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    01 StudyGuide CellAdaptandNec Latham 0820-22

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    ivankcurry
    Cellular adaptation to stress can occur through hypertrophy, atrophy, or metaplasia. Hypertrophy involves an increase in cell size while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size or number. Metaplasia is the replacement of one adult cell type with another. Necrosis is cell death due to injury and involves the loss of membrane integrity, while apoptosis is programmed cell suicide. Reversible cell injury can progress to irreversible injury and necrosis if ischemia is prolonged. Protein and other accumulations in cells can occur through various pathological processes.

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    01 StudyGuide CellAdaptandNec Latham 0820-22

    Uploaded by

    ivankcurry
    93 views8 pages
    Cellular adaptation to stress can occur through hypertrophy, atrophy, or metaplasia. Hypertrophy involves an increase in cell size while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size or number. Metaplasia is the replacement of one adult cell type with another. Necrosis is cell death due to injury and involves the loss of membrane integrity, while apoptosis is programmed cell suicide. Reversible cell injury can progress to irreversible injury and necrosis if ischemia is prolonged. Protein and other accumulations in cells can occur through various pathological processes.

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    Cellular adaptation to stress can occur through hypertrophy, atrophy, or metaplasia. Hypertrophy involves an increase in cell size while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size or number. Metaplasia is the replacement of one adult cell type with another. Necrosis is cell death due to injury and involves the loss of membrane integrity, while apoptosis is programmed cell suicide. Reversible cell injury can progress to irreversible injury and necrosis if ischemia is prolonged. Protein and other accumulations in cells can occur through various pathological processes.

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    93 views8 pages

    01 StudyGuide CellAdaptandNec Latham 0820-22

    Uploaded by

    ivankcurry
    Cellular adaptation to stress can occur through hypertrophy, atrophy, or metaplasia. Hypertrophy involves an increase in cell size while hyperplasia is an increase in cell number. Atrophy is a decrease in cell size or number. Metaplasia is the replacement of one adult cell type with another. Necrosis is cell death due to injury and involves the loss of membrane integrity, while apoptosis is programmed cell suicide. Reversible cell injury can progress to irreversible injury and necrosis if ischemia is prolonged. Protein and other accumulations in cells can occur through various pathological processes.

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    Path 1: Cell Adaptation and Necrosis

    Aug 20 and Aug 22, 2012, Professor Latham


    Accommodations: Hypertrophy, Atrophy, and Metaplasia
    Hypertrophy: Increase

    HYPERTROPHY: Increase in Organ Size


    Example

    Cellular
    Hypertrophy
    (SIZE)

    Phys or Path

    Process

    Pathologic: HTN
    increase resistance LV
    grows to compensate

    1) growth factors and vasoconstrictive agents contractile


    proteins cells get bigger
    2) genetic changes fetal
    isoforms efficient chromatin
    duplicates but doesnt divide 4N

    Gross

    Micro

    Normal: 1.5 cm thick


    LV

    -Box car nuclei: large


    blueish rectangles filled
    with chromatin

    Path: super thick LV!

    -Large myocytes

    LVH:
    Left Ventricular
    Hypertrophy

    Physiologic: normal
    response when
    breastfeeding

    prolactin Proliferation of
    glandular epithelium acinar cells
    increase cell #

    Breasts enlarge

    More epithelial acinar cells

    Lactating Breast

    Hyperplasia
    (NUMBER)

    Pathologic: adenofibromatous hyperplasia

    5-a-reductase increases
    increase metabolism of
    testosterone to DHT
    Increase in glandular tissue
    and stroma

    -Nodules
    -Compressed urethra,
    so Bladder
    hypertrophies to
    push urine

    -Infolded
    -Increase in cell number

    BPH:
    Benign Prostate
    Hypertrophy

    Rule:

    Hyperplasia happens in mitotically active cells


    Cellular Hypertrophy only happens in post-mitotic cells - cardiac and skeletal muscle

    Atrophy: Decrease
    1. Lack of nutrients
    2. Ubiquitin-proteosome degradation - ubiquitin tags a cell for degradation by ligase
    3. Autophagy: cell reduces its size reduces the nutrients it demands reduces the nutrients it receives
    bud off vesicles of ER collect cellular proteins brings it to the lysosome degradation
    Residual bodies: un-digestible proteins that form in the cytoplasm due to lipofuscin granules
    Lipofuscin: insoluble gold-brown deposit made of oxidized lipid-protein complex bound to
    ceroid; wear and tear pigment because it shows the cell has undergone metabolic stress

