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Clinical pathology > Hepatobilary and pancreas > Flashcards

Hepatobilary and pancreas Flashcards

1
Q

Definition of iatrogenic

A

induced inadvertently by a doctor
or by medical treatment
or diagnostic procedures

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2
Q

What are the three classifications of jaundice?

A

Pre-hepatic = too much bilirubin produced
Hepatic = too few functioning liver cells
Post hepatic = bile duct obstruction

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3
Q

Cause of pre-hepatic jaundice

A

too much bilirubin produced

eg. Haemolytic anaemia

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4
Q

Causes of hepatic jaundice

A

too few functioning liver cells, eg:
Acute diffuse liver cell injury
End stage chronic liver disease
Inborn errors of metabolism

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5
Q

Causes of post hepatic jaundice

A

bile duct obstruction, eg:
stone,
stricture,
tumour – bile duct, pancreas

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6
Q

What is the pathway of bilirubin metabolism?

A
  1. Bilirubin produced by red blood cell breakdown
    = unconjugated.
  2. Metabolised in liver – conjugated
    and excreted in bile
  3. Some bilirubin is re-absorbed
    from gut along with bile salts in Enterohepatic circulation
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7
Q

What symptoms are associated with pre hepatic jaundice and why?

A

Patient notices yellow eyes/skin only

Because the bilirubin is unconjugated – bound to albumin, insoluble, not excreted

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8
Q

What are the symptoms associated with hepatic jaundice and why?

A

Patient notices yellow eyes/skin and dark urine

Because the bilirubin is mainly conjugated

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9
Q

What are the symptoms associated with post hepatic jaundice and why?

A

Patient notices yellow eyes, dark urine and pale stools

Because the bilirubin is conjugated so soluble and excreted, but can’t get into gut

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10
Q

Which LFTs indicate hepatocyte damage?

A

ALT and AST

Alanine aminotransferase more specific for liver than Aspartate aminotransferase (also found in muscle and red blood cells)

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11
Q

Which LFT indicated damage to the bile ducts?

A

Alkaline phosphatase

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12
Q

How is jaundice investigated?

A

Ultrasound scan to check for dilated ducts in obstruction

Only if no dilated ducts do a liver biopsy to find out the cause of jaundice

Most (non-obstructive) cases are due to acute hepatitis

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13
Q

How does mild acute hepatitis look histologically compared to intermediate and severe acute hepatitis?

A

Mild = lobular disarray - due to injury and death of individual hepatocytes

Intermediate = Bridging necrosis - between portal tracts and hepatic vein

Severe = confluent panacinar necrosis

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14
Q

How is chronic hepatitis defined clinically?

A

‘chronic hepatitis’ is a persistence of abnormal liver tests for more than 6 months.

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15
Q

What is the progression of chronic liver disease to cirrhosis ?

A

normal
Portal fibrosis
Bridging fibrosis
Cirrhosis - hepatocytes form nodules surrounded by fibrous tissue

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16
Q

What are the hepatotrophic viruses?

A

Hepatitis A, B, C, D E
D only affects people with B

Epstein Barr virus, Cytomegalovirus, Herpes simplex virus also as part of a systemic disease, usually in immunocompromised

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17
Q

How are Hep A, B and C transmitted?

A

Hep A = faecal oral

Hep B and C = parenteral

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18
Q

How does alcohol abuse change the liver?

A

Steatosis = Fatty change
Alcoholic steatohepatitis
Cirrhosis

19
Q

What is seen in histologically in steatohepatitis?

A

fatty change plus hepatocyte injury – ballooning, Mallory Denk body, inflammation, sinusoidal fibrosis

20
Q

What is NAFLD and what is it associated with?

A

Non-alcoholic fatty liver disease

Associated with Metabolic syndrome – obesity, type 2 diabetes, hyperlipidaemia, also some drugs

21
Q

What is DILI and how is it classified?

A

Drug Induced Liver Injury

Intrinsic – anyone taking this drug is likely to get liver damage eg. paracetamol

Or idiosyncratic – depends on individual susceptibility. Rare and can be severe.

22
Q

What is the mechanism of Parecetamol toxicity ?

A

Parecetamol has two safe metabolic pathways
Too much and it is also metabolised by Cytochrome P450 pathway to a toxic metabolite, N-acetyl-p-
benzoquinone-imine (NAPQI)

NAPQI binds covalently to
tissue membrane proteins causing necrosis.

Treatment = Acetylcysteine
Increases Glutathione which neutralises NAPQI

23
Q

What three inborn errors of metabolism cause liver cirrhosis?

A

Alpha 1 antitrypsin deficiency
Hemochromatosis
Wilsons disease

24
Q

What is Alpha 1 antitrypsin deficiency?

A

The abnormal anti-protease cannot be exported from hepatocyte

It accumulates in liver cells and injures them – cirrhosis

Insufficient A1AT in blood leads to a failure to inactivate neutrophil enzymes, causing lung emphysema, especially in smokers

25
Q

What is Haemochromatosis?

