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Pathophysiology Examination Answers

Pathophysiology Examination Answers

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Published by Fırat Güllü
Pathophysiology Examination Answers
Pathophysiology Examination Answers

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Published by: Fırat Güllü on Jul 09, 2012
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1-Causes of Cell Injury
 The causes of cell injury range from the external gross physical violence of an automobile accident tointernal endogenous causes, such as a subtle genetic mutation causing
Oxygen Deprivation.
Hypoxia is a deficiency of oxygen, which causes cell injury by reducing aerobicoxidative respiration. Hypoxia is an extremely important and common cause of cell injury and celldeath.
Physical Agents.
Physical agents capable of causing cell injury include mechanical trauma, extremesof temperature (burns and deep cold), sudden changes in atmospheric pressure, radiation, andelectric shock.
Chemical Agents and Drugs.
The list of chemicals that may produce cell injury defiescompilation. Simple chemicals such as glucose or salt in hypertonic concentrations may causecell injury directly or by deranging electrolyte homeostasis of cells.
Infectious Agents.
These agentsrange from the submicroscopic viruses to the large tapeworms. In between are the rickettsiae,bacteria, fungi, and higher forms of parasites
Immunologic Reactions.
Although the immune systemserves an essential function in defense against infectious pathogens, immune reactions may, in fact,cause cell injury
Genetic Derangements
The genetic injury may result in a defect as severe as thecongenital malformations associated with Down syndrome, caused by a chromosomal abnormality,or as subtle as the decreased life of red blood cells caused by a single amino acid substitution inhemoglobin S in sickle cell anemia
Nutritional Imbalances.
Nutritional imbalances continueto be major causes of cell injury. Protein-calorie deficiencies cause an appalling number of deaths,chiefly among underprivileged populations.
Physical Agents e.g.. trauma, thermal injury
Chemical Agents e.g. poisons, environmental pollutants and drugs
Infectious Diseases caused by protozoa, bacteria, viruses
Immunological mechanisms
Inherited diseases- inborn errors of metabolism
Mechanisms of Cell Injury
Two mechanisms serve as useful models:
fatty change
fatty change is generally a reversible form of sublethal injury whereas the effects of hypoxiadepend on the severity, duration and on the vulnerability of the cell
Fatty Change
Accumulation of fat in hepatocytes depends on rate of fat synthesis, catabolism and on thesynthesis and export of lipoproteins.
Alcohol increases triglycyeride synthesis and reduces fatty acid catabolism
Malnutrition impairs protein synthesis and therefore reduces lipoprotein synthesis
Interruption of oxidative phosphorylation within mitochondria- depletion of ATP
Progressive loss of membrane functional integrity
Increased cytosolic calcium
 2Cell injury results from functional and biochemical abnormalitiesin one or more of several essential cellular components
2-Pathophysiology of cell injury.Effects and responses.
The normal cell is confined to a fairly narrow range of function and structure by its genetic programsof metabolism, differentiation, and specialization; by constraints of neighboring cells; and by theavailability of metabolic substrates. It is nevertheless able to handle normal physiologic demands,maintaining a steady state called homeostasis. More severe physiologic stresses and some pathologicstimuli may bring about a number of physiologic and morphologic cellular adaptations, during whichnew but altered steady states are achieved, preserving the viability of the cell and modulating itsfunction as it responds to such stimuli . The adaptive response may consist of an increase in thenumber of cells, called hyperplasia, or an increase in the sizes of individual cells, called hypertrophy.Conversely, atrophy is an adaptive response in which there is a decrease in the size and function of cells.If the limits of adaptive response to a stimulus are exceeded, or in certain instances when the cell isexposed to an injurious agent or stress, a sequence of events follows that is loosely termed cellinjury. Cell injury is reversible up to a certain point, but if the stimulus persists or is severe enoughfrom the beginning, the cell reaches a "point of no return" and suffers irreversible cell injury andultimately cell death. Adaptation, reversible injury, and cell death can be considered stages of progressive impairment of the cell's normal function and structure.
Cell death
, the ultimate result of cell injury, is one of the most crucial events in the evolution of disease of any tissue or organ. It results from diverse causes, including ischemia(lack of blood flow),infection, toxins, and immune reactions.There are two principal patterns of cell death, necrosis and apoptosis. Necrosis is the type of celldeath that occurs after such abnormal stresses as ischemia and chemical injury, and it is alwayspathologic. Apoptosis occurs when a cell dies through activation of an internally controlled suicideprogram.
Cellular Adaptations of Growth and Differentiation
 Cells respond to increased demand and external stimulation by
, and theyrespond to reduced supply of nutrients and growth factors by atrophy. In some situations, cellschange from one type to another, a process called metaplasia. There are numerous molecularmechanisms for cellular adaptations. Some adaptations are induced by direct stimulation of cells byfactors produced by the responding cells themselves or by other cells in the environment. Others aredue to activation of various cell surface receptors and downstream signaling pathways. Adaptationsmay be associated with the induction of new protein synthesis by the target cells, as in the responseof muscle cells to increased physical demand, and the induction of cellular proliferation, as inresponses of the endometrium to estrogens. Adaptations can also involve a switch by cells fromproducing one type of proteins to another or markedly overproducing one protein; such is the case incells producing various types of collagens and extracellular matrix proteins in chronic inflammationand fibrosis.
 Hyperplasia is an increase in the number of cells in an organ or tissue, usually resulting in increasedvolume of the organ or tissue.
 3Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ.Thus, the hypertrophied organ has no new cells, just larger cells.
 3) Apoptosis
Death of cells occurs in two ways:
--(irreversible injury) changes produced by enzymatic digestion of dead cellularelements2.
--vital process that helps eliminate unwanted cells--an internally programmedseries of events effected by dedicated gene products
Mechanisms of Cell Death
Mechanisms of cell death caused by different agents may vary. However, certain biochemical eventsare seen in the process of cell necrosis:
ATP depletion
Loss of calcium homeostasis and free cytosolic calcium
Free radicals: superoxide anions, Hydroxyl radicals, hydrogen peroxide
Defective membrane permeability
Mitochondrial damage
Cytoskeletal damage
This process helps to eliminate unwanted cells by an internally programmed series of events effectedby dedicated gene products. It serves several vital functions and is seen under various settings.
During development for removal of excess cells during embryogenesis
To maintain cell population in tissues with high turnover of cells, such as skin, bowels.
To eliminate immune cells after cytokine depletion, and autoreactive T-cells in developingthymus.
To remove damaged cells by virus
To eliminate cells with DNA damage by radiation, cytotoxic agents etc.
Hormone-dependent involution - Endometrium, ovary, breasts etc.
Cell death in tumors.
Morphology of Apoptosis
Shrinkage of cells
Condensation of nuclear chormatin peripherally under nuclear membrane
Formation of apoptotic bodies by fragmentation of the cells and nuclei. The fragmentsremain membrane-bound and contain cell organelles with or without nuclear fragments.
Phagocytosis of apoptotic bodies by adjacent healthy cells or phagocytes.
Unlike necrosis, apoptosis is not accompanied by inflammatory reaction
Mechanisms of Apoptosis
Apoptosis can be induced by various factors under both physiological and pathological conditions: Itis an energy-dependent cascade of molecular events which include protein cleavage by a group of enzymes (caspases), protein cross-linking, DNA breakdown. Apoptosis is regulated by a large familyof genes some of which are inhibitory (bcl-2) and some are stimulatory (bax).

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