中国医科大学病理学外文翻译课件10

Chapter

8The

disease

of

cardiovascularsystem8.1

atherosclerosis

(

AS

)z

characterized

by

intimal

lesions

calledatheroma

or

fibrofatty

plaques

that

protrudeinto

the

lumen,weaken

the

underlyingmedia,and

undergo

a

serious

of

complicationsz

Primarily

affects

elastic

arteries

(aorta,carotid,

iliac-arteries)

and

large

and

mediusized

muscular

arteries

(coronary

andpopliteal

arteries)8.1.1

epidemiology

and

risk

factorshyperlipemia

/

hypercholesterolemia:①

LDL/LDL-C

,VLDL,

triglycerides,cholesterol→positive②

HDL/HDL-C,

apoA-I

→negativehypertension:→early

and

severesmoking:→endothelial

damage、CO↑→

PDGF↑,SMC

proliferation

emigration→

ox-LDLDiabetes

and

hyperinsulimemia:hyperglycemia→LDL

glycolate→ox-LDL→hypertriglyceridehyperinsulimemia→SMC↑、HDL↓heredity:

200genes;

HDL-receptorgene

mutation→familyhypercholesterolemia6.

Age

and

sex：age:

age↑→ASfactors

changesarterial

wall

proliferativechangesex:

estrogen→cholesterol↑postmenopausal

female=maleOthers:Obesity

,

stressful

life

type

,

hypoxia

,

dielackofVit.

C

,

infection

ofbacteria

,

viruLack of

exercise

:Intake

of

alcohol

:Protective

role

for

moderate

intake

ofalcohol

:

HDLA

large

amount

of

intake

of

alcohol:hypertension,

cerebral

hemorrhage8.1.3

pathologic

changeselastic

arteries:

aorta,

carotid,

iliaclarge

and

medium-sized

muscular

arteriecoronary,popliteal

A1.

favorite

site:lower

abdominal

aorta,

coronary

A,popliteal

A,

the

descending

thoracic

athe

internal

carotid

A,

the

circle

of

wWhat

does

the

atherosclerotic

vessel

look

lThe

lesion

of

atherosclerosis

is

not

one

spentitybut

a

spectrum

of

arterial

changesincluding

:□Atheromatous

fibro-lipid

plaques

=

fibroplaque

=

fibrotheroma□Fatty

streaks

=

intimal

xanthoma□Intimal

cushion

lesions

=

intimal

mass

lebasic

pathologic

changes1.

fatty

streak:

the

early

lesiongross:tiny

round

or

oval

flat

yellow

dotsarranged

in

rows,

coalesce

to

form

astreak,

1-2mm,

slightly

raised,particularto

theaortic

valve

regionLM:

a

collection

of

foam

cellsfatty

streak:

multipleyellowflatspots(fatty

dotFatty

streak

(sudan

red)(3)

formation：lipid↑→engulfed

by

Mφ,

SMC

→foam

cell(two

sources)(4)

result:reversiblecould

be

seen

in

infants

and

children2.

fibrous

plaque：gross:irregular

grey-white

raisedplaqueLM:

fibrouscap,

foam

cell,lipids图8-5

主动脉粥样硬化主动脉后壁见黄白色纤维斑块lumenFibrous

capLipid

core,clefMassontrichrome(胶原纤维-蓝；肌、纤维素-红）Media

thinCalcification,neovascular3.

Atheromatous

plaqueor

atheroma(hallmarkof

AS)z

gross:white/whitish

yellow/

yellowirregularelevated

plaque(2)

LM:①

surface:

fibrous

cap（hyaline

degenerationofcollagen,

SMC

embed

in

extra

cellularmatrix）②

necrotic

center:

amorphous

necrotic

materia（cell

debris,lipid,cholesterol

crystals,

casurrounding:

granulation

tissue,

lymphocyte+foam

cells③

media:

atrophy→thinComplicated

lesions:on

the

basis

of

fibrous

plaque

and

atheromatouhemorrhage

within

plaque:acute

obstruction

of

A(

coronary

A

→myocardial

infarction）focal

rupture:lower

abdominal

aorta、iliacarteries、tempArupture→ulceration→thrombosis↓atheromatous→embolism→infarct图8-8腹主动脉粥样硬化斑块内出血粥样斑块纤维帽和坏死物质之间可见大量红细胞，坏死物内可见针形“胆固醇结晶裂隙”图8-9腹主动脉瘤肾动脉下腹主动脉粥样硬化伴局限性明显扩张，动脉瘤形成。thrombosis：obstruction→infarctioncalcification：harden,

elasticityaneurysm

formation：rupture→hemorrhageAS

focal

disruption,

thrombomosiPslaque

ruptureThe

atheromatous

plaque

and

the

dynamics

of

plaquestability(三)Lesions

in

organs

&

clinical

features1.

aortic

AS：site：abdominal

aorta>thoratic

A>aorta arch>ascending

Alesions：atheromatous

and

secondarychangesulceration、calcification、hemorrhage,abdominal

aortic

aneurysm→Rupture→Death2.

