' ,1

ULCERATIVE AND INFLAMMATORY LESIONS

Aphthos ulcers (Canker ulcers):
* Verycommon
* More commonin l"t two decades(triggeredby stress,fever,
indigestion),
* Small,round,shallow,painful,singleor in groups,covered
witlr gray-rvhiteexudate,erythemalous
rim on:

lP*t'oRAtcA\rnY,l - softpalate, -buccolabialmucosa,

L____TePFTAGUS I - lateralbordersof tongue
* Autoimmune(?),selflimitedresolvewithin feeweeks

Herpesvirus infection:

.$ Verycomnon condition,causedby HSV-I

t Transmined
by kissing

ir, Remainsdommt withingmglia (trigeminal),reactivated

by:
e;
- fever, sun
- cold exposue
- respiratoryinfection

€. Singleor multiplevesicleson lips+ shallowpainfirlulcers

t Diagosis: Tzanktest

-_\-_-/j
\- ]

Candida:

O Nommalinhabibntof oralcaviry(30-40%)

O Causesdiseasewith impairmentof tle usualprotective

mechanisrns(diabetesmellitus,glucocorticoid
therapy,
immunodeficiencv):
- Thrush: adherent white plaques anywhere u'ithin oral cavity
- May spread to esophazus and !!9q!-+ visceral lesions

OMicroscopic: budding firngal hyphae and ovoid yeast cells,

necronc mucosa

AcquiredimmunodeficiencJ'syndrome: CANCERS OF ORAL CAVITY AND TONGUE

rnf6r|4nf
ts 3% ofall cancersin USA
Advanced cases are often associated with lesions in oral car"itv:
(l) Candidiasis E 50%deathwithin 5 vears:
(2) Herpeticvesicles - Earlv metastases,
may havealreadymetastasized
beforethe
lesionis discovered
13)Microbialinfections+glossitis
(a) AIDS: Kaposi'ssarcom4 - OId ase(notbefore40 years)
E Site:Lateralmarginsoflower lips
introralpurpricnodularmmses
Floorof mouth
Lateralbordersofmotile tongue

EIN.E. : stansaW palpablemass,

malignantulcer
E Microscopic:squamous cellcarcinom4well differentiated,
keratinizing

E Clinical:as).mptonatic,
localpain,difficultyin chewing

erd' tlarqedl,+ywhnodes
ocalr-s
H.Ar.-l'l1ffitumorapyws
SALIVARY GLANDS
i yt0t4h4mA.+r-nnOf S4t i
Siaradenitis:
('l Mumps:
)

- AII salivary glandsespeciallythe parotiddiffirse interstitial

inflmmation, mononuclear cell infiltrate
- Selfiimited

ffi,w"
inchirdhood,
buri,,.aurtr-oYiJ.9#lj*i,itir-
st.''tirv
(/Er afu p! temi niQrnrS Juhrleg
(2) Autoimmme(SjoCren's
syndrome):
all salivaryglandsand
grmd.
racrimar
glaydso hearrfS tnfiltald. i rcptarcd
(3) Basterial:secondary
to ductobsauctionby stone serretrm.

*,, i
srar
Leraloccryu(ltvfis
agrntrxf+"' luoslalrnn

&l:.:-"
 Nomal aqumous mu@sa at the right (*), squmous cell cilcinoma
(LP) infiltrating submuosamd muscles

Salivaw gland tumors:

- 80%in parotid gl arlrds
4p6l
- 80%arebenigl
- Age 66-?$deiade, equalin both sexes
CfnlqV)

a' -',l6yna: "*,-v

oi rund
quhuf f Slowly growing, well demarcated,encapsulatedpainless
swelling at mgle ofia+r" fAOn&bW
latuw ,

tgltu$um f Benign, l07o recur after excision, multiple projections oftle

tumor penetrate tlre capsule-) adequate resection to prevent
Mlxoid stroma similu to cetilage with interpersd
recurence.
isleds ud strilds ofmvo@ithelial @lls
Primary or recurrent benign tuinors present for mmy yers

f" (10-20), rnalignancy may occur

\,9 el+hwqLfuntftt\,btrf SonrJrtyu

s
inUaoL[sg|"hssu-L. Quye,nJ ul
*#'
lnnuawh
bat*q

NutirnpolfaN
F,t+J, a{st,
-Trffi.y'
?t-:?w Ee'p\,ts
t

Pathogenesis:
(l ) Primary acalasia:lossof intriosic inhibitory
innewationof lou'eresophageal sphincter(unknou,n
origin)
PU
illo rrt(164
icaj cogf-s
trc.

+{ru"nncd.
inflammation and ulceration-+ s'quambdscell m;cinoma
- Clinically: progressive
dysphagi"-tad @11i.l l@fh
noctumalregurgitationandaspiratiouoffood "/
p"i"reftoatsno.J (esophoqifiG)

rnotur:
p,rbffir q":Pttry',.s
t inWbr
I)fruwtnr-ot, wvsE
o
pr rytc+1
): Herniationofdre stomachthroughfte esophageal Paraesophagea.lhemia:
hiatusin fte diaphragmdueto enlargementofheatus hemiation of part of gastric
fundus beside dre esophagus
andlaxity of comective tissuearound
i Commonlyacquiredcondition bosldL
i Unknowncause
Clinical: symptomsdueto gstroesophagealreflux:
( I ) Regurgitationof food
win
(2) Heartpain
Sliding hemia: cap ofgastric
(3) Exacerbatedin recumbentpositionthat facilitates
the reflux
"Y
cardia moves upward above
the diaphragrn Complications:
( I ) Ulceration.stricture
Urdtac etdeF (2) Bleeding
.6,p}Ff]1j;
(3)Metaplasia+Banefiesophagus

ffi 4horasc
rno.u(s Add.WFin rt+orrrlpftoeuS
PH'I-?' di'wch&6 muccis t"nar

o Complicationof longstandinggastroe6FmEffi%!ffix.
sr&kA o Replacementof ofthe squamous
mucus-secrefing
epitheliumofesophagus

eauorndttt columnarcellsepidrelium(metaplasia)
tr Most commonin lower one-dtirdof esoohazus
tflirhd,ffi o Pathology:
( t ) Lesionshows3 Spes of metaplasia
- Qg4fqc-like mucus glmds (no parietal cells or chiefcells)
- Epithelium simila to fundus of stomach (glands with
parietalandchiefcells)aleid, fr4|pirn n
S'*t'd epithelim with gobletcells
- lntestinal-like
fid
bt rohrFc

WW
(2) Inflammatorycells
(3) lJlcerationor evenstricturefomation
(4) Lesionoccursin patches or linesthe entireesophagus
(5) lncreasedrisk (30-40tines) of malisnanttansfoimation into
adenocarcinoma (periodicbiopsyis recommended)

l
''\-/-' : swel;tol mrrclsh*-ho!lc..t,r
Coilrac+p,-Jlonc f(un
U,FooWffi
rwq
S-ffikfi Wn+add WQ*a(A%L: aalotto cfra
4
 cDturnw *h*rn* carctYluvva'
,
dflAatttt -' ods{10
Ytl*a,lluSta-"
fiM1latpre ,naLiw\

ciluol
rnsl4lote Qdrno
&rdvw,tM
$fdd-to{.
lrrvd,Vl
stptd
tlr Esophagus: lower part with dad( red mucosa (Buffi)*
Dysploia with Bffim emphagus: olunnu epitheliat ells
with

ulq€r,dllP ln
vv&rcotgJ

ESOPHAGITIS (2) Ingestionof initants(acids,alkalis,hot fluids,alcohol)

(3) lnfectronssuclrasherpesandcandidaalbicansin
andUSA (10-20%of adult
Commonin Westerncountries parients Csophql ihs
immunosuppressed
popuration)
ont l in
COn ba ql} W4 | ' \,, \)-
Causes:
(l ) Refluxof gastriccontents(reflexesophagitis,themost
mostfiequen|:. - Largely limited to
- Dysphagia and
- Decreased efficiencyofesophaeeal antirefluxmechmism
- Presenceofhiatal hernia
- hcremedgastricvolume.conFibutesto the volume
ofrefluxedmaterial
- Reductionofreprative capacityofesoplrageal mucosadueto
prolongedexposure to gasricjuice

* lnges*ion lnil4 - c&.lo€r{cra-Ar{168 dn

(acids,
# ivri+an+s akoli,l, grrr-c, - trleg-

p.

v
cpr{a.o.ltum

Herpes simplex: punched ot ulers with brom-red bre,

white nomd mu@sa
 Vurni{rn4,
anhpt*tek)hc- r4p1ven1Bl*
t/ rombrned,./ ra4J@frTyl
of sphrnCler
bul,,^,t'o*l"oPgr"t '/rhcn sprtrnckrurrrlt?he.

LACERATIONS, (MALLORY-WETSS SYNDROME)

E Witlr failure ofrelaxation, the refluxing gastriccontents
overuhelrndle consricdon at gastroesophageal junction
tr Longitudinal tearsin esophagusat tle esophagogasfic leadingto massivedilationandtearofstretchedwall
junction

O Morphology:
- Longitudinaltearat gastroesophageal junction, orianted
precedes the antiperistaltic wave of contraction. parallelto lumenof esophagus
- Varies in length(severalcm)
D With failure ofrelaxation, tie refluxing gastric contents - May involve$e mm or perforatetlre*all.
overwhelrn fte constriction at gastroesophageal junction - Hemorrhage into tlremugins (accountsto 5-:0% of
leading to massive dilation and ter ofssetched wall upperGIT bleeding)
- 2ry mlecholon (ulcer.mediastinitis,
empyema)

cohnrnofla{eohotis -Srlgur4fion {gtua, r e*nf!,

Pup+cuaLrioVs:

ESOPFIAGEALCARCINOMA
(l) Squamouscell carcinoma(9004)
esofifiws (2) Adenocarcinoma

ru x a furyror
4fPtort
rX"gt*)
inf,.fion

Rsdiogmph showing squmos cell wcinom4

| -216 oFeA dlr{ns

It
Lp/lrc,aoo/qv
,)'
-ffi -
Stst- *cc$ots- \
ffi hnf,r,' tf ,!1:n""
4,('prd,f^: -ufl#'^r"t ^ flW"nt
ehawpi"
?ana51. p'5po,d
\-r-l 5;ro r'.;,ts<t
wl&ahgn 6 d't#u- bJ$lcohol*srrutr!) , lnilahm

"Y**
, AYA
c) tlPv,+4rr,oresoPhYln/-"
,
,;XTff:^
+11o,,r,
ffi Htffi':I"tffi
\Aa,,gcorcu'FoTnrl
ffi Xr'Ptfom\$tl''it'' inhib* Tinofiptsor
4+"^aff
Orcnync
6
 Y--ui I

l\ol

lP*J'sroMAcHl

AnpVg:tvtds AWIdc.Inhh 'h{ittnj5 of6lorure

.
Sttl

GASTRITIS
ACUTE GASTRITIS
Acute erosivehemonhagicgastritis- altAtt q,A[$
Transient
inflammationof mucosa,maybeaccompanied
with
trtbY;
n4tfo$P4rl hemorrhage (erosion)
sloughing
or evensuperficial
l ,{ 9 Pathoeenesis:
mfhrm
* triEili"no* ioitantstlo8l in$. ca44/'
-Jf"S - Aspirin,NSAIDs
&rQ)*q - Corticosteroids
uttsfl;n - Excessalcohol, heavysmoking
(accidental
- Ingestionofcorrosives or suicidal)

(wH I (2) StresJulcers

(traumgsurgerylhrtnt. gk6;fii|f-
(3)Hypersecretion of gastric
acicf
Stomach, nomal appwmce of ftrndal mucos: short pits (lined with (4) Impairedprotectivemechanisms: muoussecretion,
decreased
pale olmnu muu ells) leading to long glsds ( with bright pink
deficiency of prostaglandin

l"*5 drL
cells that wrete hvdrochlori

\ l' ' FFhryn

l( fumanCriyryte
l- fstrin

wrt Slrrpk,oosivo, Yemwtlli t'

Pathology:
- Widesprcadpetechialhemorrhages
- Mucosalerosion:sloughingofepithelium-+punchedout ulcers
Acrtle'
lnflanu*utt

- Mild inflammationwith neutrophils

- Healingwiftin few days

Clinical:
- Vagueabdominalpainunlesscomplicatedby massive
hemorrhageor perforation-r Petitolitt6 <r'zns:
- Acute gastritisdue to NSAIDs may show hypochromic 5r+uai/n
microcytic anemiadueto undetected bleeding
.rqni$tl
- cr$*fi t rmr Mrrv4r "F-'ts

Avrcliaot&qfid
(REsrn * .6,*tr'*"@
A:,;; :y :o
Ft *T1*
-"v4so,rrt4$6n
":::'..:i'

Chronicinflammatory diseaseofthe stomachthat variesfrom mild

nw- superficialinvolvementto s€vereatrophyandepithelial metaplasia

(t*.rffiedeg$iit$

ohvovrro
%q*" - Autoimmune process,presenceof antibodyto-ESjgtgl
cells& intrinsicfactor
rl - Processrestrictedto fundusand body ofstomach (not to the

e)
antnrm) trlqrgl@
\h
A*VoPhgoFrnacrrt mtar ln
I \,'

Wvtdl nilt4usvb6g

Notcrrvrrnan.

(gf .Iiiif€GtidMhdi,€CIbc.teq*."",r"'i..

