(GenPath) Cellular Injury

7/31/2019 (GenPath) Cellular Injury

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GENERAL PATHOLOGYGENERAL PATHOLOGY

A discipline involving basic science andA discipline involving basic science and

clinical practiceclinical practice

Devoted to the study ofDevoted to the study of andand

changes in the cells, tissues,changes in the cells, tissues,

and organs that underlie diseaseand organs that underlie disease


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GENERAL PATHOLOGYGENERAL PATHOLOGY


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DIVISIONS OF PATHOLOGYDIVISIONS OF PATHOLOGY

GENERAL PATHOLOGYGENERAL PATHOLOGY Concerned with the basic reactions of anConcerned with the basic reactions of an

injured cell to various nonspecific stimuliinjured cell to various nonspecific stimuli

SYSTEMIC PATHOLOGYSYSTEMIC PATHOLOGY

Studies and examines the specificStudies and examines the specificresponses of special cells and tissues andresponses of special cells and tissues andorgans to more or less well defined stimuliorgans to more or less well defined stimuli


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FOUR ASPECTS OF DISEASEFOUR ASPECTS OF DISEASE

PROCESSPROCESS

ETIOLOGY/CAUSEETIOLOGY/CAUSE

PATHOGENESISPATHOGENESIS

MORPHOLOGIC CHANGESMORPHOLOGIC CHANGES CLINICAL SIGNIFICANCECLINICAL SIGNIFICANCE

These form the basic CORE of theThese form the basic CORE of thestudy of PATHOLOGYstudy of PATHOLOGY


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ETIOLOGYETIOLOGY

Refers to CAUSES of the diseaseRefers to CAUSES of the disease

Two major classes of etiologic factors:Two major classes of etiologic factors:

intrinsic or geneticintrinsic or g

enetic;;

acquiredacq

uired

one etiologic agent for one disease is noone etiologic agent for one disease is no

longer significantlonger significant

MULTIFACTORIAL.MULTIFACTORIAL.


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PATHOGENESISPATHOGENESIS

The sequence of events in the response ofThe sequence of events in the response of

the cells and tissues or organs to thethe cells and tissues or organs to the

causecause

From the beginning of the initialFrom the beginning of the initial

stimulation to the ultimate expression orstimulation to the ultimate expression or

manifestation of the diseasemanifestation of the disease


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MORPHOLOGIC CHANGESMORPHOLOGIC CHANGES

These encompass the structural andThese encompass the structural and

functional alterations in cells or tissuesfunctional alterations in cells or tissues

that are either characteristic of thethat are either characteristic of the

disease or diagnostic of the etiologicdisease or diagnostic of the etiologic

processprocess


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MORPHOLOGIC CHANGESMORPHOLOGIC CHANGES

The practice of diagnostic pathology isThe practice of diagnostic pathology is

devoted to the identification of thedevoted to the identification of the

nature and progression of the diseasenature and progression of the disease

by studying theby studying the morphologic changes

in tissues and chemical alterations inin tissues and chemical alterations in

patients.patients.


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FUNCTIONAL DERANGEMENTSFUNCTIONAL DERANGEMENTS

Refer also to the CLINICALRefer also to the CLINICALMANIFESTATIONSMANIFESTATIONS

The nature of the morphologic changesThe nature of the morphologic changes

and their distribution in the body influenceand their distribution in the body influenceand affect the normal function of the cells,and affect the normal function of the cells,tissues and organstissues and organs

These influence the clinical manifestationsThese influence the clinical manifestations(signs and symptoms), course, and(signs and symptoms), course, andprognosis of the diseaseprognosis of the disease


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CELLULAR INJURY ANDADAPTATIONS

Normally, the cell is in a homeostatic,steady state,able to handle normalphysiologic stimulation

But with more excessive physiologicstresses or with pathologic stimuli, the cellwill undergo a series of events orphenomena called CELLULAR

ADAPTATIONS, inorder to achieve analtered, steady state, thus preserving itsviability.


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Remember

Whether specific types of stress induce

an adaptive response, reversible injury

or cell death depends on the nature andseverityof the stress and on many

variables relating to the intrinsic state of

the cell itself.


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Four intracellular systemsFour intracellular systems

that are prone to injury.that are prone to injury.

