The gallbladder stores and concentrates bile produced by the liver. Gallstones form when there is too much cholesterol in the bile and can lead to complications like cholecystitis (inflammation of the gallbladder). Cholecystitis can be acute, caused by a gallstone blocking the cystic duct, or chronic from repeated attacks. Symptoms include abdominal pain and fever. Untreated acute cholecystitis can cause gangrenous necrosis or rupture of the gallbladder. Chronic cholecystitis often follows repeated acute attacks and is characterized by a thickened gallbladder wall.

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.