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Last update: MUDr. Jan Pláteník, Ph.D. (04.09.2013)
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Last update: MUDr. Jan Pláteník, Ph.D. (11.11.2014)
Disorders of acid-base balance. Reactive oxygen and nitrogen species in the body, the antioxidant defence. Ageing. Non-enzymatic glycations, insulinoresistance, metabolic syndrome. Inflammation. Disorders of protein folding and their clinical consequences. Prions. Death of heart and neuronal cell: ischemia/reperfusion, excitotoxicity and neurodegeneration. |
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Last update: MUDr. Lenka Fialová, CSc. (26.09.2019)
Pláteník J. et al.: Pathobiochemistry of metabolic disorders, inner environment and limits of its maintenance, Karolinum, Prague (release scheduled for the end of 2019). Lecture presentation [online], [cit. 2019-01-02]. Retrieved from: https://ulbld.lf1.cuni.cz/en/lecture-presentations-pbch |
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Last update: MUDr. Jan Pláteník, Ph.D. (01.12.2020)
The subjects ends with an examination. A student can take an examination in a subject for three times as a maximum, i.e. the student is entitled to two re-examinations, and no extraordinary terms beyond that are allowed. In case of the second re-examination in a mandatory or elective subject the student is examined by a committee consisting of at least two examiners. If the internal faculty regulations (Article 19, Paragraph 2), permit repeated registration for the subject, the examination by the committee shall be applied only to the second re-examination in case of the repeatedly registered subject. By this a right of the faculty to enable examination by the committee in other cases, if implied by the internal regulations (Article 19, Paragraph 2), is not affected. If a student fails to answer a partial question at the exam, it is sufficient as a cause for termination of examination and classification of the whole exam as ‘failed’. |
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Last update: MUDr. Lenka Fialová, CSc. (05.11.2020)
1. Metabolic acidosis, its causes and consequences. 2. Metabolic alkalosis, its causes and consequences. 3. Combined disorders of acid-base equilibrium. 4. Relations between acid-base equilibrium and concentration of ions. Changes in ionogram in disorders of acid-base equilibrium. Changes in acid-base equilibrium in disorders of ion metabolism. 5. Principal reactive oxygen and nitrogen species: properties, reactions, main sources in the body, role in pathogenesis. 6. Physiological role of reactive oxygen species in metabolism: tissue hormones, phagocyte weapons, hydroxylases, redox signaling. 7. Lipid peroxidation as an example of oxidative damage to biomolecules. Significance of transition metals (iron, copper) in pathobiochemistry of reactive oxygen species. 8. Antioxidant defense of human body. 9. Difference between average life expectancy and maximum lifespan. Biochemical basis of ageing, sources of errors, role of genes. 10. Ageing at the level of cells and tissues: mitochondrial dysfunction, consequences of DNA damage, role of telomeres. 11. Ageing at the level of cells and tissues: cellular senescence, alteration of epigenome, collapse of proteostasis, inflammaging. 12. Theories that explain evolution of ageing. Effect of caloric restriction. Hormesis. 13. Metabolic syndrome and insulin resistance: characteristics, causes, consequences, possible therapeutic applications. 14. Formation of AGEs, interaction AGE-RAGE, potential mechanisms to reduce formation/effect of AGEs. 15. Mechanisms of hyperglycemia-induced tissue damage. 16. Carbonyl stress, its role in pathogenesis of long-term diabetic complications, atherosclerosis and renal failure. 17. Pathobiochemistry of inflammation – acute phase reactants, immunoglobulins. 18. Pathobiochemistry of inflammation – mediators of inflammation, alarmins. 19. Pathobiochemistry of inflammation – significance od complement and its activation. 20. Pathobiochemistry of inflammation – metabolic changes during inflammation, stress starvation. 21. Rules of protein folding. 22. Role of chaperones, proteasomes and lysosomes in the cell. Endoplasmic reticulum stress. 23. Mechanism of prion diseases. 24. Origins of pathological conformation of proteins and examples of clinical consequences. 25. Metabolic alterations in myocardium during anoxia and ischemia: limits of energy production, catabolism of purine nucleotides. 26. Metabolic alterations in myocardium during anoxia and ischemia: mitochondrial ATPase, myoglobin and NO, acidosis, ion gradients. 27. Reoxygenation and reperfusion injury. 28. Excitotoxicity in pathogenesis of CNS disorders.
At the oral examination student chooses by chance a doublet of questions. |
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