Flashcards for:
Understanding Cell Injury and Death

Fibrinoid necrosis is characterized by the deposition of fibrin-like material in the walls of blood vessels and is commonly seen in vasculitis, such as polyarteritis nodosa.

Caseous necrosis has a 'cheesy' appearance and is typically seen in tuberculosis (TB) infections. It is characterized by fragmented or lysed cells and a granular appearance.

In skeletal muscle, hypertrophy occurs as a physiological adaptation to exercise, leading to increased muscle strength. In the heart, hypertrophy often results from pathological stress such as outflow obstruction, which can lead to adverse effects like heart failure.

Intracellular accumulations of hemosiderin indicate excess iron, often seen in conditions like hemochromatosis, and are visualized using Prussian blue or Pearl’s stain. Copper accumulation is seen in Wilson’s Disease and is typically stained with rhodanine or rubeanic acid.

Caspases play a crucial role in apoptosis by mediating cell death through a cascade of activations. They break down key cellular components, ensuring an orderly and non-inflammatory cell death process.

The two main types of cell death are necrosis and apoptosis. Necrosis is always pathological, often resulting in inflammation and marked by different forms such as coagulative, liquefactive, and caseous necrosis. Apoptosis is programmed cell death that can be physiological or pathological, characterized by no inflammation, caspase-dependency, and it occurs via extrinsic (death receptor) and intrinsic (mitochondrial) pathways.

Calcium influx in irreversible cell injury activates destructive enzymes like proteases, phospholipases, and endonucleases, leading to severe cellular and organelle damage, including the formation of amorphous densities in mitochondria, ultimately resulting in cell death.

Metaplasia is the reversible change in cell type in response to chronic irritation or stress. A common example is Barrett’s esophagus, where normal squamous epithelium is replaced by columnar epithelium due to chronic acid reflux.

Key enzymes in necroptosis include RIPK1, RIPK3, and MLKL. Necroptosis is typically seen in conditions like pancreatitis, steatohepatitis, and various neurodegenerative diseases.

Coagulative necrosis is a type of cell death where the architecture of dead tissue is preserved for days. It is most commonly found in the heart, kidneys, and spleen.

Hypertrophy refers to an increase in cell size, often seen in muscle cells during exercise and the heart in response to increased workload. Hyperplasia involves an increase in cell number, observable in tissues like the endometrium and prostate gland during benign prostatic hyperplasia.

The intrinsic pathway of apoptosis involves mitochondrial outer membrane permeabilization, releasing cytochrome C and activating caspases. The extrinsic pathway is mediated by death receptors on the cell surface, such as Fas ligand binding to CD95, leading to caspase activation.

During reversible cell injury from hypoxia, intracellular changes include mitochondrial dysfunction, decreased ATP production, sodium-potassium pump failure leading to cellular swelling, loss of microvilli, cytoplasmic blebs, myelin figures, clumping of chromatin, and ribosomal detachment.

Hypoxia, commonly caused by ischemia, leads to decreased oxygen supply, resulting in mitochondrial dysfunction, decreased ATP production, sodium-potassium pump failure, and cellular swelling. Persistent hypoxia can progress from reversible to irreversible injury, causing severe membrane and mitochondrial damage and leading to cell death.

Reversible cell injury is characterized by minor damage where the cell can return to normal upon removal of the stressor, including changes like cellular swelling and mitochondrial dysfunction. Irreversible cell injury involves severe damage leading to cell death, marked by severe membrane damage, mitochondrial damage, calcium influx, and nuclear changes such as pyknosis, karyorrhexis, and karyolysis.