Ateneo - UPO

1) INTRODUCTION TO GENERAL PATHOLOGY
2) THE GENETIC BASE OF THE DISEASES
3) PHYSICAL AGENTS AS CAUSE OF DISEASES
4) CHEMICAL AGENTS AS CAUSE OF DISEASES
5) BIOLOGICAL AGENTS AS CAUSE OF DISEASES
6) TISSUE MODIFICATIONS IN RESPONSE TO PATHOLOGICAL CHRONIC AND ACUTE STIMULA
7) INFLAMMATORY PROCESS
8) REPAIR PROCESS
9) NEOPLASTIC GROWTH
10) SYSTEMS of ENDOGENOUS 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 aim of the PATOLOGIA GENERALE course is to understand the root causes (etiology) and mechanisms (pathogenesis) that are responsible for altering the state of health.
To this end, the molecular, cellular and super-cellular effects of endogenous pathogens (genetic and tumor diseases) and exogenous pathogens (physical, chemical and biological causes of disease) will be examined. Cell and tissue levels will then be investigated for the adverse consequences of chronic and acute pacing with pathogens (degeneration, reversible and irreversible cell damage, cell death for necrosis or apoptosis).
The local and systemic reaction to tissue damage will be described by thorough examination of the inflammatory process and consequent tissue repair.
The course of GENERAL PATHOLOGY conducted for the Student of first Degree in BIOTECHNOLOGIES within the Extended Program reported below, will examine in particular the molecular mechanisms of the various pathological conditions examined with specific references to the implications for future Medical Research activities.

The Course needs the previous knowledge of fundamental elements of biochemistry, biology, genetics and physiology acquired in previous or parallel courses, which will provide the basis for the learning of the effects of exogenous and endogenous disease agents on the cellular and tissue levels ( Cell damage and neoplastic transformation) and non-specific (inflammatory) and specific (immune) defense responses.

Lectures based on a continuous student interaction that will allow immediate verification of understanding of the topics discussed. Strongly recommended is the acquisition of notes of all the lessons directly taken by the student such notes will be essential for the preparation of the exam. All slides of the course will be available since from the first lesson.

Students with physical disabilities, Learning Disabilities or Special Education Needs can request
specific services and tools via the Staff Sviluppo e Coordinamento Carriere e Servizi alle Studentesse

e agli Studenti, consulting the University webpage: https://www.uniupo.it/en/services/services-
students-physical-or-learning-disabilities

Students with disabilities, learning disabilities or special education needs, once they have contacted
the University Staff, can refer to the tutor in charge of the course to define the examination
modalities, concerning academic aspects.

We will evaluate the students with a written examination, with questions and multiple choice answers. The questions will be distributed to cover the all program. The questions will be prepared to both verify the knowledge and the understanding of single aspects of the program.

INTRODUCTION TO GENERAL PATHOLOGY; The state of health, the concept of etiology, the concept of pathogenesis, the state of illness.

GENETIC DISEASE BASES General on genetic mutations and their causes. Examples of genetic diseases: sickle cell anemia and alterations in transport or metabolism of amino acids: Hartnup disease, phenylalaninemia, albinism.

PHYSICAL AGENTS AS A CAUSE OF DISEASE: generality about mechanical, thermal, electric power transfer pathologies. Effects of ionizing radiation (molecular, cellular and super-cellular) and the effects of exciting radiations.

CHEMICAL AGENTS AS A DISEASE: absorption and elimination routes; biotransformation reactions: phase 1 (dependent on cytochrome P450) and phase 2; adverse effects of reactive metabolites produced during biotransformation), toxicity by chemical agents . The damage caused by free radicals: production mechanisms, protective factors and cell damage.

BIOLOGICAL AGENTS AS A CAUSE OF DISEASE: Generalities on the mechanisms of damage and defense against viral and bacterial infections.

TISSUE CHANGES IN RESPONSE TO CHRONIC AND ACUTE PATHOLOGICAL STIMULES: hypertrophy, hyperplasia, hypotrophy, atrophy, metaplasia; Reversible cell damage. Irreversible cell damage: cell death for necrosis and apoptosis.

INFLAMMATORY PROCESS: Inflammatory cells and their functions (monocytes, macrophages, neutrophil granulocytes, basophils, mast cells, endothelial cells, platelets) soluble inflammatory mediators (histamine, serotonin, arachidonic acid metabolites, plasma proteases, cytokines: interleukin 1.6 [IL-1 and IL-6], tumor necrosis factor alpha [TNFalfa], transformant-beta growth factor [TGFbeta], bacterial metabolites). Alteration of the tone and vascular permeability during inflammation (exudate formation). Activity of phagocytic cells in inflammation (adhesion, diaphytesis, chemotaxis, phagocytosis, bacterial killing mechanisms); istoflogosi. Systemic effects of inflammation.

REPAIR PROCESS: regeneration (tissue proliferative potential, growth factors: epidermal growth factor [EGF], transformant [TGFbeta], similar insulin [IGF], platelet derivation [PDGF], fibroblasts [FGF], interactions With matrix and other cells) substitution with connective tissue and angiogenesis. Wound repair



NEOPLASTIC GROWTH: General characteristics of the neoplasms (information on incidence, mortality and survival, tumor classification and nomenclature); Hyperplasia, neoplasia, anaplasia and dysplasia. Viral and cellular oncogenes, oncosoppressor genes. Neoplastic phenotype: phenotypic heterogeneity and genomic instability. Initiation, promotion of the neoplastic process (carcinogenic stages or cancerogenesis as a continuous process). The progression of the neoplastic process (neoplastic latency, neoplastic invasion, metastases).
SYSTEMS of ENDOGENOUS RESISTANCE TO CELL DEATH: Cytoprotective effects of cellular and tissue preconditioning. Early and delayed preconditioning. Mechanisms involved in preconditioning cytoprotection. Molecular mediators of preconditioning. Therapeutic implications.

The student is expected to obtain the knowledge and the understanding of the molecular base of the loss of health (disease status). Specifically the student is expected to know the causes and the pathogenetic mechanisms of fundamental diseases induced by physical, chemical, biological agents and by genetic alterations; the mechanisms of cell damage, inflammation, reparation and tumor transformation.