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This document defines and describes various types of bacterial infections including infection, toxemia, bacteremia, septicemia, and pyemia. It discusses the causes, methods of spread, effects, and postmortem findings of each type of infection. Key points include that septicemia involves circulation of bacteria without localization causing severe constitutional symptoms. The spleen, lymph nodes, heart, liver, and bone marrow are commonly affected organs. Septicemia is usually fatal within days due to organ failure and shock. Pyemia involves circulation of septic emboli that become localized in organs.
This document defines and describes various types of bacterial infections including infection, toxemia, bacteremia, septicemia, and pyemia. It discusses the causes, methods of spread, effects, and postmortem findings of each type of infection. Key points include that septicemia involves circulation of bacteria without localization causing severe constitutional symptoms. The spleen, lymph nodes, heart, liver, and bone marrow are commonly affected organs. Septicemia is usually fatal within days due to organ failure and shock. Pyemia involves circulation of septic emboli that become localized in organs.
This document defines and describes various types of bacterial infections including infection, toxemia, bacteremia, septicemia, and pyemia. It discusses the causes, methods of spread, effects, and postmortem findings of each type of infection. Key points include that septicemia involves circulation of bacteria without localization causing severe constitutional symptoms. The spleen, lymph nodes, heart, liver, and bone marrow are commonly affected organs. Septicemia is usually fatal within days due to organ failure and shock. Pyemia involves circulation of septic emboli that become localized in organs.
INFECTION efinition! invasion of ! living tissue by pathogenic microorganisms. These are ! viruses, bacteria, fungi, protozoa & metazoan and development of pathological changes. "ethod# of Infe$tion : %) E&ogeno'# from patient or carrier via: 1-Sin or mucous membrane, in!ury facilitates ! infection. e.g.sin T" #$upus vulgaris%, leprosy, & . '- (ngestion #food or )ater%. e.g. Typhoid fever, cholera, bacillary dysentery. *- (nhalation: - +irectly d.t inhaled droplets from patient. - (ndirectly d.t inhalation of contaminated dust. e.g. T" & other respiratory tract infection. ,- (n!ection & blood transfusion. e.g. & , malaria, viral hepatitis, -(+S. .- se/ual Transmission. e.g. & , -(+S. 0- Transplacental from infected mother to ! fetus. e.g. congenital & , 1ubella, To/oplasmosis. () Endogeno'# d.t 1- 2ommensals: "acteria normally present in ! body & under certain conditions, they turn pathogenic. e.g.: Strept. viridans #in ! mouth%. 3neumococci #in 4asopharyn/%. 5 coli. #in ! intestine%. infection occurs )hen ! body resistance - - 6 immunodeficient states #immune suppressive therapy, prolonged antibiotic therapy% or, )hen these bacteria change their position. This is called opportunistic infection '- septic focus: as sinusitis, cholecystitis7etc 1 King of pathology )e#'lt# of Infe$tion (*a$te+ia i# ta,en a# an e&le %:
(mmunity , )ea organism subclinical infection. (mmunity , strong organism disease. "ethod# of -p+ead of Infe$tion: 1-$ocal #+irect%: via tissue ,fluid and motility of macrophage. '-$ymphatic :through the draining lymphatic. *-"lood :through the )all of blood vessel 8r from lymphatic system )9 lead to to/emia,bacteremia, septicemia and pyemia. ,--long the natural passage:5.g 1espiratory tract and lung alveoli. I. To&emia %.ef (.-o'+$e /.Type#0 %.ef! 2irculation of bacterial to/ins in ! blood )ith production of clinical & pathological manifestation. (.-o'+$e# of To&in#! 1. produced by the organism itself: :5/oto/ins from living gram ; ve bacteria. e.g. 4ecroto/in :5ndoto/in from gram -ve bacteria. 2. released from the necrotic tissue /.Type# of To&emia! 1) Acute Toxemia= Exotoxic toxemia : $arge doses of to/ins reach ! blood )ithin a short period e.g. acute infections such as diphtheria, bacillary dysentery, lobar pneumonia. 2) hronic Toxemia=Endotoxic toxemia : Small doses of to/ins reach ! blood over long period e.g. chronic infections such as T", & . 2 King of pathology 1Effe$t# of to&emia I)Clini$al ($on#tit'tional #ign# 2 #ymptom#) : fever, headache, rigor, loss of appetite, loss of )eight, tachycardia & ;; tissue metabolism II)3athologi$al ! 1-inflammation '- degeneration: acute to/emia degeneration of parenchymatous organs # cloudy & fatty change%. *- -myloidosis : in chronic to/emia ,-4ecrosis: acute to/emia hemorrhage of suprarenal glandsnecrosis & acute adrenal insufficiency .--nemia: d.t depression of b.marro) by to/ins & hemolysis of 1"2s N0B!-ap+emia! 6 to/in production by saprophytes on necrotic tissue e.g.retained placental products after labor or abortion II. Ba$te+aemia %.ef (.-o'+$e# /.Effe$t# %.ef! 2irculation of small number of bacteria e9out multiplication in the blood and e9out to/ins (.-o'+$e# of *a$te+ia! 1) Endogenous : -2ommensals : e.g. Strept veredans by tooth brushing, tooth e/traction% -Septic foci as boil, otitis media, sinusitis7etc 2) Exogenous : (n early stages of certain diseases as in typhoid fever & & /.Effe$t#! :2ommonly destroyed by body defense. :$arge dose cause disease E0g:Subacute infective endocarditis #S(5% Staph aureus cause 8steomylitis !"#$%& '()* III. -epti$emia %.ef (.Ca'#e# /.method# 4.effe$t# 5.O+gan affe$ted 6.C73 8.p+ogno#i# 9.po#tmo+tem0 3 King of pathology %.ef! 2irculation & multiplication of large number of virulent microorganism )ith their to/ins in ! blood )ithout localization & )ith production of severe constitutional manifestations & structural changes. (.Ca'#e# 2 pathogene#i#! +),redisposing factors: +ecreased body defense due to immunodeficiency states ++)Exciting factors : 3yogenic microorganisms as: : commonest is Strept. hemolyticus #in puerperal sepsis%. :Staph. aureus #in acute 8steomyelitis% :<eningococci #in septic meningitis%. :=onococci #in gonorrhea%. /."ethod#! The micro- organisms reach ! blood by: 1-(nvasion of ! systemic arterial circulation from suppurative lesion of ! lungs or left side of ! heart '-(nvasion of ! systemic venous circulation via: a->inger pric by infected scalpel at operation or autopsy of septic cases. b-Septic thrombophlebitis as in puerperal sepsis, cellulitis, osteomyelitis & septic meningitis. c-from lymphatic system as in cellulitis. 4.Effe$t# of -epti$emia !(pathology)! I)-e:e+e to&emia ;ith it# effe$t#! a- 5rythrogenic 4ecroto/in act on ! capillaries producing necrosis of their )alls )hich leads to multiple petechial hemorrhage in sin, mucous membranes & serous membranes b- >atty change, cloudy s)elling of parenchymatous, organs & ?ener@s degeneration of muscles. 2- >ocal necrosis especially in: - $ymphoid system. - $iver & heart. 4 King of pathology - suprarenal gland - acute adrenal insufficiency. II)Enzyme#! a-Streptoinase & fibrinolysin: prevent blood coagulation. b- Aemolysins #$ecithinase% dissolve ! cell membrane of erythrocytes.Aemolytic anemia !aundice & ! intima of bl vesselsstained dar red color d.t released Ab. 5.O+gan# <ffe$ted! I) -pleen! a$'te #pleni$ #;elling o+ t'mo+ (#epti$emi$ #pleen)! N7E : :5nlarged, hyperemic, very soft, friable. C7- :bulging of red pulp )hich appears red-grey & semifluid #)ashed under tap )ater%. :$ymphoid follicles are ill defined. "7E:+ilated congested sinusoids& atrophic lymphoid follicles & infiltration by neutrophils, lymphocytes, macrophage & plasma cells& $ittoral cells sho) phagocytic activity II) Lymph node#! Enla+ged 2 +e#em*le #pleen in "7E III) Hea+t! =#epti$emi$ hea+t=!. N7E 1 - Enla+ged, soft, flabby )ith dilated chambers. ! blood in ! dilated chambers & big blood vessels does not coagulate #fluidity%. '- The endo$a+di'm stained red. *- The myo$a+di'm sho) foci of suppurations #abscesses%, necrosis and degenerations #fatty change & cloudy s)elling%. ,- The pe+i$a+di'm: :is thic , dull ,opaBue and reticulated. :the pericardial sac contain yello) pus. .- The :al:e# sho) vegetations #-(5% acute infective endocarditis. "7E! the endocardium&myocardium&pericardium&cusp vegetations sho) pi$t'+e of #'pp'+ati:e inflammation #pus cells,$ongested blood vessel,e/udates rich in fibrin,neutrophils,necrosis% 5 King of pathology I>) Bone ma++o;! -t first, there is increase of immature granular cell series then later, they decreased. Therefore, ! blood picture sho)s leuocytosis follo)ed later by leucopenia. 6.C73 - 3atient is severely ill.#septicemic Shoc & fever%. - 1ed color of sin #Ab%. - Cello) color of eye #Daundice%. 8.3o#t mo+tem pi$t'+e: Sin is red, hot & Daundice may manifest. <ultiple petechial hemorrhages. >luidity of blood in ! heart & big vessels. 9.3+ogno#i#! Fatal in ho'+# o+ day# due to :acute heart failure,acute renal insufficiency and hypotension I> 3yaemia %.ef (.Type#.$a'#e# /.pathology 4.p+ogno#i# %.ef! :2irculation of septic emboli #detached septic thrombi% e9 their localization in ! organs :The responsible microorganism is usually Staph. aureus. (.Type#: I) 3'lmona+y pyemia! Septic emboli coming from different organs & circulate in systemic venous blood then pulmonary arterial circulation to be impacted in lung capillaries. Common $a'#e#! puerperal sepsis or osteomyelitis or septic meningitis. () -y#temi$ pyemia! Septic emboli coming from suppurative lung lesions or from left side of ! heart & circulate in systemic arterial blood to reach different body organs. Common $a'#e#: suppurative lung lesion & acute bacterial endocarditis. /) 3o+tal pyemia! Septic emboli coming from suppurative lesion of =.