CARCINOMA ESOPHAGUS - DR ZAHID IQBAL MIR Dr. Zahid Iqbal Mir, MBBS MS (General Surgery), DNB (General Surgery) has done his MBBS and masters in General Surgery from the prestigious Govt Medical College Jammu and DNB in General Surgery from NBEMS New Delhi. He is a passionate surgeon, earlier practising at Government Medical College, Jammu as Registrar in Department of General Surgery. Nowadays working as Senior Resident in Department of General Surgery, Government Medical College & Hospital, Sector 32, Chandigarh and a rising name in field of surgery. He is an enthusiastic, enigmatic and dedicated teacher as well. He is not just a resolute learner, but also an awe inspiring guiding light for his juniors, which makes him the most loveable and respected senior. Currently he is running “LOVE FOR SCALPEL” for PGMEE aspirants on most of the social platforms, which is gaining immense popularity among residents, medical graduates and undergraduates.

1. GALL BLADDER CARCINOMA
PATHOGENESIS
PATHOLOGY
PRESENTATION
GBC GROUPS
Ø SACHI NEGI, 78, 2K17
Dr. ZAHID IQBAL MIR (SENIOR RESIDENT)
MBBS, MS Surgery, DNB Surgery

2. PATHOGENESIS

3. Differences in the demographics, clinical presentation,
and gender distribution suggest that there are TWO
key pathways to developing GBC.
CHOLELITHIASIS
&
RESULTANT
CHOLECYSTITIS
ANOMALOUS
PANCREATICO-
BILIARY JUNCTION

4. CHOLELITHIASIS
CHOLECYSTITS
PREDISPOSE
TO
MALIGNANT
CHANGE
PROMOTER FOR
CARCINOGEN
EXPOSURE
PROMOTER IN
GENETIC PRE-
DISPOSITION
CHRONIC
IRRITATION OF
GALL BLADDER
MUCOSA
ü Seen in areas where GBC is
associated with gallstone
disease, female gender bias, and
age > 65
ü Gallstones present in 70-90 % of
patients with GBC
ü Overall incidence of GBC in
patients with cholelithiasis is
0.5-3%.
ü Higher with larger gallstones
and longer duration of
cholelithiasis.

5. ANOMALOUS PANCREATICOBILIARY DUCT JUNCTION
NORMAL
Normally, the main pancreatic duct and the
common bile duct open into the second part of
the duodenum alone or after joining as a
common channel.
The mean length of the common channel is
about 4-5 mm.
In AUPBD connection between CBD & MPD is outside the duodenal wall – LONG COMMON CHANNEL

6. üGBC - Occur at a younger age,
show less female gender bias,
lower incidence of associated
cholelithiasis.
üHigh proportion of cases of GBC
in Japan.
üKRAS mutations and relatively late
onset of p53 mutations.
AUPBD KOMI CLASSIFICATION

7. OTHER RISK FACTORS

8. GALL
BLADDER
POLYPS
PRIMARY
SCLEROSING
CHOLANGITIS
CONGENITAL
BILIARY CYSTS
CHRONIC
SALMONELLA
& H. PYLORI
INFECTION
CARCINOGEN
EXPOSURE
PORCELAIN
GALL BLADDER
OBESITY
and
HIGH BLOOD
SUGAR

9. PORCELAIN GALL BLADDER
üAka calcified
gallbladder, calcifying
cholecystitis, or
cholecystopathia
chronica calcarean.
üAssociated with
cholelithiasis in more
than 95 % of cases.
üRecent studies :-
approx 2-3% of cancer
develops in these
cases.

10. GALL BLADDER POLYPS
CLASSIFIED INTO
MALIGNANT BENIGN
NON NEOPLASTIC NEOPLASTI
C
CHOLESTEROL
POLYPS
INFLAMMATORY
POLYPS
ADENOMYOMAS
ADENOMAS
LEIOMYOMAA
• Outgrowths of the gallbladder mucosal wall.
• Usually found incidentally on USG or after cholecystectomy.

11. • The incidence of gallbladder cancer is high, upto
77% in polyps larger than 1 cm.
• Gallbladder polyps exhibit a high rate of
malignancy in patients with PSC.
• Sessile polyp (including focal gallbladder wall
thickening >4 mm) increases 7 fold risk
• Age >50 yrs has a higher incidence of malignant
polyps

12. PRIMARY SCLEROSING CHOLANGITIS
• A higher risk of gallbladder
mass lesions is reported in the
chronic inflammatory state
associated with primary
sclerosing cholangitis.
• Therefore, an annual screening
ultrasound of the gallbladder is
recommended in these
patients.

