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Glasgow Phase 3 > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What is hepatic steatosis?

A

Simple fatty liver

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2
Q

What are the categories of non-alcoholic fatty liver disease?

A
  • Non alcoholic fatty liver. This is hepatic steatosis without evidence of hepatocellular injury.
  • Non alcoholic steatohepatitis. This is hepatis steatosis WITH hepatocellular injury. This may progress to cirrhosis and liver failure where as risk of NAFL risk is minimal.
  • Difference between two is histological features.
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3
Q

What are the definitions of acute inflammation, chronic inflammation and acute on chronic inflammation for liver disease

A

Acute - Agent causes injury but is then removed. Occurs days to weeks. Fulminant can occur which is severe acute rapidly progressing to liver failure.
Chronic - Agent causes injury then persists. Months to years. May causes fibrosis then cirrhosis.
Acute on chronic - Acute exacerbation with evidence of underlying chronicity

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4
Q

What is liver cirrhosis and the common causes

A

It occurs as a result of chronic inflammation. It is a diffuse process which results in fibrosis and formation of nodules of scar tissue. Fibrosis affects blood flow through the liver causing portal hypertension.
The common causes are alcoholic liver disease, NAFLD, Hepatitis B and Hepatitis C

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5
Q

What are key history questions to ask a patient presenting with liver pathology?

A
  • Any previous jaundice, T2DM, thyroid disease.
  • Any new prescriptions, OTC, herbal remedies.
  • Drug use, alcohol use, social situation, partner.
  • Any family history of jaundice, liver tumours, haemochromatosis
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6
Q

What results are included in a standard liver function test?

A
  • Bilirubin, AST, ALT, ALP, GGT, albumin.
  • However the best way to actually test the function of the liver is via albumin, prothrombin time and bilirubin.
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7
Q

Name some acute and chronic diffuse liver diseases

A

Acute - Acute hepatitis and acute cholestasis or cholestatic hepatitis.
Chronic - Fatty liver disease, chronic hepatitis, chronic biliary/cholestatic disease, genetic/deposition disease and hepatic vascular disease

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8
Q

What are the investigatory tests for acute liver disease?

A
  • Ultrasound liver + biliary tree.
  • Look for cause of acute viral hepatitis (HAV, HBV, HEV OR CMV)
  • Look for autoimmune hepatitis (ANA, SMA, LKM or raised IgG)
  • Look for paracetamol levels. Note theraputic levels may be toxic in patients under 50kg or with alcohol misuse.
  • Look for other drug induced liver injury
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9
Q

Explain the appearence of acute liver injury in histology

A

Hepatocyte injury appears as swollen cells. Spotty necrosis can appear where cells have died. Lots of plasma cells

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10
Q

What are ANA, SMA and LKM antibodies?

A

ANA = antinuclear antibodies,
SMA = Smooth muscle antibodies,
LKM = Liver kidney antibodies

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11
Q

What are causes of acute cholestasis/cholestatic hepatitis and its histological appearence

A
  • Extrahepatic biliary obstruction, eg gallstones or pancreatic disease, or drug injury eg, abx
  • Histologically there is brown bile pigment (bilirubin) +/- acute hepatitis
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12
Q

Describe features of drug induced liver disease

A
  • Many drugs can cause liver disease and it can cause almost any pattern of liver disease, so mimics other diseases.
  • Most are unpredictable however some arent eg, paracetamol or methotrexate
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13
Q

What is a specific histological feature of hepatitis B?

A

Ground glass cytoplasm in hepatocytes due to accumulation of surface antigens

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14
Q

What are the investigations for chronic liver disease?

A
  • Ultrasound,
  • Look for viral causes (HBV, HCV)
  • Look for autoimmune cause (Autoimmune hep - ANA, SMA, LKM antibody. Primary biliary cholangitis - anti-mitochondrial antibody and raised IgM. Primary sclerosing cholangitis - Anti-neutrophil cytoplasmic antibody)
  • Look for metabolic liver disease eg, haemochromatosis, Wilson’s disease or alpha 1 anti-trypsin deficiency.
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15
Q

What are the most common cause of chronic liver disease

A
  • Fatty liver (alcohol or non-alcohol)
  • Chronic viral hepatitis (commonly hep C)
  • Autoimmune liver disease (primary biliary cholangitis or autoimmune hepatitis)
  • Haemochromatosis
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16
Q

Describe features of autoimmune hepatitis and the treatment.

