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$D% 1. 2. 3. 4. Hyperplasia is an increase in the number of cells in an organ or tissue, usually resulting in increased volume of the organ or tissue. Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ. Atrophy is the shrinkage in the size of the cell by loss of cell substance. etaplasia is defined as a reversible change in !hich one adult cell type "epithelial or mesenchymal# is replaced by another adult cell type. %ell s!elling is the earliest sign of a reversible cell in&ury. (ree radical is a chemical species that have a single unpaired electron in an outer orbit. *ecrosis is a spectrum of morphological changes that follo! cell death in a living tissue largely resulting from the progressive degradative action of enzymes on the lethally in&ured cell. *ecrosis has si, ma&or type- coagulative, %aseous, .i/uefactive, fibrinoid,gangrenous and (at. Apoptosis "1reek falling off# is defined as a path!ay of programmed cell death that is aimed at a highly regulated intracellular programme in !hich cells destined to death by activated enzyme that degrade the cell2s 3*A and nuclear and cytoplasmic proteins. orphologically an apoptotic cell sho!s5 a# cell shrinkage, b# chromatin condensation c# formation of cytoplasmic blebs and apoptotic bodies, d# phagocytosis by macrophages. Apoptosis has t!o phases a# 6nitiation phase e,trinsic and intrinsic path!ays b#7,ecution phase c#phagocytosis of dead cell
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is is defined as uni directional migration of leukocytes to!ards the site of in&ury under chemical gradient action.eukocytes Adhesion molecular families have a ma&or classes5 a# @electins "7. and divided into 9:. reaction to in&urious agents such as microbes and damaged. 1+.ecutioner caspases are mainly 3 8 '. 2$. c# 6mmunoglobulin family of adhesion molecules and d# ucin like glycoproteins. 14.travascular tissue in the HA.. 6nflammatory response consist of 9:..12. b# 6ntegrins.. 10. @electins mainly involved in rolling of leukocytes. migration and activation of leukocytes. 24. main patterns5 Acute and %hronic.udate# into the e.bim 1enes inhibiting apoptosis are bcl 2 family. 6nitiator caspase are + 8 0. A>? of acute inflammation. . %hemota. and systemic reactions. 6ncreased vascular permeability leading to the escape of a protein=rich fluid "e. <asodilatation is one of the earliest manifestation of acute inflammation. 8 A types#. ost important chemotactic agents are %$a.. 1). 23. if follo!s a transient vasoconstriction of arterioles lasting fe! seconds. 22. main components5 vascular 8 cellular. A7%A in 1'.bak. 24. transmigration and immunoglobulin family in adhesions. !hile e. a&or opsonins are5 %3b 8 (c fragment of 6g1 proteins . 13. 3ystrophic calcification is al!ays seen in damaged tissues !hile metastatic calcification may occur in normal tissues !henever there is hyperplasia. 6nflammation is a comple. (ormation of endothelial gaps in venules is the most common cause of vascular leakage.9B4 and bacterial products. 1$. 21. usually necrotic cells that consists of vascular responses. 1enes promoting apoptosis are5 ba.
.ide. leading to body infections. %lotting.> cytokines that mediate inflammation. %hediak=Higashi @yndrome is an autosomal recessive condition characterized by failure of fusion of phagosome !ith lysosome.idase !hich generates supero.ing vascular smooth muscle in ischemic conditions.C> systems involved in inflammatory responses ?inin. eota. 33. and >A*97@. 32. 31.in.=1 8 9*( are t!o of the AD.934 8 . 44. 34.ymphotactin 20. 2). 3$. %hronic granulomatous disease of childhood results from inherited defects in the components of *AA3H o. H242= A. 3'. 3). 3+..2'. 34.9%4. 6A=1. 9he ma&or mediators of pain are Bradykinin 8 Arostaglandins Aotent vasodilators are 5 <asoactive Amines. . Activated Hageman factor initiates (.=Halide systein is the most efficient bactericidal system in neutrophils.. 6. A% "%$B')+0# is the membrane attack comple. Alasma Aroteins are5 %omplement system proteins.ins are bioactive products generated from transcellular biosynthetic mechanisms involving neutrophils and platelets. 2+. . 30. fibrinolytic and complement system @>@=A "slo! releasing substance of anaphyla. %A=1. *itric o. .ipo.ide plays ma&or role in production of vasodilation by rela. Arostaglandins are vasodilators. clotting system and fibrinolytic system. a&or chemokines include5 6. !hich finally kills the bacteria.is# constitutes .974 promote vasoconstriction. <asoactive amines are histamine and serotonin !hich are the main players of early inflammation. Arostaglandins 8 *.=+. bronchospasm 8 increased vascular permeability.
