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Pathology of Cellular Injury and Death. Cellular Adaptations

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Pathology of Cellular Injury and Death. Cellular Adaptations What is disease? • A condition in which the presence of an abnormality causes a loss of normal health • Manifests in signs and symptoms subjective: e.g., pain objective: confirmed by diagnostic tests • Duration of disease: short lasting - acute long lasting - chronic • Outcome: varies; can be lethal What is pathology? • The study (logos) of suffering (pathos) • Devoted to the study of - the cause of the disease (etiology) - the mechanism(s) of disease development (pathogenesis) - the structural alterations induced in cells and tissues by the disease (morphologic change) - the functional consequences of the morphologic changes (clinical significance) • The morphologic change can be focal (localized abnormality) or diffuse Teaching program of pathology for medical students General pathology • Basic reactions of cells and tissues to abnormal stimuli, i.e. common features of various disease processes in various cells and tissues Systematic pathology • The descriptions of specific diseases as they affect given organs or organ systems The descriptions and terms used are the basis of medical language Students are expected to attend the lectures, the autopsy and histopathology practicals, and the organ demonstrations. Attendance at the practicals the attendence is always verified. There is no possibility for missed practicals to be repeated later. Students who are absent from more than 25% of the practicals, automatically fail the semester. The grade achieved in the fall-semester examinations will be calculated from the sum of the following: - the first mid-term assessment (maximum 5 points) - the second mid-term assessment (max. 5 points) - the histology examination (max. 5 points) - the autopsy examination (max. 5 points) - the final test (max. 80 points). The final grades: from 0 to 50 points: failed (grade 1), from 51 to 59 points: passed (grade 2); from 60 to 69 points: accepted (grade 3); from 70 to 79 points: good (grade 4); from 80 to 100 points: very good (grade 5). Pathology of cellular injury and death Cells react to adverse influences by 1) Reversible cell injury Changes that can be reversed when the stimulus is removed 2) Irreversible cell injury Changes that cause cell death 3) Cellular adaptation Stimuli result in new but altered state that maintains the viability of the cell Intracellular mechanisms particularly vulnerable to cellular injury • Maintenance of membrane integrity - critical for ionic and osmotic homeostasis of the cell • Aerobic respiration - oxidative phosphorilation and ATP production in mitochondria • Synthesis of enzymes and structural proteins Common cellular injuries • Hypoxic/ischemic injury • O2-derived free radicals • Others: chemical injury (acid and alkali solutions), burns, frostbite, trauma, electric shock, etc. Hypoxia Reduction in available oxygen Common causes 1. Upper airway obstruction (eg., sudden swelling of laryngeal mucosa, foreign body aspiration) 2. Inadequate oxygenation of blood in lung diseases 3. Inadequate O2 transport in blood because of decreased number of RBCs (anemia) 4. Inadequate perfusion of blood in the tissues in heart failure Aspiration of gastric content caused obstruction of airways and led to death in the patient with deep coma Ischemia • Inadequate blood supply to an organ or part of it due to impeded arterial flow or reduced venous drainage Reversible ischemic injury • Leads to hydropic change of cells • Commonly observed in kidney biopsies Pathomechanism • A decrease of blood pressure for hours • Hypoxia of tubular epithelial cells ATP depletion malfunction of Na+/K+ ATPase influx of sodium and water into tubular cells Morphologic features • Light microscopy (LM).... • Electron microscopy (EM).... LM: the tubular epithelial cells are vacuolated, and the brush border of proximal tubules is lost. Hydropic change on EM: accumulation of water in the cytoplasm, in the invaginations of the surface plasma membrane (hydropic vacuoles), in the cisterns of the RER, and in the mitochondria; loss of microvilli of proximal tubules Clinical consequence • Acute renal failure: decreased urinary output; hemodialysis is necessary • If systemic hypotension can be corrected, the renal function normalizes within days Irreversible ischemic injury and cell death • The transition from reversible to irreversible state is gradual and occurs when adaptive mechanisms have been exhausted • Depletion of ATP, influx of Ca 2+, activation of multiple cellular enzymes, such as phospholipases degradation of membrane phospholipids proteases degradation of membrane and cytoskeletal protein ATPases enhance ATP depletion endonucleases chromatin fragmentation EM features indicative of death