中国医科大学病理学外文翻译课件1

Chapter

IAdaptation

and

injuryof

cell

or

tissueCell

deathNecrosisapoptosisAdaptable

cellatrophyhypertrophyhyperplasiametaplasiareversibly

injured

celldegenerationRelationship

of

normal

cell,adaptable

cell

and

injured

cellNormal

cell一、Cell

adaptation1

.

Definition:a

non-injurious

reaction

of

cells,

tissues

and

organs

to

exogenous

and

endogenous

harmful

stimuli.§1.

Cell

adaptation

and

aging2.

Morphologic

manifestationHypertrophyHyperplasiaAtrophyMetaplasia（一）Hypertrophy1.

Definition:an

increase

in

the

size

of

atissues

or

organ

due

toincreased

size

of

individual

ce2.Types(1)

Physiologic

hypertrophy:pregnancy

→

uterus↑(endocrine

hypertrophy)Physiologic

hypertrophy

of

uterus(2)

Pathologic

hypertrophyHypertension

→

heart

hypertrophyGN

→

residual

nephron

hypertrophy3.

EMcell

components mitochondria

↑endoplasmicreticulummicrofilament↑protein

synthesis↑Myocardial

hypertrophyMyocardial

hypertrophy（二）HyperplasiaDefinition:constitutes

an

increase

in

thenumber

of

cells

in

an

organ

ortissue,

which

may

then

haveincreased

volume.Types:(1)

Physiologic

hyperplasia①

Hormonal

hyperplasia:SMC

of

uterus

during

pregnancy②

Compensatory

hyperplasia→partial

hepatectomy(2)

Pathologic

hyperplasia:excessive

hormonal

stimulationthe

effects

of

growth

factors

on

targHyperplasia

of

mucosal

epithlium(gastric

ulcer)Subacute

severe

hepatitisGastricpolypGastricpolypHepatic

cirrhosis3.

Distinguish

between

hyperplasand

neoplasia

proliferationHyperplasia:stimuli

abates→hyperplasiadisappearsNeoplasia

proliferation:

continuDefinition:Normal

formed

organ

or

tissuediminished

in

size

due

to

decreasein

the

size

of

the

parenchymalcells

or

in

the

number

of

cells.Hypoplasia:

organ

or

tissue

can’ develop

fully

to

normal

sizeAplasia:

state

of

non-developing（三）Atrophy3.

Types:Physiologic

atrophyPathological

atrophy:according

to

different

causes,divided

into

following

typesPhysiologic

atrophy

of

brain①

Insufficient

nutritive

atrowhole

body:

malignant

tumor②

Atrophy

of

disuse:decreased

workload

→

skeletalmuscle

fiber

decrease

in

number

aswell

as

in

size

when

a

patient

isrestricted

to

complete

bed

rest.③

Denervation

atrophy:damage

to

the

nerves

leads

to

rapidatrophy

of

keletal

muscle

suppliedby

those

nerves.④

Pressure

atrophy:an

enlarged

tumor

can

causeatrophy

in

the

surroundingcompressed

tissue.Endocrine

atrophy:loss

of

endocrine

(estrogen)

stimulatiatrophy

of

endometrium,

vaginalepithelium

and

breast⑥

Endocrine

atrophy:AS

→

brain4.

Morphologic

changes(1)

Gross

appearance:volume

↓weight↓Pressureatrophy

ofkidneyPressure

atrophy

of

brain(2)

Histological

changes:Decrease

in

the

size

and

number

of

cellsLipofuscin

→

brown

atrophy

(heart

or

lAtrophy

ofmyocardiumNormalmyocardiumAtrophy

of

skeletal

muscle(3)

EM:increases

in

the

number

ofautophagic

vacuolescell

debris

within

autophagicvacuolesresidual

body(membrane-bound

vacuoles)Definition:a

process

in

which

one

matured

tissue

typ(epithelial

or

mesenchymal)

is

replacedanother

matured

tissue

type.Causes:chronic

stimulation→activated

or

supprof

related

genesif

persistent→

induce

canceration（四）Metaplasia3.

Epithelial

metaplasia(1)

Squamous

metaplasia:occurs

in

the

respiratory

tractchronic

irritationdeficiency

of

Vit

Acigarette

smokerin

response

toBMColumnar

Reserveepithelium

cellsSquamousmetaplasiaHyperplasia

of

reserve

cellsin

cervical

epithelium(2)

From

squamous

to

columnartype:Barret

esophagitissquamous

cellintestinal–like

columnar

celColumnar

metaplasia

of

barret

esophagitis(3)

Glandular

metaplasiaIntestinal

mataplasia4.Mesenchymal

tissue

metaplasiaEpithelial

metaplasia

→

reversibleBone

cartilage

→

irreversibleOsseous

metaplasia二、Cellular

aging(senescencDefinition:the

maturation

and

differentiationof

the

organs

and

its

cellslead

to

the

progressive

loss

offunctional

capacity(一)Aging

clock:1.

Timing

of

the

aging

process

–the

concept

of

a

clock:①

Controlling

the

rate

and

timinof

aging

is

supported

by

theidentification

of

clock

genes.②

Telomeres:short

repeated

DNA

sequencestelomeraseensuring

the

complete

replication

ochromosomal

endsprotecting

chromosomal

terminifromfusion

andClockgenesTelomerase

activitydecreasing

(

Telomeraseactivity

is

expressed

in

germcells

and

is

present

atlowlevels

in

stemcells,

but

it

isusually

absent

in

most

somatic

tissues.)telomere

shortening（older

of

the

celland

shorter

of

thetelomere

）cell

aging(二)Metabolic

events,geneticdamage

and

agingCellular

life

may

also

be

determined

bthe

balance

between

cellular

damagerepairmentFree

radical

→

oxidative

damageMetabolic

substancesToxic

substancesDNA

damageAccumulating

ofmetabolic

substancestoxic

substancesDNA

damage

（DNA

damageis

repairedby

endogenousDNA

repairenzymes,

somedamage

persistsandaccumulatesCellular

aging§2

Injury

of

cells

and

tissu一.Causes（一）Hypoxia(commom

and

important)1.

