CONCISE PATHOLOGY FOR EXAM PREPARATION PDF
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download Concise Pathology for Exam Preparation - 3rd Edition. Print Book & E- Book. ISBN , This book has been written in a concise and easily assimilable style to enable rapid understanding of the mechanism and morphology of. Concise pathology for exam preparation (3rd edition.) By: Khanna, Geetika. Publisher/Imprint. Elsevier. Isbn/Ean. / Format. eBook.
Many different types of injuries act on tissues to cause direct parenchymal cell injury or interstitial injury. Interstitial abnormalities may cause indirect parenchymal cell injury. A variety of injurious agents act on human tissues Figure I-1 to produce tissue damage either directly or indirectly. Direct Injury A noxious agent may act directly on the tissue and interfere with its structure or biochemical function.
An example is a burn, in which the heat causes immediate direct destruction of cell membranes and other tissue components and coagulation of intracellular proteins.
Indirect Injury An injurious agent may act at some site other than the tissue in question to produce an abnormality in the immediate environment of the cell or cause accumulation of some toxic substance, which in turn causes cell damage.
Representative causes of indirect injury include accumulation of toxic products in kidney and liver failure or a change in extracellular pH, electrolyte concentrations, or core body temperature. These indirect injuries may result in cell damage in many different tissues throughout the body, eg, structural and functional abnormalities in the brain in liver failure hepatic encephalopathy.
Normal function is dependent on 1 the immediate environment of the cell; 2 a continuous supply of nutrients such as oxygen, glucose, and amino acids; and 3 constant removal of the products of metabolism, including CO2. Cellular Injury Injury to a cell may be nonlethal or lethal Figure Figure 1—1.
Mechanisms of injury leading to cell degeneration and necrosis. Individual separate mechanisms are discussed in the text. Necrosis is accompanied by biochemical and structural changes see below and is irreversible. The necrotic cells cease to function; if necrosis is sufficiently extensive, clinical disease results.
Cell necrosis should be distinguished from the death of the individual, which is difficult to define. From a legal standpoint in many countries, an individual is considered dead when there is complete and irreversible cessation of brain function.
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Many individual cells and tissues in a legally dead individual remain viable for some time after death, however, and constitute a major source of organs for transplantation. Degeneration is reversible but may progress to necrosis if injury persists.
When it is associated with abnormal cell function, cell degeneration may also cause clinical disease.
This process, through which effete cells are removed from normal tissue, is termed apoptosis. It differs from necrosis in that apoptotic cells are rapidly removed by phagocytes and there is no overt inflammation associated with their removal.
In addition, apoptosis typically is initiated within the cell by nuclear fragmentation pyknosis and cytoplasmic condensation. Cell membranes remain intact in the early stages, leading to small shrunken cells containing cytoplasmic or nuclear debris apoptotic bodies. Certain growth control genes may initiate apoptosis Chapter Neoplasia: II. Malignant Lymphomas.
ATP is produced by phosphorylation of adenosine diphosphate ADP , a reaction that is linked to the oxidation of reduced substances in the respiratory chain of enzymes. Oxygen is required oxidative phosphorylation Figure Figure 1—2. Main biochemical pathways involved in cellular ATP energy production. Abnormalities that result in failure of energy production are noted by letters that correspond to the accompanying text description.
Causes of Defective Energy ATP Production Figure Hypoglycemia Glucose is the main substrate for energy production in most tissues and is the sole energy source in brain cells. Low glucose levels in blood hypoglycemia therefore result in deficient ATP production that is most profound in the brain.
Hypoxia Oxygen reaches the cells via arterial blood but is ultimately derived from the atmosphere. Most of the oxygen carried in blood is bound to hemoglobin. Lack of oxygen in the cells hypoxia may result from 1 respiratory obstruction or disease, preventing oxygenation of blood in the lungs; 2 ischemia, or failure of blood flow in the tissue, due either to generalized circulatory failure or to local vessel obstruction; 3 anemia ie, decreased hemoglobin in the blood , resulting in decreased oxygen carriage by the blood; or 4 alteration of hemoglobin as occurs in carbon monoxide poisoning , making it unavailable for oxygen transport and leading to the same result as anemia.
