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Liver Disease Flashcards

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1
Q

Normal liver functions

A
  • Protein, carbohydrate and fat metabolism
  • Plasma protein and enzyme synthesis
  • Production of bile
  • Detoxification
  • Storage of proteins, glycogen, vitamins and metals
  • Immune functions
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2
Q

Normal structure of the liver

A
  • Vasculature: Incoming portal vein and hepatic artery. Outgoing hepatic vein to IVC
  • Parenchymal liver cells (limiting plate (interface)-sheet of hepatocytes lying against the peri-portal connective tissue). Damage to the interface = interface hepatitis, can lead to fibrosis.
  • Biliary system
  • Connective tissue matrix
  • All arranged as portal tracts (portal vein, hepatic artery and bile duct) with surrounding parenchyma in acini structure
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3
Q

Portial triad components

A

Bile Duct
Hepatic artery
Hepatic portal vein branch

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4
Q

Causes of liver injury

A 
Vascular (portal hypertension)
Infection (hep C& )  
Traumatic (obstruction to bile or blood flow) 
Autoimmune - ALD 
M- metabolic (drugs, toxins, alcohol), fatty liver disease 
Iatrogenic/idiopathic 
Neoplastic 
Congenital - genetic (haemochromatosis) 
Degenerative 
Enviromental
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5
Q

Inflammation

A

body’s response to injury

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6
Q

Acute inflammation

A

agent causes injury but its then removed

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7
Q

Chronic inflammation

A

agent causes injury but then persists

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8
Q

Presentation of acute

A

Days to weeks. N.B.

“Fulminant” = severe acute, rapidly progressing towards liver failure

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9
Q

Presentation of chronic

A

Months to years

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10
Q

Acute on chronic presentation

A

Chronic liver disease often presents with acute exacerbation of disease but with evidence of underlying chronicity e.g. fibrosis. Common presentation in autoimmune conditions also.

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11
Q

Inflammation target

A
  • Injurious agent causes cell damage and sometimes death, often with inflammatory cell infiltrate e.g. alcohol, virus.
  • Liver injury often mainly to parenchyma (hepatocytes); but bile ducts or rarely blood vessels can be the main target
  • Parenchyma, bile ducts, blood vessels and connective tissue are inter-dependent, so damage to one damages the others
  • Chronic inflammation common in liver and may increase connective tissue (fibrosis)
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12
Q

Cirrhosis 3 parts

A
  • Diffuse process with
  • Fibrosis &
  • Nodule formation

= end-stage liver disease

Main treatment and diagnosis aim 
-acute not to chronic 
-chronic not to cirrhosis 
0cirhosis not to portal hy[ertension 
-
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13
Q

Liver signs

A

hepatomegaly

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14
Q

Portal hypertension

A

ascites and encephalopathy

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15
Q

Chronic dysfuncion

A

pruritis, spider naevvi, jaundce

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16
Q

Non specific symptoms

A

nausea, falls, tremor (liver flap)

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17
Q

Abnormal biliary systen

A

o Accumulation of bilirubin (esp. acute cholestasis); jaundice
o Accumulation of bile acids (esp chronic cholestasis); pruritis

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18
Q

Abnormal parenchyma

A

o Right upper quadrant pain (RUQ)
o In chronic diseasehormone changes (gynaecomastia)
o Liver failure only occurs once

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19
Q

Liver investigations - blood

A

• LFTs:
Transaminases- ALT, AST, Alkaline phosphatase- ALK P, Gamma glutamyl transferase-GGT,
Bilirubin and albumin
• Liver-related haematology test e.g. Prothrombin time- tests synthetic function
• Synthetic function PPT and Albumin

Other tests
• Viral serology
• Autoimmune serology
• Liver metabolic/genetic diseases- iron, copper and alpha-1-antitrypsin
• Alpha-fetal protein hepatocellular carcinoma
• Radiology- especially useful for masses: Ultrasound of abdomen, CT of abdomen. ERCP/MRCP
• Biopsy - only in few cases due to significant morbidity.

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20
Q

Modes of presentation with liver disease

A

Modes of Presentation with Liver disease

  1. Asymptomatic- abnormal LFTs, abnormal imaging (Abnormalities incidental or on screening: increasingly common presentations esp. to GP)
  2. Symptomatic- classic signs (jaundice or ascites) or more general (malaise, itch, anorexia)
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21
Q

Two diagnosis of liver disease

A

Diffuse liver disease

space-occupying lesion

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22
Q

Liver disease falls into broad patterns

A 
acute hepatitis, 
acute cholestasis, 
fatty liver disease, 
chronic hepatitis, 
chronic biliary disease, 
hepatic vascular disease and deposition/genetic disease.
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23
Q

Acute hepatitis Presentation

A

short history of RUQ pain
tendereness
malaise
Elevated AST/ALT

paracetemol overdose AST/ALT in thousands, massive necrosis

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24
Q

Causes of acute hepatitis

Study These Flashcards
A

viral hepatitis
autoimmune
drug injury
(Viral, drug, autoimmune)

