Tissue and Cellular Injury
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Transcript of Tissue and Cellular Injury
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Chapter 1
Tissue and Cellular Injury
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1. Overview of cellular responses to stress and
noxious stimuli
(1)Cells are active participantsin their
environment, constantly adjustintheir
structure and function to accommodatechanin demands and extracellular stresses.
(!)Cells tend to maintain their intracellular
milieuwithin a fairly narrow raneofphysioloic parameters, that is, they maintain
normal physioloic state (homeostasis).
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(")#hen cells meet physioloic stresses or
patholoic stimuli, they can underoadaptation, achievin a new steady state
and preservin via$ility and function.
(%)The cellular principal adaptive
responses are hyperplasia, hypertrophy,
atrophy, and metaplasia. e. &iceps'pectoral muscle hypertrophy.
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()If the adaptive capa$ility is exceeded or if
the external stress is inherently harmful,cell injurydevelops (i. 1).
(*)#ithin certain limitsinjury is reversible,and cells can return to a sta$le $aseline+
severe or persistent stress results in
irreversible injuryand death of the affectedcells.
http://en.wikipedia.org/wiki/Reactive_oxygen_specieshttp://en.wikipedia.org/wiki/Reactive_oxygen_species -
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i. 1 taes in the cellular response to stress and injurious stimuli
http://en.wikipedia.org/wiki/Oxidative_stresshttp://en.wikipedia.org/wiki/Oxidative_stress -
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(-) Outline(-) Outline
Cellular /daptation
hyperplasia+
hypertrophy+
atrophy+
metaplasia.
Cellular Injury
reversi$le injury
irreversi$le injury
necrosis 0
apoptosis
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Section 1Cellular Adaptation
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Overview: Cellular adaptations tostress
ven under normal conditions, cells mustconstantly adaptto microenvironment
chanes.
/daptations are reversi$le chanesin the
num$er, si2e, phenotype, meta$olic activity,or functionsof cells in response to chanes intheir environment.
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3hysioloic adaptationsusually represent the
cellular responses to normal stimuli $y
hormones or endoenous chemical mediators
e., the hormone4induced enlarement of the
$reast and uterus durin prenancy.
3atholoic adaptationsare responses to stress
that allow cells to modulate their structure and
function and thus escape injury. uchadaptations can ta5e several distinct forms.
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There are numerous types of cellular adaptations
ome involveup or down reulation of specificcellular receptors involved in meta$olism of
certain components.
Others are associated withthe induction ofnew protein synthesis $y the taret cell.
Other adaptationsinvolve a switch $y cells
from producin one type of a family of proteins toanother or mar5edly overproducin one protein.
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Then cellular adaptation is a state that
lies intermediate $etween the normal,
unstressed cell and the injured,
overstressed cell.
Cellular adaptations have many types /trophy( decrease in cell si2e)
6ypertrophy( increase in cell si2e)
6yperplasia( increase in cell num$er)
7etaplasia(chane in cell type)
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mitosishyperplasiahyperplasia
atrophyatrophy
hypertrophyhypertrophy
ORGAN
SI!
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1.6yperplasia
(1) 8efinition Cellular num$er
increasein an
oran'tissue.which may thenwhich may then
have increasedhave increased
volume.volume.
inactive mammary glandLactation breast
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(2) Types:
Physiologic hyperplasiaPhysiologic hyperplasia::Hormonal hyperplasia,
e.. &reast ep. hyperplasia at pu$erty'
prenancy.
Compensatory hyperplasia :9esponse to
deficiency.
e.. 6yperplasia followin surical removal ofpart of liver or one of 5idney+
6yperplasia of the $one marrow in
anemia.
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Pathologic hyperplasiaPathologic hyperplasia caused $ycaused $y
excessive hormonal or rowth factorexcessive hormonal or rowth factor
stimulationstimulation.
e.. Ovarian tumor may produce estroen
and stimulate endometrial hyperplasia+ 3ancreatic islet hyperplasia in infants of
a dia$etic mother (stimulated $y hih
lucose level) +
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:otice
:eoplastic hyperplasia is the total loss ofnormal rowth4differentiation control
mechanism.
