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Surgery > Gall Bladder > Flashcards

Gall Bladder Flashcards

1
Q

Biliary tree

A

Right + left hepatic ducts = common hepatic duct (CHD)
CHD + Cystic duct = Common Bile Duct (CBD)
CBD joins with pancreatic duct = hepatopancreatic ampulla of vater
Ampulla of Vater releases bile and pancreatic enzymes into duodenum through oddi of sphincter

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2
Q

Gall Bladder blood supply

A 
Cystic artery (R. Hep. Artery -> Com. Hep. Artery)
Cystic vein into portal vein
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3
Q

Gall bladder nerve innervations

A

Parasympathetic (contraction): Vagus Nerve

Sympathetic and Sensory: Coeliac Plexus

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4
Q

Cholelithiasis

A

Uncomplicated gall stones

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5
Q

Types of gall stones and RF

A

Cholesterol gall stones: most common (90%). RF: FHx, diet (obesity, metabolic syndrome, sudden weight reduction), age, and female sex hormones.

Brown pigmented gall stones: Result of stasis and infection. Unconjugated Bilirubin and calcium salts RF:Bile ducts strictures or parasitic infestation

Black pigmented: Polymerised calcium bilirubinate (5-10%). RF: age, chronic haemolytic anaemia, cirrhosis, cystic fibrosis, and ileal disease

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6
Q

Typical presentation of gall stones

A

Most asymptomatic.
Can present with RUQ pain, sometimes after food
Constant pain, increasing intensity. Pain duration <30 mins is not biliary colic. More than 5 hrs suggests complicationor cholecystitis

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7
Q

Key investigation for gall stones

A

US initial test

If unremarkable and symptoms persists CT scan or MRCP if query choledocholithiasis (common bile duct stones)

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8
Q

Management for gall stones

A

Asymptomatic: Observe
Symptomatic: Lap. Cholecystectomy
choledocholithiasis with/without symptoms: ERCP

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9
Q

Acute Cholecystitis

A

Acute gall bladder inflammation
Lasts 3-6 hours. Fever is common
RUQ tenderness with + murphy’s sign

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10
Q

Investigation for acute cholecystitis

A

US is the definitive test

If unclear then use hepatobiliary iminodiacetic acid HIDA

CT is not as good as US for diagnosing, but it is useful when obesity or gaseous distension limits ultrasound interpretation

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11
Q

Management of acute cholecystitis

A

Supportive care (fluids, analgaesia, obs)
Oral/IV Abx-cefuroxime or ciprofloxacin and metranidazole
Lap. Cholecystectomy
If poor surgical candidate:
Percutaneous cholecystectomy drainage tube

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12
Q

Primary Sclerosing Cholangitis (PSC)

A

Chronic progressive cholestatic liver disease

Inflammation and fibrosis of intrahepatic and/or extrahepatic bile ducts causing strictures

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13
Q

PSC more commonly associated with UC or CD

A

UC

2/3rd of people with PSC have associated IBD

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14
Q

Common risk factors of PSC

A

Male 2:1 ratio
Hx of IBD
Genetic: First degree relative has PSC
Common age of diagnosis is in 40s to 50s

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15
Q

Common signs and symptoms

A 
Abdo pain (non specific RUQor epigastric)
Pruritus
Fatigue
Weight Loss
Fever (bacterial cholangitis)
Jaundice
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16
Q

Key investigations for PSC

A 
Raised ALP (bile duct injuiry or blockage)
Raised serum gGT: supports liver origin of ALP not bone
Serum aminotransferases, raised bili

May have reduced albumin if in severe liver disease stages

Abdo US
CT
MRCP or ERCP: MRCP is better diagnostically but if considering need for therapy (high suspicion of dominant stricture or cholangiocarninoma) consider ERCP

17
Q

Management of PSC

A

Asymptomatic: Observation and lifestyle change
Pruritus relief: Colestyramine (bile acid sequesterant)

Autoimmune hepatitis: immunosuppressants (corticosteroids)

Hepatic Osteopenia: Calcium and Vit D supplements
Hepatic Osteoporosis: Bisphosphonates and HRT

ERCP if cant gain access via endoscopy do percutaneous transhepatic cholangiography (PTC) can allow for biliary drainage, stent placement, and/or stricture dilation

End stage liver disease: Liver transplant

18
Q

Primary biliary cholangitis/cirrhosis (PBC)

A

Progressive chronic disease of the small intrahepatic ducts characterised by progressive bile duct damage.