- The most commoncauseof gastritisin USA

- Prevalenceof infection increaseswith age,at age of 60
almostall populalion are serologicallypositive,2l3 show
histologicalevidenceof gastritis
- The organismremainson the surface(no invasionofmucosa)
- Chronic inflammationof antrunt andbodv
e, i,
\ - Playsimportantrole in pepticulceration(all casesof
duodenalulcersand% with gastriculcers)
Increasedrisk of cancer
ar*

l'rbr
 Ulcxt'knch gfunYUffi

v,i!

ut-cEn's- d,i srupt'tt<'

PEPTIc
'1
. Mucosalulcerationsthat gdend tkough the epitheliallayer
(l) Intedinal netoplasia, the gastric epithelium is replaced by
into the submucosaordOeper.
intestinaltype
. It may occur in any pan ofGIT exposed!o acid pepsin,most
(2) Dysplasia:cytologicalalterations(shape,size, orientation, ofteninsomachan-l:4t.
;btbotg.t rrrrtl '
nuclearenlargement)-+ increasedincidenceof gastriccancer . Incidence:in USA,2.5% ofmalesand 1.5%in femaleshave
in chronic gastritis.
peptic ulcers
(3) Degeneration ofthe epitheliumofgastricglands-+marked . Age: Duodenal40-60years
reductionin their number(alropftic gastitis)
Gastric:middleagedandelderlymorethanyoung
(4) InJiltation of the macosaby lymphorytes and plasna cells

Ittt4 ocur il ewn Heeh'l's

Nver{rcrrltrm
fs"rro{*r
h,rS,brach PrulecJrva
papilcrrlcrrs .L
Pathogpnesis:: Pathoepnesis::
lmbalancebetweenacid/pepsinsecretionand mucosaldefense Imbalancebetweenacid/pepsinsecretionand mucosaldeGnse
mechanism: mechanism:
f Hypersecretionof acid )> Hypersecretionofacid
I Decreasedmucosalresistanceto acid. > Decreasedmucosalresistanceto acid.

Normally stomach protecs itself from self dige*ion by: Normally stonmch protecls ilself from self digestionby:
(l) mucussecretion (l)mucussecretion \
(2) HCOPsecretion : lli[88t;::lX-v,*uot.o ac;^7wee -- .
(3) mpid gastricepithelialregeneration (3) rapidgastricepithelialregeneration
-
(4) rich mucosalbloodflow-+ sustainsthe high metabolicand (4) rich mucosalbloodflow-+ sustainsthe highmetabolicand
regenerativeactivity regenerativeactivity feplf ao ar€ t-f,d.c.{:.
-
(5) mucosalreleaseofprostaglandin-t maintainsmucosal (5) mucosalreleaseofggEglgglgr --+maintainsmucosaF
bloodsupply bloodsupplv
ffia#*plr. \a€oditohsr.r
td jp.ltt4-- ensqr€o

iftt\lwr.,ffi, th ednfod +H@a-

talsgNao.

AggressiveFactors:
l) Helicobacter oylori,inlaCrkOn
- Isolatedfrom gastricantrum of 90%ocases with duodenalulcer
and70oloof gastriCulcer
- Treatrnentwith antibioticshelps healing& preventsrecunence.
|yle^X)
- Role:
a) intenseinflammatoryresponse, Chrg|li c' itrihlionf

*N N +
bjendotoxin
- digr wyti cn slrfto
c) urease.breakdownurea-) ammoniumchloride
dj proteases& phospholipases
cPi.tti"rliutfl
+ damagesurfaceepithelium
e) stimulates acid secretionby promoting gastrinrelease
2) NSAIDs: suppressmucosalprostaglandinsynthesis+ reduceHCCP
Jblcods'.fpy
e and mucin (aspirin,ibuprofin had adverseeffect).
3) Cigarettesmoking:impairsmucosalbloodflow andhealing
0 in&h{hn4n"n 4) Alcohol
5) Corticosteroids
6)Psycologicalstress
- {-/t /,,i);W V

&yttoskstds
on
inWbilccr\Prolil<rah
neatiS
ouc/llyd
rWrPur
 Patholos.v:

-$j@: lessercuwatureof stomach +

anteralregionT.lloric
mrera rggfon 17 Antwn
t9rt L (Erlfutl l. rolrl,,rr
-,
Ist part ofduodenum (anterior or posterior wall) - {CiJl
-Sh4pq:round,2 to 4cm in diameter,
sharply punchedout edgesand overhangingmargins
-Depth:varies,superficialor deep reachingmusclelayer

Microscooic:
a-necrotictissue- heCfot Cd.O-bne
b- inflammatoryinfiltrate
c-granufationtissue - f,to-UnS+ +rcR I
d-fibroustissueatthebase ofulcer
-&tvl"a k \

Epigastricpain(l-3 hoursaftermeals,worseat night,relieved

byantiacids
andfood
k +d Srifn4lflc- cpjStn"
rru tL - W ndtaliA' ocide /aI lcdrnV -amfr

{2)Pedbration (5% ofcase!)

(3) Pyloric obsruction,: libtb$i$
(4) Malignancy:rarefor gastriculcer(unknom for duodenal)-.
?jcfAerq - yri ld- avrevnta ot c)TDntc -
ulcevr;$*e* gPL'L2n nn,o--t

TQ ' |Atte"sottnts T 6asll ic or

cASrRrc I (,eVYu(
rr.rMoRS
Patholow:
lntestinalvariant Diffusevariant
Origin Gutric muou undergone Nomal mucoss, not B Threemacroscopicpictures:
intestinal metaplaia (chronic ssociated with chronic (l) Exophytic:solidmassthatprojectsinto thelumen
satdtis) (2) Ulcerating:shallowulcer,l-10 cm diameterwith i
Incidcnce Moreommon in high risk No significant change in induratedmargin
prcple,diminishing
in incidence over years (3) Infitrating:no tumormass,the entirewall is infiltrated,
fruumcv in USA thickened(2cm),muchfibrosis,firm
Dcgrcc of Bener differentiated Poorly differentiated (Linitis plastica,leatherbottlestomach)
dilfcrentirtion r.to Stifhta lzfififi.
Age incidence ARer 50yeus Euliv age D Microscopic : the pattemvariesfrom well differeqf4lpd
M:F
o.rn**rn--.muoutryanaplasncntmor.
2:l Absent
orcd( Some produce mucrn that drsplacesthe nucleus\

t1

Ur*b(A, Pylorust cuttln$) 5q"

ntrt(qfpn+ Iu*tor o[+tv s+uilrr& hO-lSZ;
&.
-Vvtfrlcoyyu/lo1 2'qo
' 37" pl atl cau@{ert1",vls
in4Sfl C&d'ncend
fr*rilus+bY YatnatYl3
Z rnuprrsrqica.lType-s
' fntG'hy^d.I
Vr'#r+ : onlppw,a@t6Aof ( tl.pllorf, pvgatfu
,s{tbkQd
M -..)
- fu$It,c: fh pYelt<pcr,tgkrhi. funn$orn gosfrio rnecu.scc[ts.
 FSP"tdn'lrna

*rra#"*qd
bf of
yy"ucrls
urfiCI
tmhQ\q\?
,till
d$Wu.0)
Woy,,hynfuorwhut-rlt ws,(
latce'l
dnikry
r)

snread:
pqrchdh"nll feacVxrgsmea{-
ogry).gi+gt4lunhrxd 4abd'h anneeI og
J^fpdhtDy'uun- v
(l ) Local:nearbv orsans.ovarv(Krukenberetumor)
(2) Lymphatic:regionallymohnodes(portahepa,along saC
peritoneal
curvatures,
distallvmphnodes:supraclavicular
(3) Blood:liver, lung,brain rnatJmn+Ascihs- sirdn2ttcsettt.i"lfit'r't*
'loruhqnt'cJ ett?il t%u
Clinical:
( I ) Non-specificsignsof tumorgrowth \rlt I 0e6
(2) Localsigns:vomiting,dysphagia,pyloricobstruction
(3) Ulceration-+bleeding
(4) Diatantmetastasis: supnclavicularlymphnodes,ovary
gc.rqdatf es h'vct,bran,tr

Qaz*1
W*d"rruch
ths wMg
 Fw'

,tw:
villi+yk
Colul/lnor
[P3"3I"t..t".i
Nomal appeme of smallintstinal virricow^d

w^
muosa with longvilli havingwruional
cells
b1 mmvtur

m.f;
Longitudinal smooth muscle
of colon 6 bmds, taenia @li DEVELOPMENTALABNORMALITIES

Mesacolon: distension ofthe colon more than 6 or 7 cm in diameter:

(l )goneenitalmega.colog(liir$spryne dise?se):SuIUC mcfal
- LacKoI tnnervanon
oI olstalpolttonot colon(rectum,seElnotd)-
+ aganglionic segment
- fu nctional obstruction
- massive distention of colon proximal to affected segment ,ndrtib
- wall thinned (distention) or thickmed (muscle hlpertrophy)
- delayed passageofmechoniurn. followed by vomiting.
- complications: enterocolitits, perforation of distended colon
Fat sqrrcn+
ltlkc*t6n aqniilalc
(2) Acquired mega colon:
a- Chasa disease:hnanosomes directlv invade bowel PfD{tmal
Mu@sal crypts with mily
b- Organicobstructionby hrmoror sficture AnmakA
c- Toxic mesacolon(ulcerativecolitis)
goblel ells, submu@sal
-
d- Psvchomotor disorders fe
rnd$qws
aotalssla
\etuN
atnl,4{ svqtri! atritr')N
+.lt4rrt\nd tu*.
Ffts'
*rfuahU
'tuftutLedrn
llscrprwcBowELprsEASE-l
ft+omq
(l ) Arterialocclusion(celiac,superior,inferiormesenteric
fieries) th['htf
a- Arterial$ggglgsis (severeatherosclerosis,-
systemi

b-d49rj4.g!@ derached rhrombus

from,lg&ltgg.c.
le&Atdlrtl' "Hal fibrillatibn,
LV - muralthrombusin pewiousmyocrdiai infarction.
a&trrnunc
61766 - bacterialvegetations dsgc*s
aodlic,un*FaJ
c- tntrinsicvasculr lesion:
- volwlous
- in$ssception
lfnchsprung disme. Contrastradiograph
- stangulatedhemia
showingmokeddilationof reco*gmoio

EEvE BloryA
A^st',a'
pr;iffiIattaw'r1
U$6hu'st ffurkchs
';nt^(6q larasgt$ylt*o: s'+*"[;%"^,M
+nrlsco
Clltlllz AWd)rq' @w
t[z fyat$trrgo
 lepEd!,V
- fdrrnsioVre'tilwWra*<'.

uUsprg

(2) Thrombosis ofmesenteric vein: hyercoagulability ofblood by oral

ulcrwJ contaceptives,intraperitoineal sepsis, post-operative state

ffi,,,*d,
br*|-ttta
(3) Non-occlusive ischemia: (intestinal infaction withoul occlusion):
reduced cardiac out from shock, acute rnyocardial infarction,
vasocontrictive drugs
verufrs
(2) Infarction is always heirronhagic
PaftoloeI:
(3) Muked edema, interstitial hembrrhage, necrosis, gangrene
(l ) Severity of injury varies fiom:
- transmural inftrction (involving all layers), Clinical:
- rnual infarction (mucosa and submucosa) sparing tlre muscle -Most common in later years of life
- mucosal infarction (not deeper than musculais mucosa) - Suddm onset of severepain
-Bloody dianhea
 \i

Diarrhea:
- lncreased stoolmass(in excessof250 gm) or stool freauency
or stool fluidiry
- Over I 4 liters may be lost /day in severecases
- Often accompaniedwith pain,urgency,incontinence

painfuldimhea,sraining,mucusandblood
D)'sentery:

Recfteller;iml
Ishmic 6tqitis, sall intestinal muosa with advmced nrcrosis .
Q<c+zdSPas/vlawde&
od acute inflmmation
{blusons*{lon- Sftaj

(x: arfiraribfs+ bOciffic

ENrERocolrrrs cdn'
rNFEcrrous @,li
ar irr&$u4
- Dianhealdiseaseofmicobialorigin
- Worldwide,accounts for onehalfofall dea6sin children
- excessive omotic forces exerted bv luminal solutes- youngerthan 5 years cliarrll1 ie9?*i5,ita<. SbL d$tf,
- abatewitl fasting (e.g. Mg SO,.lact1rt.lr'i;-iA@
(3)Ixrdativedia$hea:
idtAnmOfrnlin[i*la
WL
urdrrSg./r
- Etiolog-v:
- outputof purulentbloodydianhea ?Fbjld tl (l ) Viruses:rotavirus
- persistson fasting(e.g.shigel14mpylobacter))ftpgfil (2) Bacteria: Enteropathogenicstrains of E. coli, salmonella.
hs.d
(4) Malabsomtion:
#
shigell4 campylobacter, vibrio cholerae,
4U -
clostndium difficile, clostridium perfringens --
0Sctt'de
- bulky stool with increasedosmolaritl'due to mabsorbed
(3) kotozoa: Entamoebahistolytica, Girdia lamblia
c0lirlis
nutrients and exess fat (steatonhea) Dlfr+utVncr'
- usuallyabateson fasting
inlcrttu-

I
(5)..+ii!frJ
Deraneed motiliw: - E.6li: norfiat fuq,-hafifil*S lgurr&n
.,
- variable, diagnosedby exclusion of other tJ?es (e.g surgical
but ttr.lnre pdlrrynio $ains
h'$J Shol .{ rdqrs diav(he
qe=

@ {-: Malabsorptionoccursdueto:
Imoairedinnaluminaldieestionof food:
E Clinicalconditionin whichoneor moreirnponantnutrientsare &g1gfiffi"rio-n Una'blG$ dtlC* no 7'
&&chue- inadequatelyabsorbed from the srnallintestine. - Deficientbile saltssecondan'toliver diseases

d4ahn1 * Intestinalabsorptionis characterizedby t\a'ophases: Impairedabsorption:

