Apoptosis[ edit ] Apoptosis is the programmed cell death of superfluous or potentially harmful cells in the body. It is an energy dependent process mediated by proteolytic enzymes called caspases, which trigger cell death through the cleaving of specific proteins in the cytoplasm and nucleus. The cell surface is altered so as to display properties which lead to rapid phagocytosis by macrophages or neighbouring cells. Inhibition of apoptosis can result in a number of cancers, autoimmune diseases, inflammatory diseases, and viral infections.
The first light-microscopic proof that a cell is dead is Cell injury and fragmentation of the nucleus. Most necrosis results from loss of blood supply to part of the body.
Hypoxia is the inability to carry out oxidative phosphorylation. Coagulation necrosis retains the outlines of the cells.
Liquefaction necrosis is usual following total loss of blood to the brain, or when neutrophils digest tissue as in most bacterial infections. Caseous necrosis is crumbling of tissue, and is most familiar in tuberculosis.
Enzymatic fat necrosis results from the action of pancreatic lipase on belly fat. Apoptosis is enactment of a program for single-cell death, often on the instructions of a developmental program or T-killer cell, or in the setting of otherwise-sublethal cell injury, i.
Hypertrophy means cells growing bigger. Hyperplasia means cells growing more numerous. Cell injury means shrinkage of an organ. Anaplasia is bizarre cells. It means the genome has been destabilized.
Dysplasia "intraepithelial lesion", if really ugly "carcinoma in situ" is anaplasia confined to an epithelium, i. These definitions and understandings will become critical when we discuss neoplasia -- formation of new, worthless organs.
Pathology's contribution to your grade-point average and licensure exam score is important. Although the foremost quality that residency programs consider is your reliability, your demonstration of pathology knowledge on exams is still important. Further, you'll be bombarded with questions about pathology on rotations, and you'll be judged by your answers.
For a preview of what to expect, see BMJ You'll also need to know how to use the lab. We can teach you this, and we'll try to do it mostly by giving you practice.
Whether "lab use" can even be taught in the classroom in a manner that will stick is contentious: All three are our duties as teachers Pediatrics To succeed in this course, you must try to understand when applicable instead of just memorizing.
The worst advice someone can give you is: This is not impossible.
Most of us probably know more rock-and-roll lyrics than there are words in "Big Robbins". We learned the lyrics easily because we knew the tunes.
The key concepts in pathology will be the tunes that enable us to learn the "little details" that we need for patient care. You can learn because, and only because, you are able to say as you go along, "This makes sense. Your licensure exam is intended to test you ability to think, as well as your knowledge base.
Master the key concepts early. After you hear a lecture or read a paragraph in a book, try to rephrase it whisper, write in your own words. Review the material in the evening following the lecture, while it is still fresh; this will save you time.
Throw away your highlighters. Mark up the margins with your own words. Develop your own personal symbols. Talk with your friends, and explain what you're learning to each other.
|Also in this section||Injury may progress through a reversible stage and culminate in cellular death.|
|Fastest Basicmedical Insight Engine||Free radicals and cell membrane damage Free radicals are highly reactive atoms or molecules which have an unpaired electron in an outer orbit.|
|cell injury - regardbouddhiste.com - Human pathology||From Kumar V et al:|
|Cell injury | Clinical Gate||Apoptosis[ edit ] Apoptosis is the programmed cell death of superfluous or potentially harmful cells in the body. It is an energy dependent process mediated by proteolytic enzymes called caspases, which trigger cell death through the cleaving of specific proteins in the cytoplasm and nucleus.|
|CELL INJURY AND DEATH||The first light-microscopic proof that a cell is dead is shriveling and fragmentation of the nucleus.|
And look at pictures early. This seems to take more time. But it will save you time, even in the short run, because it is much more efficient. It's like running your motor with your car in gear, rather than in neutral.
A common "final pathway" in a variety of forms of cell injury, including injury brought about by inflammatory cells, is generation of free radicals, i.e., molecular species with a single unpaired electron available in an outer orbital.
Cell response to injury is not an all-or-nothing phenomenon: The stronger and the longer the stimulus, the larger the damage Response to a given stimulus depends on the type, status, and genetic make-up of the injured cell: Contrast ischemia in skeletal muscle (tolerates 2 .
REVERSIBLE CELL INJURY has two morphologic hallmarks -- cell swelling and fatty change. CELL SWELLING ("cloudy swelling"; the extreme forms are called "vacuolar degeneration" or "hydropic change") is the visible change resulting from water being pulled by .
1 2 CHAPTER 1 Cell Injury, Cell Death, and Adaptations responses are hypertrophy, hyperplasia, atrophy, and metaplasia. If the adaptive capability is exceeded or if the external stress is inherently harmful, cell injury develops (Fig.
1–1). Within certain limits injury is reversible, and cells return to a stable baseline; however, severe or per-.