Presiding Officer Training module 2024 lok sabha elections
Gall bladder disease.pptx
1. Gall bladder disease
Mahteme Bekele (MD)
Assistant professor of surgery
Emergency directorate director
Postgraduate program director
SPHMMC
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2. Objectives
• To identify
– Common diseases of the GB
– Common presenting symptoms of GB disease
– principles and options of management GB
disease
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RUQ Anatomy: GB Location
• GB lies inferior to liver
• Between the right and quadrate hepatic lobes
• Hollow viscus in the gallbladder fossa 7-10cm
• Consists of fundus, body, and neck
• Neck tapers to cystic duct
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RUQ Anatomy
Gallbladder
Left
liver
lobe
Hepatic
artery
Portal
vein
IVC
Cystic
duct
Right
liver lobe
Common
Bile Duct
Quadrate
liver lobe
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The Bile Duct System
• Liver makes bile 500-1000ml/day
• Out to common hepatic duct
• Goes to…
– Common bile duct to duodenal ampulla
– Cystic duct to gall bladder
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Gallbladder function
• Reservoir for bile ( contains 40–70 ml bile)
• Concentrates bile up to 5-10x
– water is absorbed
– bile salts and solutes become concentrated
• Secretion of mucous up to 20 ml/d
• Contract &release bile into duodenum
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Gallbladder Anomalies
• Agenesis
• Hypoplasia
• Hyperplasia
• Total reduplication
• Subtotal division of fundus
• Phrygian cap
• Septated gallbladder
• Floating gallbladder
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Cholelithiasis
Incidences
Most common biliary pathology
Prevalence: 6-10 % men, 12-20 % women
Fat, fertile, flatulent, female of fifty.
Majority of gallstones clinically silent
18-50% become symptomatic over 10-15yr
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Classification
Based on stone composition ,location& etiology.
• Composition
– Cholesterol stone
– Pigment stone
– Mixed stone
• Location
– GB
– Extra hepatic BD
– Intra hepatic BD
– Major elements – cholesterol, bile pigments, calcium.
– Others – Fe, P, CO3, mucus,debris
12. RISK FACTORS
• Age >60yrs
• Gender women b/n 20-60 2x risk
•Estrogens
•pregnancy, hormone replacement, pills
•Obesity esp. in women
•Rapid wt loss
• Fasting Diabetes
•SBS , TPN ---- increase PGS
•cirrhosis & hereditary blood disorders
•Vagotomy
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Pathogenesis Cholesterol & mixed stone
occurs in three stages
1) Cholesterol saturation
♣mixed bile acids, lecithin &cholesterol…micelles
♣ any alteration …cholesterol precipitation
♣ due to ↑ed quantity or alteration of the vehicle
…critical step
♣ supersaturation can occur due to
secretion of hepatic bile with either high cholesterol
or low bile acids or lecithin …litogenic bile
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2) Nucleation
cholesterol monohydrate crystals form & agglomerate
…macroscopic stones
promoters or retarding agents
● heat labile GP in the bile as potential pronucleating
factors (e.g GB mucus)
Stasis of bile in the GB
● ↓ GB motility & emptying
● ↑ed calcium
● ↑ PGS
● alteration in GB secretion &absorption
3) Stone Growth
● Due to cholesterol precipitation & agglomeration
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Pathogenesis of Pigmented Stones
Due to
altered solubilization of unconjugated bilirubin
with precipitation of ca bilirubinate & insoluble salts
2 types
1.Brown pigment stones
-common in Asia
-secondary to infection
-release of beta glucuronidase
2. Black pigment stones
-pts with haemolytic dd. & cirrhosis
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Clinical Presentation
I. Asymptomatic
Dx incidentally > 50% of pts with GS
25% of pts within 5 yr…symptomatic
II. Symptomatic or cxn. of GS
biliary Colic
-sudden onset (30-60min) after meal
-increased freq. & intensity with time
-6-10% risk of recurrent each year
-2% risk of comp.
