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Phase 2- GI > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What is cholecystitis?

A

Inflammation of the gallbladder

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2
Q

What is cholelithiasis?

A

Gallstone (within gallbladder)

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3
Q

What does choledocholithiasis refer to?

A

Gallstone within the bile duct

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4
Q

What is cholangitis?

A

Infection of the bile duct

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5
Q

What does MRCP stand for?

A

Magnetic resonance cholangiopancretography

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6
Q

What does ERCP stand for?

A

Endoscopic retrograde cholangiopancreatography

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7
Q

Describe the anatomy of the biliary tree

A

Biliary canaliculi, interlobular bile ducts, septal bile ducts, intrahepatic ducts, right and left hepatic duct, common hepatic duct, common bile duct

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8
Q

Where does the common bile duct pass?

A

Behind the duodenum, and through the head of the pancreas

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9
Q

What does the common bile duct join with, and what does this form?

A

Joins with main pancreatic duct to form hepatopancreatic ampulla (of vater)

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10
Q

Where does the ampulla of vater empty?

A

2/3rds down the duodenum

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11
Q

What is the function of the gallbladder, and what is its capacity?

A

Reservoir for bile and concentrates bile (reabsorbing salts and water), 30-50ml

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12
Q

Where is the gallbladder?

A

Lies in the gallbladder fossa, on the inferior surface of the right lobe of the liver

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13
Q

What are the three regions of the gallbladder?

A

Neck, body and fundus

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14
Q

What connects the gallbladder to the common bile duct?

A

Cystic duct, which joins the common hepatic join to form the common bile duct

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15
Q

What is the epithelium of the gallbladder

A

Columnar epithelium

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16
Q

What are the components of bile?

A

Bile acids, water, electrolytes, cholesterol, phospholipids and conjugated bilirubin

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17
Q

What are bile acids synthesised from?

A

Cholesterol

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18
Q

Where does bile acid synthesis occur?

A

Hepatocyte

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19
Q

What are the main primary bile acids?

A

Cholic, and chenodeoxycholic acids

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20
Q

How are primary bile acids conjugated to secondary bile acids?

A

Addition of amino acids group (taurine or glycine), before active export from hepatocyte

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21
Q

How is bile secreted from the gallbladder?

A

Vagal stimulation promotes GB contraction, and cholecystokinin mediated GB contraction and relaxation of sphincter of Oddi

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22
Q

Where is cholecystokinin released from, and what is this in response to?

A

CCK is released from the duodenum in response to presence of fat

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23
Q

What stimulates liver ductal secretion of bile?

A

Secretin

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24
Q

How is gallbladder relaxation and sphincter of Oddi closure mediated?

A

By sympathetic nerves, and by gut hormones vasoactive intestinal polypeptide (VIP) and somatostatin

