Robbins Essential Pathology PDF - Cell Injury and Cell Death
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This document is an excerpt from Robbins Essential Pathology, focusing on cell injury and cell death from a pathology perspective. It discusses topics such as physiologic and pathological hypertrophy, as well as the accumulation of abnormal substances within cells. The excerpt also touches on chronic inflammation and its relation to the subject.
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12 CHAPTER 1 Cell Injury and Cell Death A B C...
12 CHAPTER 1 Cell Injury and Cell Death A B C Adapted Adaptation: Normal myocyte response to myocyte (hypertrophy) increased load D E Fig. 1.14 Physiologic and pathologic hypertrophy. (A-C) Physiologic hypertrophy of the uterus during preg- nancy. (A) Gross appearance of a normal uterus (right) and a gravid uterus (left) that was removed for post- partum bleeding. (B) Small spindle-shaped uterine smooth muscle cells from a non-gravid uterus. (C) Large, plump, hypertrophied smooth muscle cells from a gravid uterus; compare with (B). (B and C, same magnifica- tion.) (D, E) Myocardial hypertrophy in a patient with severe hypertension. (D) Normal myocardium (thickness 1 to 1.5 cm). (E) Myocardial hypertrophy. The left ventricular wall is thicker than 2 cm. n cronc smokers and coumnar meapasa o e esopagea e subsance may be ocaed n e cyopasm, wn organees squamous epeum n paens w cronc gasrc relux (Fg. (ypcay ysosomes), or n e nuceus, and may be syneszed by 1.15). Aoug meapasa aows ces o sur vve, oten com- e afeced ces or may be produced esewere. promses er uncon; or nsance, squamous epeum n e e man paways o abnorma nraceuar accumuaons are broncus canno produce mucus and provde car y acon, wo nadequae remova and degradaon or excessve producon o an mporan uncons o norma bronca epeum a proec endogenous subsance, or deposon o an abnorma exogenous mae- e ar ways rom necon. Aso, w e perssence o rggerng ra. Some exampes are descrbed n e oowng. smu, meapasc epeum can be e se o neopasc rans- Fatty cange (steatoss). Seaoss s e accumuaon o pds (Sup- ormaon, as n e bronc (squamous ce carcnoma o e ung) pemena eFg. 1.2), mos oten n e ver oowng proonged and upper gasronesna rac (esopagea adenocarcnoma ars- acoo consumpon or n obese ndvduas as a componen o ng n e seng o Barre esopagus). nonacooc ay ver dsease (see Caper 13). Coestero and coeser y esers. Pagocyc ces may become overoaded w pd (rgycerdes, coesero, and coeser y PATHOLOGIC ACCUMULATIONS IN CELLS esers) n severa dferen paoogc processes (Suppemena eFg. Cells may accumulate abnormal amounts of various substances, 1.3), mosy caracerzed by ncreased nake or decreased caab- which may be harmless (e.g., carbon particles in the lungs and osm o pds. O ese, aerosceross s e mos mporan (see mediastinal lymph nodes of city dwellers) or may cause varying Caper 8). degrees of injury. CHAPTER 1 Cell Injury and Cell Death 13 mmunogobuns a msod and accumuae n e roug ER o some pasma ces; neurobrar y anges n neurons; and “aco- oc yane” (see Caper 13). Pgments. Pgmens o severa ypes may accumuae n ces. Lpo- fuscn s a browns, granuar maera composed o pds and pro- ens a s produced by ree radca–medaed pd peroxdaon (Suppemena eFg. 1.5). Is accumuaon n ces s a sgn o ree Basement Normal Squamous radca–medaed njur y, so s oten seen n oder ndvduas and membrane columnar metaplasia n aropc ssues. Hemosdern s a emogobn-derved brown epithelium A pgmen (Suppemena eFg. 1.6) a accumuaes n pagocyes and oer ces n condons o ncreased red ce breakdown or ron overoad (see Caper 9). Gycogen. Excessve nraceuar deposs o gycogen are assocaed w abnormaes n e meabosm o eer gucose or gycogen. Gycogen may accumuae n poory conroed dabees or n gyco- gen sorage dseases (see Caper 13). Cacum. Cacum sa deposs are seen n a varey o dsease saes. Dystropc caccaton occurs n e seng o