4brprnot^ - Innalurninaldigestionin which proteins,crbohldrates and

faS areenzlmaticallybroken down, a processtiat beginsin
- Diminishedsurfaceabsorptiveareaof small intestine(bowel
resection) hnr({,S htbf
- Unhcff{ul
hd' the mouth md continuesin small intestine. - Defectiveabsorption
e.g.Iact6seinlolqllr,ce'- I IA6{6f,,O
- Damageto epithelialcells/ .
- Terminaldigestion:_ly4lgbgilof peptidesanddissacharides
Ss by peptidasesanddisaccharidases
mucosalcellsin SI.
in brushborderof
S Clinical:
- Transepilhelialbasportofnutrients, fluid andelectrol]'tes - passage ofbulky, fiothy, greay, yellowor graystools
acrossepithelialcellsof Sl - anorexi4abdominaldistention, flatulence
rvasring
- muscfe _W.
dhhder4ol, W,
I
eAgna,
- intalwnind.'u (&lrth4,sfvn@$,
hrysfton W)
Wctrya",
l - + rA'
dtq*l WJntoaltaa'rut
udis*rh
G wwsdd tPb'Jtu*-,")
Viyeacchsrvd
pro*crngq a,.q,. + sho4 chern di'F€fh&, il ... {e}/a"' 3
ior-ornlrztclgcstroa .lrk€d &rrttruy diEetton
 q CI,
+v\0

Ulcerative
colitis
qs,
Bodr diseasesarechronic.relapsingofunknou,n etiology

lesions(inflamedsegmentsseparated
by -in{tsnnrd
ia Incidence:g1g!5$j!e more prevalent in USA, Grear Britain
md Scandanavia
$scnq
mrJaoEr
* Age: at an1'age (peak incidence in 2d-3'd decades) *rlarerc.oEq'
(4) Lumen:atmosralu,ayst4ffi$y edernaandlaterby
* Ser:&Ej{gi slightly more t}rm males
fibrosis(stringsign.thin streamofbarium,stricture)

r,ut*,.\ d Acl*e : ltrill$ notruNd\ e&na

NM
'W t ghi*usvAAl
e;rr.nic,Arrrnis

(5)Mucosa:
- al$cl+
"a"tn'"
- erly focal mucosal ulcers -+ later coalesceinto long
sementine
linearulce@

- ulcersbecomedeeper+fissuresthatpenetrate
deeplythrougl
UorL
ue u'arrone-ilerosaffi tilgraL{b
- turthe, extffi sures@d$*itr
w,
',#ffit
(6) Microscooic:
- Cbronicinflmmation of all

ffilJr"ru'rummmtriM
-'-- J
- particutarty
in colon)+ IlCoplaSiq V,JtNt
- Nodular lynphoid aggregates'
Crohn's dise6e: poximal ed di$al strictules in teminal ilom

Serln$- *fl"*

iwmur(-rns/|!'}Cd'

iritis, sclerosingcirot- g'tiij

X Clinical:
(l ) Recunmt episodes ofcrampy abdominal pain, diarrhea, fever
(2) Bleeding
(3) Initialaftackremitwith or witlrouttreafinent,followedby
(4) Complications:
- inte*inal :lEiEEtqorgbullqldon

ffi
-.$1g!qwifr otherlooFiiFintistine, bladder,vagina,skin
- abdominalgbtcessor peritonitis
- malabsorotion md malnutritionwith diffirselesionsin SI

gh - incremed
.. risk of malignancy(lesstlra UC)
:

Chrunro
cfu,4L!ryY1$elfi
$3.:
t rWntA,dry ^Y,Auw
rnuc4slnb/
;*"JC"xail*ffWmM e PtJ4
PuitDnid'6,
-'PlWrr"W
.'CP\neAStt ,
nk46Lv,lufu4Ylw, Ulvod.
tt\4UCpnu}/-I-r ,rrril
 .,d
*{$w,{' {;+,s
frt len+1 Q n Utc,,ratw-6
F]LCERATIvEflE
D'
* Ctrrons

* Incidence: -worldwide more commo{r(inUSA than

'7/loo,^>)
*+Age: anyage(peak20-25),equalincidencein both sexes

(1) Siteof lesiort*iqi@*ewdF(rectum or rectoseemoid)

-etr)
col.n
(2)lnflammatio@t
($dDffiffiHkEhn lesionbeginsin rectum,extendsproximally in
fashion for a variable distance (may be entire colon!
-ggp15ig11913l
r+t iume
,'\%
t ii
(5) Mucosa:hyperemia,edema,easy bleedingwitffiffiffiEryti,i€€Sffi
g@. Isolatedislandsof regeneratipgmucosabulgeinto
lpseudopolyps,progressive mucousalarophy.
l8r.r,brnucoSq'GrlFrf,
in nrucoscr ,nffarnntjv't
?e totvnalui
Wottno*a {o *x,c.s- il1*rs+t
\otolostruchor;
lota jrnstdrtr

(6-;Microscopic: ttntrun o{cpdlufiurnu/ *

- 111fi
n - Chronicinflammationof'beBs*&.sdbmucosa
$, - Iossandatrophyofsurfaceepithelim
' s Stluuilorro&atutc

-ffi*
Weryffi.ryS@Wry3$rlheanlky&i.srne
\\{./ spondylitis, sclerosine cholangitis)

X Clinical:
(l ) Recurent episodesofbloody diarrhea with crampy abdominal
pain, diarrhea, fever
(2) Bleeding (more widr UC thm CD)
(3) Initial attack remit rvith or without featrnenr. followed by

-.

Oran rltt.rr-'$ - C1'on'S

stury
dnt+V
MW Buium enema:finegruulaity
ofmucosa
 1
Y.,r,,l

Diverticulum:blind pouchoffdre alimentaryEact,linedby mucosa

andcommunicateswitlr the lumenof the gut., either congenital
or acquired.

's diverticulum:d4oc{

(mucosilE6fiiiffiEi
(3) Generallyasvmotomatic
(4) May be sl'mptomatic when:
- bacterial growth that depletesvitamin Br?-+ syndrome similqr
toperniciius
anem;aimocngl, uittcila:bb/o.ttr)
- contains lreterotropic gastric mucosa+ peptic uloemtion of
adjacent mucous membrane.

uJanl,m
atqah!'4 rt 6.lf
qwtoasd,
2- rnustrc.I gks a/cr, <g.ilvrrlgL$.ittturt
@tcr/v-t'
F{cc.LqJE

tlpe(Dive*icutosis):
o Acquired Vey C6yftmon
in parallel rorvs
taenlae
ffi7o), increases
in frequency (2) Formedonly ofmucosaandsubmucosa hemiateddrough
errvift age (50% above 60 years) musclelay'er(pseudodiverticula),
baseis fonnedofserosal
connective tissue.
(3) Number:variesfrom few to severalhundreds
mtreased dlmculty ln passageot rntestrnalcontent+ (4) Size:0.5-I cm
sustainedbowel contractions+ increasedinfaluminal pressure. (5) Gentrallyasvmptomatic (80%)or symptma&ri
As nervesandvesselspenetratecircular musclein between -i"t"-Grn--Trrping,continuousdiscomfortin
taeniacoli they createfocal defectsalongwhish tle mucosa theleft lowerquadrml
and submucosahemiate. - sensationofnever being ableto ernptydrerectum
completely

le not covnpttcafion:
Yt"tUr*U.
 (6) Diverticulitis:
- inflammationofdiverticulum in responseto iritation
causedby retainedfecalmaterialrq$ffirrhiort, pericolic
abscess,pertonitis
- Clinical:
- fever, persistat lower abdominal pain
- tendemess in lower left quadrant

Morecommonin smallintestine
?
Causes:

t46thq+ f0ft6dYlu[-ddr@
{r Hernias:
- Weaknessin the wall of peritonealcavity that permits
protrusionofserous-linedsacofperitoneum(hemialsac),
segmentofthe visceramay becomeFappedin them
(smallintestineor omentum).
- Pressureat dreneckinterfereswith blood supplv+ infarction
- Sites: ilgualand femoral cmais, mbilicus. surgical 5gggg

;/frndretopeitoneat I \

g$r ffir
 ::1
.-'.:

Umbilica.l hemia with small hemial

sc containing adipose tisue from
omstum

segment ofbowel into the distal one

- In chidren: due to excessiveDeristaltic activitv- and in adults
dueto a mass(tumor)
- Compression ofblood
supply+ infarction

s#+{ cffss
twIslU
WdN
 TUMORS OF SMALL AND LARGE INTESTINES

q Majority of Intestinal pollps occur sporadically:

ffi
- rnainly in colon
- lncrease in frequency with age

{
J- 'o

*ry aoM
nippleJike,
6ess'&digb:F.i1)-
tive cellsandgobletcells,

Vohulus: uisting of mesentery,

iscbemic,darkred fron infuction
entiresmallintotine bemmes lx either single or multiple

*#fi6W \tpr#N1

srHt''
Neoplasticpol!,p(adenoma): 8 b
- Very low incidence in dre small intestine, higher in colon
. *J,t[sc$dssena-
- larae uD to l0 cm in diameter
fa
- Prevalenceincreaseswith age (40-50% at age of60) ji9!s&, caulifl owerlike surface
- Familial predisposition 4 4X-. - fomed of finger-like extensionsof the mucosa, covered with
-figlL
- Most colorectal cancersrise in pre-existing adenomas dysplastic cells
-There are 3 qrpes: - cmcer is high (40%) in adenomasmore than 4 cm
(l) Tubular adsoma: mostll tubula glmds
Urlrgr Si1,t : rr*-
wr,ltOJwrrr
(2) Villous adenoma: villlous projections
(3) Tubulovillous adenona: mixture ofabove rf Tubulovillous adenoma: Mix oftubularandaveolarareas
v}@&.{*J
.
Tubularadenoma: clinical: f'1a7.
- - most conmon
W b
- as)'mptomatic usually
+
- smooth surt-ac-e- pedmculated. slender stalli I -J cm long
'"ryt"ai""
-ocetil+
- usually less than 2 cm in diarneter.
lwr* +a'n, iu
-*$
- fomed of branching disorganized glmds rvjth tall
hlperchromatic cells
- cancer is rare in adenomasless than I crn{
,/ a;rrrw*rc+ Lr. [bJ ,n<*r I
br19n

Adenomat@s pollp (tubulu adenoma)

with hemonhagic surface md long
nmow stalk
.+; ..1

Villous adfl om4 sessile,

larger thu tubuld
Adenomatous polyp (tubuld adenoma): small stalk, crowded diprg&iad adenoma (up to I 0 cm)
gluds lined uirh cells havi nuclei, less goblet c€lls,

CLORECTALCARCINOMA

- 134.000 cases/yearand about 55,000 dea$s in USA

- Peali incidence is 60-70 yeus of age
- More in males

Villous adenoms:@liflowerlike
covercd with dvsoldtic eDi
- Adenoma-Carcinoma Sequence:
(l ) Populations having hilh prevalence ofadenomas have a
high prevalence of colorectal cancer
(2) Adenomatous pol]?s antedateb), several vears onset of
colorectal cancer
(3) Patients u'ho are followed and rvho have all adenomatous
pollps removed are art decreasedrisk for colorectal cancer
due ro elongred gludultr structures

(l) Polypoidal rnass

(2) Ulcerating
(3) Infiltrative (mnular, constrictive)

Microscopic: adenocarcinom4 well differentiated

Spread:local, local llmph nodes, liver, lung, bones

Clinical:

Cilcinoma, lefl coloq onuls,

encircling od onstricting heapedup
n, ulceEted
- Change in bowel habits, abdomilal pain, reduced stool caliber

10
Adenocilcinom4 neopluticglads
with crowdednuclei,plsmorphism,
hyperchmmtism

11
1
j

Functions:
(l ) Processingofdietary aminoacids,ca6ohy&ates,lipids, and
vitamins
(2) S1'ntheses of serumproteins
(3) Detoxificationandexcretioninto bile ofendogenousu'aste
products,toxins, microbes

Greatfunctionalreserveoftbe liver masksthe clinical impact

ofearly liver damage
Removalof 75% of liverproduces little changein function+
total resenerationwithin few weeks
@
Q,rtto11
?olVt

fr
(l) Bilirubinis dreendproductofhernedegradation, derivedfrom
brealdown of old RBCsin mac.ggplggg( liver , spleen,BM).
Bile formationserves2 function:
(l) Eliminationof systemicwasteproducts: (2) Bilirubindrusis fomed outsidedreliver+ tightlyboundto
. . -^ . ^ j L j l : -. L : -\ .