acrophages and Alasma cells. and a variable amount of inflammatory cells. 40. in !hich active inflammation. 4). Fuiscent or stable cells and Aermanent *on=dividing cells. onocytes. 4+. <71( 8 fibroblast 1ro!th factor are mainly involved in angiogenesis. fibroblasts.udates# !hile ononuclear cells "!ith one nucleus are the main cells of chronic inflammation . is formed of these groups of molecules 5 a# fibronectin b# adhesive glycoproteins and c# proteoglycans 8 hyaluronic acid. 7.tracellualr matri. 9here are 3 types of cells in the body5 %ontinously dividing labile cells. Acute inflammation is defined as a rapid response to an in&urious agent that serves to deliver mediators of host defense E leukocytes and plasma proteins to the site of in&ury. 44. %hronic inflammation is defined as an inflammation of prolonged duration. %lassical tuberculous granulomas is composed of epithelioid cells. 3on2t confuse it !ith 1ranulation tissue !hich has capillaries. $4. *eutrophils are the main cells of acute inflammation "e. !hile lymphocytes are present in increased number. acrophages are the prima donna "main !orking cell# of chronic inflammation. 9here are t!o types of 1ranulomas5 6mmune 8 foreign body. 9hey are of t!o types5 embryonic 8 adult stem cells.anghan2s multinucleated giant cells. 1ranuloma is a focus of chronic inflammation.41. 42. . 4'. caseation necrosis and collar of lymphocytes. 91(=B is a gro!th inhibitor for most epithelial cells and leukocytes. potent fibrogenic agent and a strong anti=inflammatory effect.ymphocytes. ononuclear cells include . 4$. $1. . consisting of microscopic aggregation of macrophages that are transformed into epithelium like cells surrounded by a collar of mononuclear leukocytes. tissue destruction and attempts at repair are proceeding simultaneously. 43. @tem cells are cells characterized by their prolonged self rene!al capacity and by the asymmetric replication.
$0. . '1. '2.a# inflammatory reaction is more intense. $4. '4. . Heart failure cells are hemosiderin laden macrophages seen in chronic pulmonary congestion. 7dema is defined as accumulation of fluid in the interstitial tissue spaces and body cavities. $$. resulting of arteriolar dilation !hile from impaired outflo! from $3. Aetechiae are minute 1 to 2 mm hemorrhages into skin. (ate of thrombus include5 propagation embolization. < 8 G# are fibrillar and most common !hile type 6< is non fibrillar. !ith 2) types discovered so far. 9ypes 6.ines of Iahn are laminated lines produced by alternating pale layers of platelets admi. b# uch more granulation tissue forms and c# !ound contraction phenomenon. mucous membranes or serosa surfaces. $). $'. 66. !hile H3 mm hemorrhages are called Aurpura and more larger H 1 to 2 cm subcutaneous hematomas are called 7cchymoses. particular tissue leads to an active process. Hyperemia is from augmented tissue inflo! because %ongestion is a passive process resulting tissue.f the inherited causes of hypercoagulability. Accumulation of e. <ircho!2s triad include5 a# 7ndothelial in&ury b# @tasis or turbulent blood flo! 8 c# blood hypercoagulability.ocal increased volume of blood in a Hyperemia and congestion. $+.cessive amounts of collagen may give rise to a hypertrophic scar !hile if scar tissue gro!s beyond the boundaries of the original !ound and does not regress. Healing by 2nd intention differs from 1st intention in three !ays.$2. it is called keloid. organization and recanalization. dissolution. mutation in the factor < gene and prothrombin gene are the most common. .ed !ith some fibrin and darker layers containing more red cells. %ollagens is the most common protein in the animal !orld. 666. .
