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1. THE BILIARY TRACT
Lecture 30
CHOLELITHIASIS

2. Gall bladder Stores & Concentrates Bile
The commonest location of impaction of a
gallstone is Hartmann’s pouch
Hartmann's pouch is an out-pouching of the
wall of the gallbladder at the junction of the
neck of the gallbladder and the cystic duct.

3. The main function of the gallbladder is to store and concentrate the bile secreted
by the liver and then deliver it into the intestine for digestion and absorption of
fat. The concentrating ability of the gallbladder is due to its absorptive mucosal
surface that has numerous folds.

4. Normally, the liver secretes
approximately 500 ml of
bile per day and the
gallbladder concentrates it
5-10 times. The motility,
concentration and
relaxation of the
gallbladder are under the
influence of a peptide
hormone, cholecystokinin,
released from
neuroendocrine cells of the
duodenum and jejunum.
Cholesterol,
Bile Pigments,
Calcium Salts
CHOL, GALL Liver secretes 400-800 ml bile per day
Lecithin

5. Cholelithiasis
*Presence of stones in the gallbladder
is referred to as cholelithiasis (from the Greek
chol- (bile) +
lith- (stone) +
iasis- (process).
3% to 4% in Asian countries
Gallbladder (cholecyst, or biliary vesicle, bile bladder)
GALL means BILE or Chol
They are usually formed in the gallbladder, but
sometimes may develop within extrahepatic
biliary passages, and rarely in the larger
intrahepatic bile duct (Pigment stones).

6. CHOLELITHIASIS (GALLSTONES)
Epidemiology
• Gallstones afflict (badly affect)10% to 20% of adult
populations in developed countries.
• It is estimated that more than 20 million persons
in the United States have gallstones, totaling some
25 to 50 tons in weight!
Over 95% of biliary tract disease is
attributable to
cholelithiasis (gallstones).

7. *TYPES OF GALLSTONES
1.Cholesterol stones 20%
2.Pigment stones (Black & Brown) 5%
3.Mixed stones 75%
I. PURE GALLSTONES: Cholesterol stones, Pigment stones, Calcium Stones
II. MIXED GALLSTONES
III. COMBINED gallstones ( shell different & nucleus different).

8. *Pathogenesis or Lithogenesis
• Bile formation is the only significant pathway for
elimination of excess cholesterol from the body,
either as free cholesterol or as bile salts.
Cholesterol is rendered water-soluble by
aggregation with bile salts and lecithins
(Phospholipids).
• When cholesterol concentrations exceed the
solubilizing capacity of bile (supersaturation),
cholesterol can no longer remain dispersed and
crystallizes out of solution.
CHOLESTEROL STONES:

9. Cholesterol gallstone formation involves four
simultaneous conditions:
(1) Supersaturation: The bile must be
supersaturated with cholesterol;
(2) Hypomotility (Stasis): Hypomotility of the
gallbladder promotes nucleation;
(3) Nucleation: Cholesterol nucleation in the bile is
accelerated;
(4) Accretion: Hypersecretion of mucus in the
gallbladder traps the nucleated crystals, leading to
their aggregation into stones (Accretion).
Accretion within the gallbladder mucous layer.

10. Schematic pathogenesis of gallstone formation. (HMG- CoAR = hydroxy methyl
glutaryl-coenzyme A reductase; 7α-OHase = cholesterol 7 α-OHase hydroxylase;
MDR3 = multidrug resistance- associated protein 3).
Cholesterol Stones:
Imbalance between bile salts, lecithin
& cholesterol allows cholesterol to
precipitate out of solution and form
stones.
Pigment Stones: Occur due to excess
of circulating pigments (e.g.,
Hemolytic anemia.

11. The four contributing factors for cholelithiasis: supersaturation, gallbladder
hypomotility, crystal nucleation, and accretion within the gallbladder mucous layer.
A
micelle
is an
aggreg
ate of
surfact
ant
molec
ules
disper
sed in
a
liquid
colloid
1
2 3
4
Cholesterol is essentially
insoluble in water and can be
solublised by another lipid.
Normally, cholesterol and
phospholipids (lecithin) are
secreted into bile as
‘bilayered vesicles’ but are
converted into ‘mixed
miscelles’ by addition of bile
acids, the third constituent. If
there is excess of cholesterol
compared to the other two
constituents, unstable
cholesterol-rich vesicles
remain behind which
aggregate and form
cholesterol crystals.
When cholesterol
concentrations exceed the
solubilizing capacity of bile
(supersaturation),
cholesterol can no longer
remain dispersed and
crystallizes out of solution.

13. Pathogenesis – Pigment Stones
• Formation of PIGMENT stones is more likely in
the presence of UNCONJUGATED BILIRUBIN in the
biliary tree, as occurs in hemolytic anemias and
infections of the biliary tract.
• The precipitates are primarily insoluble calcium
bilirubinate salts.