- Bilirubin(endproductofhemedegpdation) --

- Excess cholesterol of albumin-freebilirubin

(2) Emulsification ofdietary fat (detergerit action ofbile salts)
is found in theplasma-r may diffirse into tissues.
iii) Thealbumin-free fractioncanincrease in severe
hemolltic disease, e.g.hemolyticdiseases of neu'boms
Nomal bilirubin value: varies, 0.3-1.2 mgolo (erytlroblastosisfetalis) + may accumulatein the brain
Systemic retention of bilirubin (more tlan 2 mgolo)+ yellow skin + severeneurologicdisorders(Kemicterus)
coloration Iaundice)

I d
(3) Obstruction
ofbile flow
(4) Conjugatedbilirubin in $e plasrnacm drereforebe excreted

Jaandiceoccuts whenewr therc is imbalaucebe*een bilirubin Physiological (neonatal)jaandice of newborns:

productbn and auetion: Becauseconjugatingandexcretingbilirubin do not fully mature
(l) Excessiveproductionofbilirubin 'l until about2 weeksafferbirdr, almostall newbomsdevelopsome
(2) Reduced (albumin degreeofjaundice dueto unconjugatedhyperbilirubinemia
hepaticuptake I Un@njugated boud)
(3) Impairedconjugation hvpeftilirubinemia
I
[-
0hotes{a-t{s,
oFuw
WftA+oF+r*J(rr.)

rS i,

Pathologv:
O Systemicretentionofnot onlybilirubin but alsoothersolutes
eliminatedin bile:bile saltsandcholesterol - Similarin obsfuctiveandnonobstructive conditions.
O Results fiom frepatocellular dvsfunction or hilnn
- Bile pignents accumulateu,ithrn liver cell
obs!ructrcn
(rnEa- or extranepahc), presenled$1th: - Bromish plugsof bile in dilatedbile canaliculi
- Obsructioninducesdistentionofupstreambile ductswirh bile
Bilirubin: Jaundice
- Proliferationofbile ducts
Bile salts: elevated bile salts
- Prolongedobsruction:focaldestruction ofliver cells.fibrosis
thatextendsandsubdiridesdre[iverprmchma. finallybiliry
+ $eir deposition in
cirhosis
peripheral tissues (skin)+
pruritus.

Cholesterol: Skin xanthoma

Elevated level of alkaline

ohosohatase
r

I
HEPATIC FAILURE
0 Themostsevereclinicalconsequence ofliver diseases
n Resultof suddenmassivehepaticdesruction,mostoften due
(3) Hepaticdysfirnctionwidrout overtnecrosis:hepatocytesare
to progressivedamageofthe liver
n 80-90%ofhepatic functionalcapacitymust be erodedbefore viable but unableto performnormalfunctions:
hepaticfailuremanifests. acutefaffy liver ofpregnancy,tetracyclinetoxicity,
Reye'ssyndrome
Categories of liver failure:
( I ) Massive heoatic necrosis:
a) tumlnmt vra neDanns
b) Drugsandchemicals:
= Acetminophen,antituberculous drugs(isoniazid, G(impaired productionby liver)
rifanpin), halothme,industrialchemicals(CC4), t
mushroompoisoning. vs tsu d l tL u r ca L - vL r c,

: Eiher dueto:
- I- l u cr sL '
toxic effect,or
4f immune-mediated
-tdirect hepatocyte
destruction -i

€ m*ftir' \ot'*traf Ull

I he tollowlns ls the heouencv of etioloeical cateeories lir'rle o@ser -6-'
mct\ ho$ rQffon=<-
/uJ\r ia $^-L
(3) Biliarydisease.
impairmentof diffirsion of solutesbetweenliver cells \ Ri* ,-aLa$ese
s-10% Ur\\qF{ Crf rh06\S
(4) Hereditaryhemochromatosis,
iron overload.59/o
/ -disruptionofbloodflowmd
a) chronicinflammation + productionof inflammatory
\aW^ /
cytokinesby Kupffercellsandendothelialcells:

Fffi*".-l fr
TNF, ll-l , toxinS
b) directstimulationofperisinusoidalstellatecells(in space
of Disse)by toxins+ fiansfom ini66ffiUhsri;t .
(8) Sphilis cells =-
'
(8) C5ptogeniccinhosis-l0-l5o/o
. v , r 1 ..^ -

\ttn nor b€ aYPeJL{

:6 rkGQgtrvn\Gir,j

i eanrres:
E Bridsing fibrous seota, delicate bands or broad scars replacing
adjacent lobules
E Paenchrmal nodules caused by by regenerationofencircled
hepatocytes,\,ar),ing fiom very small (< 3mm, micronodules)
to large (several cms. rq3qronodules) ci c f hi?.,

scarringdoesnot constitutecirhosis.
E- Disruptionofarchitectureofentire liver

- Nonspecific: anorexia, weakless and u'eight loss

Progressiveliver failure
-r: Complications relatedto portalhlpertension =
I Liver nerosis + fibrcsis+ regmmion+ fim nodulr livq cinhosis.I
 .]
l:-/:

*n

Livtr ci[hosis: regenentivenodulesofiepatoc]ts surcuded by fibrous

tissuecontaining settered lymphcyres & prclifenting bile duds

Clinical conseouencesto portal hnrertension

A
excesslrurcm pentonearca\lly
F
(2) Portosystemic venousshunts:
- veinsu,ithin tie re"tuffi
- velns aI ctroroesoDnauai_runcnon flfr-rz
- veins along falciform ligament of liver and periumbilical - ' -^
andabdominalwall collateralsIIf,

(J) Consesti\-t(increased bloodu,ithinsnleen\

(4)Hepati[

lru1ngdc+lnliit{g rn b{ud

ry?Bpn^
INFLAMMATORY DISEASES

VIRAL HEPATITIS

^t#
HepatitisA virus(HAV):

D Benign,self-limitingdisease

N fishescoDcentrate
virusin watercontatninated
by hurnan
w
Cornrfun
n hoyl$iluajs
* ctnitUren
W
 Khrciisnrt[hdbunt,?
Hepadds B virus rlIBVr, [a
El Becauseviremia is transient,bloodbornebansmissoinof HAV is
rare,so donatedblood is not specificallyscreenedfor this virus i Two billions are infectedtoday:757oin Asia andWestPacific
In USA- 200,000to 300,000neu,cases everyyear. r
Mild or aSnnptomafic
course Hdn4d relDv6
i Canproduce: \)
E Virusis not cytotoxicto hepatoc),tes,
liver injury seemsto be (l) Asymptomatic,subclinicalcarrierstate (57-
(2) Symptomatic hepatitis: l3J-
/s DNO
a) mild acutehepatitiswith clearanceof the virus, recovery9C
b) fulrninantbeoatitiswitlr massiveliver necrosis I fo
vlus ,
c) chronicheoatitis: r rpr
-asymptomaticcanier, recovery
mvetqecl
- activehepatitis:cinhosis,hepaticcarcinqna

crr(hcgr i lmportmtrole in development

of hepaticcarcinoma

\verColts- VrrrrSis prdent ro

a) B[oDd

during the active episodesin acuteandchroniclrepatitis.

Boft bloodandbodyfluidsareprimaryvehiclesof

Chronichepatitis(l 0%)
(l) Asynptomaticcariers:recovery
(2) Active hepatitis:cirrhosis,
.
trvef ro{
carcinoma pcosl
frsue ftn"as:B&Lrve
Qcrl,
rnitd l% At ggeftsn
I r r -r , (
Nuf rnSlootS.
(unti re- ttp A.''y
fiefbdes]: n.,rfl
N.E.: {-\\,l"|
Enlargedliver | \rr
Microscopic:
Multifocal areasof necrosiswith lymphocyic infiltrate
- Ballooninsdeseneration of heDatocYtes

ffif;illapente{ esinophilicshrunken
Virus is not c]'totoxic to hepatocytes,liver injury seemsto be

J Clinical:
- Prodromeoffever,headacbe,
rnyalgi4 nausea"
vomiting
- Jaundice
- Dark urine
- Enlareedtenderliver
 e-'S 3\tss
(B): balloning
Aote viml hepatiris

= baltotr|ry

Acute viral hepatitis (B): Councilmm \4ral hepatitis @), wiq state;individual
body (necrotic hepatrclte), smsll cell
with esinophilic cltoplam, pyhotic
nuclei

Cwncr

Chronic adive hepatiris (B):

mononuclw cell infiltrate in
ponal tr6 eflends into adjacent
Iobules unouding groups of
hepatocJ,tes,
mdy de undergoing
degmeration md necrosis

lnflAmrtnfrun' ril

M0crcnodJ',Jo(qcaicl-iltan Sr'--r
Potta-l tr aL+
-.^
I

. D]
' 'l('/
r \\
, r\{lr"(
D.I.' r.k
uus;r,'
Fulminmt hepatitis, eKensive |l@ of
sdJ"
nsrosis+ small liler with winkled
capsule

-J i

E*"etrt
';:#1"'ilPs"
t tl'i-=---- neLrDes
6
 ofi
Atfllduqh trrni[eC,n d,stnrka"ul
w
-_ ,J

flcpb tusn) HeoatitisC infection

.rtI|[|ni.n.|r.--.-.
2b,c,0b-3s
":!@
Wpc- - Majorroutesof transmissiffi
Transnissionanong healthworkers andbf sexualcontactis I
ltlo exhffielyrow, $gyyrf
eS

. - Penistmtinfectbn'is.gfudlfnark
g

9f HCV. fligh rateof

t "p-roqres:igltoffiiifr8ils1ma(59.70%) md cinhosis "
-r Cintrosis
(20-3s%)
II
I
X (2c"T5%)&al'*iBv r Hepatwdlulueinoma

-rp.:6-12weeks
Shor*ef *han f3
- Clinicalcourseis usuallymilderthanHBV" oftenaslmptornatic
- ChronicHCV for decades withoutprogessingto cinhosis
- Fulrninantheoatitisis rue

tc lruerdrVnsP
101' olurlo;:Chm{t
ZO-s52. clrr ho9s

Y"3,nua

dd
-u:hq
,ntl*Qarotr"{
lo'tu*"

\iort ban\5n
fr +v a^.co-\lKc-
\Ab-g' #patitispvirus(Hpv),
Dgfec'ff Vg; VrruS U
^

.$+t
-Hepatitisdeltavirur p
-Defectiveviruw
and acquires lIBs antigen coat as envelop) - Self limited
- Not associatedwith chronic liver disease
- High mortality rateamongpregnantwolnur(20%)
(ecAv(Jli
*r:r$rot
.\*S" - -ResemblesFiBV@
G virus(HCV),f,r,,r, ,;;)\
Hepatitrs
- Transmission
by AJ\k{- \
t.ttD
;SnontY
s a) contaminated bloodandbloodproducts,\',lJry.1U((r
b ) possiblyby sexualconract.esp. horno SalH.clS
-du-nnot
rnftc| do
CCIn'l 'r ,,
,q.
' - Corirnronty
:.;..
_-,.;:..:..,
i ,. - ..
infectspatientswith HIV. this dualinfection
"isrirttedfrxeaedN tfl{i'l.sT€(.ffitms}fivedtaffbt.):
t
|Ygtdtg
Ut$= tts gl
- i
*hii vi'ras tt&es -
rrnrrurno
S'rppte*Dn
9,C,and> &rnr. ];-ransrnrsftoh or,tTJli
cLM
bFFl@V
ancg I

I"IAV
 Liver abscess:
E In developing countries: common, parasitic: amebic liver abscess

D In developed counfies: uncommon, bacterial or fungal

Organisns reacb liver through:

- ascending infection in biliary tract
- blood spread by portal vein or hepatic adery,
- direct invasion fiom adjacent souce,
- penetrating injury

B Single or multiple, small or large (few mms to several cms)

E Clinical: fever, pain in right upper quadrant- tender hepatomegaly.

mdjaundice
&"tAa1rtt" oq $tory tfcct
E Surgicaldrainageis oftennecessary

- is i\e rn4lormelabolizingmd detoxifyingor-ranin rhebody.

lF Liver

i*+hjury mayresultfrdm1l ) directtoxicity,(2) lrepaticconversion

of
xenobiotic into active to\or (3) through immune mechanisms.

t* Drug-induced
\
chronichepalti(is dlniq!ly andhisrologically
simila to chronic viralpfatitis ad auto)tnqlune hepatitrs
,// -\
{e Serologicalmrpfs of viral infection ue critical for
diagnosis/./r' -\\-

* e*p9sdf to to*in or $erapeuticagentshouldalwaysbe included

iry'6edifferentialdiagmosis
of an1,form of liver disease
I Liver,mebic abwss I

k-lrohsl

N
Alcoholicliver disease:
$ thrl-\ L?'.bbs
mt+e-hsrdna
f€-6ptrar\,yf
-
a) more than I
b) causes100,000-200,000deadrVyearin USA: - Microscooic:lipid accumulates,
vesicularglobules-peripheral larUn Oxd-
\N; 5rii- mostdeaths displacement of nucleus 4"ha.4
resultof car accidents
iii- 20,000dueto endstageliver failure QstustU,a,-ql-op'nqfS{dcohol . , tre
ilih' .1. Distinctiveformsof liver diseasedueto ethanol
:

ri- alcoholichepatitis:10-350/o l::*:::t^:H^"^l

--tt-
iii- cirhosis:l0-l5o/o
arcononcrrverors^e
.i.Dairr.
ingestion
'rur€
"rl6rs#. l#,I",PryL
lcvcrg udrrag. - , .;tIEt!!.
- foci cellular su'elling and necrosrs,
- inflammatory infiltrate,
lhdr
accr{muJc-ftry}
+Crrfr"lerg'flI
J I - fibrosis Ta
ll d, rW e*h,slwcl
W rylos-^)Qd
 b) alcoholcan bemajor caloric sourcein tlre diet displacing
othernutrients-+malnutrition andt"itamindeficiency
e.g.thiaminandBI2. bl
c) impaireddigestiondueto dmage of gastricmd intestinal
mucosae

Clinical findings:
Fanyliver (steatosis):
- HepatomegalyeMlAr^Nj, b-dlf
- Mild increasebilirubinanil alkalinephosphatase

Chronichepatitis:
- Malaise,anorexia, weightloss,fever
- Enlargedtenda liver. abdominaldiscomfort
6pYgfi,u-te
- Increasedbilirubinandalkalinephosphatase (.trrhos+i

2) Hepaticfailure

ffiF \,\eirsh*nLen
"hbrosre
Uver cinfiosis.Numercusregenentivenodules,small(ess rhm 3 mm,
micrqodulu cinhosis),sepmtedby depressed rm of scatissuqe.g.
m alcoholism.biliarycinhosis.hemchromatosis

Cr vr h o ? S .
fy(tD S,*hrduJ6 23,
YY\a'v'p t " " )4 nTt
ho&deE *f*o****
Shc/-ld teoNt,\q *f61*a*wsd,
CrrfiaJv€-qn"{CISS
rtl lrnluo}a
Aloholic cinhosis:
0 Micronodulr
o Regenemting nodules of disordered
cord @lls, no qtral vein
B Nodules sunqnded by fbrous tissue
rvith chronic inflmmatory cells od
 *'t.
' -^^"sn'!totl"utfl '!tt-tor*a
6r\ Vo
1'41

INBORN ERRORSOF METABOLISM

and
PEDIATRICLIVER DISEASE

(l ) Hemochromatosis
(2) Wilson'sdisease
(3) al- mtitrypsin cleftUeXt C,/

R\l duet" qoo mil+ai16t)

@ GALLBLADDERI
I hr\ arxehi*-rt+delcnnrned
]l
fi.rloiorrvaj rAdtsstuc Chi r rrutS+
rcv. fU Wlo
Dalc4"lf5 .

