logy course 2

8/14/2019 logy Course 2

1/29

Cutsul IICellular 8 extracelular lesions

Ifltracellul^r ecculrrhiionsThercare3typesdsubdanesidldedn

ompoisG (ipids pd6'G aid(elnoi, s) and endosenous p 9d6ic6fte,Aosenous (n ieG sobdaicet orendoseno6 (Pdd lcad bY abi om3L


2/29

lnrrlcellul.rr acct,mulationsr Factorciavodng intracellu af accum ulations:! endogsnous substane ls p.oduced n a normalamountbutlhe rate of removalofce Ls is redlced (ial

r endogenous subslance accumulales becauso lican nol bemelabolized (defective eizyme) > storage diseaseD erogenous abnomalsubstance s deposled in lhe clbecaue lhe cellhas no the capaciiy lo caffy it(accumulation ol cadon a.d siica)

iret rlrlrccllular rcr.urnullnorrs(dr.turbrnces in f^t metrbo|sm)

, Liplds ln ihe body are otlhree categoresa rgylendes o' leLUa 'ats /s'eaioss. obes'v. elc)r choesteroland cholesterol este6 (ATS, etc)D phosphollpids-PL (sloragediseaset


3/29

Steatosi; (frrttr ch.rnge)Slealos s means excessrvehglycer des in parenchymalconlarn this metabolile. Stealos s occure frequenlynlhe iver whch is lhemajor organ invo vd in lipidmetaboism but aso nkidney. heart and mls.le

!-.

!. srs i.( |irn.gdlls,


4/29

I{epatic latty change/ hepatic steatosis

i.l'..,'".-:.. .. se r r! anrusGs srttrB dlr f


5/29

Cholesterol and cholestelol esters

" Manv cells are uslrg the cho eslerclior synihesis ofcellmenibranes without prcducifg an intracellularaccumllalion of cholesierol (CT) and cholesiefol esle6." lnkacellular accumu aiion ofCTls presentrn somep. 'ooqrca, pro.esses, rs ma.r'esleo b) nslologc?lIntracyioplasmic vacuoles (foamy or .thic


6/29

Cholcsrcroi and cholcsrerol esrcr r.cLn rlrtronAccumulat on of CT n phagocyl c ce s- madophages are loadd wrh tui .raitri c.ers lcelswlhE g in hypei pidem c states - Hypenlpldaemicheredtary of acq! red syndrornes

- slrawberry !a lbLadderr sk'n: &nlelasma (at ntema .nse eye)

t,11,


7/29

5rr.s\berry \csrcLe or L

n-meor ,"ioic; t !:o r'" {.b:*Eoundoilhe onqet ra bi:D m

Strawbctq, gallbaddcr

congesied nucosaL s!daceCholesterolosis resu ls lrcmexcesslve cholesierol lrom

focal co lecllons ofroamy


8/29

Xanthonras

connective lissue at the

F.rmrhal Irr pcrlrplde mi.r


9/29

l.iirr1r ./:, li,r,,.11. '' , . - i-; INeph.olic sd..* lhrough.eabsoblion at lhe evel

(6os nop-hilc) - iito cellolasma @ls. wiich rema nin RER with fomation of 'r!, ;: i.{'. .i.Jlt,.;

"ir l'.i

metabol sm of alucose ;glycosen a@umu alon i'Glycosen smorerydenl nthe

nuces o*scer).;id


10/29

i i'r'; t: !iGLti."lin'l s. endoseioG (s,nihenzed inhe bodn or. a ooenoB (brclshLf'dm od'id?orhe bodri

'^.-:-t'i

* Exogenolrs prgmenls r Endogenous pigments

Anthracosrs

macropnages !n neavyGfossly, in smoking thelungs wiLl gt b acker andAnlhracosls is the lermlsd to describe b ack


11/29

Car-boo

'l'etooProfess ona taltooeE use

ox'de or even heratoiyL i)