Benign tumors are !ell differentiated. 9he most dominant histologic characteristic of infarction is ischemic coagulative necrosis. *eoplasm is an abnormal mass. eyes and cvs. )4. 7hlers=3anlos @yndrome comprise a clinically and genetically heterogenous groups of disorders that result from some defect in the syntesis or structure of fibrillar collagen. utation is defined as a permanent change in the 3*A. 9he phenomenon is called embolism. characterized by changes in the skeleton. '$. hypovolemic. )1.tracellular glycoprotein (irbillin=1. septic. 9umor has t!o basic components5 Aarenchyma 8 stroma. Amyloid is a pathologic proteinaceous substance deposited bet!een cells in various tissues and organs of the body in a !ide variety of clinical settings.cessive manner after cessation of the stimuli !hich evoked the change. '). '0. 6nfarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue.ceeds and in uncoordinated !ith that of the normal tissue and persists in the same e. and resulting in hypotension follo!ed by impaired tissue perfusion and cellular hypo. . gro! fast and sho! invasion and metastasis. li/uid or gaseous mass that is carried by the blood to a site distant from its point of origin. neurogenic and anaphylactic. '+. @hock is the systemic hypoperfusion caused by reduction either in cardiac output or in the effective circulating blood volume. 7mbolus is a detached intravascular solid.'3. arfan2s syndrome is a disorder of the connective tissue of the body. the gro!th of !hich e. )3. ainly cause by defects in an e. gro! slo!ly and don2t sho! invasion and metastases. !hile tumors are of t!o types5 Benign and alignant.ia. )2. !hile alignant tumors range from !ell to undifferentiated. ''. )4. a&or types of shock include5 cardiogenic. '4.
. >79. . Aolycythemia by >%% and hypertrophia osteoarthropathy by %A lung. a&or antioncogenes are5 >B. a&or paraneoplastic synbdromes include. Aflato. @ingle most important feature to differentiate benign from malignant tumor is 79A@9A@6@. divided into initiation and promotion phases. ?69.>A@. %ushing syndrome. a&or oncogenes are.%A 1$=3 for %A breast. )'.ncogenic viruses include.=1. *(=1. >adiation induced carcinoma thyroid. c# apoptotic genes and d#3*A repair genes Aroto=oncogenes are changed to oncogenes by three processes5 mutation.)$. for mesenchymal tumor E vimentin. alpha fetoprotein=H%% and *on= seminomatous germ cell tumor testis. AA%. (our types of genes are normally !orking in human body5 a# proto= oncogens b# antioncogenes. malignancies include leukemias and papillary )+. %arcinomas mostly use lymphatic routes and sarcomas mostly use hematogenous routes of spread. a&or immunomarkers for epithelial tumors are cytokeratin. %A=12$ for . %7A=%A colon. +$. hypoglycemia by (ibrosarcoma and H%%. )). +4. a&or chemical carcinogens associated as include5 Asbestos !ith esothelioma. B>%A=1. +4.Human Aapilloma virus. *itrates=1astric carcinoma.varian %A . 9A$3.in !ith H%%. 7pstein Barr virus . <inyl chloride !ith Angiosarcoma . a&or tumor markers included 5 H%1 for %horiocarcinoma. Aniline dyes !ith 9%%.?aposi @arcoma Herpes viruses 8 Human 9=%ell leukemia virus "9he only oncogenic >*A virus#. %hemical carcinogenesis is a multistep process. +). A3H secretion by small cell carcinoma lung. Hepatitis B virus. %a 10=0 for %A %olon and pancreas .iver. :. . +3. for leukocyte origin tumor E leukocyte +'. translocation and amplification. Hypercalcemia by @/uamous cell carcinoma lung. AAA (or %A prostate. +2. )0. AB. 7>B=B1. +1. calcitonin for medullary carcinoma thyroid. %= J% 8 *= J%.
ic hypersensitivity. ++. 02. hypersensitivity reaction. @&ogren2s syndrome.A system is a key factor in most 9ransplant re&ection reactions. 9ype 66 cytoto.esL#. +0. >eactions are mediated by either 9 lymphocytes or by antibody. 0'. 6n type 666 immune=comple. 9ype 6 hypersensitivity "KanaphylacticL# or Kimmediate hypersensitivityL# is the result of antigen binding to 6g7 on the surface of mast cells and basophils. . a&or histocompatibility comple. usually this happens 2=4 hours after e. is present on all nucleated cells. and B# %ellular immunity=9=%ell lymphocyte mediated. 6mmune reactions are divided into t!o broad categories5 A# Humoral immunity=B=cell lymphocyte mediated via production of antibody and . %34 molecule is a high affinity receptor for H6< a&or autoimmune disease include Hashimoto2s thyroiditis.es "Kimmune comple. 9his sort of tissue in&ury is mediated by antigen= antibody comple.A molecules and release lymphokines. %34Mhelper lymphocytes5 help B cells make antibody and also help to generate cytoto. @144 for neural origin tumors and for skeletal muscle tumors E desmin.ic 9 cells.posure. 9ype 6< Hypersensitivity reaction is called Kdelayed hypersensitivityL.ften develops as a response to soluble antigens. 0). 04. 0$. ankylosing spondylitis. 9oll like receptors are membrane proteins that recognize a variety of microbe derived molecules and stimulate innate immune responses against the microbes. >heumatoid Arthritis. 03. K@oluble antigensL precipitate !ith antibodies. antibodies attach to antigens on the surfaces of a cell and then something in&ures or destroys the cell. 6t is mediated by sensitized %34M9 lymphocytes !hich process antigens in association !ith class 66 H.common antigen. 9hese instantly degranulate and release active substances into the surrounding tissue. 01. 04. 9he H.
