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Y3 Lecture week IV > Liver and pancreas pathophysiology > Flashcards

Liver and pancreas pathophysiology Flashcards

1
Q

Patterns of alcohol-related damage to the liver (pathological names)

A
  • fatty change -> steatosis
  • steatohepatitis -> fatty liver disease, inflammation + fat accumulation in the liver
  • fibrosis
  • cirrhosis
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2
Q

What are Mallory Denk bodies?

A

When we drink alcohol -> hepatocytes are damaged -> accumulate fat -> if this is chronic * then filaments in hepatocytes break down -> Mallory Denk bodies will form

mallory denk bodies (red on the picture) + neutrophils (blue on the picture) = steatohepatitis (inflammation of the liver)

(hepatocytes may recover in 6-8 weeks of stopping drinking)

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3
Q

How long does it take for a) fat b) Mallory Denk bodies to disappear after alcohol cessation?

A

a) fat: 6-8 weeks
b) mallory denk: 3 months

*but if the alcohol drinking continue - end up with fibrosis

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4
Q
  1. What is the normal surface of the liver like?
  2. What is the surface of the liver in cirrhosis?
A
  1. Normal -> smooth
  2. Cirrhosis -> nodular
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5
Q

What pathological process is the nodule in the cirrhotic liver result of?

A

hepatocytes die -> nodules = residual hepatocytes that are stretched out and pulled apart by fibrosis

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6
Q

What is the pathologist assessing in the biopsy of the alcoholic liver (degrees of damage)?

A
  1. Steatosis
  2. Steatohepatitis (fat accumulation + inflammation)
  3. Degree of fibrosis
  4. Cirrhosis
  5. Hepatocellular Carcinoma
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7
Q

What else (apart from alcohol) can cause liver damage?

A
  • non-alcoholic fatty liver disease (e.g.people with large BMI increased risk)
  • non-alcoholic steatohepatitis
  • viruses (hepatitis B, C etc)
  • drugs/toxins
  • other tumours (either hepato-cellular ca or metastases e.g. from the lung or colon)
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8
Q

Causes of liver cirrhosis in adults

A
  • alcohol
  • hepatitis B or C (chronic as inflammation and destruction of hepatocytes)
  • non-alcoholic steatohepatitis
  • immunological damage
  • genetic problems
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9
Q

x2 examples of autoimmune liver problems leading to cirrhosis

A

a) autoimmune disease - antibody against and destruction of own hepatocytes
b) primary biliary cholangitis - inflamed bile ducts in the liver -> damage and destruction

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10
Q

x2 examples of genetic liver problems leading to cirrhosis

A
  • hemochromatosis - excess of iron -> accumulation in the tissues -> damage to hepatocytes
  • alpha-1 anti-trypsin deficiency -> damage to hepatocytes -> cirrhosis
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11
Q

Causes of liver cirrhosis in children

A
  • CF
  • chronic active hepatitis
  • Wilson’s disease
  • alpha-1 antitrypsin deficiency
  • galactosaemia*

*galactosaemia - metabolic disease; body is unable to metabolise galactose -> galactose accumulates in the tissues

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12
Q

Complications of liver cirrhosis

A
  • portal hypertension (ascites, enlarged spleen, varies)
  • liver cell failure (jaundice, bleeding tendency)
  • hepatocellular carcinoma
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13
Q

General categories of causes of jaundice

A

Elevated level of bilirubin:

A. Pre-Hepatic -> excess production

B. Hepatocellular -> #conjugation

C. Post-hepatic/ obstructive -> impaired bile flow

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14
Q

What are the possible causes of Pre-hepatic reasons for jaundice?

A

Pre-hepatic - an excess of bilirubin (e.g. broken RBCs)

Causes: haemolytic anaemia, thalassemia, major haemorrhage

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15
Q

Examples of the reasons for hepatocellular causes of jaundice?

