Home >Documents >2.Patologia Aparatului Cardiovascular

2.Patologia Aparatului Cardiovascular

Date post:23-Jan-2016
Category:
View:57 times
Download:4 times
Share this document with a friend
Description:
histologie
Transcript:

PATOLOGIA APARATULUI CARDIOVASCULAR

PATOLOGIA APARATULUI CARDIOVASCULAR-Endocardita valvulara- Miocardita reumatismala- Miocardita Fiedler- Infarctul miocardic- Pericardita fibrinoasa- Ateromul- Aortita sifiliticaAnatomieBarbati m=280-340 gFemei m=230-280 gVD = 0.5 cm (1/3 VS)VS= 1.3-1.5cmAtrii = VDAparat valvular cordaje tendinoase+ muschi papilariEpicard+miocard+pericardINFARCTUL MIOCARDICDefinitieCauze

VEZI SEMESTRUL I !3

RUBIN -FIGURE 11-2. Position of left ventricular infarcts resulting from occlusion of each of the three main coronary arteries.A. Anterior infarct, which follows occlusion of the anterior descending branch (left anterior descending, LAD) of the leftcoronary artery. The infarct is located in the anterior wall and adjacent two thirds of the septum. It involves the entire circumferenceof the wall near the apex. B. A posterior (inferior or diaphragmatic) infarct results from occlusion of theright coronary artery and involves the posterior wall, including the posterior third of the interventricular septum and theposterior papillary muscle in the basal half of the ventricle. C. Posterolateral infarct, which follows occlusion of the leftcircumflex artery and is present in the posterolateral wall.4

3zile

In this microscopic view of a recent myocardial infarction, there is extensive hemorrhage along with myocardial fiber necrosis with contraction bands and loss of nuclei

5 zile

1-2 saptamani

3-4 saptamani

The earliest change histologically seen with acute myocardial infarction in the first day iscontraction bandnecrosis. The myocardial fibers are beginning to lose cross striations and the nuclei are not clearly visible in most of the cells seen here. Note the many irregular darker pink wavy contraction bands extending across the fibers.

1-2 zile -disparitia nucleilor fibrelor miocardice-inceput de inflamatie acutaClinic:Modificari EKGCreste CKMB16In this microscopic view of a recent myocardial infarction, there is extensive hemorrhage along with myocardial fiber necrosis with contraction bands and loss of nuclei

12-24hPrimele 7 zile-transmural

-necroza fibrelor musculare galben palid-hiperemie-miocard viabilENDOCARDITA VALVULARAEndocardita - infectioasa (vegetanta) -non-infectioasa(marantica, b.Liebman-Sacks, LES)Endocardita infectioasa -colonizarea cordului sau endocard mural =>formarea de vegetatiii friabile compuse din detritusuri trombotice si microorganisme asociate adesea cu distructia tes cardiac subiacent-apar prin bacteriemie-poarta de intrare->inf dentare,proceduri iv, droguriVegetatiile contin:-bacterii 65%Streptococ viridans25%Stafilococ auriu(abuz IV droguri, imunodeficienta)-fungi, ricketsii(febra Q), Clamidii+fibrina si celule inflamatoriiApar de valve NATIVE/PROTETICE (S. epidermitis)Clinic -> 2 forme1.ENDOCARDITA ACUTA-simptome brutale si severe-valve normale-mai ales S auriu-pot aparea perforatii valvulare=>aj in miocardul subiacent=> abces inelar-sursa de infectie =bacteriemia-persoane cu rist: taratii, imunodeprimatii, alcooliciiPatogenie: agresiune valvulara de catre substante toxice=>predispunere la trombi=>infectare cu organisme virulente=> deces z->s>50%=> inf. Necrotizante, ulcerative, invazive =>dificil de tratat=> necesita chirurgie2.ENDOCARDITA SUBACUTA-apare insidios-valve afectate anterior (prolaps VM,b.reumatismala, b. congenitala cardiaca, lez. Degenerative, calcificari VM, Vao-c.m. Streptococul Viridans-perforatia este rara-sursa de infectie-> dupa traume minore muc bucala, intestinala, VUPatogenie: agresiune valvulara ->trombi fibrino-plachetari sterili(non-bacterieni)-> colonizarea cu agenti infectiosi=> Endocardita subacua bacteriana vegetanta la locul unde sangele regurgiteaza in camerele cardiace.Micro-> tesut de granulatie -> fibroza/calcificari + ii cronic

