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Medicine year 1 semester 2 > Case 10- Liver Pathology > Flashcards

Case 10- Liver Pathology Flashcards

1
Q

Causes of steatosis

A

1) Alcoholic liver disease
2) NAFLD- due to metabolic syndromes like obesity, type 2 diabetes mellitus, hypertension and hypercholesterolemia
3) Drugs- corticosteroids
4) Viral hepatitis
5) IBS and Wilson’s disease
6) Gastric bypass

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2
Q

Steatosis

A

1) Liver biopsy shows hepatocytes with very large, fat filled vacuoles.
2) Nuclei is therefore pushed to the periphery
3) Inflammatory cells surround the fat vacuoles

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3
Q

Steatohepatitis

A

A type of fatty liver disease characterised by inflammation of the liver with concurrent fat accumulation. Fatty liver disease with inflammation. Evidence of cell injury/cytoskeletal disruption, cell death and accompanying inflammation in the liver.

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4
Q

Changes that occur with Steatohepatitis

A

1) Ballooned hepatocytes
2) Mallory- Denk bodies- cytoskeletal aggregates made of proteins
3) Necroinflammation- lobular inflammation with lymphocytes, macrophages and neutrophils
4) Hepatic fibrosis, when severe it is portal-portal fibrosis which appears as a chicken wore pattern of fibrosis

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5
Q

Acute liver failure

A

There is development of severe acute liver injury with encephalopathy and impaired synthetic function (INR of>1.5) in a patient without cirrhosis or a pre-existing liver disease.

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6
Q

Chronic liver failure

A

When you have symptoms for more then 6 moths

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7
Q

Liver failure

A

A condition of severe end-stage liver dysfunction that is accompanied by a decline in mental status that may range from confusion (hepatic encephalopathy) to unresponsiveness (hepatic coma). Used synonymously with fulminant hepatic failure, acute hepatic necrosis

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8
Q

Hepatitis

A

Inflammation of the liver

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9
Q

Blood test results for hepatitis

A
  • Elevation in the serum aminotransferases (ALT and AST) compared with alkaline phosphatase.
  • Serum bilirubin may be elevated.
  • Tests of synthetic function may be abnormal.
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10
Q

Characteristics of Hepatitis

A

Inflammation of the portal tracts (portal triad) and adjacent lobules. There may also be necrosis. Inflammatory cells surrounding the portal triad

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11
Q

Causes of hepatitis

A
  • Infections (viral)- Hepatitis A, B, D, HIV, EBV, CMV and HSV.
  • Autoimmune- type 1 and 2 autoimmune hepatitis, SLE.
  • Drug induced liver injury- antibiotics (isoniazid), NSAIDs and herbal preparations.
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12
Q

Hepatotropic viral hepatitis

A

Causes inflammation to the liver only. Acute hepatitis is caused by HAV (Hepatitis A virus) and HEV, through the oral route. Chronic hepatitis is causes by HBV, HCV and HDV, which is transmitted through body fluids.

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13
Q

Non-hepatotropic viral hepatitis

A

Systemic effects with liver involvement. Acute hepatitis can be caused by CMV (cytomegalovirus), EBV (Epstein-Barr virus) and HSV (herpes simplex virus).

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14
Q

Hepatitis A virus

A

It is an RNA virus transmitted via the faecal-oral route (person to person or contaminated food and drink). Symptoms include nausea, anorexia, fever, malaise, abdominal pain, dark urine, pale stools and jaundice. It is diagnosed through detection of serum immunoglobulin IgM anti-HAV antibodies. It does not cause chronic hepatitis and has a self-limited course. Lifelong immunity once infected.

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15
Q

Hepatitis B virus

A

A DNA virus with 8 genotypes. Common in Southeast Asia and sub-Sahara Africa. It is through body fluids and from mother to child. 70% of patients have no symptoms, those who do have mild-flu like symptoms like nausea, vomiting and jaundice. It is diagnosed through serum markers including Hepatitis B surface antigens. Unlikely to progress to chronic infection.

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16
Q

Treatment for Hepatitis B virus

A

Supportive treatment for acute infection. For chronic infection prescribe antiviral agents such as pegylated interferon, Entacavir and Tenofovir.

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17
Q

How to identify Hepatitis B

A

Under a microscope you will see ground glass hepatocytes

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18
Q

What Hepatitis B cause

A

Hepatitis B acute infections can lead to recovery, fulminant hepatitis and chronic hepatitis. Chronic hepatitis can lead to Cirrhosis and then Hepatocellular carcinoma.