(.T circulate in portal venous circulation to reach liver. Common $a'#e#: acute suppurative appendicitis , cholecystitis . 6 King of pathology 4.3athology (%) Capilla+y impa$tion p+od'$e# m'ltiple a$'te a*#$e##e# (pyemi$ a*#$e##e#)0 4E5: :<ultiple abscesses :8n outer & cut surface :Cello)ish #pus% :eBual in size #1-' mm% :related to a blood vessel :more or less rounded. :5ach abscess is surrounded by zone of hyperemia. <E5: as an abscess -./0 ? central bacterial colonies (() <+te+ial impa$tion $a'#e# la+ge+ fo$i of #'pp'+ation (#epti$ infa+$t#)0 (/) Clo'dy #;elling 2 fatty $hange of @ pa+en$hymato'# o+gan#0 4.3+ogno#i#! - 1apidly fatal. - 2ommonly complicated by septicemia. Infe$tion i# $la##ified to! %.Ba$te+ial! (.3a+a#iti$ /.F'ngal 4.>i+al 1 T0B 2 A(#yphili#)0 1Bilhazia#i#0 1<$tinomy$o#i# 1Lep+o#y0 1 Hydatid 2 Fila+ia#i#0 1-a+$odo#i#(g+an'loma of 'n,no;n $a#'#e)0 >i+al infe$tion 3athologi$al effe$t# of :i+'#e# B ti##'e +ea$tion to :i+'# infe$tion in$l'de! 1 - 2ellular degeneration. '- 2ellular necrosis. *-2ellular proliferation as in sin )arts 7 King of pathology ,->ormation of =iant cells. . - (ntra-cellular inclusions bodies. a%(ntracytoplasmic as: 2ouncilman bodies in viral hepatitis. b% (ntranuclear & intracytoplasmic as: in cytomegalovirus. 0- 1elease of interferon.6 antiviral molecules Type# Of >i+al Infe$tion %. <$'te :i+al Infe$tion: -s in influenza, measles, chicen po/ poliomyelitis, viral hepatitis. <ethod of infection by inhalation or ingestion. "e$hani#m! The virus proliferates in ! cells at entrance site local lymph nodes cell death release to blood stream. 3rimary viremia : ! virus circulate in the blood primary viremia constitutional symptoms fever malaise, headache, vomiting, bone aching & lymphadenopathy%. The virus multiply in all $.nodes )ith -- of constitutional symptoms. Secondary viremia : ! virus released from all body lymph node to blood forming secondary viremia )ith localization in specific organs.>or e/ample: Firal hepatitis -, ", 2 to liver cell. 3oliomyelitis anterior horn cell. 2hicen po/ & Small po/ sin. <easles lymphoid tissue. (. Latent >i+al Infe$tion! --Aerpes simple/ type(. "-Aerpes zoster in young age ! organism becomes latent in dorsal root ganglion manifest in old age. /.-lo; >i+al Infe$tion: - 2rutz field =acop disease. 4. On$ogeni$ >i+'# infe$tion a#! !&123% 455)6%& 7"829:;%& -- 3apova virus #papilloma virus%: 8 King of pathology 2ondyloma accuminata. 2ommon )art. Duvenile laryngeal polyp. "- 5pstein "arr virus: infectious mononucleosis . "uritt@s lymphoma. 4asopharyngeal carcinoma. 2- A" Firus hepatoma. +- Aerpes simples virus type (( cancer cervi/. F'ngal Infe$tion Ca'#e#! >ungi & 3seudofungi #commensal type of bacteria% Type#! (- Superficial mycosis : tinea nigra, tinea vircecolour. ((- 2utaneous mycosis : 1ing )orm. (((-+eep mycosis #subcutaneous mycosis% a-$ocalized. b-Systemic. <. Lo$alized a# : <$tinomy$o#i# : ef! -'pp'+ati:e g+an'loma )ith formation of multilocular abscess caused by pseudofungus #actinomyces israeli, or actinomyces bovis%. (+y infe$tion may be ! cause of #'pp'+ation "ethod of infe$tion! :3seudofungi are commensals in mout&intestine. :(t invade tissue through mucosal abrasion. : the superficial )ounds heal & the disease spread. 9 King of pathology -ite#! a% 2ervicofacial #0GH%. b%-bdominal #'GH%# iliocecal area% ma## in )t0 Ilia$ fo##a. #blood spread but not lymphatic% to liver multiple lesions in ! liver. c% 3ulmonary #1.H% aspiration from ! mouth abrasion lung or through diaphragm from liver infection spread to surrounding #blood%. d% Sin #.H%. N7E! %.-ite: a% 2ervicofacial #0GH%. b%-bdominal #'GH% c% 3ulmonary #1.H% d%Sin #.H%. (.-hape! Aard mass formed of multiple abscesses e9 multiple sinus discharging pus containing Sulpher lie granules colonies of actinomyces israeli "7E! Suppurative granulomas formed of: Cente+ : yello)ish bro)n fungus colonies )9 are formed of red stained clubs #rounded% and hyphae #deep blue filaments% 3e+iphe+y : neutrophils ; pus cells ; macrophages ; lymphocytes ; fibrous tissue Fate! a-1epair by fibrosis. b-Spread: 1 . i+e$t. (t is the main method and donIt respect any structure. '. Blood #p+ead #rare%. *. Lymphati$ #p+ead not o$$'+. "y$etoma ("ad'+a footC "ad'+amy$o#i#) it diffe+# f+om a$tinomy$o#i# in! - 2aused by 4ocardia # live in soil %. 10 King of pathology - Spread only locally# direct % N7E : %.-ite: in e/tremities #palm;foot%. (.-hape:<# a$tinomy$o#i# e/cept only one difference:- The $olonie# may *e ;hiti#hC*la$,C*+o;n o+ yello;0 "7E!-s actinomycosis -./0 3a+a#iti$ infe$tion %.Hydatid di#ea#e 1efinition! (t is an infective parasitic disease transmitted from animal #dog% to man. $a'#ed *y ingestion of contaminated food e9 egg of 5.granulosus by man hatch in ! intestine pass )ith portal blood to ! liver mature into larval stage #hydatid cyst%. -(t may pass to ! lung, systemic circulation brain, bone -cyst may reach 'G cm in diameter. (t is composed of: 1% - lumen contains stra) -colored fluid. '%(nner germinal layer:- that forms scolices. *%8uter chitinous laminated layer. ,%Surrounding fibrous capsule. 1$ompli$ation#! 1 %3ressure on ! surroundings. '% rupture anaphylactic shoc. *% 'ry bacterial (nfection. ,%Spread of scolices directly or by blood. (.Fila+ia#i# 1Etiology! 11 King of pathology The disease is transmitted by bites of ! 2ule/ pipiens mosBuitoes )hich inoculate micro-filaria of Juchereia "ancrofti in ! sin. These microfilaria migrate to lymph nodes & lymphatics #mostly of ! lo)er limbs & e/ternal genitalia%)here they mature into adult )orms. 13athology! %.Lymphangiti# 2 lymphadeniti# #inguinal, femoral & popliteal lymph nodes%. (nflammation is mainly produced by dead adult filaria )orms. (t starts allergic #eosinophils% then becomes chronic granulomatous. 4ecrosis & liBuefaction may occur #filarial abscess%. >ibrosis )ill finally cause lymphatic obstruction. (.Lymphati$ o*#t+'$tion!. ! lymphatics distal to obstruction become dilated #lymphatic varices% & may rupture leading to: :2hylous ascites #$ymph in ! peritoneal sac%. :2hylothora/, chylocele. :5lephantiasis: This is lymphatic edema #hard non pitting edema% of ! lo)er limb associated )ith fibrosis. ! limb becomes maredly enlarged & ! sin is e/tremely thicened. Ba$te+ial infe$tion LE3)O-D %.ef!infective granuloma caused by mycobacterium lepra. (."ethod of infe$tion! 1bacteria enter via sin#commonly% or via 1s mucosa#rare%. 1infectivity is la) infection occur by long close contact. 1(ncubation period :.-1G days. /.Type#! <)Ea+ly lep+o#y! :manifestations: anesthesia &greenish maculed on the face and limbs. :>ate: K.H recovery e9out tt. '.H progressed to established leprosy. B)E#ta*li#hed lep+o#y(Typia$l)!* types: :$epromatous leprosy#nodular%. :Tuberculoid leprosy#maculo-anasthetic%. :"orderline leprosy:- :mi/ture of ' typical forms. -unstable till change to one of the previous type 12 King of pathology Lep+omato'# lep+o#y B nod'la+ lep+o#y T'*e+$'loid lep+o#yB Ne'+al lep+o#y0 %.in$iden$e! (.Imm'nity! 4.infe$ti:ity 5.No0of *a$illi! /.Nat'+e! 6.Ne+:e infilt+ation! 8.N7E! 9."7E! E.3+ogno#i# %F.iagno#i#! commonest high high high progressive. 4o nerve infitration . (t affects: %)-,in! - multiple nodules on nose, eye lids, eye bro)s - ! lesion is symmetrical in both sides - leonine face#$oss of eye bro)s% ()e+mal #en#o+y ne+:e! - glove & stocing anesthesia loss of sensation, tissue atrophy autoamputation of fingers & toes. /) "'$o'# mem*+ane:sho) nodules in: 4ose bloced nose. $aryn/ hoarseness of voice. 4)affe$tion of inte+nal o+gan# e&$ept C0N0-0 )ea$tion! Lep+omato'# +ea$tion:- :diffuse reaction. : formed of dense infiltrate of macrophages & lymphocytes. : ma$+ophage#: contain lepra bacilli foamy macrophages called #$epra cells% & giant $ell#0 :lympho$yte#:scanty 8r absent. :! reaction ends by fi*+o#i#0 :need tt. :cause of death:renal failure. $epramin test: -ve $ess common. lo) lo) lo)
regressive.
presence of nerve infiltration. . (t affects: %) -,in!.hypopigmented anaesthetic e9 flat macules. - ! lesion is <symmetrical. -sin ulceration;'ry infection. () 3e+iphe+al (moto+ 2 #en#o+y ne+:e#)! Sho) :cord lie thicing. :paralysis. : anesthesia. /)No affe$tion of inte+nal o+gan0 )ea$tion! T'*e+$'loid +ea$tion!. $ocalized reaction:#tubercle lie granuloma : Tubercle is similar to T." formed of epithelioid cells, $anghans giant cells and lymphocytes. :giant $ell#:fe),small,e9 fe) nuclei. : lympho$yte#:plenty ,peripherally. :4o caseation #non $a#eating t'*e+$le). :! reaction ends by fi*+o#i#. :spontaneous or stationary cure. $epramin test: ;v 13 King of pathology -a+$odo#i# T0B %.ef! (.N7E! /."7E! 4. hype+$al$emia 5.+eti$'lin F+ame;o+,! 6.3+ogno#i#! 8.iagno#i#! :4on caseating granuloma of Lnno)n cause. :-ssociated e9 T-cell depression. 4on caseating lesions:- a)L0N##hilar&mediastinal% :4ot matted *)L'ng! (Honey $om* appea+an$e%: diffuse granulomas in alveolar )all e/tensive fibrosis compensatory dilatation of surrouding bronchi. :bacilli: 4o.#unno)n cause%. :4o caseation. :lymphocyte: Scanty. : giant cells:- -fe). -Schauman;asteroid inclusions -mainly central nuclei. :5pithrloid cells. ;; (ntact Lnpredictable: acute 8r chronic Temorary 8r permanent. Mveim test :(nfective granuloma due to T." bacilli. 2aseating lesions:- a) L0N##hilar&mediastinal%:matted. *)L'ng:either:-# K% :=honIs focus. :-ssmonIs simon focus. :2hronic fibrocaseous T.". :T." bronchopneumonia. :T." pneumonia. :<iliary T.". :Tuberculoma.
