cause of necrosis there are the following types of necrosis:
traumatic necrosis;
toxic necrosis;
trophoneurotic necrosis;
allergic necrosis;
vascular or ischemic necrosis.

6. Main types of necrosis
Two essential changes bring about irreversible cell injury in necrosis - cell digestion by denaturation of proteins and lytic enzymes.
coagulative necrosis develops (during denaturation of proteins ).
Liquefactive necrosis is a progressive catalysis of cell structures (during enzymic digestion). Liquefactive necrosis is typical of organs in which the tissues have a lot of lipid (such as brain) or when there is an abscess with lots of acute inflammatory cells whose release of proteolytic
Both of these processes require hours to develop

7. Zenker degeneration (waxy degeneration): This refers to necrosis of skeletal muscle in infectious diseases with high fevers (such as typhoid fever). The musculature becomes opaque and waxy, tears easily, and loses its cross-striation.

8. The liver shows a small abscess here filled with many neutrophils
The liver shows a small abscess here filled with many neutrophils. This abscess is an example of localized liquefactive necrosis.
The two lung abscesses seen here are examples of liquefactive necrosis in which there is a liquid center in an area of tissue injury. Liquefactive necrosis is typical of organs in which the tissues have a lot of lipid (such as brain) or when there is an abscess with lots of acute inflammatory cells whose release of proteolytic enzymes destroys the surrounding tissues.

9. Clinic-morphological forms of necrosis
1) Gangrene – total necrosis of the organ, reported with the external environment:
dry – at the thrombosis of arteries, an organ acquires the black coloring
moist (wet) – at the thrombosis of arteries and veins + influencing of putrid bacteria.
gas gangrene
bedsore is a type of gangrene, death of the tissue under the influence of pressure (sacral area, buttocks, great trochanter). It is trophoneurotic necrosis of the bed- patients
noma – widespread necrosis of soft tissue of person.
2) Sequester – fragment of dead tissue, which can’t be autolysed, replaced by connective tissue and which is localized among alive tissue
3) Infarction – vascular or ischemic necrosis;
4) Fat necrosis
5) Caseous necrosis
6) Fibrinoid necrosis.

10. Gangrene
This is gangrene. In this case, the toes were involved in a frostbite injury. This is an example of "dry" gangrene in which there is mainly coagulative necrosis from the anoxic injury.
This is gangrene of the lower extremity. In this case the term "wet" gangrene is more applicable because of the liquefactive component from superimposed infection in addition to the coagulative necrosis from loss of blood supply. This patient had diabetes mellitus.

11. noma – Moist gangrene of the soft tissue of the face in measels

12. Sequester in bone – fragment of dead tissue, which can’t be autolysed, replaced by connective tissue and which is localized among alive tissue

13. Fat necrosis
This is fat necrosis of the pancreas. Cellular injury to the pancreatic acini leads to release of powerful enzymes which damage fat by the production of soaps, and these appear grossly as the soft, chalky white areas seen here on the cut surfaces.
Microscopically, fat necrosis is seen here. Though the cellular outlines vaguely remain, the fat cells have lost their peripheral nuclei and their cytoplasm has become a pink amorphous mass of necrotic material.

14. Caseous
necrosis
This is more extensive caseous necrosis, with confluent cheesy tan granulomas in the upper portion of this lung in a patient with tuberculosis. The tissue destruction is so extensive that there are areas of cavitation (cystic spaces) being formed as the necrotic (mainly liquefied) debris drains out via the bronchi.
Microscopically, caseous necrosis is characterized by acellular pink areas of necrosis, as seen here at the upper right, surrounded by a granulomatous inflammatory process.

15. Fibrinoid necrosis
Sometimes the small arteries and arterioles can be damaged so severely in malignant hypertension that they demonstrate necrosis with a pink fibrin-like quality that gives this process its name - fibrinoid necrosis.