    ATROPHY: Decrease in Organ Size

    Cellular
    Atrophy
    (SIZE)

    Cell Death
    (NUMBER)

    Both
    (SIZE AND
    NUMBER)

    Example

    Process

    Gross

    Micro

    Skeletal
    Muscle
    Atrophy

    1)Disuse
    2)Denervation
    3)Decrease in functional
    need
    4)Decrease in resources
    to support it

    Lose bulk

    Smaller size
    of skeletal
    myocytes

    Cerebral
    Atrophy

    Alzheimers and dementia


    decrease in number of
    neurons and supporting
    tissue

    Atrophy
    of the
    Heart

    Autophagy (see above)


    Decrease in both myocyte
    size and cell number

    -Deep sulci, narrow gyri


    -ventricles expand
    hydrocephalus ex
    vacuo
    -Deep brown color due
    to accumulation of
    lipofuscin in cardiac
    myocytes

    See golden
    brown
    lipofuscin
    granules

    -Reduced epicardial fat

    Metaplasia: Change
    o One adult differentiated cell type is replaced by another
    o Occurs through local effects, usually chronic injury
    o Change is potentially reversible if the stress is removed
    and it is pre-cancerous
    o increases risk of cancer
    o Ex: bronchial mucosa (pseudostrat ciliated columnar w
    goblet) Smoking squamous cell metaplasia
    Question: Kidneys from a 65 y.o. man with HTN.
    o R kidney hypertrophied, L kidney atrophied
    o Hyperplasia and Cell Death most likely change in NUMBER, not CELL SIZE
    Why hyperplasia? Kidneys are mitotically active!
    Why Cell Death? Decreased blood and nutrients will kill the cells
    o L kidney atrophies due to a pathology (deficient blood supply), so the R
    hypertrophies as a compensatory means to meet demands of the renal system

    Pic

    Accumulations Cellular and Tissue


    Example

    LIPOFUSCIN

    Residual
    bodies
    resulting from
    Autophagy

    What is it

    Process

    Pathology

    Lipid-protein
    complex bound to
    ceroid

    Autophagy un-digestible proteins form in cytoplasm


    sign of wear and tear and metabolic stress

    Gold-brown deposits

    Reversible
    Fat accumulation in a
    non-adipocyte
    no membrane
    around the fat
    Hepatic
    Steatosis

    Fat accumulation in a
    non-adipocyte

    FAT

    Deranged fatty acid metabolism increase


    triglyceride stores fat accumulation
    (1) Alcohol, Diabetes, and Starvation
    increase Free FAs
    (2) Alcohol increase esterification of FA to TG
    (3) Alcohol, Hypoxia, and Toxins
    decrease oxidation of FAs
    (4) Alcohol, Toxins, Protein Malnutrition decrease
    apoprotein synthes

    Gross:
    -Yellow
    -Greasy
    -3x Weight -Round Edges
    Micro:
    Microvesicular central nucleus,
    many small globs of fat
    Macrovesicular: displaced nucleus,
    one large glob of fat

    Macrophages phagocytize necrotic cell membrane debris


    that contain lots of phospholipids foamy lipid-filled
    macrophages accumulate Crystals of cholesterol
    accumulate in plaque in thickened intima of arteries

    Foamy macrophages
    Cholesterol Crystals

    Macrophage
    Fat
    Accumulation

    ADIPOCYTE sticks between cells


    in normally fat free organs
    (DIFFERENT than other two)

    aging and atrophy lipocytes between


    myocytes from epicardium to endocardium

    See adipocyte fat cells between


    myocytes, normally in R atrium

    Fatty
    Infiltration of
    Heart

    Iron normally stored


    in hepatocyte
    (ferritin) and marrow
    (macrophages)
    IRON

    Hemosiderin
    Ferric Oxide

    Primary: genetic mutation increases iron absorption from gut


    Secondary: (1) Other causes of increased iron absorption
    (2) hemorrhage hemoglobin catabolism
    RBBCs release iron hemosiderin accumulate
    in macrophages

    granular gold-brown
    deposit

    Hyalinization of
    arterioles due to
    protein
    accumulation
    Hyaline
    Arteriosclerosis