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25
What is a function of bile acids?
Promote intestinal absorption of fats by emulsification and formation of micelles
26
Describe another function of bile acids
Enhance absorption of fat soluble vitamins
27
What is another function of bile acids?
Facilitation of the excretion of cholesterol (solubilising cholesterol within bile and by being a product of cholesterol metabolism)
28
What is the final function of bile acids?
Exert hormone like effect to influence intestinal metabolic pathways
29
What happens to bile acids after they complete their function in the intestine?
95% of bile acids recirculate via enterohepatic circulation, with reabsorption mostly occurring in the ileum by active transport into the portal circulation
30
How is faecal loss of bile acids compensated for?
Synthesis of new bile acids in the liver
31
How are bile acids transported back to the liver?
Hydrophobic bile acids are bound to albumin in the blood. Venous blood from the ileum feeds into the portal vein and then directly into the liver sinusoids
32
What are the 5fs (risk factors) of cholelithiasis?
Female, fair (caucasian), fat (BMI >30), fertile (one or more children), forty (age >40)
33
What are other risk factors of cholelithiasis?
IBS, low fibre diet and family history
34
What are the three types of gallstones?
Cholesterol gallstones (most common), bile (black) pigment gallstones and brown pigment gallstones
35
What leads to the formation of gallstones?
3 main events, often occurring together: cholesterol supersaturation, biliary stasis and increased secretin of bilirubin
36
What is the first event in gallstones pathogenesis?
Cholesterol supersaturation (high levels of cholesterol); occurs when oestrogen levels are high, and when bile acids levels are low (small bowl resection or active Crohn's)
37
Describe the second event of gallstone pathogenesis
Biliary stasis; occurs during periods of fasting or starvation, observed during prolonged total parenteral nutrition
38
Describe the third event of gallstone pathogenesis
Increased secretion of bilirubin; pigmented stones can develop when there is increased RBC breakdown (haematological conditions) and when their is failure of hepatic conjugation
39
What are some complications of gallstones in the gallbladder?
Biliary colic, actue cholecystitis, empyema, mucocoele, cancer
40
What are some complications of gallstones in the CBD?
Obstructive jaundice, cholangitis, pancreatitis
41
What are some complications of gallstones affecting the small intestine?
Gallstone ileus
42
What is biliary colic?
A stone which has impacted in the GB, usually ate the neck (Hartmann's pouch); causing pain in the epigastrium/through to the back which is provoked by eating. Vomiting is also common. LFTs are normal, no jaundice and often settles if stone moves back into GB body/fundus
43
Describe actue cholecytitis
Impacted stone in GB leading to GB wall oedema/inflammation and development of bacterial infection within GB wall. Symptoms include pain, nausea, vomiting, fever and abdominal tenderness. Raised inflammatory markers, sometimes abnormal LFT +/- jaundice. Is treated with antibiotic, analgesia and elective cholecystectomy when symptoms settle
44
What are two common causes of post-hepatic jaundice?
Choledocholithiasis and pancreatic cancer
45
What are some signs and symptoms of post-hepatic obstructive jaundice?
Pale stools, dark urine, yellow sclerae, itch (and scratch marks), features of chronic liver disease, hepatomegaly and abdominal tenderness
46
Describe choledocholithiasis
Migration of one or more stone from GB to CBD, commonly impacting above ampulla of vater, where duct narrows significantly
47
How is cholodecholithiasis diagnosed?
Ultrasound +/- MRCP or endoscopic ultrasound
48
How is choledocholithiasis treated?
ERCP to attempt stone removal, and cholecystectomy to prevent recurrence
49
How can pancreatic cancer cause obstructive jaundice?
Tumour in head of pancreas compressed CBD as it passes through pancreatic tissue
50
What happens to LFTs in biliary obstruction?
ALP is increased, often associated with a rise in GGT. Bilirubin rises steadily and level of bilirubin is indicative of duration of obstruction. AST/ALT can be elevated in obstructive jaundice but are much less prominent, and often more transient. In prolonged obstructive jaundice coagulopathy is common
51
What is the surface area of the intestines?
250 metres squared
52
How is the surface area of the intestines increased?
By villi and microvilli
53
How much water is absorbed in the GI tract?
Roughly 9000 mL
54
Where is the majority of the water absorbed?
Small intestine
55
Where is the net absorption of water highest?
Large intestine
56
How is diarrhoea treated in children?
Fluid replacement to prevent dehydration, zinc supplement to decrease severity and duration of diarrhoea, continue feeding and use more fluids
57
When might lactate containing intravenous fluids be given?
When patient is bicarbonate deficient (bicarbonate is produced in lactate metabolism)
58
What factors affect the rate of fluid replacement?
Age, cardiovascular status and renal function; as well as the severity of existing dehydration and the time it took to develop
59
When would 6L of fluid be given over a period of 24 hrs?
Emergency rehydration
60
When would 500 mL of IV fluid be given 6 hourly?
Standard regimen (rehydration)
61
When would 500 mL of IV fluid be given 8 hourly?
Slow rehydration (cardiovascular complications)
62
What is the maximum concentration for peripheral administration of IV potassium supplementation?
40 mmol/L
63
What is the maximum rate of IV potassium supplementation?
10 mmol/hr (faster only if cardiac monitoring, or a central line is available (only up to 20 mmol/hr))
64
Risk of chronic hepatitis B infection is highest in which age group?
Neonates
65
Which nerve supplies the internal anal sphincter?
Hypogastric plexus
66
From which artery does the superior rectal artery originate?
Inferior mesenteric artery

Phase 2- GI (5 decks)

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