病理學(xué)-p復(fù)旦基礎(chǔ)醫(yī)學(xué)院系

Pathology

StudiesuticEtiology(病因?qū)W)Pathogenesis(發(fā)病機(jī)制)Pathological

changes

(diagnosis)(病理改變)Consequence(prognosis

and

therguidance)(結(jié)局)病理學(xué)----研究疾病的發(fā)生原因,

發(fā)病機(jī)制,及組織細(xì)胞的

病理改變肝炎

癌

突變

肝癌肝癌大體和鏡下細(xì)胞改變Category

ofPathologyan

resection)Clinical

PathologySurgical

pathology

(biopsy

andAutopsycytologyMolecular

pathologyBasic

PathologyLaboratory

experimentAnimal

experimentResourcesResourcesKumar,

Cotran

&

RobinsBasicPathology7th

edition8th

editionContentsof

PathologyGeneral

PathologyStudyofMechanisms

ofDiseaseSystemic

(specialStudyofDiseasesbyan

system)PathologyanSystemBriefhistory 3stages:一.an

pathology(

病理學(xué)）M agni

(1688~1771) 700

cases《the

sites

and

causes

of

disease》(1761)Rokitansky

(1800~1878)30

thousands

cases

of

autopsies

performed二. Cellular

pathology

(細(xì)胞病理學(xué))19世紀(jì)30年代

microscopy

--

cellVirchow

(1821~1902)《cellular

pathology》(1859)Virchow’s

office

--

Berlin Medicine

-

History

Museum三.Ultrastructural and

molecularpathology(超微結(jié)構(gòu)和分子病理學(xué))30th

age

－electronmicroscope (電鏡)

50th

age

－ultrathin

section(超薄切片)70th

age

－molecular

biology(分子生物學(xué))Pathology

development ofChina20世紀(jì)初中國(guó)開(kāi)辦醫(yī)學(xué)院第一代病理學(xué)家協(xié)和醫(yī)學(xué)院廣州中山大學(xué)醫(yī)學(xué)院國(guó)立

醫(yī)學(xué)院1915年1926年1927年谷鏡汧1922

德國(guó)海岱山大學(xué),柏林大學(xué)19251927協(xié)和醫(yī)學(xué)院1929

中華醫(yī)學(xué)會(huì)第七次大會(huì)心的谷鏡汧性畸形一例報(bào)告動(dòng)脈之病理的研究1951

主編<病理學(xué)總論><實(shí)用病理學(xué)提綱>1954年12月中華醫(yī)學(xué)會(huì)病理學(xué)會(huì)成立Role inMedicine(Queen

of

Medicineor

as

doctors’

doctor)Bridge

between

basic

biomedical

researchand

clinical

sciencesProvide

diagnosis

of

the

diseasesServeas

oneofthegoldencriteria

formedical

service

qualitiesProvide

most

definitive

evidence

of

thedisease

processHow

to

study

well?Put

a

high

value

of

pathological

practiceMake

connections

between

general

andsystemic

pathologyLink

pathologic

changes

with

clinicalmanifestationsAlways

think

patient急性肝炎—肝細(xì)胞水樣變性----肝腫大ExamandGrading

Policies50%

Written

test

including

multiple

choices,pathology

terminology

definition

andexplanation,questions,

etc.30%

Experimental

oral

test10%

Performance

in

laboratory

course10%Mid-term

examEnglish( eneral

performance

in

pathology

course

)Chapter

I.Cell

adaptation,

Injury

and

Death(細(xì)胞適應(yīng)、損傷和

）Adverse

agents:Intrisical:

metabolic

productsischemiaEnviromental:Physical

(radiation,

violet

light,etc.)Chemical

(CO,

CCl4,etc.)Biologic

(bacteria, ,

etc.)Affecting

factors:Nature,

severity

and

duration

of

thestressCharacters

of

the

cell(vulnerability,differentiation,

blood

supply,

and

nutritional

status)Hypoxia (缺O(jiān)2)Normal

cardiomyocyte(正常心肌細(xì)胞）Adaptation（適應(yīng)）Reversible

injury（可復(fù)性損傷）Irreversible

injury（不可復(fù)性損傷）I. Cell

adaptation（細(xì)胞適應(yīng)）Definition

機(jī)體組織、細(xì)胞對(duì)內(nèi)、外環(huán)境的變化所發(fā)生的形態(tài)結(jié)構(gòu)和功能代謝的改變ClassificationPhysiologic:

