Basic Science of Cardiovascular Disease: tissue cells and signalling MED5542
- Academic Session: 2021-22
- School: Cardiovascular and Medical Sciences
- Credits: 20
- Level: Level 5 (SCQF level 11)
- Typically Offered: Semester 2
- Available to Visiting Students: No
- Available to Erasmus Students: No
This course will provide students with an in-depth and critical knowledge of the basic science underlying cardiovascular disease and provide an insight into the complex pathways and signalling processes that mediate the disease in cells, tissues and animal models.
Lectures and tutorials throughout semester 2.
Written exam (50%)
2500-3000 word essay (50%)
Main Assessment In: April/May
To provide the students with a comprehensive overview of the cardiovascular system such as the anatomy and physiology of the heart and blood vessels. In addition, the students will acquire an in-depth knowledge of the cellular, molecular and signalling processes underlying cardiovascular disease ranging from well-established mechanisms to insights into novel pathophysiology of disease. The students will also acquire a critical understanding of current research tools and techniques, models systems available for study and their limitations.
Intended Learning Outcomes of Course
By the end of this course students will be able to:
■ Undertake an in-depth and critical appraisal of the cellular and molecular pathways underlying normal cardiovascular physiology.
■ Discuss critically, and in depth, novel molecular and signalling pathways underlying cardiovascular disease with reference to the primary literature.
■ Contrast the causes and consequences of the pathophysiology pathways involved across a range of cardiovascular diseases.
■ Demonstrate a broad knowledge of the research methods and models used in basic science and applied research for investigating the cardiovascular system.
Minimum Requirement for Award of Credits
Students must submit at least 75% by weight of the components (including examinations) of the course's summative assessment.