2027 L1 Cell Injury & Types of Necrosis

Hypoxia

A deficiency of oxygen in the body that causes cell injury by reducing aerobic oxidative respiration.

Cell Injury

Damage to cells that can occur due to a variety of factors such as physical trauma, chemical exposure, hypoxia, or infections.

Responses to Cell Injury

• Atrophy

• Hypertrophy

• Hyperplasia

• Metaplasia

• Dysplasia

• Necrosis

• Inflammation

Hyperplasia

An increase in the number of cells in a tissue or organ.

Metaplasia

Change in cell type in response to stress, where one differentiated cell type is replaced by another.

Dysplasia

An abnormality in the size, shape, and organization of cells, often indicating a precursor to cancer.

Necrosis

The death of cells or tissue that occurs when they are irreversibly damaged.

Apoptosis

Programmed cell death that occurs in a regulated and controlled manner.

Inflammation

The body’s immediate response to tissue injury or harmful stimuli that can be acute or chronic.

• can be acute or chronic

• key players: neutrophils first to arrive, macrophages perform phagocytosis and initiate repair, lymphocytes mediate adaptive immune response

• mediators: cytokines facilitate cell-cell communication, chemokines guide cell movements, ROS neutralises pathogens and cause tissue damage

Fibrosis

The formation of excess fibrous connective tissue in an organ as a reparative response to injury. e.g. cirrhosis, fibrotic limb diseases - excess can compromise organ function

Cytokines

Chemical mediators that facilitate cell-to-cell communication during immune responses.

Granuloma

A focus of inflammation characterized by a collection of macrophages and other cells, often in response to infection.

Normal Cell Structure

• Confined to narrow function structure, kept in check by

  • metabolism

  • differentiation

  • specialisation

  • neighbours

• Handles demands through homeostasis

Haemodynamic Load

if increased, heart muscle adapts and atrophies but can become damaged if

• blood supply to myocardium compromised/inadequate > irreversible muscle injury

• injury not fixed > cells suffer irreversible injury and die

Cell Injury Process

• Adaptations = reversible responses to stress

• Too much stress = cell can’t adapt = becomes injured

• Leads to apoptosis/necrosis

• If cells lack nutrients, they resort to autophagy

Saponification

The process where fatty acids combine with calcium to form chalky white areas in tissues, often seen in fat necrosis.

Ischemia

Insufficient blood supply to tissues, leading to a lack of oxygen and nutrients.

Autophagy

A cellular process where cells digest their own components to survive under stress or nutrient deprivation.

Reactive Oxygen Species (ROS)

Chemically reactive molecules containing oxygen, which can damage cell structures and contribute to disease.

Physical Agents

Trauma, extreme temperatures, and pressure changes that can lead to cell injury.

Chemical Agents

Common chemicals, like glucose and salts, as well as toxic substances like arsenic and carbon monoxide, can cause cell injury.

Infectious Agents

Pathogens including viruses and large parasites that disrupt cell integrity.

Immune Reactions

Autoimmune responses that can inadvertently damage tissues while functioning to protect the body.

Genetic Abnormalities

Chromosomal issues that lead to disorders, such as sickle cell anemia.

Nutritional Imbalances

Health problems that arise from deficiencies or excesses of nutrients.

Acute Inflammation

A short-term response to injury aimed at removing harmful stimuli and beginning the healing process.

Chronic Inflammation

A prolonged inflammation response that can lead to tissue damage and various diseases.

Neutrophils

White blood cells that are the first responders to the site of injury, playing a crucial role in the acute inflammatory response.

Macrophages

Cells essential for phagocytosis of dead cells and debris, as well as initiating the healing process during inflammation.

Lymphocytes

White blood cells involved in mediating adaptive immune responses, particularly during chronic inflammation.

Cytokines

Chemical mediators produced during inflammation that aid in signaling and directing the movement of immune cells.

Chemokines

A subset of cytokines that specifically attract immune cells to sites of injury or infection.

Hypertrophy

Growth of cells in response to increased demand, leading to larger tissue mass.

Atrophy

Shrinkage of cells due to reduced workload or stimuli, resulting in decreased tissue mass.

Metaplasia

Change in cell type in response to stress, where one differentiated cell type is replaced by another.

Reversible Injury

Cellular damage that can be repaired if the stressor is removed promptly.

Irreversible Injury

Severe cellular damage leading to necrosis or apoptosis when the injury is too extreme or prolonged.

Necrosis

Uncontrolled cell death caused by injury, characterized by proteins denaturing and enzyme digestion, leading to loss of membrane integrity and leakage of cellular contents.

Myelin figures

Structures that can be eaten by other cells or transformed into fatty acids; may harden or calcify.

Coagulative Necrosis

Tissue structure remains unchanged for a few days; occurs in all organs except the brain; injury prevents breakdown of cells and necrotic proximal convoluted tubules lack nuclei but retain brush borders.

Liquefactive Necrosis

Commonly occurs in brain ischemia; digestion of dead cells results in a liquid-like mass; associated with bacterial and fungal infections leading to creamy yellow pus.

Caseous Necrosis

Found in TB infections; has a crumbly, cheese-like appearance; necrotic area comprises fragmented cells within an inflammatory border, forming a granuloma.

Fat Necrosis

Occurs mainly in breast tissues; results from enzyme release from the pancreas during acute pancreatitis, leading to fat destruction and the formation of chalky-white spots (fat saponification).

Fibrinoid Necrosis

Found in immune reactions affecting blood vessels; occurs when immune components aggregate in artery walls and combine with fibrin.

Cell Injury under Light Microscope

Cellular swelling and fatty change

Cellular Swelling

Early reversible injury resulting from disturbance of ionic homeostasis and failure of cellular energy production (pumps) in membrane, leading to an increase in cell volume.

• in major cells, pallour, rigidity and weight inc. can be seen microscopically; clear vacuoles in cytoplasm, enlarged pinches off ER