Stones of the gall bladder :

Objectives:

1-Anatomy & function.

2-pathogenisis.

3-Riskfactors.

4-Morphology.

5-Clinical picture.

6-Complications.

Anatomy:

**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.

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

Functions:

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

n.

incidence: affects 10-20% of adult population.

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.

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.

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.

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

Cholesterol stones Pigment stones

1- pure cholesterol stones:Solitary, oval, large, smooth, yellow

whiteC/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:

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.

Mucocele of the GBMucocele of GB by US

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.

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.

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.

Clinical picture:

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

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

Morphology:

Except for the presence or absence of calculi, the 2 forms are morphologically similar:

1-Gross picture: GB is distended & tense,theserosal surface is coated with fibrinousexudate,lumen is filled with pus mixed with green bile.

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

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.

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.

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 .

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 .

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.