Chapter 5 Gall Bladder Diseases power point

Chapter 5 Gall Bladder Diseases power point

1. GALLBLADDER AND
EXTRAHEPATIC BILIARY SYSTEM
Dr. Birhane

2. Bile Formation
•Bile production and secretion is one of the
major functions of the liver.
•The physiologic role of bile is twofold: first to
dispose of certain substances secreted into bile
and second to provide enteric bile salts to aid in
the digestion of fats.
•Bile is a substance containing organic and
inorganic solutes that is produced by an active
process of secretion and subsequent
concentration of these solutes.
03/05/25 2

3. 03/05/25 3

4. 03/05/25 4

5. •The concentration of inorganic solutes in bile
in the main biliary tree resembles that of
plasma
The major organic solutes in bile are
•Bile acids,
•Bile pigments,
•Cholesterol, and
•Phospholipids
03/05/25 5

6. 03/05/25 6

7. Gall Stone Disease (cholelithiasis)
•Gall stone disease is the most common
pathology of the biliary tract.
Incidence
•Female sex and old age are the common risk
factors.
•But the condition can occur in both sexes and
at any age.
03/05/25 7

8. Classification
1. Cholesterol stone (6%): usually solitary
2. Mixed stone (90%): cholesterol is the major
component(> 70%) with others like calcium
bilirubinate. These type of stones are multiple,
faceted and usually associated with infection.
3. Pigment stone: mainly composed of calcium
bilirubinate.
They are usually small,multiple and black.
Commonly associated with hemolytic disease.
03/05/25 8

9. 03/05/25 9
Mixed stones: they are clearly
faceted and consist of layers of
pigment and cholesterol.
pure cholesterol stones.

10. Pathogenesis
•Three important factors implicated in
pathogenesis of cholelithiasis are:
1.Metabolic: cholesterol is soluble in bile salt
and phospholipids.
-When bile salt is deficient or when the
cholesterol level is in excess in relation to the
bile salt, the bile formed is supersaturated or
lithogenic.
03/05/25 10

11. 2. Infection: causes increased mucus plug formation
and scarring which form a nidus for stone
formation.
-Also many bacteria deconjugate billirubin which
will combine with calcium to form insoluble
calcium bilirubinate.
3. Stasis: important for growth of stone.
-Progesterone in multiparous women is believed to
be contributory.
03/05/25 11

12. Clinical Presentation
•Most (90%) patients with gall stone diseases are
asymptomatic. Symptomatic patients present
with:
History:
- Right upper quadrant colicky pain (biliary
colicky)
- Dyspepsia, fatty food intolerance, flatulence,
abnormal post prandial bloating
03/05/25 12

13. - Symptoms of acute cholecystitis or other
complications
Physical examination:
• Right upper quadrant tenderness
• Risk factors can be identified
03/05/25 13

14. Complications of Gall bladder stone
1. In the gall bladder:
• Acute cholecystitis
• Chronic cholecystitis
• Gangrene
• Perforation
• Empyema
• Mucocele
• Carcinoma
03/05/25 14

15. 2. In the bile duct:
• Obstructive jaundice
• Cholangitis
• Acute pancreatitis
3. in intestine:
• Acute intestinal obstruction (Gall stone ileus)
03/05/25 15

16. Diagnostic workup
•Basic
•Ultrasound: detects stone in the gall bladder
•Plain abdominal film: Only 10% of stones are
radio opaque and visible on X-ray
03/05/25 16

17. 03/05/25 17

18. 03/05/25 18

19. Treatment
•Surgery: Open or
Laparoscopic
1) cholecystectomy. The
main stay of treatment
2) cholecystostomy for bad
risk patients with severe
infection.
(Severe Acute cholecystitis
or gall bladder empyema).
03/05/25 19

