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Clinical pathology > Medical liver diseases > Flashcards

Medical liver diseases Flashcards

1
Q

Jaundice definition

A
  • First visible in sclera: white of eye
  • Classified according to where the abnormality is in the metabolism of bilirubin
  • Visible when bilirubin >40umol/l
  • Commonest sign of liver disease
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2
Q

Pre-hepatic jaundice

A
  • Too much bilirubin produced
  • Haemolytic anaemia, Gilbert’s syndrome: enzyme deficiency
  • Unconjugated: bound to albumin, insoluble, not excreted = patient notices yellow eyes/skin only
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3
Q

Hepatic jaundice

A
  • Too few functioning liver cells
  • Acute diffuse liver cell injury, End stage chronic liver disease, Inborn errors
  • Mainly conjugated: soluble = patient notices yellow eyes and dark urine
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4
Q

Post-hepatic jaundice

A
  • Bile duct obstruction

- Conjugated: soluble, excreted, but can’t get into gut = patient yellow eyes, pale stool and dark urine

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5
Q

Simplified Pathways of Bilirubin Metabolism

A
  • Bilirubin produced by RBC breakdown = unconjugated

- Metabolised in liver: conjugated and excreted in bile

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6
Q

Investigation of Jaundice

A
  • Ultrasound scan to check for dilated ducts – indicates an obstruction of biliary duct
  • If no dilated ducts, biopsy to find cause of jaundice
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7
Q

Jaundice clinical features

A
  • bile salts in the skin = patient itchy
  • Jaundice in the skin, patient = yellow
  • Over time, oedema reduces and fibrosis increases
  • Characteristic appearance: Biliary Gestalt
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8
Q

Jaundice histopathological features

A
  • bile in the liver parenchyma
  • Bile salts and copper can’t get out: accumulate in hepatocytes
  • Bile pigment is visible in bile plugs
  • ## Swelling and irregularity of hepatocytes and inc activity of macrophages
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9
Q

Acute Hepatitis

A
  • Inflammation in the liver
  • acute liver injury caused by something that goes away
  • Recent onset will resolve back to normal
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10
Q

Chronic hepatitis

A
  • Inflammation in the liver
  • chronic liver disease caused by something that doesn’t go away
  • Results in ongoing liver cell injury and progressive structural liver damage of scarring and remodelling
  • Persistence of abnormal liver tests for more than 6 months
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11
Q

Causes of acute hepatitis

A
  • Damage hepatocytes, short term:
  • Inflammatory injury: hepatitis: Viral, Drugs, Autoimmune, Unknown: seronegative
  • Toxic/ metabolic injury: alcohol, drugs (paracetamol)
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12
Q

Commonest causes of severe liver cell injury in the UK =

A

alcohol and paracetamol toxicity

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13
Q

acute hepatitis pathogenesis

A
  • Mild: death of individual hepatocytes

- Rare severe end: hepatocytes die faster than replaced; rapidly progressing organ failure and possibly death

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14
Q

Causes of Chronic Hepatitis

A
  • Immunological injury: virus, autoimmune, drugs
  • Toxic/ metabolic injury: fatty liver disease, alcohol, drugs – most common cause
  • Genetic inborn errors: iron, copper, alpha 1 antitrypsin
  • Biliary disease: autoimmune, duct obstruction
  • Vascular disease: clotting disorders, drugs
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15
Q

Pathology of Chronic Liver disease

A
  • Injury to liver cells, inflammation, formation of scar tissue and regeneration of hepatocytes
  • Continuing liver damage is combined with the body’s attempts at regeneration of hepatocytes and repair: the wound healing of angiogenesis and fibrosis
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16
Q

Progression of Chronic Liver Disease

A
  • Scarring gradually increases and starts to link vascular structures (bridging) eventually transforming the liver tissue into separate nodules = end stage = cirrhosis
  • remodelling = bands of fibrosis that bridge between portal tracts and hepatic veins
  • Remodelling becomes complete, and hepatocytes form nodules surrounded by fibrous tissue
  • Portal blood entering the liver can flow through vessels in the fibrous tissue and not percolate through sinusoids, The cirrhotic liver therefore is inefficient in metabolic function
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17
Q

Viral Hepatitis

A
  • Hepatotrophic viruses (Specifically affect hepatocytes)
  • A, B, C
  • D = delta, only in people with B
  • E = waterborne
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18
Q

Alcohol and the liver

A
  • steatophepatitis
  • spectrum of fatty change associated with inflammation - can lead to cirrhosis
  • Alcohol = major cause of liver disease
  • Some patients with alcohol injury may just show fatty change: a reversible stage of liver injury that may or may not progress to steatohepatitis
19
Q

Steatohepatitis =

A

collagen surrounds cells like chicken wire, increases as well as portal tract fibrosis

20
Q

Obesity: NAFLD

A
  • Non-alcoholic fatty liver disease
  • Associated with metabolic syndrome: obesity, T2DM, hyperlipidaemia
  • commonest cause of liver disease
21
Q

NAFLD

A
  • NAFLD = liver counterpart to metabolic syndrome
  • Insulin resistance from excess of calorie intake over body’s demands means fat is stored in the body in various compartments including the liver:
  • Stored in the liver = fatty liver or steatosis
  • More serious complications include cirrhosis and steatohepatitis
22
Q