. 9igered lipid effect is seen in Herat. 140. A(B is acid fase bacillus " ycobacterium tuberculosis # and called so because it resists decolourization by %oncentrated Acids. a&or complement proteins include 5 .:all sharing is often noted. 14'.in %3a. Adenocarcinoma is characterized by back to back closely packed glands lined by pleomorphic malignant epithelial cells !ith high *N% ratio.+.?eratin epithelial pearls. 114. 142.hyperchromatic nuclei and pale cytoplasm. groups and clusters of pleomorphic malignant epithelial cells !ith high *N% ratio. umps.ive vaccineseasles. 1liomas and B%% are highly malignant but dont usually metastasize. Hepatitis A. 14$. >A@ gene protooncogene protein is 19A bound and :orks !ith 1AA in cooridination !ith 19Aase. 144. 14). 9!o types of vaccines include5 .'.psonization by %3b %hemota.hyperchromatic nuclei and eosinophilic cytoplasm. Arotooncogenes are converted into oncogenes. 143.). @/uamous cell carcinoma is characterized by sheets.intercellular bridges and individual cell keratinization are seen. >ubella. >B gene activates and :orks in hypophosphorylated form. 141. 1amma interferon is one of the cytokine to activate macrophages and also play ma&or >ole in 1ranuloma formation. %ytokines are mediators released from one cell and modulate the actions of another cell. 14+. %$a embrane breakdo!n and killing %$b. 00. Aolio etc and ?illed vaccines5 >abies.0+. 144.is by %$a Anaphylato. %4a. Aolio. p$3 !orks by 3*A repair and promoting apoptosis.0 7nhancement of antibody production %3b A% comple. <aricella.
steoclasts E bone. 7osinophils are players in allergic infections.metastasis. 113. 112. (*A% and biopsy are key investigations to early diagnose a tumor. @e/uence of events in acute inflammation is 5 9ransient asoconstriction.atypia and mitoses. immunization !ith live or killed infectious agents. e.microglia E brain.is and phagocytosis. 24 to 4+ hours accumulating. acrophages seen as a part of reticuloendothelial system include5 . to. 11'. 124. rolling. >eserve stem cells are main players in metaplasia.111.posure to microbial products "to. leprosy.@inus histiocytes E lymph nodes. 124. 114. fungal infections. ubi/uitin proteosome path!ay 8 autophagic vacuoles are mainly involved in atrophy. rabies etc. E tumor. echanical and trophic factors are involved in hypertophy. @taging of a tumor is based on 9* 124. 9uberculosis is the leading cause of granuloma in Aakistan.alveolar macrophages E lung. 11+. margination. @udden death is ma&orly linked !ith embolism. 123. cat scratch disease. 1rading of a tumor is based on differentiation.oids# Aassive immunity is resistance based on antibodies preformed in another host eg administration of antibody against tetanus. post acute inflammation .kupffer cells E liver.monocytes start 11$.nodes. 122. diphtheria. 110. Active 6mmunity is the resistance induced after contact !ith foreign antigens eg microorganisms. diapedesis.ins. adhesion. a&or granulomatous causes include5 sarcoidosis.neurofibromatosis 1astrointestinal E familial polyposis coli .vasodilation stasis. 11). 121. arfan- a&or autosomal dominant disorders include5 @keletal E syndrome *ervous E Huntington disease. chemota. botulism.
