Professional Documents
Culture Documents
R STONES
Presented by:
Amer AlQaisi
Faisal AlEnezi
:Supervised by
Prof. Kamal Gharaibeh
OUTLINES
1.Anatomy
of gallbladder
2.Anatomy of biliary tree
3.Physiology of biliary system
4.Bilirubin metabolism cycle.
5.Congenital abnormalities
6.Gallstones
7.Complications of gallstones
8.Clinical presentation & Management
9.Choledocolithiasis & cholangitis
10.
Neoplasms
Anatomy of Gallbladder
Gallbladder is a pear-shaped sac lying
on the undersurface of the live which is
7.5-12 cm long and it has a capacity
of 30-50 ml.
It is divided to :
- Fundus
- Body
- Neck
The Hartmann's pouch : is a dilatation
in the gallbladder just before the
origin of cystic duct .
Relation:
Anteriorly :
the anterior abdominal wall and
.the inferior surface of the liver
Posteriorly
:
the transverse colon(proximal)
.1st and 2nd part of duodenum
The
Blood supply:
- by the cystic artery , a branch from the
right hepatic artery .
- cystic vein which drain directly into the
portal vein.
Nerve supply:
supplied by 3 types of innervation,Theceliac
plexus supplies sympathetic innervation,
thevagus nervesupplies parasympathetic
innervation, and theright phrenic
nerveconveys sensory information.
There are a small ducts that drain bile directly into the
. gallbladder from the liver, called Duct of Luschka
PHYSIOLOGY
PHYSIOLOGY
The second main function of the gall bladder is concentration of
bile by active absorption of water, sodium chloride and
bicarbonate by the mucous membrane of the gall bladder. The
hepatic bile that enters the gall bladder becomes concentrated
510 times, with a corresponding increase in the proportion of
bile salts, bile pigments, cholesterol and calcium.
The third function of the gall bladder is the secretion of mucus
approximately 20 ml is produced per day. With total obstruction
of the cystic duct in a healthy gall bladder, a mucocele develops
on account of this function of the mucosa of the gall bladder.
Bile
Components of bile:
Water 95%
electrolytes
bile salts (like cholic acid & chenodeoxycholic acid )
phospholipids ( like licithin)
bilirubin (conjugated)
fatty acids
BILIRUBIN PRODUCTION
Heme proteins
myoglobin, cytochromes
(to 25% 20)
Hemoglobin
(to 80% 70)
Heme
Heme oxygenase
Biliverdin
Biliverdin reductase
Bilirubin
albumin
indirect
unconjugated
pre-hepatic
BILIRUBIN PROCESSING
albumin-Bilirubin
albumin
ligandin
hepatocyte
ligandin-Bilirubin
UDP-Glucuronyl
transferase
ER
Bilirubin diglucuronide
direct
conjugated
post-hepatic
BILIRUBIN EXCRETION
Bilirubin diglucuronide
glucuronate 2
liver 90%
Bacterial enzyme
Bilirubin
Bacterial enzyme
intestines
Urobilinogen
<-------kidneys 10%
20%
Bacterial enzymes
80%
Stercobilinogen
Stercobilin
Urobilin
urine
feces
CONGENITAL ABNORMALITIES
Absence of the gall bladder
Occasionally, the gall bladder is absent. Failure to
visualise the
gall bladder is not necessarily a pathological problem.
The Phrygian cap
present of septum that incompletely divides the GB.
(SINGLE OR MULTIPLE)
CHOLEDOCHAL CYST :
BILLIARY ATRESIA
- Biliary atresia (BA) is a progressive, idiopathic, fibroobliterative disease of the extrahepatic biliary tree that
presents with biliary obstruction exclusively in the neonatal
period.
- The extrahepatic bile ducts are progressively destroyed by
an inflammatory process, which starts around the time of
birth. The aetiology is unclear. The inflammatory destruction
of the bile ducts has been classified into three main types :
type I: atresia restricted to the common bile duct;
type II: atresia of the common hepatic duct;
type III: atresia of the right and left hepatic ducts.
-Associated anomalies include, in about 20% of cases, cardiac
lesions, polysplenia, situs inversus, absent vena cava and a
preduodenal portal vein.
COMPLICATIONS :
-Ascending cholangitis
Intrahepatic changes can occur and eventually
result in biliary cirrhosis and portal hypertension.
Untreated, death from the consequences of liver
failure occurs before the age of 3 years.
GALLSTONES
Risk factors :
The big 5 : five Fs : female 3:1 , forty (>40) , fat ,
fertile,fair.
less common :
-Oral Contraceptives. - Rapid weight loss.
