Robbins Essential Pathology (PDF) Diseases of Blood Vessels
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Summary
This document is a chapter from a medical textbook on diseases of the blood vessels. It covers topics like chronic endothelial injury, endothelial dysfunction, and macrophage activation. Visual aids and diagrams help with understanding atherosclerosis mechanisms.
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108 CHAPTER 7 Diseases of Blood Vessels Endothelium...
108 CHAPTER 7 Diseases of Blood Vessels Endothelium Intima Media Adventitia 1. Chronic endothelial “injur y”: Hyperlipidemia Hyper tension Smoking Homocysteine Hemodynamic factors Toxins Viruses Response to injur y Immune reactions A 2. Endothelial dysfunction (e.g., increased per meability, Platelet leukocyte adhesion), Monocyte monocyte adhesion, and migration 3. Macrophage activation, B Smooth smooth muscle recruitment, muscle cell accumulation of lipids in Fig. 7.3 Hypertensive vascular disease. (A) Hyaline arteriolosclerosis. vessel wall The arteriolar wall is thickened with the deposition of amorphous pro- teinaceous material (hyalinized), and the lumen is markedly narrowed. Fatty streak (B) Hyperplastic arteriolosclerosis (onion-skinning) (arrow) causing lumi- nal obliteration (periodic acid–Schiff stain). (B, Courtesy Helmut Rennke, MD, Brigham and Women’s Hospital, Boston.) ver or bar y excreon. C onsequeny, ger eves o HDL cor- 4. Macrophages and smooth muscle cells reae w a reduced rsk. S evera oer acors assocaed w an engulf lipid ncreased rsk o aerosceross (de, sedenar y esye, obesy, smokng, dabees) ower HDL eves or eevae LDL eves. Sa- Lymphocyte n drugs, wc nb coesero syness and suppress LDL eves, aso ower e rsk o aerosceross-reaed cardovascuar Fibrofatty atheroma dsease. Hemody namc fac tors. A eromas end o o cc ur a s es o u r- bu en bo o d ow : e os a o e x ng vess es , a maj or ar e r a branc p ons, and a ong e p oser or wa o e ab d om na aor a. Te roe o y p er e ns on n e d e veopmen o a e ro - s ceross s presumaby due o emo dy nam c e e c s on e nd o e - a unc on. 5. Smooth muscle Genetcs. Famy sor y s an mporan rsk acor or aeroscero- proliferation, collagen ss. Fama ypercoeseroema, an auosoma domnan dsease, and other ECM Lipid deposition, extracellular and mugenc dseases suc as yperenson and ype 2 dabees, debris lipid aso are assocaed w ncreased rsk. Lymphocyte Collagen Age. Sympoms rom advanced esons appear n mdde age or aer. Fig. 7.4 Summary of the morphologic features and main pathogenic he ncdence o myocarda narcon ncreases ve-od beween events of atherosclerosis. 40 and 60 years o age, and dea raes rom scemc ear dsease rse w eac successve decade. CHAPTER 7 Diseases of Blood Vessels 109 A B Fig. 7.5 Atherosclerotic lesions. (A) Aorta with mild atherosclerosis composed of fibrous plaques, one denoted by the arrow. (B) Aorta with severe, diffuse complicated lesions, including an ulcerated plaque (open arrow), and a lesion with overlying thrombus (closed arrow). FIBROUS CAP (smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization) NECROTIC CENTER (cell debris, cholesterol crystals, foam cells, calcium) MEDIA Fig. 7.6 The structure of an atheromatous plaque. G ender. Premenopausa women are reavey proeced agans e exraceuar marx (remodeng) and rombus organzaon, and aerosceross compared w age-maced men, possby because oten undergo caccaon, wc can be seen radograpcay. o e beneca efecs o esrogen and progeserone on pd pro- Acue and cronc canges n aeromas can ave serous es. consequences: Cona ematopoess. he perpera bood ces o over 10% o Rupture or uceraton exposes rombogenc subsances, nduc- adus