HPB: revision cards Flashcards

(61 cards)

1
Q

What is the pathogenesis of Gallstone formation? - list three factors

A

Interplay between bile supersaturation, nidus for crystal formation, and gallbladder hypomotility.

This refers to the processes that lead to the development of gallstones within the gallbladder.

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2
Q

What causes excess cholesterol concentration in bile?

A

Hepatic overproduction or relative reduction of bile salts or phospholipids.

These conditions can lead to the supersaturation of cholesterol in the bile.

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3
Q

What role does mucin composition play in gallstone formation?

A

Mucin is a glycoprotein that can facilitate the aggregation of cholesterol crystals, which then can act as a nidus for crystal formation.

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4
Q

How does biliary stasis contribute to gallstone formation?

A

Biliary stasis leads to prolonged retention of bile, increasing the likelihood of stone formation, via precipitation of nidus

.

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5
Q

What are the non-modifiable risk factors for Gallstone formation?

A

Genetic factors, Ethnicity, Increase age, Female gender, Oestrogen increases cholesterol secretion and diminishes bile salt secretion, Pregnant

Non-modifiable factors are those that cannot be changed or influenced by lifestyle choices.

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6
Q

List the modifiable risk factors for Gallstone formation.

A
  • Lifestyle
  • Obesity
  • Diet high in cholesterol
  • Diabetes

Modifiable factors can be influenced by changes in behavior or lifestyle.

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7
Q

True or False: Female gender is a non-modifiable risk factor for Gallstone formation.

A

True

Gender is a biological characteristic that cannot be changed.

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8
Q

Fill in the blank: Oestrogen increases cholesterol secretion and diminishes _______ secretion.

A

bile salt

This hormonal effect contributes to the risk of gallstone formation.

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9
Q

What effect does pregnancy have on Gallstone risk?

A

Increases risk due to hormonal changes

Hormonal fluctuations during pregnancy can influence gallstone formation.

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10
Q

What is the relationship between obesity and Gallstone formation?

A

Obesity is a modifiable risk factor

Reducing obesity can lower the risk of developing gallstones.

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11
Q

How does a diet high in cholesterol affect Gallstone formation?

A

It increases the risk of formation

High cholesterol intake is associated with gallstone development.

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12
Q

What role does diabetes play in Gallstone formation?

A

It is a modifiable risk factor

Managing diabetes can help reduce the risk of gallstones.

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13
Q

Which specific diseases increase the risk of stone formation?

A

Hyperbilirubinaemia, Cirrhosis, Ileal resections, Crohn’s disease

Specific pathologies that contribute to the risk of stone formation.

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14
Q

What are examples of conditions associated with Hyperbilirubinaemia?

A

Sickle cell, Thalassemia, Hereditary erythrocytosis

These conditions can lead to increased bilirubin levels, contributing to stone formation.

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15
Q

True or False: Cirrhosis is a disease that increases the risk of stone formation.

A

True

Cirrhosis is associated with metabolic changes that can lead to stone formation.

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16
Q

Fill in the blank: ________ resections can increase the risk of stone formation.

A

Ileal
Ileal resections can disrupt enterohepatic recirculation of bile salts

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17
Q

What gastrointestinal condition is linked with an increased risk of stone formation?

A

Crohn’s disease

This inflammatory bowel disease can lead to malabsorption and other metabolic changes affecting stone risk.

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18
Q

What percentage of bile acids are reclaimed via enterohepatic circulation?

A

Approx 90%

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19
Q

Where are primary bile acids synthesized?

A

In the liver

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20
Q

What is the role of the gallbladder (GB) in bile acid storage?

A

Stores and concentrates bile acids mixed with cholesterol, water, and phospholipids

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21
Q

What happens to primary bile acids after they are excreted in the duodenum?

A

They are broken down by intestinal bacteria to form secondary bile acids

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22
Q

How are bile acids reabsorbed in the small bowel?

A

Via passive transport in the jejunum and active transport in the ileum

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23
Q

What percentage of bile acids are reabsorbed in the terminal ileum (TI)?

A

Approx 95%

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24
Q

What do bile acids form to facilitate re-entry into the portal circulation?