Coronary

AS：coronary

heart

disease3.Carotid

A、Cerebral

A

ASsite：basilar

A,middle

cerebral

A,Williscirclelesion①ischemicatrophy②infarction：thrombosis→occuludetemporal

lobe,

caudate

nuclears,lenticularnucleus,thalamus③

hemorrhage：AS→aneurysm

rupture图8-10

大脑基底动脉粥样硬化

图8-11脑软化↑示动脉粥样硬化斑块

↑示筛状软化灶Renal

A

AS:sites：ostia

ofrenal

A

majorbranch,proximal

segmentlesion

：

infarctor

hypertension

AS

of

extremities:narrowing→claudication→thrombosis→gangreneSmall

intestine

AS:

infarction8.2

pathogenesis1.

Response

to

injury

theory

andinflammation

theory:---

Current

view

of

the

pathogenesis

of

ASAS

plaque

as

the

response

of

endothelial

celto

damaging

factorsdamage

factors:mechanical

denudation、

LDL、hypercholesterolemia、immunecomplex、ox-LDL、smokingz

Central

to

this

thesis

are

the

followingeventsRoles

ofLipidsEndothelial

injurySmooth

muscle

proliferationMacrophage(Mφ)zz

①

Role

of

lipidsIncrease

endothelial

permeabilityImpairendothelial

functionOX-LDLingested

by

Mφ→foaming

from

cellschemotactic

for

circulating

monocytesincrease

monocyte

adhesionstimulate

release

of

growth

factorschemotactic

to

endothelial

cells

(EC)smooth

muscle

cells

(SMC)②

Role

of

EC

injury:

initial

lesionMechanical

injurySmokingRisk

Factors

HypoxiaHyperlipidemiaHypertensionEC

injuryNon-denuding

EC

dysfunctionEC

denudingIncreased

EC

permeabilityEnhanced

monocyte,

platelet

adhesionRelease

GF→SMC

proliferationz

③

role

of

macrophage:

key

stepy

Platelet

,

EC,

Monocyte,

SMCGrowth

Factors

(PDGF,FGF,etc)emigrationproliferationadhere→emigrant

subendothelially→

foam

cellsMatrixGF→SMC↑z

④

role

of

SMC

proliferation:GF

→

SMC

proliferation

in

media→

emigration→intimaaccounting

for

the

progressive

growth

of

ASphenotype

change(constrictive→synthesis)surface

LDL

receptor→foam

cell

(SMC

derived)collagen

,

elasticfiber

protein,

proteoglycansinteraction→formation

of

AS

plaque2.

Lipid

infiltration

theory：hyperlipemia↓EC

damage→permeability↑→lipoprotein

deposit→Mφcleanup↓SMC↑↓atheroma3.

Smooth

muscle

mutagenic

theory①SMC

in

AS

plaque→monoclone②

etiology:chemical

mutagenic

agentsvirus4.

Macrophage

receptor

defect

theory(1)normal①cell

membrane:

LDL

receptor→combine

withLDL→engulf→intracellular②

intake→LDL

receptor→change

with

the

needof

cholesterol(2)

AS:

LDL

receptors↓↓→LDL

cleaning↓→LDL

in

blood↑(2)

ox-LDL①

not

be

recognized

by

nativeLDL

receptor②

engulf

mediate

by

scavenger

recept(Mφsurface）→foam

cell③

chemotactic

to

monocytes↑④chemotactic

to

EC、SMC↑GF↑8.2

coronary

AS

and

coronaryheart

diseasecoronary

atherosclerosisdistribution：①left>right，large

branch>small

branch，proximal

segment>distant

segment②

left

anterior

descending

coronary

A>rightCA>left

CA>left

circumflex

CAThe

progression

of

myocardial

necrosis

after

coronary

a.RCALCXLADfeatures：cutfacecrescent

plaquemyocardial

side，eccentric

stenosin4

grades：Ⅰ

<

25%

;

Ⅱ

26-50%;

Ⅲ

51-75%;

Ⅳ

>76%ischemic

heart

disease

(IHD)8.2.2

coronary

heart

disease

(CHD)1.