A

Hepatocellular -> anything that will # liver’s ability to conjugate bilirubin

Examples of types of damage: reduced uptake, impaired conjugation, decreased hepatocellular excretion

Examples of conditions leading to hepatocellular damage: viruses, drugs, toxins, alcohol, circulatory disturbance, autoimmune disease, cirrhosis

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16
Q

Reasons of post-hepatic/obstructive causes of jaundice

A

Impaired bile flow:

A. Intrahepatic: biliary tree disease (primary biliary cirrhosis)

B. Extrahepatic: gallstones, BD stricture, Primary Sclerosing Cholangitis, pancreatic cancer

17
Q

Simply, what RBCs break into

A
  1. RBC -> globin and heam

*globin recycled

*heam -> iron and bilirubin

*iron is reused

  1. Bilirubin bound to albumin -> travels to the liver -> conjugation -> excretion into bile
18
Q

Patient presents with jaundice, what do we enquire about in the history ?

A

Try to determine if it`s chronic or acute

19
Q

investigations in jaundice

A
20
Q

What markers may be raised in case of bile duct (cholestasis) problems that lead to jaundice?

A

Alkaline Phosphatase (ALP) and GGT

21
Q

What markers may be raised in case of hepatocytes damage/ problems that lead to jaundice?

A

AST and ALT

22
Q

Stigmata of chronic liver disease/cirrhosis

A
  • ascites
  • spider naevi
  • palmar erythema
23
Q

What is Ishak score used for?

A

To assess the degree of inflammation and fibrosis in hepatitis C

24
Q

Histological features of liver biopsy in Hepatitis C

A

inflammation and lymphocytes present

assessment of degree of scarring and fibrosis

25
Q

What is the marker of Primary Biliary Cholangitis?

A

anti-mitochondrial antibodies (AMA)

26
Q

Is Primary Biliary Cirrhosis same as Primary Biliary Cholangitis?

A

Yes. Primary biliary cholangitis is a new name for primary biliary cirrhosis

(as cirrhosis is generally thought/by public opinion/ to be associated with alcohol; when PBC is associated with autoimmune condition, it’s a bit unfair for the patients to be associated with alcohol damage to their liver)

27
Q

Histology of PBC

A
28
Q

Autoimmune hepatitis auto-antibodies markers

A

Autoantibodies:

  • ANA
  • anti-SMA
  • anti-liver kidney microsomal (LKM)
29
Q

medical treatment of autoimmune hepatitis

treatment of PBC

A

autoimmune hepatitis -> steroids

PBC -> urseodeoxyholic acid

30
Q

Causes of intrinsic cholestatic injury (damage to bile ducts in the liver)

A
  • Primary biliary cholangitis (PBC)
  • Primary sclerosing cholangitis (PSC)
  • Sarcoidosis
  • Drugs
  • Graft vs host disease (liver transplant)
  • HIV
31
Q

What process damages the bile ducts in sclerosing cholangitis?

A

Fibrosing process

32
Q

Presentation of chronic pancreatitis

A
  • chronic abdominal pain
  • steatorrhoea (reduced enzyme activity)
  • diabetes mellitus (loss of islet cells)
  • obstructive jaundice
  • ascending cholangitis
33
Q

What do you see in the chronically damaged pancreas? (histology)

A

Red fibrosing tissue between the healthy tissue and then progressive destruction of a healthy pancreatic tissue

34
Q

Causes of pancreatitis

A

I - idiopathic

G - gallstones

E - ethanol

T - trauma

S - steroids

M - mumps/ malignancy

A - autoimmune

S - scorpion bite

H - hypertriglycerides, hypercalcaemia

E - ERCP

D - drugs

35
Q

What does ‘double duct’ sign mean?

A

Dilation of both: common bile duct and pancreatic duct

Suggestive of a problem around the ampulla of Vater

36
Q
  • How does ERCP work? (what structures does it go through)
A

Scope put down into the duodenum -> cannulated ampulla -> die injected = whole biliary tree and main pancreatic duct can be seen

*if the stricture, the die would not go through it

* while ERCP also brush cytology can be taken

37
Q

Difference between Primary Sclerosing Cholangitis and Primary Biliary Cholangitis

  • -* clinical features and population profile
  • site of involvement
  • cause of obstruction
  • key microscopic feature
  • diagnostic clue
  • associations (other conditions)
  • long term complications
A
38
Q

How does Primary Sclerosing Cholangitis look like on ERCP?

A
39
Q
A

Y3 Lecture week IV (18 decks)

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