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Pulselessness (Cyanosis Petechial hemorrhages Congestion ) Hanging Strangulation | Autopsy findings in hanging | Suffocation | Traumatic Asphyxia | Drowning | Hydrocution | Immersion syndrome | Postmortem findings in drowning | Tests in drowning death #mbbs #forensicmedicine #medicos

Decomposition of human body , mummification, embalming of human corpse, Thanatopraxia , Forensic entomology #mbbs #forensicmedicine #medicos

Forensic medicine : Early postmortem changes : Eye changes , skin changes , Rigor mortis , Algor mortis , Livor mortis .

Autopsy procedures for forensic medicine students who are perusing there MBBS and right now want to revise forensic medicine. #Forensicmedicine #autopsy #mbbs #medicos

Self self editorial: Pratiyogita darpan Motivational talk Editorial UPSC motivational editorial UPSC

Rheumatoid Arthritis , Gout , Osteoarthritis, Psudogout . Robbins Pathology Book Podcast. Bone Pathology

Many diseases are caused or influenced by environmental factors. Broadly defined, the term ambient environment encompasses the various outdoor, indoor, and occupa- tional settings in which humans live and work. In each of these settings, the air people breathe, the food and water they consume, and the toxic agents they are exposed to are major determinants of health. Other environmental factors pertain to the individual (“personal environment”) and include tobacco use, alcohol ingestion, therapeutic and “recreational” drug consumption, diet, and the like. It is generally believed that factors in the personal environment have a larger effect on human health than that of the ambient environment, but new threats related to global warming (described later) may change this equation. The term environmental disease refers to disorders caused by exposure to chemical or physical agents in the ambient, workplace, and personal environments, includ- ing diseases of nutritional origin. Environmental diseases are surprisingly common. The International Labor Organi- zation has estimated that work-related injuries and ill- nesses kill more people per year globally than do road accidents and wars combined. Most of these work-related problems are caused by illnesses rather than accidents. The burden of disease in the general population created by nonoccupational exposures to toxic agents is much more difficult to estimate, mostly because of the diversity of agents and the difficulties in measuring the dose and dura- tion of exposures. Whatever the precise numbers, environ- mental diseases are major causes of disability and suffering and constitute a heavy financial burden, particularly in developing countries. Environmental diseases are sometimes the consequence of major disasters, such as the methyl mercury contamina- tion of Minamata Bay in Japan in the 1960s, the leakage of methyl isocyanate gas in Bhopal, India, in 1984, the Cher- nobyl nuclear accident in 1986, the Fukushima nuclear meltdown following the tsunami in 2011, and lead poison- ing resulting from contaminated drinking water in the city of Flint in the United States in 2016. Fortunately, these are unusual and infrequent occurrences. Less dramatic, but much more common, are diseases and injury produced by chronic exposure to relatively low levels of contaminants. It should be noted that a host of factors, including complex interactions between pollutants producing multiplicative effects, as well as the age, genetic predisposition, and dif- ferent tissue sensitivities of exposed persons, create wide variations in individual sensitivity. Disease related to mal- nutrition is even more pervasive. In 2010, it was estimated that 925 million people were malnourished—one in every seven persons worldwide. Children are disproportionately affected by undernutrition, which accounts for more than 50% of childhood mortality worldwide. In this chapter, we first consider the emerging problem of the health effects of climate change. We then discuss the mechanisms of toxicity of chemical and physical agents, and address specific environmental disorders, including those of nutritional origin.

Pathology : Robbins & Cotran : Adaptations of cellular growth & differentiation Hypertrophy| Hyperplasia| Atrophy | Metaplasia Hypertrophy Hypertrophy is an increase in the size of cells resulting in an increase in the size of the organ. In contrast, hyper- plasia (discussed next) is an increase in cell number. Stated another way, in pure hypertrophy there are no new cells, just bigger cells containing increased amounts of structural proteins and organelles. Hyperplasia is an adaptive response in cells capable of replication, whereas hypertro- phy occurs when cells have a limited capacity to divide. Hypertrophy and hyperplasia also can occur together, and obviously both result in an enlarged organ. Hypertrophy can be physiologic or pathologic and is caused either by increased functional demand or by growth factor or hormonal stimulation. Hyperplasia Hyperplasia is an increase in the number of cells in an organ that stems from increased proliferation, either of differentiated cells or, in some instances, less differenti- ated progenitor cells. As discussed earlier, hyperplasia takes place if the tissue contains cell populations capable of replication; it may occur concurrently with hypertrophy and often in response to the same stimuli. Hyperplasia can be physiologic or pathologic; in both situations, cellular proliferation is stimulated by growth factors that are produced by a variety of cell types.Metaplasia Metaplasia is a change in which one adult cell type (epi- thelial or mesenchymal) is replaced by another adult cell type. In this type of cellular adaptation, a cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment. Metaplasia is thought to arise by the reprogramming of stem cells.Atrophy Atrophy is shrinkage in the size of cells by the loss of cell substance. When a sufficient number of cells are involved, the entire tissue or organ is reduced in size, or atrophic Although atrophic cells may have diminished function, they are not dead. Causes of atrophy include a decreased workload (e.g., immobilization of a limb to permit healing of a fracture), loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and aging (senile atrophy). Although some of these stimuli are physiologic (e.g., the loss of hormone stimulation in menopause) and others are pathologic (e.g., denervation), the fundamental cellular changes are similar. They represent a retreat by the cell to a smaller size at which survival is still possible; a new equilibrium is achieved between cell size and dimin- ished blood supply, nutrition, or trophic stimulation. Cellular atrophy results from a combination of decreased protein synthesis and increased protein degradation. • Protein synthesis decreases because of reduced meta- bolic activity. • The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate ubiquitin ligases, which attach multiple copies of the small peptide ubiquitin to cellular proteins and target them for degradation in protea- somes. This pathway is also thought to be responsible for the accelerated proteolysis seen in a variety of cata- bolic conditions, including the cachexia associated with cancer. • In many situations, atrophy also is associated with autophagy, with resulting increases in the number of autophagic vacuoles. As discussed previously, autoph- agy is the process in which the starved cell eats its own organelles in an attempt to survive.

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थमती सांसे: हिन्दी साहित्य कहानी [email protected]