Excess iron is directlv toxic to tissues:

^
(l) Stimulation of collagen fomation .- hUfV-t
Excessive
accumulation of bodl*+ deposited (2)Directinteraction
ofironwithDNA+ lethalinjur1,,
predisposition
organs(mostly irilfff to carcinoma'henaj"C4
(3)Lipidperoxidadon'(Fre<_Dz R4dica-[s < dloNqa-.
Causes:
(l) Prirnan,: Patholoq.v:
- geneticdefect,autosomal
recessive - Deposition of hemosiderin in liver, pancreas,myocardim, joint.
skin, pituitary,. thyroid ..etc
ironaecmulatesoverlifetime. OlC{Srve [b - Golden-yellow hemosiderin granules in the cyoplmm ofcells.

$-,i
(2) Secondarv (acquiredl:iron overload:qi ven fe - boO.q rorl I O
- prentral iron Ypla.? need-AH Ovrt f c<Jl'ot''uer
- trmsfusions J - Pmcreas:diabetes (75-80%ofpatiens)
- hemolyic anemius- t€ tb allhq"t, fltxUlltrd
fo - Heart:interstitialfibrosis loc4. pls
w"
g
- decreased utilization,e.g,aplu.ti" ao-.mia' btgs - JEirlls:acutesynovitis'at+hn{a
coill dbrc{m
lwer* |
Crcf l v{-.rf -A-"r|iniS"l""lilqrxqonaaisf,'.,
* Bncr,lnartcoloYaj;6\
a,r1e-n orrb€JS
s
- trbro€r \J
\e\€+s-
geJa.ceI\S
elrabobs
!'mplomalrc: A R.estnc"five
(l) Hepatornegaly.abdominalpaln-7 Shnffilt{'c I
(2) Diabetesmellitus(destruction
ofpmcreaticislets)
CfprctrOfirlrr
(3) Cardiacdysfunction(arrhlthmia,cadiomyopathy)
(4) Skinoiementation Fo*L'€$
isj e',r"it! - hc dlpo? t' rn $hovr4-Qenlrr
(6) Hlpogonadism (amenonbea in females, impotence in males)

(7) Earlier clinical presentation in males, physiologic iron loss

(menstruation, pregnmcy) retards iron accumulation in
women
 Liver.hemshrcmatosis,
Kupfferells in sinusoids
full ofbrom
hemosiderin

qf+rr
* Autosomal recessive disorder rfiptaholicm+
accumulation oftoxic levels ofcopper inlnmy tissues,mostly

-
* Nomal copper physiology:
a) absorption ofingested copper (2-5 mg/day).
"'t""'
b)Piplasma
vr ralsport.
o Jr u a u 4 r JPu r "r f\ bouni- 54
c) hepaticuptake,bound "lburin
to a2- globulinasceruloplasmin
+ blobd
d) hepaticuptakeofceruloplasmin fiom plasm4lysosornal
degradation-+ secretionoffree oopperin bile

* In Wilson's disease,absorbedcopperfails to enterthe circulation

in theform ofceruloplasmin+decreased biliary excretionofcopl

Iiter uha-bL-,*o hak-Cu,UlaZ

r r, ^vd4,oc!
f,+S*u'IaM
tt' ,f,- J
 -s.ryJ,$t'^*l'$
-.x$;$*). t
* Pathoeenesis:
Increasedcoppercausestoxic liver injury:
(1) promotesformationof&eeradicals uru{ +l
(2) bindingto cellularproteins
(3) non-ceruloplasmin-bomd copperspillsoverinto circulation
-+ hemolysis,lesionsin brain,eye ...
*Treatnent:
Long-termcopperchelationtherapy@-penicillamine)
* Clinical:
- Usualonset:6 years

Parkinsonlikemanifestations
- Eye:Kayser-Fleischer
rings(browish depositsof copperin
Descment'smembrme)

d409,,"r
Ftk1fn

Wilwn's disce: accumulation

of red-brommules of
in liver. liver cinhosis

s#
T*$
B Autosomal

...,.'---:.>
al- antitrypsin

ol 0l- mbFwsln

B Main function of AAT

faaOt -ngtd,gC tQ
deficiencJ

recessive disorder, marked by fte low serum level

o The mutant protein can not be secreted by the hepatocyte, it
accumulatesas globular inclusions ofretained AAD ( sbongly
positive with PAS stain)

o Clinical:
-Newboms:10-20% exhibitchotestasis ) €arf
- Older children md adults: ptesilt u,ith:
- chronic hepatitis
't
14{ bi €

fDf groenb o Syndresized

mainlyby theliver - cinhosis

.rn\un'- kuf o Its deficiencyleadstoAf;(lack of this proreinpemits the

- emphysema

activityof neutrophiltissuedestructin
g en4m es)

r"^ \\ Uet-
31n$of,be
rnkonS*Y*alsnt
.v/
f\
-) e\cchooa
a\ao:Bd
Y-j
''\
{t
Reve'ssyndrome qounq
. Rare disease characterized 'cj'';(dteYt
-l-.
. Affects chi
vinJ
trhlrrFtlarlC\n"Ch Ftr
inkhlon
. Paftoeenesis: '
- Unlinown
'
kotrin
- Derangementof mitochondrialfunction in combinationwith viral
infection.lI tohrr#lrr
Liver: redhyalineglobulessined
with PAS,alpha-l- mtitrypsiq the
. Deadr
\,hq? ural{
Droteinis not secffied.a@umulals
ln of
. Adminisaation ofaspirin to contol fever in viral infections of
children should be avoided
in6r0runu ,
ffir'hcludtd.)
Kesf
mrDn

JI
OBSTRUCTIVEBILIARY TRACT DISEASE Jte
o Diseasecharacterizedby: inflammation,fibrosis, inegular
r€A.sbn
Lnown *-icnrresanddilationsofintrahepaticandextrahepatic bile ducts

- Prolonged obstruction ofbiliary tree

- Causes:
(l ) Extrahepatic cholelithiasistF o Males affected more than females (2:l )
(2) Strictures from previous surgery
(3) Malignatcies ofofbiliry tree and head ofpancreas

- Early lesions are reversible with conection ofobstruction

o Chronicprogressiveandoftenfatalcholestatic liver disease.
- Prolonged obstruction and secondary inflammation + periportal Non suppurative.granulomatous destructjonof mediun-sized
fibrogenesis+ scming md nodule formation (2ry biliary intrahepatic
bile ducts,portalinflammation& scming
cirrhosis)
o Cinhosisonly latein thecourseofthe disease

Prinaq' biliary cinhosis: autoimue (a!i-

F*"ltrh.dblfi;l
Mtahondial AB), chronic inflmmation in
Donal ds. bile duct destruction
losebile
prmnlrn0
'fL'bqeV
I.we tds,
Fnrtochondrfl
 - bepaticartery(40%)
- portalvein (60)

- Obstsuctionof&e main hepaticarterydoesnot alwalc produce

ischernic
necrosisof the organ.Tlrombosisof intrahepatic
branch
ofhepaticarteryby thrombosis. embolism,tumor+ mayresultin
localizedinfarct.

-Portalvein obstruction
:
- ascitis
- increasedpressurein GIT
- esophagealvarices

-hemrnorhoict"

wili
whfubr
a
- Red-blue nodule, less than 2 cm below the
- Vascular chmels. lined by endothelial cell wi$ interuening
stroma

(2) Liver cell adenoma:

- Mostly in women of childbearing age who usetr
tumor regresseson discontinuation of
hormone
-I;,
- Bile-stained, well-demarcated, usually beneaththe capsule

fltD wdnomq

ffi lJ
- Relativelyunconmonin NordrAmericaandWesternEurope
5:2o/oof all

more common

(3) Dietar-derivell from tle fungus

flams(moldygrains
orpeanuts)
* heq061s J)
(4) Chemicals e.g. dloratmst

used{o Ctr}linebilant
 - Pathologv:
N.E.:unifocalmrosivelesionor multifocal(scattered
nodules)
Microscopic:hepatocytes
arrangedin nestsor smallcords

- Clinical:
Hepatomegaly, bloody ascitis, fever, pain, weight loss

roE:nosis:
3-6monthssmival afterdiagnosis

- Liver is a common site for metastatic spread ofcancer

of primarv tumors: breast. lung, colon

€c^rosls

Cholelithiasi#r*
- Affectsl0% ofadultpopulation
in Westem
counrries.C6

- Most gall stones are silent (800/o),no biliary pain or stone

smooth
?ourrd.o{al'
ffi;g"- bM 'cvgg{al5
 Pathosenesis: ,,:chslebysri6*
in ftafffrthfn
': Aimosl al.waysinassociationr*,itli:.gdlstones
- Cbolesterol
is waterinsoluble,renderedwatersolubleby bile salts
md lecitlrins
cosecretedinlobile.
Acute calculuouscholecystitis:
- Acute inflmmation of gallbladder that containsstoneg iWadcd
- Prevalenceincreaseswith:
a) age (30oloofpeople older than SOyears); 5
oiirifr onit1446i:'!,0fii9nE$&ti
of t$FMoift s. ,rMnd
anrcdrry7
?
b) in native Americans (?5% prevalence) - Acute calculous cholecystitis is due to chemical irritahon and
c)2:l whirewomen versusmen-toC lUf pdCJ mOfCC
inflarnmation ofu,all associatedwith obstruction ofbile outflow
c)decreasedgallbladder
motilit,_
blO b0(dnd b ClL. - Acute acalculous cholecystitis (no stones).most casesoccur in
Clinical:signsandslmptomsof cholecystitis, jaundice
sometimes seriously ill patients.

gh0lr'ldft.
mrnlcolro+ Rr4tl/t+

FH3
,8\B
Paftologv:
- Enlarged gallbladder with red edematous wall
- Serouscoat covered with fibrinous or even suDpurativeexudate

.qpp-_ctrlwp.,ii,eiaf.ptiti.radidt'hgrb
shostetir;ndiich; rt
- fercr, nausea
- right subcostal
regionis tender,rigid, sometimes distended
gailbladder

,Vojrn
Sm# ofCIbrtrrn
g6n6 - Almoslalwaysassociated $'ith s'ift gall stones.Stonesdo not play
a directrole in initiationof inflammationbut supersaruration
bilepredisposes
of
to bothchronicinflammationmd stoneformation.

peY - lnfections (E. coli, Enterobacfer) in l/3 ofcases.

W
44btw'
Clinical: similr to the acute: bilitry colic, upper right quadrant pain,
epigastric distress

W Cholmgitrs:
presence
Choledocholithiasis: ofstonesin biliarytract

- Acute inflmmation of the rvall of bile ducts. almost alwavs

due lo baclerial infection. It
"-
bile florv. most cornmonly stones
,"iit6*y lesion obstructing
(choledocholithiasis).

- Bacteria enter enter Yia sphincter of Oddi, rather than blood:

^ moffrrnpf.
i;."*1.,,f
KteDsteila
t
Clostridium
Bacteroides
Enterobacter

'ffi5
GrouD D streDtococci

\ilPrasitic infeclions in certainpans of the u,orld: schistosomiasis

') r l nr..^-.
-.^t- -rr./
NMgS
@WN'YI

tumors:
- Cancer of gall bladder is rnore colnmon thil catcer aising il
bile ducts
- Slightly rnore cornrnonin rvornen | .