    HTN

    endothelial damage protein leaks from circulation


    to vessel walls
    protein accumulation in AFF ONLY

    Diabetes proteins glycosylate proteins get trapped in


    BOTH AFF AND EFF arterioles and glomeruli of kidney

    DM in Kidney
    small 80-100 A
    filamentous
    degraded protein w
    Ig light chains

    Amorphous, homogenous,
    glassy, pink appearance
    Thick walls
    Can be nodular

    HTN in Artery
    Chronic injury degenerated proteins to betasheets accumulate in heart and vessel wall
    Diabetes

    Hyaline
    Change due
    to Amyloid

    amyloid or collagen in pancreas


    islets of Langerhans

    Amorphous, homogenous, glassy, pink


    appearance

    PROTEIN

    Collagen Scar in
    Myocardium

    Amorphous, homogenous, glassy, pink


    appearance
    Myocytes drop out

    Healed myocardial Infarct

    Hyaline Scar

    Mallory Bodies
    Intracellular
    Hyaline
    Change

    Russell Bodies

    Obesity and alcohol hyaline change in


    hepatocytes
    Chronic Infection Immunoglobulins
    accumulate hyaline droplets in plasma cells

    Mallory
    Excess Calcium in
    circulation

    Dense red within a hepatocyte


    Glassy pink hyaline in plasma cell

    Russell
    Micro: Deep purple, dense, slightly
    fragmented deposits
    Gross: Firm, gritty, sandpaper

    Messed up calcium metabolism

    Metastatic
    Calcification

    Renal

    CALCIUM
    Calcium deposits at
    injured cell sites

    Lung
    Deep purple, dense, slightly
    fragmented, grainy deposits in
    damaged tissue
    Gross: aorta cracks like an egg

    activated phosphatases bind Ca ions to


    phospholipid membrane of injured cells

    Dystrophic
    Calcification

    Gross:

    Coronary Artery:

    Aorta:

    Reversible Cell Injury


    10-15 mins: Ischemia (lack of oxygen) Ox Phosph in Mitoch ATP Energy Prod --> 3 paths
    1. Na-K-ATPase Na + water + Ca enter the cell
    (Cloudy) Swelling
    Ca precip in mitochondria
    Myelin figures
    Blebs
    2. Glycolysis anaerobic support Glycogen, lactic acid pH chromatin clumping
    3. Detachment of ribosomes from RER protein synth and fat deposits
    15-60 mins: If oxygen not returned, lose plasma membrane integrity:
    1. Lose phospholipids membrane holes enzymes leak into circulation CPK and LDH mark cell
    2. Cytoskeleton breaks down cell loses shape and breaks down
    3. Free radicals generated lipid peroxidation breakdown
    4. Mitochondria Ca deposits internal membrane integrity destroyed ox phosph can no longer take place
    5. Release of lysosomal enzymes protein degradation cell and nucleus fall apart
    4-8 hours: cell death

    Cloudy Swelling: Early Reversible Cell Injury


    o Kidney: PCT cells more vulnerable to oxygen
    Micro: Swelling, pallor of cytoplasm, chromatin clumping
    Gross:swollen, pale, parboiled, bulging cortex
    o Hydropic degeneration: vacuoles of water within the injured cell
    sign of more severe cloudy swelling on its way to irreversible
    Differentiate from fat vacuoles:
    Small vacuoles that look empty
    around central vein of liver (end of Ox supply)

    Irreversible Cell Injury and Death: Necrosis and Apoptosis


    Apoptosis vs. Necrosis
    Death by
    Cause

    Necrosis
    Injury
    Disruption of homeostasis

    Energy

    Depleted

    Cell
    membrane

    Dissolves, releasing proteases and


    inflammatory substances,
    damaging neighboring tissues

    Apoptosis
    Suicide
    Death by Design, programmed
    Dependent, requires new RNA and
    protein synth
    Intact. Phagocytosis of sub-cell
    fragments removes cell without
    exposing neighboring tissues

