week 5 degenerations.pdf

Upload: otaibynaif

Post on 02-Jun-2018

219 views

Category:

Documents


0 download

TRANSCRIPT

  • 8/10/2019 WEEK 5 Degenerations.pdf

    1/25

  • 8/10/2019 WEEK 5 Degenerations.pdf

    2/25

    Degenerations

    PresentedBy

    Ahmed El-Rashedy

    Professor & Previous Headof Pathology DepartmentAl-Azhar University

  • 8/10/2019 WEEK 5 Degenerations.pdf

    3/25

    Degeneration

    Def.: An abnormal disturbance of metabolism associated

    with reversible morphological changes on exposure of aliving tissue or cells to non-lethalirritants.

    Types of irritants:

    1. Hypoxia.

    2. Chemical agents: Air pollutants & hydrocarbons.

    Hypertonic solutions.

    Poisons: Cyanide, Mercury, Arsenic.

    Insecticides.

    Fungicides.

    Industrial vapors or fibers (Asbestos, silica).

    Drugs: Narcotics.

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    4/25

    Types of irritants:

    3. Physical agents:

    Mechanical trauma or crush injury.

    Extremes of temperature (excess heat or severe coldness).

    Irradiation whether ionizing (cobalt, gamma) or non-

    ionizing (X-, ultraviolet) rays.

    Electric shock.

    4. M icro-organisms(viable agents):

    Bacteria.

    Viruses.

    Fungi.

    Parasites.

    Rickettsia.

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    5/25

    Types of irritants:

    5. Immunologic disorders:

    Hypersensitivity to a foreign protein (injectable,

    ingestible, inhaler).

    Hypersensitivity to a self- antigen as extrusion of

    eye lens protein or sperm head protein in obstructedepididymis.

    6. Genetic diseases:

    Sickle cell anemia: production of Hb-S instead ofHb-A.

    Downs syndrome (Mongolism): aberration in

    chromosome no; 21.

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    6/25

    Types of irritants:

    7. Nutr i tional disorders:

    Hyper- or Hypo- vitaminosis A & D. Protein-Calorie deficiency: Marasmic baby

    (Kwashiorkor' s disease).

    Fat-rich diet intake: Obesity & atherosclerosis.Sites of degeneration:

    Parenchymatous organs because they contain highly

    active & energy producing cells. These organs are:1. Liver (H epatocytes).

    2. Kidney (Renal tubular cells).

    3. Heart ( Cardiac muscle cells).

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    7/25

    Cloudy Swelling

    (Hydropic Degeneration=Ballooning

    Degeneration=Vacuolar Degeneration)Def.: An abnormal accumulation of water inside the living cell.

    Pathogenesis: Hypoxia (or ischemia) Early mitochondrial

    condensation Mitochondrial swelling lack in energy supply

    causing failure of sodium /potassium pump Retention ofsodium inside the cell Increase of intracellular osmotic pressure

    with imbibation of water from extracellular compartment

    producing droplets of water within the cytoplasm (fine granules

    representing swollen mitochondria = Cloudy swell ing). Then, large

    vacuoles (representing distended endoplasmic reticulum)

    accumulate within the cell Clear cytoplasm (Hydropic

    degeneration).

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    8/25

    Pathology:

    A) Gross: The affected organ becomes:

    1. Color: Pale.

    2. Size: Enlarged (Swollen).3. Weight: Increased (Heavy).

    4. Cut surface: Bulges over the capsule.

    B) L/M (in kidney):

    1. Renal tubules: Size: Swollen &enlarged.

    L ining cell s:

    Shape: Pyramidal (normally cubical).

    Cytoplasm: Pale, granular or clear.

    Lumen of tubules:

    Star-shaped or obliterated (normally patent, oval

    & regular).

    2. Capil laries in-between the swoll en tubules:

    Compressed.

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

  • 8/10/2019 WEEK 5 Degenerations.pdf

    9/25

    B) E/M (in kidney):1. Changes in cell membrane: Cellular swelling. Loosening of intercellular attachments

    (Desmosomes). Formation of myelin fingers. Blunting & distortion of microvilli.2. Changes in cytoplasmic organelles: Mitochondrial swelling with indistinct

    cristae, double short basal infoldingmembrane with bizarre mitochondria,rupture & calcification.

    Deformed Golgi zone.

    Lysosomal swelling. Dilated rough endoplasmic reticulum. Detached free ribosomes & protein

    synthesis. Cytoplasmic droplets & clear vacuoles

    of water.