W
-
- occursmostiiequentfy ril1-i . decaae- plOlglffi |I 4
- Diagnosedlale. 5 yer suruival rate ofonly | 9/o U

At*
\YdYatalo'-ro0rwffi€ ' l,/
r

Ve8/ g1n'fiLs
AcutePancreatitis:
ffif '
- Enzlmaticnecrosisandinflammationofpancreas fl
- Releaseof: fI
- lipase-+fat necrosis,
faqv acidscombineu,rthcalcium i
I
MC-
forminginsolublesalts
- Foteolyic enzf,mes -+ damageof pancreatictissueand

- Pancreatic pseudocysttnecrotic
materiallined up b1,fibrous
[to.l"r-nU
wall. no epithelialtirun\ hrrnefl
ehvahd
Sit4
It rnt*rlin

.fl"Jffi -ifts "'h"t^Sd,thdl

so7s

Aore pilcretitis: swollen with uas of hemonhagic ncrosis, loss

h,sh 6c
I
WhoJtl
I dJGUd

I Lrge pancrqtic pseudoc-vst,opened, with inegular brcm inner surface I

 W; w$QQItU
'cfu1py
chronicpancreatitis,
Qilftc cnr*ihon
at ampulla of Vater -A9Es!3939\. olsi]dJeleleEc.j4blosuq!--+ lossof
ii. Alcohol: strongpredisposingfactor (unknown mechanism) parenchyrna
+ replacement byfibroustissue-
iii. Acinarcell injury by viruses,alcohol,toxins,trauma, u,ithalcohor
-Associared abuse'aCrfraqg O$OCfffOfCdlS.
- Densely
fibroticorsanwithextensive
atl6Dhv
t+ Clinicalmanifestations: -ctrnrcatT-
i. acuteabdominal:epigastricpairi r.adidtingto upperback(d l) Persistentpain in the epigastricregion
medicalemergency) 2) Malabsorptionand steatorrhea
ii. peripheral:vascularcollapseand shocti$iiffid'.6btictiel,rlbntsge 3) diabetes(latecomplication)
hli8'ieleaseof vdsodilatitg'agents)A Sh oC& 4) predispositionto pancreaticcarcinoma

40FU €^ef
iii. Elevated seruni level ofamvlase and linase
glucosuna
iv.Hl,perglycemia. dapgtlg O f€l!t6

W
v. Hypocalcemia: calcium binds to fattl abids in abdomen

o,llumovrtmcl-thrb
F,+'
trrcyedlc o?
S

r .P\
-lr b*nitD
0rnbfnl Dl b+ + Ca+vgonDU S
Carcinomaof the Pancreas:

rrs
(precededby lung. colon, breastand prostatecancers)
8,
U,
- Risk factors:? Smoking,? diet,? chemicalcarcinogens(
evidencethat alcoholor coffeeincreases the risk)
no
rcAktkath
- Age: betrveen60 and80 years
- Malesmorethanfemales,blacksmorethanrvhites
r)
- Site:
h- (encer
[h*
rw
r 60%O,inhead oflxiirbleas,I 5% in body.59zoin tail. 20olodiffirse

- lLE.: induratedmass l " ' - \trnX-

.u.i; .i'it.."nou,"@$[E#
- lvircroscoprc: Trta !a(qatt'
ini pro::!r*c
Q'+ eo[Dn
\{g"Let l{€ad.,fruGtft1
wnf sili: s +h p0'r-,Cf$-t3
lslvuer<d,
ClinicalFeatures:
- Insidiousgrowthoveryears,remainssilenttill extension

(,Autgcera'
&ng'
ffi$e
- Bloodexamination:carcinoembryonic
antigen,CA 19.9antigen
{gold markerfor Dancreatic
-#Tuw6ru'a.f
carcinoma)
(iEs
tvl-rrdtDrer*''lo
affits
)- eAh I tl

e #orn
lr^|^..I I l- f
..l lFv '
n
lt
\. - l n .
nl\ f
v l- r -JI
.{\\\,,
d\ r '
I
[im.9+
CA bod'{ and+df
r I L vn

IJ
.a \\ \-
Lqrnilnhc,
WwU
rr
ffi
 .t}os

ENDOCRINE PANCREAS Tlpe I VersusTypeIl Diabetes

haWS Diabetes Mellitus IDDM (TypeI) NIDDM (TypeII)

gvx!* A groupofdisorders thal affect many organs,characterizedby

glucoseintolerance.
abnormalities of insulinsecretionor
metabolismleadingto hyperglycemia. glucosuriaandtendencyto
developatherosclerosis.
nephropathv andneuropathies

- No HLA association
- Foundin lessthanl0% - Foundin greaterthan
leve,l Type il Di abetesMellitus ({rdE+irisli.ltsdepeitdcnr
20%oftbem

atrl +I4EDlv4;1littd#6ffiEtSM) Gt l -N one

Jexceeds - Immunopatbologi"
mechanisms
I - Insulinresistance
| "gryfi141eq4.51rybe

banal*ula.deg'-rcilltr0c8r.rna-
+"
sf#,v**p$o * fl +r,,ryFlapsta ruf$o
Type I VersusType II Diabetes
(\pal_r IDDM (Type I)
Swrj.on\\O - No insulitrs
-on:el1 - Focal atrophyand
amyloid
in3u\in - Mild B-cell depletion

Weightloss
Trearmenr l- Insulin | -
I | -Oralhypoglycemic
I Insulilis ofan islet in a patienr who dweloped Diaberes mellitus I
 dst'*s5,f'f,
{0Y,6\.Je;qp
\_-/.J

_A Pathogenesis of MetabolicDerangement
- lnsulin is a major anabolichormone
- Derangedinsulin fimction atrectsglucose,fat and protein
metabolism
=-
- 1 glucosein blood -+ t glucosein urine (glycosuria)-r
- OIIIUSetn|cKenlngol basementmembraneot caplllanesOl
skin, skeletalmuile, retina and renal glomeruli
l,nlc6tg'["
osmoticdiuresis(polyurea)-+ intensethirst (polydipsia). - capillariesare moreleaky than normal to plasmaproteins
..-zndrno$
$r** Increasedapetite(polyphagia)developscompletingthe
classicdiabetictriad
Grmnttt"?
v) *rDi'dd&tr,Mtlti6ls:'
- occursexclusively iarype trd,iabetes
- complicatedlesions(ulceration,calcification, hemonhage,
thrombosis)lead to narrorving,occlusion,ischemiaand
c-aD.
ol&olanlvs
- severeinsulin J and t glucagon aneurysmal dilation
- excessivereleaseof free fatty acids from adiposetissue large vesseldiseaseleadto myocardialinfarction cerebral
- hepaticoxidation generatesketonebodies strokeand gangreneof lower extremities
- !$q!em!a and-I@ruria
- life-threatening
systemicmetabolicketoacidosis
. ct;a -eki< (Drr'a

5D%MI d-ta*Ls

ft n
3, Kidney: n€Phr$$: 4. DiabeticOcularComplications
- Diabetic Nephropathy,kidneysare the mos severelydamaged Visual impairmentandblindnessdueto:
organin diabetes .-a. diabetic retinopalry; hemorrhage,exudates,edema,thickening
- Renalfailureis a majorcauseofdeath of retinal capillariesand microaneurvsms
a. Glonterular involvenpnt: q. Cataracl
gGtaucomat{€ngrttrh u* eYe 9[c- el$lU.t &uc\6d'hn
Resultin progessive proteinuriaand chronic renal failure
b. l'ucular
t-
- symmehc penpheralneuropatiy
* arteriosclerosis
-r nephrosclerosisandhypertension _ - affectssensoryand motor newesoflower ertremities
c. lnfecrnn +pyelonephritis St!t{6€_ neAiAh - Schuanncell injury, myelin degeneration
#
\or -'n{oc{irrr--. - axonaldamage
- autonomicneuropathymay lead to:
* sexualimpotence
* borveland bladderdysfunction

- cxqenssof
Fanoreas
- nqsultn
- hn+i etfu
Islet cell Tumors: t 6Ul : aettfwle)tur^or
- rare comparedto tumorsofexocrine pancreas

Betacell tumors(lnsulinoma) qdOfpn"C}* t cunow cudruU

- mostcommonisletcell tumor
- producesufficient amounbofinsulin to causehypoglycemia
- attackswith serumglucoselevel belorv50 mg/dl.
fl's arrlaq.nrzB
ing^tri
- synptoms:confusion,Iossof consciousness \r1p64\r;CXim t)
- aftackspromptlyrelievedby glucosefeeding 'r -
r
'.-7aul
i
K
Acute mastitis:
D Bastenasnter tre breast6roush.
=Gt
- Fissuresin the nipple during earlystageoftrursing i
. Variousforms of dermatitisinvorlvingthe nipple :

Dl-'tt-l
i;\RTr cl Staphytooo6d'iilfecrioil.ill-derecs€iitshr6rbq,lwjbEieli*d
tpipal infl qn@.t-o.rylqhages,
*.x_N_ti,\!t1l abseosses-'+,
scamng
hgding mgy leave

Mammaryduct ectasia(dilatedjlU9l5):
o Nonbacterial infl anmation of breast
o Dilation ofmain excretorv ducts.

o Rupnne of dilated ducts + chronic inflammation

o Seenin multiparous women behveen 40 and 50

o Mistaken for cancer (palpable paiareolar mass, induation of

breast,nipple retraction and thick white nipple secretion)

Traumatic fat necrosis

I Uncommon-
historyof prior fauma

. Localto onebreast

. Centralfocusofnecroticfat cells,suroundinginflammatory
reaction,later replacedby scartissue

. Palpablemass,skin reFaction

Irumatic fat narcsis: inegulr far cells without psipheral nuclei,

interuening pink morphos nffiic matsial ed inflmmdory ells
 JI
- morethanhalfofall surgicalprocedures
on breast
- Age:2040, rre aftermenopause
- eggsc:hormonalimbalance:
Excessestrogen
Deficient progestrone
Oral contraceptives
decrease
incidenceby maintaining
balancebetweenestrogen/progestrone

{}
THREEFORMS:

women) + increase
in fibrous stroma and dilation ofterminal ducts into cvsts,
no epithelialhlperplasia (simplefbrccystic disease)
-(60-80o/oof
Cvsts:
--
- Multiforal,bilateral,vary rn size( l -5 cm),
- Brom to blue,filled with serousfluid drarmay calcify
( microcalcificationsin mammograms).
- Linedby a singlelayerof cubicalor columnuepithelium
(multilayered in focalareas),may be largepolygonalcells
with abundant granulr esinophilicc1'toplasm similarto
sweatglands(Apocrinemetaplasia)

surroundingall formsofcysts

| (l) Cysticdilararion
oftminal duds + apocrine
metaplciaof epi*reliu I
(2) hcreed fibrcusmma
|

Cystic cheges: duct ild dudules

bmne dilated. oithelium cuboidal

ta----rl
 DFrcr&feradie'6lia$ses: r
- Epithelialcell hyperplasia,frequendyaccompaniedby
cystsandfibrosis.

- holiferationofepithelialcellslining thedilatedterminalducts
-r multilayeredwith papillaryinfoldings(ductalpapillomatosis)
or filling the ductallumen(fenestrations)

- Mld h'yperplasracaries little riskof oarcinondtl.5-2 times),

at5pioal,.hyperplasia{cells
varS'ingin sizemd shape,
hlperchromaticnuclei)hassignificantlygearer risk
(5"fold.inu€aied rtdk of oareinonia) i

Mar*edducralepirhelialhyperplcia, Fibr@ystic chages, duds with

witft increreedrisk ofbrut crycinoma epithelial hyperplaia (mulrilayered),
(1.5-2timesnomal) A$?ic€l dudal epithelia.l hyperpl6i4 with increued risk of brut cucinoma
no atlua (5-fold)

&
B SclerosinLadenosis:
- Lesscommontha dreprevioustwo \pes
eNumber of aciniperteminal duct mit is increased
at leasthvice,
backto baakfdd€roslg. ;

- Markedintralobularfibrosis(sc/erosrs./+
rnaycompletely
compress the lumensof ductsmd acinicreatingsolidcords
(confusedwidr carcinoma)

- Deformedandenlargedlobularunrts

- Slightrisk ofcancer

Fibroq'stic choges: cystically dilated duds, abundmt fibrosis, small

dea of calcifi cation, sclerosing adenosis
 "j

-v.-.i
.:,
JI 0
TUMORS
Sfomaltumors - Mcroscooic:
- Loosefibroblasticstroma sunoundsductlike or glandular
€'N@ spaceslined with cellshaving intact basementmembme.
- Ductal spacesmay be open,round or oval (periductal
@ fibroadenoma)or compressed into slit-like sFuctures
- Age: young women, peaks,iq3'd decade
(intraductalfi broadenoma).

. N.E.:
l) Encapsulated,
&eelymovable,1-10cm
2) Frequentlymultipleandbilateral,

Fibroadooma, comprcssed brut onnctive rissue (*) foming capsule,

l iiu. fibroblotic woma witlr elorgared @mpressed duds lined by nomal

(2) Phvllodestumor

- Much less common drm fibroadenoma

- Varies in size: few cm (4cm) to massive size distending the breast

- Shows grossly leaflike clefts and slits (Gr. Phyllodes= leafJike)

- Usually benign. some become malignant (low gade), tends to

remain localized, may recur after removal, but only rarely
m etastasizes

.. 1
 :l

(3) Sacoma EBithelial

tumors, t^
. Similar to malignantlesionsseen elsewherein the body
e.g.liposarcoma. angiosarcoma,
changein phyllodestumor
leiomyosarcoma. sarcomatous 'l-
- 9.flg$S-ggl]u2gto*dr within &e main lactiferousducts
or smuses
! Bulky tumor masr *i6
"ryg|gg-
- Mostlysolitary,lessthm lcm
. Angiosarcoma ofbreast:arises.either: - Branchingpapillae,coveredu,ithcubicalepithelium
a) spontaneousll,,
b) ascomplicationofradiation treatrnentfor cancerbremt -e!!dsal:
(riskup to 4%,5-10yearslater) - Spontaneous
unilut"ot *, olfF
b) in the skin ofchronically edematousarm aftermastectomy - Smallsubareolurnass
(Stewilt-Trevess)'ndrome)
- Mostly benign

L
lntmductal papillona: Iuge cystic FW6F
dilared duct showing Iobulaled
ductal tr€ll
-Epidemiolqg_andBiskJactors
(l) I of8 womqr in USA develop cancer breast, l/4 will die as a
result (nearly 45,000-50,000 deathsper )'ear)+*&b$*t@f
{@ffi9s9)

(2) dgg: increaseswi*r age, uncommon under 30- with steady increase
till menopause,75oloare older &an age 50.