Maintenance of the integrity of theMaintenance of the integrity of the

cell membranecell membrane

Aerobic respiration/oxidativeAerobic respiration/oxidative

phosphorylation and ATP production -phosphorylation and ATP production -

mitochondrionmitochondrion

Synthesis of enzymic and structuralSynthesis of enzymic and structural

proteins proteins RNARNA

Preservation of the genetic apparatusPreservation of the genetic apparatus

-- DNADNA


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Considerations to remember about

cell injury..

Morphologic changes of cell injury

becomes apparent only after some

critical biochemical system within thecells has been deranged.

Injury at one locus leads to wide

ranging secondary effects


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Further considerations about cell

injury.

Reactions of the cell to the

stimuli/injury depend on the

type, duration, and severityofthe stimuli

Consequences of cell injury

depend also on the type, state,

and adaptabilityof the cell.


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BROAD CATEGORIES OF CAUSES

OF CELL INJURY

HYPOXIA

PHYSICAL AGENTS

CHEMICAL AGENTS/DRUGSINFECTIOUS AGENTS

IMMUNOLOGIC REACTIONS

GENETIC PROBLEMS NUTRITIONAL IMBALANCE


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HYPOXIA/ISCHEMIC INJURY

Main point of attack: AEROBIC OXIDATIVE

RESPIRATION

Common causes:

Impediment of blood flow by arteriosclerosisor thrombi

Inadequate oxygenation of the blood due to

cardio-respiratory failure Loss of oxygen carrying capacity e.g. anemia

and carbon monoxide poisoning


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HYPOXIA/ISCHEMIC INJURY

ACUTE CELLULAR SWELLING OR EDEMA one of

the earliest and most common manifestation of

ischemic injury

This is caused by impairment of cell volume

regulation by the plasma membrane

2 to ATP depletion => sodium will accumulate

intracellularly with diffusion of potassium out of

the cell

2 also to increased intracellular osmotic load due

to accumulation of catabolites


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HYPOXIA

Hypoxia affects oxidative phosphorylation

Hence, synthesis of vital ATP is critical

membrane damage, which may lead to lethal

cell injury CALCIUMis an important mediator of the

biochemical alterations leading to cell death


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HYPOXIC CHANGES

Cellular swelling would result whenever cellsare incapable of maintaining ionic and fluidhomeostasis

Hydropic change or vacuolar degeneration,for there are small, clear vacuoles that appearwithin the cytoplasm, which came fromdistended or pinched off in sequesteredsegments of endoplasmic reticulum

When this affects all cells in an organ, theorgan grossly has some pallor, with increasedturgor, and increased weight


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MORPHOLOGY OF INJUREDMORPHOLOGY OF INJURED

CELLS.CELLS. A. Ultrastructural ChangesA. Ultrastructural Changes

In the plasma membraneIn the plasma membrane

Cellular swellingCellular swelling Formation of cytoplasmic blebsFormation of cytoplasmic blebs

Blunting and distortion of microvilliBlunting and distortion of microvilli

Appearance of myelin figures (whichAppearance of myelin figures (whichmaybe deposited intracytoplasmic ormaybe deposited intracytoplasmic or

extracellularly)extracellularly)


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CELLS.CELLS. In the mitochondriaIn the mitochondria

Swelling, rarefaction, appearance ofSwelling, rarefaction, appearance of

amorphous densitiesamorphous densities

The endoplasmic reticulum becomesThe endoplasmic reticulum becomes

dilated with detachment anddilated with detachment and

disaggregation of polysomes intodisaggregation of polysomes into

monosomesmonosomes

Nucleolar alterations andNucleolar alterations and

disaggregation of granular anddisaggregation of granular and

fibrillar elementsfibrillar elements


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CELLS.CELLS. B. Light Microscopy PatternsB. Light Microscopy Patterns

Can be reversible injuries (in theCan be reversible injuries (in the

form ofform ofCELLULAR SWELLING ORCELLULAR SWELLING OR

FATTY CHANGE) or cell deathFATTY CHANGE) or cell death

(NECROSIS)(NECROSIS)

Fatty change- encountered inFatty change- encountered in

cells dependent on involved incells dependent on involved in

fat metabolism such as thefat metabolism such as the

myocardial cellsmyocardial cells, and the, and the


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CELLULAR INJURY

REVERSIBLE ANDREVERSIBLE AND


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REVERSIBLE ANDREVERSIBLE AND

