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Docente
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BEI ROBERTO
(programma)
DESCRIPTION OF TEACHING MODULE:
Cellular adaptations, cell injury, and cell death: cellular responses to stress and noxious stimuli. Cellular adaptations of growth and differentiation: hyperplasia, hypertrophy, atrophy, metaplasia. Overview of cell injury and cell death: causes of cell injury. Mechanisms of cell injury. Reversible and irreversible cell injury. Morphology of cell injury and necrosis. Examples of cell injury and necrosis: ischemic and hypoxic injury, ischemia-reperfusion injury, chemical injury. Apoptosis: causes of apoptosis, morphology, biochemical features of apoptosis, mechanisms of apoptosis, examples of apoptosis.
Subcellular responses to injury: lysosomal catabolism (heterophagy, autophagy); hypertrophy of smooth endoplasmic reticulum; mitochondrial alterations; cytoskeletal abnormalities. Intracellular accumulations: lipids, proteins, hyaline change, glycogen, pigments (exogenous pigments, endogenous pigments); pathologic calcification (dystrophic calcification and metastatic calcification)
General features of inflammation:
Acute inflammation: historical highlights, stimuli for acute inflammation; vascular changes (changes in vascular flow and caliber, vascular leakage); cellular events: leukocyte extravasation (leukocyte adhesion and transmigration) and phagocytosis. Adhesion molecules involved in the inflammatory response. Chemotaxis. Defects in leukocyte functions.
Chemical mediators of inflammation: vasoactive amines, plasma proteins, arachidonic acid metabolites: prostaglandins, leukotrienes, and lipoxins, platelet-activating factor (PAF), cytokines and chemokines, nitric oxide (NO), lysosomal constituents of leukocytes, oxygen-derived free radicals, neuropeptides. Disorders of the complement system.
Outcomes of acute inflammation. Morphologic patterns of acute inflammation.
Systemic effects of inflammation, consequences of defective or excessive inflammation
Neoplasia:
Molecular basis of cancer: essential alterations for malignant transformation, the normal cell cycle, self-sufficiency in growth signals: oncogenes. Insensitivity to growth inhibitory signals: tumor suppressor genes. Retinoblastoma as a paradigm for the two-hit hypothesis of oncogenesis. Selected tumor suppressor genes involved in human neoplasms. p53: guardian of the genome. Evasion of apoptosis. DNA repair defects and genomic instability in cancer cells. Limitless replicative potential: telomerase. Development of sustained angiogenesis. Invasion and metastasis. Stromal microenvironment and carcinogenesis. Dysregulation of cancer-associated genes.
Molecular basis of multistep carcinogenesis gatekeeper and caretaker genes. Tumor progression and heterogeneity. Carcinogenic agents and their cellular interactions: chemical carcinogenesis, metabolic activation of carcinogens. Molecular targets of chemical carcinogens. Major chemical carcinogens. Radiation carcinogenesis: ultraviolet rays, ionizing radiation. Microbial carcinogenesis: oncogenic DNA viruses, oncogenic RNA viruses. Host defense against tumors: tumor immunity, tumor antigens, antitumor effector mechanisms. immune surveillance. Effects of tumors on the host local and hormonal effects. Grading and staging of tumors.
Heart pathophysiology: heart failure, cardiac hypertrophy: pathophysiology and progression to failure. Ischemic heart disease. Angina pectoris. Myocardial infarction.
Liver pathophysiology: general features of hepatic diseases. Patterns of hepatic injury. Hepatic failure. Cirrhosis. Portal hypertension. Bilirubin and bile formation. Causes and classification of jaundice. Hereditary hyperbilirubinemias. Cholestasis. Viral hepatitis. Ascites.
DIDACTIC MATERIALS:
Suggested Text-Book:
Kumar et al
Robbins and Cotran Pathologic Basis of Disease 8E.
The student will be provided the slides shown in class.
REFERENCES:
Kumar et al
Robbins and Cotran Pathologic Basis of Disease 8E.
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