-large solitary stones…acute cholecystitis
-multiple stones<4 cm…acute pancreatitis
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Complications of GS
• IN THE GALLBLADDER
due to mov’t of stones & infection
cholecystitits →acute or chronic
gangrene
perforation
-biliary peritonitis
-biliary-enteric fistula
empyema
mucocele (hydrops)
carcinoma
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Cxn…cont’d
• IN THE BILE DUCTS
obstructive jaundice
cholangitis
Acute pancreatitis
• IN THE INTESTINE
acute intestinal obstruction (GS ileus)
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Cholecystitis
• Could be
acute or chronic inflammation
Calculous or acalculous
• Risk factors: obstruction and bile stasis
• Bacterial growth common but secondary
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ACALCULAS CHOLECYSTITIS
pts with major abdominal & thoracic surgery & TPN
recovering from major trauma
severe burns
Acute emphysematous cholecycistitis
serious form of Ac.
xized by gas in the lumen or wall of the GB
in the elderly pts
25% have DM
CF as AC but pts are more toxic
DX ….air in the gallblader or wall on plain abd. Film
GS in 75% of pts
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INVESTIGATION AND DIAGNOSIS
1. History & P/E
Typical biliary colic
may be associated with
fatty meal intolerances
Nausea and vomiting
Any of the atypical symptoms
Non-specific atypical symptoms like
indigestion,
abdominal bloating
Belching
although commonly reported by patients with gallstones,
are less likely to be caused by cholelithiasis since they are least likely to
disappear after cholecystectomy
28. 2. Standard base line investigation
- CBC
-LFT
-Serum Amylase ….. Acute pancreatitis
- Blood culture
3. Plain radiography
- 10% of GS are radio opaque
-not routinely indicated
-in acutely ill pts to R/O perforated viscus
- Gas in the GB or BD
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4. ULTRASOUND
primary screening
procedure
can show us….
Calculi with acoustic
shadow
thickened wall ,
distension of GB
localized
pericholecystic
collection
dilated CBD
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5. Oral cholecystography (OCG)
- replaced by U/S
- used to assess GB function
6. IV cholangiography
-to see extrahepatic biliary tree
-effective in jaundiced pts.
7. CT & MRI
- to R/O pancreatic head tumour
8. Scintography … to Dx acute cholecystitis
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9. PTC & ERCP
- in pts with comp. acute biliary dd. & jaundice
- clotting studies before PTC
- prophylactic antibiotics
indicated in pts.
- known GBS with increased bilirubin >10 mg/dl
- Sx pts with previous cholecystectomy
- pts with biliary Sx & inconclusive evidence
32. Management of GB stones
• category 1-Gallstones on imaging studies but
without symptoms
• category 2- Typical biliary symptoms and
gallstones on imaging studies
• category 3-Atypical symptoms and gallstones
on imaging studies
• category 4 -Typical biliary symptoms but
without gallstones on imaging studies
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33. Category 1
• Asymptomatic
– SYMPTOMS DEVELOPMENT
– ~3% /year ….2/3rd remain asymptomatic in
20years
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Management of acute cholecystitis
A. Conservative Rx
i. relief of pain
NSIAD
opiates & morphine
i.v fluids if DHN
ii. Control of nausea & vomiting
keep NPO
anti emetics
NG tube
iii. Control of fever
broad spectrum Abs( blood culture)
-cephalosporin's & aminoglycosides
most pts respond within 48 hrs
elective cholecystectomy after 6-8 wks
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Mx of…cont’d
B. Definitive Rx
I. Removal of GB & stones after 6-8wks
♣open cholecystectomy
♣ Laparoscopic cholecysectomy
**Emergency cholecystectomy
- pts not settling within 48 hrs
- pts with DM to prevent gangrene
II. Removal of GS alone
♣ medically dissolution agents (CDCA’& UDCA )
♣ other procedures Lithotripsy (ESWL)
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Mx of stones in CBD
• 1o stones originate in the CBD
• 2o stones -- Most CBD stones originate in the GB
• cxn of CBD stone
Obst. Jaundice
Cholangitis fever
RUQ pain Charcot’s triad
Jaundice
Charcot’s triad
+
altered mental status Reynolds’s pentad
+
shock
Suppurative cholangitis=>liver abscess
Impaired LF =>Biliary cirrhosis
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• choledochotomy
Indications
(1) palpable CBD stones
(2) If there is jaundice or
Hx of jaundice or
cholangitis
(3) dilated CBD
(4) abnormal LFT, in particular, the alkaline
phosphatase is raised