Stones of the gall bladder

1. Stones of the gall bladder :

2. Objectives:
 1-Anatomy & function.
 2-pathogenisis.
 3-Riskfactors.
 4-Morphology.
 5-Clinical picture.
 6-Complications.

3. Anatomy:

4. **The gall bladder is a pear shaped organ measuring about 9
cm in length and has a capacity of approximately 50 ml.
**located in the right upper abdominal quadrant. Hangs on
it’s bed on the visceral surface of the liver with neck lying
superiorly & fundus inferiorly .
**composed of :
1-Fundus.
2-Body.
3-Neck that tapers into cystic duct which combines with the
CHD forming the CBD which enters the second part of the
duodenum.

5. The wall is composed of :
 1- mucosal layer: of columnar smooth epithelium
which becomes larger and more numerous at the neck.
 2- smooth muscle layer of: inner longitudinal-
middle oblique-outer circular.
 3- perimuscular layer :of fibrous connective tissue.
 4-Serosal layer :incomplete

6. Functions:
 Storage and concentration of bile secreted by the
liver and deliver it into the intestine for digestion
and absorption of fat.

7. n.
incidence: affects 10-20% of adult population.

8. Types:
1-Cholesterol stones : more than 80%
A- pure: rare.
B-mixed : most common.
2-pigment stones: 20%... due to excess circulating
bile pigments eg. Chronic hemolytic anemia.

10. Pathogenesis:
 1-cholesterolsupersaturation in
bile.
 2-Crystal nucleation.
 3-Stone growth.
-Bile is composed of bile salts,
phospholipids, cholesterol.
- If there is imbalance between those
components cholesterol will
precipitate out of solution
(cholesterol super-saturation) .
- -GB hypo motility promotes
formation of mucus sludge and
nucleation of cholesterol into
filaments.
- this hyper secretion of mucus traps
the filaments permitting accretion
into stones.

11. Risk factors:
 Genetic: more in the first degree relatives.
 Sex: females are twice> the males .
 Age: more than 40.
 Diet: obesity –lack of dietary fibers.
 Hormonal: pregnancy & OCPs increase the hepatic
cholesterol uptake and synthesis.
 Drugs: treatment by hypocholesterolemic agents .
 GIT diseases e.g. crhon’s disease, ilial resection, ilial bypass
are associated with increase in hepatic cholesterol uptake.
 hemolytic anemia ( pigment stones only):increase content
of un conjugated bilirubin in bile.
 Geographically: more in western world.

12. So…it is a disease of 5 f: Fatty ,Ferile ,Female, in their Fourties
or Fifties.

13. Cholesterol stones Pigment stones
1- pure cholesterol stones:
Solitary, oval, large, smooth, yellow
white
C/S.:radiating glistening crystals.
2-Mixed: multiple faceted variable
sized
C/S :laminated alternating dark
pigment layer and and pale white
layer.
 Multiple ,small jet
black,mullberry shaped,Gb is
healthy, not inflammed and
has normal thin wall
 C/s:soft black(radioopaque)
Morphology:

21. Clinical picture:
 80% are asymptomatic, sometimes, mild dyspepsia and constant or
colicky striking biliary pain.
 Symptomatic gallbladder disease develop only when complications
develop.
 complications:
 1- Acute and chronic cholecystitis.
 2-Cystic duct obstuction at the neck leading to mucocele or
empyema.
 3-CBD obsruction …ascending cholangitis or acute pancreatitis.
 4-Fistula formation and intestinal obstruction ( gall stone ileus).
 5- Cancer of the gallbladder.

22. Mucocele of the GBMucocele of GB by US

23. Cholecystitis :
 Definition: inflammmation of the gallbladder.it may be:
1-Acute.
2-Chronic.
3-Acute on top of chronic.
I-Acute cholecystitis
 In many ways ,similar to acute appendicitis, condition begins with obstruction
leading to inflammation.
 Etiopathogenisis: based on initial mechanism, occurs in two types of situations:
1-Acute calculus cholecystitis.
2-Acute acalulus cholecystitis.

24. Pathogenisis :
A-Acute calculus: is due to obstruction of the gall
bladder neck or the cystic duct by a gall stone
,causing obstruction of the bile outflow which in turn
leads to disruption of the protective glycoprotein
layer, the inflammation is :
 Initially due to release of prostaglandins from the
wall.
 Later..by 2ry bacterial infection chiefly E.Coli.

25. B-Acute acalculus cholecystitis
 10% of cases.
 Here , inflammation is due to dehydration, Gallbladder
stasis, vascular compromise & bacterial contamination
by variety of causes:
1-Previoys non biliary surgery.
2-Burns.
3-Multiple injuries.
4-Recent childbirth.
5- Severe sepsis.
6-Torsion of the gallbladder.

26. Clinical picture:
• 1-Severe upper abdominal pain radiating to
the right shoulder with: guarding & tender
palpable gallbladder.

27. 2-Jaundice,fever, leucocytosis, are
generally presentwhen CBD is obstructed.
• N.B. :In acute acalcular ,the same except
that the symptoms are masked by the
severe clinical condition.
• course:
A mild attack subsides spontainously over
1- 10 days,while 25 %require
cholecystectomy

28. Morphology:
 Except for the presence or absence of calculi, the 2
forms are morphologically similar:
 1-Gross picture: GB is distended & tense,the
serosal surface is coated with fibrinous
exudate,lumen is filled with pus mixed with green
bile.

30. 2-Mp: the wall shows marked inflammatory
edema, congestion and exudation, may be frank
abscesses in the wall &gangrenous necrosis with
rupture of the peritoneal cavity.

35. II- Chronic cholecystitis
 The commonest type of clinical GB disease.
 Pathogenisis:
It is a GB inflammation that has lasted along time.
it almost always results from gall stones and from
prior attacks of acute cholecystitis. Sometimes , it
occurs de novo. the cause is super saturation of
bile.

36. Morphology:
1-Gross picture:
 GB is usually contracted but may be normal or
enlarged with the wall thickened.
 On cross section, opaque grey-white appearance.

37. 2-Microscopic picture:
 Thickened and congested mucosa.
 Variable degree of chronic inflammatory reaction consisting of
lymphocytes, plasma cells and microphages.
 In severe cases: Sub epithelial and Sub serosal
fibrosis and mononuclear cell infiltration .

40. Clinical picture
 Recurant attacks of constant or colicky dull
aching pain in the right hypo-chondrium or
the epigastrium.
 Nausea and vomating .
 Intolerance to fatty meals .

41. complications
 Empyema , cholangitis, sepsis
 Perforation due to gangrenous necrosis leading to local abscess
formation or diffuse peritonitis
 Intestinal fistula
 Aggravation of the pre-existing medical illness.