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Year 2 > Biliary Disease And Pathology > Flashcards

Biliary Disease And Pathology Flashcards

1
Q

What stimulates the release of bile?

A

Cholecystokinin, which is produced by i cells in the duodenum. Bile is produced by canaliculi in the liver and is stored and concentrated in the gall bladder, in order to aid in the digestion of fat

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2
Q

Where is the majority of bile absorbed?

A

Terminal ileum, to be returned to the liver.

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3
Q

What are the primary bile acids?

A

Cholic acid and chenodeoxycholic acid, which are synthesised in the liver from cholesterol. Prior to secretion into the duodenum, they are typically conjugated into glycine and taurine.

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4
Q

What are the secondary bile acids?

A

Formed by the action of intestinal bacteria on primary bile acids, to form deoxycholic acid and lithocholic acid for lipid absorption by enterocytes.

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5
Q

What does bile contain?

A

Primary and secondary bile acids
Cholesterol
Bilirubin
Phosphatidylcholine

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6
Q

What is the function of bile?

A

Absorption of fat
Eliminate unnecessary waste products such as cholesterol and bilirubin
Act as a signalling molecule to activate hormone receptors.

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7
Q

How does bilirubin form?

A

From the breakdown of RBCs, from the haem portion -> biliverdin in the spleen. Biliverdin -> unconjugated bilirubin by bilirubin reductase.

Unconjugated bilirubin requires albumin for transport in the bloodstream to travel to the liver, and become conjugated with glucoronic acid, to form soluble conjugated bilirubin which is released into the bile, and undergo changes by intestinal bacteria to be excreted in the urine and faeces.

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8
Q

What is the form of bilirubin in the urine?

A

Urobilinogen- this is formed from the action of intestinal bacteria by deconjugating bilirubin.
-.> A portion is reabsorbed in the terminal ileum to return to the liver as biliverdin.

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9
Q

What is the form of bilirubin in the faeces?

A

Stercobilin, which is formed from the oxidation of urobilinogen.

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10
Q

What is the cause of pre-hepatic jaundice?

A

Excess breakdown of RBCs
Gilbert Syndrome
Overactive erythropoeisis

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11
Q

What is Gilbert Syndrome?

A

Recessive autosomal condition where there is a defect that causes the inability to conjugate bilirubin with glucoronic acid, causing pre-hepatic jaundice.

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12
Q

What is the cause of hepatic jaundice?

A

Liver damage due to infection or cirrhosis
Drugs
Hepatic cancer
Toxins

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13
Q

What is the cause of post-hepatic jaundice?

A

Gallstones obstructing bile exit.
Cholangiocarcinoma
Strictures
Biliary atresia
Pancreatic cancer.

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14
Q

What is a cholangiocarcinoma?

A

Cancer of the bile ducts, which leads to post-hepatic jaundice. There is a low survival rate.

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15
Q

What is biliary atresia?

A

Inflammation and fibrosis of the bile ducts which prevents the flow of bile, that typically occurs in early infancy, and can be considered a congenital condition. Surgical resection is common and this leads to post-hepatic jaundice.

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16
Q

What causes both hepatic and obstructive jaundice?

A

Primary sclerosing cholangitis, when bile ducts inside and outside the liver become inflamed and become fibrosed, causing narrowing and the blockage of flow.

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17
Q

What are the types of gallstones?

A

Cholesterol and pigment- Hardening of bile in the gallbladder, due to too much cholesterol, bile salts or bilirubin.

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18
Q

What is cholecystitis?

A

Inflammation of the gallbladder due to accumulation of bile, typically due to a bilestone blocking the duct which causes pressure build up and presents as sharp pain in the upper right quadrant

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19
Q

What is mucocele?

A

Prolonged blockage of the cystic duct leads to bile outflow being blocked. The gall bladder distends and reabsorbed bile to be replaced by clear watery mucous, creating an increase in pressure that causes ischaemia of the gallbladder wall and inflammation if it progresses without relief. This stasis increases the risk of bacterial colonisation and can progress to acute cholecystitis and shock.

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20
Q

What is cholesterolosis?

A

Excessive accumulation of cholesterol within the macrophages of the mucosa and lamina propia walls of the gallbladder, creating polyps and leading to mucous villous hyperplasia.

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21
Q

What is the endocrine function of the pancreas?

A

Production of insulin and glucagon for blood glucose regulation by cells in the Islets of Langerhaan.

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22
Q

What is the exocrine function of the pancreas?

