Pathophysiology ch 01 introduction, cell injury, adaptaion, death v2

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Text of Pathophysiology ch 01 introduction, cell injury, adaptaion, death v2

  • 1. : Chapter 1. Introduction to PathophysiologyIntroduction to Cellular ChangesLearning Objectives:After studying this chapter, the student is expected to 1. Explain the role of pathophysiology in the diagnosis and treatment of disease. 2. Use appropriate terminology. 3. Explain the importance of a patients medical history. 4. Describe common cellular adaptations and possible reasons for the occurrence ofeach. 5. Identify precancerous cellular changes. 6. List the common causes of cell damage. 7. Describe the common types of cell necrosis and possible outcomes.

2. INTRODUCTION Homeostasis: Cells tend to preserve their immediateenvironment and intracellular environment.WHAT IS PATHOPHYSIOLOGY?Pathophysiology involves the study of functional Causes of cell injury: Oxygen Deprivation (Hypoxia,due to restriction of blood ischemia),or physiologic changes in the body that resultChemical, Infectious,and Immunologic agents,from disease processes. Genetic defects, Nutritional imblances, physicalagents, and aging.This subject builds on knowledge of the normal Cell injury could be reversible (e.g. adaptation), and structure, and function of the human body.cells return to a stable baseline; however, with As a disease develops, the changes in the severe or persistent stress, irreversible injury (cell death by necrosis or apoptosis) results. normal anatomy and/or physiology of the body may be obvious or maybe hidden, occurring at the cellular level. As such, pathophysiology includes some aspects of pathology (histopathology), the laboratory study of cell and tissue changes associated with disease.(Normal heart (center), Cardiac hypertrophy(left(and dilatation (right 3. CELLULAR ADAPTATION TO INJURY1- Atrophy 2-hypertrophy Shrinkage in the size of the cell by the loss ofcell substance. When a sufficient number ofcells is involved, the entire tissue or organ Hypertrophy is an increase in the size of cellsdiminishes in size. Cells are not dead.. and consequently an increase in the size of the Causes of atrophy include: organ.1- Decreased workload (e.g., immobilization of Hypertrophy can be physiologic or pathologica fractured limb to permit healing)and is caused either by increased functional2- Loss of innervation demand or by specific hormonal stimulation.3- Diminished blood supply Hypertrophy and hyperplasia can also occur4- Inadequate nutritiontogether, and obviously both result in an5- Loss of endocrine stimulation enlarged (hypertrophic) organ6- Aging. Uterine hypertrophy during pregnancy 4. .(CELLULAR ADAPTATION TO INJURY (cont3-hyperplasia 4- metaplasia. Hyperplasia constitutes an increase in theIs a reversible change in which onenumber of cells in an organ or tissue.differentiated (adult) cell type is Physiologic hyperplasia is divided into (1) replaced by another differentiatedhormonal hyperplasia, (2) compensatory(adult) cell type.hyperplasia,It might be protective adaptive mechanisme.g. cigarette smoking but it involves Most forms of pathologic hyperplasia areloss of functioninstances of excessive hormonal or growthfactor stimulation. Hyperplasia could be precancerous.Thyroid-diffuse hyperplasia Graves disease 5. Cell Damage and NecrosisThere are many ways of injuring cells in the The most common cause of injury is ischemiabody, including:where sensitive cells suffer hypoxia (reducedoxygen in the tissue) > interferes with energy(ATP) production > loss of the sodium ischemia, or deficit of oxygen in the cells,pump > increase in sodium ions inside thedue to respiratory problems or circulatorycell > cell swelling & ruptureobstruction; At the same time, in the absence of oxygen, physical agents, excessive heat or cold, oranaerobic metabolism occurs in the cell,radiation exposure; leading to a decrease in pH (acidosis) and mechanical damage such as pressure or further metabolic impairment.tearing of tissue; Cell lysis releases destructive lysosomal chemical toxins or foreign substances;enzymes into the tissue, which cause microorganisms such as bacteria, viruses, inflammation (swelling, redness and pain)and parasites;as well as damage to nearby cells. abnormal metabolites accumulating in The enzymes released from the dead cells cancells;diffuse into the blood, providing helpful nutritional deficits; clues in blood tests that indicate the type of and imbalance of fluids or electrolytes.cells damaged.