IRREVERSIBLE INJURYIRREVERSIBLE INJURY

CONSEQUENCECONSEQUENCE


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IRREVERSIBLE INJURYIRREVERSIBLE INJURY

Two critical events that consistentlyTwo critical events that consistently

characterize IRREVERSIBILITY:characterize IRREVERSIBILITY:

Inability to reverseInability to reverse mitochondrialmitochondrial

dysfunctiondysfunction

Profound disturbance in theProfound disturbance in the

membrane functionmembrane function


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Possible mechanisms of MembranePossible mechanisms of Membrane

DamageDamage

Progressive Loss of PhospholipidsProgressive Loss of Phospholipids

Due to activation of endogenousDue to activation of endogenous

phospholipases, stimulated byphospholipases, stimulated by

increased cytosolic calciumincreased cytosolic calcium

Due to also to decreased synthesis,Due to also to decreased synthesis,

the steps of which are ATPthe steps of which are ATP

dependentdependent


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Cytoskeletal abnormalitiesCytoskeletal abnormalities

Due to increased proteasesDue to increased proteases

Results in the detachment of the cellResults in the detachment of the cellmembrane from the cytoskeleton,membrane from the cytoskeleton,

rendering the membrane susceptiblerendering the membrane susceptible

to stretching and possible ruptureto stretching and possible rupture

Possible Mechanisms of MembranePossible Mechanisms of Membrane

DamageDamage


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Presence/Formation of toxic oxygenPresence/Formation of toxic oxygenradicalsradicals

Free radical production is increasedFree radical production is increased

during reperfusion=>Reperfusionduring reperfusion=>ReperfusionInjuryInjury

Radicals are produced by theRadicals are produced by the

polymorphonuclears that infiltratepolymorphonuclears that infiltratethe site of ischemia duringthe site of ischemia duringreperfusionreperfusion

Possible Mechanisms of MembranePossible Mechanisms of Membrane

DamageDamage


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Possible Mechanism of MembranePossible Mechanism of Membrane

DamageDamage

Presence of lipid breakdown productsPresence of lipid breakdown products

These have detergent-like effect onThese have detergent-like effect on

the membranethe membrane

Accumulation of phospholipidAccumulation of phospholipid

catabolic products duringcatabolic products during

degradationdegradation

In the form of unesterified FFA, acylIn the form of unesterified FFA, acyl

carnitine, and lysophospholipidscarnitine, and lysophospholipids


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My inspiration.My inspiration.


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OXYGEN DERIVED RADICALS

SUPEROXIDE

Generated either directly duringautooxidation in the mitochondrion, or

enzymatically by cytoplasmic enzymeslike the oxidases and P-450

O2 oxidase = O2-

Once formed, O2- can be inactivated bythe enzyme SUPEROXIDE DISMUTASE(SOD) to form H2O2


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HYDROGEN PEROXIDE

Produced either by the dismutation ofO2- or by oxidases present in theperoxisomes (catalase-containingorganelles)

O2- + O2- + 2H+ SOD = H2O2

+ O2


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HYDROXYL RADICALS- CAUSED BY:

Hydrolysis of H2O caused by ionizingradiation

Interaction of transitional metals(copper and iron) in Fenton reaction

Through the Haber-Weiss reaction

Eff t f th di l


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Effects of these radicals are onthe MEMBRANE, LIPID

PEROXIDATION, SULHYDRYLBONDS of proteins.

And also on the nucleotides of theDNA.


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SYSTEMS THAT MAY INACTIVATE ORSYSTEMS THAT MAY INACTIVATE OR

TERMINATE THESE RADICALSTERMINATE THESE RADICALS

Antioxidants either endogenous orAntioxidants either endogenous or

exogenousexogenous

Vitamin E, Vitamin C, sulfhydrylVitamin E, Vitamin C, sulfhydryl

containing substance amino acid likecontaining substance amino acid like

cysteine, glutathione, and D-cysteine, glutathione, and D-

penicillamine, ceruloplasmin, andpenicillamine, ceruloplasmin, and

transferrintransferrin


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EnzymesEnzymes

Superoxide dismutase convertsSuperoxide dismutase converts

superoxide to hydrogen peroxidesuperoxide to hydrogen peroxide

Catalase decomposes H2O2Catalase decomposes H2O2

Glutathione peroxide catalyzes theGlutathione peroxide catalyzes the

ability of reduced glutathione to releaseability of reduced glutathione to release