A

Acinar cells produce amylase, lipase and the protease trypsin and elastase for digestion of fats, carbohydrates and protein.

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23
Q

What controls pancreatic secretions into the small intestine?

A

Sphincter of Oddi, formed of smooth muscle.

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24
Q

Where are the digestive enzymes produced from the pancreas released?

A

Into the duct of Wirsung, which joins with the bile duct at the hepatopancreatic ampulla of Vater, at the major duodenal papilla.

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25
Q

What is an annular pancreas?

A

Congenital abnormality where a ring of extrapancreatic tissue encases the duodenum.

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26
Q

What is a heterotropic pancreas?

A

Congenital abnormality where pancreatic tissue is found outside its normal location.

27
Q

What is pancreas divisum?

A

Congenital defect of the pancreas, when there is improper fusion of the dorsal and ventral buds during the 8th week of pregnancy, with no known cause.

28
Q

What is agenesis of the pancreas?

A

Embryological deformity where there is no formation of the body or tail of the pancreas.

29
Q

What is acute pancreatitis?

A

Inflammation of the pancreas which causes acinar cell damage that leads to the release of digestive enzymes which become activated in the pancreas to cause auto-digestion of structures like blood vessels. It presents as severe epigastric pain which may radiate to the back, vomiting and nausea.

30
Q

What is a severe consequence of acute pancreatitis?

A

Fistula formation between the lungs and the pancreas, leading to pancreatic effusion.
Pancreatic pseudocyst
Hypovolemic shock

31
Q

Which enzyme is more specific for acute pancreatitis?

A

Serum lipase.

32
Q

What is pancreatic pseudocyst?

A

Occurs due to ductal obstruction in pancreatitis, where death of the pancreas causes liquefactive haemorrhagic necrosis to occur, due to ischaemia and fluid buildup. Non-epithelialised fibrous tissue surrounds this area of necrosis, and the tissue becomes filled with pancreatic juice, leading to to abdominal pain, palpable mass and loss of appetite.

NB: A true cyst is surrounded by epithelialised tissue.

33
Q

How does pancreatitis affect the blood vessels?

A

Release of pancreatic proteolytic enzymes causes inflammation of the arteries and can lead to necrosis and a pseudoaneurysm formation. This may rupture and haemorrhaging, which can result in hypovolemic shock. The inflammation and clot formation due to pancreatic vessel damage can cause systemic activation of coagulation factors which leads to intravascular coagulation that develops throughout the body.

34
Q

What are the symptoms of acute pancreatitis?

A

Central and severe abdominal pain which radiates to the back, with nausea and vomiting and a history of alcohol or gallstones.

35
Q

What are the signs of acute pancreatitis?

A

Guarding and rebound tenderness in the upper abdomen
Hypocalcemia
Cullen’s Sign
Grey’s Sign

36
Q

What is Cullen’s sign?

A

Bruising and superficial oedema around the bellybutton, due to intraperitoneal haemorrhage, typically due to acute pancreatitis.

37
Q

What is Grey’s sign?

A

Bruising around the flank, due to severe necrosis in pancreatitis.

38
Q

What are the causes of acute pancreatitis?

A

I GET SMASHED
I: Idiopathic
G: Gallstones
E: Ethanol
T: Trauma
S: Steroids
M: Mumps and Hepatitis
A: Autoimmune
S: Scorpion
H: Hypercalcemia/Hyperlipademia
E: ERCP
D: Drugs

39
Q

How does acute pancreatitis affect calcium levels?

A

Acute pancreatitis causes high levels of lipase to be released which leads to fat necrosis of cells. This releases free fatty acids which will bind to calcium and cause hypocalceimia.

40
Q

What are the investigations for acute pancreatitis?

A

Raised serum lipase and amylase
Hypocalcemia
Raised CRP and WCC
Glucose intolerance
Haemorrhagic peritoneal effusion
CT and ultrasound scan

41
Q

What is CRP?

A

C-reactive protein, indicating inflammation.

42
Q

When should an imaging scan for acute pancreatitis be produced?

A

48 hours because inflammation and necrosis may not be fully formed.
CT sound may be more developed and show inflammation, necrosis and pseudocyst.
Ultrasound will show gallstones.

43
Q

How is acute pancreatitis treated?

A

Pain management with analgesics
Supportive IV fluids for electrolyte restoration and monitoring urine output for renal failure
Antibiotics if infection occurs
Oxygen therapy to reduce inflammation

44
Q

What is ERCP?