Drug induced liver injury (DILI) classification

A
  • Classified by its hepatotoxicity
  • Intrinsic e.g. paracetamol - every time, predictable; Anyone taking this drug is likely to get liver damage
  • Idiosyncratic: rare, unpredictable, metabolic and immunological input
23
Q

Drug induced liver injury (DILI)

A
  • Acute liver injury
  • Raised liver enzymes
  • Commonest symptom of DILI = jaundice
  • Paracetamol toxicity = commonest cause of acute liver failure
  • Paracetamol toxicity = necrosis of a high proportion of hepatocytes in a predictable, zonal distribution without any inflammation
24
Q

Haemochromatosis

A
  • Inborn error of iron metabolism: bronzed diabetes
  • abnormality of HFE gene
  • Failure of iron absorption regulation, excess iron stored in various organs: liver, pancreas, joints, skin, heart
25
Q

Haemochromatosis diagnosis

A
  • high serum levels of transferrin
  • Large amounts of iron in hepatocytes cause liver injury
  • Liver biopsies are stained with Perls’ stain for iron = blue
26
Q

Haemochromatosis treatment

A

Treatment = easy, Frequent venesection

- remove blood to decrease iron usage in making more blood which will deplete iron stores to normal

27
Q

Wilson’s Disease definition

A
  • Inborn error of copper metabolism

- Causes little caeruloplasmin, a copper transport protein in blood = copper accumulation

28
Q

Wilson’s Disease diagnosis

A
  • CP levels in the blood can be tested
  • low serum copper, high urinary copper (24hr urine collection) and high copper in liver tissue
  • Rhodamine stain: copper = brown
29
Q

Wilson’s Disease treatment

A

Treatment: to chelate copper - mineral supplement that may be better absorbed and easier on the stomach] and enhance its excretion

30
Q

Alpha 1 Antitrypsin deficiency

A
  • Inborn error of metabolism results in abnormal structure of A1AT, which folds wrongly and can’t be excreted from hepatocytes. There are many types, the commonest is PiZZ
31
Q

Alpha 1 Antitrypsin deficiency diagnosis

A
  • The accumulated A1AT forms globules of glycoprotein that stain positive with PAS diastase stain
  • low levels of A1AT in the serum
32
Q

Alpha 1 Antitrypsin deficiency pathogenesis

A
  • This damages liver cells, may lead to fibrosis and cirrhosis
  • low levels of A1AT in the serum make the patient susceptible to emphysema
33
Q

Alpha 1 Antitrypsin

A

protein made in the liver excreted into blood where it functions to neutralise proteolytic enzymes, particularly from active polymorphs

34
Q

Autoimmune hepatitis definition

A

chronic liver disease due to disturbance of the immune system with recognition of ‘self-antigens’ leading to chronic inflammation and destruction of hepatocytes

35
Q

Autoimmune hepatitis features

A
  • Autoimmune hepatitis
  • Diagnosis based on auto-antibodies - raised IgG, ALT
  • prominent interface hepatitis with lots of plasma cells seen on biopsy
36
Q

Primary biliary cholangitis

A
  • Anti-mitochondrial antibodies; IgM, raised alkaline phosphatase
  • Commoner in women
  • Bile duct injury characterised by granulomatous inflammation = destruction of bile ducts
37
Q

Primary Sclerosing Cholangitis (PSC)

A
  • More sinister
  • Associated with ulcerative colitis, high ALP
  • Commoner in men
  • characteristic pruned tree on cholangiogram
  • Periductal onion skin fibrosis
38
Q

urso-deoxycholic acid

A
  • A bile salt analogue which delays disease progression

- Used to treat primary sclerosing choloangitis

39
Q

Cirrhosis definition

A

defined histologically as a diffuse hepatic process characterised by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules

40
Q

Cirrhosis pathogenesis

A
  • Liver cells still present, but portal vein blood bypasses sinusoids so liver cells cannot perform their functions
  • Pressure inside the liver increases = portal hypertension
41
Q

Cirrhosis aetiology

A
  • Alcohol
  • Non-alcoholic steatohepatitis
  • Chronic viral hepatitis: B, C
  • Autoimmune liver disease: AI hepatitis, PBC, PSC
  • Metabolic: iron, copper, alpha 1 antitrypsin
42
Q

Cirrhosis complications

A 
Structural changes, fibrosis: 
- portal hypertension
- increased blood flow
- stiff liver
- pressure rises in portal vein
Oesophageal varices:
- bleeding, can cause haemorrhage
43
Q

Hepatic failure

A
  • Liver so damaged it can’t function
  • Acute hepatic failure = rare: severe rapid liver injury
  • Chronic hepatic failure: end stage chronic liver disease
44
Q

end stage chronic liver disease clinical features

A
  • Ascites, Muscle wasting, Bruising, Gynaecomastia, Spider naevi
  • Caput medusa = variceal umbilical vein collaterals (palm tree sign – portal hypertension so blood can’t get through so tries to go around periumbilical veins causing these large caput medusae)

Clinical pathology (69 decks)

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