Scribd Logo
Upload

Welcome to Scribd!

  • 35 views

    0102 - Adaptation, Injury and Cell Death

    Uploaded by

    cipriano2
    This document discusses cell adaptation, injury, and death. It describes how cells can undergo reversible or irreversible damage depending on the degree of aggression. Irreversible damage leads to cell death through either necrosis or apoptosis. Necrosis is unregulated cell death caused by intense injury that damages mitochondria and cell membranes. Apoptosis is a regulated form of cell suicide that occurs through mitochondrial or receptor pathways and involves cell shrinkage and nuclear fragmentation without inflammation. The document compares the key differences between necrosis and apoptosis.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd

    0102 - Adaptation, Injury and Cell Death

    Uploaded by

    cipriano2
    35 views16 pages
    This document discusses cell adaptation, injury, and death. It describes how cells can undergo reversible or irreversible damage depending on the degree of aggression. Irreversible damage leads to cell death through either necrosis or apoptosis. Necrosis is unregulated cell death caused by intense injury that damages mitochondria and cell membranes. Apoptosis is a regulated form of cell suicide that occurs through mitochondrial or receptor pathways and involves cell shrinkage and nuclear fragmentation without inflammation. The document compares the key differences between necrosis and apoptosis.

    Copyright

    © © All Rights Reserved

    Available Formats

    PDF, TXT or read online from Scribd

    Did you find this document useful?

    Is this content inappropriate?

    This document discusses cell adaptation, injury, and death. It describes how cells can undergo reversible or irreversible damage depending on the degree of aggression. Irreversible damage leads to cell death through either necrosis or apoptosis. Necrosis is unregulated cell death caused by intense injury that damages mitochondria and cell membranes. Apoptosis is a regulated form of cell suicide that occurs through mitochondrial or receptor pathways and involves cell shrinkage and nuclear fragmentation without inflammation. The document compares the key differences between necrosis and apoptosis.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    35 views16 pages

    0102 - Adaptation, Injury and Cell Death

    Uploaded by

    cipriano2
    This document discusses cell adaptation, injury, and death. It describes how cells can undergo reversible or irreversible damage depending on the degree of aggression. Irreversible damage leads to cell death through either necrosis or apoptosis. Necrosis is unregulated cell death caused by intense injury that damages mitochondria and cell membranes. Apoptosis is a regulated form of cell suicide that occurs through mitochondrial or receptor pathways and involves cell shrinkage and nuclear fragmentation without inflammation. The document compares the key differences between necrosis and apoptosis.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    of 16

    Theme - 2

    Adaptation, injury and cell death

    PATHOPHYSIOLOGY
    Dr. Javier Pereda
    Table of contents
    Introduction
    1- Cell degeneration
    2- Cell adaptation
    3- Irreversible damage
    4- Basic mechanisms of cell damage and death
    5- Irreversible damage: cell death
    6- Necrosis
    7- Apoptosis
    8- Apoptosis and disease
    9- Differences between necrosis and apoptosis

    Prof. J. Pereda
    Introduction

    Normal cells are able to handle normal


    physiological stimuli.

    HOMEOSTASIS

    Prof. J. Pereda
    1- Cell degeneration (I)

    Definition:
     Regressive process in which cells deteriorate with
    changes at different levels.

    Types of cell degeneration


     Hydropic degeneration
    • Decrease of ATP, sodium-potassium pump does not
    work well. Increase of H2O.
     Intracellular accumulation of substances
    • Excessive normal substance • Exogenous substance
    • Abnormal substance
    Prof. J. Pereda
    1- Cell degeneration (II)
     Cause is cell aggression

     Consequence depends on the degree of


    aggression

    1) Reversible damage
    -
    2) Cellular adaptation
    degree of aggression
    (of degeneration) 3) Irreversible damage
    +
    Cell death
    Prof. J. Pereda
    2- Cell adaptation
    Long-term damage Not adaptations:
    Neoplasia
     Not always positive Aplasia

     Changes in size and function


    ATROPHY: HYPERTROPHY:
    decreased size (and function) Increased size (and function)

    NORMAL
    HYPERPLASIA:
    Increased number
    (in proportion to stimuli) METAPLASIA:
    Change in cellular type

    DYSPLASIA
    Disorder in cellular number and type

    Prof. J. Pereda
    3- Irreversible damage
     If the injury is too strong and cell cannot adapt:
    irreversible damage leading to cell death.