N N destroyed =ood# healing % 8r "ad # spread %. Tuberculin test. 14 King of pathology By\King of pathology( Legand Hazem ) TGBE)CGLO-I- ( T0B ) ef : 2hronic infective granuloma affecting nearly all body systems but mainly ! lungs. Ca'#e# :- <.3+edi#po#ing Fa$to+# ! En:i+onmental! 3e+#onal ! $o) socioeconomic level 2ontact e T" patient. 8ver cro)ding. 5nvironmental pollution. 4egroes. "ad general hygieneG <alnutrition. +epletating #+<% & (mmune deficiency dse B.mode of infe$tion : )ill be disscused. $.Ca'#ati:e <gent# B E&$iting fa$to+# ! : TB *a$illi : -t+'$t'+e of TB *a$illi ! * layers: 2A8, lipid & protein #tuberculoprotein%. Type# of TB Ba$illi ! 1- Auman type #<ycobacterium T"%: transmitted by inhalation from infected patient '- "ovine type #<. "ovine%:transmitted by ingestion of infected co)@s mil *- 8ther rare Types: -vian type. Cha+a$te+ of TB *a$illi ! :)ea So sensitive to direct sunrays. :aerobic O resist dryness. :4on motile- 4on invasive. :Not to&igeni$. :highly antigeni$ :e+y i++itant to imm'ne #y#tem0 1Type# of T0B ! 1-primary T." '-secondary T." )ea$tion of the *ody again#t *a$illiB t'*e+$le fo+mation B p+olife+ati:e +ea$tion B pa+en$hymato'# le#ion0 15 King of pathology -3-TA8=545S(S In %#t (4 h# from introduction of bacilli inside attraction of neutrophils to 2A8 layer of ! bacilli, but they can@t ill it & rapidly disappear. F+om @ ( nd day, attraction of macrophages & lymphocytes to lipid layer of ! bacilli. macrophages engulf ! bacilli but can@t ill it # the organism multiply inside % as <acrophages at this stage are unsensitized. Fe; ;ee,# : T-lymphocytes are attracted to protein layer of bacilli # 33+ %, T" granuloma is formed by the interaction # % macrophages & T cells :Chemi$al mediato+# of g+an'loma fo+mation: Fa$to+# +elea#ed *y ma$+ophage# Fa$to+# +elea#ed *y helpe+ T $ell# ($-1': ;; helper T cs to secrete ($-': ;; mitosis of other lymphocytes (4> : most important factor for granuloma formation : 1- ;; production of monocytes from bone marro). '- ;; production of ($-1' from macrophage *- ;; all steps of phagocytosis T4>: 1. 2hemotactic for macrophages '. -ttrctive to other lymphocytes from blood *. Fasodilator # help more macrophages & lymphocytes to reach the area% 16 King of pathology The lipid part of ! engulfed bacilli changes ! characters of macrophages to cell similar to epithelial 2s called epithelioid cells:a- "7E disscused later -./0 E": cell membranes sho) desmosomes # % 2s form a )all against spread of infection $anghan@s giant 2s:-a-formed by fusion of epithelioid cells. b- <E5 disscused later -./0 lymphocytes surround epithelioid 2s >ibroblasts appear & encircle ! tubercle by fibrous tissue So The tubercle at this stage is called Fi+m t'*e+$le <fte+ ( . / ;,# a central caseation start in ! center & ! tubercle become #oft t'*e+$le Ca#eation i# $a'#ed *y!. 1.lymphoines of sensitized lymphocytes. '. 3roteolytic enzymes from dead neutrophils. *.1elative central ischemia. ,.+elyed hypersensitivity reaction against tuberculoprotein. N7E of TB +ea$tion! Size:1-*mm 2 - Shape:at first granules then become cavity . 2olour:yello)ish . (C 2onsistency:firm then after caseation become soft "7E of t'*e+$le : A< +f =on caseating tubercle : Jell formed pale pin granuloma formed of , layers : 1 - Epithelioid $ell# : * macrophage contain T." bacilli . * ytoplasm : large, s)ollen, pale pin e9 ill defined border . * =ucleus : vesicular, eccentric . 17 King of pathology : E":2ell membranes sho) desmosomes # % 2s form a )all against spread of infection. (.Hiant $ell#! : formed by fusion of epithelioid cells. :it is of ' types: LanghanI# type! (n center of tubercle 4uclei are peripheral and may be :Aorse-shoe lie :"ipolar :1ing form Non.LanghanI# type! 4uclei in the center of cytoplasm. /.T.Lympho$yte#! :surround epithelioid cell and e/tend in P Q them. :small rounded cells e9 dar stained rounded nucleus. 4.Fi*+o*la#t laye+ B Fi*+o#i# a+o'nd g+an'loma0 ><+f caseating tubercle: (t )ill be formed of . layers: %.Cent+al $a#eation ne$+o#i# ! :(t occur due to JJJJJ0 ?"58@& -./* :appear homogenous structurless pin area. ',*,,,.: Same cells as above e&$ept only one diffe+en$e!. Little langerhans giant cells surround central caseation. N0B : a-central caseation necrosis is directly proportional to hyperseitivity So: Aypersensitivity caseation area b->ibroblast layer is directly proportional to immunity# immunity fibroblast layer% . 18 King of pathology : Type# of T0B ! 1-primary T." '-secondary T." 19 King of pathology 1ry T." 'ry T." %.ef! (."7I! /.-ite#! 4.pathogene#i# and +ea$tion again#t T0B! <.p+olife+ati:e +ea$tionB t'*e+$le fo+mation! B.E&'dati:e +ea$tion! 5.N7E! 6."7E! 8.fate! RSH :T." of 1 st e/posure. :common in childhood period. :occur in non immunized person. (nhalation. E&ogeno'# (ngestion. -liver tonsil -nose 1are lung mainly. -sin intestine -mall +ea$tion occur. :slo). :>irm. :)ell formed. 4o e/udative reaction. Colo'+ :grey. Con#i#ten$y :firm e9 no cavity. T'*e+$le# eK minimal $a#eation. <.good: Aealing by: : Small lesionfi*+o#ed :large lesion $al$ifi$ation2 en$ap#'lation. :The organism may die or remain dormant in ! healed lesion :T." of ' nd e/posure. :less common in adulthood period. -e&ogeno'#0 .endogeno'# do+mant fo$'#. -ny organ but mainly lung. (ntestine. E&ten#i:e +ea$tion!at 1ry infection 8r at "2= vaccination the ptn acBuire immunity and hypersensitivity agains bacilli the immunity protect ptn for some time then hypersensitivity reaction of body against T.". rapid occurrence,e/aggerated response softer due to more liBuefaction of caseating material. 59 more liBuefaction so it )ill form cavity and may discharge from ulcer, Sinus, fistula. E&'dati:e +ea$tion ! :occur in serous covering and in soft parenchymatous organs. :The serous covering become studed e9 Tubercles associated e9 e/udates )9 may be: - serous. -serofibrinous. -T." pus. * The E&'date Contain: neutrophils& lymphocytes & macrophages & caseous material. ! lymphocytes represent KGH of ! inflammatory 2s. absent or little <esothelial 2s. Colo'+ :yello). Con#i#ten$y :soft may fo+m $a:ity. T'*e+$le# eK e&ten#i:e $a#eation0 <.good: Aealing by fibrosis, calcification, encapsulation & cavity formation e9 epithelialization. B.*ad: 20 King of pathology
'H +isscused in pulmonaryT.". -./0 do+mant fo$'#. B.*ad: Spread by: :local#direct%:by macrophage Fia serous sac , cavities. :lymphatics:via draining $ymphatic. :along natural passage: -less than in 'ry T.". - 5.g: lung alveoli. respiratory tract. :"lood#hematogenous%: -more than in 'ry T.". -(f:fe) number phagocytosed. <oderate 4o isolated organ T." $arge 4o <iliary T.".