Enzyme Inhibition Cyanide poisoning is a good example of a chemical interfering with a vital enzyme. Cyanide inhibits cytochrome oxidase, the final enzyme in the respiratory chain, causing acute ATP deficiency in all cells of the body and rapid death. Uncoupling of Oxidative Phosphorylation Uncoupling of oxidation and phosphorylation occurs either through chemical reactions or through physical detachment of enzymes from the mitochondrial membrane.
Mitochondrial swelling, which is a common change associated with many types of injury, causes uncoupling of oxidative phosphorylation. Effects of Defective Energy Production Generalized failure of energy production will first affect those cells with the highest demand for oxygen because of their high basal metabolic rate.
Brain cells are maximally affected. The earliest clinical signs of hypoxia and hypoglycemia are disturbances of the normal level of consciousness.
Intracellular Accumulation of Water and Electrolysis The earliest detectable biochemical evidence of diminished availability of ATP is dysfunction of the energydependent sodium pump in the plasma membrane. The resulting influx of sodium and water into the cell leads to cloudy swelling, or hydropic change, an early and reversible effect of cell injury.
The cloudy appearance is due to the cytoplasmic organelles dispersed in the swollen cell. These electrolyte abnormalities may lead to disordered electrical activity and enzyme inhibition. Changes in Organelles Swelling of cytoplasmic organelles follows influx of sodium and water. Distention of the endoplasmic reticulum detaches the ribosomes and interferes with protein synthesis. Mitochondrial swelling causes physical dissociation uncoupling of oxidative phosphorylation, which further impairs ATP synthesis.
Switch to Anaerobic Metabolism In hypoxic conditions, cellular metabolism changes from aerobic to anaerobic glycolysis. The conversion leads to the production of lactic acid and causes a decrease in intracellular pH. Chromatin clumping in the nucleus and further disruption of organelle membranes then occur. Disruption of lysosomal membranes leads to release of lysosomal enzymes into the cytoplasm, which damages vital intracellular molecules.
The exact point at which cellular degeneration becomes irreversible, resulting in necrosis, is unknown. Free radicals are highly unstable particles with an odd number of electrons an unpaired electron in their outer shell. The excess energy attributable to the unstable configuration is released through chemical reactions with adjacent molecules. One of the best known interactions is that between oxygenbased free radicals and cell membrane lipids lipid peroxidation , which leads to membrane damage.
Figure 1—3. Free radicals and cell injury. The various agents that produce free radicals are shown in the left column, with mechanisms of action in the right column. Healthy cells possess a number of antioxidant mechanisms that limit the effects of toxic free radicals.
Activation of the Complement System The final compounds of the activated complement pathway Chapter 4: The Immune Response , probably a complex of C5b, C6, C7, C8, and C9, exert a phospholipase-like effect that can enzymatically damage the plasma membrane.
This phenomenon complement fixation and activation is an important component of the immune response that causes the death of cells recognized as foreign.
Lysis by Enzymes Enzymes with lipase-like activity damage cell membranes. For example, pancreatic lipases—when they are liberated outside the pancreatic duct in acute pancreatic inflammation—damage nearby cells and cause extensive necrosis. Some microorganisms—eg, Clostridium perfringens, one of the causes of gas gangrene— produce enzymes that damage plasma membranes and cause extensive necrosis.
Lysis by Viruses Cytopathic viruses cause lysis by direct insertion into the cell membrane. Other viruses cause lysis indirectly via an immune response to virally determined antigens on the surface of infected cells. Lysis by Physical and Chemical Agents Extremes of heat and cold and certain chemicals solvents may cause direct lysis of cells. Less severe injury produces localized damage, which may be repaired, although with some membrane loss.
In erythrocytes, this process leads to the formation of microspherocytes smaller and rounder red cells; see Chapter Blood: II. Hemolytic Anemias; Polycythemia. Loss of Function The plasma membrane maintains the internal chemical composition of the cell by means of selective permeability and active transport.
Damage to the plasma membrane may result in abnormal entry of water, causing cloudy swelling and hydropic change identical to that resulting from injury due to defective energy production.
Deposition of Lipofuscin Brown Atrophy Lipofuscin is a fine, granular, golden-brown pigment composed of phospholipids and proteins. It accumulates in the cytoplasm as a result of damage to the membranes of cytoplasmic organelles and is most commonly seen in myocardial cells Figure , liver cells, and neurons.
Lipofuscin causes no cellular functional abnormalities. Figure 1—4. Myocardial fiber with lipofuscin pigment in the perinuclear region. On sections stained with hematoxylin and eosin, lipofuscin has a golden brown color. Lipofuscin deposition occurs in elderly individuals, those suffering from severe malnutrition, and those with chronic diseases.