12/29

' LipofuscinLipotuscin rPre*nts the Pesenceof ry6Gom$ that h4eadcumuktedindiqesrrbre pds appeadns as yelldl\licrcspida lY, it appeac as aperinucd6ne broM (ru$us)piqment. Tris is a prciem nenliniEcylop asm o pismenl ntohepalooyts and erd dyoo$es r^ro@r s at lhe e deiy !.d swere

Hemosidcrin pigrnent

i.Hem osided n is an endoqenougresult ns irom the deodat onHemcidedn is a fom ol ircnMcrcsoprcaLy, in FlE staining


13/29

Flemositletosrsexcessive accumulatron


14/29

Local Hemosidetosrs.onditonsol chonicstasis e sr aveoa, ma(ootugesconra n nq a b6M pgme nE

! al lhe Pe(Phery or beed nsi e qblueqen pigmnr Pers

HemosidennThe brown granu ar materain a veolar macrophages isaccumLlated asa resu I or

In hepalocytes hemosdernaccumlLation s slaLftd mblue using a speclalslaiiLnq


15/29

Biluubir pigmcnrB lnubln is an endognousEsulting from degBdatLon

ex@ss ve accumulat'on ol

clinica ly manifesled bY anye low colorofsclerae and


16/29

j.ru rr.Lcclorphol o-tl-In cterus skin scerae andoans are geen sh-yelowYe low coloriums in green

Thre are rema n unsbLned

lr,lacroscop ca Ly the llveris

,\cc,.roruLatiooM'os@p'.a|iy'he|eare2

drahepalocyt-A granura'

of L, i:1. pigL,rcrrL: \ll


17/29

lhslypeof]:lndcalhedomjmnt

EliTRACLl.l,aILrl}.. Aricil LelU LrL'1 i1]l 'l3{ Hyalinosis. Hvalinosis represenls a::l,ij:.**'"- abromar acc*.r . a,io- o'nyalnilll".li;il e Amyloidosis":,"^-'"" Amvooocisischaracie-zed.;;.,;"" by an e(racellularaccumulatjon of amyLoid(nbrillar abnormal proieins) niissues and organs in a vad,Aiyofconditions


18/29

TCi'Itc I t I \tFyaln is a descriplve le.mthal describes an a tered-Anracellular prote n. whichhas an u.iform appea nce

ICH-Hyalnoss represenlsaccumulalion oi hya in.ECH Hya nos s represntsa ussu ar accumllation oi

Protein accumulation

* \.'i

(hyalinosis)


19/29

Ar\{\'LOID O SIS

r ssles arro oqans rn a

reacuon wrih starah. hen@


20/29

AIII\LOIDOSIS

by v rchotr reaclion (bY

b.own red,lhatlums ln

[rlcrcsftpilry n HE sra n ngamyroiddeposits 3 3tained nihe sameuY as hya n i Pink

I'hyslcal structure or amylorq. i; EM ihe afryLo d E iepsded by lrr ck unb.ancfred I amedts- lnis onla- rro.'s "spo-


21/29

Chcmical !irucRIre of amlloid

1. Amyloid fbrillar Ptotetn

Chemical structure of an Yloid:, 95% of the mateial consisis of amyloid librillar, lhe remaining 5% is represented bv the Pcomponent (glycoprotein - seic amyloid)

s oi amyloid P@teins 3rbrllarr'"xix".?L:il*",i"":1il?:"," 5de, d romp6ma.e slmmu^(kl

) n 3 !irqf pdei nofrE' I :.."*r'f:;1""". ; 'v;l:x':11.'"""'i':..""'3 " " *-'. i": o ""'*td",';rT flfii::t;;:"?.ii i:!is, "il r:: "5";' Jir * " *-' $m"i"s},ffi *jf:,1iil1'.r;r.f '{+J'*$}:i'+li"ii:i{r

o z.Lmd,r a^'.a *ru. Fde"c. .!o- ). I ,rlgTra o o: rc_n


22/29

2. P Component

ha6 a similar sltucture wilh C-Eacli@ p@ie n.serum componeni (PAS +)has affnity ior amioid riber and may be rquiredtoris an lselllprcrein ln IMH deiect n9 orthe amyloid in