:mainly by local spread. 4atural passage. :4o role of lymphatics. :minor role of blood spread. The important complication here is: (+y amyloido#i#. N0B:def0 of do+mant fo$'#! :(t is healed lesion in )9 organism still dormant# . AB"C DE)0 :(t become activated in case of immunity 'ry T." occur. 21 King of pathology %+y T0B (%).ef (().mode of infe$tion (/).#ite (4).Component (5).Fate0 (%).ef ! -s before0 (().mode of infe$tion ! -s before. (/).-ite !-s before. (5).Fate !-s before0 (4).Component of the %+y $omple&:- 1 p+olife+ati:e +ea$tionB t'*e+$le fo+mation in affe$ted o+gan!. #pathogenesis-4E5-<E5% -s before. 1 TB lymphangiti# of lymphati$# d+aining the a+ea! . (t forms a cord of multiple tubercles in ! )hole course. .due to macrophage tae bacilli to draining $.4 along )ay of macrophage to $.4 The bacilli cause T." lymphangitis #inflammation of lymph vessels%. :-fetr reaching $.4 bacilli cause T0B lymphadeniti#0 (+y T0B i##$'#ed *efo+e0 "ilia+y TB! %+yL(+y. in any o+gan pyemi$ a*#$e##! FG H1"I ef:due to blood#hematogenous%spread of large ef:due to circulation of small emboli infected 4o of T." bacilli e9 lo) immunity. e9 pyogenic bacteria. "ethod of #p+ead: spread of bacilli from any lesion "ethod of #p+ead:by infected emboli )9 are to the blood to reach any organ. (mpacted in capillaries and N7E: small blood vessel in any organ multiple N7E: -s before. uniform small size #* mm% tubercles separated from each other by normal tissue & not surrounded by congestion & present on outer & cut surface of organs related to a bl.v. (n lung,located mainly at the upper lobe. (n serous membranes, are arranged diffusely. "7E:-s tubercle but no giant cells or fibrosis#lo; imm'nity) "7E:-s abscess; central bacterial colonies Fate: fatal Fate: fatal %+y 3GL"ON<)D TB (%).ef (().Etiology (/)."7E (4).Component (5).Fate0 3'lmona+y T0B i# Fa:o+a*le #ite fo+ TB ( ea#y inhalation % 22 King of pathology (%).ef ! Jame as 1ry T.>. (().Etiology ! a.p+edi#po#ing fa$to+# ! -s before0 *."7I ! 5/ogenous by inhalation0 $.E&$iting fa$to+# ! Auman type bacilli0 (/)."7E ! 1"7E of t'*e+$le -./0 ? minimal $a#eation ne$+o#i#0 1T0B lymphangiti#! (t forms a cord of multiple tubercles in ! )hole course0 1T0B lymphadeniti#! (;ill *e di##$'#ed late+)0 (4).Component ! <. HhonI# fo$'# : parenchymatous lesion # disscused later %0 B. T0B lymphangiti#! (t forms a cord of multiple tubercles in ! )hole course0 C. T0B lymphadeniti# of hila+ O+ media#tinal L0N ( ;ill *e di##$'#ed late+ )0 M.HhonN# fo$'#!Oef N7E "7E Fate P
1ef ! parenchymatous lesion in 1ry pulmonary T.". 1N7E ! Size:1-'cm .-ite:Sub-pleural lo)er part of upper lobe. .(- Lpper part of lo)er lobe. Shape:oval or rounded. .No:Single0 .%C 2olour:grayish yello). 1"7E : <E5 of tubercle -./0 ? minimal caseation necrosis0 1Fate :6>ate of 1ry pulmonary T." # disscused later % (5).Fate! <.good : RSH Aealing by: : Small lesionfi*+o#ed :large lesion $al$ifi$ation2 en$ap#'lation. :The organism may die or remain dormant in ! healed lesion do+mant fo$'# B.*ad : 'H Spread by! %.di+e$t #p+ead! pleurisy,pyothora/,pneumothora/,pyo pneumothora/ and haemoptysis. (.Lymphati$ #p+ead::from hilar $.4 to hilar structure. :from mediastinsal $.4 to mediastinal structure. /.Blood #p+ead:#"acillemia% : spred of T." bacilli in blood. : a$$o+ding to the do#e:- If +ea$hed a :ein : Small doseremoved by immune system <oderate doseisolated organ T" 6 T'*e+$'loma. $arge dose generalized milia+y TB If +ea$hed a p'lmona+y a+te+y : 1eturn bac to the lung miliary T" of lung. 4.Nat'+al pa##age! 23 King of pathology a<Endogenous passage : in lung tissue &bronchi :T." bronchopneumonia: inflammation of bronchi surrounding lung tissue. :T." pneumonia: inflammation of lung tissue. :"roncho-pleural fistula. :-cute tuberculous bronchopneumonia6-cute phthisis6=alloping consumption. b<Exogenous passage : in structures above 8r outside lung:- T =ohnIs focus enlarge& then open into bronchus : T." laryngitis # T." in laryn/ % : T." tonsillitis # T." in tonsils % : T." ulcer in tongue. : intestinal T." by s)allo)ing sputum. K< Acute tuberculous bronchopneumonia =Acute phthisis = Lalloping consumption :< %.ef!: bilateral consolidated patches around terminal bronchioles more in lo)er lobes. :(t is rare complication of pulmonary T." occue )hen -- immunity &;; dose of bacilli e9 ; ;hypersensitivity (.3athogene#i#!1 =honIs focus ulcerate in bronchial tree. : (n ptn e9 -- immunity T." bacilli spread forming multiple tubercles#patches% The patches fuse together forming large caseous area on evacuation Ca:ity fo+mation0 :2overing pleura sho) T." pleurisy. :Ailar $.4 sho) hilar T." lymphadenitis. /."7E!-s <E5 of tubercle -./0 B't No giant $ell# and No fi*+o#i# ( no imm'nity) 0 4.Fate! Fatal a# +'pt'+e of the $a:ity pneumothora/, pyo pneumothora/ and T." pleurisy. T0B 'l$e+ in tong'e i# $hK *y : N7E: No:single or multiple. Size:variable in size. 'S Shape:irregular in shape. 1 "a+gin: irregular, cyanotic. 1Edge : undermined # groove % :Ba#e : hard, indurated. :Floo+ : yello)ish covered e9 caseous material. 1d+aining L04 : mildly enlarged. :It o$$'+ on tip spread deep parenchymatous glossitis. #"a$+oglo##ia ?"58& ME& %. "7E: "7E of t'*e+$le0 (+y 3GL"ON<)D TB (%).ef (().Etiology (/).In$iden$e0 (4).-ite (5).pathology0 %.ef! 1It i# ad'lthood type of p'lmona+y T0B0 24 King of pathology 1o$$'+ in % #t e&po#'+e in imm'no$omp+omized pe+#on )e.e&po#'+e to T0B *a$illi0 (.Etiology! a.p+edi#po#ing fa$to+#!-s before *."7I! 5/ogenous by inhalation0 5ndogenos by )e-activation of dormant focus. $.E&$iting fa$to+#!Auman type bacilli0 /.In$iden$e!Le## $ommon0 4.-ite! apical or sub-apical part especially in 1t than $t $ung due to: 1Hood :entilation(ae+o*i$ o+gani#m)0 1.. lymphati$# in api$al pa+t0 1na++o; )t p'lmona+y a+te+y than left .. *lood flo; ..+e#i#ten$e0
5.3athology! a.<##man #imon fo$'#0 *.Ca:ita+y T0B0 $.Ch+oni$ fi*+o$a#eo'# p'lmona+y T0B0 a.<##man #imon fo$'#! (ef.ChK.fate) 1ef! 12hronic apical lesion. :>ormed by fusion of many tubercles enlarge,caseate form large lesion e9 2entral caseation&fibrous capsule :character: :The lesion is variable in size. :4ot associated e9 lymphangitis or lymphadenitis So it differ from =ohnIs focus. :>ate: depend on amount of organism. (mmunity. Aypersensitivity. <mo'nt of o+gani#m Imm'nity hype+#en#iti:it y Effe$t :Aealing by fibrosis 8r calcification. :(t is less common. Spread rapidly rapid destruction of lung tissue # -cute T." bronchopneumonia %. : (t is less common. <oderate <oderate <oderate 2avitary pulmonary T" may # 2hronic fibrocaseous pulmonary T" %. :it is more common. 25 King of pathology B. Ca:ita+y p'lmona+y TB! - Softening & liBuefaction of caseous material coughed out 2avity formation. -The cavity may be healed 81 pass to Ch+oni$ fi*+o$a#eo'# p'lmona+y TB . C. Ch+oni$ fi*+o$a#eo'# p'lmona+y TB!. ( %.pathogene#i# (.N7E /."7E 4.Fate ) %.pathogene#i#! a-the lesion e/tends from apical focus to ad!acent bronchi &lung tissue. b- caseous material become discharged through bronchioles leaving a mother cavity fo+mation of #mall $a#eo'# a+ea0 c-these areas on evacuation leaving small cavities called # a'ghte+ $a:itie# )B <$ina+ $a:itie#0 d- Fi*+o#i# o$$'+ 6 healing e/tends in # % ! cavities lung fibrosis & bronchiectasis0 e.These small foci may be formed in the )all of blood vessel . if rupture severe Aaemoptysis. /."7E : m'ltiple $a#eating t'*e+$le# -./0 ? e/cess fibrosis ? epithelialization of cavities ?7. calcification. (.N7 E!( of the mothe+ $a:ity):- 1No: Single #single mother caviyy surrounded by smaller ones%. 1-ite:apical 8r sub apical part of the 1t lung. Size:large. 1(- Shape:irregular. : The lining is irregular & shreddy & yello)ish d.t caseous material. : The ;all sho):a-raised bands of remnants of bl.vs & bronchi. *-2aseation foci in )all of blood vessel if rupture cause haemoptysis :the #'++o'nding a+ea! the caviy is surrounded by:- a-fibrous tissue. *-multiple small daughter cavities S8 - This arrangement of the large mother cavity &small daughter cavities gives )hat is called ( $lo:e+ leaf appea+an$e )0 4.Fate!. <.good fate : healing by 5ncapsulation. 5pithelization. +ystrophic calcification. B.Compli$ation :- 1-due to tissue destruction: Aaemoptysis. 'ry amyloidosis. "roncho O pleural fistula. '-due to spread: +irect spraed. "lood spread. +isscused before -./0 4atural spread. No lymphati$ #p+ead. *-due to fibrosis : (t cause 1t sided heart failure. ,-it cause peptic ulcer either by : -nti T." drugs 26 King of pathology 3sychic causes. N0B : -ny chronic lung dse cause lung fibrosis -ny diffuse lung fibrosis cause pulmonary hypertension. -ny pulmonary hypertension cause 1t sided heart failure. Jo No you OnoP Phy chronic fibrocaseous T.> cause Qt sided heart failure R