hydrogen from sulfhydroxyl tohydrogen from sulfhydroxyl to

hydroxyl radical or to hydrogenhydroxyl radical or to hydrogen

peroxideperoxide

SYSTEMS THAT MAY INACTIVATE ORSYSTEMS THAT MAY INACTIVATE OR

TERMINATE THESE RADICALSTERMINATE THESE RADICALS


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MICROSCOPIC CHANGES OFMICROSCOPIC CHANGES OF

INJURIESINJURIES

IF DUE TO REVERSIBLE INJURY:IF DUE TO REVERSIBLE INJURY:

IF DUE TO IRREVERSIBLE INJURY:IF DUE TO IRREVERSIBLE INJURY:


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NECROSISNECROSIS

Morphologic changes that follow cellMorphologic changes that follow cell

death in a living tissue or organ resultingdeath in a living tissue or organ resulting

from the degradative action of enzymesfrom the degradative action of enzymes

on the lethally injured cellson the lethally injured cells

Secondary to:Secondary to:

1.1. Enzymic digestion of cellsEnzymic digestion of cells

2.2. Denaturation of proteinsDenaturation of proteins


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NECROSISNECROSIS

Nuclear changes associated with cellNuclear changes associated with cell

death/necrosis :death/necrosis :

Pyknosis Pyknosis nuclear shrinkage with small,nuclear shrinkage with small,

dense, wrinkled chromatin materialdense, wrinkled chromatin materialKaryolysis Karyolysis dissolution of the chromatindissolution of the chromatin

pattern due to hydrolytic action of thepattern due to hydrolytic action of the

DNASES of the lysosomesDNASES of the lysosomes

Karyorrhexis Karyorrhexis break up of thebreak up of thenucleus intonucleus into

many clumpsmany clumps


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APOPTOSISAPOPTOSIS

dropping off process- single or cluster of cellsdropping off process- single or cluster of cellswhich are round or oval masses withwhich are round or oval masses witheosinophilic cytoplasm and dense chromatineosinophilic cytoplasm and dense chromatinpattern become dropped offpattern become dropped off

These represent fragmented cells which areThese represent fragmented cells which aretaken up and degraded by phagocytic cellstaken up and degraded by phagocytic cells

This process is responsible for the destruction ofThis process is responsible for the destruction ofcells during embryogenesis, and for hormone-cells during embryogenesis, and for hormone-

dependent involutiondependent involutionRepresented by Councilman bodies seenRepresented by Councilman bodies seencommonly in liver hepatitis and toxicitycommonly in liver hepatitis and toxicity


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NECROSIS vs APOPTOSISNECROSIS vs APOPTOSIS


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Sequence of events in apoptosisSequence of events in apoptosis

The initial changes consist of nuclearThe initial changes consist of nuclear

chromatin condensation andchromatin condensation and

fragmentationfragmentation

Followed by cytoplasmic budding andFollowed by cytoplasmic budding and

phagocytosis of the extruded apoptoticphagocytosis of the extruded apoptotic

bodiesbodies

Signs of cytoplasmic blebs and digestionSigns of cytoplasmic blebs and digestion

and leakage of cellular componentsand leakage of cellular components

happenhappen


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Necrosis VS ApoptosisNecrosis VS Apoptosis


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TYPES OF NECROSISTYPES OF NECROSIS

COAGULATION NECROSISCOAGULATION NECROSIS

Most common patternMost common pattern

Shows opaque, acidophilicShows opaque, acidophilictombstone cellstombstone cells

Loss of nucleus, BUT WITHLoss of nucleus, BUT WITH

PRESERVATION OF THE BASICPRESERVATION OF THE BASIC

SHAPE AND OUTLINESHAPE AND OUTLINE

Tissue architecture is still recognizedTissue architecture is still recognized


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COAGULATION NECROSISCOAGULATION NECROSIS Seen in the following organs duringSeen in the following organs during