14. The risk factors most commonly
associated with the development of
cholesterol stones are:
1. ↑Age and Sex-F.
2. Environmental Factors.
3. Acquired Disorders.
4. Hereditary Factors.
Recently, mutation in
CYP7A1 gene has been
found that results in
deficiency of enzyme,
cholesterol 7-hydroxylase,
which has a role in bile
acid synthesis. This
mutation is associated with
hypercholesterolaemia and
gallstones.
Deficiency of dietary fibre content is
linked to higher prevalence of
gallstones. A moderate consumption of
alcohol, however, seems to protect
against gallstones

15. These factors cause enhanced
activity of enzyme, HMG-CoA
reductase, that normally
regulates cholesterol synthesis
and its hepatic uptake.
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16. Any condition in which gallbladder motility is reduced
predisposes to gallstones, such as pregnancy, rapid
weight loss, and spinal cord injury. In most cases,
however, gallbladder hypomotility is present without
obvious cause.

17. Up to 80% of people with gallstones, however,
have no identifiable risk factors other than AGE
and GENDER.
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18. Morphology – Cholesterol Stones
• Cholesterol stones arise exclusively in the
gallbladder and consist of 50% to 100%
cholesterol.
• Pure cholesterol stones are pale yellow; increasing
proportions of calcium carbonate, phosphates, and
bilirubin (Mixed Stones) impart gray-white to black
discoloration .
Pure gallstones, Mixed gallstones and Combined gallstones.

19. Morphology – Cholesterol Stones
• They are Large, ovoid and firm; they can occur
singly, but most often there are several, with
faceted surfaces resulting from their apposition.
• Most (80%) cholesterol stones are radiolucent,
although as many as 20% may have sufficient
calcium carbonate to be radiopaque.

20. Morphology - Pigment Stones
• Pigment stones may arise ANYWHERE in the biliary
tree and are classified into BLACK & BROWN stones.
• In general, BLACK pigment stones are found in
sterile gallbladder bile, while BROWN stones are
found in infected intrahepatic or extrahepatic ducts.
• The stones contain calcium salts of unconjugated
bilirubin and lesser amounts of other calcium salts,
mucin glycoproteins, and cholesterol.
• Black stones are usually small in size, fragile to the
touch, and numerous.

21. Morphology – Brown stones
• Brown stones tend to be single or few in number
and to have a soft, greasy, soaplike consistency
that results from the presence of retained fatty
acid salts released by the action of bacterial
phospholipases on biliary lecithins.
• Because of calcium carbonates and phosphates,
50% to 75% of black stones are radiopaque.
• Brown stones, which contain calcium soaps, are
radiolucent.

22. Mutation in MDR3 gene has
been found that causes defect
in phospholipid secretion from
bile (↓Lecithin), resulting in
cholesterol supersaturation of
bile and cholesterol gallstone
formation.
???

23. Black & Brown

31. RUQ
Murphy
sign

32. Clinical features
• The vast majority of gallstones
(>80%) are “silent,” and
most individuals remain free of
biliary pain or other complications
for decades.

33. Symptoms
Symptoms commonly begin to appear
once the stones reach a certain size
(>8 mm).
Symptomatic gallstone disease appears
only when complications develop.

34. PAIN

35. Pain- Biliary Colic
• The patients with gallstones develop symptoms due
to cholecystitis which include typical biliary colic
precipitated by fatty meal, nausea, vomiting, fever
along with leucocytosis and high serum bilirubin.

36. Pain during inspiration with examiner’s hand on the
GB location.

37. A cholescintigraphy scan, also
known as: Hepatobiliary
Iminodiacetic Acid HIDA, a nuclear
imaging procedure to evaluate the
health and function of the
gallbladder. A radioactive tracer is
injected through any accessible vein,
then allowed to circulate to the liver,
where it is excreted into the biliary
system and stored by the gallbladder
and biliary system.[1]
In the absence of disease, the
gallbladder is visualized within 1 hour
of the injection of the radioactive tracer.
If the gallbladder is not visualized
within 4 hours after the injection, this
indicates either cholecystitis or cystic
duct obstruction. Cholescintigraphy for
acute cholecystitis has sensitivity of
97%, specificity of 94%

39. URSODEOXYCHOLIC ACID
(Hepexa- M)

40. 1. Cholecystitis 2. Choledochlithiasis 3.
Mucocele (Hydrops) 4. Biliary Fistula 5. Gallstone
ileus 6. GB Cancer
Intestinal Obstruction
Or Hydrops GB
Inflam of BD
Pus

41. The invasion of GAS-FORMING ORGANISMS, notably
clostridia and coliforms, may cause an acute
“emphysematous” cholecystitis.

42. "Is there any reward for good, other than good?"