T B0 ENTE)ITI- Inte#tinal T0B0 Type#:1ry intestinal T.". 'ry intestinal T.". %+y inte#tinal T0B0 (Childhood type) %.Etiology (.pathology /.Fate0 %.Etiology: :E&$iting fa$to+#: mainly bovine type. 1are Auman type (.pathology: < - pa+en$hymato'# le#ion! 1 m'ltiple t'*e+$le# eK minimal $ent+al $a#eation -./0 : bacilli are engulfed by macrophage of 3eyer@s patches proliferative reaction tiny ulceration. : macrophage tae organism to draining $.4s T." lymphadenitis. : along their course to $.4s, the bacilli taen by macrophage cause T." lymphangitis. B. T0B lymphangiti#! (t forms a cord of multiple tubercles in ! )hole course0 C.T0B lymphadeniti#! :tubercles in the draining $.4s #mesenteric $.4s% :this called #Ta*e# "e#ent+i$a%. ef: T." lymphadenitis of mesenteric $.4s , as part of 1ry comple/. * <esenteric $4s are enlarged & fused together 6matted #d.t inflam of perinodal tissue% /.Fate :Hood : healing 1Bad : spread. $ocal # direct % T." peritonitis , T." salpingitis. "lood spread a# *efo+e -./0
!"S ( +y inte#tinal T0 B0( $ommon in ad'lt# ) %.Etiology (.type# /."7E %.Etiology! a. E&$iting fa$to+# : mainly Auman type. 1are bovine type0 *."7I! in human type by s)allo)ing of infected sputum. "lood transfusion. (n bovine type by drining of infected mil. 27 King of pathology (.type#! I.Gl$e+ati:e Type! # pathogenesis T =UE T VUE % 1pathogene#i# of t'*e+$'l'# 'l$e+! starts in peyer@s patches . T" reaction destruct submucosa & mucosa. ulcer )9 is at 1 st parallel to longitudinal a/is of ! intestine # tae the shape of peyer@s patches% but later d.t e/tension in lymphatic , ! ulcer tae a girdle shape ulcer #encircle the bo)el% e9 its a/is perpendicular to that of intestine :N7E B Cha+a$te+# of @ Gl$e+: No:multiple. -ite:terminal ileum. Size: as payerIs patches. (- Shape:irregular transverse girdle ulcer. "a+gin: irregular & cyanotic. Edge: undermined #destruction is more in the deeper layers% Ba#e:hard , indurated #fibrosis%. Floo+:yello)ish covered e9 caseous material. <&i#!perpendicular to longitudinal a/is of intestine. +aining L0N : not enlarged #not affected%. The pe+itoneal $o:e+ing is filled e9 multiple tubercles & appear thic dull & opaBue adhesions 1"7E! . m'$o#a ! 'l$e+ated0 . -'*m'$o#a!#ho; t'*e+$le# -./0
II.hype+pla#ti$ Type B Ileo.$ae$al T0 B! %.-ite (.effe$t /.C73 %.-ite! 1Te+minal ile'm 1$ae$'m 1a#$ending $olon0 (.Effe$t! a.the )all of previous sites is thicened e9 narro) lumen chronic obstruction b-the mucosa sho) foci of caseation and small ulcers. /.C73: presence of )t ilia$ ma##. Compli$ation of inte#tinal TB 1-inte#tinal fistula either internal PQ 'loops of intestine causing malabsorption. 5/ternal PQ loop of intestine&anterior abdominal )all causing >eacal matter goes out. '-inte#tinal obstruction : # acute d.t adhesion or chronic in hyperplastic type %. *-inte#tinal perforation : d'e to adhesions and fibrosis. Thi# $a'#e septic peritonitis #4.":caused by 5coli bacteria not T." bacilli as T." bacilli is not invasive% ,-Aemorrhage. .-'ry amyloidosis. 0-Spread: $ocal#direct% T." peritonitis , T." salpingitis # T." of fallopian tube %. "lood spread as before -./0 28 King of pathology %+y inte#tinal T0B (+y inte#tinal T0B %.<ge! (.Type /.method 4.fo+m 5.L0N# 2hildren bovine drining diseased mil tiny ulcers enlarged#tabes mesentrica% adults human 8r bovine -me 8r s)allo)ing of infected sputum. La+ge t+an#:e+#e ulcers 4ot enlarged 29 King of pathology T0 B0 3E)ITONITI- 8ccur in children & young adults. "ethod of Infe$tion : 1-direct spread:from intestine , mesentry , fallopian tube. '-lymphatic spread : from intestine , lung. *-"lood spread:from T." of other organs. Type# <. lo$alized0 B. gene+alized 5/udative & depends on @ do#e of *a$te+ia & +e#i#tan$e of @ *ody0 1. Ascetic WmoistX Pet) type : ;; dose of bacilli & - - resistance, ;; hypersensitivity 1 ?? #e+ofi*+ino'# e/udate, & ! peritoneal covering is studded e multiple tubercles. '. aseous type : - dose of bacilli. -resistance moderate -hypersensitivity :5/udate formed of $a#eo'# mate+ial0 *- Nry Wplastic) type : - - - dose - ;; resistance - - - hypersensitivity. :$ittle tubercles, ;; fibrosis adhesion # % ! loops of intestine :The omentum is thicened & contracted & rolled on itself (#a'#age #hape% Compli$ation - -dhesion acute intestinal obstruction. - >ecal fistula. - $ocalized T" peritonitis: caseous encysted type # % ! loops of intestine <#$eti$ (moi#tC ;et) type +y (pla#ti$) type %.$a'#e! (.fl'id e&'date: /.fi*+in! 4.No of t'*e+$le: 5.pe+itone'm! 6.ompli$ation#: 8.ChK #ign! ;; hypersensitivity, -- resistence $arge amount $ittle amount :moderate 4o. There is peritoneal distension :rare :------ -- hypersensitivity,;; resistence $ittle amount $arge amount :large 4o. There is peritoneal adhesions. :8bstruction -fistula -'ry infection. : #a'#age #haped ma##e# 30 King of pathology T B0 LD"3H<ENITI- ef! :(t accur as part of 1ry T.". :$.4s arenIt affected in 'ry T." but it is affected only in 1ry T.". (t is the 2ommon cause of lymphadenopathy in children. "ETHO OF INFECTION! -ite#! 1. >orm part of 1ry comple/. :Ailar and mediastinal $.4s in pulmonaty T." '. Spread through lymphatics. :<esentric $.4s in intestinal T.". *. "lood spread # rare %. :2ervical $.4s in tonsillar T.". N7E! :$4 is enlarged . :5arly T" lymphadenitis :- <ultiple non caseating tubercles at periphery then go centrally. They are separated by thin rim of nodal tissue. :$ate T" lymphadenitis :- - 2aseation starts in the tubercles fuse together replace the )hole $4 #if caseation is liBuefied by enzymes of polymorphs it is called COL <B-CE-- %. -The reaction e/tend to capsule perinodal tissue ! $4s become matted together form one mass e9 central caseation. "7E! Ea+ly TB0 LN : non caseating tubercles -./* Late TB LN : caseating tubercle -./* Fery late:$.4s are transformed to caseous material enclosed e9in fibrous capsule COL <B-CE-- F<TE YLood :Aealing by : fibrosis , calcification or encapsulation. Y>ad : 1- spread according to its site: --direct : :cervical $.4s cold abscess retropharyngeal abscess open on the surface by sinus 31 King of pathology )9 has undermined edge and discharge caseation. :Ailar and mediastinal $.4s to hilar and mediastinal structures :<esentric $.4s cause T." peritonitis. "-"lood spread : as before -./0 '-'ry amyloidosis
Cold a*#$e## %.ef (.Etiology /.N7E 4."7E 5.Effe$t %.ef! (t is soft mass formed of caseous material surrounded e9 fibrous capsule. (.Etiology: : very late T." lymphadenitis. :3ottIs disease. /.N7E: soft mass E encapsulated E UJ :sho) yello)ish , dry , friable material. 4."7E! "7E of t'*e+$le -./0 ; e/tensive fibrosis ; e/cess neutrophils. 5.effe$t! a :'ry amyloidosis. *: in 2ervical region # vertebra % retropharyngeal abscess.. - in Thoracic region# vertebra % posterior mediastinal abscess. -in $umber region# vertebra % psoas abscess. $ :"lood spread: as before -./0 T'*e+$'loma %.ef (.Etiology /.N7E 4."7E 5.Effe$t %.ef:(t is tumor lie mass formed of caseating tuberculus reaction surrounded e9 fibrous#glial% capsule. (.Etiology:due to blood spread of moderate dose of bacilli in patients e9 moderate immunity. 1T'*e+$'loma i# (+y B't it i# $ompli$ation of %+y01 /.N7E! No! single. onNt fo+get! If it i# in *+ain In $e+e*ell'm2*+ain #tem -ingle0 32 King of pathology In $e+e*+'m m'ltiple0 -ite :any organ . 1S -ize: ,. O 1G cm -'+fa$e :nodular. 2olour:grayish yello) caseous material surrounded by grayish )hite capsule. (C 2onsistency:firm. Cap#'le :encapsulated. C7- : sho) caseating center surrounded by fibrosis #o+ glio#i# if in *+ain)0 4."7E :t'*e+$le# eK e&ten#i:e $ent+al $a#eation -./* surrounded e9 fibrous# or glial if brain % capsule. 5.effe$t! :<ass effects: as pressure effect , obstructive effect ,edema,77.. :destruction of the affected organ. :Spread of infection.
TB0 of C0 N0 -0 I) T0 B0 "eningiti#! Common0 %."ETHO OF INFECTION! 1. Blood #p+ead from a 1ry comple/.: -- tubercles starts at brain corte/ & ventricles rupture reach 2.S.>.meningeal infection. "-Through choroid ple/us. 2-3art of miliary T. ". (. i+e$t #p+ead from vertebra# in 3ott@s disease% (.3athogene#i#! :yello;i#hCdiff'#e e&'date covers leptomeninges #pia-arachnoid% at ! base of ! brain due to irregular brain surface at ! base; slo) 2. S. > circulation. :T'*e+$le# fo+mation along the small blood vessel , choroid ple/us , and lining of ventricles. 33 King of pathology :a+ea of $e+e*+al #oftening due to ischemia from 5-8. :I++eg'la+ity of *a#e of *+ain 2ompression of eye nerves # *, ,, &0%. /.N7E! 1- Thic dull opaBue leptomeninges0 '- subarachnoid space are studded e9 multiple tubercles. *. 2S> circulation is a balance # % secretion & absorption #)ith no obstruction% .(f this changes;; (2T dilated ventricles. ,-2hange of 2.S.>: :clear - lymphcytes - protein - pressure. :"acilli presence - 2$ - sugar :Sho) T." pus #thic, turbid , caseous%. 4."7E! 1-poo+ly fo+med tubercles in meninges Small e9 central caseation. '-In$omplete transformation of macrophage to epitheloid cells. *-#mall or fe) giant cells. ,- C0-0F : contain T" pus & bacilli. .-E&'date formed of # caseation O $ymphocyte - 5pithiloid cells - >e) giant cells %. 5.Compli$ation! :Fibrosis:hyrocephalus&cranial nerve palsy. :(nfarction occur due to thrombosis&5-8. :Spread:direct 81 blood. II) T'*e+$'loma Le## $ommon :N7E 2 "7E disscused before. :Effe$t : there is increase intra-cranial pressure.