(3) Genetic and famill predisoosition:

- 5-10% ofbreast cancersare related to specific inherited gme
mutation (tumor suppressorgetreon chromosome l7)
- 5070 ofu'omen widr hereditary breast cancer (familial
Intraductal papillma in main predisposition) have g€ne mutation
lactifercus duct Oeneath ueola),

(4) Geosraphic influences:higherin USA andNorthernEuropethan Classification: {F

Africa andAsia (environmentalfactors)

Q Eitherhaveinvadedthebasementmembranelmy4giyg infilnainel
ot not (lglglnwivg cMcinoua in sitt/J.

i9ht,bitateral in 4ot

h" Exogmous: Post-menopausal:

estrogenreplacementtherapy

(6) Preexistingproliferativebreastdisease
Wanthe

B Locations:

(7) Cancerofcontrolateral
breast(47oofpatients)
on (8) Ionizingradiation
- Upperinner,lowerouter,lowerinnerquadrants:
l0o./o
each

'.__J &.rs\oQao.CQ\nUrO-*
\dout\utQcr"t'0irufYlo-
 ns
DISTRJBUTIONOF Tffi EISTOLoGIC T}?ESOF BREAST C{NCER

TOTALCANCERS PERCENT
!&
NONINVASIVE (IN SITI) CARCINOMAS
CONIFEDDY BASEMENTMEMBRANE,DO NOT INVADE INTO SIROMA
oRLyMpHovAscaARcHANNELs
J!: ftI1bVC
sff;e
h
:, :. Lrtraductalcarcinoma(DCIS):
w1@-:* dx-Ylor;tt^t,
w:wc$qPsry,.!!q. i. :.:i-1i:,1 ,.8e!
tobulor Lobularcarcinoma
in situ 20 mEI--'
-Much more commonftan inralobular carcinomain situ
- Arise in 0reterminal ductlobular unit
4ornocinl tre - Cells grow, fill andplug the ductsandductulesu"ith carcinoma
cellsbut remainconfinedwithin thebament membrane
RWe$gg. q,.,,,,.,;::,::,. ..:t::.ilgs,
-Variouspattems:
Lobularcarcinoma t0
a) comedocarcinoma
Mucinous(mucoid)crcinoma 2 b) noncomedocarcinoma
Medullarycarcinoma 2 c) mioopapillary
Tubularcarcinorna 6 d) Paget'sdisease

Yuttrrq{S
*F
(2) Noncomedocarcinom a:
Monomorphictumor cellilllnl, with spacesthat
areevenlydistribured md regxrlain shap@
| molitna.ytJ
Qllcgapap4ary 4$c 4J4!4!c-stsFa t trvX6t'artprtL

CJ
0Yr

w
tliltfurrl
Intraduct @inom4 nonmmedwinoma, noplmic cells surcud
holeswith sharpmrgins 6 ifpunchedout bv a cmkie cuuer

'g J
 tobular. oarcinoma in situ (LCIS):

- Monomorphiccellsin clustersin ductsandlobules

- Neverform a mass(incidentalfinding),rarelyassociated
with
calcification
- Do not distortthe tissues,
aciniremainrecognizable
- Birateratin20-40v") Oh\r/ tb-?DyO ,n
f)ClS
- Onethirdof womendevelofinvasiveLicinoini

*e% YeA
developtnva€i
bT
a$r<r Uaqcrnfi'rud
IT OT)YW
1* Lobula cilcinom4 neoplasicpmlifemtionof cellsin reminal breretduas ad
acini, small md round cells (30% risk for development of invcive reinoma)

s
INVASIVE (INFILTRATING) CARCINOMAS

- Strmulatefibrosis that replacesbreast fat (mammo$aphic density)+

hrd palpable tumor mass (scirhous carcinoma) '
t'l&rY L4(tA
- Extension ofthe growtlr may cause dimpling ofthe skin and
retraction ofnipple.
- Mcroscooic: scatterednests or cords ofmalignant cells in dense
fibrous stroma

- 2/3 expressestrogen or prcgestrone receptors

I u'hite center(desmopl6ia) md periphenl yellowish d6 ofnecrosis I

&r hrrncrps degrro Ie {iUrarstreeur,

1 o*ono-* r*.**]lli;f,
--.og*
 DrclalCArnslt*
Lu+onipCe
:-a.::

Paset's
disease
ofthebreast- 8tstn tg$i6n 0C
-Nipple lesiondueto breastcancer(l-2% ofcases) tnh

- Skin is Aequently fissured, ulcerating and oozing. Superimposed

bacterial infection is common.
- Propnosis depmds on the mderlying carcinoma, i.e. not
worsened by Paget's disease)

- Microscooic: Invasion ofepidermis with neoplastic cells (paget's

cells), scattered singly or clustered, sunounded with a clear halo
ides),associated
u,ith IDC ) invasiveor

Drnl u,r/inrlrrido rn Dur}s tz)

lnvasivelobularcarcinoma:

- Makes 5-l 0% of all breast carcinoma

- Rubbery in consistency, does not create a palpable mass.
- Cells invade individually into stroma + sfiands oftumor cells,
onecell u'idth (inthe form
- Expresshormone receptors "fq)

- ;fureq"dy rnr.tastiaSs

x m%
-Tend to be large and fleshy, sheets of large maplastic cells,
scanl sFoma
Dresenthost reaction to the
rl vr - v-v

#
S*UlroiruuleteiOnal22
- Rre, lesscommonthanmedullarycrcinoma
r Productionof[qucin intracellularlyandextracellularly
intothe
surroundingstroma+ softbulky gray-bluemasses
>Express hormonereceptors

pAoiJ .*,
r,r,rc.,n,{urrnr
crcinoma: large flehy m6s, shets ud nesis of ells snouded
strom4little dmoplsia (benerprcgnosisthm IDC &

"e
\*,,"J

b?o ntrAdrd4j
ruburarcarcinoma,
- Multifocal, in a single breast or bilateral
- Rarely presents as palpable mass
- Microscopic: well-formed tubules

- Well differentiated, rare lymphatic spread, excellenl prognosis

- ExDresshomone receDlors

I Colloid or mucinoustrcinma with abundmtbluidr mucinI

Mammoeraphy:
- hcreaseddetection
- Detectionof smallinvasivetumorsbeforebeingpalpable
- Easily directedbiopsy
- Signs:
(l ) Density
(2) Massdistortion
(3) Calcification
(4) Chmgeswith time

l$Features commonto all carcinomas;

6'ohsrtf
t' ll&rylency to adhereto-pectoralis.muscle
anddeep
lurn{
w,1\ (4) During pregnaacy,tumorsspieadvffip-idly -+ exciteslocal
inflmmatory reactionu.ithswelling,rednessmd tenderness

(5) Spread:
- Local
- Llmphatic:nodalspreadis presentin 2/3 ofcasesat
time of presentation
- Blood:favoredlocations:lung,skeleton,liver,
adrenals.brain

;
fll Fantus{ t b4et?
bl"nl cawsos (Xstt' ^{*J
puarld orarl<-T ' Wl\ahb '1: s
os
A) tgngha-t
 Themajorprognosticcriteriaaccordingto the AmericanJoi9y'
committeeon cancs: ,/
(l ) Sizeof primarytumor, ,/
(2) Lymphnodemelastases- ,/
(3) Presence ofdistantmetastases ,/
Stage0: DCIS andLCIS(5-years\riytfute:90o/.)

StageI: Irvasivec arcinona:.2gK lessin diameter.\9 nodes.

No distantrnetast?,(5-year sun'ival rate:879t)

Staee11A: - lnvasivecrlinomas 2 cm or lessin dimeter wifll

involvg/axillarynodes.OR
- lnvatile carcinornagrealerthtr 2 cm but lessthan5 cm
i2Kze with negativJlpph nodes(5-yearsunival rate:
n50a\

Staggll_B:- hvasivecarcinomas greaterthan2 crplrnsizebut less

than 5 cm witb positive lymph noy'ds,On
- Invasive carcinom a greater thaS$gin size with
negative lymph nodes (5-y.5# survival rate: 75%)

StageIII A: - Invasivecarcinomy'of_aUsize with fixed lyrnph

nodes,OR
- lnvasive car,gilfomaof any sir with nonfixed llmph
node

StageIII B: Invasly6 carcinornawith skin involvement. chest wall

or clinical inflammatory cmcinoma . or with
asesto ipsilateral intemal mammmary llrnpfi
nodes (5 year sun'ival rale 460/o\

: any cancer with distant metastasis:5-year suwival: I 3%

rreatment:
QIAAWAU Carcinoma:
(1) Surgery:mastectomyor lumpectomy
(2) Radiation,post-operative - Rare, with a &equency ratio to breast cancer in female ofof I :125
(3) Cemothl'rapy - - Becauseof dre scant mount of breast substancein males. the tumor
(4)Hormonar rapidly infiltrates the skin and thoracic wall
- -Iiunq(itn (c6mpJcs - zusk factors and patlrology ofmale breast cancer are r6markably
to cance$ seen n women.

MALEBREAST
Glnecomastia:
'
ttC nalJ'
(l ) Livercinhosis:
inability
(2)Estrogen-secreting
of liverto metabolize
tumors e.g.Sertoli
estrogen
cellcarcinoma
{vt n
(3)Estrogen therapy UCgd+eV ?ohp CA.
(4)K.tmfettusyrdrome- ,
)6q/ -Trdf6 a^rcfirA O
(5) Physiologic gpecomastia at piberq'arid in extremEold age aloVl'ttt

10
 Ic.q.srrl
| -' -*- | A. -^
70-year-old
mm sawhis physicimfor a routbe health
maintenanceexamination.On physicalexamination,therewereno
rmrarkablefildings, but a stoolsanple waspositive for occult
blood. A colonoscopywas perfonnedandshoweda 5-cm sessile
massin $e upperportion ofthe descendingcolon at 50 cm from the
TI.IEGASTROINTESTINAL
TRACT analverge. The histologicappearance at low power of a biopsy
specimenofthe lesionis shownin the figure below. The patient
refusedfurther workup andtreatment.Five yearslater, he seeshis
physicianbecauseofconstipation,microoltic anemia,and a 5-kg
weight loss over the past6 months. On surgicalexploration,thtre ls
a 7 cm massencirclingthedescending colon. Which ofthe
followingreoplasmsis he_qow mostlikely to have?
lil-l
a. (5, NOn-HoOgKrn
lympnoma
.:. (C) Villous adenoma
+ (D) Squmouscell cacinoma

ICACZ
A 70-year-old manwith a lengthyhistoryofchronic
alcoholismashadincreasing difficulty swallowingandhas
noticeda 6-kgweightlossoverthepast2 months.On physical
examination, tlere areno remarkable findings. Upper
gastrointestinalendoscopyshowsa 3-cm ulcerativemassin the
midesophagus tlat partiallyoccludesthe esophageal lumen.
Cu ilr= crcss drr@.rci'r ur.
Iesionis shownbelow. Whichof thefollowingis mostlikely to
be seenon microscopicsectionofthis mass?
{. (A) Multinucleated
*ro cellswith intrmuclearinclusions

't (C) Adenocarcinoma

.i. (D) Thrombosedvascularchannels

IC A S E3 |
For the pastyear,a 20-year-old
mm hashad.increasingly
voluminous,bulky,foul-smellingstoolsanda 1O-kgweightloss.
Thereis no historyof hematemesis or melena.He hassome
bloatingbut no abdominalpain. On physicalexamination, there
areno palpableabdominalmassesandbowelsoundsarepresent.
Which of the followinglaboratoryfindingsis mostlikely to be
presenton examination ofhis stool?

A (B) Giardia lamblia cysts

-
* (C) Vibrio cholerae
.i. (D) Entamoeba histolydca fophozoites

s)
.>\ fi
t1
*dff
U ,ft
) '
 IcASE;l IC A S E5l

A 68-year-old womm has had substernal pain after meals
for may years. For the past year, sbe has had increaseddifficulw
swallou'ing both liquids and solids. On physical examination, there
il:il:T-T:5ffj":E*n'ffihr
A 53-year-oldwomanhashad nause4vomiting, and
midepigasbicpail for 5 months. On physioalexamination,there
areno significant findings. An upper gastointestinalradiogaphic
seriesshowsgasb-icoutletobstruction. Upper sasbointestinal
;n ,i n i , ,,n w <n ,- - c a n ,,i a - .- '- ^

vvure! ur urc ruru*,rg oropr*ffiffia

- - ".t- .:- f

the foll_owing neoplasms? seen in a biopsy specimm ofthis mass?

