Molecular mechanisms of cellular adaptation and alterations of cell growth: epigenetic components and role of growth and transcription factors.
Cellular damage: general biological mechanisms (mitochondrial damage, ATP depletion, production of reactive oxygen species, loss of calcium homeostasis, loss of selective membrane permeability. Reversible and irreversible damage. Ischemia and hypoxia. Vacuolar, hydropic and turbid degeneration.
Autophagy, necrosis and apoptosis. Opportunistic double role of autophagy as a survival and as a death mechanisms. Physiopathologic aspects, mechanisms and morphology of the autophagic process.
Necrosis: mechanisms of autolysis and herolysis, nuclear alterations. Principal morphologic types of necrosis (coagulative, colliquative, caseous, fibrinoid, steatonecrosis). The consequences of the necrotic process. Apoptosis: genes that regulate apoptosis (pro- and anti-apoptotic). Hypotheses on the evolutionary origins of the apoptotic process and relationships with mitochondrial symbiosis at the dawn of eukaryotes. Molecular mechanisms: the caspases cascade (intrinsic and extrinsic pathway). Morphological characteristics and pathophysiological significance of apoptosis.
Intracellular accumulations: lipids (fatty degeneration and steatosis), proteins, glycogen and pigments. Pathological calcifications.
The physiological control of cell proliferation and its alterations. Cell cycle and its regulation. Positive and negative regulation. Action of growth factors. Cell membrane receptors. Mechanisms of transduction of the mitogenic signals. Reversible and irreversible alterations of cell proliferation and differentiation.
Hypertrophy, hyperplasia, atrophy, aplasia, hypoplasia, metaplasia, dysplasia, anaplasia. Examples of hypertrophy and hyperplasia and their physiologic and/or pathologic roles: hypertrophy of skeletal and cardia muscle, hypertrophy of the myometrium, hyperplasia and hypertrophy of the adipose tissue, hyperplasia of the hemopoietic tissue in chronic hypoxia and in chronic forms of malaria, hyperplasia and hypertrophy of the glandular components of the breast in lactation. Hyperplasia, dysplasia and anaplasia in tumorigenesis.