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19
Q

Hepatitis D virus (delta virus)

A

An RNA virus. Dependent on hepatitis B for life cycle, there is either coinfection or superinfection in a person who already has hepatitis B. It infects about 5% of hepatitis B infected patients. Acute hepatitis D is more severe then hepatitis B, it will exacerbate pre-existing liver disease due to HBV. Highest fatality rate of all hepatitis infections.

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20
Q

Hepatitis C virus

A

An RNA virus. Undergoes blood borne transmission via IV drug use, blood products and a needle stick injury. Infrequently sexually transmitted. Progresses to chronic disease in the majority of individuals, can be asymptomatic or non-specific symptoms like fatigue. Cirrhosis in 20-30%. Virus can recur in liver transplant. Successfully treated with antiviral (Sufosbuvir). 25% of all hepatocellular carcinomas are due to Hep c

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21
Q

Hepatitis E virus

A

Single stranded RNA virus, transmitted through the faeco-oral route. Found in animals. Can cause mild symptoms to fulminant hepatic failure. Has a high mortality rate among pregnant women.

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22
Q

Autoimmune hepatitis

A

Chronic and progressive hepatitis of unknown aetiology. The bodies immune system attacks the liver cell. Initially no symptoms. Leads to chronic hepatitis and therefore increased risk of cirrhosis and HCC. May be triggered by viral infections or drugs.
78% female predominance, often perimenopausal women with other immune disorders

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23
Q

Type 1 autoimmune hepatitis

A

Contains positive Antinuclear antigens (ANA), anti-smooth muscle antigens (SMA) and anti-soluble liver antigens. Normally involves adults.

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24
Q

Type 2 autoimmmune hepatitis

A

Contains anti-liver microsomal disease antibodies. Disease occurs predominantly in children.

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25
Q

Intrinsic drug induced hepatitis

A

Reactions are predictable and dose dependent i.e. paracetamol and alcohol

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26
Q

Idiosyncratic drug induced hepatitis

A

Unpredictable reaction due to individual genetic differences in the hepatic metabolites of drugs

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27
Q

The three main morphological features of cirrhosis

A
  • Bridging fibrous septa- can be portal-portal, linking portal tracts with one another or portal-central, linking portal tracts with terminal hepatic veins. Fibrosis is a dynamic process of collagen deposition and remodelling.
  • Parenchymal nodule formation- contains hepatocytes encircled by fibrosis, they vary from very small (micronodular <0.3cm) to large (several centimetres, macronodular). Nodularity results from cycles of hepatocyte regeneration and scarring.
  • Disruption of the architecture of the entire liver
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28
Q

Cirrhosis

A

Chronic disease of the liver resulting in the replacement of normal tissue with scar tissue

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29
Q

Stages in the development of cirrhosis

A

Fatty liver (fat depositions cause liver enlargement) –> Liver fibrosis (scar tissue forms, more liver cell injury occurs) –> Cirrhosis (scar tissue makes liver hard and unable to function properly)

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30
Q

Causes of cirrhosis

A

Alcoholic liver disease, Non-alcoholic fatty liver disease and Chronic viral hepatitis (hepatitis B, C).

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31
Q

Consequences of Cirrhosis

A
  • Portal Hypertension- causes Ascites (fluid build-up in the abdominal cavity), Hypersplenism (enlargement of spleen) and Oesophageal varices.
  • Synthetic dysfunction- coagulopathy (blood is unable to form clots) and Hypoalbuminaemia.
  • Hepatorenal syndrome- dysfunction of kidneys.
  • Hepatocellular carcinoma
  • Encephalopathy- damage to the brain
  • Hepatopulmonary syndrome- dysfunction of the lungs.
32
Q

The cardinal symptoms of liver disease

A
  • Jaundice- yellow skin and eyes
  • Oedema
  • Abdominal pain
  • Ascites- fluid in the abdomen
  • Dark urine, pale faeces
  • Pruritus- itch
  • Nausea, vomiting and loss of appetite
  • Bruising
  • Chronic fatigue
  • Encephalopathy- confusion.
33
Q

Primary liver cancer

A

Neoplastic transformation of normal cells within the liver

34
Q

Secondary liver cancer

A

Haematogenous (via blood) metastases from other primary malignant tumours. More common.

35
Q

Benign primary liver cancers

A

Hepatocellular adenoma (Hepatocytes), Intraductal papillary neoplasm (cholangiocytes) and Haemangioma (endothelial)

36
Q

Malignant primary liver cancers

A

Hepatocellular carcinoma (Hepatocytes), Cholangiocarcinoma (cholangiocytes) and Angiosarcoma (endothelial).