20. Acute Cholecystitis
•Acute cholecystitis is an acute inflammation
of gall bladder due to obstruction of neck of
gall bladder or cystic duct stone.
•Another rare form of acute cholecystitis which
occurs in absence of stone is called acalculous
cholecystitis.
03/05/25 20

21. Pathogenesis
•Direct pressure of calculus on the mucosa
results in ischemia, necrosis, and ulceration
with swelling edema and impairment of
venous return.
•This process increases and extends the extent
of inflammation and favors bacterial
multiplication.
03/05/25 21

22. The end result may be:
- Pericholecystic abscess
- Fistula formation between gall bladder and bowel
- Gall bladder empyema/mucocele
- Rarely, perforation of gall bladder and bile
peritonitis
•Commonly involved bacterial species in acute
cholecystitis include ;
•E. coli, Klebsiella species, Streptococci species,
Enterobacter species and Clostridial species.
03/05/25 22

23. Clinical features
•History:
• History of chronic cholecystitis or Cholelithiasis
• Women more affected than men
• Moderate to severe right upper quadrant and
epigastric pain which may radiate to the back.
• Fever and vomiting
03/05/25 23

24. •Physical examination:
• Right upper quadrant tenderness usually with
rebound tenderness
• Gall bladder or inflammatory mass due to
omentum wrapped around the GB may be
palpable.
• Murphy’s Sign may be positive: sudden arrest
of inspiration due to tenderness of inflamed
gall bladder which is palpated during deep
inspiration.
03/05/25 24

25. Investigation
•WBC: Leucocytosis
•Plain Chest or abdominal X-ray: to check for
pneumonia or radio opaque stone
•Ultrasound: detects calculi, gall bladder wall
thickening and pericholecystic fluid
•Others
03/05/25 25

26. Treatment
1. conservative
•- Admit the patient
•- keep the patient NPO
•- Start on IV fluid
•- Insert NGT
•- Analgesics
03/05/25 26

27. •- Antibiotics to cover common causative
bacteria: usually ampicillin and gentamycin are
used.
•- Follow the response to medical treatment
with clinical improvement (fever, abdominal
findings) and WBC count reduction
•- Appoint the patient to undergo
cholecystectomy after 6 weeks
2. Surgical treatment: Cholecystectomy
03/05/25 27

28. Obstructive Jaundice
•Jaundice is a yellowish discoloration of the
sclera, mucous membrane and skin.
•It becomes clinically evident when the level of
serum billirubin reaches 2.0 to 3.0 mg/dl
03/05/25 28

29. Classification
1. Medical: This type of jaundice could be
subdivided into;
•Pre hepatic: - when the cause is excessive
destruction of RBC (hemolytic)
•Hepatic: - when the cause is due to the liver
problems.
2. Surgical: when the cause is obstruction of
biliary trees (obstructive jaundice)
03/05/25 29

30. 03/05/25 30

31. Causes of extra hepatic biliary obstruction
Obstruction in the lumen
• Gall stone(the most common)
• Parasitic occlusion e.g. Ascaris
• Blood clot
Obstruction in the wall:
• Atresia (congenital)
• Stricture (post traumatic)
• Tumor of the bile duct
03/05/25 31

32. Extrinsic compression
• Carcinoma of head of pancreas(the second most
common)
• Carcinoma of ampulla of vater
• Pancreatitis
• Lymph node around porta hepatis
• Choledochal cyst
03/05/25 32

33. Clinical manifestation
•History: Helpful to differentiate surgical
jaundice from medical jaundice for
management decision
- Intermittent jaundice, if it is due to stone
- Progress of jaundice (progressively deepening
or intermittent)
- +/- Pruritis
03/05/25 33

34. - Urine and stool (clay color) color change is
indicative of obstruction
- RUQ abdominal pain
- Loss of appetite, weight loss
•- History of abdominal trauma, surgery
03/05/25 34