A

Presentation may be non specific and there is a variable presentation: Fatigue, weight loss, lethargy, weight loss, RUQ pain, acute jaundice, arthralgia or unexplained fever.
- There may be elevated AST, ALT, ANA, SMA, LKM, IgG. Biopsy is required for definitive diagnosis
- Treat with immunosuppressants (corticosteroids eg, prednisolone or azathioprine)

17
Q

What are some causes of chronic biliary/cholestatic disease and the histological appearance

A
  • Causes include primary biliary cholangitis or primary sclerosing cholangitis.
  • May appear with focal, portal predominant inflammation and fibrosis with bile duct injury.
18
Q

What is primary biliary cholangitis, its associations, presentation and treatment?

A
  • Autoimmune inflammation of small bile ducts in the liver causing cholestasis.
  • Presence of AMA,
  • Presents with tiredness, itching, jaundice. In early disease there is elevated GGT and ALP.
  • It is associated with other autoimmune diseases eg, Sjogren’s, hypothyroidism, rheumatoid arthritis
  • Treat with ursodeoxycholic acid
19
Q

What is primary sclerosing cholangitis

A

Condition where intrahepatic or extrahepatic bile ducts become strictured and fibrotic. Chronic bile obstruction can lead to hepatic inflammation, fibrosis and cirrhosis.
Association with ulcerative colitis.
Gold standard diagnosis is via MRCP.

20
Q

Describe features of Wilson’s Disease, the presentation and treatment

A
  • Autosomal recessive mutation in ATP7B gene which results in failure to transport excessive copper into bile.
  • It can present with chronic liver failure, neurological or psychiatric symptoms (parkinsonism), low caeruloplasmin, high urine copper levels and Kayser-Fleischer rings.
  • Treatment is via copper chelation (penacillamine) or oral zinc.
21
Q

Describe features of haemochromatosis, the presentation and treatment

A
  • Homozygous C282Y mutation of HFE gene.
  • It causes iron accumulation in tissue and organs. Can present with abnormal LFTs, polyarthropathy, adrenal insufficiency, heart failure, diabetes and skin pigmentation.
  • Diagnosis via liver MRI for iron.
  • Treatment with venesection
22
Q

How can you determine the difference between alcoholic or non alcoholic fatty liver disease

A

In alcoholic liver disease the AST is raised and so the AST/ALT ratio is above 1.5.
In NAFLD the AST is normal and the ALT can be raised so ratio is below 0.8

23
Q

What are the characteristics of alcoholic hepatitis and a scoring system which can be used?

A

It presents with excessive alcohol within 2 months and raised bilirubin for less than 2 months. Can present with hepatomegaly, fever, leucocytosis and hepatic bruit. Glasgow alcoholic hepatitis score can be used

24
Q

What are the tests for liver fibrosis and scoring systems

A

Tests for fibrosis = FIbroscan which measures hardness of liver, and blood tests eg, elevated liver fibrosis test and fibrotest. Different scoring systems for fibrosis exist eg, NAFLD fibrosis score Fib-4

25
Q

What is the clinical presentation of liver cirrhosis and a scoring system?

A
  • May be incidental with abnormal LFTs.
  • If decompensated then can have signs of advanced liver disease eg, Variceal haemorrhage, hepatic encephalopathy, ascites, hepato-renal failure, hepatocellular carcinoma.
  • Scoring system is the Childs-Pugh score which determines mild, moderate or severe.
26
Q

What is the diagnosis and treatment of ascites

A

Diagnostic tap to look for white cell count or lymphocytosis. Also to look for albumin level.
Treatment is via a low salt diet, diuretics eg spironolactone or furosemide, or large volume paracentesis.

27
Q

Describe features of hepatic encephalopathy (precipitating factors, presentation and treatment)

A
  • Avoid giving sedation, opioids. GI bleeds, infections, electrolyte disturbances can make it worse.
  • It can present with asterixis
  • Treatment is via non-absorbable, disaccharides (lactulose) and non absorbable antibiotics to reduce urease produced by gut.
28
Q

What are some benign non neoplastic SOL of the liver?

A
  • Cysts, eg, Von Meyenberg complex
  • Abscess
29
Q

Describe features of hepatic haemangiomas and hepatic adenomas and their importance

A
  • Differential diagnosis of metastasis hence their importance.
  • Haemangioma is a benign blood vessel tumour. Avoid biopsy because of bleeding risk.
  • Hepatic adenoma - Rare tumour of epithelium which mainly affects young women, is associated hormonal therapy and requires excision
30
Q

Describe features of hepatocellular carcinomas

A
  • Most common primary tumour of liver and commonly occurs in patients with cirrhosis, associated with elevated serum AFP.
  • Diagnosis is based on two cross sectional scans: CT AND MRI with the typical features.
  • Treatment includes: Kinase inhibitors (Sorafanib), radiofrequency ablation, TACE, resection or transplant.

Glasgow Phase 3 (148 decks)

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