-Hyperlipidemia -Gallbladder stasis.
-Family history
-Ileal diseases or resection
Types of GB stones :
1. Cholesterol 20 %.
2. Pigmented ( Black , Brown ) 5 %.
3. Mixed 75 %
Pathogenesis:
When bile is supersaturated
with cholesterol, unstable
unilamelar phospholipid
vesicles are formed.
(Cholesterol > 80%)
This leads to formation of
cholesterol crystals.
Characteristics :
Yellowish
, greasy.
Ovoid
, firm
Single
or multiple
Most
are radiolucent.
CHOLESTEROL
STONES
stones :
Brown
Stones :
Form
bile.
Associated
PIGMENTED STONES
Characteristic :
MIXED STONES
In gallbladder :
- Acute cholecystitis.
- Chronic cholecystitis
- Biliary Colic
- Empyema.
- Mucocele.
- Perforation
- Carcinoma (0.08%)
In the intestine
- Gallstone ileus
(intestinal obstruction)
BILIARY COLIC
Caused by:
- Transient obstruction of the GB by a stone in
Hartmanns pouch or cystic duct , which leads to
spasm in the wall of GB
Presentation:
pain:
S:Right upper quadrant.
O: suddenly after fatty meals
C: gripping pain, dull.
R: referred to the tip of the right shoulder and
radiate to the back
A: Associated with - Nausea, vomiting, flatulence,
dyspepsia .
T: Less than 6 hours, if more then it is acute
cholecystitis.
ACUTE CHOLECYSTITIS
Definition:
Inflammation of the gallbladder that
develops over hours, usually resulting from a
cystic duct obstruction by a gallstone.
This form of gallbladder disease usually
subsides within 1 to 7 days with a
conservative plan of treatment .
Pathophysiology
5
4
CLINICAL PRESENTATION
(ACUTE CHOLECYSTITIS)
Age : Typically 30-60 year old.
Presentation in younger patients, may be due
to congenital hemolytic anemia(sickle-cell
disease often form pigment stones, which
may precipitate an attack of acute
cholecystitis).
Gender : Females are more commonly affected
Analysis of Pain:
S: RUQ
O: sudden onset
C: sharp
R: radiates to the back (close to the inferior angle of
right scapula)
A: associated with nausea , vomiting and fever
T: continuous , Duration of pain usually >6 hours
E: aggravated by movements and breathing
S: severe
*The patient May have previous history of flatulent
dyspepsia or biliary colic .
PHYSICAL EXAMINATION
General Examination :
_ Patient appears ill
_ shallow breathing
_ Tachycardia +ve, Pyrexia +ve
PHYSICAL EXAMINATION
Abdominal Examination :
INVESTIGATION
5.
6.
7.
1.
2.
3.
4.
8.
9.
2)
3)
4)
5)
It occurs because of :
1) Dehydration
2) GB stasis
3) Vascular compromise
4) Bacterial contamination
( mostly Gram ve: E-coli , Klebsiella , Enterobacter )
CHRONIC CHOLECYSTITIS
PRESENTATION
-Upper abdominal pain after eating.
((begins 15 to 30 mins after a meal,
and last for 30 to 90 mins))
(most common complaint).
- flatulent dyspepsia(post-prandial belching)
- Heartburn
PHYSICAL EXAMINATION
Signs of jaundice
Abdomen looks normal
RHC mass and tenderness
Percussion and auscultation should be normal
MANAGEMENT
CHOLECYSTECTOMY
Usually we do it by laparoscopy,
but in the following cases we do it by Laparotomy :
1.
2.
3.
POST OPERATIVE
COMPICATIONS
1- hemorrhage
**usually the source is from cystic artery.
** the patient complains of persistent abdominal pain,
or features of hypovolemic shock
2- wound infection
3- bile leak
4-bile duct stricture
**the most dangerous complication , leads to :
cholangitis , obstructive jaundice ,
secondary biliary cirrhosis and hepatic failure.
NEOPLASMS
PORCELAIN GB
CHOLEDOCOLITHIASIS
- Stones present within the biliary tree.
- Stones may be:
1) derived from gallbladder
2) primary ductal & intrahepatic stone formation
- Asymptomatic in 10%
- Symptoms due to:
1) cholangitis (Charcots triad), biliary obstruction
(Obstructive Jaundice , Dark urine , Pale stool ,itching)
2) pancreatitis
3) Liver abscess
4) chronic liver disease with secondary biliary cirrhosis
5) acute cholecystitis
CHOLEDOCHOLITHIASIS CAN BE
PRIMARY OR SECONDARY
CHOLANGIOCARCINOMA