copper E :ilson disease lipofuscin E aging 12'.9uton giant cells E .papillary carcinoma thyroid and serous ovarian malignant tumors.. 132. a&or intracellular accumulations are 5 elanin E melanoma.g >A@. 134. 1iant cells are cells containing more than one nucleus. 12). 12+. 13+. acrophages get accumulated in chronic inflammation by continuous recruitment.is and loss of nucleus.ines of Iahn confirms a thrombus.anthoma :arthin finkeldey giant cells E measles.ymphoma (oreign body giant cells E foreign body 134. .carbon E anthracosis. 133. Asamomma bodies are lamellated bodies of dystrophic calcification seen in meningioma. 13).bile E cholestasis. 6g1 fi. 6schemic in&ury leads to coagulative necrosis. 6g7 is the allergic reaction player antibody. 6g A is found in secretions. gene is seen translocated in % .change a single nucleotide for another e.Crinary E polycystic kidney disease Haematopoietic E hereditary spherocytosis 12$. karryorrhe. 130.anghan giant cells E 9uberculosis. Aoint mutations are often caused by chemicals or malfunction of 3*A replication. (atty change is also kno!n as steatosis. . karyolysis. 13$. *uclear changes in a necrotic cell include5 pyknosis. AB.es complement and crosses placenta. a&or giant cells are 5 . e.9hey are alternate layers of platelets !ith fibrin and >B%s2 13'. 131.>eed @ternberg cells E Hodgkin . 6g is the most heavy antibody.proliferation and immobilization. 120.
but a term for necrosis that is advanced and visible grossly !ith super added putrefaction. 6n males bronchogenic carcinoma and in females breast carcinoma are at the top. !here the cell dies by s!elling and bursting its content in the area. . 1angrene "Ogangrenous necrosisO# is not a separate kind of necrosis at all. (ibrinoid necrosis occurs in the !all of blood vessels !hen endothelium and smooth muscle cells are in&ured and dying. because they can attract polymorphonuclear leukocytes. . (at *ecrosis5 A term for necrosis in fat. 6nflammatory bo!el disease. 14+.144. such as the (as receptors. !hich causes an inflammatory response. either by a physical blo! or by surgery "traumatic fat necrosis#. or in tumor necrosis. the intrinsic path!ay of apoptosis is initiated through the release of signal factors by mitochondria !ithin the cell 1$4.g. 14'. protein synthesis. Areneoplastic conditions include5 %irrhosis of liver.eukoplakia. %oagulative necrosis is characterised by the preservation of cellular and tissue architecture 143. in !hich the coagulated tissue no longer resembles the cells. tuberculosis#.i/uefactive necrosis5 Csually caused by focal bacterial infections.. located on the cell membrane. Cnlike necrosis. 142. Adenomatous colonic polyps . apoptosis is a very clean and controlled process !here the content of the cell is kept strictly !ithin the cell membrane as it is degraded.trinsic path!ay of apoptosis is initiated through the stimulation of the transmembrane death receptors. 144. but is in chunks of unrecognizable debris 14$. 14). caused either by release of pancreatic enzymes from pancreas or gut "enzymic fat necrosis# or by trauma to fat. 9he e. aerobic respiration. Atypical hyperplasia of endometrium. a&or sensitive cell components5 maintenance of integrity of cell membrane. 1$1. 140. 6n contrast. genetic integrity 141. %aseous necrosis E cheese like 5 A distinct form of coagulative necrosis seen in mycobacterial infections "e.
7. prevents platelet aggregation. 1$'.tent to !hich differentiation.atent stage. 6nitiator chemicals = %ause irreversible damage to 3*A. Benzene = . 1$0. @uppurative or purulent inflammation is characterized by the production of large amounts of pus or purulent e.ung. large intestine# b= Arsenic = .ane A2 "9GA2#. 1'1.ung d= %admium = prostate e. 6onizing radiation leads to dys&unction à random fusion à mutation. 1$$.1$2. Aromoter chemicals itself cannot induce cancer. aggregates platelets. dilates vessels.eukemia . . constricts blood vessels. 1$+.imum they can cause severe dysplasia. 1'2. 1$3. 9hrombo. An ulcer is a local defect. 1reat for !henever hemostasis is unnecessary. 1$). 6nitiation. 1'4. alignant transformation are ast cells are the main source of histamine and platelets the main source of serotonin. 1'4. hemangiosarcoma c= Beryllium = . elanomas.udate consisting of neutrophils. 16 tract "esophagus.they propagate or enhance the effects of initiators 1$4. stomach. or excavation. 1'$. Arostacyclin "A162#. 1reat for hemostasis. from the vessel !all. the tumor cell resemble its parent cell is .Hepatomas are malignant tumors. Aromotion and recognizable stages in carcinogenesis. from platelets. of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflammatory necrotic tissue 1'3.ung. @eminomas. but at ma. necrotic cells. skin. and edema fluid.posure long term of radiations lead to leukemia and thyroid cancers. ?no!n chemical carcinogens include 5A= Asbestos = mesothelioma. 7. 9eratoma is a tumor derived from more than one germ cell layer.
