Cell Injury and Death Concepts

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Questions and Answers

What is cell injury?

Cell injury is a variety of stresses that a cell encounters as a result of changes in its internal and external environment.

What are the two main types of irreversible cell injury?

Necrosis and apoptosis (correct)

Apoptosis and fatty change

Fatty change and necrosis

Inflammation and necrosis

What is fatty change?

Fatty change is the accumulation of neutral fat within parenchymal cells.

Fatty change is always irreversible.

False Signup and view all the answers

Which of the following is NOT a cause of fatty liver?

Muscle strain Signup and view all the answers

What are the characteristics of a fatty liver?

A fatty liver is typically enlarged, smooth, rounded, pale yellow, and greasy to the touch. Signup and view all the answers

What is the hallmark of coagulative necrosis?

Conversion of normal cells into 'tombstones' Signup and view all the answers

What is liquefactive necrosis?

Liquefactive necrosis is a type of necrosis that occurs due to the degradation of tissue by powerful hydrolytic enzymes. Signup and view all the answers

In which of the following organs is liquefactive necrosis most commonly found?

Brain Signup and view all the answers

What is caseous necrosis?

Caseous necrosis is a type of necrosis that combines features of both coagulative and liquefactive necrosis. Signup and view all the answers

Caseous necrosis is often associated with inflammation.

True Signup and view all the answers

What is apoptosis?

Apoptosis is a form of programmed cell death that is characterized by the orderly dismantling of the cell. Signup and view all the answers

Which of the following is NOT a characteristic of apoptosis?

Inflammation Signup and view all the answers

What is the fate of necrotic tissue?

Necrotic tissue can either be removed by phagocytosis or replaced by fibrosis. Signup and view all the answers

Study Notes

Cell Injury and Cell Death

Cell injury is a result of various stresses caused by changes in the internal and external environments.
The cell's response to injury depends on the nature, duration, severity, type, extent, and adaptability to the injury.
Cells may adapt to the changes and revert back to normal if the stress is relieved (cellular adaptations).
Residual effects of the injury may persist within the cell.
Some injured cells recover (reversible injury), while others die (irreversible injury).

Cellular Responses to Injury

Cells can revert to normal after the stress is removed.
Residual effects may remain within the cell.
The injured cell may recover or die.

Types of Cell Injury

Reversible cell injury - Cellular changes are temporary and will recover if the injurious agent is removed. Examples include fatty change.
Irreversible cell injury - Cellular changes are permanent. The cell reaches a point of no return and may progress to cell death. Examples include necrosis and apoptosis.

Fatty Change (Steatosis)

Accumulation of neutral fat within parenchymal cells.
Common in the liver, but can occur in the heart, skeletal muscle, and kidneys.
Imbalance between fat uptake, utilization, and secretion can cause fatty liver.

Etiology of Fatty Liver

Excessive alcohol consumption (most common).
Liver diseases such as hepatitis C.
Starvation.
Malnutrition.
Obesity.
Diabetes mellitus.
Chronic illnesses (like tuberculosis).
Hypoxia (e.g., anemia).
Hepatotoxins (chemicals like carbon tetrachloride, chloroform, ether, aflatoxins).
Certain drugs (e.g., estrogen, steroids, tetracycline).

Gross Picture of Fatty Liver

Enlarged liver size.
Smooth liver surface
Rounded liver borders.
Bulging cut section.
Pale yellow color.
Greasy texture.

Microscopic Picture of Fatty Liver

Numerous lipid vacuoles in the hepatocytes(liver cells).
Vacuoles begin small (microvesicular) and become larger(macrovesicular).
Nuclei pushed to the periphery (signet ring appearance).
Cell rupture and coalescence of vacuoles to form fatty cysts.

Effects of Fatty Liver

Mild fat accumulation is reversible.
Marked accumulation is irreversible, progressing to necrosis and cirrhosis.

Necrosis

Focal death of cells within a living body due to released hydrolytic enzymes.
Accompanied by an inflammatory reaction.
Causes include hypoxia, chemical agents, physical agents, microbial agents, and immunological injury.

Necrosis Pathogenesis

Denaturation of proteins. Characteristic nuclear changes in the necrotic cell.
Cell digestion by lytic enzymes. (autolysis - the breakdown of cells by its own enzymes; heterolysis - the breakdown of cells by enzymes of inflammatory cells).
Morphologically: homogeneous, intensely eosinophilic cytoplasm.

Gross Picture of Necrosis

Necrotic tissue appears opaque yellow and may be swollen.
Surrounding tissues appear hyperemic due to inflammation.

Microscopic Picture of Necrosis

Cytoplasm appears homogenous and eosinophilic.
Nuclear changes due to denaturation of proteins (pyknosis, karyorrhexis, karyolysis).

Architectural Changes of Necrosis

i. The tissue rapidly appears structureless due to cell lysis. Autolysis and heterolysis by enzymes.
ii. Protein denaturation (coagulation) may happen before cell lysis. The shape is retained (structural ghosts). The degradation happens later, and the tissue appears structureless..

Fate of Necrotic Tissue

Inflammation surrounds the necrotic area, caused by the release of inflammatory mediators.
Healing: phagocytosis of the debris, regeneration and fibrosis depending on the degree of necrotic cells; possible encapsulation or dystrophic calcification.

Types of Necrosis

Coagulative necrosis.
Liquefactive necrosis.
Caseous necrosis.
Fat necrosis.
Fibrinoid necrosis.

Coagulative Necrosis

Most common type usually resulting from ischemia.
Occurs in infarction of organs (except CNS), and also effects kidneys, heart, and spleen.
Protein denaturation precedes cell lysis. Cell outlines persist for several days.
Nuclear degeneration is gradual.

Gross Picture of Coagulative Necrosis

Early stage shows pale, firm, slightly swollen foci of the tissue.
Later stages show a yellowish, softer, shrunken affected area.

Microscopic Picture of Coagulative Necrosis

Normal cells are converted into “tombstones” (structural ghosts)
Necrotic cells are swollen and more eosinophilic.
Nuclear changes are present.
Affected tissue is structureless.
Surrounding tissue shows acute inflammation.

Liquefactive Necrosis

Due to ischemia and bacterial/fungal infections.
Degradation of tissue by powerful hydrolytic enzymes (cell lysis is more than protein denaturation).
Examples include brain infarcts and abscess cavities (pus).

Gross Picture of Liquefactive Necrosis

Affected area is soft with liquefied debris and later, a cyst wall.

Microscopic Picture of Liquefactive Necrosis

Necrotic cell debris and macrophages filled with phagocytosed material.
Cyst wall formed from proliferating capillaries, inflammatory cells, and cells (e.g. glial cells in brain, fibroblasts in abscess).

Caseous Necrosis

Found in the center of tuberculous infections.
Combines features of coagulative and liquefactive necrosis.
Usually begins as ischemic coagulative necrosis, often from endarteritis obliterans.
Hypersensitivity leads to toxin release, causing partial liquefaction of the necrotic cells.

Gross Picture of Caseous Necrosis

Foci resemble dry cheese, and are soft, granular, and yellowish.

Microscopic Picture of Caseous Necrosis

Necrosed foci appear structureless and eosinophilic, with granular debris.
Surrounding tissue shows granulomatous inflammatory reactions, composed of epithelioid cells and giant cells (e.g., Langhans).

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Description

Explore the fundamental concepts of cell injury and death, including the types of injuries cells experience and their responses. This quiz covers reversible and irreversible cell injury, as well as the cellular adaptations that may occur. Test your understanding of how cells react to stress and the implications of these changes.