norma serum ca- cum and s e deposon o cacum sas n njured ssue (e.g., n areas o caseous necross and n advanced aerosceross). Dys- ropc caccaon can ave uncona consequences, as n ca- cc senoss o e aorc vave causng et venrcuar yperropy B due o pressure overoad (Suppemena eFg. 1.7). Metastatc ca- Fig. 1.15 Metaplasia of normal columnar (left) to squamous epithelium ccaton occurs n e seng o ypercacema, wc s seen n (right) in a bronchus, shown schematically (A) and histologically (B). saes o yperparayrodsm (see Caper 16), or ncreased bone desrucon, as n cancers nvovng e bone. Measac cacca- on occurs wdey rougou e body bu prncpay afecs e Protens. Morpoogcay vsbe proen accumuaons are ess nersa ssues o e vascuaure, kdneys, ungs, and gasrc common an pd accumuaons; ey may occur wen ces ake mucosa. I usuay does no cause cnca dysuncon. up or synesze excessve amouns. For exampe, proten dropets Amyod. Amyod consss o one o many dferen proens a are vsbe n rena ubuar epea ces wen e ubues resorb assume a brar conormaon and are deposed n exraceu- excessve amouns o proens rom e urne, wc occurs w ar ssues, were ey may nerere w e norma uncons gomeruar damage eadng o e neproc syndrome (see Cap- o organs (Suppemena eFg. 1.8). Amyod deposon s oten er 11) (Suppemena eFg. 1.4). Oer exampes ncude Russe reaed o mmune processes and s dscussed n Caper 4 bodes, eosnopc ncusons comprsed o newy syneszed CHAPTER 1 Cell Injury and Cell Death 13.e1 Supplemental eFig. 1.4 Protein reabsorption droplets in the renal tubular epithelium in a patient with albuminuria. (Courtesy Dr. Helmut Rennke, Department of Pathology, Brigham and Women‘s Hospital, Boston.) Supplemental eFig. 1.2 Fatty liver. High-power detail of fatty change of the liver. In most cells, the well-preserved nucleus is squeezed into the displaced rim of cytoplasm about the fat vacuole. (Courtesy Dr. James Crawford, Department of Pathology, Zucker School of Medicine at Hofstra/Northwell.) Supplemental eFig. 1.3 Cholesterolosis. Cholesterol-laden macro- phages (foam cells, arrow) in the lamina propria of gallbladder affected by cholesterolosis. (Courtesy Dr. Matthew Yeh, Department of Pathol- ogy, University of Washington, Seattle.) 13.e2 CHAPTER 1 Cell Injury and Cell Death A B Supplemental eFig. 1.5 Lipofuscin granules in a cardiac myocyte shown by (A) light microscopy (deposit indicated by arrow) and (B) electron microscopy (note the perinuclear, intralysosomal location). A B Supplemental eFig. 1.6 Hemosiderin granules in liver cells. (A) Hematoxylin-eosin–stained section showing golden-brown, finely granular pigment. (B) Iron deposits shown by a special staining process called the Prus- sian blue reaction. Supplemental eFig. 1.7 Dystrophic calcification of the aortic valve. View looking down onto the unopened aortic valve in a heart with calcific aortic stenosis. It is markedly narrowed (stenosis). The semilunar cusps are thickened and fibrotic, and behind each cusp are irregular masses of piled-up dystrophic calcification. CHAPTER 1 Cell Injury and Cell Death 13.e3 A B C Supplemental eFig. 1.8 Amyloidosis. (A) A section of the liver stained with Congo red reveals pink-red deposits of amyloid in the walls of blood vessels and along sinusoids. (B) Note the yellow-green birefringence of the deposits when observed by a polarizing microscope. (C) In the kidney, the glomerular architecture is almost totally obliterated by the massive accumulation of amyloid. (B, Courtesy Dr. Trace Worrell and Sandy Hinton, Department of Pathology, University of Texas Southwestern Medical School, Dallas.) 