It is due to a lack of cellular antioxidants that normally prevent lipid peroxidation of organelle membranes. Lipofuscin is also called "wear and tear" pigment.
DNA controls the synthesis of structural proteins Figure , growth-regulating proteins, and enzymes. Figure 1—5. Protein synthesis.
Nucleic acids are represented as lines with multiple short projections representing the bases. Changes in the nucleotide sequence will lead to synthesis of an abnormal protein or failure of synthesis of the protein.
Amino acids are represented as A1—A4. Causes of DNA Abnormalities Inherited genetic abnormalities are passed from generation to generation, frequently in predictable fashion according to mendelian laws Chapter Disorders of Development.
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Acquired genetic abnormalities are somatic mutations resulting from damage to genetic material by any of several agents, including ionizing radiation, viruses, and mutagenic drugs and chemicals. Effects of DNA Abnormalities The clinical and pathologic effects of genetic abnormalities depend on 1 the severity of damage, 2 the precise gene or genes damaged, and 3 when the damage was sustained.
When genetic damage is inherited or occurs during gametogenesis or early fetal development, clinical effects may be present at birth congenital genetic disease. Acquired genetic disease results when genetic damage occurs postnatally. DNA abnormalities are manifested at a cellular level in several ways. Failure of Synthesis of Structural Proteins Severe damage to DNA in the nucleus—as occurs after high doses of radiation and some viral infections— causes necrosis due to inhibition of synthesis of vital intracellular structural proteins.
Less severe damage may result in a variety of effects, depending on the extent of inhibition and the type of protein synthesis that is inhibited. Failure of Mitosis Interference with mitosis in actively dividing cells eg, bone marrow cells may result in depletion of erythrocytes anemia and neutrophils neutropenia.
Similar depletion of cells may occur in intestinal mucosa, resulting in abnormal structure and function. Failure of mitosis in the testis may result in decreased spermatogenesis, manifested as infertility. Failure of Enzyme Synthesis Enzyme deficiency in the embryo may result in congenital diseases inborn errors of metabolism.
Acquired enzyme defects result in necrosis if a vital biochemical system is affected. Enzyme defects involving less vital biochemical reactions result in a variety of sublethal degenerative changes Chapter Disorders of Development.
Concise Pathology for Exam Preparation
Diagnosis of Infectious Diseases. Depending upon their severity, they may produce cellular degeneration or necrosis. Accumulation of Endogenous Substances Table Table 1—1. It is common in the liver and rare in the kidney and myocardium and occurs as a nonspecific response to many types of injury. Free fatty acids are carried in the blood to the liver, where they are converted to triglycerides, phospholipids, and cholesteryl esters. After these lipids form complexes with specific lipid acceptor proteins apoproteins , which are also synthesized in the liver cell, they are secreted into the plasma as lipoproteins.
When triglycerides are metabolized normally, there is so little triglyceride in the liver cell that it cannot be seen in routine microscopic sections. Figure 1—6. Fat metabolism in the liver cell. Numbers shown correspond with circled numbers in the section on causes of fatty liver as described in the text. When the rate of conversion of fatty acids to triglycerides in the liver cell is increased because of overactivity of the involved enzyme systems. This is the main mechanism by which alcohol, a powerful enzyme inducer, causes fatty liver.
When oxidation of triglycerides to acetyl-CoA and ketone bodies is decreased, eg, in anemia and hypoxia. When synthesis of lipid acceptor proteins is deficient. Protein malnutrition and several hepatotoxins, eg, carbon tetrachloride and phosphorus, cause fatty liver in this way.
In acute fatty liver, triglyceride accumulates as small, membrane-bound droplets in the cytoplasm microvacuolar fatty change, Figure Figure 1—7. Acute microvacuolar fatty change of the liver in Reye's syndrome. The cytoplasm of the liver cells is filled with numerous small vacuoles representing the lipid that has been dissolved out of the tissue during processing.
The nuclei are centrally located. Chronic Fatty Liver Chronic fatty liver is much more common. It is associated with chronic alcoholism, malnutrition, and several hepatotoxins. Fat droplets in the cytoplasm fuse to form progressively larger globules macrovacuolar fatty change, Figure The distribution of fatty change in the liver lobule varies with different causes Figure Grossly, the fatty liver is enlarged and yellow, with a greasy appearance when cut.