.9 37A3. *uclear damage is the hall mark of irreversible cell in&ury. tissues and organs is Aathology. etaplasia can lead to dysplasia. scanty cytoplasm and pleomorphism. 1'). 1)3. 1)). 1)+. Aerineural spread is seen by carcinoma of prostate and pancreas "2 A2s #. %arcinoma in situ is 5 (ull=thickness dysplasia e. 1'+. @cientific study of structural changes and functional conse/uences of in&urious stimuli on cells.hyperchromatic nuclei.AH6% %7. 3ysplasia can regress and does not al!ays lead to cancer. moderately.@ > *.1''.9H. 1'0. 1+4. Benign tumors never locally invade and invade the surrounding tissues. alignant tumors al!ays 1)2. Aathologic hyperplasia constitutes a fertile soil in !hich cancerous proliferation may eventually arise like bph and endometrial hyperplasia. etaplasia is a t!o edges s!ord because it can lead to dysplasia and the original function of cells is lost. include5 !ell..*.tending from the basement membrane to the surface of the epithelium. 1)$. %arcinoma of the ovary spreads through seeding of body cavities.C1H A9>. A. A malignant cells sho!s5 high *N% ratio. prominent nucleoli.9H7J 1)0. 3ysplasia 5Atypical proliferation of cells characterized by nuclear enlargement and failure of differentiation !hich falls short of malignancy 1)4. 1)'. 9he change that occurs in the stroma as tumor invades is called desmoplasia 1)1. 1+1. poorly. 1)4. %ommonest places for mets deposits are liver and lungs. AJ HA<7 36 6*6@H73 (C*%96. >anges of differentiation undifferentiated "anaplasia#.
OblandO. to occlude a systemic artery. :hite infarcts "Oanemic infarctsO. . since it tends to shut do!n organs due to microthrombi. 1+$. and also causes bleeding due to consumption of clotting factors and activation of plasmin. OverrucousO. or !hen the organ !as already very congested.. 1+). not. a birth defect#. the clotting cascades are activated throughout the body. or sterile "OmaranticO. 9ransudates are fluid accumulations that are essentially salt=!ater. 7.e. . 1++. or !hen arteries are occluded in loose tissues "bo!el# or !ith a dual blood supply. 102.also the thrombi of acute rheumatic fever#. >ed infarcts "Ohemorrhagic infarctsO. <egetations are thrombi that occur on cardiac valves. @ome people reserve the !ord OthrombusO for the ante=mortem kind. from Oan=O. less often at sites of other vascular disease or old surgery.1+2. 7mbolusO comes from the 1reek for Obottle stopperO. 1+'. >enal cell carcinoma is famous for this. and that ante=mortem diagnosis is notoriously unsatisfactory even today.ymoron but isnQt# result !hen veins are occluded.udates are protein=rich fluid accumulations. 9hey may be loaded !ith bacteria "Obacterial endocarditisO#. sounds like an o. blood# are usual !hen arteries are occluded in solid organs 103. Aulmonary embolization is one of the great killers of hospitalized patients. 9umor emboli are bits of cancer that invaded a vein and then broke off. 101. and call post=mortem thrombi OclotsO. and O=emeO. A parado. Arterial thrombi usually occur over ruptured atherosclerotic pla/ues. due to leaky vessels.ong bone fractures are the main cause of fat embolism. 1+4. 9his is bad. 6n disseminated intravascular coagulation. accumulated because of pressure problems. 104. 1+3. 1+0.ical embolus "P crossed embolus# is one from the systemic veins that passes through a right=to=left intracardiac shunt "i.
<71(. 7ndothelium gets leaky in acute inflammation due to5 1# formation of endothelial gaps in venules 2# cytoskeletal reorganization 3# increased transcytosis 4# direct endothelial in&ury $# leukocyte dependent in&ury '# delayed prolonged leakage )# leakage from ne! blood vessels . 10'. 244.104. . Histiocytes are mature tissue macrophages.ysosomal leakage confirms irreversible cell in&ury. (1(.91(. 100.71( are main gro!th factors. %horistomas and hemartomas are not neoplasms. 10$. %ell membrane damage is the first sign of irreversible cell in&ury. 10+. 10). onocytes are the largest cells in blood stream.
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