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.
Prerequisites
mandatory previous exams are decided by the Consiglio di Corso di laurea magistrale.
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.
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 (defects of nutrient transporters, cystic fibrosis)
* Hormones and receptors
* Inborn errors of metabolism (
Hyperphenylalaninemias, Urea cycle defects, Hyperomocysteinemia; Glycogenoses, Fructose intolerance, Galactosemia; Disorders of Fatty Acid Oxydation
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
- Osmotic and Volume disorders: * pathophysiology of water and sodium
disorders
* Pathogensis of edema
* Hypovolemia and shock
* Hypernatremia and hyponatremia.
* Disorders of potassium homeostasis: hyperpotassemia and hypopotassemia.
* Acid-base
disorders: acidosis and alkalosis.
* Disorders of calcium, phosphorus and magnesium.
-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.
*Obesity
* PEM
* Hypovitaminosis and hypervitaminosis
Bibliography
- Kumar, Abbas, Fausto, Aster (Eds). Robbins e Cotran – Pathologic Basis of Disease - 10 ed. Elsevier Masson, 2021
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.
- 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 nutrition.
*Obesity
* PEM
* Hypovitaminosis and hypervitaminosis
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.
Students with SLD / BSE must first contact the UNIPR CAI center.
The final summative evaluation will consist in an oral examination.
The oral examination will consist of 2 questions/student (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 evaluation 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.
The final vote will be decided jointly by the examiners. The Committee 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.
Full marks with laude will be reserved to students exhibiting, together with an
overall evaluation of 30/30, good communication skills and capability of autonomous in depth-analysis of the subject.
Other information
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