Robbins Essential Pathology PDF - Cell Injury and Cell Death

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 cronc smokers and coumnar meapasa o e esopagea e subsance may be ocaed n e cyopasm, wn organees squamous epeum n paens w cronc gasrc relux (Fg. (ypcay ysosomes), or n e nuceus, and  may be syneszed by 1.15). Aoug meapasa aows ces o sur vve,  oten com- e afeced ces or  may be produced esewere. promses er uncon; or nsance, squamous epeum n e e man paways o abnorma nraceuar accumuaons are broncus canno produce mucus and provde car y acon, wo nadequae remova and degradaon or excessve producon o an mporan uncons o norma bronca epeum a proec endogenous subsance, or deposon o an abnorma exogenous mae- e ar ways rom necon. Aso, w e perssence o rggerng ra. Some exampes are descrbed n e oowng. smu, meapasc epeum can be e se o neopasc rans-    Fatty cange (steatoss). Seaoss s e accumuaon o pds (Sup- ormaon, as n e bronc (squamous ce carcnoma o e ung) pemena eFg. 1.2), mos oten n e ver oowng proonged and upper gasronesna rac (esopagea adenocarcnoma ars- acoo consumpon or n obese ndvduas as a componen o ng n e seng o Barre esopagus). nonacooc ay ver dsease (see Caper 13).    Coestero and coeser y esers. Pagocyc ces may become overoaded w pd (rgycerdes, coesero, and coeser y PATHOLOGIC ACCUMULATIONS IN CELLS esers) n severa dferen paoogc processes (Suppemena eFg. Cells may accumulate abnormal amounts of various substances, 1.3), mosy caracerzed by ncreased nake or decreased caab- which may be harmless (e.g., carbon particles in the lungs and osm o pds. O ese, aerosceross s e mos mporan (see mediastinal lymph nodes of city dwellers) or may cause varying Caper 8). degrees of injury.  CHAPTER 1 Cell Injury and Cell Death 13 mmunogobuns a msod and accumuae n e roug ER o some pasma ces; neurobrar y anges n neurons; and “aco- oc yane” (see Caper 13).    Pgments. Pgmens o severa ypes may accumuae n ces. Lpo- fuscn s a browns, granuar maera composed o pds and pro- ens a s produced by ree radca–medaed pd peroxdaon (Suppemena eFg. 1.5). Is accumuaon n ces s a sgn o ree Basement Normal Squamous radca–medaed njur y, so  s oten seen n oder ndvduas and membrane columnar metaplasia n aropc ssues. Hemosdern s a emogobn-derved brown epithelium A pgmen (Suppemena eFg. 1.6) a accumuaes n pagocyes and oer ces n condons o ncreased red ce breakdown or ron overoad (see Caper 9).    Gycogen. Excessve nraceuar deposs o gycogen are assocaed w abnormaes n e meabosm o eer gucose or gycogen. Gycogen may accumuae n poory conroed dabees or n gyco- gen sorage dseases (see Caper 13).    Cacum. Cacum sa deposs are seen n a varey o dsease saes. Dystropc caccaton occurs n e seng o norma serum ca- cum and s e deposon o cacum sas n njured ssue (e.g., n areas o caseous necross and n advanced aerosceross). Dys- ropc caccaon can ave uncona consequences, as n ca- cc senoss o e aorc vave causng et venrcuar yperropy B due o pressure overoad (Suppemena eFg. 1.7). Metastatc ca- Fig. 1.15 Metaplasia of normal columnar (left) to squamous epithelium ccaton occurs n e seng o ypercacema, wc s seen n (right) in a bronchus, shown schematically (A) and histologically (B). saes o yperparayrodsm (see Caper 16), or ncreased bone desrucon, as n cancers nvovng e bone. Measac cacca- on occurs wdey rougou e body bu prncpay afecs e    Protens. Morpoogcay vsbe proen accumuaons are ess nersa ssues o e vascuaure, kdneys, ungs, and gasrc common an pd accumuaons; ey may occur wen ces ake mucosa. I usuay does no cause cnca dysuncon. up or synesze excessve amouns. For exampe, proten dropets    Amyod. Amyod consss o one o many dferen proens a are vsbe n rena ubuar epea ces wen e ubues resorb assume a