ischemia: KIDNEYS, HEART,ischemia: KIDNEYS, HEART,

ADRENALSADRENALS

2 to denaturation2 to denaturation

COAGULATION NECROSIS OF


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COAGULATION NECROSIS OFCOAGULATION NECROSIS OF

THE HEART TISSUESTHE HEART TISSUES


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LIQUEFACTION NECROSISLIQUEFACTION NECROSIS Occurs when autolysis and heterolysisOccurs when autolysis and heterolysis

prevail over conditions that favorprevail over conditions that favor

denaturationdenaturation 2 to hydrolytic actions of enzymes2 to hydrolytic actions of enzymes Seen in ischemic destruction of brain andSeen in ischemic destruction of brain and

kidney tissues which are converted to akidney tissues which are converted to a

cystic structure filled with cellular debriscystic structure filled with cellular debrisand fluidand fluid hallmark of areas of pasthallmark of areas of pastbacterial infectionbacterial infection

LIQUEFACTION NECROSIS BRAIN
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LIQUEFACTION NECROSIS, BRAIN,LIQUEFACTION NECROSIS, BRAIN,

GROSSGROSS

As this infarct in the brain isAs this infarct in the brain is

organizing and being resolved, theorganizing and being resolved, theliquefactive necrosis leads toliquefactive necrosis leads to

resolution with cystic spaces.resolution with cystic spaces.

LIQUEFACTION NECROSIS OFLIQUEFACTION NECROSIS OF
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LIQUEFACTION NECROSIS OFLIQUEFACTION NECROSIS OF

KIDNEY TISSUE, MICROSCOPICKIDNEY TISSUE, MICROSCOPIC


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CASEATION NECROSISCASEATION NECROSIS Combination of coagulative andCombination of coagulative and

liquefactive necrosisliquefactive necrosis Seen in tuberculous infectionSeen in tuberculous infection Microscopically: cells are not totallyMicroscopically: cells are not totally

liquefied nor are their outlines preservedliquefied nor are their outlines preservedcreating a distinctive amorphous granularcreating a distinctive amorphous granulardebris and is enclosed within adebris and is enclosed within a

granulomatous inflammatory wallgranulomatous inflammatory wall Grossly: soft, friable, whitish gray cheesyGrossly: soft, friable, whitish gray cheesy

surfacesurface


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Tuberculous Infection of the LungsTuberculous Infection of the Lungs


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Caseation Necrosis, Lung TissueCaseation Necrosis, Lung Tissue


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FAT NECROSISFAT NECROSIS SEEN AMONG ADIPOSE TISSUESSEEN AMONG ADIPOSE TISSUES Due to lipaseswhich catalyze theDue to lipaseswhich catalyze the

decomposition of triglycerides thatdecomposition of triglycerides thatleak from adjacent damaged adiposeleak from adjacent damaged adiposecells to produce free fatty acidscells to produce free fatty acids

which in return then becomewhich in return then becomecomplex with calciumcomplex with calcium formformCALCIUM SOAPSCALCIUM SOAPS

FAT NECROSIS MESENTERYFAT NECROSIS MESENTERY


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FAT NECROSIS, MESENTERY,FAT NECROSIS, MESENTERY,

GROSSGROSS

FAT NECROSIS PANCREASFAT NECROSIS PANCREAS


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FAT NECROSIS, PANCREAS,FAT NECROSIS, PANCREAS,

GROSSGROSS

FAT NECROSISFAT NECROSIS
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FAT NECROSIS,FAT NECROSIS,

PANCREAS,MICROSCOPICPANCREAS,MICROSCOPIC

Microscopically, fat necrosis adjacent to pancreas isseen here. There are some remaining steatocytes at

the left which are not necrotic. The necrotic fat cellsat the right have vague cellular outlines, have losttheir peripheral nuclei, and their cytoplasm hasbecome a pink amorphous mass of necroticmaterial.