CHD：

ischemic

heart

disease(IHD)–

agroup

of

closely

related

syndromeresulting

from

myocardial

ischemia2.etiology

and

pathogenesis：①insufficient

blood

supply:

AS、sp②

increase

in

cardiac

energy

demand:BP↑↑，overworked，excite→work

load

of

heart↑An

imbalancebetween

the

perfusion

anddemand

of

the

heart

for

oxygenated

blooangina

pectorisz

1.

angina

pectorisA

symptom

complex

of

IHD

characterized

byparoxymal

and

usually

attacks

of

substernal

oprecordial

chest

discomfort

(constricting,squeezing,

chocking

or

kinfelike)cardiac

oxygendemand↑↑acute、temporarily,comparatively

coronary

Ablood

supply2.

clinical

typesstable

or

typical

angina：reliveby

rest

or

nitroglycerin,

chronicstenosing

coronary

AS（>75%）prinzmetal

or

variant

angina:episodic

angina,

occure

at

rest,

duecoronary

spasm,

ECG：S-T

elevated,unrelated

to

BP,

rate,

activity,vasodilators

respond

promptly（3）unstable

or

crescendo

angina：occure

with

progressively

increasingfrequencytend

to

be

of

more

prolonged

durationInduced

by

disruption

of

an

AS

plaque

witsuperimposed

partial

thrombosis

andembolization

or

vasospasm

(preinfarctiangina)myocardial

infarction，(MI)concept：acute

ischemic

necrosisdue

to

severe

sustainedischemia,heart

attacktypes：95%

LV,

transmural

orsubendocardial

infarction（1）subendocardial

myocardial

infarctio①

concept：an

area

of

ischemic

necrosis

l

to

the

inner

1/3,

at

most

½

of

the

ventric

wall

(papillary

muscle,

trabeculae

carn②

lesion：multiple

different

in

size

focnecrosis③

circumferential

infarction:entire

LV

endocardium（2）transmural

myocardial

infarctiontypical

infarction：①

the

ischemic

necrosis

involves

the

fulnearly

full

thickness

of

the

ventriculawall

in

the

distribution

of

a

singlecoronary

artery

>2/3→thick

layer

infarz②

favorite

sites：LAD

40-50%Anterior

wall

of

LV

nearapex,anterior

portion

ofventricular

septrm,

apexcircumferentiallyRCA

30-40%Inferior-posterior

wall

of

LV,posteriole

portion

ofventricular

septum,

inferior-posterior

RV

free

wallLCX

15-20%Lateral

wall

of

LV

exceptat

apex3.lesion：anemic

infarct，yellow

or

gray-red，dryirregular12hr

naked

eye½-1hr

EMz4.Lab：z1/2hr:

glycogen↓z6-12hr:myoglobin

↑z24hr:

GOT,LDH,GPT,CPK↑gross½-4hr4-12hrOccasionally

dark

motting12-24hrDark

motting1-3dMotting

with

yellow-tan

infarct

center3-5dHyperemic

border,

center

yellow-tan

softing7-10dMaximally

yellow-tan

and

soft

with

depressed

red-tan

margins10-14dRed-gray

depressed

infarct

borders3wGray-white

scar,

progressive

from

border

to

coreof

infarct>2mScarring

completeLM½-4hrVariable

waviness

of

fibers

at

border4-12hrBeginning

coagulationnecrosis,edema,hemorrhage12-24hrOngoing

coagulation

necrosis,

myocytehypereosinophilia,

marginal

contraction

bandnecrosis1-3dCoagulation

necrosis,with

loss

of

nuclei

andstriation,

interstitial

infiltrate

of

neutrophils3-7dBeginning

disintegratin

of

dead

myofibers,

earlyphagocytosis7-10dWell-developed

phagocytosis

of

dead

cells,earlyformation

of

fibrovascular

granulation

at

margin10-14dWell-estabished

granulation

and

collagendeposition2-8wIncreased

collagen

deposition>2mDense

collagenous

scar图7-14心肌梗死心肌梗死48h后，心肌细胞核消失，肌浆变成均质细颗粒状，横纹几乎消失。扩大的心肌间隙中可见多量嗜中性粒细胞浸润。图7-15心肌凝固性坏死（肌浆凝集）梗死的心肌纤维肌浆内可见明显增厚的波浪状横带（收缩带）图7-16

心肌梗死心肌梗死7天后，心肌细胞核几乎消失，肌浆变成红染无结构。可见增生的肉芽组织。图7-17急性心肌梗死左心室前壁线形破裂5.complication①

myocardial

rupture：acute,severe，1-3days

or

1week（within

2weefavorite

siteresultVentricular

free

wallHemopericardium

andcardiac

tamponadeventricular

septumLeft-to-right

shuntpapillary

muscleSevere

mitral

regurgitation②

ventricularaneurysm：a

late

complication,from

a

largetransmuralanteroseptal

infarct,paradoxicallybulgesduringsystole③mural

thrombos