- * (A) Non-Hodgkin lymphoma

-ilpsiofthism .l. (B) Leiomyosarcoma
.1. (B) Leiomyosarcoma

.i. (C) Squamous cell carcinoma t'. (C) Squamous cell cucinoma

* (D) Non-Hodgkin lymphoma r-

I CA S E6l
*d-,"r,.iJ:;fii:i!ry"';":fl1:il"T,:?::1""'*1,.
arthritisofthe hipsandknees.Recmtly,he hashadepigasticpain
with nauseaandvomiting'andan episodeof henaionisis. On'
physicalexamination, thereareno remarkablefindings.A gastric
biopsyspecimenis mostlikely to showwhich of thef;llow;g
lesions?
* (A) Epi6elial dysplasia
{. (B) Helicobacterpylori infection
reASEtl
A 44-year-oldwomanhashadinueasingdifficulry
swallowingliquids md solidsfor the past6 months. On physical
examinetr'on,
her fingershavereducedmobility becauseoftaut,
nondefonningskin. A bariumswallowshowsmarkeddilationof
'JreesophaguswidJn tbedista.lportion.rvherethereis
mafl(edtunmal narrowrng.A biopsyspecimenflom drelower
esophagusshowsprominentsubmucosalfibrosis with little
inflammation.Whichof thefollowingis mostlikely to produce
thesefindings?
+ (A) Portalhwertension
A (B) Iron deficiency

't' (D) Adenocarcinoma * (C) Barren esophagus

- *
a

I CASE8 | A 35-year-old
manhashad epigastricpainfor over I lCASEel
A 2?-year-old
manhassudden onsetofmarked
abdominal
pain. Onphysical
examination,
hisabdomenis
J#il:i:i
ffi;:*".';,::::T:*..
beginsa 2-week courseof antibiotics,but on day 4, he feelsbetter
ffiemicroscooic
appearance ofa sectionlhroughtheexcisedileum is shownin rbe
next figure. Which ofthe following additionalcomplicationsis
md discontinuestreatrent. Severalweekslater,the epigastricpain
tle patientmost likely to develcpas a resultofthis disease
recurs. If the patientdoesnot seekfurther featnent, which of the
orocess?
followingcomplications is hemostlikely to develop?
.:. (A) Enterocutaneous
fistula
{'-
.:. (B) Fatmalabsorption\
.:.-
.|. (C) Hepaticmetastases a (C) Intussusception
* (D) Hepaticabscess
* (D) VitaminB, deficiency

._f)A -n
1l
r) r )c f\tl
/
2

8 ) R 1)
 ICASE
roI
A 46-year-oldwomanwith a lengthyhistoryofheart_
bum and dyspepsiaexperiencessuddenonsetofabdominal pain.
On physicalexamination,shehas severemidepigastic pain with
glarding. Bowel soundsarereduced.An abdominatnlain filrn .
radiographshowsfiee air underthe leff leafofthe diaphragrn.The
patientis immediatelytakento surgery,and a perforatedduodenal
ulceris repaired.Whichof the followioilir rnostlikely
to haveproducedthesefindings?
.:. (A) Campylobacterjejuni
* (B) Cryptosporidimpanum
{. (C) Entamoeba
histolyica

ll I
ICASE
A 59-year-old
manhashadincreasing
difficulty
swallowingduringthepast6 months. Thereareno significant
findingson physicalexaminatjon.Uppergastrointestinal
endoscopy showsareasoferythematous m-ucosaabov.thfl
A biopsyspecimenfrom tbeloweresophagus hasthemicr6Glli
appearance shoun in the nextfigure. As a consequence
of this
patient'scondition,whichofthe following complicationsis most
likely to occur?
{. (A) Hematemesis
+ (B) Squanouscell carcinoma
*
* (D) Lacerations
(Mallory-Weiss
slrndrome)

lrl
IcASE
A 49-year-old
womaaseesherphysicialbecause

q- + (B) Diverticulitis
self-iifriiffi*-md diarrhea,which haveoccurredseveraltimes
- {. (C) Primarybiliarycinhosis
during the past20 years. Eachepisodelastsabout2 weeksand
resolves withouttreabent. Findingson physicalexamination (D) Fatmalabsorption
ae
unremarkable, but a stoolsampleis positivefor occultblood. * (E) Pqirectal fistula formation
LaboratoryshJdiesshowno ova or parasitesin the stool.
Colonoscopyshowsdiffirseand uninterruptedmucosal
inflammationandsuperficialulcerationextendingfrom the rectum
to the ascendingcolon. Colonic biopsy specimensfiom the area
show a difrrse, predominmtlymononuclea, infilfate in the
laminapropria. Thepatientis at high risk of developing which of
thefollou.ingcomplications?

3
I D\ D tl\ t?)
 lcesrrg I |co'EA
A 4l-yer-old manhasbeenHIV positivefor $e past8 A 67-year-oldwomm hasexperiencedseverenausea
yearsandhasbeenreceivinghighly activeantiretroviraltherapy vomiting,erJy satiety;anda 9-kgweightlossoverthe past4 months.
for the pastyear. For the past 2 weeks,he has experiencrdpain On physicalexamination, sbehasmild musclewasting. Upper
whm swallowing.He hashadno episodes of hematemesisand gastrointestinalendoscopyshowsthat the entiregastricmucosais
no nauseaor vomiting. Thereae no remarkablefindings on croiefi tnf, nac rn erunrn,r^r'.
1E "-^-
physicalexamination.Tlte CD4+ lymphocytecountis now gastomlestinalradiographsshowthat the stomachis small and
285/pl. Whichof 0refollowingconditionsis mostlikely to shrmken. Which of the following is most likely to be found on
producethesefindings? histologicexaminationofa gastricbiopsyspecimen?
+ (A) Esophageal
squmouscell carcinoma * (A) Earlygasric carcinoma
* (B) Achalasia {. (B) Chronic atrophicgastritis ltnths
{. (C) Loweresophageal
fibrosiswith stenosis t (C) Granulomatous
inflammation VlaSheat
{-

151
ICASE
A 5l-year-old
manhassudden
onsetofmassive

ilffi*i,lH:i.;*Ti: ",ti*',i,,
blood pressure85/50mm Hg. Laboratorystudiesshow a -o
atocrit of 2 I o/0.The serologictest resultfor HBs Ag is
positive.He hashadno prior episodes ofhematemesis. The
hematemesis is mostlikely to be a consequence ofwhich ofthe
followine?

.!. (B) Barrett esophagus

-r. (C) Candidaalbicansinfection

* (D) Squamous
cell carcinoma

16l
IEASE I CASE17I
An I I -month-oldpreviouslyhealdrinfant hasnot
produceda stool for I day. The mothernoticesthat the infanfs
parn fbr I swallowsfood. Physicalexaminationshowi abdomenis distended.On physicalexamination,the infant,s
no abnonnalfindings. Uppelgashointestinal endoscopy shows0.5- abdomenis very tenderandbowel soundsarenearlyabsent.An
to 0.8-ommucosalulcersin theregionofthp middleto lower .
abdominalplain filrn radiographshowsno free air, but thereare
esoplragus.The shallowulcersareround,sharplydemarcated, and distendedloopsof smallbowel with air-fluid levels. Which of the
havean erythematousbase. Which of tlre follou.ing is mostlikely to
followingis mostlikely to prodpcethesefindings?
producethesefindings?
'!. (A) Meckeldiverticulum
* (B) Hirschsprung
disease
+ (B) Gastroesophageal
reflux disease
.!. (C) Pyloric stenosis
* (C) Candidaesophagitis
+ (D) Mallory-Weisssyndrome

laD
,rf \

lq\ r') /dA tb) A t7) D

 FASErsI I CASEle I
A 22-year-oldwomanhashad severalepisodesof
aspirationof food associatedwith difficulty swallowingduring the A 20-year-oldwomanin her ninth month ofpregnancyhas
rncreasingpain on defecationandnoticesbright red blood on the
auscultation,cracklesareheardat the baseofthe
toilet paper. Shehashadno previousgashointestinalproblems.
barium swallowshowsmarkedesophageal dilation After shegives birrh, the rectalpain subsides,andthere.isno more
ofthe loweresophageal sphincter.A biopsy
specimenfrom the lower esophagusshowsan absenceofthe bleeding.Which ofthe follou'ingis themostlikely causeofthese
myentsricganglia. Which of tbe following is the mostlikely findings?
diagnosis?
t (A) Hiatalhernia * (A) Colorectalcmcer
* (B; Plmmu-Vinsonsyndrome t'. (B) Ischemiccolitis
* (C) Barett esophagus * (C) Intussusception
.l (D) Systemic
sclerosis t-
t'(E) Volwlus

CASE20 CASE2I
A 38-year-old manwho hasbeenHIV nositivefor I 0
A 24-year-oldwoman gives birtl to an infant at term yearshashad severenauseaandvomiting for the past2 weeks, On
after an unconplicatedpregnancy. The infant's lengthandweight physicalexamination,he is afebrile. A stool samile is positivefor
areat the55epercentile.Thse is no significantpassage of occultblood. The abdornenis not distended,theri areno palpable
;riiEe davsaitrbrnn' rirenrmt vom*s ariorai massesor orgaromegaly,andbowel soundsarepresent.The
fll
leedrngs.Un physlcalexamlnation, $e infantis afebrile,but the patienthas oral thrush. Thereare severalreddisb-purple,0.5- to 1
abdomenis distendedandtcnderandbowels soundsarereduced. -
cm noduleson the skin ofthe trmk. Laboratorystudiesshow a
An abdominalultasound scanshowsmaked colonic dilation above CD4+lymphoc)4ecout of I I 8/pL. Uppergashointestinal
narrowsepent in the sigmoidregion. A biopsyspecimen from the ardoscopyshowsI 2 reddish-purple, 0.6 to I .8 crn,gastricmucosal
narrowedregion showsan absenceofganglion cells in the muscle nodules.A biopsyspecimen ofthe nodulesis mostlikelv to show
wall andsubmucosa. Whichof tbe followingis mostlikely to whicbof the followingneoplasms?
producethesefindings?
* (A) Adenocarcinoma (B) Non-Hodgkinlymphoma
*- (B)Trisomy2l
{' (C) Tubularadenoma
* (C) Volwlus (D) Colonicatresia
r- (E)Squamouscellcrcinoma
.!. (E) Intussusception

ICASE 22 | A 27-year-old manhashadintermittentcrmping

abdominalpain andlow-volumediarrheafor severalweeks. On E sErIA 49-yetr-old man has complained ..heartbum',
of affer
physicalexamination, he is afebrile;thereis mild lowerabdominal meals for the past decade, There are no remarkable findinss on
tendemess but no masses, md bowelsouds areDresent.A stool physical examination. Upper gastrointestinal endoscopy.ii.
sampleis positivefor occultblood. The symptomssubsidewithin I
week. Six monthslater,the abdominalpain recus with perimal
pain. On physicalexamination,thereis now a perhectalfistula.
themucosashou's
Colonoscopy showsmanyareasofmucosaledemaandulceration Whichof the following
and someareastlat apper normal. Microscopicexaminationof a
biopsyspecimenfrom an ulceratedareashowsa patchyacuteand
chronic infl ammatory infi ltrate, cr)?t abscesses,an{sevqral-_ t (A) Esophageal
varices

Iryglrc. which;f rhefouo*ing*:ildlffi + (B) Radiation6erapy

explainsdresefi ndings?
{. (C) Achalasia
(B) Amebas
t (C) Shigellosis (D) Sarcoidosis
+ (E) Iron deficiencymemia
.1.(E) Ulcerativecolitis

.5
\s)v n) D 20\ A ?\D AA B) D
 :t

A 65-year-oldwomm goesto her physisianfor a

ree
routinehealli maintenanceexamination. A stool sampleis A 45-year-oldwomanhashad increasingabdominat

lffifi"Sii#frffi
distentionfor the past6 weeks. On physicalexamii.t"",-O"*
i.
al abdominalfluid wave andbowel soundsarepresent.
Paracentesis yields1000mL ofslightly Uouayserous
hula.-
most likely to developin this patient? Cytologic examinationof the fluid showsrr"tign-t
consistentnith adenocarcinomalhe patient,Jmedical""ii,hisory
* (A) Adenocarcinoma
:1 indicatestlat shebashadno majormedicalillnesses
andno
'- surgrcatprocedures.Whichoftle followingconditions
is most
-:a4
= A (C) Bowelobstilction
likely to havepreceded the development
ofthe adenocarciloma?
::=
.:a:4 A (D) Malabsorption
ta (A) Ulcerativecolitis (B) Crohndisease

.!. (E) Toxicmegacolon f. (C) Diverticulosis (D) Coloncucinoma

* (E) Hirschsprung
disease
=

ICASE,;I
A 32-year-old man seesthephysicianbecausehehas
l*sEA
experien_cednauseaandvomiting for tbe iasi week. On physical
exmttrauon,he appears man
cachecticandsaysthathehasnoticeda
I 5-kg weight loss overthe past2 months. A I 0_cmnontender
massis palpablein themidabdominalregion. Aa abdominal overthepast24 hours. On pbysicalexamination. there
CT is difrrse abdoninal tendemess.n e
scanshowsthat the mass i. tyrnpaofi--'-
widrout a fluid wave,andbowel sounds "Utiorr"n
areneady abselt. Tiere
is well-healed,S-crntansversescarin the rigtrt lower quadrani
of
*
theabdmen. Thereisnocapurmedusae.,{stool
;ilL'
*(A) Bluutingatrdflatteningofvilli eontainingincreased negativefor occult blood. An abdominalplain filrn
radiopranh
numbersoflymphocytesandplasmacells showsdilatedloopsof smallbowelwith air-fluiaf"uelr,
U-uitlo"
.1.(B)Denselypackedtubularglands 1t i::::li f lparotomr, the sugeonnotices,a 20-"r p;;;
linedby dysplastic
cellswith or reqdrsb:btackilew that changesabruptlyto pink_aDDetrins
n)perchromahcnuclei
on bothdistalandproximalmargins.Tte patieni,smeiical
::wet
historvis simifienr nntvfn .-;-
"-
of the followingis mostlikely ro iave producidtbeffirfinrs? -
* (D) Irregularulcerationwith chronic inflammation -1g_!,j;;
and
Eanulomaformation

€. (A) Adenocarcinoma ofthe ileum

E
.i. (C) Croh disease

t!'(D) Vohulus
* (E) Intussusception

6
;q) ;.s) a L "\ ( ^ ar\g