Cell Adaptations and Hypertrophy

Reversible changes in a cell's size, number, or functions, in response to environmental changes.

Increase in cell size, leading to organ growth. No new cells are generated; existing cells simply enlarge.

Increase in cell number, leading to organ growth. New cells are generated.

Hypertrophy due to increased functional demand.

Hypertrophy due to hormonal or growth factor stimulation.

An example of physiological hypertrophy where the uterus grows due to estrogen stimulation and protein synthesis.

Occurs when adaptive limits are exceeded or cells experience damaging insults, nutrient deprivation, or mutations.

Hyperplasia that occurs as a normal response to physiological stimuli, such as hormonal changes.

Hyperplasia that occurs when cells regenerate to compensate for damaged or lost cells. This allows an organ to maintain its function.

Hyperplasia that occurs in response to hormone stimulation. This is a normal process during puberty, pregnancy, and lactation.

Hyperplasia that occurs in the bone marrow. This is a response to increased need for blood cells.

Hyperplasia that occurs as a result of abnormal or excessive hormonal or growth factor stimulation. This can lead to disease.

Hyperplasia of the endometrium, the lining of the uterus. Often caused by an excess of estrogen.

A reversible cellular injury characterized by accumulation of water within cells, causing swelling and distension of the endoplasmic reticulum.

The affected organ appears pale, with increased turgor (stiffness), and increased weight.

Small clear vacuoles (distended ER) appear within the cytoplasm. The cytoplasm stains red (eosinophilic) with hematoxylin and eosin.

Loss of plasma membrane structures like cilia and microvilli. Cytoplasmic blebs form at the apical cell surface. Mitochondria, ER, and Golgi complex swell or dilate. Myelin figures form due to damaged cell membranes.

An abnormal accumulation of triglycerides within parenchymal cells, often a sign of cell injury, particularly in the liver.

Alcohol abuse, diabetes mellitus, obesity, toxins, protein malnutrition, and anoxia (lack of oxygen).

Fatty change of the liver, where the liver becomes enlarged, yellow, greasy, and soft.

The organ appears yellow, greasy, and soft.

Intracellular clear fat vacuoles push the nucleus against the cell membrane.

A form of cell death that occurs from severe injury, leading to cellular breakdown and inflammation. This is almost always pathological.

A type of necrosis where cells are digested by hydrolytic enzymes, turning the tissue into a viscous liquid.

A common example of liquefactive necrosis where bacterial or fungal infections trigger leukocyte accumulation and enzyme release, forming pus.

A form of necrosis where the tissue has lost its blood supply, often involving multiple tissue planes and causing putrefaction.

A unique type of necrosis found in tuberculosis, combining features of both coagulative and liquefactive necrosis.

Death of fat cells caused by lytic enzymes, occurring in fat-rich areas of the body.

A form of cell death where the tissue architecture is preserved for days, often caused by ischemia. Dead cells appear eosinophilic with indistinct nuclei. The necrotic area is called an infarct.

A form of necrosis that is characterized by the deposition of fibrin-like material in the walls of blood vessels, seen in conditions like hypertension and vasculitis.

A programmed cell death that eliminates unwanted or damaged cells in a controlled manner. The cell shrinks and fragments without causing inflammation. This process is important for development, tissue homeostasis, and eliminating abnormal cells.

Necrosis is an accidental cell death caused by injury or disease, leading to cell swelling and lysis, while apoptosis is a controlled cell death that eliminates unwanted cells without causing inflammation. Necrosis is often linked to inflammation, while apoptosis is not.

Leakage of intracellular proteins into circulation is a hallmark of necrosis. Early detection of tissue-specific biomarkers, like troponin in heart damage or transaminases in liver injury, can help diagnose tissue necrosis.

A crucial feature in irreversible necrosis is the inability to reverse mitochondrial dysfunction. The lack of oxidative phosphorylation and ATP generation signifies cell death.

A decrease in the size of an organ or tissue due to a reduction in cell size and number.

Atrophy caused by decreased workload, like a muscle that isn't exercised.

Atrophy caused by damage to the nerves supplying a muscle.

One mature cell type is replaced by another mature cell type in response to stress.

Atrophy caused by prolonged compression of tissue.

A specific type of metaplasia where stratified squamous epithelium replaces another type, often as a response to chronic irritation or vitamin A deficiency.

This reversible cell injury, marked by swelling, is primarily caused by oxygen deficiency or toxins that damage mitochondria, leading to ATP depletion.

An accumulation of triglycerides within cells, particularly in the liver, often due to toxic injury disrupting lipid metabolism.

Early stages of injury where cells can recover if the damaging stimulus is removed, characterized by functional and structural alterations.