34 King of pathology G+ina+y -y#tem TB a),idney0 B)G+ete+ C)'+ina+y *lade+ %. Kidney T0 B! "ETHO OF INFECTION! :"lood spread :- -as a part of military T.". -T." in any organ. :-scending from lo)er L.T. Fo+m# of T0B le#ion in ,idney: 1< hronic T> pyelonephritis = surgical Oidney= hronic ulcerocaseous pylonephritis. 2<Viliary T. >. disscused before. Z.Tuberculoma. disscused before. 1< hronic T. > pyelonephritis = surgical Oidney:< 1ef0 1-ite 13athogene#i#0 1N7E 1effe$t 1Compli$ation0 1ef: T." of idney in )9 tubercles present in the renal corte/ of the idney. 1-ite! start at pyrimdal ape/ or base. : 3athogene#i#! (nfection start in corte/ tubules & peritubular lymphaticsform multiple tuberclesmultiple cavities caseous material discharge to calyces pelvis . N7E! [M\"I (any di#ea#e o$$'e in ,idneyCit# N7E in$l'de '#'ally (-ize.-'+fa$e.Cap#'le.C7-) -ize! enlarged -'+fa$e: lobulated6 bossy Cap#'le! thic adherent & difficult to be striped 9:]^* _/60 @ . C7-! irregular cavities lined by & containing caseous material 35 King of pathology ; -hape! preserved. Late!In T0B pyoneph+o#i#C ,idney *e$ome! : -ize! enlarged, : -'+fa$e: lobulated6 bossy : Cap#'le! thic &adherent & difficult to be striped . :caseating material. In (+y $ont+a$ted ,idneyC ,idney *e$ome ! 1-ize! 1-'+fa$e!irregular. 1Cap#'le:thic& fi*+o'# :2aseating material: :Fi*+o#i#: Effe$t! depends on patency of ureter: - (f 3atent ureter evacuation of caseous material fibrosis (+y $ont+a$ted ,idney. -(f Lreteric obstruction accumulation of caseous material in idney T0B pyoneph+o#i# Compli$ation ! Jpread . di+e$t : to ureter urinary bladder #discending infection%. .Blood #p+ead : a# *efo+e -./0 Qenal failure # if bilateral % (0 T0 B G+ete+ a."ode of infe$tion : from idney 81 L." 81 "lood. B.Effe$t ! 5arly:<ainly )all of upper or lo)er 1E* become filled e9 tubercles. $ate: <iddle part is affected. 36 King of pathology /0 T0B0 '+ina+y *ladde+ a."ode of infe$tion : -descending infection from idney infection start at Lreteric opening. --scending infection from prostateinfection start at bladder nec. To trigone B.Effe$t ! Tubercle formation then ulcerate discharging T" pus. (f heal by fibrosis $ont+a$ted *ladde+0 TB OF "<LE HENIT<L -D-TE" "ethod of infe$tion! 1% (f ! infection is hematogenous epididymis is 1 st site to be affected. '%(f ! infection is descending from L T prostate is ! first site to be affected. 3athology! %0 3+o#tate: -descending from L. bladder or ascending from epididymis. formation of multiple tubercles fuse enlarged prostate. -may result in urethral,rectal,or peritoneal fistula. (0 -eminal :e#i$le! (nfection from prostate or epididymismultiple tubercles & destruction of ! gland & hemospermia # blood & bacilli & sperms%. /0 T B0 #pe+mati$ Co+d (f'nni$'liti#) - <ultiple T" nodules 6Tubercles. . T'*e+$'loma `9]* 40 TB epididymiti#! (nfection from blood 81 from spermatic cord destruction of epididymis & formation of posterior scrotal sinus. & anterior 50 Te#ti# not affe$ted0 TB OF FE"<LE HENIT<L -D-TE" %.T0B -alpingiti# B T0B of fallopian t'*e! a."ode of infe$tion: :from surrounding structures. :from blood spread. *.N7E 2"7E! T." salpingitis 4on T." salpingitis %.ef! (.N7E! /."7E! 4.p+ogno#i# Tubercle in )all of fallopian tube due to direct or blood spread. :the tube appear Sausage-shaped e9 3eri-tubal fibrosis and adhesion. :)all thic. :$umen contain caseating material. -t'*e+$le eK $ent+al $a#eation -./0 :either heal or spread to near organs. : (f ! fimberial end is patent discharge caseous material to peritoneal sac. :(f ! fimberial end is closed d.t adhesion TB pyo#alpin& (#a'#age appea+an$e) 2hroic inflammation in fallopian tube. :appear funnel shape. :thin. :contain pus. .non #pe$ifi$ $h+oni$ inflammation -./0 :Aealing 37 King of pathology (.TB Endomet+iti#! +irect from ! tubes . Q 3athology ! (f female in 2"3 ! tubercles are poorly formed e no caseation d.t shedding of endometrium every month e menstruation. "ut in old age tubercles are )ell formed & discharge caseous material in ! lumen T. ". pyometria. /.O:a+ian TB! Spread from fallopian tube or T" peritonitis. BONE TB0 )o'te# of Infe$tion ! -"lood Spread. ->rom bone to !oints. TB o#teomyeliti#! Start in Aaversian canal & bone marro) destruction of bone e formation of seBustrum. a granulation tissue is formed only# no callus% because ne) bone formation needs ostoblastic 2s an involecurum is formed around. Aealing by fibrosis TB >e+te*+ae (3ottI# di#ea#e)!. %.ef :: it is T." of vertebrae : it is the commonest T. ". of bone in children & adults. (.Etiology : : mostly Aematogenous spread # blood spread %. :rarely by other methods. /.-ite#! -Thoracic vertebrae. 38 King of pathology - $umbar vertebrae. Tho+a$o.l'm*a+ :e+te*+ae is the commonest site. -2ervical vertebrae. 4.3athogene#i#: :T." start in vertebral body ad!acent to intervertebral disc then caseation necrosis 8ccur finally )ill involve the intervertebral disc. :caseation material from destruction site )ill descend along vertebral columns till 3ara vertebral gutter. : enclosure of caseous material e9in the fascia of the muscles 2old abscess formation : The transverse process & spines of vertebrae are not affected. 5.Compli$ation B Effe$t! a.efo+mity : yphosis, scoliosis, lordosis. *.Cold a*#$e## ! : infection from vertebra periosteal covering neutrophils & fluid are ;; in caseous material T" pus. < pa+a:e+te*+al a*#$e## is formed in front & sides of ! vertebraeSpread under ! anterior vertebral ligament to other vertebrae & under muscle sheath form abscesses in other areas. < in eraical region Waertebra) retropharyngeal abscess.. < in Thoracic regionWaertebra) posterior mediastinal abscess. <in bumber regionWaertebra) psoas abscess. $.3a+aplegia ! :in 1G-'. Hof cases. :$a'#e#: -2ompression of cord by collapsed vertebrae -2ompression by: T5/tradural cold abscess contain T" pus. T(ntradural abscess 39 King of pathology d. (+y amyloido#i#0 -ho+t Bone TB B TB0 da$tyliti#0 Start at medullary cavity of diaphysis. Long Bone TB0 <etaphysis & epiphysis e/tend to !oints Roint TB!. -Fertebral , Mnee, hip, )rist !oint - infection from neighboring epiphysis or hematogenous infection. 3athology! T" synovitis e multiple studded tubercles #e/udative type% effusion is serous or serofibrinous or pyogenic - Aealing fibrous & bony anylosis. "i#$ellaneo'# T B0 )HINITI- 1ry: rare 'ry from infected sputum T B0 -KIN B! L'p'# :'lga+i# 1ry infection from outside in "utchers 'ry: miliary TB0 pe+i$a+diti#0 Serofibrinous inflammation - up to T" pus. TB ton#illiti# %+y TB ton#illiti#! (nfection by bovine type from contaminated co)s mil, 40 King of pathology 1ry comple/ formed of : - parenchymatous lesion in ! tonsil. - T" lymphangitis. - T" lymphadenitis of upper deep cervical $4s. (+y ton#illa+ TB! :'ry to fibrocaseous T" of lung. :2ommon in adults :3athology:T0B 'l$e+ ch9 by: 4o:single or multiple. Size:variable in size. 'S Shape:irregular in shape. : "a+gin!Bl'i#h2nod'la+ :5dge:undermined #groove% 1Ba#e!-oft :>loor: yello)ish covered e9 caseous material. :draining $.4:mildly enlarged. Finally Se #ay that : Fo+m# of T0B in l'ng# may *e ! (8) :=honIs focus. :-ssmonIs simon focus. :2hronic fibrocaseous T.". :T." bronchopneumonia. :<iliary T.". :Tuberculoma. 41 King of pathology :T." pneumonia. Be#t ;i#he#
By7King of pathology0 42 King of pathology By\King of pathology( Legand Hazem ) -D3HILI- (A) ef! venereal 6 se/ually transmitted # ST+ % infective granuloma #chronic%due to treponema pallidum "ode of Infe$tion! +.Accuired infection : the organism penetrates ! intact mucous membranes & abraded sin. 1. #e&'al $onta$t - genital organs # glans penis, vulva, cervi/ % . - 5/tra genital organs as lip & tongue (0 Non #e&'al $onta$t - 4ipple of infected mother sucling infant. - >inger #of a doctor% touch syphilitic lesion. - "lood transfusion ++.ongenital +nfection : The organism passes from infected mother to ! fetus via placenta after ! last * months of pregnancy. 3athogene#i# ! 1-8rganism blood stream #bacteremia% to various organs & multiply in perivascular lymphatics (t affects all ! organs. '-the disease is divided to * #tage# #represent delayed hypersensitivity developed against organism Separated by f+ee pe+iod# # represent developed immunity %. *-1ry &'ry are highly infectious )hile *ry stage has very fe) organism. A (-yphiliti$ )+ea$tion! !"S d;e0 1-peri-arteritis # acute then chronic % Thic,fibrosed adventitia. '-5-8($on$ent+i$ endothelial 2 fi*+o*la#ti$ p+olife+ati:e thi$,ening of @ #mall :e##el#) thic,fibrosed intima. 43 King of pathology *- perivascular infiltration # cuffing % by chronic inflammatory cells : $ymphocytes, plasma cells (mainly) Cmacrophage and giant cells. ,-deposistion of mucopolysaccharides in the interstitial tissue hardness. .-=ranulation tissue. 0-+raining $.4s: sho) follicular hyperplasia.