over e age o 70 years w norma bood couns ave cona ng rombus ormaon (Fg. 7.7). muaons n genes a are assocaed w varous ypes o myeod Hemorrage, caused by damage o rage capares n e a- neopasms, suc as acue myeod eukema (see Caper 9). Ind- eroma, eads o rapd paque expanson or paque rupure. vduas w cona emaopoess ave a wo-od eevaed rsk o Embosm o sma ragmens o aeroma durng paque rupure dyng rom cardovascuar dsease, possby because ese mua- may cause scema n downsream organs. ons dysreguae e uncon o macropages and ereby enance Aneurysm formaton s caused by oss o easc bers and oer oca nlammaon wn aeromas. supporng srucures rom e meda ayer o e vesse wa. Clncal Features. Myocardia infarcion (ear aack), cerebra Morphology. In descendng order, aerosceross mos oten nvoves infarcion (sroke), aoric aneur ysm, and peripera vascuar dis- e nrarena abdomna aora, e coronary areres, e popea ease (gangrene of exremiies) are e major cinica consequences areres, e nerna carod areres, and e vesses o e crce o of aeroscerosis. Ws. Lesons a varous sages o severy oten coexs (Fg. 7.5). hese compcaons may sem rom sow progresson o aerosce- Aeromaous paques are we o yeow rased esons w sot pd roc esons or rom dramac acue evens, as oows: cores covered by brous caps conanng smoo musce ces and Ateroscerotc stenoss. Sowy advancng senoss may presen w coagen, assocaed w macropage and T-ympocye nraes sympoms o scema n ssues supped by e afeced vesses. he and varabe degrees o neoangogeness (Fg. 7.6 and Suppemena occuson s descrbed as a crtca stenoss wen bocks 70% o e eFg. 7.1). Macropages sufed w pd, so-caed oam ces, may be umen, because a s pon and beyond, e ssue demand oten promnen. Exraceuar coesero s oten presen, requeny n e oupaces e bood suppy. Presenaons ncude angna pectors, orm o crysane aggregaes (coesero cets). he meda benea wc ypcay appears w exeron and rems w res; cronc e paque may be aenuaed and broc, w smoo musce aropy. scemc eart dsease, w sympoms reaed o ear aure; and Paques progressvey enarge roug syness and degradaon o ntermttent caudcaton, due o eg scema w exeron. CHAPTER 7 Diseases of Blood Vessels 109.e1 L F C A B C Supplemental eFig. 7.1 Histologic features of atheromatous plaque in the coronary artery. (A) Overall architecture demonstrating fibrous cap (F) and a central necrotic core (C) containing cholesterol and other lipids. The lumen (L) has been moderately compromised. Note that a segment of the wall is plaque free (arrow); the lesion is therefore “eccentric.” In this section, collagen has been stained blue (Masson trichrome stain). (B) Higher-power photograph of a section of the plaque shown in (A) stained for elastin (black), demonstrating that the internal and external elastic laminae are attenu- ated and the media of the artery is thinned under the most advanced plaque (arrow). (C) Higher-magnification photomicrograph at the junction of the fibrous cap and core, showing scattered inflammatory cells, calcification (arrowhead), and neovascularization (small arrows). 110 CHAPTER 7 Diseases of Blood Vessels A B Fig. 7.7 Atherosclerotic plaque rupture. (A) Plaque rupture without superimposed thrombus, in a patient who died suddenly. (B) Acute coronary thrombosis superimposed on an atherosclerotic plaque with focal disrup- tion of the fibrous cap, triggering fatal myocardial infarction. In both (A) and (B), an arrow points to the site of plaque rupture. (B, Reproduced from Schoen FJ: Interventional and Surgical Cardiovascular Pathology: Clinical Correlations and Basic Principles, Philadelphia, Saunders, 1989, p. 61.) Acute paque cange. Acue paque canges, suc as rupure, Pathogeness. he pressure wave produced durng