P componeni is a glycoprctein. disilncld byiibdLs of amio d.. lscoselyassoqaGdwithflbnsof anilodinallfomsor

amyloldosis


23/29

. isro4nary heamybd s' I.1 r...;: it.r..t--\i .;,.tl$,:;ir:ilJ';


24/29

Renal amyloidosis

t_ --lcpaIc lm)1o1dosl\


25/29

Emoe.onirci "10tie-d n .-o /ed!eaf! I aso_rcv'on Lhe eBiemtr se^'lafllLodosis k,i'{o.o, /.. :in b0 omosc 5r"l 6 s.oA oo at t'd in'"ri.deoosd oaee"iui dndudLno neiemcadf;mvodcs Gn mer*r4.au5e 'mpaid condlcr ondisl!brnoa" oai, d4df/'om\na edsr"4ryoofcvP

C.rr.lirc arlvloiJo:rs

..\i,,n: .:r!r,L h\ .il.,Nnr ir((l,,,llri: ,ls({!rLr.rrPaihological crlcincadonCacilicationdiseasemeansabnormalslogeorcacumThere are 2 types of pathological calcification :r DystroPhiccalcificatio.e occure ldny in nonllabLe ordead lssues

r in ihe abse^ce of d studan in ca metabo shr Metastatic calcificalion! @cu6 in loca v ab e lissues! in se ol ncased *rum concentalonsorca. nihe pr*ence of ab^o rmaL melabolism or ca


26/29

Dr sttophic calcifi cation. Dysirophic calcincaton rnay occuf in dead tissues ncase of normal calcaemia

r Dyslroph c calcfication 6 sen in areasofnecrosis old fterenl types:coagulal on nec

! Ca dtcal on s a so present n alheromas of advancedr I asooccu6 n card ac atered valvesJ whatever lhe p ace of slorage ca cufr salts appear aswhite linegEnules ofien ooklnq cretareols

:- -- -.-

.lYletllstatlc ctlcrlrcatron' N4elastat c calcification may occur in normal tissuesin case of hypercalcaern a.. There are 4 major causes of hypercaLcaem a:! incrcased secEtionolparalhyrcd homone wlhaconsequenl bone sorbton. as n parathyroid tumors! bone tssue damagelhatoccurs in pdmarytumors olbone o dfuqF .Let.rat a"rr.td.", .9, b ede. "1("-r dsorders realed iovllamn D which ncludes poisoninq

d re.alfailure, causing tention ofphosphate which leadsto secondary hypepaGthyro dism


27/29

Nletastatic ca1cifi cation - NIorPholog,YE Locallons metaslatccalclicaton occurs anvlvhere nthebody but affecls mai.ly irtersutialt ssues oflhe gaski.mucosa kidney, pllmonary syslemc aneres and. A lhese iissleswilh difiereni localation lost acldsandthus became an aLkali.e afea predlsposing to metaslat c' Morphologically nd llese rocl oa)srmilar to thoF descfbed In dysboph c.a clficationThus, they aPpear as arnorphous non_cryslalline depositsor in the form ofcrystallline deposilse GeneralLy, mineral salt deposils are nol causlng clin cadvsf .1c-or o'roadq:olallrri,/ ca,.- espratof o-c..r'l. ri,la)s re opoo" ls ilthe kidnev herroca c Fos slmay cause renal dysi!6c1 on-r,1L"d'r. r '.. ,r^dnl!1 ."1'r'n


28/29

C.rlcitlc.l r rh-cs

PethoLogical rissue calciEcations


29/29

Prrh,,loe,crl u :ue c-rl.itrc ro ls

PrthologLcrl rissuc t'icrfi c:titurs

calc!!m sa ts stain darkblue on H&E.specialstains lke theVon Kossa ls applied i

logy course 2

Documents