General Pathology: Cell Injury, Cell Death, and Adaptations (PDF)

GENERAL PATHOLOGY PRELIMS | LESSON 2 CELL INJURY, CELL DEATH AND ADAPTATIONS Cell Injury inflammation, and enzymatic digestion of the...

GENERAL PATHOLOGY PRELIMS | LESSON 2 CELL INJURY, CELL DEATH AND ADAPTATIONS Cell Injury inflammation, and enzymatic digestion of the lethally injured cell. Remember the four (4) aspects of disease. Patterns of Tissue Necrosis: Cell injury occurs: Coagulative necrosis ○ Cells cannot adapt ○ The dead tissue retains its ○ Adaptive responses are exceeded shape and firmness for days. ○ Exposure to damaging insults, ○ This occurs because the deprived of critical nutrients or injury damages proteins and compromised mutations enzymes, preventing normal It can be reversible or irreversible. breakdown. Reversible Cell Injury ○ Typically caused by blocked ○ Characterized by functional and blood vessels and is common structural alterations in early stages in most organs except the or mild forms of injury, which are brain. correctable if the damaging stimulus ○ When it affects a localized is removed. area, it’s called an infarct. Irreversible Cell Injury ○ Cell death Irreversible Cell Injury Cell Death Two (2) principle types of cell death: ○ Necrosis Pathologic process that is the (a) Kidney with infarct; yellow. (b) N; normal consequence of severe injury. kidney, I; with infarct ○ Apoptosis Type of cell death that is Liquefactive necrosis induced by a tightly regulated ○ Differs from coagulative suicide program in which necrosis in that it involves the cells destined to die activate breakdown and liquefaction intrinsic enzymes that of dead tissue. degrade the cell’s genomic ○ This type of necrosis is often DNA and nuclear and seen in bacterial or fungal cytoplasmic proteins. infections, where microbes trigger the accumulation of Necrosis white blood cells that release enzymes to digest the tissue. Pathologic process that is the consequence ○ The resulting necrotic of severe injury. material, known as pus, is Characterized by denaturation of cellular typically creamy yellow due proteins, leakage of cellular contents through damaged membranes, local 1 | Robles  to the presence of these appearance of the necrotic white blood cells. tissue. ○ In the central nervous system, ○ Microscopic examination cell death from lack of reveals a structureless mass oxygen often leads to of fragmented cells and liquefactive necrosis. granular debris surrounded by a distinct inflammatory border, forming a granuloma. Brain with infarct Gangrenous necrosis ○ Refers to tissue death, Tuberculosis of the lungs, with yellow-white commonly in a limb “cheesy” appearance (especially the lower leg), due to loss of blood supply. Fat necrosis ○ It usually involves coagulative ○ Destruction of fat tissue, necrosis affecting multiple usually due to activated tissue layers. pancreatic lipases released ○ If bacterial infection occurs, it during acute pancreatitis. can lead to additional These enzymes break down liquefactive necrosis due to fat cell membranes and bacterial and white blood cell triglycerides, creating fatty enzymes, resulting in wet acids that combine with gangrene. calcium to form chalky-white areas known as fat saponification. Caseous necrosis ○ Typically seen in tuberculosis infections and is characterized by a cheese-like, friable 2 | Robles  Fibrinoid necrosis ○ Death of host cells that have served ○ A type of damage to blood their useful purpose. vessels often seen in immune Causes: (Pathologic) reactions. ○ DNA damage ○ It happens when ○ Accumulation of misfolded proteins antigen-antibody complexes, ○ Can be induced during certain along with leaked plasma infection, particularly viral infections. proteins, accumulate in the ○ May also contribute to pathologic vessel walls. atrophy in parenchymal organs after ○ On H&E stains, this results in duct obsruction, such as occurs in a bright pink, amorphous the pancreas, parotid gland, and appearance known as kidney. fibrinoid because it resembles fibrin. CELLULAR ADAPTATION Adaptations are reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in responses to changes in their environment. FORMS: Hypertrophy ○ When a cell increases in size, leading Wall of artery is bright pink because of inflammation to an overall enlargement of the affected organ. This occurs without an increase in the number of cells, APOPTOSIS just the size of each cell due to the Type of cell death that is induced by a tightly buildup of internal components. regulated suicide program in which cells destined to die activate intrinsic enzymes that degrade the cell’s genomic DNA and nuclear and cytoplasmic proteins. Causes: (Physiologic) ○ The removal of supernumerary cells during development. ○ Involution of hormone dependent (a) Normal uterus on right, gravid uterus on left; tissues on hormone withdrawal. (b) spindle-shaped uterine; © large plump ○ Cell turnover in proliferating cell cells from gravid uterus populations, to maintain Hyperplasia homeostasis. ○ An increase in the number of cells in ○ Elimination of potentially harmful a tissue or organ, usually in response self-reactive lymphocytes to prevent to a specific stimulus. immune reactions against one’s own tissues. 3 | Robles  This ○ process leads to the enlargement of the organ or tissue, distinct from hypertrophy, which involves the growth of individual cells. Atrophy ○ The process where an organ or tissue decreases in size due to a reduction in both cell size and number. It can be part of normal development or a result of various pathological conditions. (a) Normal brain; (b) Atrophy of brain Metaplasia ○ A reversible change where one type of mature, differentiated cell is replaced by another type that is better suited to handle a particular stress or adverse condition. (b) Metaplasia of columnar epithelium 4 | Robles