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
Q

What is a function of bile acids?

A

Promote intestinal absorption of fats by emulsification and formation of micelles

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26
Q

Describe another function of bile acids

A

Enhance absorption of fat soluble vitamins

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27
Q

What is another function of bile acids?

A

Facilitation of the excretion of cholesterol (solubilising cholesterol within bile and by being a product of cholesterol metabolism)

28
Q

What is the final function of bile acids?

A

Exert hormone like effect to influence intestinal metabolic pathways

29
Q

What happens to bile acids after they complete their function in the intestine?

A

95% of bile acids recirculate via enterohepatic circulation, with reabsorption mostly occurring in the ileum by active transport into the portal circulation

30
Q

How is faecal loss of bile acids compensated for?

A

Synthesis of new bile acids in the liver

31
Q

How are bile acids transported back to the liver?

A

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
Q

What are the 5fs (risk factors) of cholelithiasis?

A

Female, fair (caucasian), fat (BMI >30), fertile (one or more children), forty (age >40)

33
Q

What are other risk factors of cholelithiasis?

A

IBS, low fibre diet and family history

34
Q

What are the three types of gallstones?

A

Cholesterol gallstones (most common), bile (black) pigment gallstones and brown pigment gallstones

35
Q

What leads to the formation of gallstones?

A

3 main events, often occurring together: cholesterol supersaturation, biliary stasis and increased secretin of bilirubin

36
Q

What is the first event in gallstones pathogenesis?

A

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
Q

Describe the second event of gallstone pathogenesis

A

Biliary stasis; occurs during periods of fasting or starvation, observed during prolonged total parenteral nutrition

38
Q

Describe the third event of gallstone pathogenesis

A

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
Q

What are some complications of gallstones in the gallbladder?

A

Biliary colic, actue cholecystitis, empyema, mucocoele, cancer

40
Q

What are some complications of gallstones in the CBD?

A

Obstructive jaundice, cholangitis, pancreatitis

41
Q

What are some complications of gallstones affecting the small intestine?

A

Gallstone ileus

42
Q

What is biliary colic?

A

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
Q

Describe actue cholecytitis

A

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
Q

What are two common causes of post-hepatic jaundice?

A

Choledocholithiasis and pancreatic cancer

45
Q

What are some signs and symptoms of post-hepatic obstructive jaundice?

A

Pale stools, dark urine, yellow sclerae, itch (and scratch marks), features of chronic liver disease, hepatomegaly and abdominal tenderness

46
Q

Describe choledocholithiasis

A

Migration of one or more stone from GB to CBD, commonly impacting above ampulla of vater, where duct narrows significantly

47
Q

How is cholodecholithiasis diagnosed?

A

Ultrasound +/- MRCP or endoscopic ultrasound

48
Q

How is choledocholithiasis treated?

A

ERCP to attempt stone removal, and cholecystectomy to prevent recurrence

49
Q

How can pancreatic cancer cause obstructive jaundice?

A

Tumour in head of pancreas compressed CBD as it passes through pancreatic tissue

50
Q

What happens to LFTs in biliary obstruction?

A

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
Q

What is the surface area of the intestines?

A

250 metres squared

52
Q

How is the surface area of the intestines increased?

A

By villi and microvilli

53
Q

How much water is absorbed in the GI tract?

A

Roughly 9000 mL

54
Q

Where is the majority of the water absorbed?

A

Small intestine

55
Q

Where is the net absorption of water highest?

A

Large intestine

56
Q

How is diarrhoea treated in children?

A

Fluid replacement to prevent dehydration, zinc supplement to decrease severity and duration of diarrhoea, continue feeding and use more fluids

57
Q

When might lactate containing intravenous fluids be given?

A

When patient is bicarbonate deficient (bicarbonate is produced in lactate metabolism)

58
Q

What factors affect the rate of fluid replacement?

A

Age, cardiovascular status and renal function; as well as the severity of existing dehydration and the time it took to develop

59
Q

When would 6L of fluid be given over a period of 24 hrs?

A

Emergency rehydration

60
Q

When would 500 mL of IV fluid be given 6 hourly?

A

Standard regimen (rehydration)

61
Q

When would 500 mL of IV fluid be given 8 hourly?

A

Slow rehydration (cardiovascular complications)

62
Q

What is the maximum concentration for peripheral administration of IV potassium supplementation?

A

40 mmol/L

63
Q

What is the maximum rate of IV potassium supplementation?

A

10 mmol/hr (faster only if cardiac monitoring, or a central line is available (only up to 20 mmol/hr))

64
Q

Risk of chronic hepatitis B infection is highest in which age group?

A

Neonates

65
Q

Which nerve supplies the internal anal sphincter?

A

Hypogastric plexus

66
Q

From which artery does the superior rectal artery originate?

A

Inferior mesenteric artery