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    10/25

    Electron micrograph showing:

    (a) Proximal convoluted tubule cell

    with focal loss Brush Border (BB),

    numerous apical vesicles (V),numerous lysosome (L) deformed

    Golgi zone (G), nucleus (N) with

    marginal heterochromatin in dense

    cytoplasm.

    (b) Swollen round mitochondria (M)

    with indistinct cristae, vesicles (V)

    and secondary lysosome (L).

    (c) Apoptotic cell with nucleus have

    invaginated nuclear envelope andheterochromatin condensation.

    (d) Double short basal infolding

    membrane (arrows) with bizarre

    mitochondria (M)

    Prof. Dr. Ahmed Elrashedy

    f h d El h d

  • 8/10/2019 WEEK 5 Degenerations.pdf

    11/25

    Electron micrograph showing:

    (a) Part of tubule cell reveals normal

    Brush Border (BB), small lysosome

    (L), nucleus (N) and large elongated

    mitochondria (M) in-between

    extended basal infolding (arrows).

    (b) Details intact Brush Border (BB)

    and well developed vesicles (V).

    (c) Details part of nucleus (N) with

    peripheral heterochromatin,

    lysosome (L), homogenousmitochondria (M) with normal

    cristae, double membrane basal

    infolding (arrow) & free ribosome

    (R).

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

  • 8/10/2019 WEEK 5 Degenerations.pdf

    12/25

    Fatty changes (Fatty Degeneration)

    Def.: An abnormal accumulation of fat within the parenchymatous cells.

    Sites:

    1. Liver.2. Heart & muscles.

    3. Kidney.

    Pathogenesis:

    Excess accumulation of triglycerides within the liver due to one of the

    followings:

    1. Excess free fatty acid entry into the liver.

    2. Excess FFA synthesis from acetate.

    3. Increased FFA esterification into triglycerides (through

    glycerophosphate).

    4. Decreased FFA oxidation.

    5. Decreased apoprotein synthesis (Apoprotein normally conjugates

    with triglycerides to form lipoprotein).

    6. Impaired lipoprotein secretion from the liver.

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    13/25

    Causes of Fatty liver:

    1. Chronic alcoholism (Hepatotoxicmethyl alcohol drinking).

    2. Protein malnutrition (starvation).3. Diabetes mellitus.

    4. Obesity.5. Hepatotoxic chemicals: as carbon

    tetrachloride& phosphorus.

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

  • 8/10/2019 WEEK 5 Degenerations.pdf

    14/25

    Pathology:

    I) Liver:

    Gross:

    1. Mild:No abnormality.2. SevereFatty liver:

    Size: Enlarged.

    Color: Yellowish.

    Consistency: Soft& greasy.

    Outer Surface: Smooth.

    Border: Round.

    Differential Diagnosis:

    Amyloid liver :

    Size: Enlarged. Color: whitish.

    Consistency: Firm & waxy.

    Outer Surface: Smooth.

    Border: Sharp.

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

  • 8/10/2019 WEEK 5 Degenerations.pdf

    15/25

    L/M:

    1. Early:

    Small fat vacuoles in the cytoplasm nearthe nucleus.

    2. Later :

    Union of these vacuoles to give clear

    spaces displacing the nucleus into the

    periphery against the cell membrane

    (Signet r ing appearance).

    3. Late:

    Rupture of the fat-filled hepatocytes with

    union of the fat globules together giving

    fatty cysts.

    Prof. Dr. Ahmed Elrashedy

    Prof Dr Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    16/25

    II) Heart: (Tabby Cat Str iations) or (Thrush

    Breast):

    Occurs in case of chronic or severe anemia(due to a prolonged moderate ischemia).

    Gross:

    Size: Enlarged.

    Color & Pattern: Alternating layers of

    yellowishfatty myocardial fibers & dark red-

    brown congested uninvolved fibers.

    Consistency: Soft.

    Outer Surface: Smooth.

    L/M:

    Similar to those detected in the liver.

    Prof. Dr. Ahmed Elrashedy

    Prof Dr Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    17/25

    Identification of fatty globules:

    1. Hematoxylin & Eosin stain: Clear vacuoles

    (dissolution of fat by xylene used in preparing

    the slide).2. Sudan IV & Red oil stains: Bright-red globules.

    3. Osmic acid & Sudan black : Black fatty

    vacuoles.

    N.B.:Fatty ingrowth or stromal fatty

    infiltration: An abnormal accumulationof fat within the stromal C.T. cells.It occurs in obesity.

    Sites:1. Pancreas: Fat in the C.T. septa of the

    pancreatic lobules.2. Heart: Fat in the C.T. in-between the

    muscle bundles.