Endocardita non-infectioasa1.E. trombotica non-bacteriana (marantica)

-grupe de risc: bolnavi debilitati, hipercoagulabilitate, TEP/CID, ADK, lez traumatice: cateterism cardiac-vegetatii mici 1-5mm, vitroase, gri-roz-sterile, friabile nedistructive-fibrinoplachetare-localizare: linia de inchidere a valveiMicro:-trombi fata reactie ii/distr valva-sursa sistemica de embolii=> infarct secundar-rol de NIDUS pt E. bacteriana-evolutie ->organizare fibroasa=> benzi de fibrozaPatogenie: -> status hipercoagulabilitate=> activare cascada coagulare

2.E. nonbacteriana verucoasa(b. liebmann Sacksc)

-VM, VT-vegetatii mici verucoase, sterile, 1-4mm, roz granulare-orice valva-> pe suprafata expusa torentului sangvin- pe suprafata subiacenta a valveiVEGETATIIINFECTIOASE >5mmNON-INFECTIOASE 5 mm), 3) lupice (Libman-Saks) = ambele fetze4) NBTE = non-bacterial thrombotic endocarditis ( predomina proliferarea fibroblastelor si depozite de colagen interstitialDaca necroza este extensiva-> modificari ~infarct PMN+/ organizare/reparareDe obicei este insotita de pericarditaBACTERIANA- focare multiple cu ii mixt (PMN) - microabcese -> endocardita infectioasa-> emboli septici in coronareRickettsia -> vasculite extinse cu afectare coronareFungi- gazde imunocompromiseToxoplasma raspuns inflamator focal mixt (PMN+Eoz)Boala Chagas(Trepanosoma Cruzi)-> ii mixt (Li, Pl, Ma)Toxica ii perivascular + interstitial(Li, Pl, Eoz) -nu are necroza miocitara

MIOCARDITA VIRALA:I. ii interstitial (Li+PMN) si necroza a fibrelor musculareII. Predomina Li si his si se produce proliferarea tes conj.RICKETTSIA: Edem interstitial ii Focal sau in placard Anitschkow cells, mast cells and eosinophils are noted in close association with small vessels ; PMN putine (necroza=> multe PMN) Modificari vasculare endoteliul capilar si arteriolar edematiat si flebita cu trombozaArterita miocardica necrotizanta ( Tifos epidemic)MIOCARDITA REUMATISMALARAA=FEBRA REUMATICA=lez. Ii ac, recurenta,, post infectie cu streptococ hemolitic gr ACea mai imp manif a RAA= boala cardiaca reumatismala cronica ce poate produce lez parenchimatoase ireversibile si decesEtiopatogenie-r. imunologica la atg streptococice-r. autoimuna declansata de o inf streptococicaClinic-febra, poliartrita migratorie artculatii mari, pancardita,noduli subcutanati, eritem marginal, coreea Sydenham-copii 5-15 ani-latenta 1-5 s-debut: febra + poliartrita articulatii mari-cardita reumatismala 50-70% din copiii de 2-16 ani-pina la varsta adulta- 35%= un singur atac-cea mai grava leziune=miocardita reumatismala =>-aritmii(fibrilatie)-prelungirea intervalului PR-fibrilatie= trombi arteriali =>embolii-dilatatie cardiaca+insuficienta mitrala=>deformari ale aparatului valvular -atacul initial => vulnerabilitatii la reactivarea leziunii la faringite consecutive=> atacuri recurente cu aceleasi manifestariDG + : criterii JONES minim 2 majore sau 1major+2 minoreMAJORE cardita-poliartrita-coree-eritem marginal-noduli subcutanatiMINORE artralgii-febra-reactanti serici de faza acuta-pr pe ekgMorfologie lez. Inflamatorie focala cu localizari-in cord-patognomonic=granulomul reumatismal Aschoff-in miocard= localiz in tes conj-vasc- in relatie cu vasele intramiocardice=> miocitele=>leziuni distrofice /sunt distruseNodulul reumatismal1.initial- necroza fibrinoida a fb de colagen din ax conj-vasc= faza distrofic-alterativa2.Faza proliferativa= constituirea granulomului reumatismal-focarul de necroza fibrinoida e inconjurat de Li, Ma, Pl-histiocitele citoplasma amfofila abundenta-nc rotunzi/ovoizi, central-cromatina dispusa in centru3.In timp->(ani, zeci de ani)corpi Aschoff=>inlocuiti de cicatrici fibroase, ap valvular ingrosat, retractat=>deformari permanenteGRANULOMUL ASCHOFF-necroza fibrinoida-Li,Pl, Ma-macrofagele cel Aschoff= multinucleate cel Anitschikow(patognomonic)=>nc in bara dintata omida, citopl abundenta, nc central rotund/ovoid, cromatina centrala

