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
Treatment for haemochromatosis?
Regular venesection (test iron and ferritin levels)
26
What is alpha-1 antitrypsin deficiency: Dominance? Causes?
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
What is NASH/NAFLD? Associated with which metabolic syndrome? Mechanism?
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
``` Wilson's disease: Dominance? What is it? Deposition sites? Clinical signs? ```
• 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
What is hepatocellular carcinoma? Often arises in.... Aetiology?
Malignant liver tumour Often multifocal Often arises in cirrhotic liver Aetiology: - Aflatoxin (fungal origin) - Hep B and C viruses - Cirrhosis
30
6 pathologies of the biliary system?
1. Gallstones (cholelithiasis) 2. Cholecystitis 3. Cholangiocarcinoma 4. Obstruction Congenital malformations 5. Atresia 6. Cholesocal cysts
31
Cholangiocarcinoma: Location? Association? Causes?
* 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
Risk factors for gallstones? F's*
Female, Fair, Fat, Forty, Fertile | Diabetes mellitus
33
Most common gallstones?
Cholesterol (yellow), bile pigment (green) , *mixed*
34
What 6 conditions can gallstones lead to?
Cholecystitis, obstructive jaundice, cholangitis, pancreatitis, cholangiocarcinoma
35
Difference between acute and chronic cholecystitis?
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
What is an annular pancreas? | Presents as?
At 2nd part of duodenum Causes obstruction Presentation: Polyhydramnios, low birth weight, poor feeding
37
Pancreatitis: Acutely leads to? Chronic leads to?
``` 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
``` Pancreatic carcinoma: Type of cancer? Associations? Presentation? Clinical sign? Prognosis? ```
* 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