NEETMEDICALGK

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.

अनंतपुर की सवारी:हिंदी साहित्य कहानी: अशरफ़ [email protected]

थमती सांसे: हिन्दी साहित्य कहानी [email protected]