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MD3002 WEEK 4 - B > 6. Hepatobiliary and Pancreatic Disease > Flashcards

6. Hepatobiliary and Pancreatic Disease Flashcards

1
Q

What two vessels join to form the common bile duct?

A

Cystic duct

Common hepatic duct

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2
Q

Portal triad is made up of which structures?

A

Bile duct
Hepatic artery
Hepatic portal vein

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3
Q

The liver synthesises, produces and breaks down what?

A

Synthesises: Albumin, clotting factors, complement, alpha-1-antitrypsin, thrombopoietin
Produces: Bile through conjugation of bilirubin
Breaks down: Drugs, insulin, ammonia

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4
Q

What do Kupffer cells do?

A

Phagocytose old blood cells, bacteria and foreign materials from the bloodstream/gut

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5
Q

Jaundice:
What is it?
Can cause?
Classified by conjugation of bilirubin?

A

Jaundice is the yellowing of the skin and mucosal surfaces. When bilirubin levels are >40micromol/L
Can cause intense itch

Unconjugated is water insoluble. Conjugated is water soluble so can be excreted in the urine, leading to dark urine.

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6
Q

Classification of jaundice by cause: Prehepatic, intrahepatic and post-hepatic?

STARRED

A

Prehepatic: Haemolysis –> Release for bilirubin from RBCs

Intrahepatic: Liver disease –> Excess bilirubin in liver and bloodstream

Post-hepatic (obstructive): Obstruction of bile outflow –> Dark urine and pale stools

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7
Q

Main causes for acute liver injury?

A

Viral infections
Alcohol
Adverse drug reactions
Biliary obstructions

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8
Q

Consequences of acute liver injury?

A

Jaundice, malaise
Raised serum bilirubin and transaminases
Liver failure: decrease in albumin, ascites, bruising, encephalopathy

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9
Q

Patterns of hepatocyte injury, zones of injury?

A 
Zone 1 (on outskirts): Greatest blood supply so most susceptible but also most reliant 
Zone 3 (inner zone): If injury in this zone then that's when symptoms are experienced as cells cannot regenerate
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10
Q

3 forms of liver injury due to alcohol?

A

Steatosis
Cirrhosis
Acute hepatitis with Mallory’s hyaline

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11
Q

What is steatosis?

Why does Mallory’s hyaline develop?

A

Fat deposition altered by metabolism

Mallory’s hyaline builds up due to hepatocyte damage

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12
Q

What is the process of cirrhosis development due to alcohol?

A
  1. Acetaldehyde binds to hepatocytes causing damage → Inflammatory reaction
  2. Inflammation → fibrosis
  3. Fibrosis (collagen) + Regeneration → Cirrhosis
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13
Q

What are the 3 morphological classifications of cirrhosis?

A

Micronodular: Nodules <3mm
Macronodular: Nodules >3mm
Mixed

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14
Q

Complications of cirrhosis?

A
  • Liver Failure – hepatic encephalopathy (ammonia), build up of steroid hormones → hyperoestrogenism (palmar erythema and gynaecomastia), bleeding
  • Portal hypertension –↑ hepatic vascular resistance, AV shunting – oesophageal varices, haemorrhoids, caput medusae
  • Hepatocellular carcinoma
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15
Q

How does drug induced liver injury vary depending on the drug?

A

Paracetamol= Injury to liver cells (hepatocellular)
overdose

Methyl testosterone= Injury to bile production/secretion cells
(cholestatic)

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16
Q

Acute biliary obstruction:
Usually due to?
Causes?
Complication?

A
  • This is usually due to gallstones
  • Causes colicky pain and jaundice
  • Can be complicated by infection of the blocked CBD - cholangitis
17
Q

Main 4 causes of chronic hepatitis?

A

Viral
Alcohol
Drugs
Autoimmune

18
Q

Chronic hepatits, is hepatitis that lasts more than…

A

6 months

With sustained elevation of transaminases which requires liver biopsy to classify cause

19
Q 
Primary biliary cirrhosis:
Females vs males?
Stages?
Presentation?
Test results of ALP + IgM, AMA
A

Females > Males
Stages:
1. Autoimmune destruction of bile duct epithelium: Dense lymphocytic infiltration
2. Proliferation of small bile ducts
3. Architectural disturbance: Portal and bridging fibrosis
4. Cirrhosis

Presentation: Jaundice, pruritus, xanthelasmata

Raised ALP + IgM, AMA

20
Q

What is haemochromatosis

A

Iron deposition in the liver causing alteration of architecture –> Fibrosis –> Cirrhosis

21
Q

Difference between a lobule and acinar view of the liver?

