Module Details

Principles of Pathology

BT044

Course
Principles of Pathology
Code
BT044
Academic Year
2026/2027
Curriculum Year
2026/2027
Degree Programme
PHYSIOTHERAPY
Curriculum
000 - CORSO GENERICO
Course coordinator
Lecturers
Credits
3
Lecture Hours
30
Scientific Disciplinary Sector (SSD)
MEDS-02/A - Experimental Medicine and Pathophysiology
Course Type
Single-subject learning activity
Course Delivery
OBB - Obbligatoria
Year
1
Teaching period
Secondo Semestre
Campus
FOSSANO
Teaching language
Italian
Course Contents
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 ACUTE AND CHRONIC PATHOLOGICAL STIMULI
7) THE INFLAMMATORY PROCESS
8) THE REPAIR PROCESS
9) NEOPLASTIC GROWTH
Reference Texts
Patologia Generale per Corsi di Laurea in Professioni Sanitarie G.Pontieri (Ed. Piccin)
Istituzioni di Patologia Generale. M.U. Dianzani (ed. UTET)
La Professione del Medico vol.3, (ed UTET)
Learning Outcomes
The General Pathology module is part of the integrated course (Microbiology, General Pathology, and Immunology) on the Molecular Basis of Disease (for the degree programs in Physiotherapy, Radiology Technology, and Biomedical Laboratory Technology) and on the Etiopathogenesis of Disease (for Dental Hygiene), a course shared by all degree programs in the Technical Health Professions area.
Prerequisites
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.
Teaching Methods
Lectures based on continuous interaction between instructor and student, allowing for the immediate verification of understanding regarding 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 very 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.
Assessment Methods
The exam consists of a written test with multiple-choice questions covering topics in Microbiology, General Pathology, and Immunology. Specifically regarding General Pathology, questions will cover all fundamental aspects of the individual sections of the syllabus outlined above.
The exam is considered passed only if at least 50% of the questions for each of the three disciplines within the integrated course are answered correctly. The number of questions is proportional to the number of hours (and thus the scope of the syllabus) allocated to each discipline in the integrated course. A single final grade is awarded.
Detailed Syllabus
NTRODUCTION TO GENERAL PATHOLOGY: the state of health, 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 CHANGES 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, neutrophil 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).
Expected Learning Outcomes
The student must demonstrate an understanding of the fundamental mechanisms and causes of the diseases described in the course, as well as knowledge of the key aspects of the activation and development of the inflammatory process and the mechanisms of cellular damage.
Last update:21-10-2026 00:13:19