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Gastrology > Liver Disease > Flashcards

Liver Disease Flashcards

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

A

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

25
Q

Histology of acute hepatitis

A

diffuse hepatocyte injury seens as swelling throughout the liver (portal tracts, interface and parenchyma)
Hepatocyte death - acidophil body

26
Q

Management of acute hepatitis

A

remove or treat cause

liver support if severe dysfunction e.g confluent necrosis

27
Q

Acute cholestasis presentation

A

Acute onset of jaundice.

Elevated bilirubin, alk P, GGT also possibly alt/ast

28
Q

Causes of acute cholestasis

A

extra-hepatic biliary obstruction

Drug injury e.g Ab, NSAIDS, Steroids

29
Q

Histology of acute cholestasis

A

Brown bile (bilirubin)pigment with +/- acute hepatitis

30
Q

Fatty liver disease presentation

A

Acute or chronic “hepatitis” or

Asymptomatic abnormal LFTS

31
Q

Fatty liver disease Causes

A

Alcohol
Non alcholic (
Drugs (methotrexate, amiodarone, steroids)

32
Q

Chronic hepatitis definition

A

Liver inflamamtion (abnormal LFTS) for at least 6 months

33
Q

Presentation of chronic hepatitis

A

Chronic hepatitis or acute exacerbation

34
Q

Causes of chronic hepatitis

A

Viral (ep B or C)
Drugs
Autoimmune

35
Q

Aims in chronic hepatitis

A

Hep B&C have classical features. Assess grade and stage.

Liver support if severe disease. Specific treatment where possible

36
Q

Histology of chronic hepaittis

A

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
Q

Chronic hepatitis pathology reporting

A
  • 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
Q

Chronic biliary cholestatic disease

A

Chronic liver diseasepruritus due to excess bile acid

OR Abnormal LFTs- mainly alk P and GGT (for over 6 months)

39
Q

Causes of chhronic biliary cholestatic disease

A

Primary biliary cirrhosis:

Primary sclerosing cholangitis

40
Q

Histology of chronic biliary cholestatic disease

A

Focal, Portal predominant inflammation and fibrosis with bile duct injury
(granulomas in PBC).

41
Q

PBC

A
  • 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
Q

PSC

A
  • Rare, assoc with ulcerative colitis

* Risk of progression to cholangiocarcinoma

43
Q

Genetic deposition liver disease

A

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
Q

Hepatic vascular disease

A

• 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
Q

Drug induced disease

A
  • 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
Q

Masses Liver disease

A
  • for masses (space-occupying lesions and focal lesions) the main differential diagnosis is inflamm, benign or cancer
  • cancers include: metastases and primaries (HCC)
47
Q

Focal liver disease symptoms

A
  • Symptomatic- hepatomegaly, RUQ pain, jaundice

* Asymptomatic- incidental discovery by imaging or abnormal LFTs

48
Q

Focal liver disease investigations

A

imaging by- u/s, CT +/- a biopsy

49
Q

Types of focal liver lesions

A

Non neoplastic

  • development/degererative e,g cysts
  • inflammatory e.g abscess

Neoplastic

  • benigh
  • malignant
50
Q

Cysts

A

• 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
Q

Liver abscess

A
  • May arise from ascending cholangitis

* Also from Hydatid and other parasites

52
Q

Benign types of liver neoplasms

A

Benign 5%

Hepatocyte - Hepatocellular adenoma
Bile duct -bile duct adenoma
Blood vessel- haemangioma

53
Q

Malignant types of liver neoplasms

A

Hepatocyte - Hepatocellular carcinoma
Bile duct -cholangiocarcinoma
Blood vessel- Angiosarcoma

54
Q

Haemangioma

A
  • Benign blood vessel tumour

* Biopsy avoided because of bleeding risk

55
Q

Hepatic adenoma

A
  • 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
Q

Hepatocellular carcinoma

A
  • Most common primary liver tumour

* Usually rises in cirrhosis and associated with elevated alpha feto protein

57
Q

Cholangiocarcinoma

A
  • 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
Q

Liver metastases

A
  • Common
  • Mainly metastatic carcinoma especially adenocarcinoma
  • Especially from GI, Lung and Breast
  • Metastatic neuroendocrine and melanoma also common
  • Treatment usually standard chemo etc.
59
Q

How to tell the difference between intrahepatic jaundice and extra hepatic jaundice?

A

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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