. %+y A! (%+y #o+eB $han$+eBha+d $han$+e) 4Gf"^%& 4e;g%& 9#C& -not occur in blood transfusion infection & congenital &. .(+y -tage 4Gf"^%& 4e;g%& 9#C& ./+y -tage! :occur after 1G-*G years . :(t has a favorable sites cardiovascular system #SG-S.H% 2.4.S. #. - 1GH%. 1Type# of +ea$tion of Te+tia+y A! %.iff'#e syphilitic reaction: :-ite : commonest in tongue , aorta , testis. :N7E :sho) repeated necrosis & fibrosis. 1"7E : +iffuse & reaction. (.lo$alized!(H'mma) 4Gf"^%& 4e;g%& 9#C& Te+tia+y A OF C<)IO><-CRL<) -D-TE" #SG-S.H of cases% I . >a#$'la+ A (all #ize#)!. 44 King of pathology - Small bl.vs #coronary% periarteriris. - <edium bl.vs #limbs% 5ndoarteritis. - $arge bl.vs #-orta% diffuse & aortitis diff'#e -yphiliti$ <o+titi# B L'eti$ ao+titi# ! :8ccur after 'G years of 1ry infection & in male Q female *:1 :-ffect ! Thoracic aorta # -scending aorta & arch % 48T belo) ! diaphragm <the+o#$le+o#i# h/\ :occurs in this part d.t ;; vasa vasora & ;;lymph supply ;; 4o. of organisms. %.3athogene#i#! earliest changes are 5-8 ; perivascular cuffing of ! vasa vasorum by plasma 2s & lymphocytes. narro)ing of these nutrient arteries ischemic destruction of ! ela#ti$ ti##'e 2 m'#$le of the media stellate - shaped fibrous scars in ! media & fibrosis of ! adventitia. Cont+a$tion of @ median #$a+# a transverse )rinling of the intima ( t+ee *a+, ) [9i]%& j"e% # appear as longitudinal )rinling %. Sith de#t+'$tion of @ t'ni$a media, ! aorta loses its elastic support become dilated producing a #yphiliti$ ane'+y#m ; 'ry atherosclerosis of damaged areas )eaening of ! )all diffuse involvement by calcified atherosclerotic plaBue, )9 obliterates ! intimal tree barU pattern. ! presence of atherosclerotic patches in this location #thora/% is not typical for atherosclerotic aneurysm )9 is usually abdominal (.Compli$ation! a.Na++o;ing of $o+ona+y o#tia !. : due to aortitis as & doesnIt affect coronaries # no lymphatic %. : (f gradual &incomplete myocardial infarction and angina pectoris. : (f sudden complete myocardial infarction. *.<o+ti$ :al:e in$ompeten$e ( ao+ti$ +eg'+ge )!. volume overload $t ventricular hypertrophy & dilatation# heart )eightQ1GGG gm %6 $o+. *o:in'm. A> death. $.-yphiliti$ <o+ti$ <ne'+y#m!. 1ef :localized dilatation of arterial )all forming Sac. :Ca'#e :due to stretching of fibrosed media by ".3 )9 is already lost its elasticity. 1Type# : may be saccular or fusiform 1 '#'ally contain mural thrombus 45 King of pathology :;hen! aneurysmal dilation involve ! aortic valve ring -ortic valve incompetence volume overload $t ventricular hypertrophy & dilatation# heart )eightQ1GGG gm%6 $o+. *o:in'm. A> death. :Compli$ation! <ural thrombusembolization 1upturedeath. 3ressure on surrounding :- ##'pe+io+ media#tinal #ynd+ome %includes:- yspnea & 1espiratory difficulties as a result of encroachment on lungs ysphagia: difficulty in s)allo)ing due tocompression on ! esophagus ysphonia & +ry cough due to pressure on recurrent laryngeal nerve eath estruction & erosion of bone #vertebral bodies & ribs%. istended nec veins due to pressure on SF2 II. Ca+dia$ A! - 4arro)ing of coronary ostia. - -ortic valve incompetence - =umma of interventricular septum heart bloc & may septal defect. - diffuse & pericarditis. N0B! p+e$an$e+o'# le#ion of A a+e!. Le',opla,ia of tong'e 2 H'mmato'# 'l$e+0 Te+tia+y A of C0N0-! :(t occurs in .-1GH of cases. :(t is of ' types: 1< Veningo<aascular k. 2<parenchymatous k Wneuro k). 46 King of pathology +<Veningo<aascular k : :-yphiliti$ a+te+iti# of cerebral and spinal vessels lead to thrombotic occlusion and cerebral softening. 1-yphiliti$ meningiti# lead to fibrosis and compressing on emerging nerve lead to paralysis. 1"'ltiple g'mma0 ++< =euro<k W parenchymatous neurok ): male Q female after .-'G years ( T'a+tena+y #tage )0 <. Hene+aL 3a+aly#i# of in#ane ( H0 30 I ) ( ementia 3a+alyti$a )! ef : sub-acute encephalitis due to & granulation tissue ending in gliosis. N7E! %-3ia.a+a$hnoid mem*+ane: is thic, fibrosed, adherent. (.-'l$i 2 gy+i: flattened. /.>ent+i$le#: dilated e9 compensatory in 2.S.>. 4.B+ain at+ophy motor , sensory , psychotic symptoms. "7E!%.+od C# # long thic- microglial cells containing hemosiderin granules %. (.A +ea$tion. B.Ta*e# o+#ali# ( Lo$omoto+ <ta&ia )! ef! "ilateral degeneration of dorsal horns of spinal cord & posterior roots of spinal nerves =lial & fibrous tissue replace them. It may *e: $umbar Tabes # atrophy % L$ atrophy. 2ervical Tabes )asting $$ atrophy.
N7E! %.3ia.a+a$hnoid mem*+ane: is thic, fibrosed, adherent. 47 King of pathology (.o+#al #'+fa$e of #pinal $o+d: flattened. /.Cent+al $anal: dilated e9 compensatory in 2.S.>. 4.o+#al $ol'mn at+ophy :- $oss of deep sensation$ocomotor ata/ia. $oss of pain sensation chronic ulcer& neuropathic arthropathy 6 2harcot@s !oint#hype+.mo*ility%. "7E: . A +ea$tion. Te+tia+y A of @ )e#pi+ato+y! -y#tem! : 4ose destruction of nasal bridge saddle nose :$aryn/ vocal cord destruction & stenosis of laryn/, :$ung 5-8 pulmonary hypertension #-yerzas disease % =umma of lung is rare Te+tia+y A of Ha#t+ointe#tinal T+a$t! Tongue: - leuoplaia -+eep parenchymatous glossitis (ma$+oglo##ia) 0 -gumma occurs in midline on ! dorsum of ! tongue hard palate: -=umma perforation $iver: -<ultiple gumma heal by e/tensive fibrosis (rregular lobules # Aepar lobatum % enla+ged nod'la+ li:e+0 ?"58l MEl Te+tia+y A of @ Henital #y#tem! Testis diffuse & reaction #bilateral small hard tests% =umma hard large tests ante+io+ #$+otal #in'# ( TB h/\ ) 2ervi/ =umma. Te+tia+y A of '+ina+y #y#tem! - nephrotic syndrome Te+tia+yC A of Bone 2 Roint#! Bone! -+iffuse & reaction in diaphysis . (t is 8steosclerotic so pathological fracture rare -=umma of flat bone )orm-eaten appearance -4osesaddle nose -palateperforation Uoint#! -=umma destroy synovial membrane & !oint structure -Aydroarthrosis. Congenital A! (nfection from mother to fetus occur after ! 1 st trimester # 1st * months %. (f ! mother in 1 st or ' nd stage & stillbirth (f mother in *rd stage & infantile or tardive & . 48 King of pathology I. ead fet'#B#till *i+thB p+enatal o+ neonatal A!. II.Infantile A! in %#t ( yea+0 III0 Ta+di:e A!$hildhood ef!3remature labor of a dead macerated heavily infected fetus: :#,in +a#h # macule, papule, pustule,Fetilligo & maceration % :The inte+nal o+gan# : enlarged, pale, )hitish grey & firm. :L'ng # pneumonia alba%. :Lymphadenopathy0 & appear during 1 st ' years of life. :sOin lesion: as 'ry stage#a# *efo+e% -./0 ?rhagades ! # radial scars at angles of month & anus %. YVucus Vb! as 'ry stage( a# *efo+e% -./0 ? atrophic rhinitis. YThe internal organs: .Li:e+! congenital & cirrhosis it is pericellular cirrhosis6diffuse fibrosis in PQ hepatocytes # <onocellular fibrosis %. .Bone 2 Roint# ! #1%Saddle nose # destruction of nasal septum %. #'% & epiphysitis. #*% & periosteitis: Head :become sBuare-shaped head. 3halange# :is fusiform & s)ollen. Ti*ia :become thic-compressed laterally-curved for)ard#s)ord tibia% -L'ng #pneumonia alba%. .Blood:3aro/ysmal cold hemoglobinuria.
& appear from '-'G years of life. : mutchinsonns Triad: a- Autchinson@s teeth: incisors:)idely separated¬ched 2entrally. b-+eafness. c-Meratitis blindness. Y=eurok WL. ,.+.) Ymydroatherosis: 5ffusion of !oint cavity # =lutton !oint %. Y>one changes: as Zry stages.-./0 T'*e+$le H'mma : occur in 1ry ;'ry T.". :due to T." bacilli. :Ca#eation:classical#complete tissue destruction%. :Ne't+ophil#! present. 13+oteolyti$ enzyme: present. :LiT'efa$tion: occurs. :Ca:ity is formed. :)ea$tion a+o'nd!. -Epitheloid $ell# , lymphocyte , macrophage. -$angerhanIs cells of $la##i$al type e9 3e+iphe+al nuclei & la+ge+ in size. : <vascular lesion. :Compli$ation: sinus-ulcer-fistula. :occur in *ry & only. :due to treponema pallidum. :Ca#eation:-typical#No complete tissue destruction%. absent. absent. 4o liBuefaction. 4o cavity formation. 3la#ma $ell#,lymphocyte ,macrophage. -$angerhanIs cells of <typi$al type e9 Cent+al nuclei & #malle+ in size. Fascular lesion. =ummatous ulcer. 49 King of pathology Be#t Si#he# By7King of pathology0 By\King of pathology( Legand Hazem ) Bilha+zia#i# B (-$hi#to#omia#i#) ef : infective parasitic granuloma )9 is endemic in 5gypt. / #pe$ie# : J. haematobium #affects mainly ! urogenital system%, J. Vansoni o J. paponicum #affects mainly ! digestive system%. 8nly ! first ' are present in 5gypt. #S.A all over ! country & S.<. in ! +elta% "ode of infe$tion ! qr;s% [j&9I -2ercariae #in ! )ater%penetrate ! sin reach ! capillaries & circulate e ! venous blood to lungs systemic arterial circulation to different organs. 8nly ! cercariae reach ! abdominal organs drained by ! portal blood can survive . they reach liver in ! intrahepatic portal branches to mature male & female )orms. -dult )orms move as couples #male &females% from ! liver to rectal ple/us #S. <ansoni%7.. S. haematobium reaches ! vesical, porstate & utero-vaginal ple/uses. ->emale shistosoma pass to submucosa capillaries and lying do)n the eggs. -This eggs either :- 1- penetrate vein and )all of urinary blader )all then pass in urine. '- 3enetrate vein only submucosa granulomatous reaction. *- (mpact in liver "ilharzial preportal fibrosis. 3athogene#i# and +ea$tion of *ilha+zia#i#!. a)<ntigeni$ity of *elha+zia :- 1 - Ce+$a+ia type ( hypersensitivity . 2 - So+m if living not antigenic (f +ead antigenic vascular reaction . 3 - O:a if living antigenic vascular reaction . (f +ead not antigenic no reaction of immune system . 4 - <'to.<g ;K de+i:e f+om the inflamed ti##'e . !"S d;e0 *)pe+manent +ea$tion#!. H+an'lomato'# +ea$tion (delayed hype+#en#iti:ity type 5) (t occur around living 8va and may be -: 1 - Fo$al +ea$tion B *ilha+zial g+an'loma B *ilha+zial p#e'do.t'*e+$le B *ilha+zial nod'le = *ilha+zloma . ef ! nodule of granulomatous reaction consist of bilharzial 8va surrounded by $ymphocyte O plasma cells O macrophage O foreign body giant cells # chronic cells % + fibroblast O eosinophils . The cells are not arranged in layers as in T.> and necrosis is minimal . 2 - iff'#e +ea$tion : ef! heavy deposition of large number of 8va heal by fibrosis or even calcified .
