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    CELLULAR

    PATHOLOGICAL

    PROCESSES

    (DYSTROPHY, APOPTOSIS,

    NECROSIS)

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    Cellular typical processes

    1. Dystrophy;

    2. Apoptosis;

    3. Necrosis.

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    Dystrophy

    One of the manifestations ofmetabolic derangements in cells

    is the intracellular accumulation

    of abnormal amounts of varioussubstances.

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    Dystrophy

    typical cellular pathologicprocess caused by metabolic

    disturbance of general orcellular homeostasis,

    manifested by functional and

    structural changes of the cell

    internal environment.

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    Classification of dystrophy

    1. Protein dystrophy;

    2. Lipid (fatty) dystrophy;

    3. Carbohydrates dystrophy.

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    According to degree of cell

    damage, dystrophy can be:

    predominantly with functional

    disturbances;

    functional disturbances associatedwith obvious structural

    modifications;

    reversible;

    irreversible.

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    In function of provenience

    dystrophies are classified in: congenitaldystrophy,

    acquireddystrophies

    In function of metabolic imbalance

    exists protein, lipid, glycolic,mineral dystrophies.

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    According to metabolic imbalance

    dystrophy can have:

    univalent character(with

    derangement one of protein, lipid,

    glycolic, hydric or mineralmetabolism);

    polyvalent character(with

    simultaneous derangement of fewsubstances metabolism).

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    In function of dystrophic range ofdisorders dystrophies can be:

    General (comprise the majority of

    organisms tissues); Local(be evident predominantly at

    organ level).

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    The substances such proteins,

    fatty or carbohydrates mayaccumulate either transientlyor

    permanently, and they may be

    harmless to the cells, but on

    occasion they are severely toxic.

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    Etiology and pathogenesis

    of dystrophy

    1. A normal endogenous substance is

    produced at a normal or increasedrate, but the rate of metabolism is

    inadequateto remove it.

    .

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    E.g.

    - fatty change in the liver becauseof intracellular accumulation of

    triglyceride;

    - reabsorption protein droplets in

    renal tubules because of

    increased leakage of

    protein from the glomerulus.

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    2.A normal or abnormal endogenous

    substance accumulates because of

    genetic or acquireddefects in the

    metabolism, packaging,

    transport,

    secretion of these substances.

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    E.g.

    alpha1-antitrypsin deficiency, inwhich a single amino acid

    substitution in the enzyme results

    in defects in protein folding and accumulation of the enzyme in the

    endoplasmic reticulum

    of the liver in the form of globular

    eosinophilic inclusions.

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    3. An abnormal exogenous

    substance is depositedand

    accumulates

    because the cell has

    neither the enzymatic machinery

    to degrade the substance nor the

    ability to transport it to othersites.

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    E.g. Accumulations of carbon

    particles and suchnon- metabolizable chemicals

    as silicaparticles.

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    4. Heredity

    - the main cause of congenital

    dystrophies, lead to enzymatic

    disorders enzymopathies defect

    or lack of cell enzymes.

    e.g.

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    Deep deficiency in catabolic

    enzyme substrate (i.e. congenital

    lack of glucoso-6-phosphatase

    enzyme lead to impossibility of

    glycogenolysis and excessiveaccumulations of glycogen in cells.

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    4. Exogenous factors

    - mechanical,

    - physical,- chemical,

    - biological,

    - cell hypoxia,- energy deficiency,

    - transmembrane and intracellular transport,

    - disturbance of nutritive substances,

    - exocytose deficiency of intracellular

    substances.

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    Dystrophies (exception congenital)

    dont represent nosologic entities,but only syndromesin maladies

    composition.

    e.g. liver dystrophy, kidneysdystrophy , myocardium

    dystrophy.

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    In most normal nontumor cells, the

    number of cells in tissues is

    regulated by balancing

    cell proliferation andcell death.

    Cell death occurs by:

    Necrosis

    Apoptosis

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    APOPTOSIS

    A mechanism of programmed celldeath, marked by:

    shrinkageof the cell,

    condensation of chromatin,

    formation of cytoplasmic blebs,

    fragmentation of the cellintomembrane-bound bodies eliminated

    by phagocytosis.

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    APOPTOSIS

    (programmed cell death)

    It is an active processenergy

    dependent;

    Does not elicit inflammatoryresponse;

    May be physiologic or pathologic.

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    Apoptotic cell removal: shrinking of the cell structures(A)

    condensation and fragmentation of the nuclearchromatin (B and C), separation of nuclear fragments

    and cytoplasmic organelles into apoptotic bodies (D and

    E), and engulfment of apoptotic fragments by phagocytic

    cell (F).

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    Apoptosisis thought to be responsible forseveral normal physiologic processes:

    1. programmed destruction of cells

    during embryonic development;

    2. hormone-dependent involution oftissues;

    3. death of immune cells,

    4. cell death by cytotoxic T cells,

    5. cell death in proliferating cell

    populations.

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    Etiology of apoptosis

    PHYSIOLOGIC causes:

    During embryogenesise.g. removal of

    interdigital webs during embryonic

    development of toes and fingers;

    Hormone-dependente.g. endometrial

    cell loss in menstruation;

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    PATHOLOGIC causes:

    Irradiated tissues;

    Cell death induced by cytotoxic T-lymphocytes;

    Viral infections e.g. viral hepatitis;

    Cell death in tumors.

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    Mechanisms of apoptosis

    There are two mechanisms of

    apoptosis:

    Extrinsic pathway Intrinsic pathway

    M h i f t i

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    Mechanisms of apoptosis The extrinsic pathwayis

    activated by signals suchas Fas ligand(FasL) that,

    on binding to the Fas

    receptor, form a death-inducing complexby

    joining the Fas-associated

    death domain (FADD) tothe death domain of the

    Fas receptor.

    M h i f i

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    Mechanisms of apoptosis

    The intrinsic pathway(mitochondrion-induced

    pathway) is activated by

    signals, such as reactive

    oxygen species (ROS) and

    DNA damage, that induce

    the release of cytochrome

    Cfrom mitochondria into

    the cytoplasm.

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    The execution phase of both pathways

    is carried out by proteolytic enzymescalled caspases, which are present in

    the cell as procaspasesand are

    activated by cleavage of an inhibitory

    portion of their polypeptide chain.

    Apoptosis (usually) manifestations

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    Apoptosis (usually) manifestations

    Hormone-dependent involutionin the adult,

    such as endometrial cell breakdown duringthe menstrual cycle, ovarian follicular atresia

    in the menopause, the regression of the

    lactating breast after weaning, and prostaticatrophy after castration.

    Cell deletion in proliferating cell populations,such as intestinal crypt epithelia, in order to

    maintain a constant number.

    Elimination of potentially harmful self

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    Elimination of potentially harmful self -

    reactive lymphocytes

    before or after they have completedtheir maturation;

    Cell death induced by cytotoxic T cells, a

    defense mechanism against viruses and

    tumors that serves to eliminate virus

    infected and neoplastic cells.

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    Diseases-apoptosis association

    Apoptosis is linked to many pathologicprocesses and diseases:

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