of ischemic cells • Within 2 to 3 hours after the death of cells • Ruptured cell and plasma membranes • Lysis of cell and nuclear components (leakage of lysosomal enzymes result in digestion of organelles and other cytosolic components) Irreversible hypoxic injury: rupture of cell Reversible hypoxic injury membranes and lysis of chromatin LM features indicative of death of ischemic cells • Evident approximately 24 hours after the death of ischemic cells • Loss of nuclear staining • Eosinophilia of the cytoplasm Important • The cellular function is lost before cell death occurs, and the morphologic features of cell death lag far behind loss of function Injury induced by O2-derived free radicals Inflammation, radiation, chemicals, reperfusion lead to the formation of - • superoxide anion radical (O2. ) • hydrogen peroxide (H2O2) • hydroxyl radical (OH.) • nitric oxide (NO.) These molecules cause oxidative stress of cells: • lipid peroxidation membrane damage • cross-linkage of proteins inactivation of enzymes • DNA breaks blockade of DNA transcription Note Insidiously ongoing oxidative stress of cells plays a role in the process of aging Laboratory markers of irreversible cell injury Cytoplasmic enzymes released through damaged cell membranes into the blood • Creatine kinase (CK) - cardiac or skeletal muscle injury • Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) - liver cell injury • Lactate dehydrogenase (LDH) – from ruptured RBCs Necrosis - morphology of irreversible injury • Necrosis (necros, dead): death of cells in a living organism characterized by loss of membrane integrity and enzymatic digestion of cells • Histological sign: loss of nuclear staining • Healing: substances released from dead cells induce a local inflammatory reaction, which serves to eliminate the debris and initiates the repair process Types of necrosis 1. Coagulative necrosis 2. Liquefactive necrosis Grossly 3. Caseation visible 4. Fat necrosis 5. Gangrene 1. Fibrinoid necrosis Coagulative necrosis Most common form of necrosis, predominated by protein denaturation with preservation of the cell and tissue framework Arterial occlusion distally: hypoxic (anoxic) death in tissues Types: anemic infarct hemorrhagic infarct Anemic infarct Cause: occlusion of an end artery In the heart, spleen, kidney Gross: circumscribed yellowish lesion, the margins are hyperemic Circumscribed yellowish lesion, the margins are hyperemic Anemic infarct Cause: occlusion of an end artery In the heart, spleen, kidney Gross: yellowish lesion, the margins are hyperemic LM: dead cells become eosinophilic with loss of nuclear staining, the border of necrotic tissue is hyperemic and infiltrated by neutrophils LM of myocardial infarction: eosinophilia of necrotic fibers, disappearance of nuclear staining. Neutrophils in the interstitium Hemorrhagic infarct In the lungs, due to occlusion of a segmental pulmonary artery; sec. hemorrhage via bronchial arteries Hemorrhagic infarct of lung: wedge shaped, raised, dark-red area Hemorrhagic infarct In the small bowels, due to occlusion of the mesenteric superior artery; sec. hemorrhage via anastomosing arcades Hemorrhagic infarct of small bowels 36 Liquefactive necrosis The necrotic tissue undergoes softening due to action of hydrolytic enzymes Examples 1. Brain infarct 2. Abscess 1. Brain infarct Occlusion of cerebral artery leads to anemic infarct; then enzymes released from dead cells liquefy the necrotized area Brain infarct: the necrotic area is softened and pale Infarcted area Caudate nucleus Internal capsule Brain infarct. Macrophages scavenge necrotic, lipid-rich debris. Liquefactive necrosis 2. Abscess - localized purulent inflammation. Hydrolytic enzymes derived from neutrophil granulocytes induce necrosis of infected area Liquefactive necrosis: abscess Caseous necrosis • Distinctive form of coag. necrosis in foci of tuberculous infection of the lung • Grossly, caseous necrosis is white and cheesy LM features: the necrotic area is eosinophilic, amorphous, surrounded by activated macrophages (epitheloid cells) which mediate the tissue necrosis and kill the bacteria Enzymatic fat necrosis • Occurs in pancreatitis, induced by the action of lipases derived from injured pancreatic cells • Lipases catalyse decomposition of triglycerides to fatty acids, which complex with calcium to create calcium soaps The swollen pancreas displays several yellowish foci of necrosis Gangrene • This (mostly) clinical term refers to the severemost forms of necrosis • Total destruction of all tissue components; often putrefactive bacteria invade the necrotic tissue • Three types (detailed in Inflammation chapter) One subtype: dry gangrene • In the leg of patients suffering from atherosclerosis-related occlusion of the tibial arteries • The affected tissues appear black because of the deposition of iron sulphide
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