!"S d;e0 $)>a#$'la+ +ea$tion -: 50 King of pathology * acute endophlebitis 81 acute endoarteritis . * chronic endophlebitis 81 chronic endoarteritis . * thrombus formation . * organization . * -rterio-venous shunt . Biha+zial le#ion# of Hollo; o+gan# . O:a in #'*m'$o#a if penetrate mucosa : petecial Age. : ulceration. : 1ed spots. . O:a in #'*m'$o#a ( fe; n'm*e+ #) inable to penetrate mucosa Fo$al bilharzial +ea$tion0 .O:a in #'*m'$o#a (la+ge n'm*e+#) inable to penetrate mucosa 1-closed belharzial lesions. '-bilharzial polyp. *-sandy patches. %. Le#ion# d'e to fi*+o#i#: # closed bilhartial lesion % :- -(f there is severe fibrosis of ! submucosa & mucosa ova deposition in these sites stop. 4o ova pass to urine or stool # 2losed lesion %. ! ova deposition continue in ! muscle, subserous & peritoneal layers fibrosis & organ become small #contracted organ% e9 obstruction. (.Le#ion# d'e to li:ing o:a: # Bilha+zial polyp %. 4Gf"^%& 4e;g%& 9#C& /.Le#ion# d'e to dead o:a : # -andy pat$he# %. 4Gf"^%& 4e;g%& 9#C& 4. Bilha+zial 'l$e+# : 4Gf"^%& 4e;g%& 9#C& N0B:- !"Sclosed bilhartial lesion = liaing oaa u fibrosis u negatiae urine. vhile Jandy pathches = dead oaa u calcification u positiae urine. "S")w* @ [M\"I "7E of any 'l$e+ B "7E of the le#ion $a'#ing it 51 King of pathology G+ogenital Bilha+zia#i#! 4Gf"^%& 4e;g%& 9#C& Epithealial $hange# in '+ina+y *ladde+ *ilha+zia#i# !. :8ccur due to ".reaction & 'ry infection. : these changes are:- a.Epithelial hype+pla#ia : - >ocal increase in ! epithelial thicness. - +ipping do)n of ! hyperplastic epithelium.
*. B+'nne+N# ne#t# ! 1- They are sheets of the hype+pla#ti$ t+an#itional epitheli'm )9 are separated from surface epithelium & present in submucosa. '- (schemia occur hyd+ophi$ degene+ation of the center cells compress the Surrounding cells gi:e Cy#titi# $y#ti$a then glandular metaplasia of surface epithelium occur give Cy#titi# gland'la+i#. N0B! gland'la+ metapla#ia mean ( t+an#fo+mation of one type of epitheli'm to anothe+ ) -o ! The t+an#itional epitheli'm that line Cy#titi# $y#ti$a ;ill t+an#fo+m to gland'la+ epitheli'm ;K I# lined *y ( $ol'mna+ epitheli'm ? go*let $ell# ) ;K line $y#titi# gland'la+i#0 $.Cy#titi# $y#ti$a d.$y#titi# gland'la+i# .ef: hydrophic degeneration of brunnerIs nest -$arge size. -$ined by transitional 2s # flat 2s % -2ontains )atery secretion. - is due to 'ry infection. -(t is not precancerous. -glandular metaplasia of surface epithelium. -Small size. -$ined by columnar 2s ; goblet cells -2ontains mucus. -(t is due to bilharziasis. -(t is precancerous. 52 King of pathology e. at+ophi$ $hange# o:e+ the #andy pat$he# . f. #T'amo'# metapla#ia ( le',opla,ia ) : 1- eratinization very thic. '- 4E5 :- )hitish irregular patches of mucus membrane. *- <E5 :- eratinized stratified sBuamous epithelium. ,-type :- precancerous. g. malignan$y : to : transitional cell carcinoma. : sBuamous cell carcinoma. : adenocarcinoma. Othe+ '+ogenital B %) B of @ '+ete+ !. common in ! lo)er third: -8bstruction #hydroureter%. -'ry infection #pyoureter%. () B of @ ,idney !. -8va are deposited in ! interstitial tissuepyelonephritis, pyonephrosis /) B #eminal :e#i$le#: hemospermia. 4) B p+o#tate:- bladder nec obstruction. 5) B te#ti$le :- Aydrocele. 6) B #pe+mati$ $o+d:-+iffuse thicening. 8) B '+eth+a :- stricture & fistula formation. Inte#tinal Bilha+zia#i# ! 4Gf"^%& 4e;g%& 9#C& Hepati$ Bilha+zia#i# Bilha+zial p+epo+tal fi*+o#i# in li:e+ 53 King of pathology %.ef! it is diffuse hepatic affection by parasite emboli around dead )orms&living )orm of bilharzias. (t occur as $ompli$ation of inte#tinal *ilha+zia#i#. (.3athogene#i# : a) d+ained em*oli of li:ing o:a! -re drained from the mesenteric vein portal vein liver portal tract then either: :impacted in vein >a#$'la+ +ea$tion -./0 :penetration of vein Fo$al *ilha+zial +ea$tion -./0 ( x& D)w* @ angiomatoid# )
B) d+ained em*oli of dead ;o+m! :<ild cases occlusion of the affected vein intimal and sub-intimal proliferation. :Severe cases >a#$'la+ +ea$tion -./0 $)d+ained em*oli of li:ing ;o+m! :contain pigment#haemosidrine% >ibrosis. to/ins minimal tissue necrosis & minimal fatty change. N0B: &My &My !"S angiomatoids6 small vascular spaces # in liver only %. D%& z"{0 Fo$al +ea$tion D| }.~". Mw\ li:e+ and p'lmona+y only /.N7E! &My !"S % - Size :-ea+ly :slightly enlarged # inflammation % E Late:shrunen # fibrosis %. -'+fa$e : retracted. Bo+de+ : sharp. 2onsistency: firm (C 54 King of pathology 2olour:: yello)ish bile & fatty change. : bro)nish pigments. : )hitish fibrosis. Cap#'le : thicened and adherent to surface. C7- : thicened , fibrosed portal tract. 4."7E! -Li:e+ a+$hite$t'+e : preserved. -Hepato$yte#: either minimal cell necrosis E minimal fatty change. -Blood #i'#oid#: normal. -Bile $anali$'li: cholystasis. -Cent+al :ein: normal. ->on ,'pffe+ $ell# #ho;: hyperplasia & hypertrophy. -3o+tal t+a$t ( main pathology ) #ho;: :5nlarged O thicened O fibrosed. :pigments O fibrosis. :"ile duct proliferation. : Fascular reaction -./0 : >ocal bilharzial reaction -./0 ( x& D)w* @ angiomatoid#) 5.Compli$ation ( effe$t )! a)po+tal hype+ten#ion0 *)li:e+ $ell fail'+e0 a) po+tal hype+ten#ion !. Yauses : presinusoidal # >ibrosis E Thrombosis E -rterio-venous shunt %. YEffect : 1- congestion of portal drained area Splenomegally O -scitis O 4ausea,vomiting. '-opening of porto-systemic anastomosis esophageal varices O piles. *) li:e+ $ell fail'+e0 6.Type# : Aepatic "ilharziasis is of ' types:- 1->ine. '-2oarse " hepatic fibrosis. N0B: It i# $alled fi*+o#i# 2 not $i++ho#i# *e$a'#e @ le#ion i# +e#t+i$ted mainly to @ po+tal t+a$t#0 2nod'la+ a+$hite$t'+e of the li:e+ i# p+e#e+:ed 55 King of pathology Fine B0 fi*+o#i# Coa+#e B0 fi*+o#i# -ite ! In$iden$e ! inte#tinal B ! 3athogene#i# : 1-8va '-Jorm *-1epetition ,-To/in N7E ! Size Surface 2apsule 2onsistency 2ut surface "7E ! Effe$t# ! -Small portal tracts -P than .GH of cases. -<ild or moderate ->e) 4o. in small portal vein at one time -4o )orm impaction. -4o repetition of ! process. -The same in both types - decrease - finely granular - thic - firm - opaBue small portal tracts Small portal tracts sho): - >ibrosis & thicening - 8va deposition - $ittle liver cell necrosis - 3ortal hypertension - $iver cell failure -$arge portal tracts. -Q .GH of cases -Severe. -$arge 4o. in large portal vein or marginal vein -Jorm impaction -1epetition is found. -the same - mared decrease - coarsely irregular - thic - firm - opaBue, broad, irregular large portal tracts large portal tracts sho): - ;; fibrosis & thicening - dead )orms ; ova - very little liver cell necrosis - 3ortal hypertension - $iver cell failure 56 King of pathology Bilha+zia#i# of @ #pleen B Egyptian -plenomegaly (t is a syndrome characterized by:- (ntestinal bilharziasis , ". hepatic fibrosis, Splenomegaly, -nemia, leucopenia & fever. 1 -plenomegaly i# eithe+! . Ea+ly #plenomegaly Late #plenomegaly %.Ca'#e ! (.N7E ! -Size: -Shape: -capsule: -consistency: -2ES: /."7E! - 2apsule&trabeculae: -Jhite pulp 6 $ymphoid follicle: -1ed pulp: 4. Effe$t#! :8ccur e9 both types of S.haematobium & S.mansoni. :d'e to immunological inflammation response d'e to antigenic stimulation <ildly enlarged. 3reserved. : Tense. >irm 1-$ymphoid follicle enlarged. '-1ed pulp mild congestion. 4ormal. Ayperplastic & e9 prominent germinal centre. 1-<ildly congested. '-5osinophilia. *-Ayperplasia of littoral cells #macrophage%.
4o effect :8ccur e9 S.mansoni. only. :Conge#ti:e d'e to portal hypertension $a'#ed *y hepatic ". fibrosis. Augely enlarged. 3reserved. :Thicened. : )hitish due to fibrosis. :adherent to surface. :cartilaginous metaphases due to subcapsular Age 8rganization. >irm 1-$ymphoid follicle atrophied. '-1ed pulp severly congested Ayalined.. -trophied &e9 hyaline degeneration of the arterioles. 1-Severly congested. '-4o easinophilia. *- =amna =andy 6 fibrosiderotic nodules: :Component: as before #return to circulatory disorder% -./0 - 2ompression of the surroundings organs - Aypersplenism :- ef! splenomegally ; pancytopenia #anemia; leucopenia; thrombocyropenia% 57 King of pathology 3'lmona+y Bilha+zia#i# ( Bilha+zial $o+.p'lmonale ) %.ef ! it is disease result from presence of ova & )orms in pulmonary circulation coming from Lrinary bladder "ilharziasis SG H from S.haematobium E 'G H from S.mansoni (.3athology! I.O:a le#ion#:- (f 8va impaction in pulmonary vessels Fascular reaction -./0 3enetration of pulmonary vessels >ocal bilharzial reaction -./0 ( x& D)w* @ angiomatoid#) II.So+m le#ion#! The pulmonary arteries contain venous blood so )orms die rapidly necrosis of ! vessels & surrounding lung tissue causing>e+mino'# pne'monia 6 focal consolidations e9 ;; necrosis &;; eosinophils & foreign body reaction around )orm Fi*+o#i#0 /.Effe$t# 2 $ompli$ation#! 1% 3ulmonary hypertension 3ulmonary aneurysm. Ycauses : due to # fibrosis O thrombosis O --F shunt %. :Effect : Aypertrophy & dilatation of ! right side of ! heart 1.A.> # cor-pulmonale % 1ef of $o+.p'lmonale: 1t sided heart failure andEor hypertrophy )9 occur secondary to a disease in the lung.
Be#t Si#he# By\King of pathology( Legand Hazem ) 58