6yperplasia is also an important response
of connective tissue cells in wound healin,
in which proliferatin fi$ro$lasts and $lood
vessels aid in repair.
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(") 7echanisms
7ost forms ofpatholoichyperplasia are
due to excessive
hormonal
stimulation or the
effects of GFon
taret cells.
Hyperplasia of prostate gland
Normal prostate gland
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!. 6ypertrophy
(1) 8efinition
/n increase in the
si2e of cells andconse;uently an
increase in the si2e
of the oran.S"eletal muscle
normal
hypertrophy
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(!) Types 6ypertrophy can $e physioloic or patholoic
and is caused either $y specific hormonal
stimulation or $y increased functional demand.
1) 3hysioloic
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3hysioloic hypertrophy of the uterus durin prenancy./,
=ross appearance of a normal uterus (right)and a ravid uterus(left)that was removed for postpartum $leedin. &,mall
spindle4shaped uterine 7Cs from a normal uterus. Compare
this with (C)lare, plump hypertrophied 7Csfrom a ravid
uterus (& and C, same manification).
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!) 3atholoic
Overload, hormone or =
stimulation.
. the cardiac enlarementin hypertension or aortic valve
disease, >left ventricular
hypertrophy7uscle wall is over !cm and
the thic5ness of
interventricular septum
increase+ventually, it is no loner a$le
to compensate for the
increased $urden, and
cardiac failure ensues.
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#yocardial hypertrophy#yocardial hypertrophy
Normal
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(") 7echanisms of hypertrophy(") 7echanisms of hypertrophy
In hypertrophy, there are no new cell, just$ier cell, enlared $y an increased
synthesis of structural proteins and
oranelles.The mechanisms drivin cardiac
hypertrophy involve at least two type of
sinals mechanical triers, such asstretch, and trophic trier, such as
activation of ?4adreneric receptors.
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:otice
Hypertrophy & hyperplasiaare two distinct
processes, $ut they can also occur toether, ando$viously $oth result in an enlared
(hypertrophic)oran.
e.. The lare uterusin prenancy occurs as aconse;uence of estroen4stimulated47C
hypertrophy and hyperplasia.
In contrast, the striated muscle cellscan undero
only hypertrophyin response to increased
demand (overload) $ecause in the adult they
have limited capacity to divide.
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Hyperplasia is characteri2ed $y an increase in cell
num$er.
In pure hypertrophythere are no new cells, just
$ier cells, enlared $y an increased amount ofstructural proteins and oranelles.
Hyperplasia is an adaptive response in cellscapa$le of replication, whereas hypertrophyoccurs
when cells are incapa$le of dividin.
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Normal trophy
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(!) Types
1) 3hysioloice. ain+
shrin5in $reast afterlactation+ uterus after
delivery or in old ae.
!) &lood supply@O!'nutrients@
") Aoss of nerve stimulus
9eflex 'meta$olic activities
reduced. e. nerveinterruptB muscles atrophy
(anterior poliomyelitis ).
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%) ndocrine deficiency7a5e meta$olic activity
reduce. e. pituitary deficiency or hemorrhae or
necrosisB thyroid'adrenals 'onads and enitalorans atrophy.
) Inade;uate nutritione. amine Boran atrophy.
*) 3ressurean enlared tumor can cause atrophy inthe surroundin compressed tissue
-) 8isuse atrophy8emand reduction for nutrition.
e. s5eletal muscle fi$er decrease in num$er as well
as in si2e when a patient is restricted to complete
$ed rest.
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/trophy. &, :ormal $rain of a youn adult./, /trophy of the$rain in an !4year4old male with atherosclerotic disease.
/trophy of the $rain is due to ain and reduced $lood supply.
:ote that loss of $rain su$stance narrows the yri and widens
the sulci.
