Shrinkage in the size of cells by the loss of cell substance and metabolic process.
Increased permeability of the plasma membrane and nucleus, causing pallor, increased turgor, and an increase in organ weight and size.
Ischemia.
Estrogen-stimulated smooth muscle hypertrophy and smooth muscle hyperplasia.
Pyroptosis is a form of cell death involving the activation of the inflammasome, which induces caspases to produce cytokines that cause inflammation and apoptosis.
Caseous necrosis.
Fibrinoid necrosis is typically seen in immune reactions where antigen-antibody complexes are deposited in blood vessel walls and in severe hypertension.
Prognosis is the progress a specific disease will take to happen.
Permeates changes leading to neoplasia.
Reversible cell injury allows cells to return to their stable state, while irreversible injury results in cell death.
Cells first try to adapt in a limited number of ways to return to normal if the damaging stimulus is removed.
Loss of defined plasma membrane edge, eosinophilia, and loss of defined nuclear edge.
Endometrial hyperplasia during pregnancy due to hormonal causes.
Bcl-2 and Bcl-xL maintain mitochondrial membrane integrity by holding proapoptotic members Bax and Bak, preventing apoptosis.
Pathogenesis is the specific mechanism a disease needs to happen.
Mucus.
Toxins, such as those from cigarette smoke or bacteria, can be incorporated into the body and impact cellular responses, potentially leading to hypoxia.
Obesity, which might result in diseases such as type 2 diabetes mellitus and atherosclerosis.
A chain of reactions through caspases enzymes leads to cell death and formation of apoptotic bodies.
A process where the cell digests its own components through lysosomal digestion due to lack of external nutrients, leading to shrinkage and atrophy.
Neoplasia and potentially cancer.
Bacterial and viral infections can modify normal cell physiology, leading to cell injury.
Trauma can have wide-ranging effects on cells, such as burns.
The cell enters into a cellular death program, which is irreversible, such as necrosis.
Physiologic and pathologic hyperplasia.
Through the increase in replicatory machines of abnormal cells, often caused by radiation or other insults.
Myeline figures are shapes formed by the collection of membrane segments rich in phospholipids, occurring due to the disruption of plasma and organelle membranes.
Necrosis triggers an inflammation response due to the release of cellular contents into the extracellular fluid, while apoptosis does not.
They act as signals for macrophages to engulf apoptotic bodies.
Ischemia and hypoxia due to reduced blood flow.
An increase in oxidative stress, leading to damage of lipids, proteins, and nucleic acids.
It can kill the etiological agent but might further damage the cell itself, combining apoptosis and necrosis processes.
Small, clear vacuoles within the cytoplasm, known as vacuolar degeneration.
Sustained cellular damage that worsens over time, reaching a non-returning point.
1. Pyknotic nucleus (DNA condenses into a dark small mass), 2. Karyorrhexic nucleus (pyknotic nucleus undergoing fragmentation), 3. Karyolytic nucleus (DNA fragmentation fading away).
The tendency of a tissue to take a place it is not supposed to take, which can have serious consequences.
Hypoxia (oxygen deficiency) and ischemia (reduced blood supply).
Immune responses can elicit inflammatory reactions, which often cause damage to cells and tissues.
The cell becomes permanently injured but can still recover most of its normal function, making this state reversible.
An increase in the size of cells containing increased amounts of structural proteins and organelles in the cytoplasm.
Excessive hormonal or growth factor stimulation.
The replacement of sensitive cells by more resilient cells to increase protection.
Preservation of tissue structures for several days after cell death, often seen in infarcts caused by ischemia in solid organs like the kidney.
Esophagus reflux, where stomach acids are released into the esophagus.
Hyper immune response is an allergic reaction to an antigen, while hypo immune response is a lack of immune reaction to invading antigens.
Genetic abnormalities can result in the lack of certain enzymes or changes in cell physiology, leading to stress and disease.
Increased workload.
Increased functional demand (e.g., workout) or growth factor/hormonal stimulation.
'Caseous' means 'cheeselike,' referring to the friable yellow-white appearance of the area of necrosis.
The replacement of pseudo-stratified ciliary epithelium of the respiratory airways.
Sensors are activated that change mitochondrial permeability, allowing cytochrome c and other proteins to escape into the cytosol, leading to caspase-9 activation and apoptosis.
They can undergo adaptation, reaching a new steady state to preserve functions as long as the noxious stimuli is removed.
Aging diminishes the ability of cells to respond to stress and eventually leads to cell death and organism death.
A form of cell death that is a midway between necrosis and apoptosis, often associated with ischemic injuries and inflammatory reactions.
This condition is known as gangrene.
Decreased workload, loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging.
Apoptosis is the programmed death of a cell, where cells activate enzymes that degrade their own nuclear DNA and proteins.
Fatty change is the appearance of triglyceride-containing lipid vacuoles in the cytoplasm, principally encountered in organs involved in lipid metabolism, such as the liver.
Increased eosinophilia, discontinuities in plasma and organelle membranes, marked dilation of mitochondria, disruption of lysosomes, and intra-cytoplasmic myelin figures.
Squamous epithelium.
If the damage is not deep and does not enter the cellular death process, the cell can enter two reversible patterns.
The breakdown of cytoskeleton proteins.
Cardiac muscle hypertrophy due to hypertension.
Decrease in ATP level.
Fat necrosis occurs due to the release of activated pancreatic enzymes, resulting in the release of fatty acids that combine with calcium to produce white pearl areas.
The intrinsic apoptosis pathway, also known as the mitochondrial pathway, involves the release of cytochrome c from mitochondria, triggering caspase activation and apoptotic death.
Karyorrhexis is the fragmentation of the nucleus during apoptosis due to the activation of endonuclease enzymes.
Glandular epithelium.
They cause cell injury.
Death receptor pathway.
An increase in the number of cells in an organ, enlarging it.
It signals for the apoptosis process.
The two main causes of necrosis are hypoxia and ischemia.
Physiological causes include aging and normal development, while pathological causes include severe DNA damage and accumulation of misfolded proteins.
Diagnosis is the identification of a specific pathological process into a disease.
Rapid accumulation of inflammatory cells and pus, commonly occurring in the brain due to hypoxic cell death or bacterial infections.