Even when severe, chronic fatty liver is rarely associated with clinically detectable liver dysfunction. Figure 1—8. Macrovacuolar fatty change of the liver in chronic alcoholism.
The large fat globules in the cytoplasm appear as empty spaces that have displaced the nucleus to the side. The degree of fatty change varies from slight in the bottom left to marked at the top right of this photograph.
Figure 1—9. Distribution of fatty change tinted circles in the liver in hypoxic and toxic liver injuries.
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In hypoxic injury, fatty change is centrizonal; in toxic injury, fatty change occurs around the portal areas. The rules relating to this distribution, which are dependent on the mode of entry of oxygen and toxins into the liver lobule, are not without exception.
Carbon tetrachloride, for example, causes centrizonal fatty change. In chronic fatty change, bands of yellow streaks alternate with red-brown muscle "thrush breast" or "tiger skin" appearance ; this usually causes no clinical symptoms. Toxic diseases such as diphtheritic myocarditis and Reye's syndrome produce acute fatty change. The heart is flabby and shows diffuse yellow discoloration; myocardial failure commonly follows. In routine tissue sections, therefore, cells in the earliest stages of fatty change have pale and foamy cytoplasm.
Recognize, identify, and describe the anatomy of major blood vessels in the brain. Compare and contrast the different modalities used to image the brain. Recognize, identify, and describe major brain vascular pathologies and their characteristic appearance on imaging. Introduction Ever since team-based learning TBL was introduced into medical education in , increasing numbers of medical educators have implemented its student-centered, instructor-led format.
TBL is an evidence-based collaborative learning strategy that thrives by using small-group interaction to improve students' ability to apply course content. Rather than simply familiarizing students with concepts, TBL requires students to use those concepts to solve problems. Most residency programs offer daily conferences, in which residents are given didactic lectures or are exposed to a variety of case presentations.
Radiology residents are often expected to absorb a great deal of information that they will later be asked to apply in the reading room. Though this traditional educational model has been effective, we believe TBL can serve as a valuable adjunct by allowing students to immediately apply what they have learned through exercises that require them to use their knowledge. TBL integrates knowledge acquisition with knowledge application and allows students to gain a much better sense of the relevance of the material in the real world.
This module exists as part of a series entitled Diagnostic Imaging Fundamentals and is targeted to first-year radiology residents, fourth-year medical students, and residents in fields such as emergency medicine, neurology, and neurosurgery. However, anyone with an interest in brain vascular imaging would benefit from its concise descriptions and numerous examples.
By the conclusion of this module, learners will be able to recognize and describe major brain vascular injuries and create a differential diagnosis based on radiologic appearance. We believe that the module's design as a TBL exercise makes it an effective learning tool.
Students progress beyond mere acquisition of facts and achieve a depth of understanding made possible through peer collaboration and application of knowledge to real-life scenarios. Students gain an appreciation for the relevance of brain vascular imaging in real-world situations and improve their ability to make decisions quickly and confidently by practicing in a low-risk setting. This module may be implemented in a variety of educational settings: in place of traditional lectures, as part of a medical school curriculum, or informally for individuals who have an interest in neuroradiology.
The team-based format places less of a burden on the instructor, who, rather than dispensing information, acts more to facilitate the educational process. We believe the team-based approach also fosters an appreciation for the value of teamwork in solving challenging problems and facilitates camaraderie among peers.
TBL has also been shown to enhance performance on examinations. The module is the result of collaborative effort from individuals at different institutions and has been written with reference to the existing literature, compilation of unique images, and participatory feedback from residents.
Methods Students are divided into teams by the instructor at the beginning of the session.
This text contains a brief overview of brain vascular anatomy, imaging modalities, and pathology that should enable students to successfully answer all TBL questions.
The reading should be made available to students 1 week prior to the session and ought to take 3—4 hours to complete. Additional resources, though not required, are encouraged. The instructor should be a content expert.TBL has also been shown to enhance performance on examinations. The Intestines: I. Christine Ziegler. The necrotic cells cease to function; if necrosis is sufficiently extensive, clinical disease results. We will then contact you with the appropriate action.
Lipofuscin causes no cellular functional abnormalities. In addition, apoptosis typically is initiated within the cell by nuclear fragmentation pyknosis and cytoplasmic condensation.
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