    Point of no return

     Death appears as a consequence of cell damage


    mainly by:
    Ischemia (hypoxia), xenobiotics, immunity reactions, genetic
    disorders, nutritional unbalances …

    Prof. J. Pereda
    4- Basic mechanisms of cell damage and death

    1. Deficit in aerobic respiration:


    ATP depletion
    2. Loss of the intracellular calcium
    homeostasis
    3. Generation of reactive oxygen species:
    oxygen free radicals
    4. Alteration in cell permeability

    Prof. J. Pereda
    5- Irreversible damage: cell death

    TYPES OF CELL DEATH

    NECROSIS APOPTOSIS

    Prof. J. Pereda
    6- Necrosis (I)
    It is the most common type of cell death after
    exogenous stimuli. It is characterized by cellular
    disruption, protein denaturalization and organelle
    disruption.
    Cause:
     Intense and fast injury.
    Mechanism:
     Mitochondrial damage.
    –Decrease of energy.
     Membrane disruption.
    –Decrease of osmotic regulation or capacity.

    Prof. J. Pereda
    6- Necrosis (II)
    Types:
    • Liquefactive necrosis
    – No destruction of catalytic enzymes.
    • Coagulative necrosis.
    – Enzymatic denaturalization by acidosis: ischemia.
    • Caseous necrosis.
    – Typical of tuberculosis: white and friable like clumped cheese.
     When a large necrosis appears (limbs…) : gangrene
    – It may be accompanied by an infectious component.
    • Dry gangrene.
    • Wet gangrene. If anaerobics: gas gangrene
    Role in the disease:
    • Crucial role, depends on cellular type.
    • Normally associated with INFLAMMATION.
    • Difficult to treat. Not regulated.

    Prof. J. Pereda
    7- Apoptosis (I)

    Voluntary “cellular suicide” or induced by the


    elimination of non desired cells, occurring in
    embryogenesis, in physiologic and pathologic
    processes. Sometimes cohabit with necrosis.
    It has been named “programmed cell death”

    Cause:
     Irreversible damage leading not to necrosis (so it
    is a less severe aggression).

    Prof. J. Pereda
    7- Apoptosis (II)
    Cellular changes in apoptosis.
    1) Citoplasmatic volume is decreased
    2) Phosphatidilserine is externalized
    3) Zeiosis (or blebbing)

    Apoptotic bodies
    4) Characteristic changes in the nucleus
    a) First is condensed
    b) Then is located peripherally
    c) Finally is fragmented into spheres

    DNA is fragmented in regular sizes


    Destiny phagocytosis
    No release = no inflammation Prof. J. Pereda
    7- Apoptosis (III)
    Mechanisms: B) “death receptors” pathway
    e.g. TNF-α C) Direct pathway
    (granzimes)

    extracellular

    citoplasm
    A) Mitochondrial pathway

    Initiator caspases

    Executioner caspases
    Cytochrome C (most imp. caspase 3)
    - Directly Apoptosis
    - Controlled by BCL-2 execution
    family Protease activation and DFF Prof. J. Pereda
    8- Apoptosis and disease
    Important physiologic role in:
     Embryogenesis
     Cellular renewal
     Physiologic atrophies
     Immune system
    Pathologic role when:
     Apoptosis is increased:
    • Infectious diseases, degenerative diseases,
    ischemia...
     Apoptosis is decreased:
    • Virus, autoimmune diseases, neoplasia…
    great hope…
    Prof. J. Pereda
    9- Differences between necrosis and apoptosis
    Necrosis Apoptosis
    Names Cellular assassination Cellular suicide or
    programmed cell death
    Causes Exogenous Endogenous or exogenous

    Changes Citoplasmatic expansion and Citoplasmatic contraction and


    membrane disruption finally zeiosis (blebbing).
    Nucleus with secondary Nucleus with fragmented
    injuries ADN

    Resolution Inflammatory response NO inflammatory response


    Phagocytic recognition

    Meaning Pathologic Control system


    Pathologic response
    https://www.youtube.com/watch?v=witLM--V2v8
    Prof. J. Pereda

    You might also like