A

Any abnormality in the HFE gene which leads to a failure of iron absorption regulation, and excess iron is stored in various organs

Patients have high serum levels of transferrin.

Treatment = venesection

26
Q

What is Wilsons disease?

A

Inborn error of copper metabolism

Copper accumulates in
Liver - causing cirrhosis.
Eyes – Kayser-Fleischer rings
Brain – ataxia, etc.

Treatment to chelate copper and enhance its excretion

27
Q

What are the systemic effects of liver failure?

A 
Ascites
Muscle wasting
Bruising
Gynaecomastia
Spider naevi
Caput medusae
28
Q

What is portal hypertension? list its main complications

A 
Increased pressure of blood in the portal veins (a gradient of at least 12mmHg). Complications:
Splenomegaly – low platelets
Oesophageal varices – haemorrhage
Piles (perianal varices)
Part of cause of ascites
29
Q

What are the causes of portal hypertension?

A

Post-sinusoidal –
Hepatic vein thrombosis (Budd Chiari syndrome)

Sinusoidal - cirrhosis

Pre-sinusoidal - due to disease of the portal vein or its intrahepatic branches

30
Q

What are the risk factors for Hepatocellular carcinoma?

A

Cirrhosis

Male > female, Obesity, Alcohol, viral hepatitis

31
Q

What blood test can be used to detect Hepatocellular carcinoma?

A

alpha feto-protein

32
Q

What tumours commonly metastasise to the liver?

A

Few large nodules:
Large bowel

Multinodular or infiltrative:
Lung
Pancreas
Breast
Stomach
Melanoma
33
Q

What is cholangiocarcinoma?

A

Adenocarcinoma arising in the bile ducts, can be:

Intrahepatic - from small intrahepatic ducts, mass forming, presents late
RF = cirrhosis

Perihilar - from large ducts,
Causes obstructive jaundice early
RF = bile duct disease

34
Q

What are the main types of gall stones?

A

Mixed stones (most common)
Cholesterol stones – yellow, opalescent
Pigment stones – small black – in haemolytic anaemia

10% contain calcium – visible on plain Xray

35
Q

What is acute and chronic cholecystitis?

A

Acute cholecystitis – duct blocked by stone, Initially sterile, later infected.
Large, swollen, congested, ulcerated.
Complications = empyema, rupture

Chronic cholecystitis – repeated small gall stones
Complications = Fibrosis, Rokitansky Aschoff sinuses

36
Q

What are the clinical features of acute pancreatitis?

A

Sudden onset of severe abdo pain radiating to back
Nausea and vomiting

If severe:
Grey Turner’s sign – haemorrhage into the subcutaneous tissues of flank,
Cullen’s sign – periumbilicus haemorrhage

Raised serum amylase/lipase (>3x normal)

37
Q

What is the pathogenesis of acute pancreatitis?

A

Leakage and activation of pancreatic enzymes- Amylase released into blood
Mild = swollen gland with fat necrosis
Severe = + necrotic gland and haemorrhage

Hypocalcaemia (fatty acids bind calcium ions), hyperglycaemia, abscess formation, pseudocysts (collections of pancreatic juice secondary to duct rupture)

38
Q

What is chronic pancreatitis?

A

Irreversible destruction of parenchyma of pancreases, exocrine first followed by endocrine tissue, replaced by fibrosis tissue

39
Q

Aetiology of chronic pancreatitis

A

Alcohol, idiopathic cigarette smoke,

Cystic fibrosis, CFTR gene

40
Q

Complications of chronic pancreatitis

A

Malabsorption of fat due to lack of lipases, causes:
Steatorrhoea
Impairment of fat soluble vit absorption –A,D, E and K
Diarrhoea, weight loss and cachexia

Also Diabetes (late feature) and Pseudocysts

41
Q

How does pancreatic adenocarcinoma present

A

Usually between 60-80yrs
Non-specific symptoms:
Epigastric pain radiating to back, Weight loss, painless jaundice, pruritis and nausea

Trousseau’s syndrome = migratory thrombophlebitis due to hypercoagubility

Courvoisier’s sign = palpable gallbladder without pain (suggests nit stones)

42
Q

What are pancreatic neuroendocrine tumours?

A

Islet cell tumours, very rare
often produce multiple hormones but usually single hyperfunctional syndrome
eg. Gastrinoma = Zollinger-Ellison syndrome, too much gastrin causes excess acid secretion on the stomach

43
Q

What are the direct (invasive) pancreatic function tests?

A

Intubation to collect aspirates in the duodenum.

44
Q

What are the indirect (non-invasive) pancreatic function tests?

A

Pancreatic enzyme analysis in stools (Elastase)

Trypsinogen (IRT) measured in blood in CF screening

Clinical pathology (14 decks)

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