HPlec 2 Cell Injury-necrosis

7/31/2019 HPlec 2 Cell Injury-necrosis

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Lecture 2


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OVERVIEW


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Cell Injury: an alteration in cellstructure or functioning that occurs whencells are . . .

severely stressed that they are nolonger able to adapt

exposed to inherently damaging agents

suffer from intrinsic abnormalities


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General Principles of Cell Injury

The cellular response to injuriousstimuli depends on:

_______________________________.

The consequences of cell injury depend

on:_______________________________.


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Causes of Cell Injury

Hypoxia

Physical Agents

Chemicals and DrugsMicrobiologic Agents

Immunologic Reactions

Genetic Defects

Nutritional Imbalances

Aging


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PREDISPOSING FACTORS:

AgeGender

Nutritional status

GenesEnvironment

Pre-existing conditions

Immune-compromised


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Morphologic Alterationsin Cell Injury


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Reversible Cell Injury:1. Generalized swelling of the cell and its

organelles

2. Blebbing of the plasma membrane3. Detachment of ribosomes from ER

4. Clumping of nuclear chromatin


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Irreversible Cell Injury:1. Increase swelling of cell

2. Swelling and disruption of lysosomes

3. Presence of large amorphous densities inswollen mitochondria

4. Profound nuclear changes:

-Pyknosis

-Karyorrhexis

-Karyolysis


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NUCLEAR CHANGES


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APOPTOSIS

Limits neoplasmic growth

does NOT stimulate inflammatoryresponse

Apoptotic stimuli:

1. Cell membrane damage

2. Mitochondrial damage

3. DNA damage

4. Viral infection

5. Immune-mediated attack


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Feature Necrosis ApoptosisCell size Enlarged (swelling) Reduced (shrinkage)

Nucleus Pyknosis

karyorrhexiskaryolysis

Fragmentation into

nucleosome-size fragments

Plasmamembrane

Disrupted Intact; altered structure,especially orientation of

lipids

Cellularcontents

Enzymaticdigestion; may leakout of cell

Intact; may be released inapoptotic bodies

Adjacentinflammation

Frequent No

Physiologic orpathologic role

Invariablypathologic(irreversible)

Often physiologic, eliminatesunwanted cells; may bepathologic after DNA


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TYPES OF NECROSIS: According to. . .

BASIC MORPHOLOGIC CHANGES :

Coagulation Necrosis

Liquefaction Necrosis

Fat NecrosisCaseous Necrosis

Gangrenous Necrosis

ACCORDING TO LOCATION OR EXTENT:

Focal

Massive


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rapid coagulation of cytoplasm

Denaturation and precipitation of

cellular proteins

usually encountered when arterial

supply is cut off, producing Anemic orIschemic Infarction.

COAGULATIONNECROSIS


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Enzymatic digestion of the cell by its own

hydrolytic lysosomal enzymes

Necrosis of tissues rich in liquid usually

induces them to absorb fluid, leading tosoftening & liquefaction

LIQUEFACTION NECROSIS


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destruction of adipose tissue

Pancreatic lipase is released intosurrounding tissues splitting neutral fats intofatty acids & glycerol, w/o affecting cellmembrane.

FA combine w/ Ca to form soaps w/c are

replaced by phosphoric acid & carbonicacids, forming white precipitates of CaPO4& CaCO3.

FAT NECROSIS


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CASEOUS NECROSIS

characterized by a collection of soft,whitish-gray debris resembling clumpedcheese

cells are converted into a granular,friable mass of coagulated CHON & fat,with total loss of cell detail.


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GANGRENOUSNECROSIS

massive tissue death due to ischemia &superimposed bacterial infection.

combination of coagulation &liquefaction necrosis.

2 TYPES:

A. DRY GANGRENEB. WET GANGRENE


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DRY GANGRENE

Sterile necrosis Due to arterial occlusion, producing

ischemic necrosis & consequentdesiccation/ mummification.

sharp demarcation line

tissue discoloration is due to release

of blood pigments


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WET GANGRENE

venous occlusion

Bactl. infxn. + ischemic injury= putrefaction.

Offensive, foul-odored fluid

liquefaction necrosis & toxemia

no sharp line of demarcation

HPlec 2 Cell Injury-necrosis

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