Cell Injury and Cellular adaptations, Wound healing - Robbins Pathology - Chapter 1
Dr.G Bhanu Prakash Animated Medical Videos・2 minutes read
Cell injury can be reversible or irreversible, leading to adaptations or death, with different types of cell death like necrosis and apoptosis discussed. Understanding cellular adaptations, such as hypertrophy and hyperplasia, is crucial for comprehending how cells respond to stress and stimuli to maintain functionality and health.
Insights
- Cell injury is a crucial starting point in general pathology, focusing on reversible and irreversible damage distinctions.
- Mitochondrial dysfunction and sodium-potassium ATPase failure are key initial changes in reversible cell injury.
- Visible morphological changes in reversible cell injury include hydropic swelling and loss of microvilli.
- Irreversible cell injury involves severe membrane damage, leading to calcium influx and nuclear changes.
- Different types of necrosis, such as coagulative, liquefactive, and caseous, have distinct characteristics and locations in the body.
- Cell death pathways like apoptosis, necroptosis, and pyroptosis involve intricate molecular mechanisms that lead to programmed or pathological cell demise.
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Recent questions
What is reversible cell injury?
Reversible cell injury allows cells to return to normal function if damage is minimal. It initiates with a decrease in ATP levels, leading to sodium-potassium ATPase failure and cellular swelling. Visible morphological changes include hydropic swelling, loss of microvilli, and formation of cytoplasmic blebs. Electron microscopic features like myelin figures show laminated appearances due to membrane damage in swollen organelles. Membranous walls are mainly composed of phospholipids, with phosphore being the primary component, along with calcium.
What is necrosis?
Necrosis is like a murder, where cells are stressed from outside leading to cell death. Coagulative necrosis is the most common type, preserving cell architecture even after death. It is seen in heart, kidneys, spleen, and most solid organs due to infarction. Denaturation of proteins in coagulative necrosis preserves cell architecture. Brain and pancreas show liquefactive necrosis due to high hydrolytic enzymes. Cheesy appearance in lung tissue indicates caseous necrosis, a combo of coagulative and liquefactive necrosis. Fat necrosis in areas with high fat content like breasts and buttocks leads to chalky white appearance due to saponification.
What is apoptosis?
Apoptosis is a programmed cell death that can be both physiological and pathological. Examples include embryogenesis, endometrial shedding, and deletion of self-reactive T cells. Tumor cells undergo death through apoptosis, which is a programmed cell death. Anti-cancer drugs induce cell death in cancerous cells through apoptosis. Physiological examples of apoptosis include embryogenesis and endometrium shedding during menstruation. The extrinsic pathway involves an external signal binding to the death receptor CD95, while the intrinsic pathway involves stress sensors activating pro-apoptotic factors.
What is hypertrophy?
Hypertrophy is a cellular adaptation characterized by an increase in cell size due to elevated protein synthesis and transcription factors like GATA4 and NFAT. Examples include muscle growth from exercise, organ enlargement due to outflow tract obstruction, and breast and uterine tissue growth during puberty and pregnancy.
What is metaplasia?
Metaplasia is the change of one cell type into another due to stress, involving stem cell reprogramming. Vitamin A deficiency can lead to metaplasia, seen in conditions like Barrett's esophagus where squamous epithelium is replaced by columnar epithelium and goblet cells due to acid reflux. Goblet cells are not typically found in the esophagus, but in cases of gastroesophageal reflux disease (GERD), they can appear due to acid regurgitation. The presence of goblet cells in the esophagus leads to the production of mucus, contributing to the symptoms of GERD.