16. INFARCTion
Definition: A localized area of ischemic necrosis usually caused by vascular blockage.
Types of infarcts: wedge-shaped or irregular shape.
According to the propagation: total (when the whole organ is affected), subtotal (when only a part of the organ is affected), microinfarct (when observed only microscopically).
According to the color: white, white with hemorrhagic halo and red.
The causes of infarction: prolonged spasm, thrombosis, embolism.

17. Morphology of infarcts, differs with different tissues
The color of infarct depends on the features of the blood supply of the organ.
White: pale, often roughly wedge-shaped, in solid organs with single blood supply (ex: kidneys ,spleen)
Red: hemorrhagic, in organs which are soft and have dual blood supply or collaterals (ex: lungs ,bowels, liver)
White with hemorrhagic halo. If under the background of the supply through the main vessel, microcirculatory system is well developed, infarct is white with hemorrhagic halo (kidney, heart).

18. White (pale, ischemic) infarction
This is an acute renal infarction. Note the wedge shape of this zone of coagulative necrosis resulting from loss of blood supply with resultant tissue ischemia that produces the pale infarct.
Here are splenic infarcts in a patient with infective endocarditis. Portions of the vegetations have embolized to the spleen. These infarcts are typical of ischemic infarcts: they are based on the capsule, pale, and wedge-shaped.

19. Microscopically, the renal cortex has undergone anoxic injury at the left so that the cells appear pale and ghost-like. There is a hemorrhagic zone in the middle where the cells are dying or have not quite died, and then normal renal parenchyma at the far right. This is an example of coagulative necrosis.
The contrast between normal adrenal cortex and the small pale infarct is good. The area just under the capsule is spared because of blood supply from capsular arterial branches. This is an odd place for an infarct, but it illustrates the shape and appearance of an ischemic (pale) infarct well.

20. White infarction with hemorrhagic halo
The interventricular septum of the heart has been sectioned to reveal an extensive acute myocardial infarction. The dead muscle is tan-yellow with a surrounding hyperemic border.

21. Red (hemorrhagic) infarction in lung
Occlusion of a medium-sized branch of pulmonary artery can lead to a pulmonary infarction in a person with compromised cardiac or respiratory status.
A pulmonary infarct is hemorrhagic because of the dual blood supply from the non-occluded bronchial arteries which continue to supply blood, but do not prevent the infarction.

22. hemorrhagic infarction in Bowel
The small intestine is infarcted. The dark red to grey infarcted bowel contrasts with the pale pink normal bowel at the bottom. Some organs such as bowel with anastomosing blood supplies, or liver with a dual blood supply, are hard to infarct. This bowel was caught in a hernia and the mesenteric blood supply was constricted by the small opening to the hernia sac.

23. Infarction in brain
This infarct in the brain is organizing and being resolved, the liquefactive necrosis leads to resolution with cystic spaces.
The microscopic appearance of this acute cerebral infarction reveals marked edema (the pale areas).

24. At high magnification, liquefactive necrosis of the brain demonstrates many macrophages at the right which are cleaning up the necrotic cellular debris.

25. Clinical Significance of infarcts:
usually cause pain;
may cause loss of function (example: myocardial infarct may cause heart failure);
may cause hemorrhage or sepsis (examples: lung infarct causes hemoptysis, bowel infarct causes GI bleeding or peritonitis).

26. The outcomes of necrosis
Regeneration of tissues – replacement of the dead tissue with a new one;
Incapsulation – formation of the connective tissue capsula around necrotic area;
Organization – replacement of the dead tissue with connective tissue;
Petrification – replacement of the dead tissue with calcium salts;
Incrustation – replacement of the dead tissue with any other salts exept calcium;
Ossification – the formation of the bone tissue in the necrotic area;
Hyaline change – the appearance of the hyaline-like substance in the necrotic area;
Sequestration – formation of sequester;
Mutilation – spontaneous tearing away of the dead tissue;
Cystic formation.
Suppuration fusion of necrotic tissues