To show the organization of the course that includes this module, follow this link Course organization
The basic aim of the course is the acquisition of the conceptual and scientific tools to explain the causes and mechanisms of human diseases. Specifically: 1) to understand the principal chemical, physical and biological causes of cell and tissue damage; 2) to understand tissue reaction to damage, that are determinat in acute and chronic physiopathologic processes: focus on inflammation, hemostasis and tissue repair; 3) to understand aethiopathogenesis of neoplastic transformation. Particular attention will be devoted to the acquisition of scientific terms used in pathology.
2. Cellular pathology: basic mechanisms of cellular damage; biochemical lesion.
Pathogenesis of hypoxia, ischemia and oxidative stress.
Oxygen radical-induced pathologies.
Pathogenesis of radiation damage.
Biological causes of diseases: general concepts of pathogenesis of infectious diseases. Endotoxins and exotoxins: physical-chemical features, biological effects, molecular basis.
Cellular death: necrosis. Serum markers of necrosis. Necrosis pathologist classification.
3. Introduction to the immune system: cellular composition and function.
The hematopoietic system: blood cell composition; hematocrit; leukocyte formula.
Functional and morphological features of leukocyte cell populations.
The reticulo-endothelial system.
Differentiation and maturation of the lymphoid and myeloid cell populations.
Innate and acquired immune responses: general concepts.
Inflammation: causes, cardinal signs, angiophlogosis and histoflogosis.
The vascular response. Exudate: features and functions.
The cellular response: leukocyte migration, rolling, activation, firm adhesion and diapedesis.
Adhesion molecules: selectins, integrins, immunoglobulins.
Chemotaxis and chemotactic factors.
Leukocyte effector mechanisms (phagocytosis, killing and degradation of phagocytosed microbes)
Defects of innate immune cells: LAD, CGD.
Chemical mediators and regulators of inflammation.
Coagulation; Complement; chinins, plasmin.
Cellular proinflammatory mediators: (i) preformed; (ii) newly synthesized (fast); (iii) newly synthesized (slow).
Cytokines: general concepts; cytokine families; physiological role; mechanisms of action.
Chemokines: C, CC, CXC, CX3C.
Proinflammatory cytokines: TNF alpha, IL-1, IL-6: producing cells, stimuli, biological role, local, systemic and pathologic effects.
Autoinflammatory syndromes: definition, causes, therapeutic strategies.
Inhibition of proinflammatory cytokines: IL-10 and IL-1ra. Anti-cytokine therapy in autoimmune diseases.
Cytokine response in sepsis and physical exercise.
Interferons: classes, producing cells, stimuli, biological and pathological role.
Systemic effects of inflammation.
Pathogenesis of septic shock.
4. Outcomes of acute inflammation.
Chronic inflammation. Granuloma.
Resolution: Regeneration and repair.
5. Genoma ed epigenoma.
The "Histone code".
Apoptosi: estrinsic and intrinsic pathway.
6. Mechanisms regulating cellular differentiation and proliferation: pathological changes.
Metaplasia, dysplasia and neoplasia. Neoplasia (general concepts)
Morphological, molecular, metabolic, genetic and functional features of the neoplastic cell.
Cancer etiology and pathogenesis.
Cancer natural history.
Molecular bases of carcinogenesis: proto-oncogenes, oncogenes, tumor suppressor genes. Oncogenes classes: (i) growth factors (EGF); (ii) growth factor receptors (EGFR/ErbB, Her2 receptor/Neu); (III) signal transduction proteins (ras); (IV) nuclear transcription factors (myc); (V) chromatin-associate proteins; (VI) cell cycle control; (VII) microRNA; (VIII) pro and anti-apoptotic proteins (Bcl2).
Tumor suppressor genes: Cyclins, retinoblastoma, p53: physiologic and pathologic role.
The Knudson hypothesis.
Nomenclature. The TNM system.
Benign and malignant hematologic neoplasia.
Head and neck cancer.
Metastasis: molecular basis of metastasis generation ad progression.
Neoplastic cachexia and paraneoplastic syndromes.