erythocytosis

in

healthy

people

lived

in

plateau高原缺氧情況下的紅細(xì)胞增多失血情況下的皮膚、內(nèi)臟血管收縮Pathologic:Atrophy

萎縮

—

decrease

in

cellsizeHypertrophy

肥大

—increase

incell

sizeHyperplasiaMetaplasia增生—increase

incell

number化生—change

incell

typeA.

Atrophy（萎縮）Definition發(fā)育正常的 、組織或細(xì)胞體積的縮小Shrinkage

in

the

sizeof

the

cell

by

theloss

of

cell

substanceClassifications

&

causesPhysiologic:

Atrophic

thymus

in

adultAtrophic

uterus

in

old

womanPathologic:Inadequate

nutritionLoss

of

innervation(營(yíng)養(yǎng)不良)

腦萎縮(喪失神經(jīng)營(yíng)養(yǎng))

脊髓灰質(zhì)炎腿肌肉萎縮Decreased

workload

(廢用性)

骨折腿肌肉萎縮Pressure

from

surrounding

tissue,

fluid,masses( 性)腎積水皮質(zhì)萎縮Loss

of

endocrine

stimulation

(內(nèi) 減少)乳腺萎縮、腎上腺皮質(zhì)萎縮Aging(老年性)Biochemical

mechanismAffected

balance

between

synthesisand

degradationDegradationpredominanceMorphologic

changesGross:

Smaller

and

brown

(brown

atrophy)LM:

Smaller

cells(細(xì)胞變?。㊣ncreased

lipofuscin(脂褐素增多)EM:Decreased

anelles (細(xì)胞器減少)Increasedautophagic

vacuoles(自噬泡增多)ConsequenceReversible

change

(可復(fù)性改變)Diminished

function(功能降低)－Atrophic

brain-Alzheimer

disease(老年性癡呆癥)－Atrophic

pancreatic

islet

-

diabetes

mellitus

()B. Hypertrophy

（肥大）Definition

實(shí)質(zhì)細(xì)胞體積增大引起 體積變大An

increase

in

thesize

ofcells

andconsequentlyan

increase

inthe

size

ofthe

anNo

new

cells

（非新生細(xì)胞）No

cellular

swelling（非細(xì)胞腫脹）ClassificationPhysiologic:

uterus

during

pregnancy(妊娠)Pathologic:－Compensatory

or

adaptive:

hypertensive

heart－Substitutive:

enlarged

kidneyMorphological

changesGross:

Enlarged

anLeftventricular

hypertrophyLM: bigger

cellLarger

and

darker

stain

of

nucleiEnlarged

myocardial

fiberEM:

Increased

anellesIncreased

myofilamentConsequenceA

adaptivechangeAlimitedcompensationC. Hyperplasia(增生）Definition或組織中細(xì)胞數(shù)量增加An

increase

in

the

number

of

cells

inan an

or

tissueClassificationPhysiologic:Hormonal:

glandular

epithelium

of

the

female

breast

during

pregnancyCompensatory:

remaining

liver

cell

after

resecting

a

portion

of

liverPathologic:—Hormonal

（激素依賴性）如內(nèi)膜增生、乳腺增生愈合）Wound

healing

（Skin

wart

（皮膚疣）Morphological

changeIncreased

number

of

cellIncreased

mitosis

ofnuclei增生結(jié)節(jié)性增生ConsequenceAdaptive

change:proliferation

of

connective

tissuecell

in

wound

healingAdverse

effect:cancerous

proliferation(endometrical

cancer,

cervical

cancer,etc)D.metaplasia(化生）Definition一種分化成

細(xì)胞類型（上皮或間質(zhì)細(xì)胞)被另外一種成

細(xì)胞所代替One

adult

cell

type

(epithelial

or

mesenchymal)is

replaced

by

another

adult

celltype化生通常見(jiàn)于具有極強(qiáng)再生能力的組織，如上皮組織和結(jié)締組織。通常是由上述組織中具有潛在分化和增殖能力的細(xì)胞如基底細(xì)胞、儲(chǔ)備細(xì)胞、原始間充質(zhì)細(xì)胞等增生轉(zhuǎn)化所致。ClassificationEpithelial(上皮化生）Squamous:

(e.g.

squamous

metaplasia

of

respiratory

epithelium)鱗狀細(xì)胞化生Glandular:

(e.g.

interstinal

metaplasia

of

gastric

mucosa)腸上皮化生Mesenchymal(間葉細(xì)胞）Metaplasiain

connectivetissue（骨化生、軟骨化生、脂肪化生、粘液化生）ConsequenceAn

adaptive

response

（適應(yīng)性改變）to

a

adverseenviromentAdverse

effect:

（不利影響）cancer

transformationin

themetaplastic

epitheliumII. Reversible

injury（可復(fù)性損傷）Cellular

degeneration(細(xì)胞變性）細(xì)胞水腫變性脂肪變性A.Cellular

Swelling

（細(xì)胞腫脹）Mild,

reversible,

commonlesion

in

parenchymalcells(e.g.

liver,

kidney,heart,

brain)Granular

or

vacuolar

andhydropicdegenerationPathologic

changesGross:

Pallor,

increased

turgor,

and

increased

weightLM:

Cytoplasmic

visible

granule-granular

degenerationCytoplasmic

clear

vacuole-vacuolar

or

hydropic,

degeneration腎小管上皮腫脹肝細(xì)胞腫脹EM:－Blebbing,

blunting

or

distortion

of

microvilli

and

loosening

ofintercellular

atta

ent－Mitochondrial

swelling

with

formation

of

amorphous

densities－Dilation

of

Endoplasmic

Reticulum

with

deta ent

of

ribosomes

anddissociation

of

polysome－Disaggregation

of

granular

and

fibrillar

elements

of

nucleiMechanismDepletion

of

ATPNa+-K+

ATPase

injuriedMembrane

permeability

↑B.

Fatty

degeneration(脂肪變性）又名：fatty

change

(steatosis)DefinitionAny

abnormalaccumulation

of

triglycerideswithinparenchymal

cellReversible

severe

injuryMost

often

inliver,

also

in

heart,

kidney,skeletalmuscleVarious

causes

(toxin,proteinmalnutrition,diabetesmellitus,

obesity,anoxia,

especially

alcoholabuse)Pathologic

changesFatty

change

of

the

liverGross:Enlargement

and

progressively

yellow

colorIncreased

weight,and e

tuft

and

greasy蘇丹III呈橘紅色LM:Cytoplasmic

fat

vacuole,

round

and

clear

in

routing

tissue

sectionOrange

red

in

tissue

section

with

sudanIV

or

oil

red

O胞質(zhì)內(nèi)圓形空泡，大小不等，核可偏位蘇丹III呈橘紅色，鋨酸呈黑色部位可分:小葉型——淤血、四氯化碳小葉周邊型——全小葉型——嚴(yán)重、、磷、Fatty

change

of

the

heartGross:

Tigered

heart虎斑心(e.g.

anemia)

Uniformly

affected

myocytes

(e.g.diphthelia)Fatty

change

of

the

kidneyGross:

Lipid

streak

in

renal

cortexEM:round

vacuole

with

lower

electron

densityMechanismFatty

acid

accumulation—Increased

mobilization

of

fatty

acid

(e.g.

starvation)Inhibited

oxidation

offatty

acid

(e.g.

anoxia)Decreased

the

synthesis

oflipoproteins(e.g.

protein

malnutrition)Free

of

structured

lipidIII.

Celldeath(細(xì)胞

）又名：Irreversible

injury

（不可復(fù)性損傷）Two

patterns:Necrosis

（壞死）Apoptosis(凋亡）A.Necrosis

（壞死）anismDefinitionLocal

death

ofthe

cell

or

thetissuein

alivingBiological

processesSelf-digestion

or

enzymatic

digestionAutolysis

（自溶）Heterolysis

（異溶）Denaturation

of

the

proteinsMorphologic

changesNuclear

changes

（核改變）Pyknosis（核固縮）Karyorrhexis(核碎裂）Kalyolysis（核溶解）Cytoplasmic

changes

（胞質(zhì)改變）Granular

degeneration

or

fatty

change

（顆粒變或脂肪變）Eosinophilic

stain

increased

（嗜酸性增強(qiáng)）Interstitial

changes

（間質(zhì)改變）Collagen

degradation

&

stroma

deaggreation（膠原降解&基質(zhì)解聚）Inflammatory

reaction

（炎癥反應(yīng)）Necrotic

patterns

（壞死類型）a.

