Ateneo - UPO

1) Introduction to General Pathology
2) Genetic Basis of Disease
3) Physical Agents as Causes of Disease
4) Chemical Agents as Causes of Disease
5) Biological Agents as Causes of Disease
6) Tissue Changes in Response to Chronic and Acute Pathological Stimuli
7) The Inflammatory Process
8) The Repair Process
9) Neoplastic Growth
10) Endogenous Systems of Resistance to Cell Death

Patologia e Fisiopatologia Generale di Pontieri, Russo, Frati (Ed. Piccin)
Istituzioni di Patologia Generale. M.U. Dianzani (ed. UTET)
La Professione del Medico vol.3, (ed UTET)

The specific objective of the General Pathology course is to understand the fundamental causes (etiology) and mechanisms (pathogenesis) responsible for the alteration of health status. To this end, the course examines the effects—at molecular, cellular, and supra-cellular levels—of endogenous pathogenic agents (genetic diseases and tumors) and exogenous ones (physical, chemical, and biological causes of disease). It also studies, at the cellular and tissue levels, the damaging consequences of acute and chronic exposure to pathogenic agents (degeneration, reversible and irreversible cellular damage, and cell death via necrosis or apoptosis). Finally, local and systemic reactions to tissue damage are described through an in-depth analysis of the inflammatory process and subsequent tissue repair.
The General Pathology course for Biotechnology Bachelor’s degree students—conducted according to the extended syllabus below—focuses on the molecular mechanisms of the various pathological conditions examined, with specific reference to implications relevant to future medical research activities.

The course requires a foundational understanding of biochemistry, biology, genetics, and physiology—acquired through prior or concurrent coursework—which will serve as the necessary basis for learning about the effects of exogenous and endogenous disease-causing agents (cellular injury and neoplastic transformation) at the cellular and tissue levels, as well as non-specific (inflammation) and specific (immune system) defense reactions.

ILectures based on continuous interaction between instructor and students, allowing for immediate verification of the understanding of the topics covered. Students are strongly advised to take their own notes during all lectures, as these will be used for exam preparation. All course slides will be available starting from the first lecture.
Additional information

Students with disabilities, Specific Learning Disorders (SLD), or Special Educational Needs (SEN) may request specific services and tools tailored to their needs by contacting the Student Career Development and Coordination and Student Services Staff and

consulting the dedicated page on the University website: https://uniupo.it/it/servizi/servizi-studenti-disabili-e-dsa

Once they have contacted the University staff, students with disabilities, SLD, or SEN may contact the course instructor to discuss the specific arrangements for exams and other teaching-related aspects.

Learning will be assessed via a written exam consisting of multiple-choice questions covering all topics in the syllabus. The questions are designed to test both knowledge and understanding of the mechanisms and causes of diseases induced by exogenous and endogenous pathological conditions, their effects (cellular damage, inflammation, and neoplastic transformation), and their progression (restoration of health, chronic disease, or death).

INTRODUCTION TO GENERAL PATHOLOGY: health status, the concept of etiology, the concept of pathogenesis, the disease state.
GENETIC BASIS OF DISEASE: Overview of genetic mutations and their causes. Examples of genetic diseases: sickle cell anemia and disorders of amino acid transport or metabolism (Hartnup disease, phenylalaninemias, albinism).
PHYSICAL AGENTS AS CAUSES OF DISEASE: Overview of pathologies resulting from the transfer of mechanical, thermal, and electrical energy. Effects of ionizing radiation (at molecular, cellular, and supra-cellular levels) and effects of non-ionizing (exciting) radiation.
CHEMICAL AGENTS AS CAUSES OF DISEASE: Routes of absorption and elimination (biotransformation reactions: Phase I—dependent on the cytochrome P450 system—and Phase II; injurious effects of reactive metabolites produced during biotransformation), toxicity of chemical agents. Free radical-induced damage: production mechanisms, protective factors, and cellular damage.
BIOLOGICAL AGENTS AS CAUSES OF DISEASE: Overview of mechanisms of damage and defense regarding viral and bacterial infections.
TISSUE ALTERATIONS IN RESPONSE TO CHRONIC AND ACUTE PATHOLOGICAL STIMULI: hypertrophy, hyperplasia, hypotrophy, atrophy, metaplasia; reversible cellular damage. Irreversible cellular damage: cell death via necrosis and apoptosis. THE INFLAMMATORY PROCESS: cells involved in inflammation and their functions (monocytes, macrophages, neutrophilic granulocytes, basophils, mast cells, endothelial cells, platelets); soluble mediators of inflammation (histamine, serotonin, arachidonic acid metabolites, plasma proteases, cytokines: interleukin-1 and -6 [IL-1 and IL-6], tumor necrosis factor-alpha [TNF-alpha], transforming growth factor-beta [TGF-beta], bacterial metabolites); alterations in vascular tone and permeability during inflammation (exudate formation); activity of phagocytic cells in inflammation (adhesion, diapedesis, chemotaxis, phagocytosis, bacterial killing mechanisms); tissue inflammation; systemic effects of inflammation.
THE REPAIR PROCESS: regeneration (tissue proliferative potential, growth factors—epidermal [EGF], transforming [TGF-beta], insulin-like [IGF], platelet-derived [PDGF], fibroblast [FGF]—and interactions with the matrix and other cells), replacement with connective tissue, and angiogenesis. Wound repair.

NEOPLASTIC GROWTH: general characteristics of neoplasms (overview of incidence, mortality, and survival; tumor classification and nomenclature); concepts of hyperplasia, neoplasia, anaplasia, and dysplasia. Viral and cellular oncogenes, tumor suppressor genes. The neoplastic phenotype: phenotypic heterogeneity and genomic instability. Initiation and promotion of the neoplastic process (multistage carcinogenesis vs. carcinogenesis as a continuous process). Progression of the neoplastic process (neoplastic latency, invasiveness, and metastasis).
ENDOGENOUS SYSTEMS OF RESISTANCE TO CELL DEATH: Cytoprotective effects of cellular and tissue preconditioning. Early and delayed preconditioning. Mechanisms involved in preconditioning-induced cytoprotection. Molecular mediators of preconditioning. Therapeutic implications.

Students must acquire knowledge and an understanding of the molecular basis of the loss of physiological health, and thus of the mechanisms and causes underlying disease states. Specifically, students must learn the mechanisms and causes of certain fundamental diseases induced by physical, chemical, and biological agents, as well as by genetic alterations; they will also gain knowledge of the key aspects of cellular damage, the activation and progression of the inflammatory process, repair mechanisms, and neoplastic transformation.