    Prof. Dr. Ahmed Elrashedy

    Prof Dr Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    18/25

    Hyaline Change (Hyaline Degeneration)Def.: Abnormal accumulation of Proteinaceous

    homogenous structureless translucent materialinside the living cell.

    Cause: Disturbance in the protein metabolisminside the cell.

    Chemical Nature:Protein-Phospholipid Complex.

    Examples:1. Kidney:Hyaline droplets within the proximal

    renal convoluted tubular cells.2. Liver: Hyaline droplets within the

    hepatocytes in alcoholic cirrhosis (Mallory

    bodies).3. Brain: Cytoplasmic round, oval or bullet shaped inclusion viral particles called Negribodies in the neurons.

    4. Plasma cells: Hyaline spherical droplets

    withinthe plasma cells calledRussell bodies.

    Prof. Dr. Ahmed Elrashedy

    Prof Dr Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    19/25

    5. Diaphragm & Rectus abdominis muscle:

    (Zenkers Degeneration)

    Cause:

    A complication of typhoid fever.Pathology:

    A) Gross:The involved muscle is:

    1. Friable.

    2. Pale.3. May rupture giving minute hemorrhages.

    B) L /M :

    I ) Early:

    1. Swollen homogenous pink muscle fibers.2. Loss of striations.

    I I ) Late:

    Necrosis with loss of the cellular details

    with fragmentation or lysis of their nucleus.

    Zenkers

    Degeneration

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    20/25

    Prof Dr Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    21/25

    Damage of F ibers

    1. F ibrosis

    Def.: Excess formation of mature collagen fibers.

    Examples:

    1. Nodal fibrosis: in L.N. draining an area of

    chronic infection.

    2. Bilharzial liver fibrosis.

    3. Liver cirrhosis.4. Pulmonary fibrosis.

    2. Elastosis

    Def.: Formation of elastic fibers.

    Examples:1. Normal Skin following a prolonged exposure

    to ultraviolet light.

    2. Skin cancer following a prolonged sunlight

    exposure.

    Bilharzial liver fibrosis

    Pulmonary fibrosis

    ( Masson trichrome)

    Elastosis

    Prof. Dr. Ahmed Elrashedy

    Pro . Dr. A me E ras e y

  • 8/10/2019 WEEK 5 Degenerations.pdf

    22/25

    3. Hyalinosis (Extracellular H yaline Change)Def.: Abnormal extracellular accumulation of hyaline

    material.

    Pathogenesis:

    A. C.T. Hyalinosis: Fusion of the collagen fibers.

    B. Vascular Hyalinosis: Leakage of plasma proteins

    through the damaged endothelium into the interior of

    arterial wall.

    Examples:I) C.T. hyalinosis:

    1) Hyalinosis of collagen fibers in old scar.

    2) Hyalinosis of splenic capsule & trabeculae in congestive

    splenomegaly.

    3) Neoplastic Hyalinosis: e.g. as secondary change infibromyoma (leiomyoma).

    II) Vascular hyalinosis:

    1. Arteriolar wall hyalinosis: in renal benign HPT & in

    diabetes.

    2. Glomerular hyalinosis: in chronic glomerulonephritis.

    . D . m E y

    Prof Dr Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    23/25

    4. F ibrinoid Necrosis

    Def.: It is a descriptive process including:

    1) Swelling of the collagen fibers.

    2) Fragmentation of these fibers.

    3) Degeneration of the collagen fibers (increased

    eosinophilia).

    Examples:1. Collagen Diseases: as

    Systemic Lupus (SLE).

    Systemic sclerosis.

    Rheumatoid arthritis.

    Polyarteritis nodosa (PN).

    2. Malignant Hypertension.

    3. Rheumatic endocarditis (Ashoff Nodules).

    Ashoff Nodules

    Prof. Dr. Ahmed Elrashedy

    Prof. Dr. Ahmed Elrashedy

  • 8/10/2019 WEEK 5 Degenerations.pdf

    24/25

    Damage of Matr ix

    Myxomatous Degeneration

    Def.: Pathological condition characterized by increase in

    the ground substance + degeneration of the stromal

    fibers.

    Pathology:

    Gross:

    Soft, jelly-like tissue resembling

    Wharton jelly of the umbilical cord.L/M:

    Star or stellate-shaped branching

    cells interlacing with each other found in a faint blue

    mucopolysaccharide matrix.

    Example: Myxomatous degeneration occurring as a 2ry change in

    fibromyoma.

    D.D.: Myxedema:

    Only an increase in the ground substance appearing as

    homogenous blue material.

    y

  • 8/10/2019 WEEK 5 Degenerations.pdf

    25/25

    Prof. Dr. Ahmed Elrashedy