sysoe produces nrapaque emorrage, or weakenng o e brous cap by proeases maxma wa sress and urbuence n e nrarena aora, e mos reeased rom nlammaory ces, oten ave serous consequences. common se o AAAs. hese wa sresses are exacerbaed by yperen- Supermposed romboss and rapd, compee occuson may ead o son, wc enances e rae o expanson o AAAs once ey orm. myocarda narcon and sroke, medca emergences a mus be here s a srong assocaon w smokng a s no we undersood, dagnosed rapdy and reaed w ancoaguans (parcuary an- bu may be reaed o an eevaed rsk o yperenson and aero- paee drugs) and romboyc agens or endovascuar sens. Oer sceross, as we as e efecs o oxns n obacco smoke. Aneur ysma mes, paque rupures ead o ncreased scema, parcuary n e daons oten concde w areas o aerosceross, wc, as aready ear, wou narcon, a cange marked by ncreasngy severe dscussed, can conrbue o meda scarrng. hese acors, aone or “unsabe” angna, wc may srke even wen e paen s a res. n combnaon, may ead o oss o smoo musce and exraceuar marx componens, weakenng e vesse wa and seng e sage or aneur ysma daon. ANEURYSMS AND DISSECTIONS Aneurysms and dissections are caused by congenital or acquired Morphology. Abdomna aorc aneur ysms ypcay occur beween defects in the walls of blood vessels or the heart. e rena areres and e aorc burcaon; ey can be saccuar Aneur ysms are oupoucngs a nvove a ree ayers o an or usorm n sape and up o 15 cm n dameer and 25 cm n arer y (nma, meda, and advena) or e aenuaed wa o e eng (Fg. 7.8). In mos cases, exensve aerosceross s presen, ear, and may sem rom nered deecs, yperenson, aerosce- w nnng and oca desrucon o e underyng meda. he ross, or ransmura myocarda narcons. Dssecons occur wen aneur ysm sac usuay conans band, amnaed, poory organzed g-pressure arera bood gans enr y o e arera wa roug a mura rombus, wc can muc o e daed segmen. surace deec and puses apar e underyng ayers. Aneur ysms and dssecons cause sass and romboss and ave a propensy o rup- ure—oten w caasropc resus. he mos common and mporan vascuar aneur ysms and dssec- Clncal Features. Mos AAAs are asympomac un an acue comp- ons nvove e aora and are descrbed nex. caon deveops. Pysca examnaon may revea a pusang abdom- na mass. hey are dagnosed and szed by magng sudes, mos Aortic Aneurysms oten abdomna urasound. Acue compcaons o AAAs ncude e Aortic aneurysms most often occur in the abdomen and are prone oowng: to catastrophic ruptures, which often prove fatal. Obstructon of a brancng vesse (e.g., e rena, ac, verebra, or Aneur ysms n e orax and ab domen ave dferen r sk ac- mesenerc areres) due o expanson, exenson, and oten super- ors: horacc aor c aneur ysms are rea vey uncommon and are mposed romboss, resung n dsa scema o e kdneys, ass o cae d w n er e d dee c s n e ex race u ar ma r x, as n egs, spna cord, or gasronesna rac E ers-D an os syndrome, Mar an syndrome, and cardovas c u- Embosm rom a rupured aeroma or a mura rombus ar syp s (s e e C aper 6), w ere as ab domna aor c aneur ysms Impngement on adjacent structures (e.g., compresson o a ureer or (AAAs) are muc more common, p ar c u ary n ma es and n adu s eroson o verebrae by e expandng aneur ysm) over e age o 60 ye ars w o smoke. A eros ceross and yp er- Rupture no e peronea cavy or reroperonea ssues, eadng enson are mp or an pre dsp osng cond ons. I s es mae d a o massve, oten aa emorrage approxmaey 1,000,000 ndvdua s n e Une d S aes ave an Women are ess key o ave AAAs, bu ose a occur n women AAA and a b ewe en 0.5% and 1% o es e esons w r upure are more key o rupure. he rsk or rupure s deermned by sze: e ac ye ar. he ds c usson a o ows s o c us e d on AAAs. Aneur ysms 5 cm n dameer or arger are consdered