cod. 08707

Academic year 2018/19
3° year of course - First semester
- Ovidio BUSSOLATI - Valeria DALL'ASTA - Bianca Maria ROTOLI - Roberto SALA
Academic discipline
Patologia generale (MED/04)
Patologia generale e molecolare, immunopatologia, fisiopatologia generale, microbiologia e parassitologia
Type of training activity
42 hours
of face-to-face activities
6 credits
course unit

Learning objectives

Once completed the Course, the Student will have a thorough knowledge and understanding of the etio-pathogenetic factors underlying the basic structural and functional alterations in humans, and the relative response mechanisms, at the different levels of integration (molecules, cells, tissues, organisms).
Students are also expected to be able to apply this knowledge, integrated with information from previous Courses, to the comprehension of the pathophysiology of common human pathologies.


Sufficient bases of cytology/histology, anatomy, biochemistry, microbiology, immunology, oncology and physiology are required.

Course unit content

The Course will provide scientific bases to the practice of medicine, defined as the capability to identify clinical conditions affecting human beings and to promote preventive or therapeutic to implement individual and community health. The Course will concern:
- Cell Pathology
- Molecular Pathology
- Tissue responses to cell injury: inflammation, hemostasis, repair
- General pathophysiology

Full programme

1)Molecular pathology
- Monogenic Mendelian disease (with relevant examples)
* autosomic dominant
* autosomic recessive
* X-linked
- Monogenic non-mendelian diseases (with examples)
- Polygenic multifactorial diseases (with examples)
- Chromosomal alterations
- Disorders of gene expression and phenotypic effects of mutations
- Examples of protein disorders
*structural proteins
* hemoglobinopathies and thalassemias
* channels and transporters
* hormones and receptors

2) Cellular pathology
- Cell damage: reversible vs. irreversible
- Protein misfolding: ER stress and UPR
- Intracellular accumulations: protein accumulation, steatosis, glycogenosis, lysosomal diseases
- Extracellular accumulations: amyloidosis
- Oxidative stress and the cell response
- Biotransformations and ethanol toxicity
- Ischemic and hypoxic stress. Cell and tissue adaptation to hypoxic-ischemic stress
- Types, biological significance and mechanisms of cell death
- Cell aging, organism aging and progeroid syndromes

3) The response to tissue damage
- Hemostasis and its mechanisms
- Hemorrhagic disease
- Thrombosis (mechanisms, Virchow's factors, evolution and consequences)
- Embolia (concept, types, consequences)
- Infarction
- Innate immunity and inflammation triggering
- Acute inflammation: phenomena, cells, mediators, types
- The inflammatory exudate (mechanism of formation, types)
- Mediators of the inflammatory response (exogenous vs. endogenous; cellular vs. plasmatic; preformed vs. neosynthesized; the complement system; the kinine system; histamine; eicosanoids; the cytokines; nitric oxide; antiinflammatory mediators)
- The resolution of the acute inflammatory response
- Chronic inflammation (the infiltrate, mechanisms, cells, evolution)
- Inflammatory lesions: abscesses, ulcerae, granulomas
- Systemic phenomena in inflammation (leukocytosis, acute phase response, the inflammatory stress, metabolic changes)
- Fever
- Defects of the inflammatory response
- Autoinflammatory diseases
- Mechanisms of tissue repair
- Derangements of tissue repair mechanisms
- Fibrosis
- Atherosclerosis

4) Pathophysiology
- Edema: exudates and trasuìdates
- Shock
- Thermoregulation
- Endocrine disorders
* Endocrine defects (hormone deficits, receptor defects, post-receptorial defects)
*Endocrine hyperactivities (hormone excess, receptor hyperactivity, excess of signal transduction)
- Pathophysiology of metabolism:
*alterations of purine metabolism
* alterations of lipid metabolism
* Diabetes Mellitus: etiologic factors, types, pathophysiology of metabolic alterations and complications
* Porphiries and jaundice
* Iron and copper. Iron deficiency and overload.
- Pathophysiology of nutrition.
* Hypovitaminosis and hypervitaminosis


- Kumar, Abbas, Fausto, Aster (Eds). Robbins e Cotran – Pathologic Basis of Disease - Elsevier Masson, 2015
- Pontieri, Russo, Frati. Patologia Generale. 5° Edizione, Piccin, 2015.
Additional references will be suggested during the lectures.

Teaching methods

Interactive oral lectures, based on the explanation of the main conceptual frame of each subject, supported by graphical presentations which will be available to the students on the Elly platform. This material will be useful to support the individual learning process but, by no means, should be considered sufficient for the preparation of the exam. Examples taken from the medical practice will be provided together with bibliographic references so as to stimulate students to raise questions, to go in depth in subjects of interest or to provide answers to simple problems presented by the teacher. The course will be integrated with optional laboratory practice.

Assessment methods and criteria

No interim summative evaluation is programmed, while valutative or diagnostic evaluations will be possible.
The final summative evaluation will consist in an oral examination.
Questions/student: 2 (from different examiners). Each question will concern a pathologic process enlisted in the detailed program. The examiner will enunciate the process, using a subject enlisted in the program, or will delineate a situation of clinical relevance in which a pathologic process is clearly involved.
In the first case, the candidate shall provide the definition of the process and will discuss causes, mechanisms and involvement in human pathology with the examiner.
In the second case, the candidate shall identify the process involved in the clinical situation and will discuss it with the examiner.
Failure to answer to one of the two questions, or the verified uncapability to define or identifying correctly the pathologic process, will prevent the successful completion of the exam.
The outcome will be also negative if, during the discussion, the student will exhibit severe pitfalls, not compatible with an adequate understanding of the subject.
After each question, the examiner will give an evalaution expressed in marks:
A. Very good knowledge and understanding. Very good capability of
applying knowledge to bio-medical problems. Corresponding to 30/30.
B. Good knowledge and understanding. Good capability to apply knowledge to biomedical problems. Corresponding to 27-29/30.
C. Average knowledge and understanding. Average capability of applying knowledge to bio-medical problems. Corresponding to 24-26/30
D. Sufficient knowledge and understanding. Sufficient capability of
applying information to bio-medical problems. Corresponding to 21-23/30.
E. Barely sufficient knowledge and understanding (with evident pitfalls).
Scarce capability of applying knowledge to bio-medical problems.
Corresponding to 18-20/30.
Full marks with laude will be reserved to students exhibiting, together an
overal evaluation of 30/30, good communication skills and capability of autonomous in depth-analysis of the subject.
The final vote will be decided jointly by the examiners, who will have the possibility to decide a vote not higher or lower than three grades from the best or the worst vote derived from the mean of the two individual votes.

Other information

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