19
Q

Difference between PSC and PBC

A

PSC involves sclerosis of the hepatic biliary ducts resulting in back of bile in the liver causing cholestatic liver disease

PBC involves the small intrahepatic ducts and not the biliary ducts so no association with biliary duct sclerosis.

20
Q

Cause of PBC

A

Believed to be autoimmune, mainly antimitochondrial antibodies found in 95% of patients. Common Ab is pyruvate dehydrogenase complex E2 subunit (PDC-E2) Can also be seen on ANA

21
Q

Pathophysiology of PBC

A

damage to, and progressive destruction of, the biliary epithelial cells lining the small intrahepatic bile ducts

Bile duct loss is progressive and in the end stages of the disease there can be a complete loss of small intrahepatic ducts. Loss of bile duct cross-sectional area within the liver leads to cholestasis with variable and progressive bile acid retention.

Result is over time liver cirrhosis

22
Q

Pathophysiology of PSC

A

inflammation and injury of the medium- and large-sized bile ducts leading to fibrosis and multi-focal stricturing of the ducts.

23
Q

Common risk factors for PBC

A

Female 10:1 ratio

Peak incidence between 45-60 yrs old

24
Q

Common signs ans symptoms for PBC

A

Hx/FHx of autoimmune disease
Hx of hypercholesterolaemia (cholestasis. H. HDL and lipoprotein X)
Pruritus
Dry eyes and mouth (sjogren’s syndrome-autoimmune)

In late stages (liver disease):
Jaundice
Metabolic changes
Portal hypertensive features (ascites, variceal bleeding, splenomegaly)

25
Q

Diagnosis of PBC

A

Cholestatic LFTs: (ALP, gGT, raised bili in late stages)
Autoantibody profile: antimitochondrial antibody (AMA) or PBC-characteristic ANA
Compatible/diagnostic liver histology

26
Q

Treatments for pruritus

A

1st: Cholestyramine (bile acid sequesterant)
2nd:
Rifampicin (Antibiotic inhibits DNA dep. RNA Poly)
Naltrexone (opioid receptor antagonist)

27
Q

Management of PBC

A

Bile acid analogue ursodeoxycholic acid or obeticholic acid (has mild hepatic impairement use with caution)

Treat autoimmune hep. overlap with corticosteroids

If end stage liver disease then liver transplant

28
Q

Ascending cholangitis

A

Infection of the biliary tree most commonly caused by obstructions

29
Q

Charcot’s triad

A

Fever, jaundice, RUQ pain

30
Q

Causes of ascending cholangitis

A

cholelithiasis leading to choledocholethiasis
Surgical inj. leading to stricture
Primary and secondary sclerosing cholangitis

31
Q

Management of ascending cholangitis

A

Antibiotics: piperacillin/tazobactam or imipenem/cilastatin:

ERCP with drainage stenting or PTC if can’t access via endoscopy

32
Q

Reynold’s pentad

A

Fever, jaundice, RUQ pain
AND
Hypotension, altered sensorium

33
Q

Complication of ascending cholangitis

A

Sepsis-> septicemia

34
Q

Bouveret’s syndrome

A

Commonly in elderly patients. It is an uncommon type of gall stone ileus as a result of cholecystoduodenal fistula formation
Diagnosed on Abdo X-ray by air in the gall bladder wall

35
Q

Mirizzi’s syndrome

A

Rare complication where gall stone in the hartmann’s pouch compresses the CBD or the CHD resulting in obstructive jaundice
Type 1- No fistula
Type 2-Fistula present

Surgery (7 decks)

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