Coagulative

necrosis

（凝固性壞死）Predominant

denaturation

of

proteinStructured

necrosisCommon

in

heart,

kidney,

liver,

spleen,etc.b. Liquefactive

necrosis

（液化性壞死）Predominant

self-digestionLiquefactive

lesionCommon

in

brain,

spinal

cord,

etc.c.

Specific

pattern

of

necrosis

（特殊類型壞死）Caseous

necrosis(干酪樣壞死）MostofteninT.B.infectionDry

and

yellow

cheesyfocigrosslyStructureless,

amorphous

granular

debrisFat

necrosis

（脂肪壞死）Typically

occuring

after

pancreatic

injuryChalky

white

areas

grosslyNecrotic

fat

cells

with

basophilic

calcium

depositInflamatory

infiltrationFibrinoid

necrosis

（纖維蛋白樣壞死）Mostly

occuring

in

hypersensitivity

reactionSmuday

eosinophilic

and

homogeneous

masses(Fibrin,

Ig,

and

plasma

proteins)ansorGangrene

（壞疽）又名：gangrenous

necrosis

（壞疽性壞死）－Attached

by

bacterial

infection

in

infarctedtissues (ofteninopened

ans)Presented

with

dark

or

black

color

in

necrotic

areas(Fe2+

+

H2S

FeS)Divided

into

3

categories

(dry,

wet

and

gas)CausesA

occlusion

A+V

occlusionDeep

wound

+aerogen

infectionMorphologicfeature

of

lesionConsequenceDry,

demarcatedMild,

localWet,

poorlydemarcatedSevere,

systemicWet,

poorlydemarcated,bubble

formationTab

1.

Comparison

of

3

Types

of

GangreneDry

Wet

GasConsequence(結(jié)局)Resolution

and

absorption（溶解吸收）Deta ent

and

discharge

（分離排出）Ulcer

（潰瘍）（空洞）—

Encapsulation

（化）anization（機(jī)化）Calcification

（鈣化）B.

Apoptosis

（凋亡））又名：Programmedcell

death

（程序性細(xì)胞DefinitionMainly

bephysiologicDetermined

by

intrinsic

geneA

pathway

of

cell

“suicide”機(jī)體局部組織內(nèi)在遺傳或

決定的、自身破壞機(jī)制所引起的細(xì)胞。凋亡細(xì)胞?？杀灰暈樗拗鞑恍枰募?xì)胞?！げ∽儥C(jī)制：生物化學(xué)改變：胱冬肽酶參與，裂解支架和激活內(nèi)核苷酶活化轉(zhuǎn)谷氨酰胺酶——蛋白質(zhì)交聯(lián)，形成凋亡小體DNA被內(nèi)核苷酶裂解成碎片和寡核苷酸特異性電泳帶細(xì)胞或小體表面分別有磷脂酰絲氨酸或血小板反應(yīng)蛋白表達(dá)——為吞噬細(xì)胞所識(shí)別Morphologic

changesRound

or

oval

masses

with

intensely

eosinophiliccytoplasm

in

single

cell

or

clusters

ofcellCondensed

nuclear

chromatin

with

karyorrhexis

andformation

of

apoptotic

bodiesApoptotic

cell,

their

fragments

could

bephagocytosedordegradedNo

inflammationTab2.

Comparison

between

apoptosisand

coagulationnecrosisCoagulation

NecrosisApoptosisStimuliHistologicappearanceDNA

breakdownMechanismTissue

reactionHypoxia,

toxinsCellular

swellingCoagulation

necrosisanellesDisruption

ofRandom,diffuseATP

depletionMembrane

injuryFree

radical

damageInflammationPhysiologic

and

pathologicfactorsSingle

cellsChromatin

condensationApoptotic

bodiesInternucleosomalGene

activationEndonucleasesProteasesNo

inflammationPhagocytosis

of

apoptotic

bodiesIV.