2 Inflammation and Repair O U T L I N E Overview of Inflammation, 14 Mediators of Inflammation, 20 Causes of Inflammation, 14 Clinicopathologic Features of Acute Inflammation, 23 Sequence of Events in Inflammation, 14 Outcomes of Acute Inflammation, 25 Features of Acute and Chronic Inflammation, 15 Chronic Inflammation, 26 Cells of Inflammation, 15 Cellular Reactions of Chronic Inflammation, 26 Acute Inflammation, 16 Clinicopathologic Features of Chronic Inflammation, 27 Vascular Reactions, 16 Tissue Repair, 27 Cellular Reactions, 17 Angiogenesis, 28 Resolution of Acute Inflammation, 20 Clinicopathologic Features of Tissue Repair, 28 OVERVIEW OF INFLAMMATION Infec tons (b ac er a , v ra , u nga , p aras c ) and m crob a ox - Inammation is a host response to infections and tissue damage ns are among e mos common and me d c a y mp or an c aus es that brings cells and molecules to the sites where they are needed o n amma on. D eren n e c ous p a ogens e c a range o to eliminate the cause of injury (e.g., microbes or toxins) and the n ammaor y resp ons es , rom m d ac ue n am ma on a c aus e s consequences of such injury (e.g., necrotic cells and tissues). e or no as ng d amage, o s e ve re s y se m c re ac ons a c an e medaors o deense ncude eukocyes (we bood ces), be a a , o proonge d cron c re ac ons a c aus e e xe ns ve ssue anbodes, and compemen proens. Mos o ese normay crcuae njur y. n e bood, were ey are sequesered o preven damage o norma Immune reactons occur wen e normay proecve mmune sys- ssues, bu ey can be rapdy recrued o any se n e body. Some em damages e ndvdua’s own ssues eer by aackng se an- o e ces nvoved n nlammaor y responses aso resde n ssues, gens (auommune dseases) or reacng o envronmena subsances were ey uncon as sennes on e ookou or reas. (aerges). Inlammaon s a major cause o ssue njur y n ese In cnca medcne, muc o e empass on s useu response dseases (see Caper 4). Because e smu or e nlammaor y as been on s armu consequences (e.g., pan, ever, and uncona responses n auommune and aergc dseases canno be emnaed, mparmens), bu s mporan o noe a an appropraey regu- ese reacons end o be perssen and dcu o cure and are oten aed nlammaor y response s a crca par o norma ea and s- assocaed w cronc nlammaon. sue manenance. he sux ts ater an organ denoes nlammaon n Necross rom any cause, even sere njur y as n narcon caused a se (e.g., appendcs, conjuncvs, menngs). Inlammaon by oss o bood suppy, ecs nlammaon due o moecues reeased can be damagng : rom necroc ces. I s nadequatey controed Foregn bodes (e.g., spners, dr, suures) may ec nlammaon, I s msdrected (e.g., agans normay armess envronmena and even some endogenous substances smuae poenay armu subsances [as n aerges] or commensa mcrobes, or agans se nlammaon arge amouns are deposed n ssues (e.g., urae cr ys- ssues [as n auommune dseases]) as n gou and coesero cr ysas n aerosceross). he smuus s persstent and canno ready be emnaed (e.g., e mycobacerum a causes ubercuoss) Sequence of Events in Inflammation Too e nlammaon, wc s ypcay manesed by ncreased The inammatory response consists of sequential events involving suscepby o necons, s aso probemac and s mos oten caused vascular reactions and recruitment of leukocytes. by quanave or quaave deecs n eukocyes, wc may resu he major seps n e response are recognon, recrumen, rom repacemen o e marrow by cancers, desrucon o norma remova, reguaon, and repar (e 5 Rs), descrbed nex (Fg. 2.1). eukocyes by cancer erapes, or use o mmunosuppressve drugs. hese seps are medaed by e coordnaed acons o cemca Ater e noxous smu and e damage ey cause are emnaed, medaors a w be descrbed aer. e nlammaor y reacon ses n moon e process o repar, wc 1. Recog nton o e noxous agen a s e n a ng s mu us resores ssue negry. or nl amma on. he ce s a r g ger nl amma on ( ssue- resden s en ne ce s, pago c yes, and o ers, des cr b e d aer) are e qupp e d w re cepors a re cog nze mcrob a pro duc s and Causes of Inflammation subs ances ree as e d rom d amage d ce s. C e u ar re cepors or The major causes of inammation are infections, immunologic mcrob es c an be o c ae d n p asma membranes (or ex race u ar reactions, tissue necrosis, and environmental substances. 14