25
Histology of acute hepatitis
diffuse hepatocyte injury seens as swelling throughout the liver (portal tracts, interface and parenchyma) Hepatocyte death - acidophil body
26
Management of acute hepatitis
remove or treat cause | liver support if severe dysfunction e.g confluent necrosis
27
Acute cholestasis presentation
Acute onset of jaundice. Elevated bilirubin, alk P, GGT also possibly alt/ast
28
Causes of acute cholestasis
extra-hepatic biliary obstruction | Drug injury e.g Ab, NSAIDS, Steroids
29
Histology of acute cholestasis
Brown bile (bilirubin)pigment with +/- acute hepatitis
30
Fatty liver disease presentation
Acute or chronic "hepatitis" or | Asymptomatic abnormal LFTS
31
Fatty liver disease Causes
Alcohol Non alcholic ( Drugs (methotrexate, amiodarone, steroids)
32
Chronic hepatitis definition
Liver inflamamtion (abnormal LFTS) for at least 6 months
33
Presentation of chronic hepatitis
Chronic hepatitis or acute exacerbation
34
Causes of chronic hepatitis
Viral (ep B or C) Drugs Autoimmune
35
Aims in chronic hepatitis
Hep B&C have classical features. Assess grade and stage. | Liver support if severe disease. Specific treatment where possible
36
Histology of chronic hepaittis
appears like acute combined with fibrosis (masson stain) -often appears mainly at portal tracts with lymphoid aggregates In viral hepatitis B- ground glass cytoplasm in hepatocytes due to accumulation of sAg (one of three main HB viral antigens)
37
Chronic hepatitis pathology reporting
* Activity (grade); degree of inflammation and sites: Portal, interface & parenchymal inflammation. Guides treatment * Yields histological summary and numerical score e.g. chronic hepatitis with mild activity and mild fibrosis, Ishak score grade 4/18 and stage 2/6 * Facilitates follow-up and monitoring of treatment including clinical trials
38
Chronic biliary cholestatic disease
Chronic liver diseasepruritus due to excess bile acid OR Abnormal LFTs- mainly alk P and GGT (for over 6 months)
39
Causes of chhronic biliary cholestatic disease
Primary biliary cirrhosis: | Primary sclerosing cholangitis
40
Histology of chronic biliary cholestatic disease
Focal, Portal predominant inflammation and fibrosis with bile duct injury (granulomas in PBC).
41
PBC
* Middle aged woman * Autoimmune disease with serum anti-mitochondrial antibodies (AMA) and high IgM * Despite the name is not cirrhotic from the outset, it is progress from fibrosis to cirrhosis * No cure but ursodeoxycholic acid eases symptoms and slows progression; liver transplant at end stage.
42
PSC
* Rare, assoc with ulcerative colitis | * Risk of progression to cholangiocarcinoma
43
Genetic deposition liver disease
Haemochromatosis - Iron Wilsons disease - coppper Alpha-1-anti-trypsin deficiency-lack of secretion from an accumulated in liver • May mimic other forms of liver disease • Due to uncontrolled iron or copper accumulation in liver and other organs; easily treatable by increased removal
44
Hepatic vascular disease
• Main form= hepatic vein outflow obstruction 1. Major form = budd-chiari syndrome causing hepatic vein thrombosis a. Often fatal due to pro-thrombotic tendency b. Early identification permits anti-coagulant therapy 2. Lesser degrees are more common and milder e.g. nodular regenerative hyperplasia
45
Drug induced disease
* Drugs can cause almost any pattern of liver disease so usually enter differential diagnosis, esp. acute hepatitis and acute cholestasis/cholestatic hepatitis * Most drug hepatotoxicity is idiosyncratic (rare but usually single clinical pattern) thus hard to investigate Augmentin, co-amoxiclav (cholestatic) * Occasionally predictable liver damage e.g. methotrexate, paracetemol * Don’t forget non-perscribed drugs
46
Masses Liver disease
* for masses (space-occupying lesions and focal lesions) the main differential diagnosis is inflamm, benign or cancer * cancers include: metastases and primaries (HCC)
47
Focal liver disease symptoms
* Symptomatic- hepatomegaly, RUQ pain, jaundice | * Asymptomatic- incidental discovery by imaging or abnormal LFTs
48
Focal liver disease investigations
imaging by- u/s, CT +/- a biopsy
49
Types of focal liver lesions
Non neoplastic - development/degererative e,g cysts - inflammatory e.g abscess Neoplastic - benigh - malignant
50
Cysts
• Usually developmental or degenerative • Single or multiple (if many, normally part of a syndrome e.g.polycystic kidnay disease) • Commonest= Von Meyenberg complex= simple biliary hamartoma o Important as it can resemble a metastases but no treatment is required
51
Liver abscess
* May arise from ascending cholangitis | * Also from Hydatid and other parasites
52
Benign types of liver neoplasms
Benign 5% Hepatocyte - Hepatocellular adenoma Bile duct -bile duct adenoma Blood vessel- haemangioma
53
Malignant types of liver neoplasms
Hepatocyte - Hepatocellular carcinoma Bile duct -cholangiocarcinoma Blood vessel- Angiosarcoma
54
Haemangioma
* Benign blood vessel tumour | * Biopsy avoided because of bleeding risk
55
Hepatic adenoma
* Relatively rare * Mainly in young women, often associated with hormonal therapy esp. OCP * No background cirrhosis * Risk of bleeding and rupture * Treatment: excision if large
56
Hepatocellular carcinoma
* Most common primary liver tumour | * Usually rises in cirrhosis and associated with elevated alpha feto protein
57
Cholangiocarcinoma
* Adenocarcinoma of the bile ducts- intra or extra hepatic * Diagnosis on imaging and cytology (hard to distinguish from metastatic adenocarcinoma) * Poor prognosis * Curative surgery or palliate
58
Liver metastases
* Common * Mainly metastatic carcinoma especially adenocarcinoma * Especially from GI, Lung and Breast * Metastatic neuroendocrine and melanoma also common * Treatment usually standard chemo etc.
59
How to tell the difference between intrahepatic jaundice and extra hepatic jaundice?
In hepatic jaundice or liver disease ALT>AST, with a high bilirubin In post hepatic jaundice ALP>AST with a high bilirubin (obstructive jaundice) Remember ALT is predominantly found in the in the liver hepatocytes

Gastrology (19 decks)

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