13. GALL STONES
ACT AS PERSISTENT NIDUS
FOR INFECTION
CHRONIC INFECTION
AND INFLAMMATION
CHRONIC SALMONELLA INFECTION

14. CHRONIC H. PYLORI INFECTION
ü Helicobacter bilis - gallbladder disease,
including GBC
ü Detection of Helicobacter-derived cytotoxins
and surface proteins

15. CARCINOGEN EXPOSURE
üPeople working in the oil, paper, chemical,
shoe, textile, and cellulose acetate fiber
manufacturing industries.
üMiners exposed to radon
üCigarette smokers

16. PATHOGENESIS & PATHOLOGY
• Adenocarcinomas involving the gallbladder
progress from dysplasia to carcinoma in situ, and
then to invasive cancer.
• Gallbladder adenomas are rarely found in the
context of dysplastic changes

17. TUMOR TYPE % OF TOTAL
ADENOCARCINOMA (Mc) 76%
PAPILLARY 6%
MUCINOUS 5%
ADENOSQUAMOUS 4%
SQUAMOUS 2%
OAT CELL 0.5%
NON SPECIFIED 8%

18. ØAdenocarcinomas originate as mucosal
lesions invading the gallbladder wall as they
grow
ØThe lack of a well-defined muscularis layer
permits early vascular, lymphatic, and neural
invasion.
ü Grossly, GBC can appear infiltrative, nodular,
papillary, or a combination
ü Papillary carcinomas - most favorable prognosis

20. CLINICAL PRESENTATION

21. üEarly invasive GBC - most often asymptomatic /
nonspecific symptoms that mimic cholelithiasis or
cholecystitis.
üAmong symptomatic patients, the most common
complaint is pain, followed by anorexia, nausea, or
vomiting.
üPatients who present like acute cholecystitis more
often have earlier stage disease and a better long-
term outcome

22. Direct invasion of
the biliary tree.
Metastatic disease
to the region of the
hepatoduodenal
ligament.
unresectability
üThis diagnosis should be particularly suspected if a compression of the common
hepatic duct by an impacted stone in the gallbladder neck is identified (i.e. Mirizzi
syndrome)
üInvasion of tumor into the porta hepatis may also result in duodenal obstruction
May also present with OBSTRUCTIVE
JAUNDICE
CAUSE?

25. COURVOISIER’s LAW
Courvoisier's sign or Courvoisier-Terrier's sign, or Courvoisier syndrome
If gallbladder is palpable in a jaundiced patient, it
is unlikely to be due to gallstones
However, there are exceptions to this rule :-
(eg, chronic pancreatitis, parasitic biliary obstruction, congenital
choledochal cyst, common hepatic duct obstruction proximal to
the takeoff of the cystic duct)
Diagnostic utility of this historical sign is limited now

26. • Rarely, patients present
with extra-abdominal
metastases (lung, pleura)
• Hepatomegaly
• Ascites
• Paraneoplastic
syndromes (eg, ectopic
hormone secretion or
acanthosis nigricans)
ACANTHOSIS NIGRICANS

27. Gall Bladder Cancer
GROUPS
üObvious clinical
üSuspected imaging
üUnsuspected at operation
üIncidental at histology
üMissed at follow up
Kapoor. J HBP Surg 2007;14:366-73

28. 28
Gall Bladder Cancer
OBVIOUS
Symptoms
and signs
of GBC
are features of
advanced disease.
Look for mets!
Palpable GB lump
Umbilical nodule

29. Gall Bladder Cancer
SUSPECTED
Liver mets

31. 31
Gall Bladder Cancer
UNSUSPECTED

32. AC LN SMA LN
Gall Bladder Cancer
UNSUSPECTED

33. 33
Gall Bladder Cancer
INCIDENTAL
Incidental gallbladder adenocarcinoma detected in a gallbladder
with focal thickening. A well differentiated morphology.

34. Gall Bladder Cancer
MISSED

35. PATTERNS OF SPREAD
Spread of gallbladder cancer occurs via four routes:
üLocal invasion of the liver or other nearby structures.
ülymphatic dissemination.
üPeritoneal spread.
üHematogenous spread.
Direct extension of gallbladder cancer typically involves
the liver (segments IV and V), bile duct, duodenum, colon,
parietal wall, and/or abdominal viscera

37. REFRENCES

38. THANK YOU !