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Normal myocardial!"## $yocardial trophy!"##
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atrophy of cardiac muscle
lipofuscin
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%&eletal m'scle
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$ressure atrophy of "idney
(pelviectasis of hydronephrosis)
vol'me eight
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(") 7echanisms of atrophy
/trophy represents a reduction in the
structural components of the cell.
This process are varied $ut ultimately
affect the $alance $etween synthesisand
deradation.
8ecreased synthesis, increased
cata$olism, or $oth may cause atrophy.
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:otice
a. /lthouh the atrophic cell si2e ets small and
their function ets low, they are not dead and
reversi$le.
$. /trophy represents a reduction in the structural
components of the cell.The cell contains fewer mitochondria,
endoplasmic reticulum, and increasin in the
num$er of autophaic vacuoles.c. /trophy results from decreased protein synthesis
and increased protein deradation in cells.
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d. The fundamental cellular chanes of atrophy
($oth physioloic and patholoic) are identical.
e. /trophy implies that a new $alance is achieved
$etween cell si2e and diminished $lood supply,
nutrition, or trophic stimulation.
f. ome cellular de$ris within the autophaic
vacuole may resist diestion and persist as
mem$rane $ound residual $odies in the
cytoplasm. #hen present in sufficient amounts,they cause a $rown discoloration to the tissue,
e. myocardium $rown atrophy (Aipofuscin).
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%. 7etaplasia
(1) 8ef. One adult cell type(epithelial or
mesenchymal) is replaced $y another adult
cell type.
It may represent an adaptive su$stitution of
cells that $etter a$le to withstand the
adverse environment.
It is thouht to arise $y enetic
DreproramminD of stem cells.
pithelial and mesenchymal metaplasia.
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(!) Causes
1) Chanes in environment
e.. tones in $ile duct and ureter lead tochane from columnar4ep. into s;uamous
ep.
!) Inflammation e.. In lon ciarettes smo5er, the columnar
ciliated ep. of trachea'$ronchi replaced $y
stratified s;uamous ep. focally or widely. Chronic atrophic astritis astric mucosa
ep. replaced $y intestine mucosa ep. (o$let
cell).
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(")inificance pithelial metaplasia is a two4ededsword.
1) The function is lost (7ucus'sputum can cleandust).
!) Aead to tumorienesis (esp. s;uamous cell
carcinoma).
(%) :otice
7etaplasia may also occur in mesenchymal
cells. e. $one or cartilae metaplasia in fi$rousct. This occurs particularly in the foci of injury.
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$etaplasia of normal col'mnar (left) to s*'amo's epitheli'm (right)
in a bronch's+ shon () schematically and (,) histologically
The s;uamous metaplasia of tracheaThe s;uamous metaplasia of trachea
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Normal bronch's m'cosa HE pse'dostratifiedcol'mnar ciliated ep.
The s;uamous metaplasia of tracheaThe s;uamous metaplasia of trachea
or $ronchi columnar epitheliumor $ronchi columnar epithelium
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;uamous metaplasia of trachea '$ronchi mucosa
columnar ep. and the lamina propria hyperemia. 6
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mesenchymal metaplasiamesenchymal metaplasia
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mesenchymal metaplasiamesenchymal metaplasia
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u$cellular responses to adaptation
Includin the chanes oflysosome
endoplasmic reticulum,
the mitochondrial
cytos5eletal a$normalities, etc.
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ummary
Hyperplasia:increased cell num$ers in response
to hormones and other =s+ occurs in tissues
whose cells are a$le to divide.
Hypertrophy:increased cell and oran si2e, often
in response to increased wor5load+ induced $y
mechanical stress and $y =s+ occurs in tissuesincapa$le of cell division.
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Atrophy:decreased cell and oran si2e, as a result
of decreased nutrient supply or disuse+ associated
with decreased synthesis and increased proteolytic
$rea5down of cellular oranelles.
etaplasia:chane in phenotype of differentiated
cells, often a response to chronic irritation that
ma5es cells $etter a$le to withstand the stress+
usually induced $y altered differentiation pathway oftissue stem cells+ may result in reduced functions or
increased propensity for malinant transformation.