Электронная библиотечная система КОНСУЛЬТАНТ СТУДЕНТА
ЭБС "КОНСУЛЬТАНТ СТУДЕНТА"
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2. CELL INJURY AND CELL DEATH

Questions to prepare for classes and examination

1. The notion of cell injury. Causes of cell injury.

2. Typical forms of cell injury.

    a) Dystrophy.

    b) Dysplasia.

    c) Derangement of the subcellular structures and components.

    d) Necrosis, apoptosis.

3. General mechanisms of cell injury.

    a) Derangements of the energy supply and utilization.

    b) Loss of the integritiy of the cellular membranes.

    c) Ionic and water dysbalance.

    d) Changes in the cellular genome or disorders of its realization.

    e) Disorders of intracellular regulatory mechanisms.

4. Three main etiopathogenic variants of cell injury.

I. Ischemic and hypoxic injury.

II. Free radical-induced injury.

III. Toxic injury.

5. Reversible and irreversible ischemic/hypoxic cell injury.

6. Ischemia/reperfusion injury.

7. Antioxidative system of the cell.

8. Components of apoptosis.

    a) Signaling pathways that initiate apoptosis.

    b) Control and integration.

    c) Execution phase.

    d) Removal of dead cells by phagocytosis.

9. Adaptive mechanisms operating during cell injury.

N 6

A technician of the chemical laboratory was not careful working with a toxic volatile chemical. He dropped a flask containing the toxic substance and smashed it. Before he left the room, he had inhaled noxious vapours of the chemical. Two days later he was admitted to hospital with the following complaints: malaise, somnolence, headache, nausea, back pains, blood in the urine. Blood analysis: erythrocytes 2.7x1012/L, Hb 80 g/L, platelets 120x109/L, leukocytes 3.1x109/L; compensated acidosis (metabolic and renal). The resuls of the special blood biochemistry analysis: an increased concentration of free fatty acid, lipid hydroperoxides, and adenosinephosphate; an elevated total creatinephosphate kinase (CPK) activity and potassium content.