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MD3002 - GI Disease/Pathology > Hepatobiliary and Pancreatic Disease > Flashcards

Hepatobiliary and Pancreatic Disease Flashcards

1
Q

What does the liver synthesise?

A

albumin, clotting factors, complement, -1-antitrypsin, thrombopoietin

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2
Q

What is produced in the liver?

A

bile through conjugation of bilirubin

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3
Q

What does the liver break down?

A

drugs, insulin, ammonia

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4
Q

What is the action of Kupffer cells?

A

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

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5
Q

What is jaundice?

A
  • Yellowing of skin and mucosal surfaces – bilirubin >40mol/L
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6
Q

What can jaundice cause?

A

itch

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7
Q

Unconjugated =

A

water-insoluble

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8
Q

conjugated =

A

water-soluble (can be excreted in urine)

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9
Q

What is the result of excess conjugated bilirubin?

A

dark urine

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10
Q

Describe a prehaptic cause of jaundice

A

haemolysis  release of bilirubin from RBCs

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11
Q

Describe a intrahepatic cause of jaundice

A

liver disease; excess bilirubin in liver and bloodstream

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12
Q

Describe a post hepatic (obstructive) cause of jaundice

A

obstruction of bile outflow –> dark urine and pale stools

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13
Q

What are the main causes of acute liver injury?

A

o Viral Infections o Alcohol o Biliary obstruction (gallstones) o Adverse drug reactions

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14
Q

What are the main symptoms of acute liver injury?

A
  • Jaundice, malaise
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15
Q

What biochemical factors are altered in acute liver injury

A
  • Raised serum bilirubin (location determines the type of bilirubin) and transaminases
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16
Q

What are the main characteristics of acute liver failure?

A

decreased albumin, ascites, bruising, encephalopathy

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17
Q

What zone of liver cells are affected in acute liver injury?

A

Zone 3 = closest to the central vein so have the least oxygen. Less reserve for survival when infected with a toxin

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18
Q

What are the major characteristics of alcoholic liver injury?

A

 Steatosis  Cirrhosis  Acute hepatitis with Mallory’s hyaline

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19
Q

What processes occur in steatosis that lead to fibrosis?

A

Acetaldehyde binds to hepatocytes causing damage ⇒ inflammatory reaction

Inflammation ⇒ fibrosis

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20
Q

What processes pccur in cirrhosis?

A

fibrosis (collagen) + regeneration –> Cirrhosis

Fibrosis tries to heal the area by preventing any further damage so inflammation cannot spread. As a result this area of the liver has no function and is stiffer

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21
Q

Causes of cirrhosis

A
  • Alcohol
  • Hep B + C
  • Iron overload
  • autoimmune liver disease
  • gallstones
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22
Q

What are the main classifications of Cirrhosis?

A
  • Morphological
    • Micronodular – nodules <3mm
    • Macronodular >3mm
    • Mixed
  • Aetiological
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23
Q

What are the three main complications of cirrhosis?

A
  • liver failure
  • portal hypertension
  • hepatocellular carcinoma
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24
Q

What are the common features of liver failure?

A

hepatic encephalopathy (ammonia), build-up of steroid hormones ⇒ hypoestrogenism (palmar erythema and gynaecomastia), bleeding

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25
Q

What are the common features of portal hypertension

A

increased hepatic vascular resistance, AV shunting – oesophageal varices, haemorrhoids, caput medusae

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26
Q

Describe drug induced liver injury

A
  • 10% of all drug reactions involve the liver
  • Injury to liver cells (hepatocellular) – paracetamol overdose
  • Injury to bile production/secretion cells (cholestatic) – methyl testosterone
  • Always take a full drug history from a patient with deranged LFTs
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27
Q

What is the most common cause of acute biliary obstruction?

A

gallstones

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28
Q

What are the symptomns of acute biliary obstruction?

A

causes colicky pain and jaundice

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29
Q

What can be the main complication of acute biliary obstruction?

A

complicated by infection of blocked CBD - cholangitis (medical emergency)

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30
Q

What can chronic liver failure follow on from and what can it result in?

A
  • A common clinical problem
  • Can follow a clinical evident episode of acute liver injury
  • May have insidious onset without symptoms until later stages
  • Many forms culminate in cirrhosis
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31
Q

What is chronic hepaitis?

A
  • inflammation of the liver lasting more than 6 months
  • Sustained elevation of transaminases – require liver biopsy to classify cause
32
Q

What are the main causes of chronic hepaitis?

A
  • Viral
  • Alcohol
  • Drugs
  • Autoimmune
33
Q

What are the three main classifications of chronic hepaitis?

A

Type – aetiology

Grade – degree of inflammation

Stage – degree of fibrosis

34
Q

What is NASH/NAFLD?

A

Non-alcoholic steatohepatitis/Non-alcoholic fatty liver disease

35
Q

What are NASH/NAFLD associated with?

A

Associated with metabolic syndrome (DM II, hypertension, decreased HDL cholesterol, ­increased triglycerides)

36
Q

What can fat deposition in hepatocytes lead to?

A

cirrhosis

37
Q

Who is autoimmune chronic hepatitis likely to occur in?

A

Females > Males

Usually present in mid to late teens

38
Q

Describe the main features of autoimmune chronic hepaitis

A
  • Interface hepatitis - hepatocytes at the interface between the bloodstream and the main hepatic substance
  • Plasma cells and swollen hepatocytes
  • Fibrosis
  • ANA, SMA, raised serum IgG and transaminases, anti-LKM (liver-kidney microsomal)
  • Patients may benefit from steroids
39
Q

Who is primary biliary cholangitis more common in?