g rsk and CHAPTER 7 Diseases of Blood Vessels 111 requre surger y. Tmey ner venon s crca: e moray rae or Pathogeness. Aorc dssecon many occurs n wo sengs: (1) eecve procedures s approxmaey 5%, wereas e rae or emer- men 40 o 60 years o age w aneceden yperenson (>90% o gency surger y ater rupure s rougy 50%. cases) and (2) younger paens w genec dseases o connecve ssue, suc as Maran syndrome and Eers-Danos syndrome (see Aortic Dissections Caper 6). he aoras o agng yper ensve paens sow meda Aortic dissection occurs when arterial blood penetrates the intima yperropy o e vasa vasorum (e sma vesses a suppy e and splays apart the media to form a blood-lled channel within vesse wa); s may dmns peruson o e meda, eadng o oss the aortic wall. o smoo musce ces and degenerave canges n e exraceuar Aorc dssecon may produce aa emorrage e bood rup- marx. Wa naes e nma earng s unknown, bu once bood ures roug e advena and escapes no adjacen ssues. gans access o e vesse wa unnes roug e meda aong e pa o eas ressance. Morphology. he nma ear markng e orgn usuay s ound n e ascendng aora wn 10 cm o e aorc vave (Fg. 7.9A). he dssecon pane wn e meda can exend rerograde oward e ear or dsay, occasonay as ar as e ac and emora areres (see Fg. 7.9B). Exerna rupure causes massve emorrage, or resus n cardac amponade occurs no e percarda sac. In some nsances, e dssecng bood reeners e umen o e aora roug a second dsa nma ear, creang a vascuar canne wn e meda (doube-barreed aorta). Hsoogcay, cystc meda degeneraton, caracerzed by oss o smoo musce ces, easc ssue ragmenaon, and accumuaon o abnorma proeogycan-rc exraceuar marx, may be seen (Suppemena eFg. 7.2). In mos nsances, no specc deec s dened. Clncal Features. Pa ens ypc a y pres en w e sud d en ons e o excr uc a ng e ar ng or s abb ng p a n , b e g nn ng n e aner or ces and rad a ng o e m d d e o e b ack. R e rog rade d ss e c - on no e aor c ro o may d s r up aor c v a ve u nc on , c aus e myo c ard a narc on by compre ss ng e c oronar y ar er e s, or e ad A B o massve emor rage no e p e r c ard a sp a c e. O er comp c a- Fig. 7.8 Abdominal aortic aneurysm. (A) External view of a large aortic ons are re ae d o exens on o e d ss e c on o e g re a ar e r es aneurysm that ruptured at the site is indicated by the arrow. (B) Opened o e ne ck or o e rena , mes e ne r c , ac, or sp na ar e r es, any view, with the location of the rupture tract indicated by a probe. The o w c may b e come obs r uc e d. R ap d d ag nos s , an yp e r ens ve wall of the aneurysm is attenuated, and the lumen is filled by a large, layered thrombus. * A B Fig. 7.9 Aortic dissection. (A) An opened aorta with a proximal dissection originating from a small, oblique intimal tear (identified by the probe) associated with an intramural hematoma. Note that the intimal tear occurred in a region largely free of atherosclerotic plaque. The distal edge of the intramural hematoma (black arrows) lies at the edge of a large area of atherosclerosis (white arrow), which arrested the propagation of the dissection. (B) Histologic preparation showing the dissection and intramural hematoma (asterisk). Aortic elastic layers are black, and blood is red in this section, stained with Movat stain. CHAPTER 7 Diseases of Blood Vessels 111.e1 A B Supplemental eFig. 7.2 Cystic medial degeneration. (A) Cross section of aortic media from a patient with Marfan syndrome, showing elastin fragmentation and areas devoid of elastin that resemble cystic spaces but are actually filled with proteoglycans (asterisks). (B) Normal media for comparison, showing the regular layered pattern of elastic tissue. In both A and B, elastin is stained black.