(e.g. diagnostic test ofmyocardial infarction) 6. Irreversible Cell Injury: 1- NecrosisDefinition: denotes death of a group of cells. It is characterized2- Liquefactive necrosis. Characteristic of focal bacterial or fungal by cell swelling, denaturation of cytoplasmic proteins, and infections, due to accumulation of white cells, and hypoxic death enzymatic digestion of the cell.within the central nervous system. Liquefaction completelyMorphology:digests the dead cells.Early: Common changes are: cell swelling + nuclear changes- Gangrenous necrosis is ischemic coagulative necrosis (frequently (pyknosis, Karyrrhexis, Karyolysis) of a limb> dry gangrene); when there is superimposed infection with a liquefactive component, the lesion is called "wetLate: different types of necrosis: gangrene. Gangerenous tissue must be removed surgically.1- Coagulative necrosis. Implies preservation of the basic3- Caseous necrosis in tuberculous infection. The term "caseous" is structural outline of the cell or tissue for a span of days. The derived from the cheesy, white gross appearance of the central injury or the subsequent increasing acidosis denatures not necrotic area. The necrotic focus is composed of structureless, only the structural proteins but also the enzyme proteins, amorphous granular debris within a ring of granulomatous thus blocking cellular proteolysis. The process of inflammation. The tissue architecture is completely lost. coagulative necrosis, with preservation of the general tissue architecture, is characteristic of hypoxic death of cells in all 4- Fat necrosis. Focal areas of fat destruction, typically occurring tissues except the brain. after pancreatic injury > release of activated pancreatic enzymes into adjacent parenchyma or the peritoneal cavity. The released- Infarction is coagulative necrosis resulting from hypoxia. fatty acids combine with calcium to produce grossly visible chalky white aresas (fat saponification) Kidney infarct exhibiting coagulative necrosis, with preservation of basic Fat necrosis with saponification in the outlines of glomerular and tubularmesentery. White-yellow chalky deposits.represent calcium soap formationA tuberculous lung with a . architecture. large area of caseous necrosis 7. Irreversible Cell Injury: 2- APOPTOSIS (PROGRAMMED CELL DEATH)It is single cell death in the middle of living tissue due to activation of internal suicide program with . characteristic morphology (cell shrinkage) that does not cause tissue disruption or inflammation Causes, importance (It occurs in): http://www.youtube.com/watch?v=witLM--V2v8&feature=related1- embryogenesis, organogenesis, and developmentalhttp://www.youtube.com/watch?v=i0SuQrJUi-4&feature=relatedinvolution2- Hormone-dependent physiologic involution. Somatic Death3- Cell deletion in proliferating populations, such as Specific types of cells die at different rates.intestinal crypt epithelium, or cell death in tumors4- Deletion of autoreactive T cells in the thymus. Brain cells die quickly (4 to 5 minutes) when5- Deletion of virally infected cells. deprived of oxygen, whereas heart muscle6- Mild injury (heat, radiation, cytotoxic cancer drugs, etc.) can survive for approximately 30 minutes.that cause irreparable DNA damage (e.g., via the tumor Formerly, death of the body (somatic death)suppressor protein TP53). was assumed to occur when heart action and respiration ceased. Now, because cardiac and respiratory function can be maintained artificially, the diagnosis of death is more complex. Currently, brain death provides the criteria for somatic death. Brain death is based on the lack of any electrical activity in any neurons in the brain as demonstrated by electroencephalography (EEG) and by the absence of responses (see Chapter 22).