GENERAL PATHOLOGY
cod. 08707

Academic year 2022/23
3° year of course - First semester
Professor
- Ovidio BUSSOLATI - Martina CHIU - Bianca Maria ROTOLI - Roberto SALA
Academic discipline
Patologia generale (MED/04)
Field
Patologia generale e molecolare, immunopatologia, fisiopatologia generale, microbiologia e parassitologia
Type of training activity
Characterising
60 hours
of face-to-face activities
6 credits
hub: PARMA
course unit
in ITALIAN

Integrated course unit module: GENERAL PATHOLOGY AND HISTORY OF MEDICINE

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.

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Prerequisites

Adequate 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 Module will concern:
- Endocrine and nutritional 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) CELL PATHOLOGY
- Cell damage: reversible vs. irreversible
- Protein misfolding: ER stress and UPR
- Intracellular accumulations: protein accumulation, steatosis, lysosomal diseases
- Extracellular accumulations: amyloidosis
- Oxidative stress and the cell response
- Biotransformations
- 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
- Hemostatic mechanisms
- Hemorrhagic disease
- DIC
- 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
- SIRS
- Autoinflammatory diseases
- Mechanisms of tissue repair
- Derangements of tissue repair mechanisms
- Fibrosis
- Atherosclerosis

4) PATHOPHYSIOLOGY
-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
* Porphirias and jaundice
* Iron and copper. Iron deficiency and overload.
- Pathophysiology of nutrition.
*Obesity
* PEM
* Hypovitaminosis and hypervitaminosis

Bibliography

- Kumar, Abbas, Fausto, Aster (Eds). Robbins e Cotran – Pathologic Basis of Disease - Elsevier Masson, 2021

- Mainiero, Misasi, Sorice (Eds.) Patologia Generale e Fisiopatologia Generale,
2 vol. VI edizione
Piccin, 2019.

Altucci, Berton, Moncharmont, Stivala (Eds.)
Patologia e Fisiopatologia Generale, 2 vol.
Ildeson-Gnocchi, 2018

Additional references will be suggested during the lectures.

Teaching methods

Lessons will be on site in compliance with safety standards, provided that further instructions on the ongoing health emergency are not implemented.
Lectures will be interactive and will be carried on through a dialogue between the teacher and the students. Examples of true-life situations and clinical cases will be also provided so as to raise the interest of the students.
Supporting didactic material will be available on the specific, student-reserved platform (Elly) and will include slide presentations and audio-video aids.
Slide consultation will be necessary but NOT sufficient for students preparation.

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 the oral examination of the Integrated Course.
For further information see the Integrated Course.
In case of the persistence of the health emergency, the exams will be conducted remotely, as follows:
remote oral questions, through the Teams platform (guide http://selma.unipr.it/).
Students with SLD / BSE must first contact Le Eli-che: support for students with disabilities, D.S.A., B.E.S. (https://sea.unipr.it/it/servizi/le-eli-che-supporto-studenti-con-disabilita-dsa-bes)

Other information

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