A

Micelles

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25
What does the liver do after bile acids re-enter the portal circulation?
Extracts the bile acids and re-circulates them in the biliary caniculi
26
In addition to stones, how else are small fractions of bile acids handled by the body?
Taken up systemically or excreted by urine
27
What are the important surgical anatomical landmarks during Cholecystectomy?
Before dissection Fundus of GB Roveure sulcus Segmental 4/Facilform Bile duct Duodenum ## Footnote These landmarks are crucial for identifying the anatomy involved during the surgical procedure.
28
What forms the hepatio-cystic triangle?
Inferior edge of Liver, Cystic duct, Common Hepatic duct
29
Fill in the blank: The _______ duct and the common hepatic duct are part of the hepatio-cystic triangle.
Cystic
30
List three structures that are important anatomical landmarks during a Cholecystectomy.
* Base segment 4 * Hepatic structures * Bile duct
31
What is the embryological origin of the pancreas?
Endodermal origin
32
What are the two separate buds that develop into the pancreas?
Dorsal and ventral buds
33
What happens to the ventral bud during pancreas development?
It rotates approximately 180 degrees to fuse with the dorsal bud
34
What does the ventral bud give rise to?
Head and uncinate process of the pancreas
35
What does the dorsal bud give rise to?
Neck, body, and tail of the pancreas
36
What persists as the Accessory duct of Santorini?
The dorsal duct
37
What is the main duct of the pancreas called?
Pancreatic duct or duct of Wirsung
38
What is pancreatic duct divisum?
Failure of fusion of ventral and dorsal ducts
39
What is the consequence of pancreatic duct divisum?
Main duct drains the majority of pancreas via the minor ampulla
40
What percentage of the population is affected by pancreas divisum?
Approximately 5%
41
What types of pancreas divisum are there?
* Classical * Completely separate * Absent ventral duct * Incomplete with separation with rudimentary connection
42
What is annular pancreas?
Pancreatic tissue encircles the duodenum
43
What causes annular pancreas?
Failure of ventral bud to migrate in unison around the duodenum
44
What can annular pancreas result in?
Duodenal stenosis
45
Fill in the blank: The pancreas develops as two separate buds: _______ and _______.
[dorsal bud], [ventral bud]
46
Where is the head of the pancreas located?
In the c-shape concavity of the duodenum
47
Which major structures are located posteriorly to the head of the pancreas?
* IVC * Renal veins * Aorta * Right crus of the diaphragm
48
What runs behind the head of the pancreas?
Distal CBD
49
What is the uninate process of the pancreas?
An inferior-posterior projection of the head of the pancreas
50
Where does the uncinate process lie in relation to the SMV/SMA?
Behind the SMV/SMA
51
In which direction does the splenic artery run in relation to the pancreas?
In a tortuous fashion along the superior border
52
Where does the splenic vein run in relation to the pancreas?
Behind the body and tail of the pancreas
53
How mobile is the tail of the pancreas?
Relatively mobile
54
What is the typical distance of the pancreas tail from the splenic hilum in approximately 70% of patients?
Within 1 cm
55
What is the relationship of the pancreas tail with the splenic hilum in approximately 30% of patients?
Touching
56
What care must be taken during splenic preservation in distal pancreatectomy?
Ligate vessels as close to the splenic hilum as possible
57
What risk is associated with improper ligation of vessels during distal pancreatectomy?
Injury to tail and risk of pancreatitis
58
What is the differential for a pancreatic cystic lesion?
Neoplastic and non-neoplastic
59
What are the non-neoplastic pancreatic cystic lesions?
Pancreatic pseudocysts ## Footnote Pancreatic pseudocysts are typically due to inflammation or injury.
60
What are the types of neoplastic pancreatic cystic lesions? list five
Serous cystic neoplasms, Mucinous cystic neoplasms, IPMN, Solid pseudopapillary neoplasms, Cystic degeneration of solid pancreatic cancer (NETs or Adeno) ## Footnote Each type has distinct characteristics and implications for treatment.
61
What are the subtypes of Intraductal Papillary Mucinous Neoplasm (IPMN)?
Main duct, side branch, mixed ## Footnote IPMN can vary significantly in behavior and management based on its subtype.