37
Q

The most common types of liver cancer

A

Hepatocellular carcinoma and Cholangiocarcinoma

38
Q

Hepatocellular adenoma

A

Extremely rare. Mostly incidental and in females. Risk factors are the oral contraceptive pill, anabolic steroids and pregnancy. It is a large adenoma with risk of haemorrhage and bleeding. It has a minor risk of malignant transformation. There are 5 different types.

39
Q

Differential diagnosis for Hepatocellular adenoma

A

Important to differentiate it from the malignant cancer HCC and focal nodular hyperplasia (FNH). FNH is non-neoplastic nodular overgrowth of the liver tissue.

40
Q

Pathology for Hepatocellular adenoma

A

Soft, well circumscribed, tan coloured tumour. Under a microscope it appears with sheets of bland hepatocytic cells without normal portal triads/tracts.

41
Q

Hepatocellular carcinoma

A

Solid tumour of malignant hepatocyte cells. It encompasses 80-90% of malignant liver tumours. 90% of these cases occur in cirrhosis.

42
Q

Risk factors for Hepatocellular carcinoma

A

Risk factors are Hepatitis B, Hepatitis C, Alcohol and non-alcoholic fatty liver disease. There are also hereditary risk factors. Most common in sub-sahara Africa and Asia due to the presence of Aflatoxin (fungal toxin) which is a risk factor for the disease. The toxin is often found in wheat stores.

43
Q

Clinical presentation for Hepatocellular carcinoma

A

Usually no symptoms except for chronic liver disease, important to continually survey patients with chronic liver disease in case cancer develops, normally done through ultrasound at regular intervals. It will present with upper abdominal pain, palpable mass and weight loss, but this will only happen when its very advanced.

44
Q

Pathology for Hepatocellular carcinoma

A

It appears round, soft, haemorrhagic and tan/green. There are often multiple tumours in cirrhosis. Under a microscope you can see abnormal hepatocytic cells in a mostly trabecular arrangement with intervening endothelial lined spaces. It stimulates the normal liver and produces bile.

45
Q

Cholangiocarcinoma

A

Malignant tumour of the epithelial cells lining the bile duct. Can affect any part of the bile duct, inside or outside the liver. Less common then HCC, higher prevalence South-East Asia. It is an adenocarcinoma so is composed of glands with mucin production, arising from the bile duct.

46
Q

Intrahepatic Cholangiocarcinoma

A

Occurs within the liver inside the bile duct

47
Q

Extrahepatic cholangiocarcinoma

A

Occurs outside the liver

48
Q

Hilar Cholangiocarcinoma

A

Occurs at the site where the bile duct exits the liver

49
Q

Causes of Cholangiocarcinoma

A

Cirrhosis, smoking, NAFLD Hep B/C, Alcohol, Inflammatory conditions of the bile duct

50
Q

Clinical presentation of intrahepatic Cholangiocarcinoma

A

Very late presentation, similar to HCC. Vague and insidious. Most people have pain without jaundice. Intrahepatic Cholangiocarcinoma can be differentiated into small duct and large duct. Small duct Cholangiocarcinoma occur in the peripheries of the liver and form mast cells. The large duct Cholangiocarcinoma’s tend to be near the hilum of the liver.

51
Q

Pathology of intrahepatic Cholangiocarcinoma

A

Firmer and whiter because lots of stroma, Scalloped margins, expansive

52
Q

Clinical presentation of hilar cholangiocarcinoma

A

Jaundice due to bile obstruction, abdominal pain, weight loss, itch and fever

53
Q

Pathology of hilar Cholangiocarcinoma

A

Infiltrating, ill-defined borders and fibrous

54
Q

Secondary liver tumours (metastases)

A

They are 20 times more common than primary tumours. The dual blood supply and fenestrated endothelium in the liver contribute to the high incidence of liver metastases. The most common type is metastases from intrabdominal primary tumours due to portal venous drainage: large bowel (colorectal), breast and lung carcinoma.
Tend to be well circumscribed lesions which make them easy to remove. In the bowel it forms an adenocarcinoma with high levels of necrosis and some mucin production.