    Cell
    physically

    Explodes

    Shrinks

    Distribution

    large area of tissue induced by


    injury

    one cell or small cluster of cells


    induced by signaling

    Apoptosis
    Step

    What Happens

    Notes

    Picture

    (1) Extrinsic Pathway: signaling by death ligands TNF


    and FAS activate initiator caspases
    -One cell labeled
    for death
    (1) Induction
    and Signaling

    -Enzyme
    activation and
    synthesis

    (2)Intrinsic Pathway: radiation, toxins, radicals,


    Growth factor
    mitochondria permeable DNA
    damage p53 tries to repair damage but its too
    overwhelmed cytochrome C apoptosis
    (3) Cytotoxic T cells: virally infected cells
    activate execution caspases

    directly

    (2)
    Execution

    Executioner
    Caspases activate
    proteases and
    endonucleases

    -Caspases: family of proteases with cysteine at active


    cite that cleave proteins at aspartic acid sites
    - executioner caspases 3, 6 activated = point of no
    return
    -Eosinophilic cell condenses, dark nucleus fragments

    (3)
    Degeneration

    Formation of
    Apoptotic bodies

    Small membrane bound subunits of cytosol with a bit


    of nuclear content

    (4)
    Phagocytosis

    Apoptotic bodies
    cleared by
    Macrophages

    Apoptotic bodies have ligands for macrophage binding


    and uptake

    Above: Characteristic of an apoptotic cell in


    a man with chronic Hep C viral infection
    (1) Densely Eosinophilic
    (2) Isolated cells are affected, not
    everything around it
    (3) Viral

    Necrosis Irreversible Change Indicators:


    o Mitochondrial Changes: severe swelling, cristae gone, Ca precipitate, electron-densities appear
    o Nuclear Changes indicating irreversible cell death:
    Nuclear change

    Whats happening?

    What does it look like?

    Pyknosis

    Balling up of chromatin

    opaque round basophilic density in


    cloudy swelling cells

    Karyorrhexis

    fragmentation of nucleus
    into debris

    Karyolysis

    Picture

    Small, dense basophilic fragments (dust)


    in cells that have begun to lose
    architecture

    Dissolution of nuclear fragments by DNAse

    Nuc

    No

    Arch

    Look

    Cause

    Effect

    Mechanism

    Example

    Uniform flat
    pink quality

    Sudden Ischemia
    (NOT gradual no
    time to adapt)

    Infarct

    so sudden that
    proteolytic enzymes
    that normally
    dissolve the tissue
    are denatured

    Gangrene: extremity
    infarction, many tissue planes
    Dry: No infection
    Wet: Infection, superimposed
    liquifactive necrosis

    Yes

    No

    Debris, fluid, no
    parenchyma

    Abcess:
    Infection neutrophi
    l influx
    Brain: Hypoxia

    Abscess: pus
    Brain: Cyst

    Complete lysis of cell

    Abscess: Neutrophil enzymes


    digest
    Brain: Mech unknown

    No?

    -no membrane
    on fat cells
    -dark dystrophic
    calcification
    (white on gross
    exam)

    Acute
    Pancreatitis

    Injured acinars Panc


    lipase leaks
    digest
    lipocyte membrane
    TG to FA precip Ca
    fat saponification

    Acute Pancreatitis

    Coagulative

    No

    Liquifactive

    No?

    Enzymatic /
    Fat

    Alcohol,
    Gallstones

    No

    Caseous

    No

    -Gross: cottage
    cheese debris
    -Micro: pink
    amorphous
    granular debris
    -macrophages
    and/or fibrosis

    Mycobacteria
    Tuberculosis

    Not empty, but


    no arch. Between
    Coag and Liqu

    Granuloma apoptosis
    necrosis of
    macrophages at center
    TNF and CD8 activation of
    Fas Fas

    Mycobacteria Tuberculosis

    see margin of macrophage


    -Eosinophilic (red)
    amorphous fibrin
    strands in vessel walls
    -varying Sm Musc
    Fragmentation
    -neutrophils (inflamm)
    Fibrinoid

    Injury to Arterial Walls:


    (1) Injury to vascular
    walls (immune complex)
    (2) Hypertension
    endothelium damage

    Vessel wall injury


    leak protein and
    fibrin from circ
    entrapped in wall

    Vascularitis:
    entrapped immune
    complexes activate
    complement
    vascular injury

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