A

Females > Males (~40-50 years old)

40
Q

What are the stages of primary biliary cholangitis?

A
  • Autoimmune destruction of bile duct epithelium – de3nse lymphocytic infiltration and granulomas
  • Proliferation of small bile ducts
  • Architectural disturbance – portal and bridging fibrosis
  • Cirrhosis
41
Q

What are the main clinical and biochemical features of primary biliary cholangitis?

A

Jaundice, pruritis, xanthelasmata

Raised ALP + IgM, AMA

42
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Age/Gender

A

PBC = >50years, NOT children, F > M

PSC = Wide age range, M > F

43
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Disease associations

A

PBC = other autoimmune diseases e.g. Sjorgens, thyroid

PSC = IBD; UC

44
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Serum immunoglobulins

A

PBC = increased IgM

PSC = no signficant increase

45
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Autoantibodies

A

PBC = AMA, ANA (centromeric)

PSC = non-specific, AMA rare

46
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Colangiography

A

PBC = normal extrahepatic and large ducts

PSC = stricturing and beading

47
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Bile duct injury

A

PBC = small ducts

PSC = large ducts

48
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Portal inflammation

A

PBC = prominent

PSC = less prominent

49
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Obliterative fibrosis of larger ducts

A

PBC = absent

PSC = characterisitc feature

50
Q

Compare primary biliary cholangitis and primary sclerosing cholangitis:

Periportal copper

A

Present in PBC and PSC

51
Q

What is haemochromatosis?

A

Iron deposition in the liver causing alteration of architecture ⇒ fibrosis ⇒ cirrhosis

52
Q

AMA =

A

antimitochondrial antibody

53
Q

ALP =

A

alkaline phosphatase

54
Q

What are the main types of haemochromatosis?

A

Primary/secondary

Primary = Autosomal recessive – HFE gene

Secondary = from repeat blood transfusions

55
Q

What is the treatment for haemochromatosis?

A

Regular venesection – test iron and ferritin

56
Q

What causes alpha-1 antitrypsin deficiency?

A

Autosomal recessive disorder

Low levels of a-1-antitrypsin in the blood but high levels in the liver

57
Q

What is the pathogenesis of a-1-antitripsin?

A
  • Proteins build up in hepatocytes as hyaline
  • Can lead to cirrhosis
  • Associated with emphysema
58
Q

What type of condition is wilson’s disease?

A

autosomal recessive

59
Q

What is the pathophysiology of Wilson’s disease?

A
  • Failure of the liver to excrete copper in bile ⇒ build-up of copper in the liver ⇒ cirrhosis
  • Copper also deposits in brain tissue ⇒ neurological dysfunction
    • Kayser-Fleischer rings
    • Low ceruloplasmin
60
Q

What are the main type of developmental/Hamartomas liver tumours?

A

Cysts

Haematomas

61
Q

What are the main type of benign liver tumours?

A

Incidental finding

Adenoma, haemangioma

Liver cysts

62
Q

What are the main type of maligant liver tumours?

A
  • Metastases – common (from colon)
  • Primary
    • Hepatocellular carcinoma
    • Cholangiocarcinoma
63
Q

What are the main causes of hepatocellular carcinoma?

A
  • Aflatoxins – fungal origin
  • Hepatitis B + C viruses
  • Cirrhosis (any cause)
64
Q

What are the main pathologies assoicated with the biliary system?

A
  • Congenital malformations
    • Atresia
    • Choledochal cysts
  • Gallstones (cholelithiasis)
  • Cholecystitis
  • Cholangiocarcinoma
  • Obstruction
65
Q

Where does cholangiocarcinoma arise from anf what is it associated with?

A

Arises from bile duct epithelium anywhere in the biliary system (intra- and extra-hepatic)

Associated with ulcerative colitis (PSC also at risk)

66
Q

What are the symptoms and clinical complications associated with cholangiocarcinoma?

A
  • Causes obstructive jaundice, itch, weight loss and lethargy
  • Can lead to rupture of common bile duct or gallbladder – prognosis poor
67
Q

What are the main risk factors for gallstones?

A

Female, Fair, Fat, Forty, Fertile

Diabetes

68
Q

What can gallstones cause?

A

cholecystitis, obstructive jaundice, cholangitis, pancreatitis, cholangiocarcinoma

69
Q

What are the main features of acute cholescysitis?

A
  • Usually caused by gallstones
  • Initially sterile then becomes infected
  • May lead to abscess/rupture
  • Symptoms
    • RUQ pain (biliary colic), fever, nausea/vomiting
70
Q

What are the features of chronic cholecystitis?

A

Invariably related to gallstones

Chronic inflammation with wall thickening

71
Q

What is annular pancreas?

And what can this cause?

A
  • Embryological malformation - part of the pancreas rotates the wrong way
  • 2nd part of duodenum
  • Causes obstruction – polydramnios, low birth weight, poor feeding
72
Q

What are the main features of acute pancreatitis?

A
  • Causes catastrophic metabolic consequences
  • High serum amylase – diagnostic
  • Massive fluid losses –> SHOCK
  • High mortality rates
73
Q

What are the main causes of acute pancreatitis?

A
  • mumps
  • gallstones
  • shock (decreased BP)
  • hypothermia
  • alcohol
  • trauma
  • scorpion sting
74
Q

What are the biocehmical markers of acute pancreatitis?

A

decreased calcium and albumin, increased glucose

75
Q

What are the main features of chronic pancreatitis?

A
  • Multiple episodes of acute
  • Causes fibrosis of pancreas – may lead to diabetes mellitus
  • Reduced production of enzymes – require supplements (creon)
76
Q

Describe the main features of pancreatic carcinoma

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 - GI Disease/Pathology (11 decks)

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