35. Physical examination:
- General appearance: obesity, emaciation.
- Depth of jaundice/pallor
- Hepatomegaly, splenomegaly
- Ascitis
- Palpable gall bladder
- Liver mass.
- Skin scratch marks
03/05/25 35

36. •Note the following distinctions of various
causes of jaundice
 Surgical jaundice is characterized by
• Yellow green icterus
• Pruritus of the skin more during night time
• Clay colored stool due to absent bile
• Dark brown urine due to conjugated billirubin
in the urine
03/05/25 36

37.  Jaundice due to choledocholithiasis is
characterized by,
•history of chronic colicky right upper
quadrant pain
• Intermittent jaundice
• Risk factors for gall bladder stone formation
or
• History of gall bladder stone (Diagnosed )
• Usually impalpable gall bladder
03/05/25 37

38.  Jaundice of Neoplastic cause is characterized
by,
• Progressively deepening jaundice
• Anorexia, weight loss, and pallor
• Palpable gall bladder with mild or no pain
03/05/25 38

39. Investigations
- Hemoglobin: anemia suggests malignancy
- Urinalysis: billirubin/urobilinogen
- Serum billirubin: total and direct
- Serum alkaline phosphatase
03/05/25 39

40. - Ultrasound: stone, cyst, dilated bile duct,
tumor
- Liver function test
- Prothrombin time
Treatment
•Surgical: The patient should be sent to a
hospital for surgery.
03/05/25 40

41. Choledocholithiasis
Common bile duct stones are secondary sth primary
Clinical manifestation:
May be silent or can present with biliary colic, cholangitis, gallstone
pancreatitis, or obstructive jaundice.
Diagnosis: US, MRC, ERCP
Treatment:
Choledochal Exploration:
choledochotomy followed be T-tube.
Choledochal Drainage Procedures
Endoscopic sphincterectomy.
03/05/25 41

42. Cholangitis
Is an ascending bacterial infection in
association with partial or complete
obstruction of the bile ducts
Clinical presentation:
Charcot's triad and Reynolds pentad .
fever, right upper abdominal pain, and
jaundice,
mental status changes and sepsis
03/05/25 42

43. Treatment:
*intravenous antibiotics and fluid
resuscitation
*the obstructed bile duct must be drained as
soon as the patient has been stabilized
03/05/25 43

44. Acute Pancreatitis

45. Definition & Incidence
•is an inflammatory disease of pancreas that is
associated with little or no fibrosis
•can be initiated by several factors: gallstones,
alcohol, trauma, infections
•complications include sepsis, shock, and
respiratory & renal failure
•pathophysiologic mechanisms remain
incompletely understood

46. Etiology
•Biliary tract stone disease & alcoholism account
for 80 to 90%
•Idiopathic disease
•Trauma
•Surgery
•Drugs
•Heredity
•Infections
•Toxins

48. Severity
•STAGE 1: Pancreatic Injury
–Edema
–Inflammation
•STAGE 2: Local Effects
–Retroperitoneal edema
–Ileus
•STAGE 3: Systemic Complications
–Hypotension/shock
–Metabolic disturbances
–Sepsis/organ failure
SEVERITYSEVERITY
MildMild
SevereSevere

49. Symptoms
•Severe, constant mid-epigastric or left upper
quadrant (LUQ) pain, radiates to the back
•"knifing" or "boring through"
•relieved by leaning forward & sitting up
•Associated with nausea & vomiting
•Low-grade fever
•Tachypnea

50. Signs
•Tachycardia, tachypnea, hypotension,
hyperthermia
•Voluntary & involuntary guarding over epigastric
region but no rebound
•Bowel sounds are decreased or absent-paralytic
ileus
•Usually no palpable masses
•Abdomen may be distended with intra/retro
peritoneal fluid
•May have pleural effusion (Lt)
•Hyperglycemia, hypoalbuminemia