brar conormaon and are deposed n exraceu- excessve amouns o proens rom e urne, wc occurs w ar ssues, were ey may nerere w e norma uncons gomeruar damage eadng o e neproc syndrome (see Cap- o organs (Suppemena eFg. 1.8). Amyod deposon s oten er 11) (Suppemena eFg. 1.4). Oer exampes ncude Russe reaed o mmune processes and s dscussed n Caper 4 bodes, eosnopc ncusons comprsed o newy syneszed  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 tons (b ac er  a , v ra ,  u nga , p aras c ) and m  crob a  ox - Inammation 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  ammaor y resp ons es ,  rom m d ac ue  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 se m  c re ac   ons  a c an e medaors o deense ncude eukocyes (we bood ces), be a a , o proonge d cron  c re ac   ons  a c aus e e xe ns ve  ssue anbodes, and compemen proens. Mos o ese normay crcuae njur y. n e bood, were ey are sequesered o preven damage o norma Immune reactons occur wen e normay proecve mmune sys- ssues, bu ey can be rapdy recrued o any se n e body. Some em damages e ndvdua’s own ssues eer by aackng se an- o e ces nvoved n nlammaor y responses aso resde n ssues, gens (auommune dseases) or reacng o envronmena subsances were ey uncon as sennes on e ookou or reas. (aerges). Inlammaon s a major cause o ssue njur y n ese In cnca medcne, muc o e empass on s useu response dseases (see Caper 4). Because e smu or e nlammaor y as been on s armu consequences (e.g., pan, ever, and uncona responses n auommune and aergc dseases canno be emnaed, mparmens), bu  s mporan o noe a an appropraey regu- ese reacons end o be perssen and dcu o cure and are oten aed nlammaor y response s a crca par o norma ea and s- assocaed w cronc nlammaon. sue manenance. he sux ts ater an organ denoes nlammaon n Necross rom any cause, even sere njur y as n narcon caused a se (e.g., appendcs, conjuncvs, menngs). Inlammaon by oss o bood suppy, ecs nlammaon due o moecues reeased can be damagng : rom necroc ces.    I s nadequatey controed Foregn bodes (e.g., spners, dr, suures) may ec nlammaon,    I s msdrected (e.g., agans normay armess envronmena and even some endogenous substances smuae poenay armu subsances [as n aerges] or commensa mcrobes, or agans se nlammaon  arge amouns are deposed n ssues (e.g., urae cr ys- ssues [as n auommune dseases]) as n gou and coesero cr ysas n aerosceross).    he smuus s persstent and canno ready be emnaed (e.g., e mycobacerum a causes ubercuoss) Sequence of Events in Inflammation Too e nlammaon, wc s ypcay manesed by ncreased The inammatory response consists of sequential events involving suscepby o necons, s aso probemac and s mos oten caused vascular reactions and recruitment of leukocytes. by quanave or quaave deecs n eukocyes, wc may resu he major seps n e response are recognon, recrumen, rom repacemen o e marrow by cancers, desrucon o norma remova, reguaon, and repar (e 5 Rs), descrbed nex (Fg. 2.1). eukocyes by cancer erapes, or use o mmunosuppressve drugs. hese seps are medaed by e coordnaed acons o cemca Ater e noxous smu and e damage ey cause are emnaed, medaors a w be descrbed aer. e nlammaor y reacon ses n moon e process o repar, wc 1. Recog nton o  e noxous agen  a s  e n  a ng s mu us resores ssue negry. or nl amma on. he ce s  a  r g ger nl amma on ( ssue- resden s en ne ce s, pago c yes, and o ers, des cr b e d  aer) are e qupp e d w   re cepors  a re cog nze mcrob a  pro duc s and Causes of Inflammation subs ances ree as e d  rom d amage d ce s. C e u  ar re cepors or The major causes of inammation are infections, immunologic mcrob es c an be o c ae d n p asma membranes (or ex race u  ar reactions, tissue necrosis, and environmental substances. 14