A

Endoscopic retrograde cholangiopancreatographym, used to diagnose pancreatic or biliary duct issues.

45
Q

Which drugs cause acute pancreatitis?

A

Azathriopine
Oestrogen
Tetracycline
Sulphonamide

46
Q

Which cells in the pancreas produce bicarbonate fluid?

A

Ductal cells

47
Q

How does alcohol cause acute pancreatitis?

A

Alcohol increases zymogen secretion from the acinar cells and decreases ductal bicarbonate secretion, which results in thick pancreatic secretions that can cause plugs to form. Alcohol also causes inflammation and recruitment of neutrophils for ROS damage, and leads to zymogen fusion with lysosomes that causes activation and auto digestion by trypsin. Protein plugs form which have calcium deposits.

48
Q

What is chronic pancreatitis?

A

Inflammation of the pancreas due to irreversible structural changes such as atrophy, fibrosis or calcification, which occurs with repeated bouts of acute pancreatitis. There are misshapen ducts, with fibrosis and calcium deposition in protein plugs but the endocrine cells are relatively spared.

49
Q

What is the most common cause of chronic pancreatitis in children?

A

Cystic fibrosis, where the ion channel dysfunction creates thick pancreatic secretions which impairs transport in the duct and leads to obstruction and fibrosis.

50
Q

What is the consequence of chronic pancreatitis?

A

Leads to pancreatic insufficiency, where cells cannot produce digestive enzymes and leads to malabsorption of Vitamins A, D, E, K and proteins. Diabetes mellitus may develop due to damage to Islet of Langerhaan cells. Weight loss will occur and steatorrhea is a symptom.

Pancreatic cancer is a rare but possible progression.

51
Q

Which causes of acute pancreatitis lead to chronic ancreatitis?

A

Trauma to pancreas
Tumours
Cystic fibrosis
Hypercalcaemia
Hyperlipidaemia

52
Q

How is the structure of the pancreas affected in chronic pancreatitis?

A

Stellate cells produce collagen which creates fibrosis, and this causes ductal dilatation and increase in pressure which can cause pseudocyst formation. Acinar cell atrophy may occur, with calcium deposits forming at these sites.

53
Q

How is chronic pancreatitis diagnosed?

A

CT and Ultrasound
ERCP will show ‘chain of lakes pattern’ as a result of alternating stenosis and duct dilatation.

54
Q

How is chronic pancreatitis treated?

A

Pain relief
Managing risk factors like alcohol, meat and weight
Vitamin supplementation
Insulin therapy for diabetics

55
Q

What is pancreatic cancer?

A

Adenocarcnoma which mainly occurs in the head of the pancreas, and quickly metastasises to the liver, peritoneum and bones. There is a poor prognosis and greater diagnosis in late middle-aged to elderly smokers, but cause is unclear.

56
Q

What is the presentation of pancreatic cancer?

A

Painless, obstructive jaundice with palpable mass and exacerbation of existing or development of new Type 2 diabetes. Trousseau’s syndrome may occur which is migratory thrombophlebitis with acancothis nigricans. Weight loss and back pain are symptoms.

57
Q

How is panacreatic cancer treated?

A

Surgery and chemotherapy, but median survival is 2-3 months.

58
Q

What is peritonitis?

A

Inflammation of the peritoneal cavity which occurs due to:
Spontaneous peritonitis
Secondary peritonitis

59
Q

What is spontaneous peritonitis?

A

Bacterial infection due to fluid build up in the abdominal cavity which is a complication of liver cirrhosis or kidney disease. This occurs in the absence of abdominal rupture.

60
Q

What is secondary peritonitis?

A

Occurs due to surgical intervention that introduces bacteria into the peritoneal cavity or contamination from the GI tract.

61
Q

What are causes of peritonitis unrelated to bacterial infection?

A

Aseptic peritonitis, which is caused by exposure of peritoneum to sterile fluids like gastric, bile, urine or foreign materials.

62
Q

What are the GI-related causes of secondary peritonitis?

A

Ruptured appendix
Perforated colon
Stomach ulcer
Trauma to abdomen
Crohn’s and ulcerative colitis
Pancreatitis

63
Q

How does peritonitis present?

A

Belly pain and tenderness
Bloating
Fullness in abdomen
Fever

64
Q

What are the causes of chronic pancreatitis unrelated to acute pancreatitis?

A

Biliary tract disease
Haemochromatosis
Cystic fibrosis

Year 2 (212 decks)

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