A

Lobule: Blood on outside going inwards
Acinar: Blood supply in between

22
Q

Causes for cirrhosis?

A 
Alcohol
Hep B and C
Iron overload
Gallstones
Cirrhosis
Autoimmune liver disease
23
Q 
Autoimmune chronic active hepatitis:
Gender incidence?
Age incidence?
Feartures?
Treatment
A

Females > Males

Usually presents in mid-late teens

Features:

  • Interface hepatitis
  • Plasma cells and swollen hepatocytes present
  • Fibrosis
  • ANA, SMA, raised IgG and transaminases, Anti-LKM (liver-kidney microsomal)

Treatment: Patients may benefit from steroids

24
Q

Which gene codes for the protein involved in haemochromatosis?

A

HFE (autosomal recessive)

25
Q

Treatment for haemochromatosis?

A

Regular venesection (test iron and ferritin levels)

26
Q

What is alpha-1 antitrypsin deficiency:
Dominance?
Causes?

A

Autosomal recessive disorder
Leads to low levels of alpha-1 -antitrypsin

Leads to protein build up in hepatocytes as hyaline as transport protein is deficient
–>Cirrhosis
(associated with emphysema)

27
Q

What is NASH/NAFLD?
Associated with which metabolic syndrome?
Mechanism?

A

Non-alcoholic steatohepatitis / Non- alcoholic fatty liver disease
Associated with Metabolic Syndrome (DM II, hypertension, ↓HDL cholesterol, ↑ triglycerides
Mechanism: Fat deposition in hepatocytes – can lead to cirrhosis

28
Q 
Wilson's disease:
Dominance?
What is it?
Deposition sites?
Clinical signs?
A

• Autosomal recessive disorder
• Failure of the liver to excrete copper in bile → build up of copper in liver → cirrhosis
• Copper also deposits in brain tissue → neurological dysfunction
Clinical signs: Kayser-Fleischer rings

29
Q

What is hepatocellular carcinoma?
Often arises in….
Aetiology?

A

Malignant liver tumour
Often multifocal

Often arises in cirrhotic liver

Aetiology:

  • Aflatoxin (fungal origin)
  • Hep B and C viruses
  • Cirrhosis
30
Q

6 pathologies of the biliary system?

A
  1. Gallstones (cholelithiasis)
  2. Cholecystitis
  3. Cholangiocarcinoma
  4. Obstruction
    Congenital malformations
  5. Atresia
  6. Cholesocal cysts
31
Q

Cholangiocarcinoma:
Location?
Association?
Causes?

A
  • Arises from bile duct epithelium anywhere in the biliary system (intra- and extra-hepatic)
  • Associated with ulcerative colitis

Causes: obstructive jaundice, itch, weight loss and lethargy
Can lead to rupture of common bile duct or gallbladder – prognosis poor

32
Q

Risk factors for gallstones? F’s*

A

Female, Fair, Fat, Forty, Fertile

Diabetes mellitus

33
Q

Most common gallstones?

A

Cholesterol (yellow), bile pigment (green) , mixed

34
Q

What 6 conditions can gallstones lead to?

A

Cholecystitis, obstructive jaundice, cholangitis, pancreatitis, cholangiocarcinoma

35
Q

Difference between acute and chronic cholecystitis?

A

Acute –
• Usually caused by gallstones
• Initially sterile then becomes infected • May lead to abscess/rupture
• Symptoms – RUQ pain (biliary colic), fever, nausea/vomiting

Chronic –
• Invariably related to gallstones
• Chronic inflammation with wall thickening

36
Q

What is an annular pancreas?

Presents as?

A

At 2nd part of duodenum

Causes obstruction

Presentation: Polyhydramnios, low birth weight, poor feeding

37
Q

Pancreatitis:
Acutely leads to?
Chronic leads to?

A 
Acutely leads to: 
• Causes catastrophic metabolic consequences –
↓ calcium, ↓ albumin, ↑ glucose 
• High serum amylase – diagnostic
• Massive fluid losses → SHOCK 
• High mortality rates

Chronic leads to;
• Multiple episodes of acute
• Causes fibrosis of pancreas – may lead to
diabetes mellitus
• Reduced production of enzymes – require supplements (creon)

38
Q 
Pancreatic carcinoma:
Type of cancer?
Associations?
Presentation?
Clinical sign?
Prognosis?
A
  • Adenocarcinoma
  • Associated with smoking and diabetes mellitus
  • Presents with painless, progressive jaundice
  • Weight loss
  • Poor prognosis
  • May be operable if small and close to ampulla

MD3002 WEEK 4 - B (9 decks)

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