PANCARDITA -> miocardul este cel mai sever atinsMIOCARDITA REUMATISMALAENDOCARDITA cel mai caracteristic si agresic efect-tipic->numeroase veruci 1-2mm,rosietice, compus din material fibrinoid-pot da focare de endocardita ulcerata=>proliferare mezenchimala c. AschoffPERICARDITA=> fibrinoasa=tartina cu unt desprinsaEFECTE VALVULARE: -cuspe greoaie, deformate de fibroza-comisuri fuzionate, calcificari valvulare,neovascularizatie-cordaje tendinoase groase, scurtate, unite-aspect de bot de peste32HP-organizare fibroasa a inflamatiei acute-foite valvulare=>ingrosate retractate=> deformare permanenta-VM/VT=ingrozarea foitelor, fuzionarea comisurilor scurtarea si fuzionarea cordajelor -fibroza densa + neovascularizatie-inlocuirea corpilor Aschoff cu cicatrici fibroase-cea mai frecventa cauza de stenoza mitrala-+/- VAo,rareori VP, sau VT-aspect de gura de peste=> punti fibroase in jurul comisurilor valvulare si calcificari-st M -> dilararea AS=> trombi murali-HVD=> congestie pulmonaraVs-> normal in SM izolata

ACUTE:-Granuloame Aschoff -Inflamatie- Celule Anitschkow si Aschoff-Pancardita-Vegetatii pe cordajele tendinoase la jonctiuneCHRONIC:VALVE INGROSATEFUZIUNEA COMISURILORCORDAJE TENDINOASE SCURTATE, INGROSATE

Robbins34CLINICPoliartrita migratorieMiocarditaNoduli subcutanatiEritem marginatCoreea Sydenham (St. Vitus Dance) -> cautati pe youtube!!!!!

35

36MIOCARDITAINFLAMATIA MIOCARDIULUIFrecvent microbianaCOXACKIE A & B, CMV, HIVTrypanosoma cruzi (B . Chagas ), 80%TrichinelozaToxoplasmozaB. Lyme (5%)DifteriaIMUN: Post-viral, reumatic, LES, hipersensibilitate medicamentoasaalfa-metil dopa, sulfati

37

II Li tipic , ocazional eoz, CG 38Alte MiocarditeAdriamicinCiclofosfamidaCatecholamine (Pheochromocitom)Amiloidoza sistemica sau primar cardiacaRosu de Congo: birefringenta verde in lumina polarizataHemochroma

Click here to load reader

Embed Size (px)
Recommended