51. Differential diagnosis
•Perforated peptic ulcer
•Gangrenous small bowel obstruction
•Acute cholecystitis

52. Investigations
•Amylase
–A level three times the upper limit of normal is 75%
specific and 80–90% sensitive for pancreatitis
–High amylase associated with acute, not chronic
pancreatitis
•Lipase:
–A level two times the upper limit of normal is 90%
specific and 80–90% sensitive
•Elevation in urinary amylase, amylase–creatinine
clearance ratio

53. Imaging
•Plain abdominal x-ray: "sentinel loop" (dilated
proximal jejunum), calcification and "colon
cut-off sign"(colonic spasm)
•U/S: best for evaluating biliary tree (67%
sensitivity, 100% specificity)
•CT scan with IV contrast useful for diagnosis
and prognosis (90% sensitive & 100% specific)

54. Ranson’s Criteria
•Admission
–Age > 55
–WBC > 16,000
–Glucose > 200
–LDH > 350
–AST > 250
•During first 48 hours
–Hematocrit drop > 10%
–Serum calcium < 8
–Base deficit > 4.0
–Increase in BUN > 5
–Fluid sequestration > 6L
–Arterial PO2 < 60
5% mortality risk with <2 signs
15-20% mortality risk with 3-4 signs
40% mortality risk with 5-6 signs
99% mortality risk with >7 signs

55. Treatment
Goals:
1.Hemodynamic stability
2.Analgesia
3.Oxygen
4.Stop progression of damage – difficult
5.Treat local & systemic complications

56. Complications
–Necrosis possibly with
infection
–Pancreatic fluid collections
–Colonic necrosis
–Gastrointestinal haemorrhage
–Splenic rupture
–Hypovolaemia and shock
–Coagulopathy
–Respiratory failure
–Renal Failure
–Hyperglycaemia
–Hypocalcaemia
Local Systemic

57. Chronic Pancreatitis
•is an incurable, chronic inflammatory
condition that is multifactorial in its etiology,
highly variable in its presentation, and a
challenge to treat successfully
•5 to 27 Persons Per 100,000
•the overall incidence of the disease has risen
progressively over the past 50 years

58. Definition
•Irreversible damage to pancreas
characterized by:
1.Pancreatic cell loss (from necrosis)
2.Inflammation
3.Fibrosis

59. Etiology
•Alcohol consumption & abuse is associated with
chronic pancreatitis in up to 70% of cases
•Tropical (nutritional)
•Idiopathic disease-20%
•Other, 10%
–Hereditary
–Hyperparathyroidism
–Hypertriglyceridemia
–Obstruction
–Trauma
•Never gallstones - cause acute pancreatitis only

60. Classification
1.Calcific pancreatitis
2.Obstruction pancreatitis
3.Inflammatory pancreatitis
4.Auto immune pancreatitis
5.Asymptomatic fibrosis
6.Tropical pancreatitis
7.Hereditary pancreatitis
8.Idiopathic pancreatitis

61. Signs & Symptoms
•Steady & Boring Pain
•Not Colicky
•Nausea / Vomiting
•Anorexia Is the Most Common symptom
•Malabsorption & Weight Loss
•Apancreatic Diabetes

62. Investigations
Lab
–increase in serum glucose
–increase in serum ALP
–serum amylase & lipase usually normal
AXR: looking for pancreatic calcifications
U/S: calcification, dilated pancreatic ducts, pseudocyst
CT: calcification, dilated pancreatic ducts, pseudocyst
MRCP or ERCP: abnormalities of pancreatic ducts-
narrowing and dilatation

63. Treatment
•Analgesia
–Most common problem is pain, difficult to control
–Celiac ganglion blocks
–Time - pain decreases with time as pancreas
"burns out
•Total abstinence from alcohol
•Surgical Therapy
• Endoscopic Management

64. Complications
•Pseudocyst
•Pancreatic Ascites
•Pancreatic-Enteric Fistula
•Head-of-Pancreas Mass
•Splenic & Portal Vein Thrombosis