Hyaline

degeneration（玻璃樣變性，簡(jiǎn)稱玻變）又名：Hyalinosis

（透明變性或玻璃樣變性）ConceptionAmorphologicaltermPresenting

eosinophilic

and

homogenous

depositsinHE

stained

sectionOccuring

incell,

interstitium

and

vascularwallCategoryIntracellular

hyaline

droplet

（細(xì)胞內(nèi)玻璃樣小滴）—

orviral

granuleNegri

body–hydrophobia

（狂犬?。〤MV inclusion–CMV

infection

（巨細(xì)胞）Ig）Proteinsabsorbed

orsynthesizedAbsorbed

protein

－Nephritis

（腎炎）Russsel

body

－Ig

synthesized

in

plasma

cell

（漿細(xì)胞Accumulated

cytokeratin

intermediated

filments性肝炎）Mallory

body

–

alcoholic

hepatitis

（—

Apoptosis

or

coagulative

necrosisCouncilman

body

–

viral

hepatitis

（性肝炎）Hyaline

degeneration

of

cardiomyocyte–diphthelia

（白喉）Hyalinosis

ofvascular

wall

（血管壁玻變）Hyalinosisof

connective

tissue

（結(jié)締組織玻變）Scar

（疤痕）Atheroma

（粥樣斑塊）Sclerotic

glomerulus（硬化性腎小球）ConsequenceDepending

on

their

causes,

mechanismand

biochemical

constituentV.Amyloidosis

（淀粉樣變）ConceptionProteinaceous

material

(amyloid)

deposited

intissueinterstitiumor

vascularwallPresenting

brown

color

after

reacting

toiodineChemical

natureAmyloid

light

chain

(AL)protein

（免疫球蛋白輕鏈）produced

by

plasma

cellassociated

with

some

form

of

monoclonal

B-cell

proliferationAmyloid

associated

(AA)protein（淀粉樣相關(guān)蛋白）－Aprotein

of

8.5

kD

molecular

mass

（76

amino

acid

residue)Derived

from

12kD

SAA

(serum

amyloid-associated)synthesized

in

the

liverDeposited

in

thesettingofchronic

inflammatory

statesMorphologic

changesAmorphous,

eosinophilic,

hyaline

extracellular

substance

with

HE

stainPink-red

deposits

with

Congo-red

stainYellow-green

birefringence

by

polarizing

microscopeAmyloid

fibril

(7~10

nm)

on

EM

examinationConsequencePressure

atrophy

ofdeposited

ans(kidney,

heart,

etc.)VI. Pathologiccalcification（病理性鈣化）ConceptionAbnormal

deposition

of

calcium

salts,together

with

smallamounts

ofiron,magnesium

and

othermineralsClassificationA. Dystrophic

calcification（營(yíng)養(yǎng)不良性鈣化）Deposition

of

calcium

salts

in

dead

or

dying

tissues(necrotic

foci,

thrombus,

atheroma,

tumor,

etc.)Absence

of

calcium

metabolic

derangementFormation

of

crystalline

calcium

phosphated

due

tolocally

increased

Ca2+,

PO42-

locally沉積于病變組織，如壞死灶、血栓、粥樣斑塊、腫瘤、蟲(chóng)卵等ATP

酶有機(jī)磷酸脂

PO2-4+Ca2+

=Ca（PO4）2pH↓B.

Metastatic

calcification

（轉(zhuǎn)移性鈣化）Deposition

of

calcium

salts

in

normal

tissue(vessel,

lung,gastric

mucosa,

kidney)

Some

derangement

in

calcium

metabolism

(hypercalciemia)due

to:Increased

secretion

of

parathyroid

hormoneDestruction

of

boneVit

D

related

disordersRenal

failure沉積于骨外正常組織，尤其是酸性環(huán)境的胃粘膜、腎小管、肺等組織.MorphologicfeaturesFine,

white

granules

or

clumps,grosslyBasophilic

deposits

histologicallyHeterotopic

boneformation,

sometimesConsequenceA

causeof an

dysfunction—

Compromised

valve

motion

(cuspa