55
Q

Liver function tests (LFT)

A

Measure hepatocellular damage rather then function, often difficult to interpret

56
Q

Blood tests used to examine hepatocellular damage

A
  • The transaminases: Alanine transaminase (ALT) / Aspartate transaminase (AST)
  • Alkaline Phosphatase (ALP)
  • Gamma glutamyl-transferase (GGT)
57
Q

Blood tests to evaluate the synthetic function of the liver

A

Tests how well the liver is working. Includes Bilirubin, Albumin, Coagulation screen and glucose

58
Q

How much bilirubin is needed for jaundice to occue

A

> 2.5mg/dl

59
Q

Transaminase

A

ALT and AST. Enzymes that metabolise amino acids. Some are found in the blood but most are in the hepatocytes, damage to the hepatocytes will cause transaminase to leak out and enter the blood. Elevated levels indicate hepatocellular damage. If they are raised on a LFT panel this is described as hepatitis/hepatocellular.

60
Q

Moderate elevation of the transaminase (ALT and AST)

A

<5 times upper limit of normal (ULN). are seen in most acute and chronic liver diseases e.g. alcohol and autoimmune related cirrhosis

61
Q

Extreme elevation of the transaminase (AST and ALT)

A

> 15-25 times ULN are seen in drug toxicity, acute viral hepatitis, ischaemic liver disease or sepsis.

62
Q

AST/ALT ratio

A

An AST/ALT of more then 2:1 suggests alcoholic liver disease. Most other causes result in a bigger increase in ALT.

63
Q

Alkaline phosphatase (ALP)

A

Found within the cells of the biliary tree (both intra and extra-hepatic). Raised blood concentration suggests cholestasis i.e. a decrease in bile flow due to impaired secretion by hepatocytes or an obstruction in the biliary tree.

64
Q

When does raised ALP suggest Cholestasis

A

Raised serum ALP is also found in states of high bone turn over e.g. osteoporosis or bone metastases. A combination of raised gamma glutamyl-transferase (GGT) and high ALP suggests a cholestatic/obstructive diagnosis. Whilst a raised ALP alone suggests high bone turnover.

65
Q

Bilirubin

A

Bilirubin is a breakdown product of red blood cells that is produced in the reticuloendothelial system. It is subsequently bound to albumin and transported to the liver to be conjugated. Conjugated bilirubin is then excreted via urine and bile, and this is what gives urine and stool its yellowish and brownish colour. Unconjugated bilirubin is insoluble and will not be excreted.

66
Q

Pre-hepatic bilirubin changes

A

Excessive amounts of Bilirubin going to the liver. For example, haemolytic anaemia which increases the levels of un-conjugated bilirubin in the blood.

67
Q

Hepatic bilirubin changes

A

Damage to the Hepatocytes leads to decreased ability to metabolise and conjugate bilirubin, leading to increase conjugated or un-conjugated bilirubin.

68
Q

Post-hepatic bilirubin changes

A

Biliary obstruction, leading to increased conjugated Bilirubin

69
Q

Albumin

A

Synthesised by the liver. Low plasma albumin concentrations suggest either decreased production (liver disease) or increased secretion (i.e. in nephrotic syndrome). As albumin has a relatively long half-life it is useful for monitoring chronic liver disease.

70
Q

Coagulation tests

A

Most clotting factors are synthesised by the liver, so when the liver is damaged less are produced. So it will take more time for blood to clot which can be used as a synthetic function test. Clotting factors have a short half life so can monitor liver on an hour-to-hour basis which is useful in life threatening situations.

71
Q

Prothrombin time (PT)

A

Normal range for PT is determined by the local lab. PT can be measured in seconds but can vary between labs depending on the method used. Measures how long it takes for blood to clot

72
Q

Internalised normalised ration (INR)

A

The INR reference range is based on the entire population to allow comparison between labs, its expressed as a ratio with 1.0 being normal. INR should only be used for warfarin monitoring. Measures how long it takes for blood to clot

73
Q

Pancreas blood tests

A

Amylase, Lipase

74
Q

Amylase- blood test

A

Produced by the Pancreas and secreted into the Pancreatic ducts which flow to the duodenum. If the Pancreas is inflamed or damaged, amylase can leak into the blood. Serum amylase is a biomarker for Pancreatic function.

75
Q

Lipase- blood tests

A

Produced by the Pancreas and leaks into the blood if the Pancreas is damaged. Is a slightly more sensitive biomarker of pancreatic function then Amylase.

76
Q

Acute Pancreatitis symptoms

A

1) Sudden epigastric/ LUQ pain
2) Pain radiates to the back
3) Nausea and vomiting
4) Anorexia
5) Sometimes pleural effusion

77
Q

Chronic Pancreatitis symptoms

A

1) Epigastric/LUQ pain
2) Pain is dull and radiates to the back
3) Pain is relieved when sitting forward and worse 30 mins after eating
4) Steatorrhoea, weight loss and nausea
5) 10% have jaundice

Medicine year 1 semester 2 (61 decks)

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