Ischemia2.

HeartLung

failure3.

Loss

of

the

oxygen

–

carrying

capacof

the

bloodinadequateoxygenation(二)Physical

agentsMechanical

traumaExtremes

of

temperature

:burns

or

exceeded

coldChanges

in

atmosphericpressureRadiation（三）

Chemical

agents

and

drugsAll

chemical

agents

and

drugsSimple

chemicals

(

glucose

or

saltinhypertonic

concentrationsCell

injury（四）Biologic

agents(most

common)virusesbacteriaothers：fungi

(fungus);

parasite（五）Immunologic

reactionsAnaphylactic

reaction

to

foreign

prdrugsEndogenous

self-antigen

→autoimmundiseases（六）Genetic

defectChromosomal

aberration

or

gene

mutationErrors

of

metabolism

arising

fromenzymatic

abnormalities（七）Nutritional

imbalanceNutritional

deficiency:

protein

,VitaminNutritional

excesses Excesses

of

lipid

→

AS Fat↑→

obesityVitamin

D

→calcificationATP

depletionIrreversible

mitochondria

damageLoss

of

membrane

permeabilityOverload

of

intracellular

calcium

an loss

of

calcium

homeostasisAccumulation

of

free

radicals二.Mechanisms

of

cell

injuryCauses

of

cell

injuryMechanisms

of

cell

injury三.Morphologic

changes

of

cell

inj(一)Reversible

injury(DegenerationDefinition:Morphologic

changes

of

cell

orextracellular

stromal

damage

due

ofmetabolic

disorderthe

deposition

of

some

abnormal

substanexcessive

normal

substance

in

cell

or

st(二)Substance

accumulation

inintra(extra)cellular

spaceExcessive

normal

substance

in

cell

orstromaWater,

lipid,

proteinThe

deposition

of

some

abnormalsubstanceInfectious

products,

mineral

substanc1.

Hydropic

degeneration(cellular

swelling

)The

first

manifestation

of

cell

injuThe

common

site:

liver,

kidney

,

heartCauses:hypoxia,infection,intoxicationMi

injury

→Na+-K+

pumpdysfunctionNa+,

H

O↑(3)

Pathologic

changes

:①

Gross

appearance:increased

in

the

weight

of

the

orgacutting

surface

pallor

in

colorcapsule

tense,

section

bulgy,cutting

edge

bulging,Cellular

swelling

of

liver②

LM:cell

swellingfine,

red-stained

granules

withincytoplasmsmall

clear

vacuolesBallooned

change

clear

cytoplasmcell

swelling

obviousl③

EM

MitochondriaERswellingCellular

swelling

of

hepatocyteBallooned

changeSwelling

of

endoplasmic

reticulumCellular

swelling

of

hepatocyte(EM2.

Fatty

change

(steatosis):(1)

The

common

site:liver,

heart

,

kidney,

muscle(2)

Causeshypoxiainfectionintoxicationobesity(3)

Definition:abnormal

accumulations

of

fat(triglyceride,

cholesterol,

phospholwithin

parenchymal

cells.(4)

Morphology①

Gross:

enlarged,

yellow,soft,greas②

LM:

clear

vacuoles

in

the

cytoplasmaround

the

nucleusAccumulation

of

fat,

glycogen,

watervacuolesPAS(Periodic

acid-schiff)

(+)

→glycogenOil

Red-0

(+)Sudan

Ⅲ

(+)③

EM:liposomemembrane-bound

round

bodyfat(1)

Fatty

liver

:most

often

seen

in

the

l①

Causestoxinsprotein

malnutrition

,diabetes

,

obesityalcohol

abusein

industrialized

nationsthe

most

common

cause②

Gross:Enlarged

,

yellow

,

soft

(section)

→greasy③

LM:

Small

vacuoles

around

nucleus↓coalescelarge

vacuoles

that

displace

the

nucleus

to

theperiphery

of

the

cell.Fatty

liver

（SudanⅢ

stained）(2)

Fatty

change

of

myocardium①

Local

typeThe

common

siteSubendocardiumleft

ventricle

papilary

muscleGross:

Tigered

effectapparent

bands

of

yellowed

myocardiumalterating

with

bands

of

darker,

red-brown(uninvolved)

myocardiumLM:

string

of

bead-like

smalldropletsnear

the

nucleus②

Diffuse

type:Cause:

severe

hypoxia

or

poisoningLesion:

diffuse

light

yellowFatty

change

of

myocardiumMyocardial

fatty

infiltration:Different

from

myo-fatty

change:In

subpericardial,

excessive

fataccumulating

and

inserting

amongmyocardial

bandles.Causes:

obvious

obesity,

alcohol

abuSudden

deathMyocardial

fatty

infiltration(3)

Fatty

change

of

renaltubule

epitheliumCauses

lipoprotein↑reabsorption

of

lipoprotein↑LM:

droplets

within

proximal

tubuleepithelium(4)

Cholesterol

or

cholesterol

e①

Atherosclerosis:

cholesterol

crysta②

Xanthoma:

Macrophage

phagocytecholesterol

foam-like③

Inflammation

and

necrosi