FAT NECROSIS BREASTFAT NECROSIS BREAST
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FAT NECROSIS, BREAST,FAT NECROSIS, BREAST,

MICROSCOPICMICROSCOPIC

In this view of fat necrosis at high magnification, someIn this view of fat necrosis at high magnification, some

lipid-laden macrophages are seen between the necroticlipid-laden macrophages are seen between the necroticadipose tissue cells. The most common etiology is trauma,adipose tissue cells. The most common etiology is trauma,but fat necrosis of the breast can also occur with surgerybut fat necrosis of the breast can also occur with surgeryand radiation therapy.and radiation therapy.
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GANGRENOUS NECROSISGANGRENOUS NECROSIS Applied to the lower extremities which hasApplied to the lower extremities which has

lost its blood supplylost its blood supply

Coagulative necrosis modified byCoagulative necrosis modified byliquefaction action of the bacteria andliquefaction action of the bacteria andWBCsWBCs

If coagulative process predominates: DRYIf coagulative process predominates: DRY

GANGRENEGANGRENE If liquefactive process predominates: WETIf liquefactive process predominates: WET

GANGRENEGANGRENE
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DRY GANGRENE, GROSSDRY GANGRENE, GROSS

This is gangrene, or necrosis ofmany tissues in aThis is gangrene, or necrosis ofmany tissues in abody part. In this case, the toes were involved in abody part. In this case, the toes were involved in afrostbite injury. This is an example of "dry"frostbite injury. This is an example of "dry"gangrene in which there is mainly coagulativegangrene in which there is mainly coagulative

necrosis from the anoxic injury.necrosis from the anoxic injury.
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WET GANGRENE, GROSSWET GANGRENE, GROSS

This is gangrene ofthe lower extremity. In this case theThis is gangrene ofthe lower extremity. In this case theterm "wet" gangrene is more applicable because of theterm "wet" gangrene is more applicable because of theliquefactive component from superimposed infection inliquefactive component from superimposed infection inaddition to the coagulative necrosis from loss of bloodaddition to the coagulative necrosis from loss of bloodsupply. This patient had diabetes mellitus.supply. This patient had diabetes mellitus.

GANGRENOUS NECROSISGANGRENOUS NECROSIS
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GANGRENOUS NECROSIS,GANGRENOUS NECROSIS,

MICROSCOPICMICROSCOPIC

Gangrenous necrosis involves the tissues of aGangrenous necrosis involves the tissues of abody part. The inflammation seen here isbody part. The inflammation seen here isextending beneath the skin of a toe to involve softextending beneath the skin of a toe to involve softtissue (fat and connective tissue) and bone.tissue (fat and connective tissue) and bone.Because multiple tissues are non-viable,Because multiple tissues are non-viable,amputation of such areas is necessary.amputation of such areas is necessary.
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OTHER FORMS OF INJURYOTHER FORMS OF INJURY

Chemicals induce cell injury by one ofChemicals induce cell injury by one oftwo general mechanisms:two general mechanisms:

1.1. Chemicals can actChemicals can act directlydirectlyby cmbiningby cmbiningwith some critical molecular componentwith some critical molecular componentor organelleor organelle

2.2. Chemicals need to be converted toChemicals need to be converted toreactive toxicreactive toxic metabolites or by productmetabolites or by productwhich will act on target cellswhich will act on target cells


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CHEMICAL INJURYCHEMICAL INJURY

Carbon tetrachloride poisoning prototypeCarbon tetrachloride poisoning prototype

of chemical injuryof chemical injury

Toxic effect is due to conversion of CCl4Toxic effect is due to conversion of CCl4

by P-450 to the highly reactive toxic freeby P-450 to the highly reactive toxic freeradical CCl3radical CCl3

CCL3 initiates lipid peroxidationCCL3 initiates lipid peroxidation

membrane damagemembrane damage


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OTHER FORMS OF INJURYOTHER FORMS OF INJURY

CELLULAR CHANGES ARE SECONDARY TO: 1.CELLULAR CHANGES ARE SECONDARY TO: 1.

CYTOLYTIC/CYTOPATHIC EFFECTCYTOLYTIC/CYTOPATHIC EFFECT

2. Oncogenic effect stimulation of host cell2. Oncogenic effect stimulation of host cellreplication and may produce tumorsreplication and may produce tumors

DIRECT CYTOPATHIC EFFECTS HAVE HIGHDIRECT CYTOPATHIC EFFECTS HAVE HIGH

DEGREE OF SPECIFICITY BECAUSE OFDEGREE OF SPECIFICITY BECAUSE OF

MEMBRANE RECEPTORS ON HOST CELLSMEMBRANE RECEPTORS ON HOST CELLS


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SUNSET over Salt Lake City


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GOOD DAY!!!!

Documents

(GenPath) Cellular Injury